Title

REFERENCE PAPERS ON BHOPAL

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The disaster that took place on the 'ark, wintry night of
2/3 December 1984 in Bhopal is the worst, man made environmental

accident in recorded history* The shocking, official estimates

of 2800 human deaths, an equal number of dead cattle and the
physical and mental disablement of over two lakhs people, b

a

.'dr.

of too ic-

' rk‘^

ses including Isocyanate (.1), d© not

adequately express the tragedy that has occurred.

The relief efforts, initiated imr.ediately, were handicapped

and hampered by the lack of authentic information on the nature

of the gases relocsedjhby the unwillingness of the Union Carbide
to relc?se information and by the lack of relevant information

among the State and Central authorities.
The doctors at the Hemidia Hospital, Bhopal, where hundred;
of the victims rushed, were faced with an acute emergency which

they never anticipated, of whose exact nature they had no
inkling, and for the treatment of which they had no ready sources

of information.
Since the nature o; the toxic gases released into the atmosphere

had not been made public cither by th. Unio.: Carbide or by the-

Centre (which sent high 1-vel technical expeits to Bhopal), this
had to be a conjecture based on reason and visible evidence.
Soon, two theories emerged to account for the varied

syBqptomatolocy and stunnin

mortality of the victims. The

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development and testing of thgse theorie , ha. they been done
properly, would undoubtedly have ad ’ed i •’ nsoly to scientific
knowledge. What is more important is that it would have relieved
the sufferings of thousands of peo.-le. The loci realities have, ho . e
ver, revealed the power struggles in the medical community and hov; it

ignores in the process, the victims; the lack of human concern

leading to withholding of probable proper tr< -?tment; the
indifference of our medicalon : scientific com-unity to

communicate with our largely illiterate but not.unintelligent
masses.

The Two Theories

The protagonists of the first theory, the •pulmonary*
theory heli ve that isocyanates of which MIC is one, damages
only those tissues with which they come into direct contact and

cannot be carried by.blood to internal tissues and organs. Thus
MIC can damage only the lungs, eyes and skin and thisy ~

.......

explains the predominant involvement of the eyes and lungs

in the Bhopal victims. They also believe.that symptoms, if any,
t..- 'xj L ■■ -<

related tc other systems must be due to hypoxia caused by lung
damage. This theory is strongly supported by a dominant faction
o.: ,<i
Iks i >icxbxI c*’i > m x<_• <_: -1-'
in the Gandhi Medical College,^ Bhopal. They believe that early

deaths were due to carbon monoxide poisoning——one of the
constituents of the released gases. They adamantly refuse to

examine any alternative theory.

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This theory cannot fully explain the varied symptoms of
the victims* nor the fact of multi—systemic involvement without

lung involvement seen in many patients. While another isocyanate,
^TDI'jhas been shown to cause brain damage, the protagonists of the
present theory arc silent as to why MIC cannot do so, too. Public

Health specialists in the U.S. say that even this can lead to
permanent lung involvement and blindness. This is in contrast

to the Union Carbide which maintains that MIC can have no lasting
damaging effects.

The main protagonist of the second theory, the ’Enlarged
Cyanogen Pool* theory, is the Indian Council of Medical Research

(ICMR). In fairness to t ds body, it must be stated at the very
cutset that it does not reject the first theory but believes that
both, have important roles to play in explaining the varied
symptomatology.-

This theory stemmed from the observation that the tissues
and blood of the dead victims were bright red in colour. This

occurs both in cyanide and carbon monoxide poisoning. Haematological
(blood) studies by ICMR ruled out the possibilities of carbon­

monoxide poisoning. No doubt that carbon monoxide is also one of

the breakdown products of MIC at high temperature. However, being
lighter than air it travels upwards and hence cannot kill in
an open atmosphere.

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Cyanide on the other hand might have been inhaled directly
as hydrogen cyanide or might have been released in the body

after the breakdown of the MIC molecule,
pool in the bo?

counts of cyanide during

into relatively harmless thiocyanates by a liver enzyme called/kv

rhodanase. ^Cyanide easily prevents the utilization of oxygen /
by cell:: of all the •

in rapid deaths dt .

The protagonists
attached to the haem: globin and slowly releases
cyanide to

rw enlarged cyanogen pool &S the body.

In these circumstances, its conversion to thiocyanate by
rhodanase, can be accelerated by administration of sodium

thiosulphate (NaTS). This is the rationale

using NaTS

as an antidote for cyanide poisoning. The resultant thiocyanates

are excreted in urine, and this can be used to test the proposed
theory itself,
.....
The ICMR conducted a double blind clinical trial in January.

Majority of patients who received NaTS showed significant

improvement and 10 cut of the 19 patients showed an eight fold
increase in urinary thiocyanate levels. Unfortunately, and

lue to reasons best kn wn to itself, the ICMR has not made the
details of the findings of this crucial trial, public. The

opponents of the theory too daim-to-h ve conducted a trial

- not double blind — which they say does not confirm the
hypothesis. They too have withheld their findings from public

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The Study by mfc

The mfc had decided at its annual meet, held at the end of
January 1985, to respond to a series of appeals from various

non-governmental organisations (NGOs) and citizen's forums to
undertake an epidemiological investigation, so as to support

the victims and the NGOs in their struggle for proper relief and

a more meaningful rehabilitation process. Seme members of
mfc visited Bhopal ir. mic—February to assess the situation and

the actual epi: iemiological survey was conducted between 18—25
March 1985 by 11 members of mfc and 3 friends from the Baroda

Medical College.

It must be admitted that the mfc had neither the human power
nor the material resources to launch a full scale investigation.
Our initial, fact finding survey revealed (i) official secrecy
regarding all information on the disaster;

(ii) absence of open

scientific debates; (iii) lack of encouragement to NGOs.. The mfc

ther fere decided to (i) make an epidemiological assessment of

the current health status and health problems of the people;
(ii) to examine the findings in the light of the t.o controversial
theories; (iii) to evolve a critique of the medical research

and relief programme; (iv) to make recommendations for a more
meaningful relief and rehabil:tation policy.

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The ICMR summaries of re s arc?; undertaken and press
r leases available to us were inadequate and sketchy, '.e

decided that we would go primarily by the broad range of
symptomatology with which the patients in the community were
presenting. We supplemented this byja thorough physical

examination and undertook hemoglobin estimations and lung

function tests. A criticism ag inst this approach of reliance
::ainly on symptoms could be th..t it lacks objectivity. However,

we believe that a thorough study of symptoms is a perfectly
valid method of study as has been accepted in a whole range

of medical conditions like chronic bronchitis, ischaemic
heart disease, arthritis etc.

The study population
Two slums were selected for the study:

(i) J P Nagar ,jj^s

situated in the close vicinity of the Union Carbide factory

and the worst affected by the gas leak, (ii) Anna Hagar, 10 km
away with the least exposure, which served as the control.
There was no area which was similar to JF Ka ar in socio­
economic and environmental characteristics and yet escaped

exposure and, ther efore, Anna Na.ar with the least

the best control tha

exjxssure was

could be chosen.

Rapport was es.-.ablished with the people by explaining to

them our objectives and making it very explicit/ tha.- we were

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not there to offer any financial compensation, medical

treatment etc. The slum dweller:, were given a h nd out in Hindi
explainin

the role of mfc and a commitment was made that the

salient findings of our study and our r.corne-nc'.ations would
be made available to them.
Sample Selection

The families for the study were selected by random
Co-w.

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sampling. Only subjects above 10 years of age were selected.

Those less than ten years wer^ excluded in

iew of their

probable inability to report symptoms correctly. All details

were entered in a pre—designed proforma. In addition, lung

function tert:- were dore by ; .andard procedur s usin

a

portable spirometer by a doctor fully familiar with measuring
these under field conditions.

Observations

The two slum populations were similar in age and sex

ccmpjsition, in the number of smokers and of people with long
standing respiratory problems like asthma. Tuberculosis etc.
The JP Ha; ar resident- who were the more a footed, were

slightly better off economically

ut this is.^no significance

in so far as morbidity rates in JP Hagar are concerned. (For
details of actual figures, see our Report).

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The subjects described a broa:3 range of symptoms. Each

T

symptom was described in such graphic detail that it was
obviously based on the patient’s own experience and could not
be malingering or wild imaginations as some are apt to allege.
Since these symptoms could arise due to different causes and since 1 ?

the residents of Anna Na ar, the controls, were also exposed to the /
cas, albeit to a small extent, the latter also reported those
Aleyev

symptoms. However, JP Nagar r sidents had ^statistically highly

I® Ahuj'-(

significantjinci..ence of these symptoms
_

The common st symptom was breathlessness on accustomed
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exertion. In additio. ^^huy ccmplafanecHef cough, chest pain/^----- y .J
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Jjcaw blurr;..

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v.<.KstzJU(7m^ui:

vision, head ache, fatigue,^ loss of memory for recent

events, abdc«i».-.l pain, nausea, waLwcfaag-of--ayer eHd=topotbnee
It i< important to note that this survey waconducted more, than
slTD
muoji J I®
three month' after the disaster, and ottil the victims suffered

with so many affects. Moreover every individual in the JP Nag r

sample reported atleast one serious symptom but many in the
Anna Nagar sample did not report nny such. Probably the most
crucial fin ing of significance was that 35% of the patients

Women in the reproductive a e group reported menstrual

irregularitie

such as shortened menstrual cycles, altered patern

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of discharge, pain durin

menstruation and excessive white discharge.

These symptoms'were compared not only between the two populations,

hut also

ith respect to the pattern in the same group before the

gas disaster.—1—

c c>_<CG^

Nearly half of the nursing mothers in JP Nagar reported
LXXS_>A_t<vj

lactation

rvv/vl

<X"

Salient Findings
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‘

. (expressed in perce:

Number of cases are s’s own in bracket

SI No

Symptom

J P Nagar

Anna Na ar

P Value

1

Breathless on usual

exertion

87.16 (129)

35.50 (49) /<$>. 0.001

2

Chest Pain/tiyhtness

50.0 (74)

26.08 (36)

«0.001

3

Weakness in extremeties

65.54 (97)

36.95 (51)

<<0.001

4

Fatigue

81.08 (120)

39.85 (55)

<<0.001

5

Anorexia

66.21 (98)

28.26 (39)

<<0.001

6

Nausea

58.10 (86)

16.66 (23)

«0.001

7

Abdominal pain

53.37 (79)

25.39 (35)

<<0.001

8

Flatulence

68.91 (102)

25.36 (35)

<<0.001

9

Blurred vision/
photcphobic

77.02 (114)

38.40 (53)

«0.001

Abnormal distant vision

42.0

21.88

<0.001

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Salient findings contd,

Si No

Symptoms

JP Nagar

Anna Nagar

P Value

11

Loss of recent memory

45.27 (67)

11.59 (16)

0.001

12

Ingling & numbness

54.72 (81)

20.28 (28)

0.001

13

Headache

66.89 (99)

42.02 (58)

0.001

14

Muscle ache

72.92 (108)

36.23 (50)

0.001

15

Anxi ety/depre s s i on

43.92 (65)

10.14 (14)

0.001

16

Impotence

8.10 (12)

0.72 (01)

0.05

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Hemoglobin (M)
(meani»s®grr£4)

14.68 (1.79)*

12.70 (1.35)* 0.01

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Hemoglobin ( P)
(mean gm%)

12.7 1(1.46)*

10.79 (1.34)* 0.001

* Standard deviations

8% of the men reported impotence,
The number of pregnant women in the sample is s too small ■end
^77?S"
A
ev^
— Cx^ie^-c i^-P
iend- to- study^pregnancy outcome ■cepe-rx-

Many residents had symptoms of anxiety, and some had
frank depression. Many had loss of memory for recent events.

Mean pulse rates and respiratory rates were not significantly
different in both sexes in JP Na; ar and Anna Nagar. Mean hemoglobin
concentrations in both males and females were significantly higher

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The mean values of lun : function tests were lower 331 JP Nagar

as compared to Anna Nagar particularly in the age group 15-44
and 45-60. The pattern was primarily restrictive.
An important findings of grave significance is that 65% of ,

the working persons in JP Nagar experienced a drop in income fir.in'
20% to 100% as opposed to 9% in Anna Nagar. This reflects the way
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ot/Ji oZ/eAS

in which physical/mental disability of the people; has affected wcrking
capacities.

The causative factor
The presence of such varied symptoms -suggests the involvement

of more org.ns and body system?; than the lung: alone. These cannot
be explained by the pulmonary theory alone even though pulmonary
lesions can cause peripheral hypoxia and herce muscular fatigue

On the other hand,' the^Gyanide-theory can better explain
and apparently unconnect-d symptomatology^However, the

IC2CR has not tested the^hypothesis vigorously. It has stu .led only

vsly ill, hospitalised patients an

concentrated r inly

on the lung symptoms. They do not say whether the non-pulmoncry
symptoms (symptoms not related to lungs) were also relieved by NaTS

and curiously has not ma e its findings public. One, therefore, may

also cue tion whether the iyXj&tde'theory is fully valid.
It must be stressed here that the mfc is not rejecting the
-vJcr-v'Cp; X pax ■

<*yan4xe theory. It is only to point out that the country’s main
medical r s arch body has failed to be rigorously scientific in

testing its own hypothesis.

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Sodium thiosulphate therapy
;.P:

all ad: explained how codturn thiosulphate (NaTS)

will GJ^-sr cyanide/radicals from the body. If the cyanide
theory has been established, evers as one of two causative factors

the victims should receive NaTS treatment. Some of the local
Oi-vzj jx£j2i^-cC-'u5XS

doctor,-^avriled themselves of this, after the cyanide theory was

pro

itx

-Ma 7fcE

ia>CAj2-

The ICrIR at a meeting held on 4 Feb 85, issued guidelines for

NaTS tratroent. The mecical group of Bhopal, which was opposing the

treatment, was also present at the meetings, according to the
minutes. Yet they opposed the treatment with the argument that they

arc not convinced its efficacy. The question is not of a doctor’s

convictions. A doctor’s choice of tr ttment cannot alee be arbitrary.
The question is whether there is scientific evidence in favour
of NaTS therapy and whether there is e ually strong, if not stronger,
“evidence against the use of NaTS in thi.

situation.

NaTS with its specific action is a better therapeutic agent than
tee non-specific remedies that are being used for the lung symptoms.

A dominant section of the doctors of Bhopal are thus guilty of
delaying treatment and by not revealing the findings of its clinical
trial, the ICMjR too has to accept pare of the blame for the continuing

suffering of the victims.
After a few weeks of controversy the NaTS therapy has now been

accepted but mass detoxification is still being strongly opposed.
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The trial with NaTS is not the only study launched by the

ICMP,. It has sponsored many other studies on the Bhopal victims,
but they lack an integrated approach. Thus lungs, eyes etc., are
being examined independent of each other, by different investigators
and the ICMR is unwittingly lending support to the first theory,

namely, that MIC gas damages only tissues with which it cones into
direct contact.

What exactly happened to the gas victims?
So ' any months after the disastrous gas' leak, one still does

not know what exactly happened to those who inhaled the gases and

ar., still surviving. This is not because all attempts to unravel
the my^ter, have foiled but because an integrated approach hud
not been ta.;en tc do s».

after tuc ux^u^tex, ueus oi t>«c>w.,ai<ds

of the survivors are still suffering from debilitating symptoms
which pr vent them from going back to work.

The medical community and the officildom have been adhoc in
their efforts to render adequate su cour to these hapless victims.

A powerful medical lobby in Bhopal r<4th-un-.cd.-ent-i-feie--bigotry

have opposed NaTS, a treatment, with good potential to the
patients. They have no convincing argument for their stand. The

IMA, the organisation which ha:

authority over the medical

profession, has remained totally mute. The doctors as well as the

ICMR have concentrated entirely on those who were hospitalised
and have not. evolved a holistic, corer-unity approach to understanding
the problem. The ICMR sponsored local studies with the exception

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of the NaTS trials have lacked the rigour and the epidemiological

orientation that are nee Esary in arriving at a meaningful
understanding of the problem.

A point of utmost significance is that the victims of the
Bhopal gas disaster mostly belong to the lowest strata of the
society and not in a position to fight for their rights, be it

medic-1 aid or monetary compensation. It is, therefore, not
very surprising that the government and its organlsationsjiave
shown marginal interest in the after effects. It also reveals
a lack of interest amen; our sci ntific community in investigating
an environmental disaster of an unprecedented nature. On the other

hand, one can observe the striking contrast with which all attempts
were made to retrieve the Black Box of Kanishka, whose mid-air
explosion resulted in the d-ath of only 326 persons but needless

to remind of the upper socio-economic class.

RecommendatIons
Research

1.

The r search an ' follow up studies should shiftfocus from
hospital/dispensary based studies of seriously ill patients

to family/community based ambulatory patients.

2.

Well designed clinical trials should be further initiated
using sodium thiosulphate as a therapeutic and epiedemiolo..ical

tool to further establish the significant role it could play
in mass therapy.

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Care,Surveillance and Rehabilitation
3.

Psycho social assessment and consequentcounselling and.
rehabilitation arc urgently required.

4.

Mass treatment with sodium thiosulphate should be initiated
maintaining good medical records.

5.

A surveillance programme should be undertaken to

assess risks to pregnant mothers, unborn babies and new born

babies. There should also be close monitoring o£ the gynaecological
problems of women.

6.

It is necessary to have a long term surveillance of lung

function in view of the postulated damage to lungs and
r suitant lun

fibrosis. Similarly eyes should be examined

regularly.

7.

A comprehensive listing of all gas disat er victims is a

long overdue task nec ssary for mass treatment, compensation
and rehabilitation. This must be done immediately.

Communication^

8.

There is urgent need for evolving a continuing education

strategy for allhealth personnel including doctors working
in both governmental and non-governmental centres. These could

be throu h newsletters, handouts and informal group
meetings, ^'he areas identified are? (i) sodium thiosulphate

therapy? (ii) identification and management of psycho-social
stre.s? (ill) risks to mothers and unborn foetus and need

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for surveillance? (iv) family planning advice till completion of

detoxification; (v) role of respiratory physiotherapy; (vi) management
of ladation failure; (vii) caution against overdrugging; (viii) need
for open minded surveillance of high risk groups; (ix) importance
of medical records,

9.

There is also urgent need for a dynamic cr ative non-formal

health education of the affected community through group
meetings*posters and pamphle-s with information and messages
built around their life style, culture anr

existing socio­

economic situation.

The areas identified are; (i) sodium thiosulphate therapy;
(ii) ongoing research programmes and informed consent; (iii)

risk to unborn and new born babies; (iv) Family Planning advice;

(v) r-spiratory physiotherapy; (vi) management of lactation
failur. including low cost weaning foods; (viii) importance of

r cords and regular check ups,

10,

Occupational Rehabilitation an: compensation.

In the ultimate analysis care of illness, health education,
psychosocial counselling would be inadequate measures if they
were not- backed by adequate monetary compensation and urgent

occupational rehabilitation of the disaster victims. This would
have to be imaginatively done keeping their previous occupations

and the residual disabilities in mind.

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Coordination
11.

The government machinery alone cannot handle

such a massive task. The government must adopt
a policy of enlising the help of all non-governmental

agencies and groups wishing to work in Bhopal. This
enlistment must be active and supportive.

and finally

12.

It is imperative that the victims as well as the entire

country must be provided with all the details of how the
Accident occurred, of the nature of the chemicals

released and of the.reasons why the detoxification by t
sodium thiosulphate has been so badly mismanaged.

OH I

2

NARMADA PROJECT AND THE TRIBALS*

—don't let them drown in despair

PREAMBLE
We are three voluntary groups working since 1980 amongst
the tribals who have been ousted from their traditional

homelands by the Sardar Sarovar Project on the Narmada river
undertaken by the Government of Gujarat. Our experience
regarding th,e problems of these tribal rehabilitees has raised

many questions and issues in our minds which we would like

to share with you.
When ambitious developmental projects like the Narmada
Project are undertaken, a large number of families are
asked to leave their lands, houses, familiar surroundings

and settle elsewhere. This is justified on the basis of
'public purpose' which is essentially

hat much larger

benefit accrue to much larger populations who would otherwise

live at a low standard of living. This, of course, must imply
that those who give up everything so that the project can
become a reality, must also not suffer a drop in their

standard of living. In fact it is necessary that they too
improve their lot commensurate with similar improvements

in the standard of living of the beneficiaries of the project.
2

♦An appeal from Chatra Yuva Sangharsh Samiti, Rajpipla
Rajpipla Social Service Society
Action Research in Community Health, Mangrol;
February 1984.

2

Our concern is focussed pn the social and economic

suffering that these oustees are going to face if the
governments rehabilitation policy on paper does not
match with the actual programme in the field. We have

reason to believe that certain ambiguities in policy

and trends in implementation seen in that area are going
to seriouslypffeet the health, life and future of these
people.

BACKGROUND
About 220 villages in the three States of Gujarat,

Maharashtra and Madhya Pradesh are going to be affected
by the inundation of large tracts in this area. Among
them we have worked with the illiterate tribals of 19
villages in Gujarat and most of the facts and issues

discussed derive out of this experience. The main occupation

of tribals in this area i$ agriculture. The income from

agriculture is supplemented through collection of forest
produce, hunting and other forms of labour.
Due to cultural reasons and administrative hurdles at
local levels, the overwhelming majority of tribals have

joint holdings

for generations together. Thus a seemingly

large land holding (more than 5 acres)

in the name of one

person in reality may mean that two or more families are
actually earning their livelihood from it.

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There are X ^ew landless labourers. Even these earn
their livelihood by cultivating government owned fallow

.forest land or other waste land. It is not possibb to
estimate the amount of land brought under such cultivation

since this is treated as unauthorised cultivation. Whatever

,

the technicality of such a situation, it is an established

fact that they have been living and cultivating such lands for
many years and they are entitled to compensation for the loss
of this only source of living.

Water Dispute Tribunal
A tribunal was set up to study the problems arising

out of the project implementation. Its fiward took into
account the factors of total dependence on land of these

tribals as well as the responsibility of the rehabilitation
programme in removing the poverty of the 'oustees'. It,

therefore, provided land for land compensation (ie., if more

than 25 percent of land owned by any family was acquired for
the project they were to be given an equal amount of irrigable

land). It also made a specific provision of a minimum of 5 acres
of irrigable land to all those whose land holding was less

than 5 acres of land. It also stated that first preference
would be given for rehabilitation within the command area of

the project. However, if the 'oustees' did not want to settle
there, they were to be settled in their respective states on
a similar basis. In addition, it was decided that the agricultural

lands were not be provided free of cost,but the occupancy
price should be r-covered from them in 20 yearly interest free

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instalments; the first instalment being half the compensation

received by the 'oustees*. The tribunal has also made the
proviso that if an individual is losing atleast 75 percent

of his land he should have the option of surrendering the
rest of his land as well. This award on the face of it seemed
a relatively fair policy and it was hoped that with proper

implementation, it would tackle all the grievances of the

tribals.
Some ambiguities

1.

The Narmada Tribunal being an inter-state water

dispute tribunal took into account the rehabilitation
of oustees from Madhya Pradesh and Maharashtra. No

refer nee was made to those from Gujarat.Clearly the

thatAapplies to Maharashtra and Madhya Pradesh should
apply to.oustees of Gujarat as well; but the government

of Gujarat has not earmarked any land in the command
area of the project for this rehabilitation. Even though
these tribals will be the first to be affected they are
expected to buy their own land and only after^they do so
other basic amenities like wells, schools and roads

are to be provided.
2.

There is a government resolution (G.R.) of June 1979

of the Irrigation Department of the Government of

Gujarat which states that a minimum of 5 acres of land
should be provided for each oustee family for their

rehabilitation. There is of course no provision to
produce irrigable land in the command area of the

project in this resolution.

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3.

In the cost estimates in the project report prepared

in 1980, the Government has made no provision for
the cost of acquiring the total of 40000 acres of land

that it would have to acquire to rehabilitate all the

oustees. It has instead provided for only 1310 acres of

land which is clearly meant for roads and house sites
only, whereas in fact the agricultural land to be

acquired should be clearly more than the actual emount
submerged, especially because a significant^proportion

of oustees who own less than 5 acres of land are to be
provided atleast 5 acres as per the directive of the

tribunal. The argument that the land is not to be given
hence
free of cost,and^its cost of acquisition need not be

mentioned is not tenable, since clearly some initial
investment will have to be made by the government. No

mention seems to have been made in the proposals on

this matter.

4.

The usual analysis of land records do not show the
reality of land holdings in a tribal region where joint

holdings are significant. We reanalysed the land
holdings not by the units as they are officially

recorded but by the number of families who are
actually dependent on the land. We found that there

were 624 land holdings in the 18 villages surveyed
whereas the number of families actually dependent on

them are 2109,since most are joint holdings. Also if

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their whole social and cultural life disrupted.

Naturally they rejected such outrageous propositions.
When the oustees refused the land as was the

ii.

experience of 5 villages which are affected by Rock filled
dykes the government asked them to purchase land from

private land owners from their compensation money. The
consequences of this were:
5

(a) the oustees with less than

acres of land could not buy 5 acres of land which

they were entitled to;

(b) some could not even buy the

land equal to what they had been, originally cultivating;

(c) the amenities that they were entitled to could not
be had asper the law because of the wild scattering.
iii.

It has not been possible for the illiterate tribals to

deal on an cequal footing with the high caste land owners

in these land deals thrust upon them by t e governments
inaction. They have been/are bound to be cheated and
exploited. In the beginning the Additional Collector

gave active help and.the deals were made relatively
easily. However, even now these deals are not yet

xompletely registered and the ownership of lands still
rests with the original land owners. The whole matter

depends on the goodwill of the concerned government
official and in our experience there has been a general

aloofness and reluctance on their part to get too involved.

.8

8
iv)

The Government of Gujarat has been pleading from the
very beginning that it is virtually impossible to give
agricultural land to the oustees as no surplus land is

available. Forest lands cannot be given as only a few

forests are left and other waste lands are scarce.

However the government could instead purchase or acquire
private lands in large tracts so that proper rehabilitation

can be carried out and rehabilitation of the oustees itself

could be proclaimed to be a ’public purpose' in this respect.

v)

In some villages the situation has arisen where 80%

of the village land has been acquired. The land acquisition
authority is refusing to acquire the remaining 20% of the
land. This land is owned by 20-30 familiesjof these families,

4-5 of them happen to retain practically all their lands.
to
If these lands are not/be acquired the isolation of these
families will be near total. They will be cut off
physically, socially and culturally. They will be
deprived o

other amenities like school, schops and health

services. The land acquisition authority is taking a very

rigid view of the land acquisition procedure which states

that only land under submergence can be acquired.
vi)

All the tribals in the affected villages of Gujarat have
so far voluntarily surrendered their lands and other

villages are ready to follow suit. There is, however,

still widespread uncertainty about the amount of
compensation they would be paid. Since all the villages are

,9

9

losing their land under the same project, it is only

fair that they should get a uniform and generous compensation.
The State Government has not yet made up its mind and is

vascillating on the issue.The traditional way of computing
the amount of compensation by taking current market values

for the land is clearly not applicable to tribal land feince

for many years no sale deeds have been concluded in this
area. In its cost estimates the government has put an
estimate of average cost of land acquisition at a rate of

Rs.2000-00 per acre. This is totally unsatisfactory.
This computed average compensation is so low that most
of the villagers will be deprived of their land in
exchange for a paltry sum insufficient to buy adequate

alternative land to survive. The consequence of such
myopic action of the government can only be that the
•oustees’ will become poorer.

To summarise the situation as it exists today, the
government has abandoned its primary responsibility of providing

land for land as directed by the tribunal; it-has offered a

totally inadequate sum of compensation; it has shown no
aptitude or willingness to keep down the prices of the
surrounding private lands which may have to be acquired by

the oustees; it has used 'holding* as the unit and not 'family*
in its computation thus hiding a concrete reality of the

tribal regions; and its grave lack of responsibility has

10

10

resulted in the ousted tribals becoming a prey to high caste

land owners and their brokers. In brief with a policy implemen­
tation that is insensitive to the human problem of these tribals
it has made the tribunals recommendation of the objective of

abolition of poverty of the oustees a myth.

Among others the main claim for this inadequate implementation
of the tribunals recommendation has been the cost factor. The

government has claimed that land acquisition of the type
recommended■will push up the cost of the project. The following

facts about the governments lop-sided sense of proportions
is cost provisions for certain other aspects of the project

is not only disturbing but show how hollow the claim is in
the first place.

The project report shows that the cost estimate of
the whole rehabilitation programme including compensation

for lands, houses' etc., in all the 220 villages in the three
States is Rs.19.83 crores, while the cost, estimates of the

construction of the staff buildings at Kevadia Colony alone

will be Rs.23.45 crores. Added to this cost the miscellaneous
and establishment costs of the same magnitude and we begin to
sense how distorted is the government's sense of proportion.

The scales which the government holds in its hand give more

than twice the weigh age to the temporary needs of providing

houses only to a few hundred families of the project in one

colony alone. In compariscn to this, the entire rehabilitation
cost of 10 to 12 thousand families scattered over 220 villages

of

the three States, which can make or mar their entire lives.

gets less than half the weightage. What is more surprising that

11

the staff quarters, the water lines, t e electricity lines,
guest homes, the roads in the Kevadia Colony have already

been built while the staff are yet to arrive. In contrast the

notices to acquire lands from the people to be ousted has already been
served but the vital issue of compensation for imminent land

loss is still unresolved.

In acountry like India, with a high population

density and high level of poverty, virtually every
ecological niche is occupied by some occupational or cultu­

ral human group for its sustenance. Each time an
ecological niche is degraded or its resources appropriated

by the more powerful in society, the deprived, weaker

sections become further impoverished. For instance, the
steady destruction of our natural forests, pasture lands
and’inland and coastal water bodies has not only meant

increased economic poverty for millions of tribals, nomads
and traditional fisherfolk, but also a slow cultural and
social death: a dismal change from rugged self-sufficient
human beings to abjectly dependent landless labourers and

squalor-stricken urban migrants. Current development can
in fact be described as the process by which the rich and
more powerful reallocate the nation’s natural resources

in their favour and modern technology is the tool that
subserves this process.

--- The State of India’s Environment, 1982

.12

12

Suggested Changes in Policy

Having worked with the tribals in the 19 villages of
Gujarat since 1980, we as a group have just begun to understand

the problems from the perspectives of the tribals. We suggest

the following changes in the policy of rehabilitation to
make it sensitive and relevant to the socio-economic, cultural,
psychological and ecological needs of these oustees who are

as much the ’public’ as any other.

i.

The amb?lguities in the rehabilitation proposals

must be clarified immediately
— the rehabilitation of displaced people in all

three States is of equal importance;

— the land for land compensation with the minimum

provision of 5 acres should be implemented
efficiently;
— the land offered being irrigable, agricultural and

as far as possible within the command area of the

project and preferably in their respective States.

ii.

The government should either buy or acquire private
lands in large tracts As it does not have any surplus

within its own possession. Under no circumstances should

the oustees be asked to purchase their own lands.
iii.

The government should take a family as a unit (and not

•holding') and provide minimum of 5 acres of irrigable

land to each oustee family irrespective of the fact
whether they legally own their land or not or the government

cab conduct a detailed survey in the villagesto find
out the amount of forest land and/or other waste lands
13

13

they are actually cultivating and provide them with

alternate land in appropriate amounts.
Not
iv.

only must individuals whose land is acquired more

than 75% be given the option of surrendering the rest
but this rule must also be extended to the villages as a
whole as well if they are going to loose atleast 75% of
their total agricultural land.
v.

The compensation for land acquired must be adequate and
sufficient to buy new lands of atleast equivalent size

keeping the basic objective of rehabilitation ie., abolition

of poverty of the oustees in mind.

The forest issue
Following our recent contacts in the interior villa es

of Gujarat and Maharashtra, we have come to understand another
important dimension of our main demand of land for land, al.hough

this factor was not totally lost sight of by us earlier. The tribals
especially Dungari Bhils who, through centuries have lived in

these forests, cannot simply imagine that they can survive
outside the forests. Forest is so much a part of their life

that outsiders like us who are quite sympathetic also cannot

fully appreciate or understand their attachment to the forests,
let alone the aloof and faceless bureaucracy of the Narmada Project.

For these tribals, forests are not on y the fountain of their
material needs, but also an integral part of their social,

14

14

cultural and religious life. You have to be with them to
understand what forest means to them. No wonder that the inhabitants

of these villages are refusing to move outside the forest area.
Even those oustees who agree to resettle on non-forest lands,
would opt for forest land, if the option is offered to them.

Why is then the Government so adamantly refusing to release

forest land for resettlement?

The re-evaluation of the

government's blanket policy with regard to forest land is

urgently called for. The Government's argument is based 1

on the laudable objective of conservation of forests. The
plausibility of this argument is only superficial. It is clear

now that the Government itself is destroying large tracks of

forest in the name of 'development'. It also sanctions felling of
the forest in the name of 'satisfaction of market needs'.
Only when it comes to giving forest lands to tribals, the

Government raises the bodjey of 'Conse vation of forests'. Hidden
in this argument is the unfounded charge against the tribals
that they are the culprits behind the massive deforestation. The

facts if examined closely would reveal exactly the opposite
story. The tribals have in fact protected the forests and
their needs of forest wood is so small in comparison to the

unsatiable hunger of the urban centres for timber that it is
sheer perversion to say that they are destroying the forests.

We therefore make a demand that these tribals must be
resettled in forest land only so that t ey can preserve their

forest bound culture and way of. life. In raising this demand we

are not at all pitting ourselves against the 'conservation of
forest’objective.

.15

15

If forests are in danger, the tribals living in forests are not
basically responsible for it. The objecgive of 'conservation of
forests'

and that of resettling the tribals in forest are not

incompatable. Indeed they could with imagination become
complementary objectives. We, however, challenge these so-called
developmental schemes which are both destroying forests and

the defenceless tribals.

CONCLUSION

Through this note we have tried to bring to your notice
the plight of these oustees of the Narmada project andthe
ambiguities and insensitivity of the government rehabilitation

policy. Our attempts to bring about appropriate changes in the
policy have made very little progress. We need your help to

tackle this problem. We must act and act decisively if we do not
want to let the tribals down in despair.

With their forest-based life styles destroyed,

the tribals are becoming human cannon fodder
for the country's modernization: poor, unskilled
and viciously exploited.
—The State of India's Environment, 1982

©H\ ■ 3

"THE TJ;.. LL,.. u-

HUJJKiJ liJHn''

A summary of the environmental and health hazards

c| dcu-r^

BENEFITS
Electricity for industry (half our total electricity produced today)
Water for irrigation (26.6 million hectares (1979-8O) of surface

irrigation potential)

Hi V EiSTMENT
From JO dams in 19^7 to 1JJ4 in 1979.
From storage capacity of 1J650 million c. metres

to 173000 million c. metros (1979).
Bs.10,566 crores invested until 1979 ie., 14% of total

planned expenditure.

HAzjifiDjS

Evacuees

Large numbers of people/villages are moved - mostly
tribals, adivasis and forest dwellers. Thirteen dams
produced 5*77 lakhs and 4j0 villages of ’oustees’.

Rehabilitation usually insensitive to socio-economic,
cultural and psychological complexities of process.
Silting

Reduces life span of dam?aed- corrodes banks and affects
aquatic flora and fauna downstream. Water loses fertilizing
value. Siltation rates have varied from Bhakra^JO^ increase}
to Nizam Sagar (AP) 1<.(i600j5 increase?)

,2

2

Earthquakes
Correlation well established. Have been reported with

respect to Mangalam (196?), Parambikkulam (196?), Koyna (1967)
Sinnerjani (1969), Hula (1972), Idukki (1977 & 1978> and also

Ghirni, Sharavati, Sholayar and Ukai dam.
l.'ater logging

Estimated that 6 million hectares of cultivated land is
severely affected by water logging due to increase—in ground
A

water table.
Soil salinization

Estimated that 7 million hectares of fertile fields are

affected by soil salinity affecting crops and plant growth.

Health
Increase in mosquito/fly populations. Spread of malaria

filaria and Japanese encephalitis (well documented for
Thungabhadra and Sathanur dams). Changes in levels of

fluoride, calciura and trace metals due to rise in ground
e3

water table causwsg crippling diseases like genu valgum
(knock knees) and fluorosis. Reported from Nagarjunsagar

and Parambikkulam Aliyar dams./
-X

'

rorests
Loss or sharp reduction of forest cover affecting flora,

fauna and ecological balances. Between 1951-1972 estimated
loss of 4 lakh hectares of forest lands.

<=•

flsanxo

/ecd /o

S/Jxead. csf

Ap haic.

Ko

TJo-m

gc^w/s

he* v<_

3iljho.i-z.io. Ircwisrru rfed /A rcT-tx^-A snculs

<>>

Kke. VblKc.
o/’

nvO b/^cL^e^o

toel^Ycdt

3

Ecology
Apart from deforestation, river and reservoir silting

and health hazards already mcntioncd?ecological changes
include - increased water evaporation affecting micro-climate;
proliferation of harmful acquatic weeds (Eupatorium, Lantana,

Milkania) which smother acquatic growth, are unpalatable
to herbivores, increase fish mortality and choke feeder

systems, irrigation outlets and block hydro-electric
installations,

floods
7&Destruction of vegetation which retains water during rainy

season.,adds to flood problem. Excessive discharges to avoid

damage to dams}cause

flash floods downstream (Hirakund, 1980)

financial drain

The cost escalation over initial cost estimates for important
projects in India have varied between 150-1 JOO percentage ..

c-ost—escalation. Apart from the additional drain on the
exchequer9cost reduction exercises are affected by inadequate

provisions for rehabilitation of oustees and inadequate
accounting of costs due to loss of forests, farm lands,

fishing and ecological changes,

ALi'ilBiLvi'IVx^ TO xAkGE DAi-id
Mini and micro hydro electric plants.
Bio-mass plants utilizing forest produce
Wind and solar energy conversions

Use of small dams, barrages and bunds

Revival of traditional tank irrigation systems.

,4

4

PEOPLES PROTESTS
Tehri Bundh Virodhi Sangharsh Samiti

Silent Valley Project protest spoai'headed by KSSP.

Bedti Project opposition.
Save Mannar Agitation (Mannar High Dam).

Jungle Bachao, Manav Bachao Andolan (Inchampalli Dara).
Mitti Bachao Abhiyen (Save the Soil campaign).

TO DAM OB NOT TO DAH IS THE QUESTION

—Summarised from ’Temples of Modern India’ by ’Madras group’ in

Patriotic and People Oriented Science and Technology Bulletin

(PPST Bulletin) Vol.4, No.1, June 1984.

(BSsSqsKadr aS-^G/o-lv 'V-tjayalakshnii,_15L South—Nada .Street,
Trinlicane, Madras- 600005) .

d> H 1

.

MEDICAL RESEARCH IN BHOPAL
— Are we forgetting the people?

Concern for man himself and his safety
must always form the chief interest of

all technical endeavours. Never forget

this in the midst of your diagrams and
equations.
—Albert Einstein

Preamble

In a tribute to the medical relief workers involved in

service to the Bhopal disaster victims the ICMR has noted
that 'a disaster of such magnitude, of such suddenness and

caused by the release of a highly toxic chemical methyl
isocyanate (MIC) into a densely populated habitat is

unparallelled in human history. The doctors, medical students,

civil servants, governmental, public sector and voluntary
bodies and the people themselves rose to the occasion in a
human gestux_e equally unpara 11 elled'...

In the absence of authoritative information on the released
gas; the unwillingness of the company to part with authentic
information; the unpreparedness of the local bodies and the
government health authorities to understand the consequences of
the disaster; and the absence of technical or toxicological

expertise on MIC among our scientific community, it was
imperative that a national body like the Indian Council of

Medical Research through its own initiative would have to harness

2

the scientific medical expertise in the country including the
local medical college community to meet this challenge. Considering

that the affected population was over 2 lakhs and that the dead
were over 6000 (though official estimates are 2000!) this research
initiative had to be equally unparallelled in meeting the phenomenal

challenges of the world’s worst recorded ecological disaster. Do
the records of events in the past four months since the disaster

bear this out?
The Plan

A report on the first nine days of the Bhopal disaster

identified

three objectives for the ICMR’s research

programme:
1.

To establish a clinical and patho-physiological profile

of the hazard which would also provide clues for improved
patient management and clinical outcome

2.

To study the long term sbquetae of toxin exposure to

lung, tissues, foetus, genes and cancer induction
3.

To obtain a basic understanding of the biological

alterations associated with MIC exposure.
Strangely enough there is no mention in this report of a

strategy by which conclusive research data as and when available
would be transmitted to the relief and rehabilitation effort

in Bhopal, ie., to the treating doctors and through a health

education effort to the affected public,
A report of projectization of ICMJ? supported research effort

lists out 17 study projects which covers acute and long term

(2)

3

health effects, lung functions, follow up of children aged 5-15
years, occular changes, pulmonary and neurological changes, growth

and development of new horns, clinical and forensic toxicological

studies, pathological and microbiological investigations, radiological
studies, biochemical and immunological studies,

carcinogenicity,

mutagenicity, teratogenicity and chromosomal changes, data managment

information system, hospital based cancer register, cytofluorometric
studies and blood gas analysis. The studies ranging from a time

span of 6 months to 5 years would incur a total financial outlay of

1.07 crore rupees.
Some surprising omissions in the list were the assessment of
psychological stress and its manifestations in the affected families,

studies on health of women (not obstetrical outcome but gynaecological

effects) and the assessment of medico social effects like reduced
earning capacity and functional disability which would affect rehabilitat­

ion efforts. Though there were references to an epidemiological and

community based outlook the research endeavour atlea'fet as on paper

did not seem to be a coordinated holistic effort on understanding

the total problem but basically a series of vertical research
programmes initiated and funded according to the interests of the
professors involved in the exercise.

Results

It is four months since the tragedy and about

three

months since many of the research programmes got underway.
As far as a communication strategy goes three press releases

it
and two lectures by the director generals and a minutes

of the meeting on the thiosulphate controversy are the only

freely available literature on the research (3-8) efforts.
From these all that any member of the scientific community
or the general public can gather are:-

i.

that there is no evidence of irreversible eye
damage or blindness

ii.

that the autopsy findings are indicative of

severe respiratory damage caused by pulmonary
odeme and asphyxia
iii.

that studies of exposed persons with lung symptoms/
signs have shown obstructive and or restrictive

abnormalities

iv.

that a double blind clinical study undertaken using
sodium thiosulphate and a placebo has established that

sodium thiosnlphate administration results in symptomatic

improvement and in increased excretion of thiocyanates
in the urine. On the basis of clear cut results, the

State government has been advised to administer sodium

thiosulphate to the exposed population and detailed
guidelines have been drawn up and circulated.

v.

that two visiting psychiatrists have found that 10-12%

of the affected individuals attending the medical clinics
in Bhopal are presenting with psychiatric manifestations—
symptoms of anxiety and depression are foremost.

5

Why this secrecy? or is it administrative over caution?
A more updated report prepared in mid March collating

all data as of that date has again become a casualty in the
commitment to secrecy (caution!) and no press release has

followed.

Issues of concern
An mfc fact finding teem which visited Bhopal in mid

February at the request of various non governmental agencies
and action groups published a report on the realities of

medical research and relief which has been widely circulated
and is now well known
16

(9)

. In mid March an mfc team of

members camped in Bhopal and undertook an

epidemiological

survey which included detailed history taking, physical
examination, lung function tests, haemoglobin estimation of
a 10 person sample of a severely affected area and a control

area <10>.
The team also met decision makers, relief and service

providers, medical teams of voluntary agencies and others,
apart from undertaking a survey of the people’s perceptions

of relief services and an overview of the services itself. The
reported
findings of the team are being analysed and will be/shortly
(a press release is published in this issue) but the experience

of the third week of March in Bhopal strengthened the findings
of the earlier fact finding team and identified a whole series

of issues of concern in the ways in which research efforts
were becoming exploitation of peoples' suffering rather than

expressions of supportto programmes of human welfare.

6

Lack of dissemination of technical guidelines
1.

The medical relief services continue to be starved of
authentic and authoritative scientific medical information
to support clinical judgment and patient management.

In the absence of clear cut guidelines from the seniors in
the profession treatment continues to be adhoc, symptomatic
and unstandardised. Findings of autopsies,lab investigations
and x-rays and other tests are not available to the treating
doctors. Doctors have not been alerted to the fact that

a wide range of symptomatology like fatigability, weakness,
memory problems are all part of the MIC syndrome. In the

absence of such information peoples’ sufferings have often been
passed off as malingering or compensation neurosis.

2.

Pill distribution
The treatment basically consists of a whole series of
pills which are efficiently and actively prescribed to the

people in a sort of conditioned reflex. In the absence of

proper record linkages each patient is collecting large

amounts of pills and not feeling the better for it apart

from the dangers of over drugging. Other form of care and
non-drug therapies have not been thought of and counselling.
f----

3.

The (thiosulphate controversy: Even after the ICMR studies
establishing the validity of thiosulphate administration and

the preparation of clear cut guidelines for its administratioA8<

zovse A
the^uaix-of- this specific antidote is not being dene as effectively
as it should be. It has become a casualty in a medical controversy

7
between d cyanogen and

/ob/oi'oo
carbon monoxide Lobby and the victims

rather than being informed and helped are being confused and

neglected.
4.

Women's health: The mfc fact finding team had highlighted the

problems of women who have suffered abortions, still births,
diminished foetal movements, suppression of lactation, abnormal
vaginal discharges and menstrual disturbances. The studies

undertaken by two Qagy doctors of mfc reported in this bulletin^^

establish the magnitude and severity of the problem. It, however,
continues to be neglected by the concerned authorities.

5.

Absence of Health Education efforts
Whatever the validity of the research efforts^in the ultimate

analysis it should get translated into a strategy of health

education and awareness building of the affected people. As
of date there are no”^guidelines or efforts in this direction.
The range of areas is phenomenal—advice to mothers of the risk
to the foetus and preparation for consequences inciting

options for MTP, advice to couples on contraception till

detoxification is over, breathing exercises and antismoking
advice to those with fibrosis of lungs, avoidance of overdrugging

of pregnant mothers, advice to mothers regarding feeding of
infants/children due to lactation suppression, availability
of

thiosulphate and other medical relief measures. None

of this has even been recognised as being necessary.

6.

Poor epidemiological and medico social orientation of problems
assessment

The general impression is that research and relief efforts are aMM
suffering from an acute clinical and institution based orientation

u

j

-L-

ccrrom c^Ky »<xe-e«-. <-7

r-oJI'\e^>'-

^niotcs^:c^\ onanYaY\an .
j

Only if all data is field based and is related to known

available morbidity patterns (or comparison with controls)

can early problems and special trends be identified and urgently
acted upon. The danger of getting into the pursuit of a very

neat and fool proof epidemiological planning exercise can be
equally counter productive.

7.

Lack of informed consent:

The people are not being informed about the

tests being done. Nor is consent being taken for being included
in the studies or for procedures to which many of them are being

subjected to. This is a minimum medical ethic.

8.

Lack of coordination:

This is a universal problem and the

ultimate casualty are the disaster victims themselves. This
t5

incordination is between government services and research efforts
in the medical college,between the different research workers themselvs'

between government and non-government relief efforts, between voluntary
agencies involved in action, relief, rehabilitation and of all

these groups with the disaster victims themselves.

While a more detailed report is awaited we in the mfc appeal to
government decision makers in Bhopal, medical college professors, ICMR

scientists, IMA, voluntary agencies, action groups that there is an

urgent need^to be actively met :
* Need to evolve a bold, imaginative and open communication

strategy to all the doctors and health workers treating the

disaster victims who are presently starved of authentic

technical/medical information hampering clinical judgment

References

1.

ICMR, The Bhopal disaster - current status (the first nine

days) and programme of research.
2.

ICMR, Projectization of ICMR supported Research

3.

ICMR, Medical Research problems in Bhopal (V Ramalingaswami)

4.

ICMR, Pathology and clinical toxicology of the Bhopal disaster

(S Sriramachari)
5.

ICMR, Medical research on Bhopal Gas Tragedy—press release

12

6.

Feb 1985

ICMR, ibid, press release, 12 Feb 1985

7.

ICMR, ibid, press release 27 Feb 1985.

8.

ICMR, Thiosulphate therapy in MIC exposed - minutes of
meeting at ICMR, 14 Feb 1985

9.

mfc, Medical Relief and Research in Bhopal—the realities
and recommendations.

10.

mfc^ Approach document of a project to evolve a strategy
of medical relief and rehabilitation which best meets the

peoples' medico social needs and expectations.
11.

Rani Bang, Effects of the Bhopal disaster on the women's
health—an epidemic of gynaecological disease: reports I & II.

12.

Lancet editorial. Calamity at Bhopal, 15 Dec 1984.

468
Anton-Culver, Culver, Kuros,
British Journal of Industrial Medicine 1988:45:469-475
is consistent with the fact that the IgM mediated
exposure and nonmalignanl pulmonary abnormality in Qua
primary' humoral response subsides with continuing
chrysotile workers Arch Environ Health 1985:40:80-7.
2 Finkelstein MM. A study of dose-response relations for ash—
.
-.
rexposure to an antigen. Our finding that both shipyard
groups had significantly higher levels of IgG than the
3 Acheson ED. Gardner MJ. Winter PD. B enn«?c.cancer
Red Cross controls (table 4) is. however, consistent
factory using amosite asbestos. Int J Epidemiol I984’1343.i!^'^a
.
-i
•
t\1
1
with the idea that asbestos behaves in the body as a
4 Liddell FDK. Thomas DC. Gibbs GW. McDonald JC p!
persisting antigen. Immunoglobulin A was also found
exposure and mortality from pneumoconiosis, respiratory
J
J
x
to be higher in shipyard workers than in the Red Cross
abdominal malignancies in chrysotile production in Quefc.
JrX^S^dM^^^^dERSSON,1 M KERR MUIR,2 V MEHR A,’ AG SALMON1
controls. The immunoglobulin levels in shipyard
experimental subjects were similar to those in shipyard
--.vofthe.mp'epopu'ationaged 50-59 years. BrJtndjf
Deoartment of Occupational Health.' London School of Hygiene and Tropical Medicine. London
control subjects. Of interest here is the observation of
6 Hilt B. LangardIS." Andersen A. Rosenberg J. Asbestos exposufn C/£™T- Moorfields Eye Hospital.2 London ECI 2PD. UK. and Chattisgarh Eye Hospital. Raipur. MP.
Huuskonen et al that patients with asbestosis have
smoking habits, and cancer incidence among production au ra
higher IgA values than controls.14 They concluded that
maintenance workers in an electrochemical plant. Am J/ndAc’0
.
.
the increase in humoral immune response could be
1985:8:565-77.
ctract In the two weeks immediately after the Bhopal disaster a community based survey was
used for the evaluation of patients with pulmonary
7
out in a series of eight exposed and two non-exposed clusters of
fibrosis.
499-504.
concern was the effect of the gas (subsequently identified as methyl isocyanate) on the eyes ot the
When we looked at Th and Ts cells, both types were
s Kubota m. Kagamimori s. Yokoyama k, Okada a. Rcdun
but data were also sousht on respiratory status and the first symptoms of the exposure. No
present in significantly greater numbers in the two
b"; mJ .S^5:4iXTS from pa"cnls W,,h asbes,oi Jise of blindness was encountered that could be attributed to the gas. The most frequent symptoms
shipyard groups compared with the Red Cross blood
donors, the Ts excess being considerably greater than
9 Lemaire i. Dubois c Grondin c. Gingras d. immunoreguiatu,renorted were burning of the eyes, coughing, watering of the eyes, and vomiting. Among these, the
of
lung
fibroblast
growth
aiterauon
,n
asbestos-induced
p
.
p
of cough most closely followed the rate of death in the different clusters. Although much
the Th excess (table 3). The greater excess of Ts cells
results in Th/Ts mean ratios that are smaller than 10 Kaga°n" t'jacobson rj. Yeung k"-y, Hmda^DL Nachnani GErarer overall, the frequency of reported diarrhoea appeared to bear a stronger relation to death rates.
those found in the Red Cross controls, a condition also
Asbestos-associated neoplasms of b cell imeage Am j Mt Renorts of photophobia and the clinical finding of superficial interpalpebral erosion ot tne cornea
found in immunodeficient people. Our findings are H Ge,1’e7nTR3^y°MG.U1hayakumarS,Newia„dAC.RuddRk.were more frequent where the death rates were lower. Thu
similar to those of Lew et al who found raised Ts but
Lymphocyte subpopulations m bronchoalveolar lavage fluidiconsistent with different effects of the gas at different doses (as estimated from
not raised Th cells in workers exposed to asbestos.asbestos workers. Am Rev Respir Dis 1985:132:824—S
Although statistically significant differences were 12 Doll NJ. Bozelka BE. Goldbah S. Anorve-Lopez E. Salvaggio Jt ,delor“>'
found when comparisons were made in several of the
Asbestos-induced alteration of human peripheral bloo.
laboratory tests, their biological importance remain to
monocyte activity int Arch Allergy. Appi Immunol I982:6t The release of a gas cloud from the Union Carbide of effects among survivors. Results of slit lamp
be determined. It is also recognised that many compar­ n
o, , iu o
ms c
factorv at Bhopal. India, on the night of 2 '3 December examination by two ophthalmologists were reported
isons were made and that differences can occur as
a. Natural killer «li aci.viw
NS4 resulted in numerous deaths and injuries among earlier.'■’ A preliminary assessment of the area of
random events and not the result of real effects. Study
workers. Am Rev Respir Dis 1985:131:831 —1
the surrounding population. It isnow believed that tne exposure and the effects suffered was made by talking
hypotheses were selected before inspection of the data, 14 Huuskonen MS. Rasanen ja. Harkonen H. Asp s. Asbesic immediate cause of the disaster was that water entered
to people who lived at varying distances and directions
exposure asa cause of immunological stimulation Scamlinm>a tank where 41 tonnes of methyl isocyanate (MIC) from the plant. From this it was possible to map out
and thus results are not selectively reported.
journal of Kespiratorv Disease 1978:59:126-V
.
,
.
- ■ „ tl.
In conclusion, our observations of the humoral 15 Hanmann dp immunological consequences of asbesle "ere stored, causing a runaway chemical reaciion. 1 he
preliminary exposure zones according to reports of
immune response as measured by changes in IgG and
exposure. Survey of immunological Research 1985:4.65-8.
heal of the reaction, possibly augmented by reactions
human and animal deaths, symptoms, and perceptions
IgA. the cellular immune response as measured by­ 16 Warheit db. George G. Hill lh. Snyderman R. Brody AR with other materials present in the tank as contamin- of the presence of the gas. Cases seen in the community
rntracranH-mXmnh01®
'b'™ anls- produced vapourisation of such momentum that
mitogen stimulation and the disproportionate increase
before the start of formal survey were not included in
attractant for macrophages. Lab Invest 1985:52:505- 4
,,
,
r
t
c.
in Ts cells and decrease in Th Ts cell ratios may. one 17 Fahey
JL. Prince H. Weaver M. et al. Quantitative changes ini11 COuId n°l be contained by the safety systems which the study, although they provided valuable informa­
day. serve as clues to the early diagnosis of suscep­
helper or T suppressor/cytotoxic lymphocyte subsets tha- may in any event have been defective or of inadequate tion regarding the limits and nature of the exposure.
distinguish acquired immune deficiency svndrome from othr Capacity (S Varadarajah. report IO the Council of
tibility for asbestos caused malignancy. The test to
Eight housing clusters were selected with the
18 ScZr Sta^nodc0o±ris- w / 1A,^'98I4;76;95 -I100’
Scientific and Industrial Research. India. 1985). There exposure zone, covering a range of different severities
these clues will depend on a prospective study.
la bchwab R, Staiano-Coico L. Weksler ME. Immunological stucie*
•••
....
- •
-*
of aging. IX. Quantitative differences in T lymphocyte subset ir is still considerable confusion about what effects of exposure as judged by the preliminary inquiries. A
We thank the Office of Naval Research for their
young and old individuals. Diagn Immunol 1983:1:195-8
ine
SUFVlVOrS
Can
DC
atiriDUiea
IO
exposure
iu
household
survey was carried out in the second week
among the survivors can be attributed to
to
support and funding under contract No NOOO14-80-C- 19 Wagner MF. Brown DG. Campbell mj. Coles rm. Edwards RE the
gas. In the two weeks immediately after the disaster after the release of the gas. Two non-exposed clusters
0571: Lorraine Wrazen. Corinne Aragaki. and Lee
Scott MP. Immunological monitoring of an asbestos-exposec a •----- n . ..
.
.
< — out a were selected, having apparently similar socioecon­
population. Arch Immunol Ther Exp (Wars:) 1982’30 ">01-^ r, team of Indian and British doctors carried ...........
Burke for their help in coding, computerisation, and 120 Ueki
A. Oka T. Mochizuki Y Proliferauon stimulat^Xs'o. U
..... - ™un.iy
iormal
community uaseu
based epiucnuo.ugwu,
epidemiological »uu,
study v
of omic status to the exposed groups but located 14 and
data analysis; Dr Nicholas Sargent. LAC/USC
chrysotile and crocidolite asbestos fibres on B lymphocyte cel! cx
POSCd
the ~::s
mass
17 km away from the plant, where no one reported
"T
—4 and
_..2 unexposed
........ r___ 2 populations before th:
Medical Center. Los Angeles, for reading the chest 3
lines. Ciin Exp Immunol 19X4:56:425-30
'
txodus
symptoms of gas exposure within several kilometers.
exodus from
from the
the CllV
city.
.x ray films: Cynthia Laudon and Paula Sweet for their 21 Rola-Pleszczynski M. Gouin S. Begin R. Pulmonary and systemic
Starting with one arbitrary selection, houses were
immunoregulatory changes during the development oi \Uthndc
help and cooperation with the study team: and Frieda
contacted consecutively in each cluster, moving from
expenmental asbestosis. Clin Exp Immunol 1984:58:325-34.
cl,,oaS
van Schijndel for secretarial help in preparing the 22 Lew
F. Tsang P. Holland JF. Warner N. Selikoff IJ. Bekesi JG
door to door with a questionnaire drawn up for the
manuscript.
High frequency of immune dysfunctions in asbestos worker •Several of the worst cases in two hospitals were purpose. All inhabitants present in each dwelling at
and in patients with malignant meNOlhelioma. J Clin Immuno.
examined in the days immediately after the disaster to the lime of the visit were examined following a
1986:6:225-33.
References
23 Kagan E. Jacob>on RJ. Asbestos exposure, immune stimulation “''lain an initial indication of the nature and severity standard format. The British doctors used an inter­
^9 ,>mpho,d malignancy. Advances in Pathology 1982.2
1 Copes R. Thomas D. Becklake MR. Temporal pauerns of
preter. The initial survey lasted from 5 to 12 Decem­
ber. after which time the entire exposure area was
Wd 22 June 1987

Pxnosure and response to methyl isocyanate: results of
rnTHHlUnity
DaSeO SUFVCy 1H BhOpal
CO* A**AA

469

470
deserted as people left in case the plant was restarted to
"neutralise” the remaining stock of MIC.
The first survey day was spent by the participating
doctors practising the administration of the question­
naire and the examination in an attempt to ensure
consistency. The questionnaire inquired about name,
age. duration of exposure based on experience of acute
symptoms and presence in the exposed areas, deaths in
the household, the first four symptoms perceived after
the exposure, eye symptoms, and treatment received to
date. The first four symptoms were requested without
prompting by the interviewer, whereas for the eye
symptoms a checklist was read out after the first four
symptoms had been recorded. A rapid clinical assess­
ment of respiratory signs was recorded (obvious
tachypnoea, audible wheeze, use of accessory muscles)
so far as possible without alerting the interviewee to
this. The initial focus of the inquiry was the eye
consequences and to lay a baseline for future possible
deterioration of sight.
Data were coded and sorted using the standard
SPSS statistical package. Analysis was done using the
Mantel Haenszel procedure for combining data from
different strata’ and the Mantel extension of this test/
Statistical results are reported as the chi-squared
statistic,’ odds ratio (OR), and confidence interval (CI)
for a stated level of probability
Results
Examination of severely affected hospital inpatients
indicated that the main symptoms which were con­
sidered life threatening were those involving the
respiratory system. The worst eye cases brought
forward for slit lamp examination at Ghandi Medical
College by two ophthalmologists showed no case of
deep corneal damage?
Travel by foot, tricab, and taxi allowed the outer
limits of the exposure zones to be mapped out, as
shown in the figure. People were affected (mostly
burning eyes and coughing) over 1 km north of the
factory, despite the light north wind. No deaths were
reported to the north of the factory. People from this
area tended to flee northward, rapidly getting away
from the gas cloud. For analytical purposes, data were
available from questionnaires of 379 people in the
eight exposed clusters and 119 people in the two
unexposed clusters (an average 2-32% of the estimated
population in the area surrounding the study clusters).
All study clusters were south of the factory. Table 1
shows the age distributions in these clusters. The age
distributions of exposed and unexposed groups show
some differences, which are most pronounced in the
extremes of age. A reporting bias was noted in
exposure cluster 7. a factory compound, where men
conspicuously understated their ages relative to the

Andersson, Kerr Muir, Mehra, Salm<, Exposure and response to methyl isocyanate: results of a community based survey in Bhopal

estimate of the interviewers (presumably to protec
their employment). Sex ratio in the two population
was similar (exposed group 41-7% women, unexpose.
group 42-9% women). The sex of about 15% o
respondents in each group was not recorded.
The duration of exposure across all the exposei
groups (n = 379) was as follows: 1 % left the areas n
which symptoms of gas exposure were reported with!
one hour, 15% were exposed for one hour, 165
between one and two hours. 16% for two hours, 8"„
for two to three hours, and 2% for three hours. I
further 29% said that they had been present in the are,
throughout the exposure period (estimated to be abou
four hours). No details regarding individual exposun
were obtained on 13%. three quarters of whom wen
children under the age of 10 years. Between cluster
where deaths occurred (1 to 6) and the remaining tw<
exposure clusters there was no apparent difference ir
the average duration of exposure nor in the proporti or
who fled from the exposed area (jr = 0-25).
Each interviewee was asked how many people hac
died in their household. The results of this are showr
in table 2. Deaths were recorded in clusters 1, 2, 3,5.
and 6. Numerous deaths were known to have occurred
in cluster 4. in households where there were n<
survivors, but the limitations of the study methoc
meant that these numbers could not be recorded on i
questionnaire. A total of 51 deaths was reported in thi
houses where the 379 survivors were examined. Basec
on the estimated population in and around eacl
cluster (800 in 6: 1500 in 1: 2000 each in 2. 3. and 7
3000 each in 4 and 5: and 4000 in 8). it is possible it
calculate that about 1850 deaths occurred in anc
around the eight clusters used in this study. Thicovered about 70% of the exposed area.
The most frequently mentioned first symptorr
among the survivors in all the study clusters waburning eyes. In answer to the open question regardin!
sequence of symptoms, 56% mentioned burning eyefirst, 15% mentioned it second. 7% third, and 3% as
the fourth symptom (total 81%). The second mos
commonly reported symptom was coughing. The nex:
two most frequently mentioned symptoms were water
ing of the eyes and vomiting (see table 3).
Table 3 shows the relation between initial symptom:
and death. It would appear that burning eyes do no:
have a particularly high reported prevalence in thosr
clusters where death was common. The frequency o:
reporting cough as one of the first four symptoms
however, follows closely the distribution of deaths
This trend was significant at the 5% level (/ = 4-32
using the Mantel extension as a test of trend wilt
1 DF). Using 25 mortality as a cut off point, clusters 1
2. and 6 were stronelv associated with reported count
(/ = 8-39; OR ='217; 99-5% CI = 1-02-4-59)
Diarrhoea and shortness of breath among ih<

Figure Map of Bhopal showing location of Union Carbide plant ( UC) and of exposed 1IS I and unexposed
' K Uh clusters. Scale is indicated by 1 km bar: area shown is about 6 km x 9 km.

471

472
Table 1

Andersson, Kerr Muir, Mehra, Saln^ £Xpos<ire an^ resPonse 10 methyl isocyanate: results of a community based survey in Bhopal

^jc 3

Age distribution in the study clusters

Death rates in relation to early symptoms

Cliisirr
Kjt four symptoms (%).
7( Burning eyes
Coughing
r Watering eyes
Vomiting
ft other symptoms (/.):
pholoi’hobia
S -Hard to open eyes
Diarrhoea
5: short of breath
Chest pain
II Nausea
Unconsciousness
5.' Dizziness
Choking
41 Headache
Twitching
Convulsions
6< dumber reported dead in each household visited divided by total examined plus number reported dead.
I Number of deaths not known
54 ’includes both volunlered information and direct questioning.
5S
15-3

61
16 1

79
208

61
16-1

Total exposed
44
42
11-6
||j

16
4-2

24
20-2

23
19-3

30
25-2

14
IIS

Tom/non exposed
8-4
67

25

5
1-3

I
0-3

survivors had a notable relation to the occurrence of
eyes could not be opened (see table 5). Survivors in th
death. Diarrhoea was reported with increasing
clusters where deaths had occurred (1-6) were near!
frequency across clusters with increasing mortality (-f
12 times more at risk of SIPE than other expose
= 10-3 using the Mantel extension as a test of trend
people: in clusters 1-6 there were 52 cases out of 22with 1 DF). Shortness of breath, on the other hand.
survivors compared with two among 101 survivors)
showed a strongly inverse relation with clustering of
clusters 7 and 8 (■/; = 17 49; OR = 11-7; 99-9% CI =
deaths
= 12-3 by the same test).
1-69-81-4).
Examination of the eyes showed different patterns
There was no evidence of eye problems other thain the various clusters (table 4). Red eyes were more
SIPE and redness in the exposure clusters compare
common among the exposed compared with unex­
with the non-exposure clusters (9 and 10). There wa
posed people overall, a finding that was statistically
no difference in the occurrence of corneal opacity t
significant at the 90% confidence level
= 31: OR
= 0-05). Bitot spot (■/; = 0-14). active infection (y; = 1-71: 90% Cl = 1-04—2-08). The characteristic
0-83). and evidence of past trachoma (f = 0-13
superficial interpalpebrai erosion of the cornea and
Pterygium
= 17-6: OR = 3-3) and cataract (^ conjunctiva (SIPE) associated with exposure to MIC
was observed in seven of the eight exposure groups
Table 2 Deaths by cluster
with differing frequency. This sign was most frequent
in clusters 4 and 6 (36% and 50% respectively). These
People
Households
were the two clusters where the lowest proportion of
Cluster
examined
with deaths
people actually reported burning of the eyes as a
i
-IT
70
symptom immediately after exposure. The possibility
17
3
To
i
69
of the coincidence of SIPE with low reporting of
50
—+
burning eyes having occurred by chance may be
i
6
excluded with greater than 99-9% confidence (y; 18
55’
0
o
59-66 with 1 DF). The apparently inverse relation
8
48
0
0
between burning and SIPE was not found between
•W orks compound: only men ol working age examined.
SIPE and reported watering of the eyes but it was
♦In cluster 4 al least Inrec households were encountered where de.' it
apparent with photophobia and the sensation that the
had occurred These were not included in the survex.

2-3; OR = 3-1) were more common in the non-exposed
population. These differences were calculated over all
age groups and disappeared with age stratification.
There was an increase in fundal changes (dilated
retinal vessels or haemorrhages) in the clusters where
deaths had occurred (clusters 1-6: 80/272) by compar­
ison with those where no deaths had occurred (clusters
7 and 8: 18/103). Data on four subjects were missing.
These findings indicate a positive association, sig­
nificant at the 2-5% level, between clusters where
deaths occurred and fundal changes on ophthalmos­
copy (z: = 5-5; OR = 1-97; 97-5% CI = 1-03-3-76).
Unfortunately, the respiratory examination was
omitted or no record was made for 55% of exposed
survivors. Among the 45% who were examined, 25
(15%) were.judged to be in “respiratory distress” on
the grounds of a conspicuously increased respiratory

Table 4

rate, an audible wheeze at rest, or use of the respiratory
accessory muscles. Overall, there was no hint of an
association between fundal changes and obvious res­
piratory distress (jr - 0-04). which probably indicates
lack of representativeness of the available 45% of the
respiratory examination data. Considering only those
people on whom a respiratory examination was recor­
ded, 16 were considered to be in obvious respiratory
distress out of the 131 who were normal on fundoscopy and nine were deemed to be in respiratorydistress out of the 40 with abnormal fundi. Fundal
changes were thus twice as common among people
deemed to be in respiratory distress. This finding.
however, was significant only at the 12% level (jr =
2-6; OR = 2-09. for 1 DF). Respiratory distress was
observed nearly six times more often in clusters 1-6
where deaths had occurred (22/105) than in the other

Signs on physical examination
10
54

.Vo

70

17

69

50

52

18

55

48

65

N'ormai

30
TT
9

6
4
j

48

19

37

2

21

33

44

30

6
9

6
18

6
9

IS

—
—

6

6

9
—

9

17

Red eve
SIPE’
Bitotspot
Pterygium
Corneal opacity
Cataract
Discharge
Trachoma
Respiratory distress
Examined

4
o
1
g
18

14

4

5

4
5

—
2

—
—

3
2

1
—
1

—
1
I

t
16

4
10

?
10

<5
18

0
11

3
—
—
7
43

—

—

2

Note'- dumber of'mns^each duster max- exceed the total number of people in the duster. Some individuals exhibited more than one sign.
People. „ot eyes, were counted—for example', four red eyes equal four people with one or two red eyes each.

474

Andersson. Kerr Muir. Mehra, Saint.

Table 5 Relation between early eye symptoms and clinical
eye damage (Cluster number, in descending order)

Frequency of:
Burning
Photophobia
Difficulty in opening eves
SIPE ‘

7
7
2
6

8
1
7
4

1
2
5
3

5
8
8
1

2
5
1
5

3
3
3
2

6
6
6
7

4
4
4
8

SIPE, superficial interpalpebral erosion.

two exposure clusters (3/66), a finding that was
significant at the 0-5% level (/ = 9-3; OR = 5 8;
99-5% CI = 1-15-29-6). No abnormal afferent
pupillary reflex was detected in any of the clusters.
Discussion

The urgency of implementing this study so soon after
the disaster, in substantially less than ideal working
conditions, imposed several obvious defects in the
data set. It is difficult to extrapolate from the number
of deaths reported in this community based survey to
the likely number of overall deaths that resulted from
the disaster. Although the household survey in each
cluster was started from an arbitrarily selected house.
after which it proceeded from door to door, there mayhave been a tendency for some of the teams to move
towards the worst affected areas in each community.
Overall, however, the patterns of death were consis­
tent with the reported wind directions: first northerly
then moving westerly. The highest mortality was
observed close to the plant and on the south east side,
presumably reflecting the change in wind direction.
Allowing for the varying levels of exposure across the
reported 100 000 people in communities with quite
different density of housing, the official estimate of
2000 to 2500 deaths seems consistent with these data.
Perhaps the most sinking impression from the
affected communities in the days immediately after the
episode was the large number of people with cons­
picuous difficulty in breathing. Some of these had been
too disabled even to attend the local hospitals for
treatment. During the two month follow up it was
noted, again informally, that many of the children seen
during the first visit still had conspicuous breathing
difficulties. Such necropsy reports as are available
indicate that some deaths were related to acute
pulmonary oedema. Failure to record some basic data
on respiratory status for the whole study population
lost the unique opportunity offered by this survey.
carried out so soon after the event. The afferent
pupillary reflex indicates damage to the optic nerve
and impairment of this reflex could be taken as
evidence of neurotoxicity. The fact that this reflex was
normal in all groups cannot be taken as evidence that
neurotoxicity did not occur. The test may provide a

response to methyl isocyanate: results of a community based survey in Bhopal
pOsure and
i

475

be confounded by the fact that only the first four
useful baseline, however, for study over a lont
,hvl isocyanate can react with methylamine, the
symptoms were requested. Later symptoms, however
period.
"’ duct of its initial reaction with water to produce
important their relation to pathology, were not re­
Our analysis of symptoms related only to UjLcthyl urea.3 Various other oligomeric or polymeric
corded. It should also be reiterated that these initial
clusters where the deaths occurred, not to lj .,\ducts have been identified in the residues in the
symptoms were not directly associated with death of
individuals, so their interpretation in this context storage tank (S Varadarajan, 1985). Any of these
the individual with the symptom but only with the
limited. During the longer term follow up of survi«0 * u|d have had effects that are distinct from those of
areas where death rates were higher.
now in progress the predictive value of these synv \<]C. There could also be reactions between endogenDespite these caveats, there appear to be several
toms in relation to prognosis could possibly be teste. nUs substances and MIC or its breakdown products.
geographical contrasts in the survivor population of
The reported mortality in this study involved relative Thus people living in different areas could have
Bhopal. The most obvious contrast is between the
small numbers in each cluster. None the less, t| svmptom/pathol°gy patterns relating to exposure to
exposure and non-exposure clusters. Secondly, there
difference between clusters may provide a basis ft different chemical species. A counterindication to this
appears to be a contrast in findings between clusters
further inquiries into the distribution and frequencyt suggestion is our observation that although liquid
where deaths occurred (1-6) and the remaining two
immediate and delayed deaths and the prognosis! phase reactions between MIC and water are rapid, the
clusters. Thirdly, table 5 indicates that in certain
symptoms among survivors.
vapour reactions are (as would be expected) much
clusters (notably 4 and 6) relatively few survivors
The association of high death rates with reporlt slower and consistent with the persistence of a concenreported burning eyes and shortness of breath,
cough and diarrhoea among the first four symptoms trated cloud of MIC in its original form tor some
whereas cough, diarrhoea, respiratory distress, and
difficult to reconcile with the apparently inverse rel; hours.3
....
SIPE were more common. In clusters 3, 5, 7, and 8
lion between clusters where death was common it
On the other hand, laboratory toxicological
deaths were more uncommon as were clinical findings
those where shortness of breath was a frequer experiments have shown distinct symptom/pathology
of SIPE but a different pattern of symptoms was
symptom among survivors. A similarly curious findir croups al different dose levels for animals expose to
evident. Burning of the eyes, shortness of breath,
was the inverse relation between reported burning ( pure and continuously generated atmospheres o
photophobia, choking, twitching, and convulsions
the eyes as an early symptom of exposure and th MIC.5 Broadly speaking, these may be classified into
were all more frequent.
clinical finding of SIPE. Clusters 4 and 6, where SIPi neuropharmacological (anaesthesia and increased
The long term follow up of survivors should allow
was most commonly observed and burning of the eye sensitivity to subsequent anaesthesia), eye irritation
us to test the predictive value of these signs and
least frequently reported, were investigated by lu and damage (including a form of SIPE similar to a
symptoms associated geographically with high death
different teams. This implies that the apparent! seen in Bhopal survivors), and lung damage (acu e
rates, information which may be of substantial value
inverse relation is not the result of an observer induce bronchoconstriction and tachypnoea, pumonary
in preparing for and coping with the longer term
bias.
oedema, and in the longer term, fibrotic and mtlamhealth consequences of the disaster. The groups of
In some clusters the death rates may have been hig matory reactions). All these effect groups occurred at
symptoms with different patterns of death/survival in
enough for most people who had respiratory sy:t[ characteristic and different exposure leve s. in par
the various clusters implies that the gas has different
toms to have died, leaving alive only those who ver licular. sensory and neurological responses were
effects on people at different concentrations (or at
relatively free of symptoms. If this was so th noticed at relatively low doses, the eye damage w
different distances from the factory). This appears to
apparently direct relation with another respirator apparent at intermediate exposures, and the more
be a feature of the concentration dependent interac­
symptom (cough) would be difficult to explain. I obvious and life threatening manifestations o P
tion of the gas and its reaction products with human
could be argued that the excess SIPE observed i monary damage appeared at higher dose levels, it
tissue.
survivors from the clusters where deaths had occurre. these differences are considered capable o ex rapo
could result from their running away from th lion to the responses seen in the Bhopal survivors
This work was partly funded by the Royal Common­
exposure, as was done by many thousands of peopli differing distribution of symptoms between exp
wealth Society for the Blind. We acknowledge
This might increase the exposure of their eyes anc groups (and by implication, severity of exposure) may
gratefully the help of Dr Kalyani Madan tn execution
theoretically, their chances of survival. In reality, mo' ** interpreted as the complex response to varying
of the field work. We are humbly indebted to the
people who ran away went southward from the plan' degrees ofexposure in a gas cloud compose mi y
survivors of the disaster for their participation.
They thus moved with the cloud, not away fron i: cntirc!;. of MIC.
which would probably reduce rather than inercas
The surface of the eye is moist un er
V
their chances of survival. There was also no evident circumstances, so damage to this
References
of a difference between clusters where death rales wer reactive with water will be associated with damage to
I Andersson N. Kerr Muir M. Mehra V. Bhopal eye. Lancet
high and other exposed clusters in respect of pattern c other moist surfaces, including those of the lungs. The
survivors in clusters where deaths had occurred were
I984;ii:148l.
exodus immediately after the release of gas.
2 Andersson N. Kerr Muir M. Salmon AG. er al. Bhopal disaster.
The second and more plausible explanation is th! indeed at 12 times the risk of SIPE and six times the
eye follow-up and analytical chemistry. Lancet 1985:i:761 -2.
the relation between dose and overall response is mor risk of respiratory distress compared with other
3 Mantel N. Haenszel W. Statistical aspects of the analysis of data
exposed
people.
This
leads
us
to
the
tentative
con
­
from retrospective studies of disease. J Natl Cancer Inst
complex than the usual log-linear relation. Thcr.
1959:22:719-48.
appear to be at least two relatively distinct symptom clusion that the deaths resulting from the exposure,
4 Mantel N. Chi-square tests with one degree of freedom: extensions
reportedly pulmonary oedema, are associated geograpathology complexes which result from the exposur
of the Mantel-Haenszel procedure. Journal of the American
Phicali;.
with
cough
and
diarrhoea
as
early
symptoms,
(see tables 3 and 4). This could be because differcr
Statistical Association 1963:58:690-700.
•{nd
with
SIPE
and
respiratory
distress
as
clinical
5 Salmon AG. Kerr Muir M. Andersson N. Acute toxicity of methyl
pathological reactions occur at different doses.
isocyanate. A preliminary study of the dose response for eye and
It is theoretically possible that the gas cloud r.ia' ■mdings among the survivors.
other effects. Bril J Ind Med 1985:42:795-8.
The picture emerging from symptom patterns may
have had different constituent components after
certain time or in certain regions. We have shown th!

journal of Industrial Medicine 1990;47:553-558
You Xue-Yun, Chen Ji-Gang, Hu Yong.^

552
its effect on frequency of tumor recurrence. J Um lr
epidemiological information concerning the effects
of job difference on the incidence of bladder cancer in
those manufacturing benzidine derived dyes, and the
first report of a cohort study about cancer experience
among the users of these dyes. The results suggest
that the risk of bladder cancer exists mainly in the
presynthesis process of dye manufacture and the
benzidine derived dyes do not appear to be as
strongly carcinogenic as benzidine. This supports a
study that compared cases of bladder cancer in those
exposed to benzidine with those working in the dye
industry.25 It is too early to make firm conclusions
based on our results; however, it is necessary to
conduct cohort studies in various industries where
these dyes are used, and more experiments on their

„ .S’

■'

pelayed eye and other consequences from exposure
ip methyl isocyanate: 93% follow up of exposed and
i ■jnexposed cohorts in Bhopal

14

DHEW National occupational hazard survey—survey a>^tl
1? DHb
fntai tables. Cincinnati: US Dept of
Education and Welfare, Public Health Service, Onin k,
‘ Control National Insututc for Occupauorul Str
?„d HeaS wi.YDHEW (NIOSH) publ No 78-114
,. nSr» H-week subchronie toxicity uud.es of Area blurbs.
16 D Ml Is and direct brown 95 dyes. Cmcinnau: US
,
Heitb Edumffon and Welfare, Public Health Sen,
National Cancer Insututc, Division of Cancer Caux
Prevention^ Carcinogenesis Testing Program. 19,8 1-:.• rnHFW oubl No (N1H) 78-1358.)
17 Gbiva^es

metabolism; such studies are now in progress.

Department of Epidemiology, Shanghai Cancer Institute, « al.
Analysis of cancer incidence, mortality, and survival rates in
Shanghai urban area during the period of 1972-1979. Tumor
1982;2:385-91.
(In C,
Chinese.)
Waterhouse
J, Muir
Correa P, Poweu J. Cancer incidence in
five continents. Vol III. Lyon: International Agency for
Research on Cancer, 1976. (IARC sci publ No 15.)
- Haley TJ. Benzidine revisited: a review of the literature and
problem assodated with the use of benzidine and its
congeners. Clin
Toxicol
13-42.
I International
Agency
for f975;8:
Research
on Cancer. Monographs,
suppl 1. Chemicals and industrial process associated with cancer
in humans.
Vols 1-12.
Lyon: IARC, 1979.
5 Sakari
T, Marita
T, Marja-Liise
K, Erkki J. Cancer of the
urinary in Finland association. Int Arch Occup Environ Health

1960;46:43-51.
Wyndcr
E, Onderdonk J, Mantel N. An epidemiological inves­
tigation of cancer of the bladder. Cancer 1963;16:1388-407.
Anthony HM, Thomas KM. Tumors of the urinary bladder, an
analysis of 1030 patien” ui Leeds, England. J Natl Cancer Inst

1970;45:879-95.
- Yoshida
O, Harada TM. Bladder cancer in workers of dyeing
industry. Igaku no Ayunti 1971;79:421-2. (In Japanese.)
> Scott TS. The incidence of bladder tumours in a dyestuff
factory.
J Ind Med 1952;9:127-32.
) Ishizu SK.BrAdministration
of occupational bladder cancer with
unnary cytological diagnosis. Tokvo: Chemical Industrial Co,
1975:5—T,
13.the Japanese research group of bladder carcinoma.
1 Ishikawa
Clinical application of 2,5-di-acetyl-/?-glucaro(l-4)(6-3)
dilactone (SIA) to the bladder tumor, with special reference to

^dersson, M K Ajwani, S Mahashabde, M K Tiwari, M Kerr Muir, V Mehra, K Ashiru,
J) Mackenzie

istract
(follow up study three years after exposure to
sibyl isocyanate in 93% of exposed survivors
j “control” residents in 10 Bhopali comamities showed an excess of eye irritation,
^^J^^gen-earc -did infection, cataract, and a decrease in
S“S?ood W1S speew reference to highly mutagenic
aui acuity among the exposed people.
btathlessness was twice as common in the
arily exposed clusters as those with lower
1977:1561-77.
Prival MJ, Valerie PM. Analysis of a method for testing in. >- insure, a trend that could not be explained
for mutagenic activity in salmonella ryphimuniLT c e different age or smoking patterns (OR 2-05,
presence offlavin mononucleotide and hamster liver S. .Vm.
CI 1-36-3-08). Case referent analysis of
ResXue-yun,
1982;97:103-16.
i You
Zhou Yong-gui, Ye Xin-liang. Study cr. =. ’-•patient attendances at Bhopal Eye Hospimethod of the mutagenicity test for benzidine aa: r
iconsidering patients with severe refractive
derivatives. Chinese Journal of Industrial Hygiou *
*»■
Occupational Disease 1987;5:146-59. (In Chinese.
rrersand astigmatism as “controls,” showed
1 Thomas MR, Kenneth CM, Ching YW "'Charlr
n'—-*- W
'C 10 H7--M*)% increased risk of trachoma, 36%
Conversion of Congo red and 2-azo?”:
ceased risk of other lid infections, and 45%
following in vitro reduction by who!.
-ceased risk of irritant symptoms among
tnously exposed people. “Bhopal eye syn^Hygiene
-Kne” may thus include full resolution of the
-6al interpalpebral superficial erosion, a
3'«|uent increased risk of eye infections,
irresponsive
phenomena
(irritation,
“rkig, and phlyctens), and possibly
Igaku ~to Sebursugaku
■
tracts. It remains to be confirmed whether
•reflects a more generalised disease as a
•‘fluence of previous exposure to methyl
'laaate or whether it is only the eye that is
Accepted 17 July 1989

•Catenary Institute of Tropical Medicine, Lon.p®°ol of Hygiene & Tropical Medicine, London
Ashiru
Eye Hospital, Bhopal, Madhya Pradesh,

, '•'•at, S Mahashabde, M K Tiwari
t "^2^' °C Ophthalmology, St Thomas’ Hospi* Stair
^°®P5tah Fafudih, Raipur, Madhya
"ST" of Pathology, Michigan State UniverMI 48824 USA

The release of methyl isocyanate (MIC) on the night
of 3 December 1984 resulted in the death of at least
1700 people, most of them, it is thought, from acute
pulmonary oedema resulting from the burns occur­
ring during the exothermic reaction of MIC with the
water content of lung secretions and tissues.1’5 Dur­
ing this rapid chemical reaction, faster in the liquid
than vapour phase, MIC breaks down to methyl­
amine and the toxic dimethyl urea4; on its own, MIC
is probably capable of alkylating with a variety of
tissues containing amino (NH,) and hydroxyl
(OH) groups. The consequences of this on the
human eye were studied in eight clusters of exposed
households and two clusters of broadly comparable
but unexposed households in Bhopal, where all
occupants were first examined by a team of Indian
and British ophthalmologists in the two weeks
immediately after exposure before the mass exodus
from the city that occurred when the plant was
restarted a fortnight after the incident.5
Despite initial fears, no case of blindness attribut­
able to exposure to MIC was found in the clinical
examinations immediately after the disaster. The
early eye lesions found in Bhopal survivors, typically
a superficial interpalpebral erosion (SIPE) of the
cornea and conjunctiva,6 appeared to heal without
notable scarring within three months. Follow up at
one year confirmed this resolution of the initial
superficial erosion, but the complaint of excessive
watering and irritation was noted during follow up.4
Andersson and colleagues studied further the com­
plaint of excessive watering by comparing 989 cases
and 532 referents from outpatient records of the
Bhopal Eye Hospital. This confirmed that increased
risk of irritant eye symptoms was related to duration
of exposure to the gas and could not be accounted for
by age or social class. The conjunctival epithelium of
cases complaining of excessive watering appeared
normal on slit lamp examination and no abnormality
of tear drainage could be detected using crude duct
patency tests/
Parallel to the epidemiological follow up of the
survivors in Bhopal, a toxicological model of the eye
damage and other effects was developed by Salmon at
the London School of Hygiene and Tropical

Andersson, Ajwani, Mahashabde, Ttwari, Kerr Muir, Mehra, Ashiru, Maciu
l^jeye and other conseguencesfrom exposure to methyl isocyanate

Medicine using Lister hooded rats, in which species
the initial eye lesions closely resembled the human
lesions observed in Bhopal survivors.’0 Changes 14
months later included an eosinophilic and lym­
phocytic infiltrate in the conjunctival mucosa and in
the perilimbal regions, more prominent in animals
that were more heavily exposed.” A subsequent
larger study in rats confirmed chronic inflammation
of the glands of the eyelids which included cystic
changes and degeneration of these organs, alterations
that were more pronounced in more heavily exposed
animals and which increased with time."
We describe here the three year follow up of eight
exposure and two non-exposure clusters in Bhopal
and the results of a case-control monitoring scheme
established at the Bhopal Eye Hospital immediately
after the disaster, which now permit evaluation of
accumulating clinical evidence that these eye changes
noted in exposed animals may also occur among man.

Methods
Eight exposed and two unexposed clusters of house­
holds, where all surviving residents were examined in
the two weeks after the disaster, were followed up
over three years. Selection of the clusters and details
of the initial examination have been described else­
where. People examined after the initial two weeks
who were not part of the original population of the
community eye programme have been excluded from
this analysis. Children bom to mothers in the original
exposure or non-exposure cohorts were included in
the analysis, as were people who died in the course of
follow up if a “verbal necropsy ” from two neigh­
bours or relatives confirmed the likely cause of death.
All examinations followed the same format and
were carried out by the same observers. A brief
questionnaire was administered in Hindi, inquiring

Table 1

about age, exposure history, main health probl
eye problems, medical treatment, and smok
habits. The eye examination was detailed, includ
slit lamp and fundoscopy of all residents of
clusters in the Bhopal Eye Hospital com:..unity
programme.
One
ophthalmologist
examined nearly 70°o of participants at least tu.
over the three years. Vision was tested with
without the use of a pinhole; colour vision
afferent pupillary reflexes were measured to test i"
damage to the optic nerve. Standard definitions v,-.
used to describe opthalmic conditions encounter-Data were analysed using standard statist!procedures.12"14
. Results of this cluster cohort analysis genera-hypotheses for testing on the much 'arger ba~
derived from the Bhopal Eye Hospitr
:h, over <
months, received some 50 000 new Outpatients. Soafter starting the hospital, which provides relief:
gas exposed victims with eye problems, a recce.
system was inaugurated allowing rapid mana
extraction of large series of cases of the eye condiucc
in question to consider their exposure histon. aand sex, and presenting complaints. Referents crtrols) were people from the same community an.
attending hospital with eye problems who
found to have a refractive error greater than r:
diopters or astigmatism (and no other defect. Ar
and sex were taken into account in
inalysu r
stratification. Social class is a compue-ted issue r
India and was only taken into account in as mu~ r
both cases and referents presented voluntarily s: trhospital from the same catchment area complain-'
of eye problems.
Results
.Table 1 portrays the age and sex distributive
people followed up in the 10 cluster cohorts c-

Age and sex distribution of 10 cluster cohorts: follow up December 1984—April 1988 (Malelfemc

corroborated by formal testing ofvisual acuity, under
conditions where neither subjects nor observers
knew the outcome of the baseline 1984 tests (table 3).
The differential loss in visual acuity between exposed
and unexposed people could not be explained by
different age structure of the populations. People in
the higher exposure clusters were more than twice as
likely to suffer deterioration in visual acuity than
people in the lower exposed clusters (OR 2-2,
Zmh 2-9,95% CI 1-29-3-75, stratified for age).
Among the other symptoms volunteered in res­
ponse to the open question “Do you have any other
health problems?” chest pain, breathlessness, and
vomiting or nausea were more frequent among
exposed than non-exposed people and more common
aiisofthc data missing by the end of three years of
among the heavily exposed than those who lived in ■
clusters that received lower exposure (table 4). The
xs up. Data could not be obtained on only a small
-piruon of the original cluster cohorts and some
complaint of breathlessness was more pronounced
among the more heavily exposed and could not be
x. «ere seen at least once during the three years or
rj died during the follow up period. Only one
accounted for by different age structures or smoking
habits in the different exposure categories (table 5).
-non refused follow up examinations, in cluster 5.
Stratifying for age and smoking simultaneously,
□cog the 379 original residents in the eight
xsed clusters, all but 15 (4%) were examined
people in higher exposure clusters were twice as
likely to report breathlessness as people in the lower
jo or had died during the three years. Among the
I (originally unexposed people, all but 20 (17%)
exposure clusters (OR 2-05, zmh 3-453, 95% CI
1-36-3-08) and 2-7 times more likely than those in the
' n re-exammed during three years of follow up,
cist all of them between April and October of the
no-exposure clusters (OR 2-73, zmh 3-69, 95% CI
iyear.
1-6-4-66).
hr symptoms reported by people followed up
More acute inflammatory trachomatous changes,
1 x three years in response to the question “Do you
trachomatous injection (TI) and follicular trachoma
(TF), were found among the higher exposure than
-any eye problems?” (table 2) indicate an excess
mtant eye symptoms (OR 1-91, zmh 2-98,
lower exposure clusters (OR 3-165, zmh 2-11,
CI 1-25-2-92) and of the complaint of loss of
95% CI 1-085-9-23). In the three years of follow up
« (OR 1-65, zmh 2-29, 95% CI 1-075-2-53)
5% of the unexposed people developed cataracts,
rithe highly exposed compared with the lower
whereas 8% of those with lower exposure and 10% of
’’Bi clusters. The complaint of loss of vision was
those with higher exposure developed cataract. The
risk of developing cataract in the higher exposure
clusters was nearly twice that in the other groups
41 Visual acuity loss* by age group in the cluster
^■follow I. - December 1984-April 1988. i percentage
(OR 1-99, zmh 2-001,95% CI 1-014-3-9). There was
among each age group j
no new case of altered afferent pupillary reflex or loss
of colour vision.

clusters

Louexposure
clusters

Cluster type

In = 201 f

>n = 161J

Breathlessness
Chest pain
Cough
Vomiting nausea
Diarrhoea
Headache
Abdominal pain
Weakness lethargy

109(54%!'
75(37%'
67 (33-..)
48(24",.)
35 (16%) J

57(35%'
19(12%)
32(20%)
10(6%)

12 (6%)

14(9%)

High

Small discrepancies in totals in clusters 1,2,4, 5, and 9 are due to births in these communities.

No
exposure
clusters
9,10
in = 97)

0
14(14%)
5(5%)
U(ll%)

10 ‘he qUCS"011: ‘'Do
have any other health
+ I rend with increasing exposure, / 22-03 2df p = 0-000

Andersson, Ajwani, Mahashabde, Tiwari, Kerr Muir, Mehra,

eye and other consequences from exposure to methyl isocyanate

556

557

Table 5

Breathlessness by age group in the cluster cohorts: follow up December 1984-April 1988. (percentage affected

among each age group)

'

--------- _---------------------------- _-------------------------------------No exposure clusters
Low exposure1 clusters
9,10
3,7,8
(n = 97)
(n = 161)

High exposure clusters
Cluster type

(n = 201)

No breathless

109 (54%)

Smokers

Non-smokers

fr-

6+

b-

Smokers
6+
b—

12
10
12
7
7
1
1

9
21
15
15
16
4
6

0
0
5
0
!
4
0
4
8
H
3
4
4
o
0
114
1125
0
1
0
0

b—

6+

b—

0
1

0
0

11
12

3°
15

0
0

o
1

a

7
g
?

15
?
5

7
7
5

3
0
3
0

3
5
4
2

■
3

’
blon-smokeri
~b+
7T

Smokers
b+

Age (y)
0-9
10-19
20-29
30-39
40-49
50-59
60-69

28 (29%)

57 (35%)

Non-smokers

*

'

—

b+ = Breathless; b— = not breathless.
Stratifying
simultaneously
for age and
smokingRR of people
with higher exposure
compared
with lower exposure OR 2-05, yrnh 3 45, 95% Cl 1 -36-3-08.
RR of people with higher exposure compared with no exposure OR 2-73, ymh 3-69, 95% CI 1 -6-4-65.
RR of people with lower exposure compared with no exposure OR 1 53, yrnh 1-47, 95% CI 0-87-2-69.
The suggestion from the cluster cohort analysis of
an association between exposure to MIC and eye
infections, irritation, and cataracts was confirmed in
the case-referent (case-control) analysis of first
attendance outpatients at the Bhopal Eye Hospital.
Over the period January 1987 to June 1988, acute
infection of the eyelid (blepharitis, chalazion, and
sty) was proportionally more common among people
exposed to MIC than among those non-exposed. To
derive an estimation of relative risk, given that many­
exposed people attended the hospital for complaints
potentially related to MIC, cycatricial trachoma
(TC) and tarsal plate involvement (TT) was chosen
as a reference entity for acute eyelid inflammation. If
these conditions are delayed consequences of
exposure then they are unlikely to have developed in
the short period since exposure to MIC. This
comparison produced a 47% excess risk of acute fid

Table 6 Signs found bv examination of the eye .-follow up
December 1984-April 1988. (percentage affected)

Cluster type
Trachoma (TI, TF)
Trachoma (TT, TC, CO
Conjunctivitis
New pterygium
New corneal opacity
New cataract
Loss of visual acuity
Abnormal colour vision
Abnormal afferent
pupillary reflex

High
exposure
clusters
1.2.4-6
tn = 201)
15(7%)
10(5%)
62(31%)
8(4%)

exposure
clusters

No
exposure
clusters
9,10

(n = 161)

19(12%)

10(10%)
10 (6%'

48 (24%)

Numbers represent people affected (one or two eyes).
A single subiect may present more than one sign.
“New" indicates occurrence during three years of follow up,
derived by subtracting signs detected in 1984.

inflammation among the exposed (/mh 2-72,95-. C
1-114—1-94). Comparison of cases of new trachccj
(inflammatory and follicular) and advanced l-«
choma (TT, TC) illustrated a preponderance of nrtrachoma among previously exposed pay.(OR 1-25,/mh 1-99,95% CI 1-18-1-45). This am
of recent trachoma infection was sustained w—
severe refractive errors and astigmatism- were usee i
a reference entity, stratifying simu:
usly for it
andsex(OR l-42,zmh3-83,95% Ci 1 .9-1-7, u.7).
Over the same 18 month period, the nsi c
phlyctenular keratoconjunctivitis was higher
people exposed to MIC than among those
exposed. Using pterygium, a non-infeca’conjunctival lesion, as a comparison entin. relative risk of phlyctens among exposed people ••
2-6 times that in non-exposed people (OR 2-W. P2-76, 95% CI 1-22-5-26) when the data
stratified for age and sex. There v- also
that people exposed to MIC wer
e
unexposed people to complain v. ..-arenas •
irritation as a presenting symptom, using the plaint of watering alone as the reference (OR 1-3, /mh 6-16, 95% CI 1-18-1'451 or
refractive errors and astigmatism (OR 1 5,7"’95% CI 1-33-1-58) as a reference group .
stratified for age and sex. Although there
apparent excess relative risk of cataract
people of al! exposure categories together, therr
statistically significant difference between ■ __ .

higher exposure and those with I-' ’.•portrayed in table 8 (OR 1-3, .
1 -23-1 -5), using refractive errors as : eren-

Discussion
oinni"
The cohort analysis of clusters in tne

ns achieved, suggests a threefold excess of eyelid
dammation, twofold increase of new cataracts, and
ess of visual acuity among the more severely exposed
jesters. Heavily exposed people were twice as likely
? complain of breathing problems as people with
ti: exposure, and three times more likely to do so
anunexposed people.
Although it was clear who had been exposed and
•bo had not, by virtue of their residence (nongvsed clusters were 11 km and 14 km away from
st Union Carbide plant), neither examiners nor
First attendees at Bhopal Eye Hospital with
'^K!:,y,au-rcf‘r‘ni monitoring, January 1987-June
11G exposure history, less than or greater than one

participants knew how the exposed clusters had been
classified as lower and higher exposure. This clas­
sification was based on early deaths associated with
exposure in these areas,’ not on distance from the
Carbide plant or on subsquent long term clinical
findings. Clusters 1, 2, and 4-6 were classified as
higher exposure whereas clusters 3, 7, and 8 were
regarded as having a lower exposure. Thus whereas it
is impossible to exclude observer or participant bias
between exposed and non-exposed clusters, it is
highly unlikely that the differences between higher
and lower exposure clusters can be explained by this
possible observer bias.
The case-referent analysis confirms an excess of
recent infections and irritant symptoms in people
exposed to MIC. If this phenomenon is limited to the
eye it could possibly be explained as iatrogenic.
Indiscriminate and long term use of eye drops,
including those containing steroids, has been a
notable feature since the disaster. It is virtually
impossible, under field conditions, to obtain accurate
and detailed medical histories on previous use of
medication, which makes this plausible explanation
difficult to exclude. Almost everyone attending the
Bhopal Eye Hospital reports using some previous
medication for their eye problems. Yet the findings of
continued irritation and recurrent infections in peo­
ple previously exposed to MIC are in keeping with
histopathology from the toxicology experiments,’-11
where evidence of dose related and progressive
chronic inflammation (eosinophil and lymphoid
infiltrates in the conjunctival submucosa and, in the
eyelid glands, epithelial dysplasia and chronic
inflammatory infiltrates) was found in the absence of
any medical treatment. Effects of MIC on the
immune system could provide a coherent explanation
for the different findings.15
In its response to MIC the eye could be considered

Andersson, Ajwani, Mahashabde, Tiwari, Kerr Muir, Mehra, Ashiru, Mackcn^

yph Journal of industrial Medicine 1990;47:559-565

Assessment of urinary protein 1 and transferrin as
early markers of cadmium nephrotoxicity

a “sentinel organ” for more general phenomena in R K Bagia in the fieldwork and manual analysis of ththe rest of the body. So far, there is no evidence of outpatient data from Bhopal Eye Hospital. Thhospital and the community eye care services^ frodamage to central or peripheral nerve tissue, as tested
in the eye by colour vision and afferent pupillary which the clinical records and cluster coh ns werreflexes.11’ Fundoscopy, which permits direct derived, are supported bv the Royal Come, nwealSociety for the Blind. The opinions expressed in th?
appraisal of arteries and veins, has not yet shown any
Bernard, H Roels, A Cardenas, R Lauwerys
abnormality associated with exposure to MIC. This article, however, are our views and not necessarii.
corresponds with the absence of cardiovascular find­ those of the Society.
ings in Salmon’s animal toxicology model.6-11
The acute superficial interpalpebral erosion is
probably similar in chemical nature to the “bums”
lbstract
urinary proteins which reflect the functional
caused to the lung by the exothermic reaction of MIC
transferrin and protein 1, a sex linked a2- integrity of the tubule or the glomerulus according to
1 Kamat SR, Mahashur AA, Tiwari AKB,« al Early observance
with water in mucous secretions. In the eye this
on pulmonary changes and clinical morbidity due io re
nicroprotein, were assayed in urine from 58 their size. Low molecular weight proteins such as fl2isoevanate gas leak at Bhopal, J Postgrad Med 1985;31-.63-TZ
lesion heals rapidly, apparently without scarring
writers exposed to cadmium (Cd) in a non- microglobulin (/J,-m),’ retinol binding protein
e Dave JM. The Bhopal methyl isocyanate incident: an ovctvkv
(tables 6 and 7). Toxicological study of the lungs
In: Schiefer HB, ed. Highly toxic chemicals: daecnm m
jrrous smelter and from 58 age matched (RBP),’6 or Zi-microglobulin’ are currently used for
showed severe and progressive changes including
protection methods. Proceedings of an intern.:-symponm.
-ferents
These two new markers of screening for proximal tubular injury’ whereas the
September 19S5 Saskatoon Canada. Can
nvenuv e
neoplastic and cystic change of the bronchial epith­
rrphroto'cicity were compared with urinary assay in urine of a high molecular weight protein such
Saskatchewan, Toxicology Research Cent:
- 5.1-37
elium, dramatic increases in peribronchial lymphoid
3 Karol MH. Respiratory effects of inhaled isocyanates. CRC O.
j.-microglobulin (/i,-m), retinol binding as albumin permits the assessment of glomerular
Rev
Toxicol
1986;16:349-79.
tissue, and abnormal syncitialising activity of the
-rotein (RBP), albumin, and ^-N-acetyl- filter selectivity, at least before tubular function is
4 Andersson N, Kerr Muir M, Salmon A, er al. Bhopal duaurr
epithelium inside pulmonary tissue.11 Similar chan­
eve follow up and analytical chemistry. Lancet 1985a;7al-:
pucosaminidase (NAG). The response of compromised.6’ According to recent studies the
5 Andersson N, Kerr Muir M, Mehra V. Bhopal eye. Lamr
ges in man, if these can be confirmed in postmortem
xotein 1 to Cd tubulotoxicity was similar to urinary activity of /i-N-acetylglucosaminidase
studies, may be related to the complaint of breathles­
6 Andersson N, Ken Muir M, Mehra V, Salmon AG. ExnoieeSat of /l.-m, RBP, and NAG. In Cd workers, (NAG) is also a sensitive indicator of excessive
sness in the cluster cohorts, more frequent with
and response to methyl isocyanate: results of a canc.rrotein 1 had a correlation with urinary Cd absorption of Cd.1011
based suXev in Bhopal. Br J Ind Med 1988:45:460-75
increasing severity of exposure and which is not
r=0-56) similar to /L-m (r = 0-48), RBP
7 Andersson Nj Kerr Muir M, Ajwam MK, Manashabec 5
In this study we have assessed two new potential
Salmon A, Vaidyanathan K. Persistent eye watenng nx;
accounted for by smoking or age.
r = 0-58), and NAG (r = 0-49). Values of these markers of incipient Cd nephropathy, urinaryBhopal survivors. Lancet 1986;ii:l 152.
If the apparent excess of cataracts found in this
iree low molecular weight proteins and of protein 1 and transferrin. Protein 1 is an r8 Salmon AG, Kerr Muir M, Andersson N. Companwe r
study is confirmed by larger investigations now
toxicology and epidemiology for methyl isocyanate at Bwx
\AG were increased only in workers with microprotein (molecular weight 20 000) which may
Hum Toxicol 1987;6:410-411. (Abstract.
under way a possible explanation may be found in the
trinary Cd higher than 10 pg/g creatinine. be the equivalent in man of the androgen dependent
9 Salmon AG, Kerr Muir M, Andersson .
dramatic kidney and liver damage found in the
methyl isocyanate: a preliminary studv o: ’.rinary transferrin and albumin were rat a2u-globulin.12 It is a sex linked protein that is
toxicological model developed by Salmon.11 These
eve and other effects. Br J Ind Med 198o;-- < - ’-o
__
onilarly affected by exposure to Cd. Their excreted in greater amounts in the urine from men
10
Gassert
T,
Mackenzie
C,
Kerr
Muir
M,
Andersson
N.
Si=^
effects were more advanced in animals that experi­
■sponse, however, was clearly more sensitive after puberty. The origin of urinary protein 1 is
AG. Long term pathology of lung, eye and other
enced higher doses of MI C and progressed with time.
following acute exposure of rats to methyl isocyanate, ljsban that of low molecular weight proteins. unknown but the data we have so far collected
1986;ii:1403.
„
., ..._
v
The apparent increased occurrence of infections, and
btvalences of positive values of these two high suggest that it might constitute a new marker of
11 Mackenzie CD, Andersson N, Cameron K, Kerr
allergic/inflammatory complaints in the human eye,
Salmon A, Gassert T. Longer term
Sonx
Mlecular weight proteins were not only impaired tubular reabsorption.12
isoevanate
exposure
in
Lister
hood
rats,
possib
.
p
m the light of increasing evidence of multisystem
other but also tended to rise at lower concenUrinary transferrin was determined because
for Bhopal disaster victims. 4m J Expl PartaHi V
damage in toxicological models, raises the possibility It Mantel
rations of Cd in urine or blood. This finding recent studies suggest that it may be a more sensitive
N. Chi-square tests with one degree
extensions of the Mantel-Haenszel procedure
of generalised systemic long term consequences
’Rests that in some subjects subtle defects in index of glomerular barrier defect than the micro­
StatisticalAssociation
„
statistical
Association 1963,58^690-70^
lvoo;50:o’y-' “'_
resulting from exposure to MIC. To exclude this, it 13 American
Mantel N,HaenszelW.S.at.sncal aspects of mejmaly-s^
ktnerular barrier function may precede the albuminuria test.1’1’ These two markers have been
is necessary to study formally the occurrence of
from retrospective studies of diseases. J
’"et of proximal tubular impairment after assayed in the urine from workers exposed to Cd in a
1959;22:719-748.
, c.m.-minfections, allergies, and deaths from these condi­
-runic exposure to Cd. It remains to be asses- non-ferrous smelter and compared with urinary fl214
Oleinick A, Mantel N Family studies r
tions. Much light will be shed on the issue when
Whether these subjects are more at risk of m, RBP, albumin, and NAG. The relation between
1970:22:617-625.
. . . r,. cesystematic evaluation of human postmortem material 15
Karol MH, Kamal SR. The antibody
■"doping renal insufficiency.
these biochemical markers and indicators of
isoevanate experimental and chmeal Im ■
from lungs, spleen, liver, and kidneys becomes
exposure to Cd was also examined.
Phvsiopathol Respir 1988;23:591-1, , colour”*1'
16
Mergler D, Blain L, Lagace JP. Solv“O.-rar h-"
available.
loss: an indicator of neural damage? Ini A
'*
early
nephrotoxic
action
of
cadmium
(Cd)
in
Health 1987;59:313-21.
We acknowledge the support of Dr A K Dube, Dr A
*■ on be detected on the basis of several urinary or
Materials and methods
Dale, T P Yadav, S K Tiwari, G S Kushwaha, and Accepted 5 February 1990
‘’’ibome markers.1-’ Tests that are currently
STUDY POPULATIONS
The study was conducted on 58 male workers
.'^'-•bended for the health surveillance of populaexposed to Cd rely on the measurement of exposed to Cd in a non-ferrous smelter. The control
group consisted of 58 age matched men recruited
from a factory with no risk of exposure to Cd or other
heavy metals. None of the exposed workers or
■tq^y Industrial Toxicology and Occupational referent subjects was occupationally exposed to lead
s*2.t|?e’ Catholic University of Louvain, Clos or mercury as shown by the concentrations of these
*'Cy^-aux-Champs, 30.54. B-1200 Brussels,
metals in blood (<35pg.T00ml) and urine
(< 5 ngig creatinine). The characteristics of the two
H Roels, A Cardenas, R Lauwerys
populations are summarised in table 1.

©hU £

Jtoumal of Experimental Biology
^August 1987, pp. 531-534

| Acute Toxicity of Methyl Isocyanate and Ineffectiveness of Sodium
Thiosulphate in Preventing Its Toxicity
R VDAYARAGHAVAN & M PKAUSHIK’
■

Department of Toxicology and Chemistry*, Defence Research and Development Establishment,
Gwalior 474 002, India
Received 15 September 1986; revised22 May 1987

pfc lDj0 (mgJtg-1 body wt)of pure methyl isocyanate (MIC) when given subcutaneously was 328.6 and 261.3 in male
&
ind female rats, and 81.9 and 85.3 in male and female mice respectively. The oral LDS„ in male rats was 51.5 mg.kg-'.
8L The LC» for 30 min exposure in a static chamber was 1046.5 mg.m-3 in rats (female) and 267.6 mg.m-3 in mice (male).
Sodium thiosulphate, given before or after MIC treatment had no beneficial effects. Estimation of cyanide in plasma,
K’ lh-er and brain did not show any significant increase in MIC treated rats when compared to controls, while 1/40 LDJ0
K of potassium cyanide given subcutaneously, produced significant elevation of cyanide level.

’ jjahyl isocyanate (MIC) an intermediate in the pro'jttion of carbamate insecticides appears highly le[3H. Surprisingly very little information is available
[&tbe toxicity of MIC1-5. Therefore, in this study
[ Sy toxicity of pure MIC in experimental animals
investigated by different routes of administration.
for sodium thiosulphate (STS) has been reported
an effective antidote when administered to
I'lBC victims its role if any, in pure MIC poisoning in
I as has also been investigated.

' Js Mserials and Methods
-Animals—Wistar rats (120-140 g) and Swiss albi® mice (18-22 g) bred in the laboratory were used.
T Se animals were housed in polypropylene cages
*> rats per cage or four mice per cage of same
.
®with dust free rice husk as the bedding material.
laocn chow (Hind Lever feed) and tap water were
■
libitum. Before the experiment the animals
'
^lasted overnight while water was given ad libii
• -J*

■

tai capacity was 21.5 1 including all the tube connections. The inner diameter of the mouth was 100 mm
so that a hand could pass through easily for keeping
the animal (rat or mouse) or taking it out. The flask
was fitted with two B-14 joints at the sides, one was
used as an inlet and the other was used as a port for
monitoring inside temperature, humidity, etc. The
outlet was at the top of the flask. A closed circuit
pump with a displacement capacity of 30 lanin-1
connected to the flask ensured mixing of the air.
MIC was loaded using a microlitre syringe in the
side test tube on a piece of Whatman grade I filter
paper kept in it. When the pump is switched on MIC
vapourises instantaneously and diffuses into the in­
halation chamber. The pump was switched on every
five min for 15 sec, for thorough mixing of the air in­

and chemicals—AH chemicals used were of
gradesynthesised6 was of above
^•Purity (gas chromatographic analysis). STS
i?*IO'ution) was obtained from Dr Franz Kohler

“ru*GmbH-

^ministration of MIC—MIC was administered
- -Si Subcutaneous (sc), oral (po) and inhalation
sc route, MIC was dissolved in olive oil,
Cr1 '* was found to be-stable for at least one day
-•> E^wnatographic analysis) and injected dorsal-

12*

route’ MIC was fed through a 20 gauge
needle.
■^cr t0 have a beter safety and also to lower
^•consumption a static chamber was used for
Jt® toxicity, consisting of a 20 1 flat bottomed
. a flat flange joint at the top (Fig. 1). The to-

Fig. 1 —Assembly for inhalation exposure static type

INDIAN J EXP BIOL, VOL. 25, AUGUST 1987

side the chamber. A teflon joint with a silicone di­
aphragm fixed at the top was used for sampling the
chamber air. As MIC is highly reactive, only silicone
tubes were used for the connections and silicone
grease for the joints. At a time, only one rat or three
mice were exposed (loading complement < 1%)
and the duration of exposure was only 30 min. Once
the exposure was over MIC was neutralised by turn­
ing the three way cock, and removing the test tube
connection with the pump on. The chamber air was
passed through a gas wash bottle containing sodium
hydroxide solution.
Analysis of chamber atmosphere—Three different
concentrations (100, 200 and 400 ppm) of MIC
were developed inside the chamber without animal
to find the effeciency of the inhalation assembly. A
20 ml sample of the chamber atmosphere was with­
drawn at intervals of 2,5,10,20 and 30 min. The
samples were taken in chilled toluene and injected
in gas chromatograph using OV-17 column. More
than 90 % recovery was obtained in all the con­
centrations and intervals. But for all calculations,
only theoretical concentration was used i.e. weight
of agent injected to volume of the chamber.
LD50 calculation—MIC was administered as a
single dose or single exposure and the animals were
observed for mortality up to 48 hr. For each dose/
concentration between 5 to 8 animals wre used.
LDS0 and LC50 were calculated by probit analysis7.
STS was given (ip) either immediately after or 10
min prior to MIC administration and protection in­
dex calculated.

TV
. ,
LDso with STS
Protecnon index (PI) = —----- —------ —LD50 without STS
Estimation of cyanide—Cyanide was estimated in
plasma, liver and brain in female Wistar rats. The an­
imals were lightly anaesthetised with ether and max­
imum blood was collected in heparinised vials from
the retroorbital plexus. After cervical dislocation,

liver and brain were removed and homogenised in
0.1 ANaOH (5% homogenate). Cyanide was esti­
mated spectrophotometrically8. The analysis was
carried out immediately after collecting the blood
and tissue samples.

Results and Discussion
LDi0 studies—Immediately after sc injection the
animals looked sedated. Hind limb paralysis and de­
creased respiratory rate were noted. Higher doses
produced gasping (mouth breathing). Mostly death
occured after 6 hr. In doses higher than LDJ0 the an­
imals showed severe convulsions and gasping and
died within 1 or 2 hr. By po route the symptoms
were similar to that of sc route, except that the gasp­
ing was more prominent. When the animals were
subjected to MIC vapour inhalation, irritation of the
eye was the first symptom observed in both rats and
mice. Within 5 min after exposure, gasping started
and was more prominent in rats. By inhalation expo­
sure also, death occured only after 6 hr. Piloerection
was observed in rats. Rectal temperature was mar­
kedly reduced and was very low in animals given
MIC sc and po than by inhalation. Post mortem (imTable 2—LCJ0 Values with MIC in Female Rat
and Male Mouse

Log
Cone.

Cone.
(mg.m-3)

No. of
animals/
experiment
Female Rat

No.
died

Monalitv
%

2.85
3.00
3.10
3.20

707.9
1000.0
1258.9
1584.9

5
8
6
5

0
4

5

0
50.0
66.7
100.0

1
2
A
6

66.7
100.0

Male Mouse
6
6

199.5
223.9
316.2
562.3

2.30
2.35
2.50
2.75

6

Table l-LD50 of MIC by Different Routes
Route of
administ­
ration

Species

Sex

sc
sc
sc
sc
po
inh
inh

rat
rat
mouse
mouse
rat
rat
mouse

M
F
M
F
M
F
M

'LC51, (t - 30 min) in a static chamber. Values mg.m-3
M = male; F=female

532

’

LDso
(mg.kg ')

95%
confidence
limit

328.6
261.3
81.9
85.3
51.5
1046.5’
267.6’

319.0-338.6
229.9-296.8
80.3-83.5
80.7-90.2
49.5-53.6
903.6-1211.8'
215.5-331.6’

16.7

VUAYARAGHAVAN & KAUSHIK: ACUTE TOXICITY OF METHYL ISOCYNATE

^ ' mediately after death) showed blood clots and edeW" ma 111 t^e I™1®5 ™
three routes, both in rat and
X mouse. Kimmerle and Eben1 also reported acute
Si lung edema as the cause of death in MIC inhaled
W rats. A very prominent oozing wound with necrosis
W of the adjoining skin at the injection site was found
W jo days after sc injection in all survived animals.
S Table 1 shows LD50 and LC50 of MIC by different
gk routes. The various concentrations used for the lef thality study by inhalation and the percentage of
L death in each is given in Table 2. MIC is more toxic
S' t0 mouse than rat. This is contrary to the findings of
’£ Dodd et al9, though the concentration time product

of LC50 of mouse is more or less same in both stud­
ies (present study; 8010 mg.min.m~3 and Dodd et
ah 10102 mgjnin.m-3). As MIC is a highly reactive
compound, it reacts very quickly with —OH, - SH
and - NH2 groups10. That is why MIC injected sc is
less toxic. As it is also a highly corrosive agent parti­
cularly to the mucus membranes1, it may cause ex­
tensive damage leading to death. This may be the
reason that MIC is more toxic by po route and in­
halation.
Effect ofSTS—SIS was given (ip) immediately af­
ter administering MIC to rats and mice. Only in
mice it gave considerable protection (H = 2.2).

Table 3—Shift of LD50 with Sodium Thiosulphate Treatment
Route of
administ­
ration of
MIC

Species

Sex

Dose of
STS
(mg.kg-1)

Route of
administ­
ration of
STS

LD,„
(mg.kg->)

337.3
(315.6-360.4)
186.0
(170.8-202.6)
940.8***
(797.8-1107.0)
243.1 •**
(208.8-283.3)

sc

rat

F

250

ip*

sc

mouse

F

50

ip*

inh

rat

F

250

ip**

inh

mouse

M

10

iv**

PI

1.3

2.2
0.9

0.9

'.i F«female; M = male
■STS given immediately after MIC.
"STS given 10 min prior to inhalation.
~LCM(t = 30 min) in a static chamber. Values are mg.m”3.
Figures in parantheses are 95% confidence limit.

Table 4—Cyanide Levels in Plasma and Tissues After Potassium Cyanide and MIC Treatment

Dose
<mg.kg-')

Sacrificing
time after
poison (hr)

Cyanide level

No.
Plasma
Ag-dl~‘

Liver
Ag-g-1

Brain
Ag.g-1

6

0.70
±0.12

3.10
±0.25

1.37
±0.09

5

1.89**
±0.24
5.59—
±0.51
45.03***
±2.52

3.73*
±0.12
4.13**
±0.21
4.65*
±0.60

1.90
±0.30
1.66
±0.25
2.85—
±0.21

1.04
±0.21
0.95
±0.15
0.81
±0.20

3.40
±0.24
3.17
±0.17
3.49
±0.21

1.50
±0.21
1.75
±0.30
1.33
±0.10

7

d

5
5

5

hire; Values mean ± SE
-^‘"’'.Omg.kg-'sdSax")

,

llw6-5 mg.m 3 for 30 min exposure.
<0.001

533

INDIAN J EXP BIOL, VOL. 25, AUGUST 1987

Where MIC was administered by inhalation STS
failed to protect (Table 3) and even the LD50 was not
shifted significantly (PI = 0.9). Further raising the
dose of STS was not beneficial in protecting the ani­
mals when MIC was given by inhalation.
To further confirm the results, female rats were
given LC50 dose of MIC by inhalation and were sac­
rificed at different time intervals. The amount of cy­
anide in plasma, liver and brain were estimated. For
comparison KCN was given sc at three different
doses of LD50 (1/40, 1/4 and 1). The results (Table
4) show that the level of cyanide in MIC treated ani­
mals was similar to that of the control. But KCN giv­
en at a very low dose of 1/40 LD50 produced signifi­
cant raise in the amount of cyanide both in plasma
and in liver. Nemery et al2 also showed that STS
could not ptotect against MIC poisoning. Thiocyan­
ate in urine was shown to be decreased rather than
increased by Nemery et al.2 and Salmon et al4. The
present results show that there is no evidence of cy­
anide produced in the body following administra­
tion of MIC (1 LC50) which explains the finding that
STS has no beneficial effect in MIC toxicity.

for his keen interest and encouragement and to Dr
R K Srivastava for his valuable suggestions. The au­
thors are thankful to Dr B R Gandhe for GC analy­
sis, to Messrs M Srinivasan and Hari Afley for fabri­
cating inhalation exposure chamber and secretarial
assistance respectively.

Acknowledgement
The authors are grateful to Dr PK Ramachandran

11

534

References
1
2
3
4
5

6
7
8

9

10

,

Kimmerle G & Eben A Arch Toxikol 20 (1964)233.
Nemery B, Sparrow S & Dinsdale D, lancet, ii (1985) 1245
Nemery B, Dinsdale D, Sparrow S & Ray D E, BrJ Ind Med.
42(1985)799.
Salmon AG, Kerr Muir M & Andersson N, BrJ Ind Med. 42
(1985)795.
Ferguson J S, Schaper M, Stock M F, Weyel D A& Alarie Y
Toxicol Appl Pharmacol 82 (1986) 329.
Raguveeran C D & Kaushik M P, J Chromatogr, 34 6 (1985)
446.
Finney D J, Probit analysis (Cambridge University Press.
London) 1977.
Feldstein M & Klendshoj N C. J Lab Clin Med, 44 (1954)
166.
Dodd D E, Fowler E H, Snellings WM, Pritts IM & Baron R
L, Fundam ApplToxicol 6(1986)747.
Cohen S & Oppenheimer E. in The chemistry of cyanates
and their thio derivatives, edited by S Patai (John Wiles
and Sons, New York) 1977,923.
Sax N I, Dangerous properties of industrial materials (Van
Nostrand Reinhold Co, New York) 1984,2273.

fHE LANCET, JUNE 3, 1989

1259

the Cancer and Steroid Hormone (CASH) group’s data proves
correct, as seems probable, one would agree with him that “the
results of all major studies thus appear to be consistent with some
jicrease in risk in women aged up to about 35"?
The Committee on Safety ofMedicines (CSM) makes a “bottom
jjfie” statement {Current Problems no 26) that there is no need for a
change in prescribing practice. I agree, bur only ifthis is interpreted
that we continue to present the risks and benefits as fairly as we can
p young women but leave to them the decision whether to use the
method. This should now mean raising the cancer issue routinely in
counselling, not omitting the protective effects against at least two
malignancies (ovary and endometrium). The contraceptive and
Dan-contraceptive benefits of combined oral contraceptives may
seem so great to many as to compensate for almost any likely lifetime
risk of breast cancer, especially as the UK NCCS group has already
shown this to be lower for modem low oestrogen pills. One of the
luthors of UK study (M. C. Pike, personal communication)
hypothesises that the risk could be lower still or absent after use of
the currently most popular brands with the new progestogens
oesogestrel and gestodene since they raise sex-hormone binding
globulin.
The main findings suggest that the incidence under age 36
changes from one in 500 to one in 300-350 for users of combined
oral contraceptives for four or more years. Dr Elizabeth Wilson of
the National Association of Family Planning Doctors proposes to
explain this as follows: imagine a meeting-hall filled with 1000
iverage young women. 2 will have to receive treatment for breast
cancer before their 36th birthday. Now fill the .hall with 1000
women who have all taken the pill for four or more years before this
age and there will be 3 under treatment—2 who would have
developed breast cancer by then anyway, and 1 who, if she had used
a different contraceptive, would either have avoided the disease or
(possibly) would have had it later. This helps to put things in
perspective: though as Dr Malcolm Pons has said “the jury is still
om on the whole matter of the pill and breast cancer”.
Mirgaret Pyke Centre for Study

Ito Square,
Lmdoc W1V 51 W

J. GlIlLLEBAUD,
Medical director

l.Pno J. Oral contraceptives and breast cancer: is the CASH study really negative?
Lmcrr 1989; i: 552.
LONG-TERM EFFECTS OF METHYL ISOCYANATE

Sir,—The focus on hydrogen cyanide (HCN) in your Round the
^orld correspondent’s report (April 29, p 952) regarding the
fi»pal disaster is potentially misleading. The release of methyl
sxxanate (MIC) resulted in at least 1700 deaths—most of them, it
1thought by clinicians who were in Bhopal soon after the event,
acute pulmonary oedema resulting from the bums during the
k tijhly exothermic reaction of MIC with water in lung secretions
5“ tissues, and not HCN. During this very rapid reaction MIC
Ct®ks down to methylamine and the toxic dimethylurea: it is also
P'fbable that, on its own, MIC can alkylate a variety of tissues that
°xnain amino and hydroxyl groups. In vitro MIC itself can also
Jfoduce “cherry red blood”, due to the formation of methylamine?
^Poiments with laboratory animals produced evidence
ftc°cnpauble with cyanide involvement in the fate of Bhopal
^ivors.3-4 Cyanide is not necessary to explain any of the acute
<5cas- Acutely MIC is several times more toxic than HCN, but the
danger of . a mistaken emphasis on cyanide is .the
^^stimation of long-term effects. Cyanide is unlikely to
^uce long-term effects while MIC exposure is associated with
^“dtrabie long-term effects.
survivors from Bhopal chronic effects on the lungs have
documented up to two years after the event? A large
Control study confirmed that increased risk of persistent
eye symptoms was related to duration of exposure to the
•^Similar long-term ocular effects were found by other
■jj^ians.7 Several studies of Bhopal survivors suggest long-term
logical effects, including the potential of MIC to produce
P’^itivity reactions? Developmental and reproductive

effects seem probable940 and neuromuscular complications may also
be a problem area.7
Few toxicological studies have been done on the long-term
consequence of exposure to MIC, but the evidence is not
encouraging. ECG abnormalities were found in rats four months
after a single exposure. Chronic respiratory damage and chronic eye
inflammation appear to be important features. Formal
immunological studies indicate persistent bone marrow
suppression, suppression of the lymphoproliferative responses of
splenic leucocytes to B and T cell mitogens^ and decreased
thymus/body weight ratios. MIC is also mutagenic, and increased
fetal deaths and reduced placental weights and fetal body weights
were observed in mice exposed to MIC during gestation.
Carcinogenicity studies are underway.
The evidence from human and toxicological studies is not easily
explained by the presence or absence ofHCN. It now seems certain,
however, that there are long-term multisystem consequences of the
exposure to MIC. Further research is best directed at MIC and its
degradation products, with special attention to immunological
consequences of exposure. To exclude such consequences among
survivors formal study of infections and allergies is required. Much
light will be shed on the issue when systematic evaluation of human
post-mortem material becomes available.
For further references see Environ Health Perspect 1987; 72: pp 35,95,133,
139,143,149,159,169,183,189. A full list of 32 papers on the toxicology of
MIC is available.
TUC Centenary Institute
of Occupational Health,
London School of Hygiene
London WC1E 7HT

NEIL ANDERSSON

1 Andersson N, Kerr Muir M, Mchra V, Salmon AG. Exposure and response to methyl
isocyanate: results of a community based survey in Bhopal. BrJ Ind Med 1988; 45:
469-75
2. Salmon AG. Bright red blood ofBhopal victims: cyanide or MIC? BrJ IndMed 1986;
43:502.
3. Nemery B, Dinsdale D, Sparrow S, Ray D. Effects of methyl isocyanate on the
respiratory tract of rats. BrJ Ind Med 1985; 42:799-805.
4. Bucher JR, Gupta BN, Adkins B, et al. Toxidty of inhaled methyl isocyanate in
F344/N rats and B6C3F1 mice. Acute exposure and recovery studies. Environ
Health Pcrspca 1987; 72:53-61.
5. Kamat SR, Patel MH, Pradhan PV, et al. Sequential respiratory psychologic and
immunologic studies in relation to MIC exposed subjects at Bhopal. interim report
of analysis after two years followup. Bombay, India: Department of Respiratory
Medicine, Seth GS Medical College.
6. Andersson N, Kerr Muir M, Ajwaiu MK, Mahashabde S, Salmon A, Vaidyanathan
K. Persistent eye watering among Bhopal survivors. Lancet 1986; ii: 1152.
7. Misra NP, Pathak R, Gauri KJBS, et al. Clinical profile of gas leak victims in acute
phase after Bhopal episode. Indian J Med Res 1987; 86 (suppl): 11—19.

clinical findings. Bull Eur Physiopaihol Resp 1988:23:591-97.
9. ICMR. Health effects of the Bhopal gas tragedy. New Delhi, India: Indian Council of
Medical Research, 1986.
10. Kanherc S, Darbari BS, Shrivastava AK. Morphological study of placentae of
expectant mothers exposed to gas leak at Bhopal. IndianJ Med Res 1987; 86 (suppl):
77-82.
DIFFICULTY IN DETECTION OF HERNIA AND
HYDROCELE IN CRYPTORCHIDISM

Sir,—To avoid treatment of retractile testicles, boys suspected
of undescended testes should be examined by experienced
investigators? But how accurate is the expen in identifying
concurrent inguinal abnormalities such as hernia and hydrocele,
which represent contraindications to hormonal treatment?
We examined 121 consecutive boys (135 testes) who were found
to be truly cryptorchid by a consultant in paediatric surgery.
Median age was 6 years (range 0-15). The preoperative position was
compared with the intraoperative finding, and classified as not
palpable, ectopic, intracanalicular, in the superficial ring, pubic, at
the penile base, and just above the scrotal base. In 7 cases, a hernia
was found preoperatively and a hydrocele was found in 1 patient.
The intraoperatively found positions correlated significantly with
preoperative findings (Spearman’s rho = 0-72, p <0-001), but a
further 24 inguinal hernias were found and 6 other boys had
unexpected hydrocele (table).
The frequency ofhernia is similar to other series? The diagnostic
probabilities indicate that palpation alone is not sufficient as a test

©hi : Y

-

rassegne

Health effects
of the Bhopal
gas teakr
B F6VI0W

Ramana Dhara
Dept, of Environmental & Community
Medicine Umdnj - Robert Wood
Johnson Medical School - Piscataway,
NJ 08S54

Introduction

The world’s worst industrial disaster
occurred in India on the night of Decem­
ber 2-3, 1984. The accident took place at
the Union Carbide plant situated in Bhopal^
(pop..900,000) the capital city of Madhya
Pradesh, one of the largest states in India.
The accident was apparently initiated
by the introduction of water into the met­
hyl isocyanate (MIC) storage tank resul­
ting in an uncontrollable reaction with
liberation of heat and escape of MIC in
the form of a gas. Safety systems like the
flare tower (to burn excess gas), caustic
soda scrubber (for neutralization) and the

refrigeration unit were either hot functio­
ning or inadequate to deal with the large
volume of escaping chemical [1].
This paper reviews health' effects of gas
exposures from published human studies
and discusses some of the clinical and epi-'
demiological issues being debated. Because
of the relative paucity of information, the
author has also reviewed unpublished
data from studies conducted by local phy­
sician groups. Some of these studies have
helped to highlight specific health pro­
blems from the disaster and initiate more
organized research to address these pro­
blems. The reader may also wish to con­
sult articles by John Bucher [2] and Mehta
et al. [3] for reviews on human and animal
toxicology.

Manufacturing Process
Methyl isocyanate (CH3-N=C=O) is an
intermediate product in the manufacture
of carbaryl (Sevin), a carbamate pesticide.
The process begins with a mixture of car­
bon monoxide, and chlorine to form pho­
sgene. Phosgene is then combined with
monomethylamine to form methyl iso­
cyanate. Methyl isocyanate is further
mixed with naphthol to produce the end­
product, carbaryl.

Chemical and Physical Properties
Ricevuio: febbraio 1992
Vcrsione dcfiniliva acceiiata: ottobre 1992

2g

Epidemiologia e p/eeemione n. 52, 1992

MIC is a clear, colorless liquid with a
pungent odor (b.p.: 39’C, f.p.: -80°C, s.g..-

0.96, m.w.: 57.1, vapor pressure of348 mm
Hg at 20°C). It is moderately soluble in
water and hydrolyses on contact to form
carbon dioxide and methylamine. When
MIC is ■ pyrolyzed in the temperature
range of 427-548°C, decomposition pro­
ducts like hydrogen cyanide and carbon
dioxide are formed [4].

Toxicological Properties

MIC is highly irritant to the skin, eyes
and mucus membranes of the respiratory
tract. This irritant property is based on its
reactivity with water which enables it to
penetrate tissues and interact with pro­
tein. Absorption through the skin is
known to occur [5], Because the ACGIH
TLV of 0.02 ppm is less than the mucus
membrane irritation threshold, p> 0.4
ppm), and the odor threshold (> 2 ppm),
the compound is considered to have poor
warning properties [6]. t

Exposure Conditions

It is estimated that about 27 tons of
methyl isocyanate escaped from the two
tanks in the plant during a period of one to
two hours [1]. The release occurred
around midnight with adverse prevailing
atmospheric conditions (inversion and a
low wind speed) which prevented disper­
sion of the gas [7], Eyewitness accounts
report that a cloud of gas enveloped the
area and moved slowly along.
Because of the unexpectedness, time
and brief period of release of the gas, air
monitoring was not possible nor was it
subsequently attemptted.
Based on quantity of the chemical
released and area of spread, (40 sq. km)
the Central Water & Air Pollution Con­
trol Board estimated MIC concentration
to be about 27 ppm (7], a figure which is
about 1400 times that of the OSHA work­
place standard of 0.02 ppm for 8 hrs. This
calculation, however, assumes equal con­
centration over the whole area of conta­
mination and does not account for varia­
bility of concentration with distance.
Using an analytic dispersion model, Singh

RASSEGNE

and Ghosh have provided simulations of
exposure concentrations at various distan­
ces downwind of the plant [8]. Twenty
seven sites were identified with ground
level concentrations ranging from 85.6 ppm
to 0.12 ppm with a median of 1.8 ppm.
Factors contributing to variability in
human exposure include distance of resi­
dence from the plant, duration of expo­
sure and activity during exposure. No
systematic attempts have been made to
reconstruct individual exposure based on
these criteria. In the actual incident, acti­
vity during exposure to the gas was cer­
tainly a major dose-regulating factor. The
Ante irritant effects of MIC created panic,
^reat anxiety and disorientation, resulting
in people running out oftheir homes. The
running resulted in increased ventilatory
rates in these people, thereby increasing
the dose of the chemical delivered to the
respiratory system. The Medico Friend
Circle study reports exposure history and
safety measures taken by people at the
time of the gas leak [9]. In a study sample
of 158 persons, 124 ran out oftheir homes.
Only 12 persons used a wet towel or blan­
ket as a safety measure.
Major organs of exposure to the gas
were the eyes and respiratory tract. Signi­
ficant amounts of MIC were also, most
probably, dissolved in saliva and swallo­
wed into the gastro-intestinal tract. Skin
exposure certainly took place but was less
clinically important than the respiratory
tract.
A cohort of 80,021 has been registered
Am the population residing around the
onion Carbide plant and classified as
mild, moderate and severely exposed
based on mortality rates in each area [10],
An unexposed population in Bhopal was
used to select the control group of 15,931
individuals.

Characteristics of the exposed population
In the exposed areas, about 53% of the
population comprise of Hindus, 45.6% are
Muslims and the rest are Christians and
Sikhs. In 1985, the monthly income of
80% of the population was below Rs 145/
month ($6) and only 1.25% earned over

Rs 465/month ($18). By 1988, 65% of the
population was earning below Rs 145/
month, indicating some improvement in
economic level. However, the above figu­
res indicate that most of the exposed
people are close to the government-defi­
ned poverty level of Rs 300/month ($12).
Ten percent of the population are smo­
kers, 1.4% alcoholics and 5.5% chew
tobacco. Only 34% of the population live
in a ‘pacca’ (permanent) house [10].

Mortality
Of the more than 200,000 persons expo­
sed to the gas, the initial death toll within
a week following the accident was over
2,500. In Nov. 1989, the Dept, of Relief &
Rehabilitation, Govt. ofMadhya Pradesh,
placed the toll at 3598 [11). Dr. SR Kamal,
a pulmonary physician who has conduc­
ted studies on a large number of gas vic­
tims, states that most of the later deaths
appear to be occurring from respiratory
complications (personal communication,
1990). Mortality rates are declined but
were still slightly higher in the severely
exposed area (8.75/1000) in comparison
with the control area (7.5/1000) during the
period May 1989-Mar90 [10].

Overall Morbidity

Symptom prevalence surveys conduc­
ted by the Indian Council of Medical
Research (ICMR) indicate that morbidity
was higher in the exposed areas (26%) as
compared with the control area (18%)
during the period Nov 1988-Mar 90.
About 11% of people experienced 2 or
more spells of illness in a 1-year period.
Respiratory, ocular and gastro-intestinal
symptoms account for most of this morbi­
dity. This trend appears to be persistent in
the survey conducted in the latter part of
1990 [12].

Ocular Problems

The intensely irritating effect of MIC
on the cornea resulted in severe ocular

burning, watering, pain and photophobia
[13]. Examination of the eye showed
involvement ofthe corneal and conjuncti­
val epithelium with redness of the eye,
corneal ulceration and lid swelling. Fortu­
nately, the corneal ulceration in most
cases turned out to be limited to the
superficial layers of the cornea. Slit lamp
examination showed discrete lesions in a
band across the interpalpebral area, punc­
tate keratopathy, conjunctival chemosis
and some pigmentary deposition on the
cornea [14], Relatively few cases of iritis
were seen [15]. Treatment at the initial
stage consisted ofsalinc eyewashes, pupil­
lary dilatation and topical antibiotics.
Andersson and others performed a fol­
low-up study on the eyes of survivors 9
months after the accident and reported
that no case of blindness could be found
that could be attributed to gas exposure
among the nearly 20,000 persons atten­
ding the Bhopal Eye Hospital [16]. Howe­
ver, they did find persistent cycrwatcring
and other chronic irritant symptoms like
burning, itching and redness. Raizada and
Dwiwedi [17] studied eye pathology
among 1140 exposed persons and found
that the main chronic lesions were chro­
nic
conjunctivitis, deficiency of tear
secretion and persistent corneal opacities.
Animal experiments conducted by Sal­
mon [18] on male Lister hooded rats indi­
cate that the most severe effects on (he
eye occur al exposure levels of 65 ppm.
Andersson et al. [19] performed a fol­
low-up of93% of exposed and unexposed
Bhopal residents 3 years after exposure. .
Their findings indicated an increased risk
of eye infections, hyperresponsive pheno-1
mena, (watering, irritation, phlyctens),
excess cataracts and resolution of the cor-/
neal erosions in exposed persons. These
phenomena have been characterized as
the ‘Bhopal eye syndrome’. The authors
state “in its response to MIC, the eye
should be considered a ‘sentinel organ’
for more general phenomena in the
body”.
Though there is no evidence that severe
damage to the eye’s external and internal
structures has occurred, the single acute
exposure seems to have resulted in a chro­
nic inflammatory process. The problems

Epidemiologia e preventions n. 52, 1992

23

RASSEGNE

of persistent eye watering in some cases
and tear secretion deficiency in others
coupled with chronic conjunctivitis indi­
cate that there is some damage to the eye
epithelium. It is conceivable that housing
conditions in the Bhopal slum areas like
overcrowding, poor ventilation and expo­
sure to dust and smoke may exacerbate
the ocular effects causing irritation and
infections.

Respiratory Toxicity
Acute symptoms ofthe respiratory tract
were mainly due to the irritant action of
MIC on tissues. Because MIC is modera­
tely soluble in water, lesions were seen in
both the upper and lower respiratory tract.
Predominant symptoms were cough
accompanied by frothy expectoration, a
feeling 6f suffocation, chest pain and
breathlessness [20], Other symptoms
included dryness and irritation of the
throat and rhinorrhea.
Autopsies on 300 victims revealed
severe necrotizing lesions in the lining of
the upper respiratory tract as well as in the
bronchioles, alveoli and lung capillaries.
Enlarged and edematous lungs, con­
solidation, hemorrhage, bronchopneu­
monia and acute bronchiolitis were seen
[211.
Follow-up studies were conducted 2.53 months after the accident by a team
from the Industrial Toxicology Research
Centre (ITRC) at Lucknow, India [22].
Exposed persons were contacted and
requested to come forward voluntarily to
be examined. A total of 1279 men, women
and children were examined. In these
studies, radiological examination of the
lungs was carried out on 903 subjects to
assess damage to the respiratory tract.
Out of 164 abnormal X-rays, 65 were
determined to have specific radiological
changes which were considered to have
occurred or aggravated as a result of gas
exposure. These were classified into two
groups:
Group A (48 subjects) were those with
radiological abnormalities thought to
haye occurred as a result of gas exposure.
These changes were haziness in different
24

Epidemiologia e pfevenaione n. S2, 1992

zones of the lung, hilar prominence, fine • nued to be exposed for a few days to trap­
mottlingand reticulation. 16 ofthe 48 sub­
ped gases in victims. This 60-yr old nonjects had respiratory symptoms (cough,
smoker had no respiratory symptoms
chest pain/tightness, breathlessness) cli­
(other than bouts of cough) till the begin­
nical signs (adventitious sounds) and
ning of 1989 when he started complaining
abnormal lung function. Twenty subjects
of severe cough and breathlessness on
had respiratory symptoms but clinical
exertion. Pulmonary function showed a
examination and lung function were nor­
mild obstructive ventilatory defect and
mal.
CT scan revealed subpleural thickening,
Group B (17 subjects) showed abnor­
punctate lesions and bilateral septal scars,
malities suggestive of old disease which
suggesting that extensive pulmonary
was aggravated (symptoms appearing
fibrosis had occurred.
after exposure) by exposure to the gas.
Though isocyanates are known to be
These abnormalities were tuberculosis,
allergenic in the lung [26] the respiratory
chronic bronchitis and pneumonitis.
toxicity of MIC appears to be primarily
Spirometry was carried out on 783 sub­
due to its irritant nature. Follow-up stu­
jects from the above sample to determine
dies with lung biopsies done six months
after exposure showed evidence of inter­
respiratory impairment [23]. Vital capacity
(VC), forced vital capacity (FVC) and for­
stitial fibrosis and bronchiolitis oblite­
rans. These findings were similar to those
ced expiratory volume in 1 sec (FEV,„,
found in ^gveral animal studies [27,28]
FEV,) were the main parameters recor­
ded. Impairment was classified as restrict
thus revealing the close association bet­
five (VC or FVC < 80% of predicted),
ween animal data and clinical findings in
Bhopal victims.
obstructive (FEV/FVC < 70%) and a
combined pattern (FVC < 80% of predic­
ted and FEV./FVC ratio < 70%).
'
The results showed that 39% of the , Reproductive Toxicity
sample was found to have some form of
Concerns that the gas leak had effects
respiratory impairment. The combined
on reproductive health were raised early
pattern of impairment (obstructive and
restrictive disease) had the highest preva­
in 1985 when reports indicated that men­
strual cycle disruption, leucorrhea and
lence in the sample (22%). Smoking had
no effect on the prevalence of this impair­
dysmenorrhea had occurred in gas-exposed women [29]. Risk to the fetus was con­
ment. Females suffered more mild and
sidered because of exposure to the gas and
moderate impairment. Severe impair­
factors like stress, anoxia and ingestion of
ment was equally distributed (2.4%)
various prescribed drugs like antibiotics,
among the two sexes.
Broncho-aivcolar lavage fluid was ana­
bronchodilators, and analgesics.
lyzed in 36 mild, moderate and severely
An epidemiological survey by Varma
[30] showed pregnancy loss and infant
exposed persons and 12 unexposed nor­
mal controls 1-2.5 years after exposure
mortality to be high in gas-exposed
[24], The results indicated that severely
women. In a sample of 865 women who
lived within 1 km of the plant and who
exposed smokers and non-smokers sho­
wed a significant increase in alveolar
were pregnant at the time of the gas leak,
43% of the pregnancies did not result in
macrophages. Based on these results, the
live births. Of the 486 live births, 14% of
authors concluded that an inflammatory
alveolitis may be present in severely
babies died in the first 30 days as compa­
red to a death rate of 2.6% to 3% for
exposed subjects and that long-term
follow-up must be done to determine if previous deliveries in the 2 years prece­
further impairment of lung function
ding the accident in the same group of
occurs.
women.
Sharma el al. [26] report the interesting
A pregnancy outcome survey of gascase of a resident of the gas-exposed area
exposed women [31] using historic con­
who, in his professional capacity, conti­
trols, demonstrated a four-fold increase in

RASSEGNE

different. The authors concluded that
pal, there was concern amongst the health
though the results.may indicate a residual
authorities that the population might
experience an increased rate of infections.
effect on T-cell precursors, further studies
are required to demonstrate an exposurePossible reasons for this increased susccp;,
tibility included depressed immune func­
elfect relationship. .
Short-term tests using Chinese hamster
tion from chemical effects, psychological
and physical stress, disruption of normal 1
ovary cells showed induction ofSCEs and
life (particularly during the 2 mass migra­
chromosomal aberrations both without
and with activation by S-9 mix from Arotions out of Bhopal), and pulmonary ,
clor-induced rat liver [37]. Sex-linked
injury.
recessive tests in Drosophila and the
Immune function was studied [35] in
Ames test were negative. The Ames test
exposed subjects from the ITRC sample
was also found to be negative by Shelby
two and a half months after exposure to
[38]. Meshram and Rao [39] using a diffe­
ascertain whether any change had occur­
rent pre-incubation procedure for the
red in the immune status. Humoral
immunity was assessed by quantitation of
Ames test (10°C for 60 min instead of the
immunoglobulins (IgG, IgM, IgA) in over
independent of maternal pulmonary
standard 37°C) found MIC to be weakly
300 exposed and 10 non-exposed persons.
damage and that MIC could be directly, mutagenic.
Shelby et al. [38] performed genetic
Cell-mediated immunity (CMI) was
fetotoxic. In the Bhopal situation, results
assessed by phagocytic activity of lympho­
from the animal studies, when considered
toxicity testing on B6C3F1 mice exposed
cytes and quantitation ofT-cell rosettes in
with the findings from human epidemio­
to MIC by inhalation. Analyses on lymp­
hocytes, bone marrow and lung cells were
19 exposed and 8 non-exposed persons.
logy, suggest that exposure to MIC is feto­
Results from this study showed that no
toxic and that this is probably the result of
done using single and multiple exposures.
difference in mean immunoglobulin
a direct effect on the fetus.
Multiple exposure experiments in the
mice showed increased frequencies of
levels was found when compared to con­
SCEs and chromosomal aberrations which
trols. The T-cell population (28%) was
found to be less than half that found nor­
were not seen in 2 hr exposures. Delay of
Genotoxicity and Carcinogenicity
cell-cycle time was also reported [40,41],
mally in the Indian population (65%).
Significant depression of phagocytic acti­
Chromosomal studies were done two
While animal and in vitro studies
and a half months after the gas leak to eva­
demonstrate MIC’s potential for genoto­
vity of lymphocytes was found as compa­
xicity, it is not clear that such toxicity has
luate genetic damage among the sample
red to controls.
of gas-exposed survivors studied by (he
Concurrent with the human studies,
actually occurred in exposed humans.
ITRC [35]. Blood was collected from 31
To assess carcinogenic potential, rats
immunotoxicological evaluation of rats
exposed adults and a similar number of
and mice were exposed to MIC for 2 hrs
exposed to MIC showed a number of posi­
age and sex-matched unexposed controls
by inhalation. Marginal increases of
tive results (44). Alveolar and peritoneal
to assess the occurrence of chromosomal
pheochromocytomas of the adrenal
macrophage function was depressed and
Serrations (breaks and gaps) in lymphomedulla and adenomas of the pancreas
exposed rats were susceptible to E. coli
"tes. The results show a significantly. were seen but these tumors were-tjot consi­
endotoxin. Delayed type hypersensitivity
increased (p < 0.001) number of breaks
dered clearly related to the exposure [42],
was assessed by injecting sheep RBC’s
and gaps In the exposed subjects. No fol­
A population-based cancer registry has
into the foot pads and was found to be
low-up studies were done to see if this
been established in Bhopal in 1986 to
impaired. Based on these results, the
effect was persistent.
study possible carcinogenic effects of the
researchers concluded that the gas had a
Cytogenetic studies were done 3 years
gas leak. All cases of cancer are being regi­
suppressive effect on cell-mediated
after exposure on a sample of 40 male and
stered and categorised by exposure area
immunity.
43 female exposed persons [36], Results
[10]. Though it has been predicted that
Karol and Kamat [26] found MlC-specifrom this study showed statistically higher
MIC has a significant potential for cancer
fic antibodies in guinea-pigs injected with
frequencies of chromosomal aberrations
induction [43], it is not expected that the
MIC as well as in 12 of 144 human survi­
in the exposed group as compared to 46
onset of gas leak-related cancers, if any,
vors. This showed that MIC was capable
age and sex-matched unexposed controls.
will occur before the 30-40 yr lag period.
of eliciting an immunogenic response.
The aberrations were in the form of
The antibody titers in the human studies
breaks, gaps, dicentrics, rings, tri and quawere low and transient suggesting a weak
dri-radial configurations and were more
Immunotoxicity
response.
pronunced in female subjects. Sister chro­
Limitations of the human studies
matid exchanges were not significantly
Following exposure to the gas in Bho­
include the relatively small sample sizes,

spontaneous abortion rate. Alteration in
menstrual cycle lenght was also observed.
Animal experiments conducted by Schwetz [32] and Varma [33] exposing pre­
gnant mice to MIC by inflation showed
that this exposure does indeed havea fetotoxic effect. Varma observed a concentra­
tion-dependant increase in embryo loss,
decrease in fetal and placental weights
and a 20% reduction in length of mandible
and bones of the extremities.
Varma et al. [34] studied the contribu ­
tion of maternal hormonal changes and
pulmonary damage to fetal toxicity of
MIC in rats and mice. Their findings sho­
pped that fetal toxicity of MIC was partly

Epidemiologia e prevenzione n. 52, 1992

25

RASSEGNE

choice of control groups and unclear
exposure ascertainment. The above limi­
tations make it difficult to arrive at defini­
tive conclusions regarding immunotoxi­
city from MIC exposure for the gas vic­
tims.

numbness, a sensation of pins and needles
in the extremities and muscle aches.
To assess whether MIC was toxic to
muscle, Anderson et al. [47] evaluated the
effects of MIC on rat muscle cells in cul­
ture. Al lower doses, the formation of
muscle fibers was prevented. At higher
doses, death of fibroblasts and myoblasts
was seen. The findings suggested either
an effect on muscle differentiation or
selective toxicity to myoblasts.

symptoms of syncope, and extreme weak­
ness. Autopsy studies done by Dr. Heeresh Chandra at the local medical college
showed two features considered to be cha­
racteristic of cyanide poisoning. These
were cherry-red discoloration of the blood
and other organs, and the unpleasant odor
of “bitter almonds” when the lungs were
Psychological and Neuro-behavioral Toxi­
opened [48],
city
A double-blind clinical trial was perfor­
med by the ICMR 2 months after expo­
Srinivasamurthy and Isaac [45] noted
sure to determine the efficacy of sodium
that psychological problems of Bhopal
thiosulfate as an antidote to the poisoning
survivors fell into four major categories.
Clinical Problems
[12]. The trial was done on 30 gas-exposed
1.
Post-traumatic
stress
disorders
symptomatic patients who were admini­
which occurred as a result of the tremen­
Paucity of information on the toxico­
stered sodium thiosulfate, a cyanide anti­
logy of MIC had created a great deal of
dous emotional stress of the disaster.
dote, intravenously. The results showed
confusion and debate about the manage­
Symptoms were anxiety, emotional recall
alleviation of symptoms with an 8-10 fold
of the event, restlessness, sleep disturban­
ment of the gas victims. The medical
increase in thiocyanate excretion in the
system in Bhopal was severely tested by
ces and generalised weakness and fatigua­
urine for 10 out of 15 patients and served
the twin factors of large numbers of inju­
to fuel suspicion that cyanide poisoning
bility. j
2.
Pathological grief reactions charac­ red people streaming into hospitals and
was involved. (Thiocyanate is the water­
terised by intense grief, depression, suici­
the absence of a definite protocol for treat­
soluble detoxification product of cya­
ment of the poisoning. Patients were trea­
dal ideation and guilt feelings arising out a
nide).
sense of failure to protect their family.
ted on a symptomatic basis. For ocular
On the basis of this study, the ICMR in
February 1985 recommended the use of
3.
Emotional reactions to physical pro­ problems, alropinizntion of the eye, local
blems: victims with ocular, lung and other
antibiotics and padding were used [14].. sodium thiosulfate on a mass scale for
Respiratory problems were treated with
detoxification of symptomatic gas-expo­
problems developed feelings of depres­
bronchodilators, steroids, diuretics, anti­
sed persons. Union Carbide denied the
sion, hostility, insecurity and helpless­
biotics and oxygen administration.
possibility of cyanide poisoning and toxi­
ness.
4.
Exacerbation of pre-existing psy­
Questions of clinical importance, some
cological experts around the world were
of which still persist to this day, are:
either unsure or skeptical about cyanide
chiatric problems.
In a psychiatric out-patient serrvice pro­
- Were there toxins other than MIC
[1].
gram set up specifically for gas victims,
In this atmosphere of confusion, the
released in the accident?
Sethi el al. [46] detected 208 persons suffe­
- What were the specific antidotes?
local health authorities in Bhopal failed to
ring from mental problems. Of these, 45%
- Did cyanide poisoning occur in the
carry out The recommendations of the
were suffering from neuroses, 35% from
victims and, if so, how was it manifest and
ICMR on a widespread and systematic
anxiety states and 9% from adjustment
what was the source of the cyanide?
basis.
reactions.
- Docs MIC enter the blood-stream and
The scientific hyphoteses seeking to
Neuro-behavioral tests were conducted
cause multi-systemic disease?
explain the source of the cyanide poiso­
on 350 exposed subjects two and a half
- What were the risks to exposed pre­
ning and the apparent effectiveness of
months after the accident [22], Auditory
sodium thiosulfate fell into three catego­
gnant-women and the unborn child?
aqd visual memory, attention response
- There is no doubt that MIC was
ries:
speed, and vigilance were found to be
clearly the major toxin released in the
1.
Cyanidefrom an external source: That
significantly impaired in this group as
accident. However, the circumstances lea-- the entry and mixing of water with MIC in
compared to controls. No effect was seen
ding to the release (hydrolytic and exot­
the storage lank resulted In a violent exot­
on manual dexterity.
hermic reaction of water with MIC) raised
hermic reaction al high temperatures (>
the possibility of impurities (phosgene) or
420°C)) which led to the decomposition of
decomposition products (hydrogen cya­
MIC to hydrogen cyanide, carbon mono­
Neuromuscular Toxicity
nide, nitrogen oxides, carbon monoxide)
xide and nitrogen oxides. This reaction
being present in the gas cloud.
was first discovered by Blake and MaghNeuromuscular symptoms in Bhopal
Suspicion that some of the early deaths
soodi in 1982 and was documented in the
survivors have persisted since the gas leak
were due to cyanide poisoning arose from
NIOSH Occupational health guidelines
[10]. These symptoms are mainly tingling,
the reporting of rapid fatalities and acute
for MIC [49].

RASSEGNE

2.
Cyanidefrom an Internal source'. That cyanide may result in an underestimation
of the long-term effects of MIC.
the MIC was being converted to some
Persistent multi-systemic symptoms
form of cyanide after being absorbed into
the body resulting in enlargement of the
have been reported by Bhopal survivors.
That exposure to MIC can produce repro­
body’s cyanogen pool. .
3.
Thiosulfate effective against MIC: ductive health problems has been shown
in human and animal studies [55]. Fergu­
That sodium thiosulfate was alleviating
son and Alarie [56] have demonstrated
the symptoms caused by MIC toxicity.
that there may be a physiopathological
(Sodiurq thiosulfate was hitherto unk­
basis for the persistence of multi-systemic
nown as an MIC antidote).
symptoms in Bhopal survivors. Their stu­
Investigators from India [50] investiga­
dies on experimental anirqals have shown
ted the first of the three hypotheses by
that radio-labeled MIC is capable of being
pyrolysing MIC at 350°C and found that
absorbed and distributed throughtout the
cyanide was produced even at this lower
body. These findings have been confir­
temperature as a decomposition product.
P'hey further injected the decomposition
med by Bhattacharya el al. [57] who have
shown that MIC binds covalently to tissue
products into rats and found that brain
proteins in its active form and not as its
cytochrome oxidase activity (the bioche­
breakdown product, methylamine.
mical basis for cyanide toxicity) was signiThere is no known antidote for MIC
•ficantly depressed.
toxicity. If further studies confirm that
There has been no evidence to date to
MIC is indeed distributed in the body,
support the second hypothesis that MIC is
converted to a form of cyanide in the
there is a need to develop a method of
treatment for MIC poisoning.
body. Animals exposed to MIC by inhala­
tion have not shown any evidence of cya­
nide in the blood [51].
Epidemiologic Considerations
Animal studies testing the third specu­
In the early period following the acci­
lation have not shown that sodium thio­
dent, clinical treatment of the injured
sulfate has any protective effect against
direct MIC toxicity [52,53].
took priority over the planning and con­
duct of epidemiological studies. This was
If one accepts the possible efficacy of
thiosulfate in alleviating symptoms of gasparticularly true given the limited health
care resources available for a large num­
exposed persons, it must be in the light
of the first hypothesis that the cya­
ber of affected people and the general lack
nide poisoning came from an external
of experience in dealing with a disaster of
source.
this nature.
Studies to determine chemical compoA few cross-sectional studies (Table 1)
0tion of the MIC tank residues are cur­
were done during the early recovery
rently being undertaken by the ICMR and
period (6 months) for various systemic
may shed some light on the toxins relea­
health end-points. Virtually all of the epi­
sed in the accident [10]. Whether cyanide
demiology for the late recovery period is
was actually released may never be known
being conducted by the Bhopal Gas Disa­
with absolute certainty as it involves re­
ster Research Centre, a branch of the
creation of the actual conditions leading
Indian Council of Medical Research.
About 10 different epidemiological stu­
to the accident.
In the Bhopal situation, administration
dies were initiated to monitor long-term
of an essentially harmless drug like
trends in morbidity and mortality. Results
sodium thiosulfate on a mass scale, with
from these studies are currently being
adequate follow-up, would have enabled
awaited. As Bertazzi [58] notesKthe select
gathering data which would confirm or
tionofacohort rather than using a popula-j
reject the usefulness of the drug.
tion registry for epidemiological studies1
avoids two major biases: dilution of expo-1
Andersson [54], however, points out
that acute MIC exposure is more toxic
sure prevalence and selective migration of
than cyanide and an undue emphasis on
people out of the disaster area. ■
I

The early cross-sectional studies suffer
from a number of defects in study design,
resulting in bias and consequent difficulty
in clearly establishing causal relations­
hips. In one follow-up study performed 3
months after the accident, exposed per­
sons were contacted and requested to
come forward voluntarily for examination
[22]. This method ofsubject selection may
have resulted in severely exposed/affected subjects being examined and a conse­
quent over-estimation of health effects. If,
however, the severely affected victims
were unable to present themselves for
examination due to illness, an under-esti­
mation of health effects may have occurred.
Relatively crude methods like mortality
rates or distance of residence from the fac­
tory have been used in defining commu­
nity exposures. Koplan et al. [59] stated
that epidemiologic studies following disa­
sters should accurately estimate exposure
to enable correct dose-response relations­
hip modeling. These data are useful fora)
■identifying exposed and ill persons, b)
determine long-term effects and c) link
exposure and effects for litigation and
compensation.
For the Bhopal gas victims, there is a
need to do epidemiological studies to
determine morbidity prevalence in the
population stratified by estimated pulmo­
nary doso. Such an approach will allow
scientifically valid and detailed studies of
different health end-points to be perfor­
med on relatively small sample sizes [60],
Exposure-based stratified random sam­
pling will also reduce bias due to self­
selection and exposure misclassification,
as well as permit dose-response and inte­
raction relationships to be understood.

Conclusions
Clinical and toxicological studies have
shown that MIC is a potent toxin. Chronic
inflammation of the eye and respiratory
tract account for a major portion of the
morbidity. Certainly the potential exists
for these damaged organs to be more
susceptible to other environmental insults
like infections, irritants, and allergens.
For e.g., a person with airway damage

Epidemiologia e preventions n. 52, 1992

27

RASSEGNE

.
.c si.luxe unu dust. i'ulmonary function limitation may preclude
survivors from working on jobs which
require moderate or strenuous activity.
Progressive pulmonary fibrosis and
restrictive lung disease appear to be a
major cause for concern among the gasbxposed. Given the completely unexpec­
ted and devastating nature of the disaster
and the resultant stress, it is expected that
p number of survivors will suffer from
post-traumatic stress disorders for many
years. Establishment of a specialised
medical center for dealing with health
problems from the gas leak will permit a
co-ordinated method of investigation and
treatment for the injured.
It is a striking fact that much of the mor­
tality and morbidity could have been aver­
ted by the simple expedient of covering
the face'with a wet cloth. MIC would have
been decomposed on contact with the
water. Unfortunately, the community was
pever informed of the existence of such a
potent chemical in the factory and contin­
gency measures to be taken in the event of
a leak.
For a disaster of this magnitude, there is
a relative paucity of knowledge based on
epidemiological and clinical investiga­
tion. Some of the medical studies done on
the survivors suffer from unscientific
design and it is difficult to utilise informa­
tion from these studies with confidence.
Stratified sampling techniques using iso­
pleths of exposure from dispersion
models may be one way of conducting an
epidemiological study without including
the total exposed population.
/
It is imperative that long-term monito-

1 ring of the affected community be done
> for at least the next fifty years. Formal stu­
dies of ocular, respiratory, reproductive,
Immunological, genetic and psychologiital health must be continued to under­
stand the extent and severity of long-term
effects of the disaster.

Acknowledgements

The author wishes to thank the following persons
for their helpful comments and criticisms: Carol and
28

Epidemiologic o provomione n. 52, 1992

Tabelia 1 - Studi degli effetti sulla salute umana dell'incidente di Bhopal

Author

Study Period
(time after
gas leak)

Major findings

Design

(cases/controls)

Andersson et al.,
IOIM, M)

Case-series

8000 exposed

8 days

chomosis, cornnnl t.lcorn,
watering photophobia,
no blindness

Andersson et al.,
1988, (13)

Crosssectional

261/ 99

2 weeks

photophobia
corneal erosions

Dwivedi et al.,
1985, (15)

case-series

232

a few weeks

Andersson et al.,
1985, (69)

case-series

490

2 months

cornoal scars
no blindness

Maskati,
1986, (61)

Crosssectional

261/106

104 days

conjunctivitis
corneal opacities

Andersson et al.,
1986, (10)

Case-series

989

9-12 months

persistent watering

Raizada,’
& Dwiwedi
1987, (17)-

Case-series

114.0

2 years

corneal opacities, chronic
conjunctivitis

Ocular Studies

chemosis, redness
watering, corneal ulcers

Respiratory Studies
Mishra et al.,
1987, (70)

Case-series

978

2 days

resp. distress, pulm.
edema, pneumonitis

Sharma & Gaur,
1987, (62)

Case-series

500 X-rays

> 72 hrs

pulm. edema, emphysema,
pneumothorax

Misra & Nag
1988, (20)

Case-series

33

1 week

Dyspnea, upper and lower
respiratory tract irritation,
pulm. edema, pneumonia

Bhargava et al.,
1987, (63)

Case-series

224

1 -4 months

Obstructive &
rostriclivo lung disease

Gupta et al.,
1988, (22)

Crosssectional

1109

2.5 months

65 subjects with
+ve X-ray changes

Kamal et al.,
1985, (64)

Case-series

113

3 & 6 months

Emphysema, pulm.
hypertension
pleural scars,
interstitial depositis

Medico Friend '
Circle
1986, (9)

Crosssectional

136/137

4 months

Survey

865

9 months

486 live/births/
historic controls

9 months

38 l/ltislorio
controls

9 months

-

Reproductive Studies

Varma,
1987, (30)

Medico Friend
Circln
1900, (31)

Obstructive &
restrictive lung disease

Suivoy

Increased pregnancy
loss,
increased infant mortality
Increased spent.
abortion rale,
alteration of
menstrual cycle

RASSEGNE

Table 1 - Human health effects studies on the Bhopal Gas Leak
Tabella 1 - Studi degli effetti sulla salute umana dell’incidente di Bhopal

Design

(cases/controls)

Study Period
(time after
gas leak)

Kanhere el al.,
1987, (66)

Crosssectional

134/24

9 months

Decreased placental
& fetal weight

Daniel et a|„
1987 • (67)

Crosssectional

18/10

6 months

No effect on
spermatogenic function

Deo et al., 1987
(68)
^ftxena et al.,
”88, (35) ■

Crosssectional

22/13

11 days

Cell cycle delay

Crosssectional

31/31

2.5 months

Increased chromosomal
aberrations

Ghosh et al.,
1990, (36)

Crosssectional

83/46

3 years

Increased chromosomal
aberrations

Deo et al.,
1987, (68)

Crosssectional

67/15

4-8 weeks

Decreased response
to T & B coll mitogens

Saxena et.al.
198B, (35)

Crosssectional

44
19/8

2.5 months
2-5 months

Decreased T-cell
population, decreased
phagocytic activity

Karol et al„
1987, (26)

Case-series

144

1 -12 months

Transient MIC
antibodies in
12 subjects

208

2-6 months

Neuroses, anxiety
stalos & adjustment
reactions

350/100

2.5 months

Impaired auditory
& visual memory,
vigilance & attention
response speed

Author

Major findings

Genetic Studies

Immune Function

Psychological Studies

Sethi et al.,
1987,(46)

Case-series

Neurobehayioral Studies

Gupta et al.,
^988, (22)

Crosssectional

Gerard Nalarclli. Rosaline Dhara. Drs. Sloven Marko­
witz, Rashid Sheikh. David Kriebel and David Weg- •
man.
Drs. Michael Gochfeld and Meredelh Turshen pro­
vided support and guidance during the writing of this
paper.

Riassunto
II peggior disastro industriale della storia si verified
in India la nolle tra il 2 e il 3 dicembre 1984 a Bhopal.
cilia di 900000 abitanti e capitale dello stalo di Madhya
Pradesh. L’lpcidenle fu probabilmente inizialo dal1'introduzioije di acqua nelle cisterne deposito di Melilisocianato (MIC) e dalla conseguente reazionc in-

controllata con libcrazione di calore e di MIC solto
forma di gas. 1 sislemi di sicurczza o non funzionarono o furono inadeguati per il grande volume di sostanza chimica coinvolta nella reazionc.
Queslo lavoro passa in rassegna gli effetti dcH'csposizionc al MIC cosi come sono conosciuti da siudi
umani e discuie alcuni degli aspetii clinici ed epidemiologici dibatluti.
Per quanto riguarda I’esposizione della popolazione si slima che circa 27 tonnellate di MIC fuoriuscirono dalle cisterne in un arco di 1-2 ore [lj. L’incidente
avvenne intorno a mezzanolte in condizioni metereologichc avverse che prevenirono la dispersione del gas
e fecero ristagnare sulla zona una nube tossica [7].
Slime basaie sulla quamita di sostanza fuoriuscila e
sull’area interessata (40 miglia quadrale) pongono la

concentrazione di MIC ncll’area a 27ppm, circa 1400
volte lo standard OSHA per i luoghi di lavoro di 0.02
ppm durante le 8 ore [7J. Simulazioni che lenessero
conto della variability di concentrazione di MIC identificano 27 aree con concentrazioni variant! da 85.6
ppm a 0.12 ppm con una mediana di 1.8 ppm [8]. La
dose assunta dipese anche dai comportamenti indivi­
dual! al momento dell'incidente. In uno studio su un
campione di 158 persone, ad esempio, 124 fuggirono
dalle case (aumentando quindi con la ventilazione
polmonare la quantita di sostanza assunta) e solo 12
utilizzarono stofl'a umida davanti alia bocca come for­
ma di protezione (9).
Una coorte di 80021 soggetti fu identificata nella po. polazione residente intorno allo stabilimento della
Union Cirbidc c cbssilicola come csposta in modo
lieve, moderate e severo sulla base dei dati di mortalila
delle diverse aree. Un gruppo di popolazione di Bho­
pal non csposta (15931 soggetti) venne identificalo co­
me conirollo. Nelle aree cspostc rispcllivamcnlc il
53%, 46% c 1% crano di religionc indu, musulmana,
cristiana o sikh. L’80% della popolazione aveva un reddito infcriorc a 6 dollari al mese c solo I’ 1% supcriorc a
18 dollari. La soglia di poverty c slabilita dal governo in
12 dollari al mese. Solo il 34% della popolazione viveva
in una casa stabile (“pacca" house) [10].
Delle 200000 persone esposte 2500 morirono nella
scltimana succcssiva all’incidcnle. Al novembre 1989
risultnva un lotnlc di 3598 viuinic dcccdulc prcvalenlemcntc per complicazionl rcspiraloric. Nel periodo
maggio 1989 - marzo 1990 la mortality generate risuliava essere piu elcvata nolle aree esposte (8.7$/1000) relativamcnte alle aree di conirollo (7.5/1000) [10].
Surveys sulla prevalcnza di sinlomi indicano una
morbidity piu elevala nelle zone esposte (26%) rispetlo alle Sree di conirollo (18%).
L’articolo e la labella 1 passano in rassegna i lavori
condoiti sulla patologia oculare, respiratoria, riproduttiva, sulla genolossicita, carcinogenicity e immunotossicila del MIC suite popolazioni cspostc cd i problem!
psicologici c di tossicila ncuroambicntalc c neuromuscola.e. Vengono infinc valutati i problem! chimici
collcgnii ad una possibilc lossicith di altri prodotti pre­
sent! nella nube lossica c potcnzialmenlc formalist
durante la reazionc di idroliiicn cd csoiermica.
Considcrazioni general! riguardanti gli studi epide­
miologic! condotli nell’area di Bhopal sono:
1.
Nel periodo immediatamente seguente l’incidente
la totality degli sforzi mcdici si conccntrarono sulla cura del numcro clcvalissimo di inlossicati e solo in un
sccondo periodo vennero pianificati studi al fine di valutarc gli effetti cronici cd acuti dcll'csposizione alia
nube tossica.
2.
Gli siudi Irasvcrsnli, i primi nd csscrc discgnali, soffrirono di numcrosi problem! ncl disegno dello stu­
dio. Gli studi prospcttici vennero discgnali con maggiorc altcnzionc agli aspclii delle dislorsioni di sclc-

3.
E imporlante ricordare che larga parle della morta­
lity e morbidity avrebbe poluto essere evilala con misure di prolczione individuate molto semplici, quale il
coprirsi il viso con un panno bagnalo. Purtroppo laconiunili non era mai slata informata n6 dalla presenza
di lossici cosi potenti nello stabilimento, nd di forme
di protezione individuate da applicare in caso di incidente.
Summary

The meihyl isocyanate (MIC) gas teak from the
Union Carbide plant al Bhopal, India in 1984 was the
worst industrial disaster in history. Exposure estimaEpidcmiologia e prevenzione n. 52, 1992

29

RASSEGNE

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son m. Jameson cw. Thigpen JE, SCHWETZ
34. Varma DR. GUES I1, SMI II1S. MUI.aY S. Dis­
, 16. ANDERSSON N. KERR MUIR M. AJWANI MK.
BA. Toxicity of Inhaled Methyl Isocyanate in F344/N
sociation between maternal and fetal toxicity of met­
^Mahasiiahpe S. Salmon a, vaidyanathan k.
Rats and B6.C3FI Mice. 1. Acute Exposure and Reco­
hyl isocyanate in mice and rats. J Toxicol Env Hlth
Persistent eye watering among Bhopal survivors. Lan­
1990; 30: 1-14.
very Studies. Environ Health Perspect 1987; 72: 53-61.
cet 1986:2; 1152.
/35ySaxena ak. Singh kp. Nagle SL. ,Gupta
52. Nemery B. Sparrow s, dinsdale d. Methyl
les of gas concentrations In the area range front 85 to
0.12 ppm. Of the approximately 200.000 persons expo­
sed. 3598 deaths have resulted as of November 1989.
Chronic inflammatory damage to the eyes and lungs
appears to be the main cause of morbidity. Reproduc­
tive health problems in the form of increased sponta­
neous abortions and psychological problems have
been reported. Questions about the nature of MIC to­
xicity have been raised by ttye persistence of multi-sy­
stemic symptoms in survivors. Animal studies using
radio-labeled MIC given by the inhalation route have
shown that the radio-label is capable of crossing the
lung membranes and being distributed to many or­
gans of the body. This paper reviews health effects of
gas exposure from published studies and discusses so­
me of the clinical and epidemiological issues being de­
bated. .

30

Epidemiologia e prevenzione n. 52, 1992

RASSEGNE

Isocyanate: Thiosulphate does not protect. Lancet
I9$55>2: 1245-1246.
X’53. VlJAYRAGHAVAN R. KaUSHIK MP. Acute toW&iiy6f methyl isocyanate and ineffectiveness of so­
dium thiosulphate in preventing its toxicity. Ind J Exp
Bloj-Aus 1987; 25: 531-534.
/34jXNDERSSON N. Long term effects ofmethyl isocyupnic, Lancet 1989; 1: 1259.
*
55. DllARA VR. On the bioavailability of methyl
isocyanate in the Bhopal gas leak. Editorial. Arch Env
Health 1992 ; 47: 385-386.
56. Ferguson js, Kennedy al. stock mf.
Brown WE. ALARIE Y. Uptake and distribution of
,4C during and following exposure to (14C] methyl iso­
cyanate. Toxicol Appl Pharmacol 1988; 94: 104-117.
57. BHATTACHARYA BK. SHARMA SK. JAISWAL
DK. In vivo binding of (,4CJ methylisocyanaic to va^k rious tissue proteins. Biochem Pharmacol 1988; 37:
2489-2493.
58. BERTAZZI PA. Industrial disasters and epide­
miology; a review of recent experiences. Scant! J Work
Emjmn Health 1989; 15: 85-100.
'( 59}K0PLAN JP. Falk H. GREEN G. Public Health
Lessons from the Bhopal Chemical Disaster. JAMA
1990; 264: 2795-2796.
60. DllARA VR. KRIEBEL D. The long-term health
consequences of the Bhopal gas disaster: dose-re­
sponse studies. Apha 120th Annual Meeting Exhibi­
tion Abstracts. Washington. D.C.. 1992; 130.
61. Mask ATI QB. Ophthalmic survey of Bhopal vic­
tims 104 days after the tragedy. J Postgrad Med 1986;
32: 199-202.
62. SllARMA PN. GaUR KJBS. Radiological spec­
trum of lung changes in gas exposed victims. Ind J
MejJRes 1987; 86 (Suppl): 39-44.
Xb<jBHARGAVA DK. VaRMA A. BATNI G. MlSRA
vx NPfTlWARI UC. ViJAYAN VK. JAIN SK. Early obser­
vations on lung function studies in symptomatic ‘gas’exposed populations of Bhopal. Ind J Med Res 1987; 86
(Suppl); 1-10.
64. KAMAT SR. MAHASHUR AA. TIWARI AK.
POTDAR PV. Early observations on pulmonary chan­
ges and clinical morbidity due to the isocyanate gas
Iciik-Aii Bhopal. J Postgrad Med 1985; 31: 63-72.
65. Kamat SR. Patel MH. Koliiatkar vp; DaVE-aA, MaHASHUR AA. Sequential respiratory
^k changes In those exposed to the gas leak at Bhopal. Ind
V J Med Res 1987; 86 (Suppl): 20-38.
.'66. KanhereS. Darbari BS. Shrivastava AK.
x// Morphological study ofexpectant mothers exposed to
gas leak ill Bhopal. Ind J Med Res 1987; 86 (Suppl): 7782.
^67, Daniel CS. Singh ak, Siddiqui p. mathur
BBL. Das SK. AGarwal SS. Preliminary report on
spermatogenic function of male subjects exposed to
gas at'Bhopal. Ind J Med Res 1987; 86 (Suppl): 83-86.
68. Di-0 MG. GANGAL S. Bl USEY AN. SOMASUNC DARAM R. BALSARA B. GULWANI B, DARBARI BS.
BHIDE S. MaRU GB. Immunological, mutagenic and
genotoxic investigations in gas exposed population of
Bhopal. Ind J Med Res 1987; 86 (Suppl): 63-76.
69. Anokrsson N, Kerr Muir M. Salmon AG.
Wi lls QJ, Brown RB, cl al. Bhopal Disaster: Eye folJowaup and analytical chemistry. Lancrt 1985; I: 761-

P

, / .70JlJSRA NP. PATHAK R. GAUR KJBS. JAIN
’
SC. YES1KAR SS. MANOR!A PC. el al. Clinical pro­
file of gus leak victims in acute phase after Bhopal epi­
sode. Ind J Med Res 1987; 86 (Suppl): 11-19.

La Cooperativa Epidemiologia e Prevenzione annuncia il

TERZO CORSO DI PIANIFICAZ1ONE, GEST1ONE
E VALUTAZIONE DEGLI SCREENING
IN ONCOLOGIA
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Napoli, lunedl 6 - venerdi 10 settembre 1993
Programma prowisorio

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Le conoscenze eziologiche:
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Rischio attribuibile e rischio prevenibile
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Un. Federico II, Napoli)
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Epidemiologia e prevenzione n. 52. 1992

31

oh

I :8

irnmentary

f

public Health Lessons From
jje Bhopal Chemical Disaster
1984 CHEMICAL disaster in Bhopal, India, was first
jiremost a terrible human tragedy. For those who were
jgtind even for those at considerable distances who read
it, the reality of 2000 or more persons dead and many
— of thousands poisoned by a toxic cloud is horrifying.
poorer, in its particulars and complexities, Bhopal’s chemi^fcaster can also serve as a case example for almost any
taught in a school of public health. The disaster has
^nts of acute and chronic epidemiology, industrial hy^e, toxicology, environmental pollution and planning, diatff preparedness and management, health economics,
j&a] ethics, and environmental protection law, to name a.
< Mehta et al1 review the literature on the Bhopal disaster
aJ its aftermath and focus on the long-term health effects.
5^ recognize the incomplete nature of much of the data and
aierious methodologic limitations for study that the cirasances of the event engendered. What conclusions can
taw from this event? What can we learn to better prepare
sselres for similar events that might occur in the future?

See also p 2781.

There is an inherent catch-22 in doing a health evaluation of
‘iffitsr. The time period just following the event—when
remains considerable chaos, confusion, and inaccessibil?<means of transport, communication, and data collecp-is the very best time to try to establish information that
*ib«ome invaluable in determining the health effects. This
,<3re is common to natural disasters such as the Mount
^Helens volcano eruption or man-mediated ones such as
y or the nuclear contamination at Chernobyl. This im-

postdisaster time period is also when it is most
^^,t0 organize systematic and valid epidemiologic
^information that is usually of most interest relates to
and morbidity (ie, the public health impact), expoenvironmental damage. Depending on the setting,
J^oiogic studies following environmental disasters may
some or all of the following: (1) accurate estimates of
(2) correlation of environmental and human expo-

relationship of exposure (or dose) to observed
•v^fects; (4) the potential interaction of other risk fac­
lor Disease Conlrol. Atlanta. Ga (Drs Koplan and Falk): me All
a/3 M«lical Sciences. New Delhi(DrRamalmgaswami): and the Harvard
. Boston, Mass (Dr Green).
to Center for Chronic Disease Prevention and Health Promotion,
•$Control (A37), Atlanta. GA 30333 (Dr Koplan).

Sf 5.1990-Vol 264, No. 21

tors with exposure in producing health effects; (5) the natural
history of the disaster-related illness (especially if, as with
methyl isocyanate [MIC], such illness has not been well docu­
mented in the past); (6) impact of therapy or progression of
disease (particularly in situations where the therapeutic ap­
proach is uncertain—in Bhopal this arose because of ques­
tions concerning possible toxic effects of cyanide); (7) effec­
tiveness of screening and diagnostic tests (in determining
who was affected and to what extent); (8) identification of
markers of prognosis (in Bhopal a critical issue was who
among the many individuals with acute respiratory problems
would ultimately develop chronic pulmonary toxic effects); (9)
evaluation of the effectiveness of disaster plans (including the
implementation of warning systems, evacuation procedures,
and the provision of emergency medical services); and (10) the
psychosocial impact of the disaster on the affected
population.3
These data are needed for several purposes: (1) to identify
exposed and clinically ill persons to provide long-term care
and monitoring for their own well-being; (2) to improve con­
tingency planning for future disasters; (3) to determine the
short- and long-term health effects; and (4) to link exposure
and health consequences for litigation and reimbursement.
The acquisition of scientific knowledge is not an intellectual
exercise. Rather, it provides information that can help pre­
vent or better control a similar disaster in the future.1
A rough estimate of deaths can sometimes be obtained in a
disaster setting in a developing country by conducting a
survey at the site soon after the event.1 In Bhopal, this meant
that in the first 5 days after the event, sample surveys might
have been conducted in selected areas of the city. While there
was some disruption of families, much of the local population
was still present up to 10 days after the event. Available
interviewers with appropriate supervision could have been
given brief training and a data collection form and sent out to
obtain rough rates of death and illness, along with other
variables. In disaster situations there are often many practi­
cal impediments to collecting what would otherwise seem to
be readily available information. For instance, in Bhopa] on
the night of the disaster, so many patients were seen at the
major hospitals that even rudimentary medical records were
not available for most patients; this would complicate unbi­
ased sample selection for clinical epidemiologic studies of
hospitalized patients. Such practical constraints ranged from
the unavailability of death certificates or medical records to
the lack of prior census data, very limited numbers of on-thescene epidemiologists or investigators, and insufficient envi. Commentary

2795

ronmental data (or even the equipment to collect such data).
The constraints to the conduct of health studies were especial­
ly severe in Bhopal because of the enormous scope of this
environmental disaster.
Determining health .effects, particularly long-term ones,
requires a knowledge of the amount of exposure. Without
such information, diseases and conditions that develop over
time in a population tend to be more readily noticed, added
together, and ascribed to the presumed exposure. Comparing
such a newly measured incidence of an adverse health event
with a neighboring nonexposed community or with the same
community at a time prior to the disaster is problematic. Even
neighboring communities often may have characteristics that
are different from the case community, such as differing
customs, different environmental exposures (the case com­
munity may have other toxic hazards in addition to those
associated with the disaster), and different food or water
sources. A comparison with an earlier time period is often not
possible due to the lack of carefully collected data on the
health condition in question prior to the disaster and 'the
problem of recall bias. Measuring exposure is made consider­
ably easier when a biomarker of exposure, such as a blood
chemistry level or determination of the level of radioactivity,
can be obtained.
For the exposure to MIC at Bhopal, such a marker had not
been identified. An alternative approach is to establish a dose­
response relationship between a measure of environmental
exposure and a health event. In the aftermath of the disaster
at Bhopal, this was not possible, because wide-scale environ­
mental measurements of MIC (or breakdown products) could
not be obtained in time. Approximations were based on less
precise measures of exposure such as how close an individual
lived to the plant. Actual exposures would be affected by
many other factors, such as the height of the patient from the
ground, the degree of ventilation of the house, and the shield­
ing of the patient from the MIC vapors. It was also noted that
degrees of damage to local vegetation could serve as an ap­
proximate, albeit imprecise, indicator of environmental expo­
sure. Indeed, several investigators of the Bhopal disaster
used a simplified dose-response approach in looking at late
health events. They chose a community within 2 km of the
plant and a farther one (approximately 8 km from the plant)
and found higher rates of decreased pulmonary function,6
increased acute ocular symptoms,’ and increased pulmonary
symptoms in children8 for the individuals living closer to the
plant. However, these studies were conducted 3 to 4 months
after the disaster, and we have no longer-term follow-up data.
What might have been done epidemiologically, especially in
ideal circumstances, is therefore a moot point for Bhopal. The
immediate medical response to the disaster appeared to be
swift, appropriate, and effective. The epidemiologic response
could not be a priority at the time.
Thus the information we have today, 6 years after the
event, is not profoundly different from that available in the
first weeks after the gas leak; there were considerable acute
pulmonary toxic effects with bronchospasm and pulmonary
edema, severe irritation of exposed mucous membranes and
the cornea, and little evidence of residual ocular effects.
However, careful study would be needed to determine the
long-term pulmonary damage and damage to other organs.
The article by Mehta et al confirms these early observa­
tions, suggests that long-term pulmonary damage has oc-

2796

JAMA. December 5.1990-Vol 264, No. 21

curred, and raises the issue of teratogenic and fetal danfrom MIC, although not proving it. Their statement “noi^
the data on morbidity and mortality are firm” is disappear *
for their desire to present (and the readers to receive) a
rich scientific review. But more important, this lack of
data extends the tragedy by denying some damaged indiyj?
uals proper restitution, confounding follow-up and care fr,
exposed individuals, and minimizing the new informal,.
available to better prevent and control future MIC exp
sures. Health authorities in industrial and chemical disaspJ

must first focus on provision of care for the ill and injured b
also must see as an urgent priority the establishment of.
surveillance and epidemiologic study system that will addre."
the aftermath of the acute exposure.
We readily perceive disaster planning and preparedness;
encompass chemical plant operating conditions and safer
systems (the cause of the disaster), and procedures to warn
evacuate, and protect nearby populations. The provision Gemergency medical services is obvious. But the ability t
conduct effective and valid postdisaster epidemiologic am
health evaluations also depends on prior planning and avC
able infrastructure. In Bhopal, support came promptly from;
variety of local and national resources, including the India;
Council for Medical Research. The article by Mehta et i
highlights the importance of the public health response, par­
ticularly epidemiology and health surveillance, in disaster
planning.
Finally, it is impossible to elose a discussion of the Bhow.
disaster without reemphasizing the importance of preven­
tion. While there are many lessons to be learned from t
careful and thorough investigation of the health effects result­
ing from the Bhopal disaster, what a terrible price was pat:
for these lessons. Many difficult issues remain to be addresser
to assure that similar disasters do not occur. Among these an
how to prevent such potentially dangerous plants from beir_r
located in heavily populated areas, how to ensure the saroperation and maintenance of technologically complex fad­
ties, and how to develop effective disaster plans to better
protect workers and nearby residents."
Jeffrey P. Koplan.'MD.Mr-'
Henry Falk, MD, MPH
Gareth Green, MD
The authors wish to thank Vulimiri Ramalingaswami, MD. DSe. FRCP. ft
for his assistance with this paper.
1. Mehta PS, Mehta AS. Mehta SJ. Makhijani AB. Bhopal traged.rtj*1effects: a review of methyl isocyanate toxicity. JAMA. 1990;264:2781-27c2. Parrish RG, Falk H, Melius JM. Industrial disasters: classification, in”*
gation, and prevention. In: Harrington JM, ed. Recent Advances in
tional Health, HI. New York, NY: Churchill Livingstone Inc: '•
155-168.
3.
Joint Report of the Scientific Group on Methodologies for the Safety I''*'
tion of Chemicals. Health assessment and medical response. In: Bouroe*Green G, eds.- Methods for Assessing and Reducing Injury Front Che^
Accidents. New York, NY': John Wiley & Sons Inc; 1989:45-65.
4. Gregg MB, ed. The Public Health Consequences of Disasters. Atlant*
Centers for Disease Control; 1989.
..
5. World Health Organization. Emergency Preparedness and
id Health Assessment in Chemical Emergencies. Geneva. Switz--:’ and
Health Organization; January 1990. Publication ERO/EPR/90.1.9. Lmerr
Relief Operations.
6.
Naik SR. Acharya VN, Bhalerao RA. et al. Medical survey o. ■
isocyanate gas-affected population of Bhopal. Il: pulmonary effects m
victims as seen 15 weeks after MIC exposure. J Postgrad Med. 1986:32: IN'
7.
Maskati QB. Ophthalmic survey of Bhopal victims 104 davsafterthe
dy. J Postgrad Med. 1986:32:199-202.
8.
Irani SF, Mahashur AA. A survey of Bhopal children affected by
isocyanate gas. J Postgrad Med. 1986;32:195-198.
—
9.
Bhopal Working Group. The public health implications of the BhoP*1
ter. Am J Public Health. 1987;77:230-236.

• -■

Co"'0*'*’

C^-GQ
British Journal of Industrial Medicine 1986: 43:502-504

Correspondence
Bright red blood of Bhopal victims: cyanide or MIC?

Sir.—Several anecdotal observations have con­
methaemoglobin was inhibited by ajj
tributed to the general perception of the nature of the
quantity of sodium dithionite. On addit"
toxic effects suffered by the victims of the Bhopal
amount'of methyl isocyanate (20-50
disaster.There have now been various reports of
lion) a vigorous reaction was observed '
evolved: this was the expected result of tfe?
scientific investigations of the toxic effects of methyl
isocyanate, the substance believed to have been
reaction, the first stage of which sene™?
amine and carbon dioxide.4 It was also ot>2.
released in the accident, and also various analyses of
although the main Sorel band absornti*
what conditions might have led to the explosive
release of the substance. It has generally been found
haemoglobin (ca 430 nm) was unaffected
that symptoms observed in exposed people may be
peak in the visible region (ca 550 nm) disarm
explained by what is now known of the toxicity of
pale red colour remained in the solution rnC
the long tail of the ultraviolet peak. The J?
methyl isocyanate.12 On the other hand, some have
claimed that other toxic compounds were involved.
was observed when a small amount of mak_
was added to a solution of haemoglobin [S
especially cyanides (organic or inorganic). So far as I
lions also caused a shift in pH of the solution?
am aware, no analytical data indicating the presence
of such substances as a result of the accident have been
the alkaline range (methylamine beingquite o,
presented. The observation of raised thiocyanate con­
basic), but when sodium hydroxide was added
centrations in the urine of both survivors and sub­
duce a similar shift no change in the spectn.
sequent visitors to the region has been claimed as
seen. Such spectral changes in haem protrinsm
evidence of cyanide exposure. While this observation
means unexpected when molecules capable of i
may well be accurate, it appears unlikely to be related
as iron ligands arc added: indeed, this is met
to methyl isocyanate exposure on the basis of labora­
mechanism responsible for the colour dift
tory investigations of rats exposed to this sub­
between haemoglobin and oxyhaemoglotia.'
stance.1 2
spectroscopic change induced by methylamwij
One particular observation that has been quite
identical with that produced by oxygenation?
widely quoted was made during postmortem studies
does it correspond to methaemoglobin form
immediately after the disaster. It was said that the
which would be prevented by dithionite: in fie
blood (and possibly myoglobin) of victims of acute
presence of this compound had no effect ci
poisoning was bright red such as is usually associated
modified spectrum.) It does seem possible,bm
with oxygenated (arterial) blood. This might be char­
that the methylamine induced spectral changes.
acteristic of cyanide poisoning where tissue uptake of
be mistaken for this well known phenomenon b"
oxygen is inhibited. On the other hand, n seems
observer using the naked eye. which is acrudetc
unlikely that human victims of methyl isocyanate poi­
such tasks.
soning would have had oxygenated blood: Nemcry
If this suggestion is accepted then theevide
el al specifically measured oxygen levels in the blood
involvement of cyanide or other substances
of exposed rats and found them to be low. due to lung
MIC. slim as it is. is further reduced.
- Q
damage and bronchoconstnction impairing the
exchange of blood gases.2 One might therefgre con­
TUC Centenary Institute of Occupational Hea
clude that some other substance was present either as
London School <>/ H vytene and Tropical Medic
a degradation product or impurity in the gas to which
Keppel St. London iVCIE 7HT.
the Bhopal victims were exposed.
References
’ISB
To evaluate this possibility we looked at the effect
1 Salmon AG. Kerr-Muir M. Andersson N. Acute toriotyw
of methyl isocyanate on the ultraviolet/visible absorp­
isocyanate: a preliminary studv of the dose response fcr<
tion spectrum of haemoglobin? A sample of blood
other effects. Hr J Ind Sled 1985:42:795-8.
MP
obtained by heart puncture from a rat was diluted into
2Ncmery B. Dinsdale D. Sparrow S. Ray DE. Eifaxi4
isocyanate on the respiratory tract of rats. Or I
10 mM sodium citrate buffer. pH 6-5: this was
1985:42:799-805.
designed to produce a haemoglobin solution (by hae­
molysis of the erythrocytes) of suitable concentration
2. pari A. New York: Academic Press. 1954:296. J V
lor measurement of the absorption spectrum in a
‘Andersson N. Kerr Muir ,M. Salmon AG. el al. Bhoplto1**1
follow-up and analytical chemistry. Lancet I985a:l®l'Perkin Elmer 124 UV/vis spectrometer. Formation of
502

■IE 1985

telTISH MEDICAL JOURNAL

failed to
hey saw
is in line
d with a
uprising
tie whole
>ie means
adorable
he mean
hree area
entering

VOLUME 290

1883

minimal course of treatment with antidepressant drugs, yet the
outcome of our unrecognised patients was worse. ,
Failure to recognise depression seemed to be related to general
practitioners’ basic knowledge of diagnosing depression and not
only to their skills in interviewing or their attitudes towards patients
with emotional disorder.
The work reported here was funded by the Medical Research Council. We
oft an immense debt to the cooperating general practitioners, their staff,
od the patients

,ise these
advantage
patients,
predicted
'e claimed
leprc
agnosi^n

: clues. In
were more
depression
essed way.
ers’ lack of
ctable to a
gnificantly
. year, and,
ontributing
-nore likely.
nore than a
reluctant to
eve affected
icse patients
e. If general
ed for a year
r depressive

My Student Elective
in eyewitness in Bhopal
10IRA SUTCLIFFE

e underwent
This indicates
■ressibn in the
did not refer
e prepared to
Inesses might
ncrease their

Iw to Bhopal from Delhi on Sunday 2 December 1984 to begin
jelective, which I had arranged to spend in the paediatric
pnment al Hamidia Hospital. In the next .two frocks 1337
ddreo were admitted to the department. Of these 119 died and
opal became a household name. As the only outsider 1 was in a
ijue position to observe the reaction of the cit^ and its medical
atrees to the world’s worst industrial disaster. This report
i aims my impressions of how the hospital and staff coped with
i*
titioners werffl :disaster and describes some of the clinical features of the toxic
an increased.; tjoisoning.
> confront the. Ispent the first night of my stay with Dr Bhanduri, the professor
pediatrics. At
Al about 1 au
30 am 1I was woken by thd
ringing
a matter of soli
the repeated nr.
D...o
self ptwiamcs.
ed by knowing, ibe doorbell followed by the entry of several people who were
■e only a short 4hmg violently. At the same time I noticed a sfreerish smell, my
" ,oj*| twere mysteriously stinging and watering, and my throat felt
ptoms, five
epressed mdtjtj t.lheard the distant sound of a siren, bur this being my first night
in appetite M Bhopal I thought nothing of the incident and went back to sleep.
/ or weariness to I woke the next morning I heard that there had been a major
ink from the Union Carbide insecticide plant about a mile from
asure in
o concentrate 0| hospital, but the nature of the gas was not yet known. At first the
or suicide.
eire relating .tm

nised depress^
from the follov
mpleted even |( i[oBtcii«ii>:lfcMliBari.»i.M»u..rK<ud,<;..nns,<>«

local news reports knew little mote than we could deduce from
seeing the numbers of affected people who had flooded into the
hospital grounds. The earliest reports suggested that about 30
people had died. With each subsequent news report wc listened
with disbelief as further details about the horrifying story began to
emerge. Even after the first full day we were unable to believe the
estimate from the BBC World Service of 2000 dead—later even this
proved to be conservative.
The dead and dying arrived by-the truckload, others came by
rickshaw or were carried by relatives. For some the effort of the
journey itself proved too much, ahd they died soon after arrival.
Many families were split up during the initial panic, everywhere
there were people looking for missing relatives. There were long
queues of people trying to identify Relatives in the mortuary. From
an early stage when the mortuary whs full, other unidentified bodies
were laid out on a nearby lawn and finder hastily erected shelters.

Facilities overwhelmed

The facilities in the hospital and the manpower became increas­
ingly overstretched as the enormity of the disaster became apparent.
The doctors were quite overwhelmed. I felt even more helpless;
having arrived only the day before 1 had been unable to see inside
the hospital or be introduced to thl- staff, and was unable to speak
the language. For the first few days I was frustrated that I was not
able to do more to help. Without a doctor to interpret for me there

1884

BRITISH MEPICAL JOURNAL

VOLUME 290

22 JUNE 1985

wax little that I could do on inv own. I joined up with a group of
other medical students to help administer eyedrops, give injections,
set up drips, and distribute food.' Doctors worked around the clock
giving repeated injections; there was no time to rcstcrili.se needles
between patients. The doctors were unable to spend much time to
help any one child, dividing their time between the ill and the dying.
Later on I was able to examine the children as they arrived and
suggest treatment. I also helped to ventilate dying children and
attempt cardiac massage.
Many hundreds of victims died within the first few hours of the
gas leak, death being caused by respiratory failure resulting from
the severe pulmonary oedema, 'flic main complaints of those who
survived were of a sensation'of intense heat, burning eyes,
blindness, vomiting, choking, coughing, breathlessness, and a
feeling of suffocation. At first the precise toxic effects of the gas were
not known so treatment was symptomatic—with antibiotic eye­
drops, oxygen inhalation, and intravenous frusemide, steroids, and
aminophyllinc to relieve respiratory distress.
'fhe most severely affected children were attended to in the
intensive treatment room, which was about 20 feet square and
supplied with only one sink and.an electric socket. Rows of infants
and older children on drips filled the couches, while others lay on
the floor or were held by their parents while they received
treatment Two or three children would be receiving oxygen
through nasal cannulae delivered from the same gas cylinder. Most
of these children admitted to the intensive treatment room died of
respiratory failure within the next few days.
The wide corridors of the hospital were packed with victims,
several members of each family requiring urgent treatment. The
luckier ones had a bed—for the whole family. By the Wednesday
these families who had been camping in the ward corridors were
being moved out to tents erected nearby by the army Relief
agencies provided food for the victims—milk, bananas, and
biscuits. By the Thursday the initial rush of people coming in had
slowed though the death toll wqs still rising: the official figure now
exceeded 2000.
Of the 119 deaths in the paediatric department from 3-14
December, 106 occurred in the first four days after exposure. The
cause of death in most cases .was cardiac arrest associated with
respiratory failure. On examination these children with toxic lung
damage were breathless and hyperventilating but not cyanosed.
Many had audible wheezes and grunts, and widespread rhonchi and
crepitations were heard with t|ic stethoscope, 'fhe children were
treated with intravenous fruseqpide and steroids to help reduce the
severe pulmonary oedema, qpd aminophyllinc to relieve the
wheezing. After about a week ’about 15 children a day were still
being admitted to the wards, plainly with respiratory complaints
—cough, breathlessness, an<| respiratory infections, 'fhe eye
problems, which had caused widespread distress in the first few
days, had been due to the direct chemical irritation, causing painful
watering eyes, local oedema, aqd photophobia. The irritant gas had
caused superficial ulceration,' which led to temporary corneal
opacity in some eases. Prophylactic neomycin eye drops helped to

keep the rate of infection low, and atropine drops were also given to
prevent the formation of posterior synechiae, though it caused
further problems of blurred vision and occasionally induced acute
glaucoma. Fortunately, the corneal ulceration was superficial and
generally healed.- without scarring,. The mobile preventative
ophthalmology uqits played an important role in the follow up of the
eye complications in the community. Some children also showed
signs of convulsiops, hemiparesis, and coma.
On 8 December a German toxicologist. Dr Daundcrer, visited
Bhopal and reinforced the views held by the head of the forensic
medicine department. Dr Heereshchandra, that the effects of the
methyl isocyanate gas were mediated via its breakdown into
cyanide and other toxic amines. If this were the case there was a
specific antidote, sodium thiosulphate. 'Fhe drug was thought lobe
harmless, but its efficacy was not proved so its widespread use in the
treatment of the victims was vetoed. Sodium thiosulphate was
administered to a few patients, some of whom showed marked
improvement, bqt by the lime a controlled trial had been startedit
was too late to expect any effect from an immediate antidote.

W'hat is the current state oj knowledge of ecological illness or total allergy
syndrome? Is there an immune basis (o this condition?

removed from their environment improvement can be remarkable. The
term “total allergy syndrome" is valueless. These arc patients with multiple
sensitivities, so eiilled “universal reactors ,“ as described above, who an
difficult to treat, and in whom immunological abnormalities have baa
found.-* Their symptoms are not all in the mind, and in environmental units
as seen in the United States many of these patients return to normal healthWe know little of what causes this syndrome but environmental factorsare
clearly important. Much work needs to be done before we have a dor
understanding as to what is happening in possibly a considerable propxwt
of the population.—J hrosioi I, reader in clinical immunology, London.

Chemicals as well as pollens can cause sensitivity. This has been discussed by
the World Health Organisation and its conclusion was that this is a
considerable health problem and that we know little about it.1 Many patients
feel “dis-cased,” complaining of lethargy, myalgia, aching joints, abdominal
symptoms, depression, fluctuating weight, etc. They arc often referred to a
psychiatrist because no tests show abnormal results. These arc obviously a
heterogeneous group which we pow know contains patients with food
allergy, the postviral syndrome, those with chemical sensitivity, and some
with primary or secondary psychological problems, or indeed a mixture of all
these, 'fhe pioneering work of Randolph has delineated a group of these
patients who arc sensitive to chemicals and gas fumes and when these arc

Tragedy attracted world attention

For the next.,few weeks the world’s attention focused on Bhopal,
Rajiv Gandhi and Mother Teresa came to visit the city, meeting the
gas victims in hospital and also in the affected slums around the
plant. Newspaper and television reporters arrived from all over the
world within a diiy or two of the tragedy. Everyone was anxious to
send back pictures of the carnage in the slum areas, record the death
throes of babies in the paediatric wards, and recount the tragic
stories of so many left widowed or orphaned by the gas. Some
television teams would film patients in the wards, regardless of
whether they had been affected by the gas or not.
I he next few \yecks were spent trying to cope with the immediate
toxic effects of t|ic methyl isocyanate gas and later to predict the
medium and long term complications likely to arise. 'Fhe most likely
problems expected are thought to be respiratory, especially pul­
monary fibrosis,* though doctors arc also anxious to follow up any
neurological, opjithalmological, and intellectual sequelae that may
emerge. Another ^car >s l^c effect of the gas on early pregnancy.
Methyl isocyanate exposure was blamed for a marked increase in the
rate of premature labour and abortions on the night of the gas leak
and in the subsequent few weeks.
I had expected the experiences of my elective period to include a
range of the usual childhood diseases—polio, tuberculosis, and
diphtheria. Instead it was as if I had arrived during the filmingofa
disaster film—except it was real.

1 am grateful to the following for allowing me access to their departments:
Dr N R Bhandarj, professor of paediatrics; Dr L P Mishra, professor of
medicine; and Dr Mittal, department of ophthalmology.
t
•AatruJZMay MS'

BRITISH MEIX

Occa
When
Startii
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Abstract
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have import
practice van
than by knm
influence of
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withdrawing
epilepsy.

Introductior

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convulsions b
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it. Current pi
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drugs in the I
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D CHADWICK.
Department ol
EHREYNOLD

Coerespondenre

1245

THE LANCET, NOVEMBER 30,1985

to know what proportion of doctors do believe in an honest
approach to their patients, and what proportion of those use the
proper terms rather than euphemisms such as growth or rumour.
which many patients do not realise are synonyms when used for
cancer.

John Squire Kirkham
MISCARRIAGE OR ABORTION
Sir,—We support Professor Beard and his colleagues’ suggestion
{Nov 16, p 1122) that doctors—like their patients—should use rhe
word “miscarriage” for a spontaneous abortion, thus reducing the
distress caused to couples who have a miscarriage. Statistical
confusion in Parliament and public debate would also be reduced.
In February this year Mr Nicholas Winterton, MP, an opponent of
abortion, asked how many deaths were due to abortion. The
Minister ofHealth gave the unintentionally misleading reply that in
1983 in England and Wales there were eight abortion deaths but did
not go on to say that all eight were due to miscarriage and none to
induced abortion.

Caroline Woodroffe.
DOGS AND PAGET’S DISEASE

Sir,—Dr O’Driscoll and Dr Anderson report that ownership of
dogs in rhe past was more common among 50 patients with Paget’s
disease than among 50 age and sex matched diabetic controls (Oct
26. p 919). This case-control comparison was done m Manchester.
They suggest that “a canine. viru$(possiblycaninedistempcr)might
be tha^imary infective agent” in the disease.

the town with the highest recorded prevalence of Paget's disease in
any country, and the other in Siena, Italy, which has a low
prevalence.1 Questions about household pets during childhood
were included in the interviews. In Lancaster 37 cases were
compared with 74 controls matched for sex and age to within five
years. Cases and controls were identified from a sequential sample
of stored radiographs in a general hospital. In Siena 27 cases from a
hospital register were matched with two sets of controls, one
comprising patients attending a rheumatology outpatient clime and
the other inpatients on medical wards. Other than for the inpatient
controls in Siena all the interviews were at the subjects’ homes.
The table shows the numbers of cases and controls who reported
having had a dog as a household pct during childhood. Only case­
control sets in which the case and at least one control was traced and
could reply to the question arc included. Matched analysis by the
Mantel and Haenszcl method was used. 55% ofsubjects (cases and
controls) in Lancaster and 45% in Siena had had a dog as a
household pet during childhood. The differences between the cases
differences in exposure to other household pets, including cats and
birds. These findings do not support those from Manchester.
I-uboratory evidence in support of the canine distemper
hypothesis has been sought in the past but not found.2 The
prevalence of Paget's disease is higher in Britain than in any other
Western European country? Only in France do the rates approach
those in Britain. However, the dog population in Britain is
estimated as 10-4 per 100 people, while values for eleven other
European countries range from 17-2 tn France to 5*3 in
: extreme rarity of Paget’s disease there.
numbers ofcases of pagets disease and controls in

U.N< LASTER AND SIENA WHO HAD DOGS AS PETS DURING CHILDHOOD

We suggest that no firm conclusions be drawn from the
Manchester study until there is additional evidence, including that
from a large, adequately controlled case-control study in another

Soultampion SO9-IXY

D. J. P, Barker
F. M. Detheridge

Sir,—Although Dr O’Driscoll and Dr Anderson’s results show
that dog ownership was commoner in patients with Paget’s disease
than in diabetic patients, it is premature to suggest from these
findings that the primary infective agent might be a canine virus.
O’Driscoll and Anderson note that the survey’ provides only
circumstantial evidence to implicate dogs in the cause of Paget’s
disease and stress the need for further studies. The lay press,
however, tends to be less discerning; for example, The Times ofNov
8, 1985. under the heading of“Distemper jabs to help the family’’,
reported that dogs were probably carriers of Paget’s disease. Such
reporting only serves to provide ammunition (irrespective of
whether it turns out to be live or blank) for anti-dog groups and
tends to alienate members ofthe veterinary’ profession who are faced
with distraught dog owners.
It would be of interest to survey the incidence of Paget's disease in
the older veterinarians. Such veterinary’ surgeons will have been
exposed to sick dogs far more than any other group and at times
available or less widely used. It would be expected, therefore, that
veterinary surgeons should be over-represented amongst patients

.METHYL ISOCYANATE: THIOSULPHATE DOES NOT
PROTECT
Sir,—Various sources15 suggest that, after last December’s
methyl isocyanate (MIC) disaster at Bhopal, in India,4 there is
controversy about cyanide poisoning in some of the victims. It
has been claimed that sodium thiosulphate (Na,S2O;) was
therapeutically effective. However, no hydrogen cyanide seems to
have been released with MIC and it is unlikely that MIC is
metabolised to or leads to the release ofcyanide in the body. On the
other hand, Na,S,Oj could have therapeutic effects apart from its
action as a cyanide antagonist. No published work throws light on
this important issue.
While studying rats exposed by inhalation to MIC5 we evaluated
the effects of Na,S,O} on the clinical evolution and daily urinary
thiocyanate excretion during one week after exposure to MIC.
Eighteen male LAC-P rats of 130-150 g initial body weight were
used. Twelve rats (two groups ofsix) were statically exposed for I h
in a 50 litre glass tank to MIC at an initial concentration of 0’25
mg/1 (about 100 ppm). This corresponds to a time-weighted average
level of between 20 and 30 ppm, causing extensive damage (mainly
to the airway epithelium) and leading to severe respiratory distress,
but no acute deaths? Four of these rats received an intraperitoneal
injection of 0-25 ml Na,S,O} m saline (673 pmol per rat) 15 min
before exposure to MIC and then daily until the sixth day after
exposure; the other eight rats similarly received injections of 0-25
ml saline. Six rats were left unexposed to MIC, three receiving
Na,S,O, and three saline injections. After the exposure, the rats
were housed individually in metabolism cages for 24 h collection of
urine (on 50 pl gentamicin 10 mg/ml) and they*were weighed daily.
Survivors were killed 7 day’s after exposure, blood was taken, and

THE LANCET. NOVEMBER 30,1935

EFFECTS OF SODIUM THIOSULPHATE ON BODY WEIGHT (AS % OF
INITIAL BODY WEIGHT) AND URINARY THIOCYANATE LEVELS (pg IN
24 h URINE) AFTER EXPOSURE OF RATS TO .METHYL ISOCYANATE

the lungs instilled via the trachea with Bouin’s fixative. Urine and
plasma thiocyanate levels were measured in Louvain, Belgium (Prof
R. Lauwerys) by a modified p-phenylenediamine method.
No clinical differences between Na2S2O, treated and salinetreated rats were observed. Contrary to expectation, some rats died
in the first 48 h after exposure to MIC (four deaths ofthe eight saline
treated animals, and two of the four Na2S20j treated animals). A
third Na2S20j treated rat was moribund on the fifth day and was
killed. The deaths could have resulted from an exposure level higher
than intended (the dose-response curve being rather steep) or from
the isolation of the animals after exposure. Body weights, a good
index of an animal’s wellbeing, were no better in the Na2S2O}
animals than in the controls (table). One control Na2S20j-treatcd
rat lost weight during the first 4 days for no obvious reason. Total
urinary thiocyanate excretion was lower in the rats receiving
Na2S2O) than in those receiving saline, but it was also lower in MIC
exposed rats than in non-exposed rats (table). The progress of
urinary thiocyanate excretion was directly related to that of body
weight. Plasma thiocyanate concentrations on day 7 did not differ
between the four groups. The histological appearance of the lungs
and airways 7 days after MIC did not appear to be influenced by the
Na2S20j treatment. Bronchioles from both treated and untreated
animals showed a hyperplastic repair epithelium with fibrosis and
peribronchiolar inflammatory infiltrate.
This study suggests that Na;S2Oj does not protect rats from the
acute and subacute effects of MIC and that cyanide intoxication is
not involved in the clinical syndrome seen after exposure to pure*
MIG
Wc thank Mr C. J. Vesey (St Bartholomew’s Hospital. London) and Dr
W. N. Aldridge for advice and Mr J. Casters for thiocyanate measurements.

.MRC Toxicology Unit.
Cinhilion, Surrey SAM 5EF

B. Nemery
.$• SPARROW
D. D1NSDALE

SODIUM DIETHYLDITHIOCARBAMATE INDUCING
LONG-LASTING REMISSION IN CASE OF JUVENILE
SYSTEMIC LUPUS ERYTHEMATOSUS

Sir,—Remissions of systemic lupus erythematosus (SLE) are
sometimes obtained with steroid therapy, but with a high risk of
steroid dependency and serious side-effects, such as severe
infections or growth failure. We have been evaluating a T-cell
restorative drug,1'2 sodium diethyldirhiocarbamate (Imuthiol;
Institut Merieux, Lyon), in a 14-year-old girl whose first symptoms

were limited to non-erosive arthritis of the knee joints. A secondary
discoid rash with erythematous patches and adherent keratof
scaling and follicular plugging developed. Fixed erythema over the
malar eminences tended to spare the labial folds.
When first seen (April, 1984) this girl was neutropenic anj
thrombocytopenic(lessthan80 000/pl). Laboratory tests confirm^’
SLE: homogeneous antinuclear antibodies at the 1/1000 serum'
dilution and positive anti-Sm antibody by immunofluorescence
assays, in the absence of treatment with drugs associated with druginduced lupus syndrome. Total haemolytic complement was vmf
tow (CHS0<7 • 7 units), as were C5 (56 • 6 mg/dl, normal 70-145)^.
C4 (4 • 92 mg/dl, normal 13-40). Severe leucocyturia was found, not
associated with proteinuria. Her HLA phenotype was A3/Bw35 j
Aw32/B". B cells were normal in number, with a mild decrease in-E
cells. Labial biopsy was characteristic ofSLE. There was no family*
history, except for a grandmother with an ill-defined connective
tissue disease.
Treatment with prednisone 2 mg/kg daily was started in’AjjfiS?
1984. A serious Cushingoid syndrome promptly developed, ahdllSi
September, 1984, we decided to try imuthiol (5 mg/kg, orally, dnggH
week) to see if we could lower the dosage of prednisone. Withinfg!
weeks we could reduce the steroid dose and after the patient
been on imuthiol for 3 months a complete remission was achie^ra
and prednisone was stopped in April, 1985. Today, a year after iEm
start of treatment with imuthiol and more than 6 months afteji
prednisone had been stopped, the girl is well and labortory testsaxeE
normal (table). No side-effects have been noted in a yearaia
continuous administration of imuthiol.

LABORATORY FINDINGS (APRIL. 1984. TO SEPTEMBER, 198®?
April, 1984

March, 1985
(LooMj

In children
systemic illness (such as renal, neurological, or
involvement) prednisone 2 mg/kg daily is usually
Severe side-effects, that can be lethal, have
other treatments. Immunosuppressive agents have
conclusive results in SLE? The use of
immunotherapeutic agent such as imuthiol might
approach to the treatment of connective tissue
association with reduced dosages of steroids or
therapy.

THE LANCET, DECEMBER 13, 1986

1403

Rapid hydrolysis of urea has been reported to be a useful test for
C pyloridis, so urea broth was inoculated with tissue homogenate.
Where the bacteria are present in large numbers in the biopsy

hours and is dqi time-consuming. However, in the 10 culture­
positive cases the urea test was positive within 2 hours in only 4 and
within 8, 24, and more than 24 hours in a further 1, 2, and 1,
respectively. Furthermore, urea testing to 24 hours or more resulted
in 3 false-positive reactions (out of 7 culture negatives).
University of Uppsala,

Lars Engstrand
Carl Pahlson

Uppsala University Hospna)

Sven Gustavsson

LONG TERM PATHOLOGY OF LUNG, EYE, AND
OTHER ORGANS FOLLOWING ACUTE EXPOSURE
OF RATS TO METHYL I SO CTANATE

Sir,—A year after the leakage of gas, mainly methyl isocyanate
IjffiMIC), at Bhopal, India, in 1984, as many as 320 000 people were
affected,1 and an increased mortality among those exposed
isted. Long-term effects of MIC exposure include irritation
ival/comeal alterations and restrictive pulmonary defects—
ve suggested the possibility of longer term sequelae.
In a pilot study* rats exposed to 31,21,11, or 0 pans per million
) of MIC vapour for 2 h have now been observed over 14
months. Two MIC exposed animals (one 31 ppm and one 11 ppm)
(died 6 and 8 months, respectively, after MIC exposure following
: -sudden onset of respiratory distress. Macroscopic and microscopic
!. (examination of the six animals killed at 14 months revealed a history
’ jof mild respiratory infection in all animals. MIC-exposed animals
; 'had at least four times the amount of lymphoid aggregates found in
['{control animals: lymphoid tissue averaged 0-219 mnr per mm2 total

lung tissue in the animal exposed to 31 ppm, 0 025 mm2 in the two
21 ppm rats, 0-039 mm2 in the 11 ppm animal, and 0-005 mm2 in the
two controls. This lymphoid hyperplasia (see figure) was adjacent to
bronchiolar airways and consisted largely of lymphocytes, plasma
cells, and macrophages. A mild infiltrate of eosinophils was present
in the bronchial mucosa of both 21 ppm animals and the 31 ppm
animal. There were no eosinophils in the lung tissues of either
control. Mild interstitial fibrosis in the peribronchiolar regions was
seen in all treated animals.
The major finding in the eyes was an eosinophil and lymphoid
infiltrate in the mucosa of the conjunctivae of the eyelids and
perilimbal regions. This was most prominent m the 21 ppm
animals.
Liver, kidney, and spleen were normal.
These findings suggest that long-term changes in the eyes and
lungs may result from a single 2 h exposure to acute sublcthal doses
of MIC vapours, and indicate that the immune system is most
probably directly involved. Immunological effects in man have
been observed,5 which might be causally related to pathological
changes or increased susceptibility to infections. Enlarged tonsils
and lymphoid hyperplasia were seen in patients 4-6 weeks after the
Bhopal incident, and antibodies to proteins modified by reaction
withMICwas noted. Kamat ct al'also suggested the possibility of
interstitial fibrosis in many of the 82 people examined. Lung biopsy
in 5 cases showed fibrosis (no controls). Hyperreactivity pneumo­
nitis after exposure to various isocyanates has been reported,7 and
low concentrations of isocyanates stimulate lymphocyte prolifcrauon.M Presence of eosinophilia has been demonstrated’ in
animals exposed to aliphatic isocyanates. MIC, when linked to
albumin, can elicit an antibody response in guineapigs.10 The
long-term finding of lymphoid hyperplasia seen in our animal study
may be due to cither to persisting exposure-related antigens or to an
increased susceptibility to other immunostimulating agents follow­
ing MIC exposure.
We conclude that the possibilities of persistent antigen/antibody
activity and hypersensitisation of the airways of individuals exposed
to MIC are worthy of further investigation, and may help uncover
the causes ofcontinuing respiratory and eye problems and reports of
delayed sudden deaths experienced by Bhopal gas victims.

Wc thank Dr J. C. Wagner for examining the lung sections and Mrs
Christine Moore for technical assistance in the preparation of histopathology

and 1 ropical Metiicine,

and T topical Medicine

T. Gassert

C. Mackenzie

Department of Ophthalmology,

M. Kerr Muir

Department of Occupational Health,
London School of Hygiene
znd Tropical Medicine

N. Andersson

1985:63(48): 18-32.
Andersson N. Kerr Muir M.Arwani MK.MahashabdeS, Salmon AG, Vaidyanathan

6. Salmon AG, Kerr Muir M, Andersson N. Acute toxicity of methyl isocyanate; a

human lymphocytes. Toxicol Appl Pharmacol 1978; 44:617-41
hematoxylin and eosin; x 20. j

Inhalation Toxicity Studies of Methyl Isocyanate (MIC) in Rats:
Pan I—Pulmonary Pathology and Genotoxicity Evaluation
K K DUTTA, G S D GUPTA, ANIL MISHRA. ANIL JOSHI, G S TANDON & P K RAY"
Industrial Toxicology Research Centre, Lucknow 226 001, India
Received 30 December 1987
A single exposure of MIC at 3.20 mg/1 chamber concentration for 8 min. through whole body inhalation chamber to
awqi* ■ male albino rats, caused severe imucon of eyes, lacrimation, corneal opacity and conjucrival hyperaemia. irritation of
tx®" respiratory tract and gastrointestinal tract, pennasal, penoral wetting, frothiness, gasping and dyspnea. Necropsy revealed consolidation of two small lobes of lungs and baloomng of the gastro-intestinal tract Microscopically, penpher'4 '
al emphysema was well marked after -18 hr of exposure, and persisted up to 14 days though exhibiting a trend of reI’jST duced severity after 3 days. Congestion of the blood vessels, edaematous changes, cellular reacnon and hyperplasia of
PS '
the lymphoid follicles became marked and persisted up to 14 days. The postexposure (7-14 days) thickening of the
alveolar septa and around the penbronchials was progressively noticeable and quite pronounced on 14th day. Food
.JJ.' L and water consumption and body weights of the animals initially reduced followed by a gradual recovery. No significant
" micronudeus formation was observed In rat bone marrow preparations 7 and 14 days after exposure. Exposure to
'-/g-.r. higher concentration of MIC. using 10.97, 21.95 and 43.90 mg/l resulted in extensive reaction, pronounced clinical
;'.Sfe:symptoms and death of all exposed rats within 24 hr. It appears from these observations that histopathological injury to
lungs and extensive monalitv in rats is a consequence of necrotizing/corrosive action of the direct inhalation exposure
'
to mic

‘ S) Methyl isocyanate (MIC. mol. wl 52.05. sp. gravity
i
09230) is a colourless, highly volatile, inflammable
-3 i, a^^rong odorous liquid used in the manufacture
ofcarbamate insecticides, such as carbaryl, carbofhran baygon, kaldicarb, and warfare agents. It
reacts violently in presence of moisture, acids, alkalies, etc. It is a hazardous chemical by all routes of
contact, irritating skin, eyes and mucous membranes. The possibilities of inhalation and subse2? quent hazards are greatly enhanced because of its
high vapour pressure1. The leakage of toxic gas. in:'IF) eluding MIC, from an industrial reservoir at Bhopal
?_.L.on 2/3 December, 1984, led to widespread morbidHH ity and mortality in humans and several species of
animals in and around the area2. An accident also
occurred in U.K., but of less severity affecting only
HI 35 firemen3. The horrifying experience of the iU-

:

nesses and deaths in humans exposed at Bhopal and
U-K-, prompted extensive toxicological studies in
animals world over. The reports of experimental
toxicological studies on MIC, using laboratory ani?• ; mak’tlave rcvealed the acute and sub-acute patho5 s Meal injury in the form of extensive necrosis, eroJ./J 53011 °f respiratory and olfactory epithelia, haemorT
e<fema. presence of cellular debris, inflammag; fc “JRlls and fibrin in the airways, chronic alveolitis
g -- and atelactasis4"10. We initiated toxicological studS >es on rats exposed to MIC right after the Bhopal
» episode with a view to comparing the results with
"Correspondent author

observations made by us on toxic gas affected pa­
tients in Bhopal (see our data on human patients).
Detailed studies were undertaken in order to under­
stand1 the acute and sub-acute toxicity potential of
MIC2, the spectrum of clinical and pathological
manifestations3, metabolic biochemical mechanisms
of biological reactivity of MIC and subsequent injury/lethality. Inhalation route was considered to be
the preferred mode of exposure akin to the environmifiital situations and rats were selected as the ex­
perimental animals for these studies.
This report presents our observations on toxico­
logical manifestations, pathological abnormality,
genetic toxicity, and relative mortality in male albino
rats exposed to MIC.

Materials and Methods
A sample of MIC, with a 99.9% purity (confirmed
by Mass spectroscopy) was procured'from Regional
Research Laboratory (CSIR), Hyderabad. All other
chemicals and reagents used in this study were of
analytical grade obtained from BDH or E. Merck,
India.
Experimental protocols—The all glass whole
body inhalation chamber of 21 litres capacity having
an internal diam. of 30 cm was used in the present
study. The chamber had two parts, (a) upper and (b)
lower. The upper part was detachable with 3.130 li­
tres capacity, having arrangements for placing ther­
mometer for recording the chamber temperature,
and to fit nebulizer, etc. The lower portion was of

177

INDIAN J EXP BIOL. VOL. 26. MARCH 1988

17.870 litres capacity, with 4 ports (two on each 20%) and exposed animals showed distinct sigtf
side). One port was connected with a compressed and symptoms of toxicity over a period of time. 4
air tube and through this tube the required amount
Similar arrangements were made to expose ani­
of MIC was injected into the chamber with a Hamil­ mals with cpmprcssed air only and these animal:
ton micro syringe; the second was for collecting air served as cqntrol. Clinical symptoms, food and wrj
samples of the chamber; the third was of vacuum ter consumption, body weight and mortality rati,
line and the fourth was provided for attachment to were observpd during and after the exposure for if
the other monitoring devices or for being connected days.
with other gases in case the same chamber is to be
Histopathology—Animals were sacrificed 48 hr,used with more than one gas. The middle of the low­ 72 hr. 7 days and 14 days after exposure. Lungwii'
er chamber has a perforated teflon plate where ani­ fixed by inflating with the fixative 10% buffered form­
mals can be placed- The bottom of the lower cham­ aline, dehydrated with ethanol, embedded in paraf­
ber is designed for independent collection of stool fin and 4-5 jam thick cut sections were stained Wil
and urine (Fig. 1).
haematoxylip-eosin12 for routine histopathology,
This type of chamber is appropriate for short­ and Gomorj's silver nitrate staining was done fa
term toxicity studies in static condition with micro reticulin13 examination.
amount of MIC in test chemicals10. The entire sys­
Genetic toxicology— Genotoxicity potential ol
tem is being kept ipside a fuming hood fitted with a MIC was evaluated in bone marrow preparation!
positive pressure exhaust system so that the work from both femurs of exposed rats according to the
environment is safe. The whole set up was checked procedure of Schmid14.
for being leak proof before each exposure.
The animals were acclimatized in laboratory con­ Results and Piscussion
Gross observations—1Gross observations during
dition for 7 days prior to MIC exposure. Each time
6
albino rats, adult, male (6-7 weeks) of 150-180 g and immediately following MIC exposure were hi
body weights from 1TRC (Ghent) animal colony perexcitability, lacrimation, perinasal and perioral
were exposed to various concentrations of MIC and wetness, respiratory difficulty, gasping, decreased
analysed by aspiring appropriate samples at various activity and ptaxia. 2-3 animals in each batch had
intervals from a side port and estimating through a nasal, oral and eye bleeding during the exposure.
GLC, model No. Sjiimatzu GC-7AG. An average Except in 2 rgts which became completely blind the
chamber concentration of MIC in this set was 3.30 postexposure manifestation included continued fro­
mg/1 maintained for a period of 8 min. This was thiness and severe dyspnea even up to 12 hr,conjucused for all further toxicology studies reported in tival hyperemia in nearly 50% of animals on 3rd
Parts Il-V. Since it gave only a partial mortality (10- day, development of corneal opacity in both eyesoa

Fig. I —The whole body inhalation chamber placed inside the exhaust system

178

DUTTA et aL: INHALATION TOXICITY OF MIC IN RAIS-1

foUowcd by clearing of eyes on 10th day.
^^^Jwater consumption of the exposed aniB
negligible up to 48 hr and improved in
t^ys. Body weight of the animals initialB i2SS± and was foUowed by a 8radual hnproveimproved water and food intake. In most
'
severity of above manifestations was diMsaifelated to the amount of exposure to MIC. Si>
observations have been reported by other
;

using MIC4'10, phosgene and nitrogen di-

KgaSandTOI'6’17? "^j^Wirv—In our experimental set up, exposure
■ Toe resulted in 100% mortality of rats at a dose
435 mg/1 within 30 min, at 21.95 mg/1 within 12
' ' ixsnd 10.97 mg/1 within 24 hr. Exposure to 4.39
f 7' <m/1 of MIC resulted in 30-40% mortality within 72
| - hr It is highly probable that the observed lethality

' wi a consequence of pulmonary insufficiency
cased by edema, haemorrhage and narrowing of
^itfrwavs4-7’’

^BESuiopisy-Dead animals or those which were in
Rgibund condition, when autopsied, had typical
^fflfelooning of the gastro-intestinal tract which was
yljjill of a brownish fluid, had enlarged lungs though
fgafr^jdier organs did not show any noticeable
Two small lobes of lung were consistently
■(consolidated and the other lobes were enlarged and
SSeddish in colour. Consolidation of the lobes was
■More pronounced in the moribund animals.
^BgHistological observations —Within the first 48 hr

■Sifter exposure, severe emphysema was observed in
grateperipheral area of the lobes (Fig 2). Congestion
S£was prevalent in the alveolar capillaries with diapeSueas, pneumocytes were hypertrophied, and large
■mononuclear cells were lying loose in the alveoli.
■Moderate lymphoid hyperplasia and presence of in»fianunatory infiltrates were observed in the perisgf bronchial areas. Desquamated bronchiolar epithelW tai cells along with inflammatory mononuclear cells
were found inside the bronchiolar lumens (Fig. 3).
Ef'After 72 hr peripheral emphysema reduced, alveKdar congestion persisted, hypertrophied pneumogjcytes increased in number, alveolar septa slightly
■thickened, edema and the changes of bronchioles
■more pronounced. These changes were more in^nse in consolidated lobes (Fig. 4).
■p^fter 7 days of exposure emphysema was reconsiderably with persistent congestion and
of numer°us inflammatory cells. Some of
alveolar septa were thickened. Bronchiolar ep■£“™ai cells were completely denudated exposing
■p decper layer and had inflammatory exudate.
■r-pPhoid aggregation in the peribronchial areas
■0. prominent. Polymorphonuclear cells were largR m number than mononuclear cells in the intersti­

tial area. Increased laying down of reticulin was also
seen in the peribronchial and perivascular areas
(Figs 5 & 6).
After 14 days of exposure, emphysema was signi­
ficantly reduced as compared to those observed ear­
lier. Many alveoli- were apparently unaffected,
whereas some isolated foci of cellular reactions
comprised primarily the polymorphonuclear leuco­
cytes and occasionally mononuclear cells were still
evident in association with haemorrhage and edema
(Fig. 7). Alveolar septa were thickened and there
was significant reticulation in the foci of cellular
reaction (Fig. 8). Peribronchial edema, inflammato­
ry cellular infiltration and fibrosis were also evident
along with the exfoliation of bronchiolar epithelium
affecting the deeper layers of bronchioles (Fig. 9).
Severe bioreactivity due to exposure to MIC and
progressive regeneration during postexposure re­
covery appears to be responsible for above observ­
ations. Our histopathological studies indicate that
the primary target of MIC induced injury in respira­
tory tract was in proximal airways, and then, to
some extent, also in alveoli. These findings are con­
sistent with the reports of acute toxicity from
MIC4"10 and toluene di-isocyanate16-17.
Since MIC is a highly irritant, reactive and necro­
tizing agent, the initial injury could be because of its
direct corrosive action on pulmonary tissue. Lung,
in its neutral physiology, has a very humid environ­
ment where MIC can react violenty, so that the con­
sequent generation of heat can substantially contri­
bute to its necrotizing action. The extent of pulmon­
ary injury observed in our studies at a chamber con­
centration of 3.20 mg/1 for 8 min varies from that in
other studies utilizing 0.02-10 mg/1 for 1 hr4-8 or
0:32-1.04 mg/1 for 30 min10, possibly due to a grea­
ter amount of MIC entering the lung and reacting
with all available moisture of the upper respiratory
tract to escape and reach alveolar areas of lung.
Genetic toxicity potential, tested after 7 and 14
days of exposure, did not exhibit significant induc­
tion of micronucleus formation in normochromatic
erythrocytes (0.166 ±0.02%) when compared to
that among controls (0.133 ±0.02%). Thereafter,
genotoxicity of MIC in this short term study is not
substantiated through our observations and this is
consistent with a recent report of McConnell et al?,
although we feel that no definitive conclusions
should be made at this time in the absence of data
from longterm studies. Investigations are underway
to study the long term effects of MIC exposure in
rats.
From the above it appears that the exposure to
MIC primarily induces pulmonary injury due to its
necrotizing/corrosive action. The pathological ab-

179

INDIAN J EXP BIOL, VOL. 26, MARCH 19SS

, *

r

Fig, 2—Section of lungs, showing peripheral emphysema. Two day post-exposure or WGC
Fig. 3—Section of lungs showing desquamation of epithelial cells into the lumen of bronchiones. ceiiii^ar rnSkrancm into the peribn*
chiolara^a. Two day post-exposure of MIC. H & E •< *<0.
J
Fig. 4—Section of lungs showing alveolar congestion and presence of edaematous fluid. 3 daw post-soo^ar-e of MjC. H&E x 130.J
Fig. 5—Section ot lungs showing desquamation of lining epithelial cells into die bronchioles ana jnoac nf inflammatory exudate
7 day post-exposure of MIC. H & E x 110.

180

rpost-exposure of MIC. Gomori’s silver nitrate x 110.
EL "■Section of rat lungs showine emphvsema. focal cellular reaction and thickening of the interalveolar septa. 14 day post-expo”
sure of MIC. H& Ex 110.
jfe: rhot°nucrograph of the same of the area of Fig. 8. Showing focal area of increased laying down of reticulin. 14 day post-exposure of MIC. Gomori’s silver nitrate x 110.
. SecOon of rat lungs showing desquamation of bronchiolar epithelial cells exposing deeper layer with marked presence of in­
flammatory cells in the bronchiolar area. 14 day post-exposure of MIC. H & E x 80.
181

INDIAN J EXP BIOL, VOL. 26, MARCH 1988

normalities and lethality are dependent upon the
dose of MIC exposure. The epithelial erosion is re­
parable during the postexposure recovery period
even though the process of regeneration brings
about fibrinogenic response and may be responsible
for chronic pulmonary dysfunction. It is expected
that these findings will help in understanding and
management of toxicosis induced on exposure to
MIC in future.
The observations made in this may provide sug­
gestive explanations regarding the abnormal respir­
atory functions noticed in our human study where
we have observed prevalence of combined obstructive-cum-restrictive ventilatory impairment, bron­
chial obstruction, and restrictive pulmonary
defect18.

Acknowledgement
The authors are indebted to Dr S. Varadarajan for
his critical review and comments on the manuscript.
The technical help of Mr BJG Maji and Mr SJHLN.
Naqvi is acknowledged. Thanks are due to Dr Ravi
Shanker for histopathological interpretations and to
Dr Deepak Kumar Agarwal for critical evaluation of
the manuscript.
References
I Kimmerle G & Eben A, Arch Toxicol, 20 (1964) 235.

182

Mamath S R, Mahashur A A, Tiwari A K B, R>td^j
Gaur M, Kolhatpar V P, Vaidya P, Parmar D, Rup^
Chatterjee T S, Jain K, Kelkar M D & Kinare S G <
palJ Postgrad Med, 32 (1985) 63.
4
Axford A T, McKerrow C B, Parry J A & Le Quesnc P
Br J Ind Med, 33 (1976) 65.
4
Nemery B, Dinsdale D, Sparrow S & Ray D E, BrJInd '
42(1985)799.
Dodd D E, Fowler E H, Snellings W M, Pritts IM
RL, Fundam Appl Toxicol 6 (1986) 747.
Fowler E H & Dodd D E, Fundam Appl Toxicol 6 (1
756.
Noorman G A, Brown R, Gupta B N, Uraih L C & Bud3
R, Toxicol Appl Pharmacol 87 (1987) 446.
73
Dinsdale D, Nemery B & Sparrow S, Arch Toxicol^
(1987)385.
McConnell E E. Bucher J R, Schwerz B A, Gupta B N, She
by M D, Luster M I, Brody A R, Boorman G A, Rid
C, Stevens M A & Adkins B (Jr), Environ Sci Techn
21(1987)188.
i
Pant S C, Srivastava R K & Vijararaghavan R, Bull Envit,
Coruam Toxicol 38 (1987) 876.
:1|
FarlandHN, Fund Appl Toxicol 3 (1983) 603.
McManus J F A & Mowry R W, in Staining methods,
logic and histochemical(Happer and Row Publishers, 44
East 33rd Street, New York), 1960.
<
-M
13 Goman G, Am J Path, 13(1937)993.
14 Schmid W, Mut Res, 31 (1975) 9.
AlarieY,
CRCCrit
Rev
Toxicol!
(1973)299.
9
15
16 Ducan B. Scheel L D, Fairchild E J. Killens R & Graham?
Am IndustrHygAssocJ, 23 (1962) 447.
Kaufman J & Burkons D, Arch Environ Hhh, 23 (1971)2^
Rastogi S K, Gupta B N. Hussain T, Kumar A. Chandra
Ray PK, Indian J Exp Biol 26 (1988) 161.

■

gpecial Communication

©Hl : |t\-

i
Rhopal Tragedy’s Health Effects
^Review of Methyl Isocyanate Toxicity
K !.
EpaS. Mehta, MD; Anant S. Mehta; Sunder J. Mehta, MD; Arjun B. Makhijani, PhD
S YEARS AGO, on December 3,

j£j, a toxic gas leak at a Union Carbide
.gccide plant in Bhopal, India, re­
used methyl isocyanate (MIC) and its
^edon products. The number of per“exposed” and “injured” remains
iasruin.1 Official estimates from the
yian government place the dead at
psmd 1800/ Others estimate mortal^to have been between 2500 and 5000
ad the number of injured to have been
?to200000.M

See also p 2795.

-Until the Bhopal incident, neither
iths nor cases of toxic effects from
EC exposure had been recorded in
Mo Medicus.** We have extensively
ttreyed the medical literature con=nng effects of MIC exposure on the
®bms of the disaster and laboratory
safe in animals. A great deal has
ta learned, but many questions still
•sain unanswered.

BHOPAL PLANT
j^.'969, the Union Carbide Corpora*Wlt a formulation plant in Bhopal,
to mix and package pesticides imfrom the United States. The
*twas expanded in 1980 to manufaccarbamate pesticides from chemiy®ermediaries produced on site."
the capital of the State of Mag.Pradesh, lies 744 km south of New
jj?and has a population of about
t^?peop'e- The railway station was
_ bom the plant, and a sizable popu^Ihat worked in the textile mill
,/^~jnthearea around the station.2

*t

Aurora, Colo (Dr P. S.
1^2’°' 01 Business. University olTexas. Austin

5760 s Gcneva St Englewood.
gfe,1|D,pS. Mehta).

5er5.1990-Vol264.No.21

In 1984, squatters’ rights were granted
to those in the burgeoning settlements
surrounding the plant.16 The Indian
Council of Medical Research estimated
that 100 000 people lived within a 1-km
radius of the plant at the time of the
tragedy.
Methyl isocyanate, produced at the
plant, was stored in liquid form in two
steel tanks, each holding 57120 L , and
was used as needed to produce carbaril
pesticides.8-’ For safety reasons, MIC
storage tanks at plants in Belgium, the
Federal Republic of Germany, Japan,
Korea, and the United States (West
Virginia) have smaller capacities, hold­
ing an estimated 17 500 L with allowable
filling of 50%.M

MIC CHEMISTRY/TOXICOLOGY
Methyl isocyanate is a colorless liquid
with a molecular weight of 57.1, boiling
point of 39°C, specific gravity of 0.96,
and vapor density of 2.1011 Contact with
water causes an exothermic reaction,
resulting in the formation of carbon di­
oxide, methylamine gases, and A7, Ndimethyl urea.8-’ The reaction is en­
hanced in the presence of acids, alkalis,
and amines. Contact with metals and
certain catalysts causes violent poly­
merization, and fire involving MIC re­
sults in hazardous decomposition prod­
ucts such as hydrogen cyanide (HCN),
oxides of nitrogen, and carbon monox­
ide.’-” The National Institute for Occu­
pational Safety and Health’s 1978 publi­
cation” sets forth the following safety
and warning guidelines for MIC: (1) The
permissible exposure limit of MIC is
0.02 ppm averaged over an 8-hour work
shift, which is also expressed as 0.05 mg
of MIC per cubic meter of air. (2) The
documentation of threshold limit values
states that at 2 ppm no odor is detected
but subjects experience eye, nose, and
throat irritation and lacrimation. At 4
ppm the symptoms of irritation are
more marked. Exposure is unbearable

at 21 ppm. (3) MIC is regarded as a
material with poor warning properties.
In 1964, Kimmerle and Eben” first
reported on acute toxic effects of in­
haled MIC in animals, establishing the
lung as the primary site of injury. Up
until 1984, data provided by industries
using MIC in pesticide and herbicide
manufacturing processes mainly dealt
with chemical properties rather than
toxicology.11 Since the Bhopal incident,
however, priority was assigned to MIC
toxicology assessment.18,11

THE BHOPAL INCIDENT
The widely accepted explanation for
the cause of the release of MIC and its
reaction products from the Bhopal plant
was the entry of water into tank 610,
which contained approximately 40900
kg of MIC. This resulted in an exother­
mic reaction causing approximately
24 545 kg of MIC and 12 800 kg of reac­
tion products to escape within a few
hours.68 Estimated time of release of
MIC and its reaction products was 12:30
am on December 3, 1984. By 2 am, most
of the contents of tank 610 had escaped,
spreading as a cloud over a large, dense­
ly populated area of approximately 40
km=. The first deaths were reported to
the police by 3 am and by morning, more
than 1000 people were reported dead,
some as far as 8 km from the plant.
Meteorological conditions at the time
of the MIC leak aggravated the effects
of its toxicity. The temperature that
night was 10°C and the air was dry. The
winds were from north to northwest at 1
to 2 m/s (3 to 4 mph) in the direction of
settlements located in the vicinity of the
plant. Temperature inversion also re­
duced the dilution of the gas cloud.
Thus, the area with the largest number
of dead and severely injured was ap.proximately 6.65 km2 south of the
plant.”
Ninety thousand patients were seen
within the first 24-hour period at nearby

Bhopal Tragedy's Health Effects—Mehta et al

2781

■!

hospitals, clinics, and small area health
facilities.” Bhopal has four major hospi­
tals and several clinics that provide pri­
mary health care. Three hundred physi­
cians staff these 1800 beds.18 Little was
known about possible treatment for tox­
ic effects due to MIC exposure, and sev­
eral days after the accident it was still
uncertain whether the effects being ob­
served from the gas leak were due to
MIC, phosgene, HCN, or other MIC
reaction products.2’” Treatment of the
exposed population was thus limited to
symptom management because no sci­
entific agreement could be reached on
what might constitute an appropriate
antidote.

ACUTE TOXIC EFFECTS
About 200 000 people were acutely af­
fected by the MIC leak. In all, 2500 are
estimated to have died during the first
week. Immediate health effects ob­
served were respiratory problems and
eye irritation.2’” Six thousand people
suffered from acute respiratory dis­
tress, plus symptoms involving the cir­
culatory, gastrointestinal, and central
nervous systems. Total exposure time,
concentration levels of MIC, age, sex,
and physical condition of victims played
a major role in the development of acute
and chronic disease. ”’2°’21 There is no
consensus on MIC concentration levels
in Bhopal’s atmosphere immediately
following the gas leak. None of the data
on morbidity and mortality are firm.
Hydrogen cyanide has been implicat­
ed in the acute injury caused by the gas
leak.22 Blake and Ijadi-Maghsoodi 23 and
Bhattacharya et al21 have shown that
pyrolysis of MIC at high temperatures
(350°C to 540°C) resulted in the forma­
tion of HCN and other degradation
produdts. The cherry-red color of the
blood and viscera of the victims, in­
creased urinary thiocyanate levels in
some survivors, and reported symp­
tomatic relief by administration of sodi­
um thiosulfate are cited as evidence sup­
porting the causative role of HCN.22,21’26
Others dispute this evidence.2’’31 In vi­
tro, MIC itself can produce “cherry-red
blood" due to formation of methyl­
amine.2’’28 Experiments with laboratory
animals produce evidence incompatible
with cyanide toxic effects in Bhopal vic­
tims.” Elevated urinary thiocyanate
levels in Bhopal victims, often mea­
sured months after the exposure, can­
not be equivocally attributed to the
original toxic gas exposure because of
the relatively rapid clearance of thiocyanate.30’31 High thiocyanate levels also
may be explained by other factors such
as water contamination, smoking, and
dietary habits of the affected popula­
tion.31 As a result, the role of HCN as a

causative factor remains ill-defined at
this time.
No attempt has been made to re­
create the incident experimentally to
examine effects on animals. However,
animal inhalation exposure studies
mimicked the gradation of human re­
sponses that occurred at different dis­
tances from the chemical plant. Overall
objectives of these studies were to de­
termine the consequences of injury fol­
lowing acute exposure to high MIC va­
por concentration and to elucidate the
pathogenesis of early mortality. In one
study, rats and mice were subjected to
lethal and sublethal concentrations of
MIC by inhalation.32 Exposure to a 20to 30- ppm concentration of MIC for 2
hours caused severe dyspnea and weak­
ness followed by death within 15 to 18
hours. A second wave of deaths oc­
curred 8 to 10 days later, preceded by
respiratory distress. Exposure to a 3ppm concentration caused no respira­
tory abnormalities, while at 10 ppm, ob­
structive airway lesions were evident
even 13 weeks after exposure. These
phases corresponded to those seen in
Bhopal victims. Lethal exposure stud­
ies done on rats, mice, and guinea pigs
revealed
extensive
degenerative
changes in epithelial lining extending
from the nasal cavity to the level of the
bronchioles with mucus, fibrin, and
sloughed-off epithelium plugging the
airways.3”8

RESPIRATORY EFFECTS
Involvement of the respiratory sys­
tem was the most common and serious
health problem of the victims. Misra et
al“ retrospectively reviewed charts of
978 patients admitted to Hamidia Hos­
pital during the first 3 days after expo­
sure. In 544 victims, symptoms includ­
ed breathlessness (99%), cough (95%),
throat irritation or choking (46%), ehest
pain (25%), and hemoptysis (12%). Cya­
nosis was conspicuous by its absence. A
more detailed report from the same in­
stitution37 on the range of radiologic pul­
monary changes in 500 victims during
the first 3 days of exposure described
interstitial edema (41%), alveolar and
interstitial edema (41%), and destruc­
tive lesions with cavitation, pneumome­
diastinum, or emphysema (8%).
Kamat et al38 studied 82 individuals
with persistent symptoms between the
seventh and 55th days after exposure.
Seventy-eight percent showed a re­
strictive pulmonary functional defect
which in one fourth improved with bron­
chodilator therapy, suggesting a sec­
ondary obstructive element. Inability
to maintain normal maximal-minimal
ventilation and oxygen uptake at rest
was seen in 45 individuals (55%). Twen­

ty-four subjects had impaired abiljt...
increase oxygen uptake on exejj

and in 78 there were extensive
genographic changes suggesting jj?
stitial depositions. Flow volume stuZ
<
of 35 individuals showed change
t*
small airways in 12 and incoordinate
central airways in 15. Blood carboy^
moglobin levels measured in 69 indiv* ;
uals were raised in 66, while methe^ ’
globin levels measured in 80 were raj^
in 63. In a separate study,83 the autL J
reassessed victims over a 6-month p.
od. Of 78 subjects studied at 3 mott?
results of pulmonary function teJl—
were unchanged in 46%, improvejjT
38%, and worsened in 12%. Only 50;! v1

52 subjects studied at the end
months showed improvement. PatdIS
al“ did sequential measurements I ■
maximal expiratory flow volume on -I •

above subjects for 18 months and fo, ■'
chronic respiratory disability with (»
volume reductions due to restrict' ,
lung disease with alveolitis.
Two months after exposure, the>
suits of demographic and clinical s»
ies41’42 of 1109 subjects supported the>
suits of the studies noted above. Thin
nine percent of 783 patients shr
ventilatory impairment by lung spin
etry tests, with females exhibits/’’
higher prevalence (44%) of abnoro
ties in comparison with males (31
Naik et al“ reported pulmonary f
tion studies on 569 persons. Grot
comprised 446 persons residing vr.
0.5 to 2 km of the plant, and grai
comprised 123 persons who lived;
ther than 8 km from the plant. At 1(»
109 days after the exposure, 72*group 1 had respiratory symptoms!
showed persistent and, in some cs
worsening pulmonary function ter
suits. In group 2, 17% suffered ?■ ,
respiratory ailments, a much highs' ,
cidence than would be expected ii
control population. Six to 8 months!
the exposure, lung biopsies don?
three of the victims revealed alw
wall thickening, interstitial fibr
and exudative reaction in terr
bronchioles with bronchiolitis oh
ans. Pulmonary hypertension rete
obstructive functional defect was
detected in some victims.4,88
Experimental studies done by ft
al44 on rabbits and rats after exposMIC at concentrations of 3 art
mg/L, respectively, revealed infl*'
tory reaction, destruction of alveo
chitecture, and pulmonary edeir
the majority of animals, epithelial:
of the bronchioles was extensive!*
aged. These findings suggest^
MIC predominantly damaged lur
sue due to its corrosive action. Ar
and Dutta et al48 showed that a■

Bhopal Tragedy^ Health Effects-M*

,]evel exposure to MIC immediatethe cell lining of the respiratory
r in both mice and rats. Animals that
the exposure showed excess
, tissue occluding the airways and
Bering oxygen exchange. Alarie et
^posed Swiss-Webster mice to
; jt a 5 to 7.6 ppm for 90 minutes and
ed MIC to be a more potent sensotant of the upper respiratory tract
/formaldehyde, chlorine, or ammoIt was a strong pulmonary irritant
dmost the same concentrations,
ingMIC a chemical with poor warodiaracteristics. Nemery et al" con­
ed the highly irritating properties
[C. In longer-term studies done by
eman et al,"-" mice were exposed for
ars to MIC concentration levels of 0
trol), 3, 10, and 30 ppm, and fold up for 91 days. At 30-ppm concenions, extensive necrosis of the respitract, including trachea and main
ochi, was observed. Though regen­
ion of ^fcielium occurred rapidly,
Jwninaraid mural fibrosis of the
o bronchi persisted in many of the
. at the conclusion of the 91-day
iy. Uraih et aln assessed the ultractural changes of nasal and respiraepithelium and confirmed the
helial necrosis and gradual regenere with persistent fibrosis in experi■ital animals. Tepper et al“ studied
iiopulmonary
effects
in
rats
o 6 months after MIC exposure
0 ppm for 2 hours and found evi« of pulmonary hypertension. This
t documented by electrocardiogram
ages and supported by postmortem
ysis that showed right ventricular
ertrophy. Srivastava et al” exposed
to sublethal concentrations (137
dor 30 minutes) of inhaled MIC so as
•raid the induction of pulmonary edeuid then studied lung morphologic
acteristics and mechanisms. Maxi■ dynr^h surface tension de»od whiRotal lung capacity, lung
■dag, and compliance increased,
ags that correlated with histologic
of emphysema. In a study on
structure of respiratory tract in
exposed to 0.25 mg/L of MIC for 1
■ Hinsdale et al" showed a “raft” of
® and fibrin lining most of the airouring the first week after expo­
rt with repair well advanced
2 to 3 days. The majority of the
Vs were lined with normal epithe■*ithin 3 weeks of exposure, but
foci of hyperplasia and occluded
* Persisted.
e clinical studies described above
'■’ethodological problems. They
^■respective; lack suitable conhave biases in history taking,
• “teping, and patient responses.

' -’■eember 5,1990-Vol 264, No. 21

mmnmmmmi

Radiologic and pulmonary function
tests are limited and poorly organized.
Nevertheless, there appears to be ade­
quate evidence of fibrosing bronchiolitis
obliterans as an effect of long-term inju­
ry, but there is no credible evidence
regarding its frequency in the exposed
population. Well-designed animal ex­
periments corroborate the development
of acute lung injury and chronic restric­
tive lung disease along with persistent
airway obstruction.

OPHTHALMIC EFFECTS
On the first day of the disaster, 6000
people were seen as outpatients and an­
other 2000 were seen as inpatients by
the Department of Ophthalmology, Hamidia Hospital." Presenting manifesta­
tions included severe watering of the
eyes, photophobia, profuse lid edema,
and corneal ulcerations. Survivors with
the most severe eye effects were stud­
ied by a team of Indian and British phy­
sicians under the auspices of the Royal
Commonwealth Society for the Blind."
A week following exposure, several vic­
tims were still experiencing photopho­
bia, while a minority had eyelid swell­
ing. In all cases, slit-lamp examination
revealed a discrete superficial interpalpebral erosion of the cornea and con­
junctiva with the typical whorling pat­
tern of new epithelialization. Blindness
or irreversible eye damage was not
seen. In the 2 weeks immediately after
the disaster, the same investigators"
carried out a community-based epide­
miological study of eight exposed (379
subjects) and two unexposed (119 sub­
jects) clusters of households. The sam­
ple represented 2% of the estimated
population in the area surrounding the
study clusters. There was no evidence
of eye problems other than superficial
interpalpebral erosion and redness in
the exposure clusters compared with
the nonexposure clusters.
Dwivedi et al" reported on ocular
disease in 232 children admitted to Hamidia Hospital. Symptoms included se­
vere ocular burning (100%), eye swell­
ing (95%), redness (94%), watering of
the eyes (89%), ocular pain (76%), and
photophobia (44%). Ninety-three per­
cent had only mild involvement, with
conjunctival vascular engorgement and
chemosis; 6% had corneal involvement
ranging from punctate keratopathy to
epithelial denudation; and only 1%
(three patients) had more severe in­
volvement, with stromal haze and iritis.
Approximately 15 weeks after
exposure,
Maskati"
studied
two
groups from similar socioeconomic
backgrounds. Group 1 comprised 261
subjects residing within 2 km of the
plant, and group 2 comprised 106 people

residing 8 km from the plant. Findings
included burning eyes (38%), dimin­
ished vision (19%), corneal opacities
(6.5%), cataracts (4%), and night blind­
ness (1.5%) in group 1 subjects, as com­
pared with 10%, 7.5%, 2%, 2.8%, and
0%, respectively, in group 2 subjects.
Eleven people in group 1, compared
with three in group 2, were suffering
from cataracts (six of the 11 were be­
tween 21 and 50 years of age).
Raizada and Dwivedi" evaluated
chronic ocular lesions in 1140 patients
who had been hospitalized earlier with
acute oculorespiratory symptoms. Main
lesions noted were chronic conjunctivi ­
tis (14%), refractive changes (35%), de­
ficiency of tear secretions (5.6%), and
persistent corneal opacities (0.5%). No
changes were seen in the iris, lens,
vitreous, or retina that could be attrib­
uted to MIC exposure. Khurrum and
Ahmad" also studied 2280 patients 2 to 3
years after their acute eye injury. Ob­
served abnormalities included chronic
conjunctivitis (15%), refractive vision
changes (3.5%), deficiency of tear secre­
tions (6.7%), and persistent corneal
opacities (9%).
Prior to Bhopal, Pozzani and Kinkead" showed that MIC application to
rodent eyes caused severe necrosis. In
experimental studies, low molecular
weight ethyl and methyl isocyanates
have been proven to be skin and eye
irritants.After the Bhopal incident,
Harding and Rixon” induced opaci­
ties in young rat lenses incubated in
50-mmol/L MIC, thereby speculating
that MIC could induce cataracts. Gupta
et al“ exposed rats to 10- to 30-ppm
concentrations of MIC for 2 hours, doses
sufficient to cause pulmonary injury or
death. Eye irritation developed, but
there was no irreversible eye damage.
All of the clinical trials were observa­
tional studies of the case series design
with descriptive accounts of the eye in­
juries that occurred in a sample of pa­
tients exposed to MIC. The studies
were susceptible to selection and mea­
surement bias. The need for Bhopal
area residents to have kept their eyes
open while fleeing from the disaster
may have been responsible for the high­
er eye injury rate as compared to the
rates seen in rats. From these studies,
we can conclude that MIC causes acute
eye injury and probably does not cause
permanent serious eye damage.

MATERNAL-FETAL,
GYNECOLOGICAL, AND
GENETIC EFFECTS
Varma" conducted an epidemiologi­
cal survey of 3270 families 9 months af­
ter exposure to MIC. Retrospective
medical history of the same families for

Bhopal Tragedy's Health Effects—Mehta et al

2783

2 years prior to the incident served as
the control, thereby minimizing vari­
ables such as cultural differences,
language barriers, and socioeconomic
factors. Forty-three percent of 865
pregnancies in the exposed group ter­
minated in fetal loss, representing a
threefold to fourfold greater incidence
of fetal loss as compared with the nor­
mal incidence of 6% to 10% in Bhopal as
estimated by the Indian Council of Med­
ical Research. The spontaneous abor­
tion rate appeared to be higher in those
exposed to MIC while in the first tri­
mester of pregnancy. Of 486 live births,
14% of infants died within 30 days as
compared with a 3% rate recorded for
1983 and 1984 in the same group. Shilotri et alK surveyed 100 women of child­
bearing
age
residing
within
a
10-km distance from the plant. Of 38
women who were pregnant at the time
of the disaster, 29 had spontaneous
abortions and two had premature deliv­
eries. Both surviving infants had multi­
ple anomalies: spina bifida, meningo­
myelocele, limb deformities, and heart
disease. Autopsies revealed lung dis­
ease. similar to MIC-induced lung
changes described in adults.
Deo et al67 studied immunologic, mu­
tagenic, and genotoxic effects on the
exposed population and concluded that
MIC, being highly reactive, interacted
with enzymes involved in DNA replica­
tion and repair and, thus, may be the
cause of serious repercussions in the de­
velopment of the embryo. Kanhere et
al6" studied the morphologic characteris­
tics of 134 human placentas in pregnant
women exposed to MIC, following full­
term and premature births, and after
medical termination of pregnancy. An
increase in hydropic degeneration of
placental tissue was noted after medical
termination of pregnancy. Some in­
crease in calcification was noted in pla­
centas of infants bom prematurely.
Even though these changes were not
statistically significant, they were in­
dicative of poor perfusion and anoxia.
Fifteen weeks post-MIC exposure,
Naik et al68 measured blood and urine
thiocyanate levels in 310 subjects resid­
ing within 8 km of the plant. As com­
pared with healthy, nonsmoker con­
trols, thiocyanate levels in the exposed
population were significantly higher. In
the 1940s, hypothyroidism and thyroid
goiter were discovered as complications
of thiocyanate treatment for hyperten­
sion.30 Maternal hypothyroidism can
cause serious sequelae in the infant.70
This is an aspect of fetal toxic effects
that has not been studied, and epidemio­
logical studies on infants bom several
months following the disaster will be
needed to uncover such effects due to
2784

JAMA, December 5,1990—Vol 264, No. 21

MIC exposure.
Fifteen weeks after MIC exposure,
Shilotri et al“ surveyed 198 women who
resided within 10 km of the plant. One
hundred women complained of gyneco­
logic symptoms and had an increased
incidence of leukorrhea, abnormal uter­
ine bleeding, and abnormal Papanico ­
laou smears. In another study, Deo et
al” studied semen samples of 19 subjects
100 to 120 days after MIC exposure and
reported normal sperm counts, morpho­
logic features, and motility. The au­
thors acknowledged that the survey
may have been too late to detect damage
to mature sperms because the duration
of spermatogenesis is 74 days in man.
Using lymphocyte culture methods,
Goswami" studied chromosomes for
chromosomal aberrations and sister
chromatid exchange frequencies, pa­
rameters regarded as good indicators of
genetic damage. As late as 12 months
after the exposure, 71% of the exposed
population showed evidence of chromo­
somal damage as compared with 21%
incidence in a control population resid­
ing 20 to 50 km from the plant.
Animal experiments were done to
study MIC’s effects on pregnant mice
and rats. Varma et al73 reported 80%
resorption of implants when pregnant
mice were exposed for 90 to 180 minutes
to 9 to 12 ppm of MIC on the eighth day
of gestation. Schwetz et al73 reported
increased dead fetuses and decreased
neonatal survival when pregnant Swiss
mice were exposed to 1 to 3 ppm of MIC
for 6 hours a day during the 14th to 17th
days of gestation. These studies63,73 also
revealed a higher incidence of fetal mal­
formations, such as reduction in ex­
tremity bone length, diaphragmatic
hernia, myocardial thinning, cleft pal­
ate, and hydrocephalus, as compared
with controls. Ib determine if maternal
pulmonary irritation was essential for
the development of fetal toxic effects,
MIC was injected intraperitoneally in
pregnant mice.63 Increased resorption
of fetal implants, even without pulmo­
nary irritation, indicated the involve­
ment of nonpulmonaiy factors. Bhattacharya et al7' reported covalent binding
of MIC tagged with carbon 14 (“Q to
brain, liver, kidney, and lung proteins
when administered intraperitoneally or
by inhalation to female Wister rats.
Ferguson et al73 studied uptake and dis­
tribution of “C during and following ex­
posure to ("CjMIC in pregnant mice and
found UC in all tissues examined, includ­
ing uterus, placenta, and fetus.
Genotoxic and mutagenic studies
were carried out using a variety of in
vitro and in vivo assays. Mason et al76
were unable to demonstrate MIC-in­
duced mutation by Salmonella rever­

sion assay or Drosophila sex-linkfr;
cessive lethal assay. There j
increased sister chromatid extf*
frequencies and chromosomal al*
tions in mammalian cell culture off
nese hamster ovary cells. Studied
Kligerman et al,77 Tice et al,76 and Siu
et al73 showed that MIC induced chjy
somal damage in actively dividing (,
marrow cells, thereby indicating}^
potential to induce systemic genov
and/or cytotoxic activity.
All of the clinical studies on mater
fetal, gynecologic, and genetic e£were retrospective cohort stud.
However, well-controlled animal
perimental studies support the clit ‘
observations. Radiolabeled “C c,'
show carbamylation and MIC’s abj
to cross the blood-tissue barrier.
forms of “C distributed in blood a,
tissues have not been identified and.
their toxicity remains to be establish
Preliminary evidence from genetic u,
mutagenic experiments emphasizes
need for case-controlled, cohort stud-.
of the victims.

PEDIATRIC EFFECTS
In the first 2 weeks after the disast,
the Hamidia Hospital Pediatric Depzment had admitted 1337 children :•
treatment of MIC toxic effects." fchundred nineteen deaths were report
in the first 12 days, with 1<‘6 dear
occurring in the first 4 days of exposer
The majority of children presented ve
symptoms of breathlessness, cot*
painful watering eyes, photophobia. arrhea, and vomiting. Some had conr.
sions, hemiparesis, and coma. Bhanrand Bharucha31 reported on neurolor-’manifestations. Twenty-four of 47 cdren had lost consciousness for
periods up to 24 hours. Three chiic-f
had convulsions. An interesting ob*"
vation by physicians who hat'. exais’’’
the children early in the illness wasr'
eralized hypotonia and weakness.
Irani and Mahashur73 studied 211
dren who were exposed to MIC anc sveyed them 100 days following th^
leak. Group 1 comprised 164 ch>-_
residing within 2 km of the plar.t1
group 2 comprised 47 children n*.
ing more than 8 km from the P1*";^
group 1, cough (83.5%), eye symp-.
(79.8%), and breathlessness
were the most common syrnp-^
These symptoms were found
8.5% of the children in group 2. > r
1,40% to 45% of the children hadr,
tent pulmonary symptoms an<>
Eye symptoms of the children in P
decreased from 79.8% to 34.ar (/;end of the 100-day study. S°n*-»
children exhibited psychologic*?.^. •
and psychiatric problems 1*
Bhopal Tragedy's Health Effects"

-ir medical status and social disjtitions.
All the pediatric clinical studies were
^ervational in nature and have serijs methodological shortcomings in
jjdv design. Lack of attention to this
^illation is unfortunate, since it is the
,jdren who may have long-term toxic
ffects.

umunologic EFFECTS
fwo and one-half months after expo-re. Saxena et al83 studied humoral im-aiity (measurement of serum immujjglobulin levels) and cell-mediated
ainunity (measurement of T-cell ro­
utes and phagocytosis) of exposed vicjas and found suppression of cell-medi£ed immunity only. Karol et al81'85 found
jansient, low-titer, MIC-specific anti■odies in 12 of 144 exposed persons as
spared with no such antibodies in
sritrol^Although the titers were low
nd tra^Pht. the results suggest that a
ogle exposure to MIC was capable of

I educing antibodies that were maini ined for several months.
Dwivedi et al86 studied immunologi»a! response in rats 7 days after MIC
t iiposure and found impaired alveolar
’ nd peritoneal macrophage function and
npaired delayed hypersensitivity re­
alises. Karol et al6* injected guinea
izs with MIC in its reactive isocyanate
rin and showed antibodies specific to
SIC hapten 3 weeks later. Tucker et al87
noosed female mice subacutely to MIC
9to 3 ppm of MIC for 6 hours a day for 4
msecutive days) and failed to show pri=n- immune system toxic effects with- 5 days of exposure when antibody
■sponse to sheep erythrocytes, natural
Cercell activity, and lymphoproliferap? responses to mitogen were studied.
distance to infectious agents, Lismc iM^cytogenes, mouse malaria
^-tsid^md influenza viruses, or to
•■saspiantable tumor cells was not com*><nised. Using the same model, Hong
examined bone marrow paramein two groups of mice, receiving 1
^3 ppm of MIC, respectively, on days
and 21. after a 4-day inhalation
(6 h/d). Myelotoxicity was inas evidenced by hypocellularity
2 suppression of pluripotent stem
Panulocyte-macrophage progeni.' and erythroid precursors. Hema**tic parameters returned to nor-

kS • ^a-vs 'n th® 1-PPm d°se group,
m the 3-ppm dose group, indicatbone marrow toxic effects perf°r a relatively long period at
3 Ppm even when there was no
^unical abnormality.
dumunologic toxicity studies of
«
been reported. Further studDteded to clarify whether injury

toer 5.1990—Vol 264, No. 21

to the human immune system is caused
primarily by MIC or is secondary to
lung disease, and to establish its biologi­
cal significance.

HEMATOLOGICAL AND
BIOCHEMICAL EFFECTS
Two and one-half months after the
incident, hematological and biochemical
studies on 695 MIC-exposed victims
showed hemoglobin levels greater than
7.4 mmol/L and a higher total RBC
count in 78%.“ Though WBC counts
were normal in most victims, polymor­
phonuclear leukocytosis (11.9%), lym­
phocytosis (40%), and increased eryth­
rocyte sedimentation rate (36.4%) were
noted. Blood glutathione level was sig­
nificantly lowered in 40% of the popula­
tion examined. Serum ceruloplasmin
level was generally about twofold high­
er. Results of routine liver function
tests were normal. Fifteen weeks fol­
lowing exposure, blood carboxyhemog­
lobin, methemoglobin, and thiocyanate
levels were significantly higher in MICexposed victims as compared with con­
trols. This persistence was attributed to
consumption of food and water contami­
nated by breakdown products of MIC.
Fifteen weeks following the incident,
Naik
et
al® found
thiocyanate
levels from Bhopal lake and tap waters
to be twice as high as in water supplied
for domestic consumption in Bombay
(720 km from Bhopal). At the end of 9
months, thiocyanate levels had re­
turned to baseline levels.
In rats and guinea pigs, neither intra­
venous injection of MIC nor in vivo ex­
posure to 1000 ppm of MIC by inhalation
resulted in any inhibition of erythrocyte
choline esterase activity or alteration in
hemoglobin electrophoretic mobility.
This suggests that neither erythrocyte
choline esterase inhibition nor structur­
al alteration of hemoglobin was a major
contributing factor to death resulting
from MIC exposure.*' Bucher et al91 ex­
posed rats and mice to 0,1,3, and 6 ppm
of MIC for 6 hours on 4 consecutive
days. No significant changes were ob­
served in red blood cell indexes, platelet
count, total leukocyte count, or serum
creatinine, blood urea, or methemoglo­
bin levels. Counts of segmented neutro­
phils increased while lymphocytes de­
creased. These researchers attributed
the slight changes in the hematological
picture to pulmonary injury caused by
MIC at these exposure levels.
Hematological and biochemical toxic­
ity studies were minimal. If MIC were
to gain entry into the bloodstream, sys­
temic toxic effects with abnormal
changes reflected in hematological and
biochemical values might be expected.

However, no significant abnormalities
were noted in Bhopal area residents.

NEUROMUSCULAR EFFECTS
Bharucha and Bharucha81 reported
neurological manifestations in 129
adults and 47 children affected by MIC
exposure. Of 129 adults screened, 50%
were reported to have lost conscious­
ness in the initial hours following expo­
sure. Other symptoms reported includ­
ed muscle weakness, tremors, vertigo,
ataxia, and fatigue. In another study,”
33 victims who were 0.1 to 8 km from the
plant were clinically evaluated. Eigh­
teen persons fainted after inhaling the
toxic gas and remained unconscious for
a variable duration. Three of them had
prolonged unconsciousness and hyper­
reflexia; one had features suggestive of
encephalopathy.
Experimental studies were carried
out on cell cultures isolated from muscle
of 2-day-old rats after exposing them to
MIC concentrations of 0.025 to 0.5 p-L
per 5-mL culture. Light and electron
microscopic studies of nuclei of both cell
types (fibroblasts and myoblasts) were
carried out. At higher concentrations,
both cell types were killed. At lower
concentrations, myoblasts appeared to
be more susceptible to MIC toxic effects
than fibroblasts. This study concluded
that MIC directly affects muscle tissue
and prevents differentiation in in vitro
situations.” Sethi et al9* studied the ef­
fect of acute exposure on rats to 3.52 and
35.32 ppm of MIC. Along with known
acute ophthalmological and pulmonary
signs, animals were observed to have
progressively increasing ataxia, unco­
ordinated movements, and immobility.
Clinical studies on neurological ef­
fects of MIC toxicity were simple obser­
vations susceptible to many possible bi­
ases related to subject selection and
characteristics observed. No valid con­
clusions can be drawn. Animal experi­
mental data on neuromuscular effects of
MIC are also minimal.

PSYCHOLOGICAL EFFECTS
Sethi et al” collected data on psychiat­
ric problems from patients attending an
outpatient clinic located in a severely
affected area for a 4-month period (Feb­
ruary' 1985 to May 1985). Of208 patients
with psychiatric symptoms, 45% were
diagnosed as haring neurotic depres­
sion, 35% suffered from anxiety' states,
and 9.7% were found to have adjust­
ment reaction. Psychoses were uncom­
mon. Cumulative data were also ob­
tained from 10 satellite government
clinics set up in moderately and severely
affected areas. Of 855 patients report­
ing with medical problems, 193 adults
(22%) also had psychiatric symptoms.

Bhopal Tragedy's Health Effects—Mehta et al

2785

Diagnostic categories included neurotic
depression (37%), anxiety states (25%),
adjustment reaction—prolonged depressive type (20%), and adjustment reaction with predominant disturbance of
emotions (15%). Again, psychoses were
uncommon.
It has been recognized that disasters
can have substantial effects on the mentai health of victims. The most commonly recognized disturbance is posttraumatic stress disorder (PTSD). In the
general population, this is rare, occurring in less than 1%.“ Studies have suggested that 15% to 35% of Vietnam veterans developed PTSD, about 30% to
59% of people may do so after natural
disasters, and 80% may develop PTSD
after man-made disasters.57,98 During a
follow-up period of 2.5 years, the prevalence of PTSD in a group of 459 fire
fighters exposed to the 1983 Ash
Wednesday brush fires in Southern
Australia varied little from 30%, there­
by emphasizing the long-term psychiatric morbidity after a natural disaster.99
The number of factors producing
stress, as well as previous studies of
PTSD and stress due to economic factors, suggest that psychiatric morbidity
in Bhopal is expected to be high as compared with populations not exposed to
group trauma."1” Regrettably, the clinical studies of psychological effects
among the Bhopal survivors were uncontrolled observations on a small sampie of the population, and therefore valid conclusions cannot be drawn.

CONCLUSION
The Bhopal tragedy has fallen from
the public spotlight, leaving pressing
questions still unanswered. We do not
have reliable figures on the number of
persons who died or were injured; nor
do we know why the gas leaked or
whether MIC was the only culprit. Most
of the clinical studies on the victims
were observational in nature and uncontrolled. Bias was pervasive and there
was insufficient information to allow
careful operational definition of crucial
matters, such as criteria for inclusion
and exclusion of subjects and controls,
and effects of independent and depen-

dent variables on study outcome. Data
quality therefore could not always be
ensured. Initially, systematic study
was prevented by the chaos and trauma
that followed the disaster; later, inadequate resources compromised study design. On a strictly scientific level, these
observational studies do not conclude
causality. However, many of the conclusions are supported by experimental
studies, and by analyzing both clinical
and experimental studies much can be
learned about MIC’s effects on the
2786

JAMA, December 5.1990-Vol 264. No. 21

1
health
of the people of Bhopal.
The Bhopal tragedy has raised a num­
1
ber
of public health issues, in terms of
]policy in regard to accident prevention,
<
contingency
planning in case of disas­
t
ters,
and actions to be taken before and
t
after
disasters that would minimize
<death and suffering/15 Comprehensive
iright-to-know laws, providing commu­
i
nities
and governments with public in­
i
formation
about the character and ex­
1tent of releases of toxic materials from
i
industrial
processes, need to be en­
:
acted.
Multinational corporations need
f operate under a minimum set of stan­
to
<
dards,
even if local laws are weak. It is
i
important
that governments act both
i
within
their own countries and through
1
the
United Nations to create the mini­
i
mal
regulations that will be needed to
j
prevent
future disasters, create contin­
f
gency
plans, and produce sound risk
:
assessments.
International funds need to be estab­
1
lished
for research in this area. Primary
<
objectives
should include the provision
< the facilities needed to obtain immedi­
of
;
ate
epidemiologic data at the onset of a
i
major
toxic disaster, monitor the health
< the surviving victims, provide what
of
1
treatment
is possible, study the causes
< toxic effects, develop a cure, and plan
of
1
for
future prevention. We need a clear­
i
inghouse
for information about industri­
: activities so as to make communities,
al
i
workers,
and the health professionals
:
aware
of health and safety precautions.
As we engage in an assessment of
Jchemical technology’, the lesson learned
from Bhopal is that the tragedy of man­
i
made
disasters can be reduced by en­
<
couraging
and planning for competent
i
medical
and scientific analyses. Such re­
s
search
should be done promptly with
i
appropriate
methodological designs and
iwith full public disclosure of the re­
sults.
101 Data and knowledge from such
s
t
analyses
can be used to treat and ade­
<
quately
assess the condition of victims
and,
it is hoped, prevent tragedies of
:
this
magnitude from occurring in the
t
i
future.
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2787

ThcLm^
1988. pp. 161-164

Zfou'rncd

vf t’X'fW'mvtrr? fay
f i6i-

Effect of Exposure to Toxic Gas on the Population of Bhopal:
Part n-Respiratory Impairment
s K RASTOGI. B N GUPTA. TANVEER HUSAIN. A KUMAR. S CHANDRA & P K RAY*
Industrial Toxicology Research Centre, Lucknow 226 001, India
Received 30 December 1987

■ ’

.

:Th«.resoiratorv status of 783 cases, of either sex exposed to the toxic gas was investigated. Lung spirometry reZ«L39% prevalence of vennlatory impairment in the affecled population. The female population exhibited a higher
l%)of pulmonary abnormalities in contrast with the male population (33.9%). The toxic gas inhalation
three patterns oi respiratory disorders as indicated by simple spirometric tests. Bronchial obstruction was rein 3 7% male and 3.6% female population respectively, while restrictive pulmonary defect was noticed in 13.4%
The combined obstnicuve-cum-restricuve ventilatory disorder was observed in 222% population. The possible
anisms involved in the pulmonary dysfunction induced by toxic gas are discussed.

‘-Tv^mnoire to the toxic gas caused vanous pulmonary
ESgfenrmiipcs resulting in a number of respiratory
ffljffiffiiflTms, viz. cough, dyspnoea, chest pain. etc. in
pffijScpopulation of Bhopal. No epidemiological study

(FEVO,S); 4, Forced expiratory volume in 1 sec
(FEV,); 5, FEV,/FVC ratio; 6, Indirect maximum
breathing capacity (IMBC); 7, Air velocity index
(AVI).

.- jllip hr reported in the literature involving exposure
ffiaSfe human population to the toxic gas. Some studbeen conducted with isocyanates'
CurnuHiye effect on lung function of the persons exposed
Sfifoluene diisocyanate (TDD has been report-

The population exposed to toxic gas was asked to
perform tn the manner demonstrated to them, at
least three VC and FVC manoeuvres. The values
from the largest of the three reproducible curves
were taken into consideration and expressed at
body temperature and ambient pressure saturated
with water vapour (BTPS). IMBC was calculated
from FEV0 7J by multiplying it by 40. AVI was calcu­
lated from the predicted VC and IMBC values as
fqllows:

Significant decrease occurred in FVC. FEV,,
FEF50% of VC on account of TDI expo1S. A recent study16 has suggested that infil­
led lung diseases with pulmonary function abnormay occur in workers exposed to TDI.

and Methods
Spirometry was performed in 783 cases (371
and 412 females) examined in the respiratory
programme during February/March 1985
KBhopal Thesubjects who were unable to perform
rometric manoeuvres were excluded from the
' A™°ng the 371 male cases, there were 179
non-smokers and 172 (51.7%) smokers
female population there were no smo-

/ . The sP*rometric lung functions were recorded usaMgEjgforcMed Vitalograph Spirometer in standing
a8P°*l0°n wth nose clip on. The spirometer was regufor ^hration of volume and speed
dynamically by air displacement meth(^rPS (norinal barometric pressure of 760 mm

saturated with water vapour). The following
gg^^eters were recorded:

capacity (VC); 2, Forced vital capacity
~3’ Forced expiratory volume in 0.75 sec
« author

% of normal IMBC

% of normal VC

Normal value of AVI was considered to be 1.0.
Higher values indicated restrictive pattern and low­
er values obstructive pattern of respiratory impair­
ment. The FEV,/FVC percentage between 70 and
80 was considered normal and values less than 70%
indicated central airway obstruction.
Peak expiratory flow rate (PEFR) was recorded
with Peak Flow Meter (Wright Standard Model,
UK) and the highest of the three values attained was
recorded.

The predicted normal values for the various lung
function tests were derived from the regression equ­
ations laid down for healthy north Indian popula­
tion17. For the female population, the predicted va­
lues were calculated from the predictiion equations.
laid down for healthy women18. The pulmonary im­
pairment was classified according to Rastogi et aL'1
as follows:

161

BlUL, VOL. 26. MARCH 1988

thropometric measurements of the population suf,
fering from respiratory impairment are shown j.
Table 2. In the male population, the mean age of the
cases with restrictive lung disorder was significantly
3 Combined
(P<.05) less than the mean values recorded in ofe.
structive and mixed lung abnormality cases. Whi]e
FVC less than 80% of the
or mixed
predicted value and FEV,/ in the female population, the mixed respiratory in,.
pairment cases were older than the other cases.
FVC ratio less than 70%
Data in Table 3 show no significant difference in
Further classification! of pulmonary impairment the prevalence of pulmonary abnormality between
the smokers I 37.5%) and non-smokers (31.1%).
was done as follows:
1
Mild respiratory impairment, between 61 and Prevalence of obstructive respiratory impairment
in the study population is detailed in Table 4. Sex­
80%.
2
Moderate respiratory impairment between 40 wise no significant difference was observed in the
prevalence of airway obstruction in the lungs.
and 60%.
3
Severe respiratory impairment, less than 40%.
Smoking exhibited a significant influence on the
Statistical procedure—The lung function test re- prevalence of bronchial obstruction (P< 0.05). Mild
sui^vere analysed by applying student’s paired/un- airway obstruction was noted in 3% of the popula­
paWi t test in the study population. Chi square test tion examined. Mild bronchial obstruction was
was used for the determination of the significance of equally prevalent in the male and female population.
the prevalence of various categories of respiratory Smokers exhibited a significantly higher prevalence
impairment in the male and female population ex­ (5.7%) in comparison with non-smokers (P<0.05).
Sexwise, it was noted that both male and female po­
posed to the toxic gas.
pulations were equally affected by the severe bron­
cho-spasm.
Results
The physical characteristics of the male and fe­
Prevalence of restrictive respiratory impairment
male population studied for lung function tests are is presented in Table 5. 13.4% population suffered
detailed in Table 1. Sexwise no significant differ­ from lung restriction. However, sex and smoking
ences were observed in their mean ages. In the male habits had no effect on it. Mild restrictive lung im­
population, the age and height differences between pairment was prevalent in 12.3% cases. The results
smokers and non-smokers were noticed (P<.001 showed a significantly higher prevalence of restric­
and P<,05 respectively). The mean values of an­ tion in the male population (P<0.05). Moderate

VC or FVC less than 80% of
the predicted values
FEVj/FVC ratio less than
70%

1 Restrictive

2 Obstructive

Table 1

^ysical Characteristics of Population Exposed to the Toxic Gas

Sex and smoking habits

N

Male Population

Non-smokers

371
179

Smokers
female population

192
h J?

Age (yrs)
X 2. SE (X)

Distance from
x • SE(x)

Height (ems)
X ± SE (X)

Weicht (kgs)
X *_ SE(X)

33.8 *_ 0.60
30.8 * 0.82

162.5 ♦ 0.35

0.50

54.5 X ~5
55.2 + 0.7

2.5 > 0.06
2.6 *0.09

36.7 ± 0.81

161.7 ♦ 0.4”

33.9 * 0.6

2.4 * 0.07

32.9 * 0.55

149.3 * 0.29

48.3

0.5

2.7 * 0.05

163.5

UCIL

Table 2 Physical Characteris'-lcs of the Population showing Respiratory Impairment

Males (N = 126)

Physical characterstics
Obstructive
(N = 1A)
X
SE(X)
Age (years)

40.4 ♦_ 3.3

Restrictive
(N=55)
X . SE(X)

female (N = 182)
Mixed
Obstructive
(N=57)
(N.15)
X . SE(X) X _* SE(X)

Restrictive Mixed
(N=50)
(N=117)
X_.SE (X) X . SE(X)

161.2 ♦_ 1.7

34.6 ♦ 1.7
163.7 0.9

39.2+1.7 31.0*2.6
161.9 * 0.8 149.7 ± 1.3

36.4 ± 1.6

Height (C ms)

150.1 2 0.8

147.6 _♦ 0.6

Height (kgs)

52.1 *■ 2.5

54.1 j. 1.5

54.2+1.5, 47.4 + 2.1

50.6 * 1.5

48.3

Distance from UCIL
ractory (Kms)

1.9 * 0.5

2.4 ♦ 0.14

2.' *0.15 2.8 *0.3

2-7 + 0.1

2.6 ♦ 0.1

39.9 * 1.0

0.7

RASTOGI er al.: EFFECT OF EXPOSURE TO : ■ >.UU GzXS ON POPULATION OF BHOPAL—I!

severe lung restriction was recorded in 0.3%
• d 0 6°/o population respectively.
frlixed respiratory impairment was recorded in
■ 22 2% 1116 P°Pulation studied (Table 6). Its pre■ valence was significantly higher in the female popu*TQn (P<0.05). Smoking did not make any differce in the prevalence of mixed respiratory impair­
ent The mild category of mixed respiratory imnairment was observed in 14.9% cases. Sexwise, it
^5 the female population which suffered more
,p< Q.oi)- 4.8% and 2.4% of the study population
- suffered from moderate and severe types of mixed

respiratory impairment (Table 6). Sexwise moderate
category was more prevalent in the female cases
(/’<0.01), while severe mixed impairment was
equally present in both sexes.

Discussion
Various types of pulmonary impairment were re­
corded in the population exposed to the toxic gas. It
was observed that the study population suffered
from three types of impairment, viz. obstructive,
restrictive and combined. The majority of the popu­
lation suffered from the mixed type of respiratory

Table 3 Prevalence of Respiratory Impairment In Population Classified According to

4b Sex and smoking

Total

habits

Persons with
normal spirometry

Sex and Smokino habits.

Respiratory Impairment

Total
---------- ••• impairment
Persons with Persons with
restrictive
mixed type
impairment
of impairment
N
%
N
% N
%

Persons with
obstructive
impairment
N
%

Male population

371

Mon smokers

179

125

14.8
14.5

57
25

15.3 126
13.9 54

33.9
30.1

Smokers
Female population

192
412

120
230

15.1
12.1

32
117

16.6 72
2 8.3 182

37.5
44.1

Total

703

475

13.4

174

22.2 30.8

39.3

2*5

• ffv./fvCX less than 70%
FVC less than 80% of the predicted values
FVC less than 80% of
predicted value and FEV^/FVC ratio less than 70%
Table 4

Prevalence of Obstructive Pulmonary Impairment in thePopulation Exposed to the Toxic Gas
Total

Male population

245

Non smokers

371
179

125

69.8

Smokers

192

120

62.5

Female population

412

230

Total

783

475

Table 5

Obstructive pulmonary impairment
Total
Mild
Moderate
Severe Impairment
N
N
N
N

Persons with
normal spirometry
N

Sex and smoking
habits

%

X

%

%

%

-

-

1

2
11

3.5
1.1

1

0.2 14
0.5 14

5.7

-

-

-

-

55.8

11

2.6

5

0.7

1

0.2 15

3.6

60.6

24

3.0

3

0.7

2

0.2 29

3.7

66.0

3.7
1.6

11

Prevalence of Restrictive Respiratory Impairment in Population Exposed tn the toxic Gas

Sex and smoking
habits

Total

Persons with
normal spirometry
N
%

N

Restrictive Respiratory Impairment
Mild
Moderate
Severe
%
N
% N
X

371

245

66.0

55

14.8

-

Non smokers

179

26

14.5

-

192

125
120

69.8

Smokers
Female population

62.5

29

412

230

55.8

42

10.1

Total

783

475

60.6

97

12.3

Male population

-

Total
Impairment
N
X

-

55
26

14.8
14.5

-

-

29

15.1

3

0.7

5

1.2

50

12.1

3

0.3

5

0.6

105

13.4

163

..ULAN J EXP BIOL. VOL. 26, MARCH 1988

Table 6 Prevalence of Mixed Respiratory Impairment in Population Exposed to theToxic Gas a *

Sex and smoking
habits

Total

with
spirometry

Mixed Respiratory Impairment

N

X

Mild
N

X

total
Ifnalr.^

Severe
X

Male population
Non smokers
Smoxers
Fe m ale population

371
179
192
412

245
125
120
230

66.0
69.8
62.5
55.8

42
16
26
75

11.3 6
8.0 4
13.52
18.2 32

1.6
2.2
1.0
7.7

9

10

2.7
2.n
2.4

Total

783

375

60.6

117

14.938

4.8

19

2.4

impairment followed by the restrictive type. The re­
sults indicated that toxic gas inhalation caused a
mild form of pulmonary impairment.
Spirometry studies revealed that majority of the
pulmonary functions were subnormal. The spirometrie parameters, i.e. VC. FVC. FEVO75, FEV,,
FEV,/FVC ratio and IMBC revealed decreased
mear. observed values in contrast with their respec­
tive reference values.
Thus the present study provides ample evidence
of pulmonary hazard in the population exposed to
the toxic gas as indicated by the decreased respira­
tory function values and high prevalence of respira­
tory impairment. The physiological mechanisms re­
sponsible for causing lung impairment induced by
toxic gas inhalation are not yet clear. Some investi­
gators1’ believe that isocyanates have an acute irri­
tating effect on the respiratory tract resulting in the
bronchospastic reactions, while others20. suggest
that isocyanate induced respiratory disease may be
immunlogically mediated. A third hypothess21 is
that the isocyanates are pharmacologically active
and on inhalation may react with components of the
lung tissue leading to changes or to the inhibition of
biological functions. Two types of pulmonary re­
sponses to isocyanate exposure have been suggest­
ed22. One is the direct irritant response due to trig­
gering of normal protective mechanism of the upper
respiratory tract and the second is host generated
and truly allergic.

164

Moderate
N
X

5

____ N

57 11
25 43
32
11-7

2&5?i

174

References
1 Bmgsch H G & Elkins H B. .V Eng J Med. 268 (1963]
2 Zapp J A. Arch Induslr Health, 15 (1957)324.
3 Stokinger H E & Scheel L D. J Occup Med. 15 (191
4 Dodson V M, J Occup Med. 13(1971)238.
J
5 Munn A. Ann Occup Hyg, 8 (1965) 163.
6 Gandevia B. BrJ Induslr. Med, 20 (1963) 204.
7 Peters J M. Proc Royal Soc Med. 63 (1970) 372. 5
8
Paggiaro P L,Loi AMO,Rossi B. FerranteFP,Ra
& Baschieri L, ClinAlergy, 14 (1984)463. 'i
9
Wegmann D H. ftters J M. Pagnotro L & Fine L?
dustr Med. 34 (1977) 196.
‘
10
Adams W G F, BrJ/ndurrrA/ed 32 (1975)72.
11
Diem J. Jones R N & Hendrick D J, Am Rev Reep
(1982)4.20.
12 Maxon F G. Arch Environ Health, 8 (1964) 755.
13
Peters J M. Murphy R L H & Pagnolto L D & Van
F. Arch Environ Health. 16 (1968)642.
.j
14
Wegmen D H. J Occup Med, 16(1974)258.
15
MekerrowCB. Davies H J & Parry Jones A, Procl
.Wed 63 (1970) 376.
16
Charles J. Bernstein A. Jones B. Jones D J. Edwi
Seal R R M E & Seaton A. Thorax. 1 (1976) L
17
Rastogi S K, Mathur N & Clerk S H, Indian J Chen.
lied Set. 25 (1983) 186.
18 Bhattacharya A K. Banerjee S. Indian J Med Rei,
62.
19
Baur X. Romme H H & Fruhmann G. Respirarion,3»
289.
20
Karol M H. Lose! HH&AlaireYC. Am Ind HygAs
(1978)454.
21
ButcherBT. KarTRM&O'NeilCL.JAZZezgyCZui/r
64(1979)146.
22
Rye W A, J Occup Med «5 (1973) 306.

3

54

rimenta) Biology
iTvss'.pp-165-172

OH I ■ 18
Fffect of Exposure to Toxic Gas on the Population of Bhopal:
b Assessment of Toxic Manifestations in Humans—Haematological
and Biochemical Studies
^b.eTAVA B N GUPTA. M ATHAR. J R BEHARL R S DWIVEDI. S K HASAN, R S BHARTI. A SINGH,
ckaUVASlAVA.
MMISRA&PKRAV
Industrial Toxicology Research Centre, Lucknow 226 001, India
Received 30 December 1987

haematological parameters like total RBC count total and differential leucocyte count, haemoglobin con. cell volume, erythrocyte sedimentation rale and various biochemical parameters like blood urea.
h°'ne (GSH) glutamic oxaloacetic transaminase (GOT) glutamic pynrvrc transaminase iGPT). ceruloplasmin, toKwHndrin. glutamic transpepudase(y-GTP) in blood, creatinine and GPT in unne were studied in the population ex■C™L. toxic gas in Bhopal 21 months after the gas disaster. In a majority of subjects studied (67.1%) haemoglobin
were higher than 12 gr 100 ml and the total RBC count was on the higher side in 77.8% subjects. Total leucocyte
k»nr did not reveal anv abnormality. Increased polymorphonuclear leucocytosis was found in 11.9% subjects. A lym^■nbocvte count of more than 40% was found in 31.6% cases. An eosinophil count of more than 6% was observed in
subjects The ESR was found elevated in 36.4% subjects of the overall population. Blood glutathione was found
FSniftranily lowered in about 40% of the population examined. Serum ceruloplasmin rose to about 2 umes of the high: Srcponed value in the controls in a significant number of exposed subjects. Creatinine content in urine was also
in these subjects. Other biochemical parameters were found to be within the normal range.

■K"

KMEfeay the effect of the toxic gas on the haemoMptic system of the exposed population various
Svvfiiiiiatological parameters like total RBC count, to■
differential leucocyte count, haemoglobin
■BEfentage, pacKed cell volume, erythrocyte sedi'imitation rate and blood urea were studied during
gEttifphase I (11 Feb to 3 .March 1985) and phase II
(March to 10 April 1985) studies at Bhopal. DeTFfew papers describing clinical and experifindings there is still no agreement on the biigical mechanism responsible for the gross effects
ibe humans. Various biochemical parameters in
serum and urine in male and female popul.exposea to the toxic gas were studied to find
changes that occurred in these parameters
|*>d whether the biochemical changes can be inter^vted to postulate a theory of the possible mechanjg“°f action of the toxic gas in the human system.

(fMMerials and Methods
EP11* 1109 persons exposed to the toxic gas 695
gpio volunteered themselves for haematological and
p’^Oienucal studies were examined during phase I
H studies. These subjects comprised persons of
age groups including children, of either
ff^belonging to different religions and having had
K“y>ng degrees of exposure to toxic gas on account

indent author

of their living at different distances from the Union
Carbide Factory at the time of gas leakage.

Blood from medial cubital vein was obtained with
the help of sterilized syringes and various haemato­
logical parameters were studied, using standard
methods in haematology. Haemoglobin value was
measured by Alkaline Haematin Method1, RBC
count and total and differential leucocyte counts
were done according to the methods described by
Dacie and Lewis1 and packed cell volume and er­
ythrocyte sedimentation rate were studied by Wintrobe method. Blood urea was estimated by Ness­
lers method as described by King and Wootton2.
The following biochemical parameters in blood
and urine were estimated.

Blood: Reduced glutathione (GSH)
Serum Glutamic oxaloacetic transaminase (GOT
EC 2.6.1.1), glutamic pyruvic transaminase (GPT
EC 2.6.1.2), ceruloplasmin, total bilirubin, and yglutamyl transpeptidase (y-GTP EC 23.2.2).
Unne. Creatinine, glutamic pyruvic transaminase.
The biochemical assay of blood or urine samples
were performed using standard methods.

GSH—EUman3 modified by follow4; CP—Curzon
and Vallet5; GOT—Reitman and Frankel'’; GPT—
Reitman and Frankel0: y-GTP—Orlowski and
Szewezuk’;
Bilirubin—Wootton3;
Creatinine—
Wootton8.

165

.^. .e cmJL. VOL. 26, MARCH 1988

(77.8%). Agewise distribution pattern of pers,
having total RBC count of more than 4 tnillion/nj.
was 87.1, 82.9,77.1,74.3,70.1 and 72.0% respi
ively in subjects in age groups of less than 15,16-2
26-35,36-45 and more than 56 years.
Total RBC count of less than 3 million/mm3 y?

Results and Discussion

Estimation of haemoglobin—A majority of the
population (67.1%) had haemoglobin values of
higher than 12 mg/100 ml, while one-third of the
population (32.5%) had values between 8 and 12
mg/100 ml. The percentage of population having
haemoglobin level of less than 8 g/100 ml was 0.4.

observed in a very small percentage of populate
The percentage of population in different
groups which had an RBC count between 3 andk
million/mm3 was between 12.9 and 28.0. A very
small percentage of population had a total RBq
count of less than 3 million/mm3. No significant
feet of the distance from UCIL factory was noted®
the red blood cell count (Table 3).

When haemoglobin values were correlated with
different age groups, no significant pattern was ob­
served. The percentage of population having more
than 12 g/100 ml haemoglobin ranged from 61.9%
in the 26-35 years age group to 75.3 in the 16-25 ye­
ars age group (Table 1).

The increased haemoglobin and high RBC count
suggest the effect of the toxic gas on the bone mar
row leading to polycythenin type of disorder it
haemopoetic system. Such a disorder is also caused
by various chcmicals/drugs which are known to re­
duce the oxygen capacity of blood. Inspite of the I
high RBC count the normal value of PCV probably |
suggested the shrinkage of RBC.
®I

There was a direct relationship between haemog­
lobin level in the individuals residing at different dis­
tances from the Union Carbide Factory. The per­
centage of cases having haemoglobin level of more
than 12 g/100 ml was 65.5.67.3 and 82.2 in persons
residing within 2.2-4 and 4-6 km respectively.
Out of the total population residing within 2 km
from the factory 65.5% revealed a haemoglobin le­
vel of over 12 mg/100 ml and a similar trend was
observed in 80% of the population living beyond 4
km (Table 2). A haemoglobin level of more than 12
g/100 ml was recorded in a higher percentage of
male population than in the female in different age
groups. However, the difference was statistically in­
significant.

Total leucocyte count—TLC count was high (more
than 10,000/mm3) in 11.6%ofovcrallpopulation.Bi
was almost similar in males and females being 103
and 12.6% respectively. The percentage of popula­
tion having TLC of less than 5,000 was 6.4.
leucocyte count (less than 5.000) was more m fer
male (8.2%) than males (4.6%). The TLC (more than; •
10.000) has similar distribution in each populationgroup residing between 2. 2-4, 4-6 km and more;
than 6 km from the factory (Table 4). LeucocytosS?

Red blood cell count—RBC count was more than
4 million/mm3 in a majority of the population

Haemoglobin (gm X)
Total

Total

Total

Female

Total
20

(27.3)

16-25

(30.0)

(70.0)
128

(0.9)

(0.6)

(29.9)
20
(26.7)

109

101

29

(24.2)

(29.8)

(27.8)

(32.0)

(75.8)

(58.3)

(68.5)
25

Total

(0.*)

(27.3)

f igures in parenthesis indicate percentage of population studiea.

166

(68.0)
205
(72.7)

282

(62.2)

57?

SRIVASTAVA et aL: EFFECT OF EXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL—III

Fable 2-Haemoglobin values in Relation to Distance from the Factory (sex wise)
Haemoolobin( oms %)

parenthesis indicate percentage of population studied.

Table 3 —RBC count According to Distance from the Factory (sex wise)
RBC count
Billion/ m m

££ Total

______________
<2

17
(10.0)
153
(89.4)

53
70
(27.6) (19.3)
129 282
(67.2) (77.7)

171

192

363

Distance from the Factory (km )

F

Total

Total

M

r

2
(2.1)
11
(11.3)
84
(86.6)

24
...
(2.) (2.)
29 40
4
4 4
1
3
4
(29.3X20.4)
(22.2)
(25.0) (42.8) (36.4)
68 152
10 14 24
(68.7)(77.6) (100.0X77.7X^5.7) (75.0X5712) (63.6)

97

99

Total

196

h

10

Total

18 28

TC

?

"nL

F

Total

3
12
15
(1.1) (3.8) (2._5)
29
89
118
(10.3) (28.2) (19.2)
250
215 465
(88.6) (88.0) (77.8)

282

316

598

Male

female total

/inures in parentnesis are the percentages from the column totals.

Taole 4—Total Leucocyte Count in Relation to Distance from the Factory

Total

13
26
(4.6) (8.2)
240
250
(85.1) (79.1)
29
40
(10.3) (12.6)
282

316

39
(6.5)
499
(Bl.?;
69,
(H.6)
5?8

167

INDIAN J EXP BIOL. VOL. 26. MARCH 1988

was maximum (28.0%) in age group over 56 years.
The respective percentage in the age groups less
than 15, 16-25, 26-35, 36-45, 46-55 were 6.4, 8.2,
16.6, 8.6 and 8.8 respectively (Table 5).
Differential leucocytes count—All the cases stud­
ied were divided into two groups, i.e. those having
less than 70% polymorphs and those with more
than 70%. Increased polymorphonuclear leucocytosis was found in 7.1 subjects (11.9%) of the overall

population. Similarly the cases were divided in tw0
groups having less than or more than 40% lympho,
cytes. The number of subjects showing lymphocyte
sis more than 40% was found to be 188 (31.6°/^
Eosinophils were found to be more than 6% in 17 j
subjects (28.7%) (Table 6).
The percentage of cases showing increased poly,
morphonuclear leucocytosis was almost similar in
different age groups, i.e. 16.1. 11.1, 11.4, 14.4 and

5 - Age and sexwise Distribution of total Leucocyte count

Table

Age group

Total Leucocyte Count
Hale

<5000
Fema^

Total

$15
16-25

1
(1.4)

(10.1)

(6.7)
4
(5.4)

(9.1)

10
(5.9)

26 - 35

36-45

(8.0)

46-55
(9.1)

(12.5)

10
(7.1)
6
(10.5)

£ 56
—
Total
(4.6)

26
(8.2)

(6.5)

Male

5000-10000
Female

11
(100.0)
61
(85.9)
60
(80.0)
67
(90.5)
27
(81.8)
14
(77.8)

240
(85.1)

> 10000
Male remate Total

Total

20

31

(8.2) 71
29
75
(16.6)
74
(13.7) (8.6)
33
(8.8)
(8.3)
18
•3
(28.0)

99
100

17?
175

(79.2)
•4
(72.0)

(9.1)
4
(22.2)

250
(79.1)

490
(81.9)

29
40
(10.3) (12.6)

(77.2)

Total
Femsle Total
H

29
(93.5)
146
(85.9)
133
(76.0)
118
(84.3)
46
(80.7)
18
(72.0)

18
(90.0)
85
(5.8)
73
(73.0)

(10.0)

(6.4)

(12.7) (5.0)
19
10
(13.3) (19.0)
(4.0)

69
282
(11.6)

66

140

24

57

7

25

316

598

ise Oistnixition of Differential Leucocyte count Values

Age group
<70

|

^’5

Male

Female
16 - 25

26 - 35

36 - 45

46-55

56

■>8

Total
Male
Female
Total
Male
Female
Total
Male
Female
Total
Male
Female

Total
Male
Female

8
18
26
64
87

151
68
87
155
64
53
20
31
22
53
17

Poly morons
> 70

2
5
7

12
19
13
20
10
10
101

2
~>

4
1

<40
10
14
24
48

60
108
51
70
121
54
47
36
24
11
35

Total

22

3

12
6
18

Total

524

71 (11.9%)

407

2

Ly monocytes
>40

Eosinophils
>6

1
6
7

12
19

23
39
62
24
30
54
20
16
102
9

49
70
119

13
22
6
1

53
74
127
59
43
35
26
14
40
11

4
8
12
22
29
51
22
26
48
20

7

6

10
17
7
1

7

17

a

188(31.8%)

424

171(28.7 %)

.5

--

SRIVASTAVA er aL: EFFECT OF EXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL-III

,7 o% in age gr0UPs uPt0 15> 16-25- 26‘35’ 36-45
1 d more than 56 years, respectively, except in the
a” group 46-55 years where only 7.1% subjects
^oweti polymorphonuclear leucocytosis (more
than 70%)*
Lymphocyte count of more than 40% was found
• 22 6% and 26.3% of subjects up to 15 and 36-45
earn age groups. High lymphocyte count in age
Loups 16-25. 26-35,46-55 and more than 56 years
found to be 36.4. 30.8.38.6 and 28.0% respect­
ively.
The maximum number of cases showing eosino­
phil count more than 6% was found in age group up

•

to 15 years (33.8%) as compared 30.0, 26.5, 20.2
and 32.0% in age groups 16-25. 26-35. 36-45 and
more than 56 years respectively.
The differential leucocyte count was not found to
be significantly affected in groups of population re­
siding at different distances from the factory.
Erythrocyte sedimentation rare—ESR was found
elevated (more than 20 mm in females and more
than 10 mm in males) in 36.4% of the overall popu­
lation. It was raised in 39.2 and 33.8% males and fe­
males respectively. .The distance from the factory
had no significant effect on ESR values in the study
population. ESR values were raised in 36.9, 38.2,

Table 7— ESR values in Relation to Distance (Sex wise)
Erythrocyte Sedimentation Rate (ESR)

Distance

<10
42

100
(58.4)

2-4

60
(61.8)

Male
> 10

Total

71

171

(41.6)
37

97

< 20

(38.2)

Female
>20

129
(67.2)
61
(61.7)

63
(32.8)
38
(38.3)

(83.3)
4*

(16.7)

Total
192

99
18

10

4-6
> 6
Total

(80.0)
2

(20.0)
0

170
(60.7)

110
(39.3)

2*

209
(66.1)

280

3*

7*

107

316

(33.8)

Figures in parenthesis are percentages of row totals
* Percentages are not worked out where denominator is less than 10

•

Table 8-Age and Sex wise Distribution of ESR Values
Age group

ESR mn/lst Hr (Wintrobe)

Male

(Years)

< 10

>10

4 15

16 - 25
26 - 35,

36-45

46-55
>

56

Total

Female

Total

<20

11
69

13
(65.0)
74

75

(74.7)
63

(36.0)
25
(25.3)
37

(63.0)
40
60.6

(37.0)
26
(39.4)

14
(58.3)
5*

10
(41.7)
2*

(63.6)
45

(36.4)
24

(65.2)
46
(61.3)
41
(55.4)

(34.8)
29
(38.7)
37
(44.6)

23
(69.7)

10
(30.3)
10
(55.6)

33

(44.4)
170
(60.7)

110
(39.3)

280

74

18

209
(66.1)

>20

Total
20

107
(33.9)

99

100

66

7
316

Figures in parenthesis are percentage of row total
• Percentaoe are not workout where denominator is less than in

169

BiOL, VOL. 26, MARCH 1988
17.8 and 33.3% population residing less than 2,2-4,
4-6 and more than 6 km from the factory respect­
ively. The age group of more lhan 56 years had max­
imum number of persons (48.0%) having elevated
ESR- This was followed by 42.1, 37.7, 35.1 and
29.1% prevalence of elevated ESR values in age
groups 36-45. 26-35 less than 15,46-55 and 16-25
years respectively (Table 7 and 8).
Blood urea—The majority of cases with raised
blood urea values (more than 40 mg/100 ml) were
found in persons in age group 36-45 years followed
by age group 16-25 (25.0%) and 26-35 (21.2%).
The overall prevalence of raised blood urea was

found to be 20.5% in males and 12.7% in
with an average of 16.3% subjects showing
values (Table 9).
-31
The distance from the factory did not havJW
significant effect on the partem of abnormal f
urea values (Table 10).
sSl
Reduced glutathione—GSH level was signified
reduced in 30% of the exposed population.
pressed level of GSH in RBC may be due to thei
hibitory effect of the toxic gas on the bioswqg
sis of various SH dependent and other related,.
zymes of glutathione synthetic pathway. Prolog
decrease in the GSH content even after 21 mqu^

t

Tanle 9— Age ana bex wise Blood urea Levels

(years)

Male

< 15

16 25
26 -35

36-45
46-55

> 56

(100.0)
50
(81.9)
38
(82.6)
52
(76.5)
20
(76.9)
8
(64.3)

< 40
Feamle

Total

20
(95.2)
78
(89.9)
78
(89.7)
39
(78.0)
14
(82.3)

29
(6.7)
128
(86.6)
116
(87.2)
91
(77.1)

(83.3)

Blood urea (mg X)
>40
Hale
Female

0
(0.0)

Total

Male

Total
Female Total '5

9

21

30

61

87

148

46

87

133

68

50

118

26

17

43

14

6

20

(4.8)
(10.4)

(18.1)

20
(13.5)

(17.3)
16
(23.5)

(103)
11
(22.0)

(79.1)

(23.1)

(17.7)

(20.9)

(70.0)

(35.7)

)16.7)

(30.0)

Total

Male

.>40
Female

Total

Male

236
(79.2)
152
(90.5)

33
(22.9)
13
(18.4)

29
(18.8)

62
(20.8)

144

154

298

71

97

168

5*

12*

17

4*

5*

9*

224

268

492

^12.8)
27
(22.4)

totals

factory (km)
Male

<2

2-4
4-6

(77.1)
58
(81.6)
5*

<40
125
(81.2)
94
(96.9)
10

>6

4*

5*

(88.2)
9»

Total

178
(79.5)

234
(87.3)

412
(83.7)

Total

(9.5)

(11.8)
-

46
(20.5)

Figures in parenthesis are me percentage of row totals
• Percentages are not wanted out as the denominator is less than 10.

170

(3.1)
2

Total

34
(12.7)

80
(163)

•

■

SRIVASTAVA “ aL: EFFECT 0F EXP0SURE TO TOXIC GAS ON POPULATION OF BHOPAL-IU

■' re to the toxic gas may lead to the impair^*redox potential of the biological system as
■V. detoxification mechanism (Table 11).
L-uc oxaloacetic transaminase (GOT)—The
°fsenim GOT was found to be almost normal

populations and there was no significant difbetween males and females or persons of
at age groups (Table 12).

Glutamic pyruvic transaminase (GPT'r-The va­
lue of GPT was also found to be within normal
range of 5-35 I.U/ml and no significant difference
was observed in the values in respect of age and sex
of the exposed population (Table 12).
Ceruloplasmin—The ceruloplasmin content was
found significantly raised in more than 45% of the
population examined. In about one third of the pop­
ulation examined (35%) it was even more than one
and a half to two times higher than the highest nor­
mal value of 50 mg/100 ml reported in literature. In
10% population the value was raised by 5-14% only.
The elevated ceruloplasmin level was found in both
the sexes but it was more prominent in ±e female
population (Table 13).
Ceruloplasmin, an acute phase reactant protein, is
found raised in various diseases including inflam­
matory disorders. It is also responsible for the incor­
poration of iron into transferrin which is ultimately
taken up by the bone marrow for the synthesis of
haemoglobin. Significant increase in the ceruloplas­
min content observed among 40% of the exposed
population surveyed may be an indication of inflam­
mation in the body tissues and a cause of high levels
of haemoglobin in these subjects. The enzyme is al­
so responsible for the transport of copper into var-

171

»O1_ 26. MARCH 1988

(B.B2 . 0.7*
IMS . OM
(>*.65~ 77.61 ) llljf 2X27)

(20)

2OBS * 0.7S
(1M2 72X60)
(27)

(1.W3.W)
(27)

ious organs including brain as well as for the regula­
tion of copper into various biogenic amines. A per­
sistent increase in its level may cause higher trans­
port of copper to various organs including brain and
may disturb the level of biogenic amines. It may also
lead to various neurological disorders.
Total bilirubin—Total bilirubin content was found
within the normal range in 314 subjects exposed to
the toxic gas. The values ranged between 0.1 and 1.4
mg/100 ml (Table 13).
•/-Glutamic transpeptidase (y-G7P)—The values
of y-GTP were found to be within normal range.
The values in 314 subjects, both male and female,
ranged from 26.9-521.7I.UVml (Table 12).
The normal value of GPT. GOT. y-GTP and bilir­
ubin in serum of these subjects suggests the normal
functioning of their liver.
Urinary creatinine—The value of creatinine in
urine of these subjects was found to be significantly
higher than in the control subjects. It ranged be­
tween 2.20 and 5.04 g/24 hr in males and 1.99 and
3.89 mg/24 hr in females with an average value of
3.30 and 2.95 g/24 hr respectively (Table 14). No

172

change was observed in the urinary enzynw-ij
GOT and GPT in these subjets after 24 tna^3
The release of creatinine in ’trine of these.i^g
indicates an increased breakdown of
phosphate (a high energy phosphate comn^g
a result of muscular distress produced after ■
sure to the gas. The data are tn accordance m
general observation of the subjects at Bhopa*
they reported whole body pain. Creaunine
is also markedly intensified in disease states^S

diabetes, exophthalmic gortre, polimyetitis.
thenia gravis and progressive muscular in i
the absence of a significant change in senm^y

significant change in urine enzymes level. it
suggested that liver and kidney possibly may
target sites for gas toxicitv.
Acknowledgement
The authors are grateful to Dr S.
his critical review of the manuscript.

King E J & Wootton I D P. Microanaivjs tn

3 Ellman G L. Arch Biochcm Biophvk 82 i 959 70.
Pharmacology, 11(1974* 151.
5 Curzon G & Vallct L. Biochem J. ~4

edited by G G Duncan. 5th tooon. 1965.98.

'i

ExpenmeniaJ Biology
201-204

A Clinical Study of Toxic Gas Poisoning in Bhopal, India
UKMISRA&DNAG
Neurotoxicology Unit, Department of Neurology
PNATH
Department of Pathology
K.G. Medical College. Lucknow, India

Industrial Toxicology Research Centre, Lucknow 226 001, India
Received 5 February 1988

- The results of a clinical study of the victims of toxic gas released from Union Carbide Plant at Bhopal, India are present^-■^•^teThuty three patients, 22 males and 11 females were studied: their mean age was 38.3 years (range 8-60). AH the patients
'^^®^^Ped close to the Union Carbide Plant, where the accident took place (0.1-3 km). Eye and respiratory tract irritation were
tjje raost important clinical features and resulted in keratitis in 18% and pneumonia in 79% patients. 55% patients fainted
'after inhaling the toxic gas and remained unconscious for a variable duration; three of them who had prolonged unconsdousness. had hyperreflexia and extensor planter response and one patient had features suggestive of encephalopathy.
-. fblymorphonuclear leucocytosis (77%) and raised blood urea (67%) were commonly observed. The patients who lived
||lfo.'.\dose to the site of accident had significantly higher frequency of fainting (P< 0.05) and respiratory involvement (P< 0.1).
■
’ ’ Long-term follow-up studies are recommended to assess the sequelae of toxic gas poisoning.

Results
Around midnight, on the day of accident, most of
the patients woke up because of severe burning in the
eyes, irritating cough, dyspnoea, suffocation which
soon became intolerable. Some patients in anxiety
and panic ran for a safer place and medical help (14
patients), while other stayed in their houses and wait­
ed for the crisis to passover( 19 patients). Ophthalmological and respiratory involvement dominated the
clinical picture and in the severely affected patients
neurological involvement was also observed.
erials and Methods
he study was conducted within a week of the acciOpthalmological manifestations—Mi the patients
Ion33 patients (22 malesand 11 females)who experienced
,
„ the eyes
, associated
.
severe burning
with
: admitted in the medical wards of Hamida Hos- ■ watcringand redness. 73%patientscomplained ofdi­
[Kpo^^jjopal. Their mean age was 38.3 years (range minution of vision and photophobia, and 24% had
?‘8-6(^Rrs) and they belonged to low or middle socio­ pain in the eyes. At the time of examination all the pa­
-economic status. At the time of the accident these pa­ tients had marked congestion of the eyes. Keratitis
rents were present within 0.1 to 3 km from the Union was present in 6 cases and was bilateral in 2.The cor­
^Carbide Plant. These patients were subjected to de- neal opacity was of macula grade in 4 patients and leu­
F*ailed medical history and physical examination be- coma grade in 2. Characteristically only the exposed
*lemat°logica! investigations which included portion of the cornea was affected being directly ex­
.xpemoglobin estimation, blood counts, bleeding and posed to the toxic gas. On fundus examination, super­
.^coagulation time, blood sugar, blood urea, scrum ficial flame shaped haemorrhages were observed in 2
ft^atinine, serum bilirubin. SGOT, SGPT and alka- cases, in both of them they were in the superior tem­
Ph°sPhalase- A follow-up study was conducted poral region. In majority of the cases symptoms im­
- aner 3 months of the initial examination when the pa- proved by 3rd day (range 2-7), except in 2 in whom
gnents were subjected to a symptom checklist and clin- they persisted till 2nd week due to severe keratitis.
g^L^amination.
Respiratory manifestations—All the patients had
severe cough; irritation and dryness of throat, rhinorg-Corra’Pondem author
rhoea, suffocation and breathlessness. 81% patients
: On second and third December, 1984 in one of the
^biggest and most unfortunate industrial accidents of
gjbe century at Bhopal. India, a highly toxic gas stored
Se Union Carbide Plant leaked, affecting large num^ber of population and claiming anumberof lives. In
y'-this communication the results of a clinical study of
the affected patients in the first week of the accident
siandashon term follow up of some of the patients for 3
gFmonths are presented.

201

JfKJU VOL. 26. MARCH 1988
complained of chest pain because of tracheitis and
73% had excessive frothy expectoration. 91% pa­
tients were markedly dyspnoeic. Pharyngitis and lar­
yngitis were present in 12% patients and were asso­
ciated with difficulty in swallowing and hoarsness re­
spectively. Crepitations and rhonchi were present bil­
aterally in 94% patients. In 64% patients dyspnoea
improved by 4th day (range 2-7) but inspite of the
treatment 46% patients were dyspnoeic at rest in 2nd
week.
Neurological manifestations— Severe cough and
dyspnoea were followed by fainting tn 55% patients.
Theduration ofunconsciousness ranged from 30 min
to 3 days. One patient had prolonged unconscious­
ness. he also had myoclonic jerks localised to the right
upper extremity and generalised hyperreflexia. His
clinical picture was suggestive of encephalopathy.
Three patients who had prolonged unconsciousness
(more than 12 hr 1 had brisk deep tendon jerks and ex­
tensor planter response. Weakness of the legs was
present in 2 patients, it was more marked in the proxi­
mal muscles; one patient had difficulty in getting up
from the squatting position and the other had difficul­
ty in walking. In both these cases the deep tendon
jerks were absent and sensations were normal. Mild
to moderate headache (55%), giddiness 146%), burn­
ing sensation in hands and feet (9%) and hypoaesthesia (3%) were also noted.
Miscellaneous manifestations —Shortly after exposuretotoxicgas64%patientshad 1-3 vomitings. 15%
had 1 -2 loose motions and 6% complained of pain in
abdomen. The patient with encephalopathy deve­
loped gastric haemorrhage on 4thday. Three cm liver
enlargement was present in a patient but he did not
have jaundice. 91% patients had sinus tachycardia
which persisted in the first week. Generalised body­
ache and fever were also present in 12% patients dur­
ing the first week. A summary of the physical signs in
these patients are presented in Table 1.
By the end of 2nd week, 3 patients were free of
symptoms and were discharged from the hospital. 29
patients had varying degree of illness and were still in
the hospital.
To study the effect of extent of exposure to the toxic
gas on the clinical picture, the physical activity under­
taken by the patient at the time of the accident and the
distance from Union Carbide Plant were associated
to the severity of the clinical picture. Dyspnoea at rest
on 7th day and history of loss of consciousness were
taken as the indicators of the severity of the clinical
picture. The statistical analysis was done by the chi
square test. The proximity of the patient to the acci­
dent site was found to be significantly associated to
the severity of the clinical picture, i.e. dyspnoea at rest
( P< 0.1) and loss of consciousness ( P< 0.05).

202

The results of the laboratory investigations are^S
sented in Table 2. The chest x-ray films of 19 patient
were examined; bilateral patchy consolidation su«i
gestive of pneumonitis was present in 15 patients,bj.
ateral airspace consolidation suggestive of pulmor£
ary oedema and prominent bronchovascular ntajra
ings were present in 2 each. Left sided pneumothorax
in addition to pneumonia was present in one patient'-'
Follow-up studies—Three months after the initi^fexamination; one fourth of these patients could be Ml
lowed up. By this time all the patients were discharged*
from the hospital but most of them still required media
cal supervision and treatment (88%). Rawness jj1

Table 1 —Phvsical Siens in Patients 1 n = 33) Exposed to a
Toxic Gas
Physical signs

Respiratory
Dyspnoea at rest
Laryngitis
Crepts and rhonchi
Ocular
Congestion
Keratitis
Retinal haemorrhages
Neurological
Altered sensorium
Pyramidal signs
Myoclonic jerk
Muscle weakness
HyporeOcxia

At the lime of
admission

On lOlhdayof J
exposure

90.9

Table 2—Laboratory Investigations in Patients Expose^/.
to Toxic Gas
No. of J
Mean
abnormal*
values (%)

Investigations

Haemoglobin
8-14.6
12.8
22
(gm/100 ml)
’ Total leucocytes
->-> 13645.5 9200-24000
(count/mm3)
52-93
75.8
Ftolymorphs<%)
Platelets
6 221667 150.00-400.00
(count/mm3)
1-2.5
1.8
Bleeding time (min) 6
Coagulation time
3.95
2.5-4.5
6
Blood urea
51.6
22-93
18
{mg/lOOmll
Serum creatinine
0.4-1.2
0.6
18
(mg/100 ml)
Serum bilirubin
0.4-0.8
0.5
19
tmg7100 ml)
29.7
6-110
19
SGOT(UZL)
17.41
17.4
19
SGPT(U/L)
Alkaline
8-92
21.4
phosphatase (KA) 9

72'7 .o>

0 51
0 4

66j i

'"/is:
-uf LT
0 rttjK.
26.3
5.3
°

33.3

MISRA et aL CLINICAL STUDY OF TOXIC GAS POISONING

. dyspnoea, cough, reduction in visual acuJ£7/\e burning in hand and feet, depression
i'^bility were the commonly reported symp-

1

one patient diabetes mallitus was discovered
follow-up period.

J?fe^Jbjects included in this study resided close to
■

Carbide Plant (0.1-3 km) and were heavily exto the toxic gas. Eye and respiratory system in!?\anent dominated the clinical picture. The ophS^mological involvement was characterized by conS-tivitis and keratitis. Comeal opacity in 6 patients

; fFJjj study suggests serious injury to cornea, howjeer in the absence of slit lamp examination the freof lesser degree of comeal involvement and
■ mnrtate keratitis can not be commented. Irntant tox■'fBklikeTDI (toluene diisocyanate)and MIC(metfwnsocyanate) have been reported to cause comeal
erdema by producing alteration in the metabolism of
corneal epithelium tn human1 and permanent eye daBuiige in animals2 respectively. Superficial retinal
.//hemorrhages which were present in 2 cases in the
present study may be attributed to hypoxia following
■ ' -.exposure to toxic gas. The mechanism of haemorj. /rhage in the funds isusually by diapedcsis of red blood
I /'Tcells through the capillary endothelium whose permEfeetbility has been altered by hypoxia-1.
f'O^The respiratory involvement in the patients of this

't&Mudy included irritation of the upper respiratory
- tract, bronchitis, and pulmonary oedema. The radio■ '.-logical picture was also suggestive of bilateral patchy
^Sjneumonia (79%) and pulmonary oedema (10.5%).
animal studies inhaled isocyanate vapours have
jjKfe01 reported to cause respiratory irritation at low
Maiconcentration (2 ppm ) and coagulation necrosis at
Tfijkigb concentration (5 ppm). The histopathological
jjggPpure was suggestive of peribronchial pneumonia4.
SRhe respiratory effects observed in the present study

compared10 that produced by several irritant
/-.ff^Kke nitrogen dioxide, sulphur dioxide, chlorine.
iSEffisgene, carbon monoxide and hydrocarbons
which produce actute pulmonary oedema. However.
^pulmonary oedema is transient and no more than a

u.n®s reacts to the insul t. The mo re serious and
basing effects are fibrinous bronchiolitis, peri-

O XuI1fihi°litiS fibrosa oblilerans and severe airway obpatients in the present study faint^■■n,and remained unconscious for 30 min to 3 days.
sfe’■ °re who had prolonged unconsciousness had hytienheXia an<i extensor P^ter response. One.pa■EthvW"11 cbn*ca* P'cture suggestive of encephalopaKsJ' "fl Otber 'IT’tant gases like TDI poisoning hyHggiJ re"exia, extensor planter response and coma

have been reported6. In another study onTDI poison­
ing in which 35 firemen were exposed while combat­
ing a fire in a polyurethane plant a majority of the pa­
tients had irritation of respiratory tract, half of them
had gastrointestinal and neurological symptoms, the
latter included euphoria, ataxia, headache and loss of
consciousness. During next 3 weeks difficulty in con­
centration, poor memory and confusion were report­
ed by 61% patients’. Similar studies have also been
carried out by ICMR8 ’.
In view of the suggestion of MIC as a possible com­
ponent of the toxic gas an experimental study gives an
idea about the dose response relationship. 0-4 ppm
MIC for 1 -5 min produces no effect, only the odour
can be perceived; 2 ppm produces lacrymation, irrita­
tion of nose and throat; 4 ppm produces more marked
irritation and at 21 ppm the exposure is intolerable10.
The patients of the present study who were close to
Union Carbide Plant probably inhaled a large quant­
ity of toxic gas and developed more severe illness as
evidenced by respiratory involvement (P< 0.1) and
loss of consciousness (P< 0.05). The results of a de­
tailed follow up study conducted after 2-3 months
subsequent to the exposure of the toxic gas have al­
ready been reported11',4. The results ofa further fol­
low up study conducted after 15 months of the expo­
sure will be presented later which would highlight a
comparative account of the clinical profile
in the acute phase and that during the follow up
period.
Acknowledgement
The authors acknowledge the help of Prof. N.P.
Misrtt. Principal and Head of the Department of Med­
icine. Gandhi Medical College, Bhopal for his per­
mission to examine the patients. Thanks are also
due to Dr. S. Varadarajan, Consultant, Planning
Commission for his critical review and comment on
this
manuscript.
References
1 Luckcnbach M & Kielar R, Am J Ophthabn. 90(1980)682.
2 Zang C. Isocyanates quoted in Developments in occupational
medictne.Vfcu Book Medical Publisher.Chicago) 1980:
365.
3 Michelson 1 C Textbook of the fundus of the cry. Hied (Chur­
chill Livengslone. London) 1980.127.
4 Bernstein L. All Clin Immunol 7011982)24.
5 Fraser R G & Prae JAP, Diagnosis of the diseases ofthe chest,
lledDN B Saunder’s Co. Philadelphia) 1978,1259.
6
BrugschHG&ElkinsHB.New£ngU.W«!.268(1963)353. .
7
Quesne P, Axford A T. KckerrowC Bi Jones A P. BrJ Ind
•Wed, 33 (1976) 72.
8
Misra N P. Palhak R. Gaur K J B S. Jain S C. Yesikar S S. Manoria P C. Shanna K N. Tripalhi B M. Asthana B S.Trivedi
H H. Shanna V K. Malhotra Y. Verma A. Bhargava D K i
Balm G, Indian!Med Res. (SupplH 1987) 11.

86

203

INDIAN J EXP BIOL. VOL. 26. MARCH 1988

9 Bharucha E P & Bharucha N E, Indian J Med Res. 86 (Suppl)

12

Rastogi SK. Gupta BN,
S & Ray P K. Indian J Exp Biol,

(1987)59.
10 B.R.MjX Isocyanates in industry, operating and medical code
ofpractice, (British Rubber Manufacture Association Ltd,

13

Birminghum) 1977.
11 Gupta B N. Rastogi S K, Chandra H, Mathur A K, Mathur N.
Mahendra P N, Pangtey B S, Kumar S. Kumar P, Seth R K,
Dwivedi R S & Ray P K, Indian J Exp Biol, 26 (1988) 149.

Srivastava R C, Gupta B
Hasan SK, Bharti
an J Exp Biol. 26(1988)

14

Saxena A K. Singh KP, NagieS
an J Exp Biol, 26(1988)173.

204

[f'trt' 2-6 , (YlO/r

f-P

i J Expend'51 Biology

6H I

I Effect of Exposure to Toxic Gas on the Population of Bhopal:
Sc
Part IV—Immunological and Chromosomal Studies
A K SAXENA. K P SINGH, S L NAGLE. B N GUPTA & P K RAY*
Industrial Toxicology Research Centre, Lucknow 226 001, India
and
R K SRIVASTAV, S P TEWARI & RANDHIR SINGH
G.S.V34. Medical College, Kanpur, India

Received 30 December 1987

0i^’; The present une response

studies were conducted in Bhopal 2 ‘ months after the gas tragedy to find out whether the toxic gas had
the imm
and caused chromosomal aberrations in the exposed population. Immunological studies
|*y: i^nwed a significant depression in phagocytosis and T-cell rosettes whereas no deviations in immunoglobulin levels
found. This indicated that the toxic gas had suppressed the cell mediated immune status and did not alter the huimmunity of the exposed population. Chromosomal studies were performed on 31 adult subjects of either sex
random age groups. The buffy coat lymphocytes of peripheral venous blood were cultured. 100 metaphase plates
each culture were observed for frequency of chromatid breaks and gaps. Appropriate control studies were also done.
ft^Staosdcally significant differences were observed in respect of chromosomal aberrations in the two groups.

•erntfy several reports have shown adverse pharledtogic, toxicologic and physiologic effects of
ferent toxic gases. In spite of available literature
1MC and its effects on eye. lungs, behavior and
innmune system in rodents1
there is a paucity
data on the effects of MIC on immune system of
■Pan beings. Preliminary reports indicated sensitifiod of animals by inhalation of p-tolyl isocyanate
toluene diisocyanate and the detection of specific
Bbodies within 2 week of exposure5, respiratory
ttress, pulmonary oedema, abnormalities of the
meal epithelium and the immuno modulatory ef­
ts after single or repeated exposures of MIC1 ~4•6.
Jbe present study an attempt has been made to asf the effect of toxic gas on immune system of hu­
bbeings.
Ihe present studies were conducted during Febuy to April, 1985 on the population exposed to
’ toxic gas to ascertain whether the toxic gas had
cred the immune response of the subjects. The
“oral immunity was assessed by quantification of
“cnoglobulins (IgG, IgA and IgM) and cell rnedio immunity (CMI) by T-cell rosettes and phagocaberrations in the peripheral
"od lymphocytes were recorded in the exposed
P“anon for the assessment of genetic and carcinpotential of the gas.

“«rials and Methods
gipheral blood was obtained from the exposed

Sj^pndent author

subjects by using plastic disposable sterilized sy­
ringes and needles. Each blood sample was divided
into two portions, one was kept for serum separa­
tion and the other taken into heparinized tubes for
lymphocyte separation.
Lymphocyte separation—Lymphocytes were sep­
arated from peripheral heparinized blood using Ficoll-Hypaque (Pharmacia. Sweden) density gradient
centrifugation. Mononuclear cells at the buffy inter­
face were gently removed and washed three times
v/ith RPMI 1640.
Phagocytosis—One ml lymphocytes (1X106
cells/ml) were taken into petri dish containing cover
slip and incubated at 37’C for 2 hr. The cover slips
were washed twice with warm PBS to remove non­
adherent cells. One ml opsonized sheep erythro­
cytes (SRBC) (1 x 108 cells/ml) were added and fur­
ther incubated at 37’C for 1 hr. After incubation.
the cover slips were washed thrice with warm PBS
and then fixed in methanol for 10 min. Dried cover
slips were stained with Leishman’s stain and mount­
ed on microscope slides. 200 cells were counted, us­
ing light microscope, to determine the percentage of
phagocytosis.
T-Cell rosettes—It was determined by spontane­
ous resetting of lymphocytes with SRBC in 44 sub­
jects. Equal volume of 0.5% SRBC in media with
5% fetal calf serum (FCS) was added to lymphocyte
suspension (2 x 10” cells/ml) and incubated at 37”C
for 15 min. The tubes were centrifuged at 1000 rpm
for 5 min and left at 4°C overnight. Cells (200) were
counted under light microscope to determine the
percentage of T-rosettes.

173

INDIAN J EXP BIOL, VOL. 26, MARCH 1988

Immunoglobulins (IgG, IgA and 7gM)—Serum
immunoglobulins were estimated by the single radi­
al immunodiffusion method. The wells of tripartigen
plates were filled with 5 pi of serum and left for in­
cubation at 37°C. For IgG and IgA the minimum dif­
fusion time given was 50 hr whereas for IgM it was
80 hr. The standard control sera and triparugen
plates supplied by M/s Hoechst India.
Chromosomal studies—Cytogenetic study was
performed on 31 adult subjects of either sex and
random age group. Peripheral venous blood (5 ml)
was drawn in a heparinized disposable syringe. The
buffy coat lymphocytes were obtained by incubating
the blood sample held in the syringe at 37°C at an
inclination of 70° for 45 min. These lymphocytes
were suspended in media TC 199 at 37°C for 68 hr
in presence of phytohaemagglutinin-P (PHA-P. Difco) and homologous serum. 8 Drops of colchicine
(0.01%) was added three hours before harvesting.
The cultured lymphocytes were treated with
0.667% hypotonic solution for 20 min and fixed in
3:1 methanol glacial acetic acid at 37°C for 15 min.
The air dried slides were prepared and stained with
4% buffered Giemsa for 30 min and trypsin-G
banding was done according to methods of Kato
and Yoshida’. 100 well-spread metaphases from
each subject were studied for chromosomal aberr­
ations. The results were compared with 31 control
cultures from residents of Bhopal who were not ex­
posed to the toxic gas.
Statistical analysis—The results are expressed as
mean ± SE. Comparisons were made with appropri­
ate controls using student’s t test. Differences were
considered significant at P< 0.05.
Results and Discussion
Experiments on phagocytosis were conducted to
study whether the toxic gas had altered the ability of
peripheral blood mononuclear cells to engulf and
process the micro-organisms. It is the first line of
defence in a host against pathogens. Increased pha­
gocytosis by phagocytic cells may contribute to the
elimination of microbial infection. In subjects suffer­
ing from toxic damage of bone marrow by chemi­
cals, the normal mechanism of bacterial killing and
digestion by phagocytic cells does not take place.
This study was conducted on 19 exposed and 8
control subjects. 57.9% of the subjects showed sup­
pression in phagocytic ability of peripheral blood
mononuclear cells when compared to controls. The
phagocytosis was found to be 17.2 ± 3.0% in the ex­
posed group whereas in controls it was 32.5 ±0.9%
(Table 1). Whether these reductions in phagocytic
response are due to the decrease in actual cell num­
bers for phagocytes in the exposed population or

174

.3
due to a reduction in their functional ability is
clear. More studies will be required for finding
able answer for the same, particularly because
used same amount of whole blood cells for do»
phagocytosis. Any reduction in number of phag
cytes will show a relative increase in other cell pc,
particularly in PMNs, lymphocytes etc. The cell u.
diated immune system is under the influence of tin
mus and the cells are referred to as thymus-depenj
ent or T-cells. They are also responsible for the el
mination of spontaneously developing neoplasi
cells which might be a potential threat to the individ
ual. Cell mediated immunity is responsible for the
protection of the host against various infective
agents. The T-cell rosettes were estimated to study
whether there was any effect on the cell mediated
immune response of the gas exposed victims. The
T-cell population in exposed subjects was found to
be 28.6 ±0.5%. It is reported to be 65.1% in the
normal Indian population8. The suppression of
T-cells in the exposed population was found to be'
statistically significant.
w
It has generally been observed that the immunof
globulin levels in a normal healthy individual are.:
fairly stable. The deviation in immunoglobulin
vels may indicate the presence of infection or closes
relationship to a causative agent. Quantification o£"
immunoglobulins (IgG. IgA and IgM) was carrier^;
out to ascertain whether the toxic gas had altered^
the humoral immune response of the exposed popu£;:
lation (Table 2). Immunoglobulin G was estimated...
in the sera of 389 subjects exposed to gas. The mean,..

Table 1—Phagocytosis of SRBC by Penpheral Bic
Mononuclear Cells
Control ®
Exposed
group
group
32.5 ±0.9
ftreent phagocytosis (Mean ±SE) 17.2 ± 3.0
29.1-38.0
5
Range
1.0-39.2
Number of cases
19
Suppression in percent of cases
57.9
P value
<0.001
Table 2—Immunoglobulin Profile of IgG, IgA and IgM
Exposed group

IgG

Mean±SE
(mg/lOOml)
Range
No. of cases

1242 ±123

Control group
Mean±SE
mg/100 ml)
Range
No. of cases

IgA

IgM
177.0 ±5.0

300-3474
389

20-364

39.0-436.7'*!
309
-*5

1184 ±88.9

216.9 ±22.8

111.5 ±12J

600-1726
10

90.9 ±3384
10

40.0-192.0
10

SAXENA et aL EFFECT OF EXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL-IV

f und to be 1242 mg/100 ml with a range
4 mg/100 ml. Four per cent of the exshowed raised IgG levels, i.e. 2747.5
^00 ml (range 2334 to 3474 mg/100 ml),

(5^ ■

7% die cascs sdowed l°w feG values, i.e.
irMrag/100 1,11 with a range of 300’to 620 m&/

mlta the case of control group, it was found to
Cii84 mg/100 ml (range 600 to 1726 mg/100 ml).
Immunoglobulin A was estimated in the sera of
$12 exposed cases and the mean value was found to
be^l3.9 mg/100 ml with a range of 20 to 364 mg/
W0 ml- Lower values, i.e. 70.8 mg/100 ml (range 20
to 118 9 mg/100 ml) were observed in 7% of the
-ses. In control group, IgA was found to be 216.9
t mg/g^nl (range 90.9 to 338.4 mg/100 ml).
' IiSStoglobulin M was estimated in 309 exposea
and the mean value was found to be 177.0 mg/
. ng) ml with a range of 39.0 to 436.8 mg/100 ml.
The higher values, i.e. 390.0 mg/100 ml. were found
in 8% of the exposed cases (range 294.7 to 436.8
t mg/100 ml) whereas in 2% it was low, i.e. 39.2 mg/
100 ml (range 39.0 to 39.5 mg/100 ml). In the con­
trol group, the mean value was found to be 111.5
.mg/100 ml wi± a range of 40.0 to 192.0 mg/100 ml.
. Our studies indicated that the mean values of immu7 noglobulin (IgG, IgA and IgM) in the exposed popu---htinn were not significantiy different from that of
■^controls (Table 2).
„;v;; In chromosomal studies metaphase observations
were recorded and analysed for the presence of
’ breaks and gaps. The number of breaks and gaps in
t - i 100 metaphases of each subject were.noted. The da’. ,ta are presented in Tables 4 and 5.
:
. The present study shows that exposure to the tox.■ tc gas caused a significant degree of chromosomal
agaberrations. Our studies support the findings of Anet
who, in a standard Ames test, found
: Tt'tn^luene diisocyanate and 4,4-methylenediphenjSrisocyanate are mutagenic for bacteria (Salmonella
iggLtyphirnurium) in the presence of a conventionally

The present studies were conducted 21 months
after the gas tragedy at Bhopal. The CMI status of
the exposed subjects as studied by the estimation of
T-cells and phagocytosis indicated that the toxic gas
nad suppressed the phagocytic ability of the peri­
pheral blood mononuclear cells. The T-cells were
also found affected by the toxic gas showing that the
toxic gas had significantly lowered the CMI status of
the exposed population. The marginal deviations in
immunoglobulin profile may be due to non-specific

Table 4—Breaks and Gaps in 100 Metaphases in Each
Exposed and Control Subjects

!

Exposed

Subject

16

10
16

18

18
18

16

20
18
20

16
19

19
22
23

16

26

19

28

19

20
18
18

"Prepared microsomal fraction (S9).

a
’ j High

Table 3—High/Low Immunoglobulin Values tn
Population Exposed to Toxic Gas

IgG
Mean±SE
2847.5 ±0.9
(mg/100 ml)
B Range
2334-3474
Rircent of cases

f^Mean±SE
te-WlOOml)

g-.^cent of cases

407.4 ±:
300-620

IgA

IgM

30
31

Table

19

5—Analysis

390.9 ±10.4

294.7-436.8

Control

Gaps

Breaks

’

Number
Mean±SD

of Chromosomal
(Breaks)

Control

Exposed

5.61 ±0.99

15.19±230

Aberrations

20.82
(PC 0.001)

Analysis of Chromosomal Aberration (Gaps)

70.8 ±5.8

Control
39.0-39.48

Number
Mean ± SO

5.68 ±0.87

Exposed

(PC 0.001)

175

-. 20. MARCH 1988

infections. It can be concluded from the present
studies that the toxic gas had suppressive effect on
CMI while it had no effect on humoral aspect of the
immune system.
The chromosomal study was conducted at a time
when the clinical signs and symptoms were well
marked. A follow-up study should be performed af­
ter such time as the clinical signs and symptoms
have subsided to ascertain the residual effects of the
exposure to the toxic gas on chromosomes.

Acknowledgement
The authors are indebted to Dr S Varadarajan for
his critical review of this manuscript.

176

References
/
1
Nemery B, Dinsdale D, Sparrow S & Ray D E, j I
42(1985)799.
2
Salmon A G. Kerrmuir M & Andersson A. BrJfaj'1
(1985)795.
3
Ferguson J S, Schaper M. Stock M F. Weyel D A & * j
Toxic Appl Pharm. 82 (1986) 329. *
.«
4
Luster M I. Tucker A N. Germolec D R. Silver M T,T§
Y, Vore S J & Bucher J R, Toxic Appl Pham &

14°.

3l

Karol M H. Dixon C. Brady M & Alarie Y, T<S
Pharm, 53 (1980) 260.
6 Verma D R. in Hazard assessment of chemicals, Vol?
by Jitendra Saxena (Hemisphere Publishinr-1
Washington), 1987.
xjJ
7
Kato & Yoshida. Chromosoma, 36 (1973) 270.
8
Singh S & Nath I. Indian J Med Res. 72(1980) 385.
9
Andersen M. Binderup M L. Kiel P, Larsen H &
ScandJ Work Envir Hlth. 6 (1980) 221.
5

fi/Mou'akon

'~Tou'rnoJ

— y—

V&1-

73

rxjf n.

f h^u-a^.

pic

mj~

eg ^ncLe.

’.

ealth and sc 0RIAL

are reluctar
BHOPAL TRAGEDY - A YEAR LATER
■irnption of v
ects. Such c
Atlantic indie
GS Sainani, VR Joshi. PJ Mehta & P Abraham
’ harmful fi
>d that gem
inued or be
dertaken in )n the night of 3rd and 4th December 1984.
tion, U.S.A., in its guidelines for treatment of MIC
lusive.
rorlds worst industrial disaster occurred A
reservoir released a cloud of forty tonnes of

RB Sir sous methyl isocyanide (MIC), leaving behind
ief Consults lands dead and affecting the health of over
search Cent Hundred thousand people in the vicinity. At
Moradabad lime very little was known about MIC and its
gical affects. This increased the magnitude of
ragedy. Are we wiser now?

from various medical and non medical
y of vitamin ds, it is clear ttiat MIC not only produces an
e illness but due to its irritant nature, causes
sunlight and ise inflammation of the skin, the eyes, the
adults. Brit M the throat and the lungs . Many died as a
iV> It of pulmonary oedema. The affected indivirtCDiseaVaSCU s comP'a'ned °f d'y cough, throat irritation.
Ls_e®s.e^’ noea on exertion and chest pain. There are
■82, pp 31-59,.
’ ’ j u’stent rales in the chest with evidence of
jq ratory obstruction. In almost one third cases.
'
■ symptoms could be graded as severe. Chest Xhj showed evidence of interstitial, alveolar and
ral pathology. Lung functions have shown a
ion. I he obstruction may be at the small and
large air-ways. There is reduced arterial
jenation The acute effects go beyond local
ition. There is central nervous system dysfunii.
Immediate loss of consciousnessMoss of
incter control, confusion, memory defect.
, euphoria and paraesthesiae have been
Gastrointestinal manifestations consisted
uampy abdominal pain, nausea, vomiting and
hoea2. Abortions and premature deliveries
rred. Kidneys and liver have been variably
ted.

"iff?

There had been some confusion over the
chanism of toxicity of MIC. This really comnded the tragedy, hampering effective theratic relief. The big question was whether MIC
cause cyanide poisoning ? The evidence avaiso far suggests, such a possibility. MIC can
se hazardous decomposition products i e
gases and vapours such as hydrogen
ide, oxides of nitrogen and carbon monoxide.
n involved in fire)’. Union Carbide Corpora1985, Vol. 33. NO. 12

toxicity, states amongst other measures, "if
cyanide poisoning is suspected use. amyl nitrite; if
there is no effect, use sodium nitrite and sodium
thiosulphate IV." Examination of the urine with
picric acid gave some indication of excretion of
thiocyanates produced by the host's detoxifying
mechanism1. Patients who received thiosulphate
showed remarkable improvement. Prof. Heeresh
Chandra of Bhopal has. based on autopsy studies
of over 300 patients, postulated that death is due
to poisoning by irrespirable gases resulting in
cytotoxic or histotoxic death. Myocardial cells
show not only pigmentary changes, but flocculent
changes of the mitochondria, which are believed
to be characteristic of cytotoxic death ’.

At autopsy the lungs are grossly increased in
size and weight. There is tracheitis with denu­
dation of mucosa Mecrotising bronchiolitis; is
present at places Alveolar septa are congested oi
destroyed. The most important finding however is
p.ilmonaiy oedema with little evidence of inflam
motion

Brain shows oedema, blood vessel conges
tion sub-arachnoid and intraventricular haemor
rhage and petechial haemorrhages in the white
matter and the cortex . Kidneys have shown acute
tubular necrosis Liver has shown necrosis in
some cases

Venous blood of victims has been uniformly
described to be red oi cherry red in colour Tms
colour can be due to carbon monoxide, cyanide.
aliphatic and aromatic nitrites and organic thio
cyanates MIC can increase cyanogen pool lead
ing to chronic cyanide poisoning . Another pos
sible mechanism is carbamylalion of terminal
ammo gioups of the chains of haemoglobin resjf
ting in shift to the left of the Bohr effect This is an
impoitant mechanism as the effect can be revei
■sed by more potent sulfui donors
The question of chronic toxicity or after
effects is yel to be answered Affected people
have continued to complain of burning and water
mg of the eyes Many have diminished vision
There is macular oedema and central serous retino-

rounul °f Experimental Biology
1988. pp-191-194

,sf- inhalation Toxicity Studies of Methyl Isocyanate (MIC) in Rats: Part
£ iv—Immunologic Response of Rats One Week after Exposure:Effect
'e.<
on Body and Organ Weights, Phagocytic and DTH Response
• h_

P D DWTVEDI. ANIL MISHRA. G S D GUPTA. K K DUTTA. S N DAS & P K RAY*
Industrial Toxicology Research Centre. Lucknow 226 001. India
Received 30 December 1987

ymmunotoxicoloacaj evaluation of rats exposed to MIC was done on animals after 7 days of exposure to it. Initial
and final body weights, percent organ weights and alveolar and peritoneal macrophage functions were evaluated. No
increase in the body weight was found in treated animals after 1 week of exposure whereas percent thymus and liver
^^^hts were significantly enhanced. Both alveolar and peritoneal macrophage functions were significantly impaired in
^^■Lxposed animals as compared to controls. Delayed type hypersensitivity, enumerated against sheep red blood cells
was found significantly impaired in MIC exposed animals as compared to the controls.
s Currently investigation on the toxicological effects
. of chemicals on the immune system is gaining im’ portance, since the complex immune system1 with
■i several types of cells is working independently or together to carryout homeostasis to provide resistance
. against infections caused by bacteria, fungi and virus, and also against toxic chemicals, carcinogens2"'
J etc.The rationale behind monitoring of immunotoxJicological effects of a chemical is (a) that the basic
'"process of host defence mechanism is well undcrjr.stood, (b) that it represents a system in which diffcrg ait cells from the system can be removed easily and
4 their functions examined in vitro, and (c) that even a
| small dose of a toxicant can have a significant effect
jron the immune system of the body much earlier than
any other system6.
g- JAn extensive study of the toxicological effect of
smethyl isocyanate (MIC) has been undertaken in
Broiir laboratories after the disaster in Bhopal, where
■ a toxi^as leakage took a toll of thousands of lives.
S A” it^Pcal but smaller accident occurred in Kern
E ti967), where 35 firemen were exposed to isocyan. ate fumes. They were studied for neurological and
lung function abnormalities7,8. However, there is no
| ?®ni®cant data on the immunotoxic effect of MIC.
Previous studies on human indicated that in low

concentration isocyanate stimulates lymphocyte
proliferation, while it inhibits T-cell blastogenic re­
sponse with mitogens in the spleen and lymph nodes
ot mice . The limited data have shown increased air- Way sensitivity leading to asthma in isocyanate
* workers10,11, and hyperactive pneumonitis12 which
pave been related to the immunotoxic effects of
’ 'socyanate. In our study of Bhopal population ex,; Posed to toxic gas we have found significant in-

p 'Correspondent author

crease in absolute lymphocyte counts, T cell counts,
DTH response and phagocytic response13.
The present study has. therefore, been carried out
to investigate the early effect of MIC (7 day post ex­
posure) on the immune response of the experimen­
tal animals with reference to phagocytic response,
delayed type hypersensitivity ;DTH) and percent
organ weights of all immunologically important
organs.

Materials and Methods
This study was done on random bred Wister
strain male rats of between 130 and 155 g body
wgight. Three sets of animals were evenly arranged
in terms of their total group body weights and were
exposed to an acute dose of MIC inside the inhala­
tion chamber. The animals were marked for identifi­
cation, maintained at 21°-24°C and weighed daily
for the change in their body weight, and a complete
record of food and water intake maintained. The an­
imals were checked twice a day for behavioral
changes and morbidity. Control groups were made
from age, sex and weight matched normal rats maintamed on similar diet and placed in inhalation
chamber with air only for the same period. The ex­
posed animals were weighed and sacrificed after 1
week. One set of exposed and control group was
used for body weight and organ weight evaluation,
another for alveolar and peritoneal macrophage
function test and the third group of exposed and
normal animals, for DTH determination. Immedi­
ately after sacrifice, a complete necropsy was per­
formed and thymus, spleen, liver, peripheral and
mesentric lymph nodes, adrenal gland and kidney
were removed, trimmed and weighed.
For phagocytosis mononuclear cells were ob­
tained from peritoneal cavity and lungs by flushing
191

DWIVEDI « al: INHALATION TOXICITY OF MIC IN RATS-IV

Table 2—Percent Organ Weight in MIC Treated Rats as Compared to Control
[Values are mean ± SE. Figures in parentheses represent number ol animals]
PValue
< 0.001
NS
<.01
NS
NS
NS
NS

Normal controls
Treated
0.182 ±0.004 (14)
Thymus
0.123 ±0.019(9}
0.407 ±0.031 (15)
0.364±0.02I (8)
Spleen
4.74 ±0.240 (9)
3.550 ± 0.200 (9)
Liver
0.107 ±0.016 (9)
0.071 ±0.012(5)
LN.(P)
0.299±0.064(5)
0.430 ±0.057 (9)
L-N.(M)
0.029±0.0056(9)
0.025 ±0.0023 (81
Adrenal
0.784 ± 0.026 (9)
0.737 ±0.037 (5)
Kidney
Lymph node (paneutl);LJI. (M) - Lymph node (Mesentnc)

Table 3—Macrophage Function in MIC Exposed Animal as Compared to Control
Groups

(Figures in parentheses are number of animals]
Phagocytosis (%)

Alveolar

Pentoneal
Mean±SE
26.16 ±2.65

Control
(9)

P Value
. water intake, it was found to be impaired and this
3Bmay have caused some weight reduction in treated
jfjimrnals. However, there was no significant change
Li percent organ weight of animals exposed to MIC
SSn comparison to control except in case of liver and
u thymus. The increase in liver and thymus weights
could have resulted from hypertrophy of these orjiggjgns due to toxic effects of MIC.
Sgfi- Lymphoreticular system plays an important role
. t?i '10st defence against foreign invaders and toxiifecmts- Macrophage actively clears the foreign body
■jg-.-from the system on one hand, and on the other pro•,j.. duces die B cell differentiation factor15. Phagocytojjfine of the most important functions of macro'
Macrophage undoubtedly plays an import^_ant role in host resistance to many microorganisms.
^..Macrophages also make a diverse group of pro. <^_dncts16 as a result of external stimuli due to lipopol^;'-^accfaande’ Phngocyuc panicles, immune com)irirp'exes
tymphokines etc. Macrophages also par;?.■ “Pnfe in formation of a variety of complement
' i -mL'”115’ ‘nterferon and interleukin-1 (IL 1).
Though by studying phagocytosis alone one cannot
- 7 ' pnpoint die defect in immune system, grossly reL&L’tteerc^'CreaSed Phng^ydc function may indicate
f.ja-..' . anility of macrophages to perform abnormally
~ or m an activated form.
fetii bo h
present study the functional capacity of
founa*16 alveolar nnd peritoneal macrophages was
ggra, °und to be significantly impaired in rats exposed to

Mean±SE
17.0-39.0
(7)
8.23 ±24.07
(7)

0.01

MIC as compared to that in the normal untreated
controls, indicating a gross impairment in the mac­
rophage related immune response of the exposed
animals. The observation is consistent with those in
the previous reports of Tse" and White et aL'1 who
observed eosinophilia, lymphopenia and neutrope­
nia in animals after exposure to aliphatic isocyanate.
An impaired macrophage function in MIC, there­
fore. has an immunosuppressive effect and animals
may become more susceptible to various infections,
as reported by Howard18 about immunosuppressed
animals and also shown by endotoxin sensitivity test
by Saxena et al'9.
Cellular immune parameters have been widely
used in toxicological evaluation of various chemi­
cals because immune system represents an integrat­
ed system of host defence and also because changes
in the immune response appear long before the in­
volvement of any other system of the body6. DTH
has proved to be one of the sensitive parameters of
cellular immune competence. The rationale behind
the DTH response assay is that the in vivo testing
reflects systemic immunity of the host more closely
than the in vitro test. Evaluating the cell mediated
immunity (CMI) using foot pad assay requires both
afferent arm (antigen recognition and processing)
and the efferent arm (lymphokine production and
increased permeability) for adequate function of the
immune system17. Any defect therefore, in efferent
or afferent arm leads to impairment in DTH re­

193

INDIAN J EXP BIOL, VOL. 26. MARCH 1988

them with 5 ml of cold minimum essential medium,
containing 10 units of heparin/ml. The peritoneal
and alveolar fluids were collected in silconized glass
tubes. Viability of peritoneal and alveolar exudate
cells was studied using trypan blue dye exclusion
test.
Phagocytosis—The phagocytic activity of perito­
neal cells was carried out using sheep red blood cells
(SRBCs) according to the method of Koller et aL'J
with minor modification. Briefly, the cells from peri­
toneal and alveolar exudate (1 x IO6) were carefully
layered over glass microslides (22 mm2) kept in
plastic petridishes of 4.0 cm diam. The cells were al­
lowed to adhere to the surface of the microslide by
incubating for 1 hr at 37°C in humidified atmos­
phere of 5% CO,. The microslides kept in petrid­
ishes were flooded with 5 ml PBS (pH 7.2) and the
nonadherent cells were removed by sucking out the
fluid with pasteur pipene. The process was repeated
thrice.
SRBCs were coated with anti-sheep red blood
cells anti-bodies (anti-Sheep Hemolysin 1:500 dilu­
tion) by incubating it at 37°C for 1 hr and washed by
PBS at the end of the opsonization process (2000
rpm. 15 min), and finally a SRBC suspension (1%)
was made by phagocytic assay.
The adherent cells on microslides kept in petrid­
ishes were covered with 1 ml of processed SRBC
suspension and further incubated for 1 hr at 37”C.
The microslides were washed with PBS, stained
with Giemsa and examined under oil immersion in
the light microscope.
The assay of macrophage function was carried
out by its capacity to phagocytose SRBCs. A macro­
phage was considered positive for phagocytosis if
three or more SRBCs were seen engulfed. The num­
ber of such macrophages was counted along with
non-phagocytic macrophages microscopically, and
their percentage determined.
DTH response— DTH response to SRBCs was
done by the following protocol. Sensitization of rats.
was done on 1st day on the abdominal side with
1 x 108 SRBCs in 0.1 ml of Hank’s balanced salt so­
lution (HBSS). On 5th day, rats were challenged in
the left hind foot pad with 1x10’ SRBC in a volume
of 0.05 ml. Diameter of foot pad was measured with
caliper before challenge injection and then 24 and

48 hr after injection to observe induration. A
volume (0.05 ml) of normal saline was ink

way with the caliper to determine non-sp^?
swelling. The non-specific swelling was substr^j*
from the left foot pad induration to determine^
actual swelling caused by hyper-sen.srtiviry^
sponse. The above control protocol was foft^
for controls as well as animal exposed to MIC^
induration in rats exposed to MIC was comparai^
that in the controls.

Results
Control and experimental values of the
weight of the animals have been shown in Tabled
control group there was a significant gain in fn®;
weight after 7 days of air exposure, whereas inti
perimental group there was a reduction in weigfe.
range although the mean weight did not show 3^
significant change. The organ weights have beertet
pressed in gm organ weight/100 g body wt inlaife
2. Only thymus and liver showed statistically signScant increase in weight Results of phagocytin
against SRBCs presented in Table 3, showed signfficant impairment in rats exposed to MIC when com­
pared to control rats. Phagocytosis was significantly
lowered in both alveolar and pentoneal maouf
phages Both range and mean values of phagocytow
were significantly low in rats exposed to MICSt
compared to normal controls.
-ey
Results of DTH in MIC exposed as well as contni
rats showed that there was a significant impainnar
of DTH response (P< 0.001) in MIC exposed »
mals as compared to normal controls. The DTH re­
sponse (cm) in control (n = 8) and experimental ani­
mals
(n=10)
being
0.2009 ± 0.007
aS
0.0037 ±0.007 respectively.
Jg

Discussion
Inununotoxic effect of MIC was studied after 1
week of exposure. There was a significant increase
in the body weight of the normal control annuals,
whereas in the group exposed to MIC the weigM
range after treatment decreased, although no sign®'
cant change in the mean body weight was observed.
In fact, during the regular monitoring of food and

Table 1 —Change in Body Weight in MIC Treated Rats as Compared to Control
Groups

Control
Treated

192

No. of

6
8

Initial body wt(g)

Range
145-150
130-155

Mean±SE
146.610.40
138.0 ±3.87

Final body wt(g)
Range
150-175
115-147

Mean±SE
162.5 ±3.56
139.37 ±3.61

<0.001
NS

2CDLAN ; EXP BIOL, VOL. 26, MARCH 1988

sponse. DTH is primarily an in vivo manifestation of
the activation of specialised T cell subsets. These T
cells are called Tdh:°- Td„ subset can respond to a
diverse array of antigens. Any change in T ceil func­
tion which is one of the most important parameters
of CMI can. therefore, be measured by DTH assay.
In the present study a significant impairment of
DTH response was observed tn rats exposed to
MIC as compared to that in normal rats, which
clearly shows a defect in CMI and T cell function. It
must be mentioned here that C?.LI and humoral im­
munity are inter-related and that when CMI gets af­
fected humoral immunity too must invariably be af­
fected. Similarly in our studies .tn the human sub­
jects1’ exposed to toxic gas at Bhopal a phytonemogglutinin and purified protein derivative mitogenic
response was found decreased in exposea subjects
when compared to that in normal controls. A de­
crease in phagocytic response of human subjects ex­
posed to toxic gas was also observed by us. These data
are consistent with the observations made in rats ex­
posed to MIC.

Acknowledgement
The authors arc grateful to Dr. S. '.aradarntan for
his critical review of the manuscript.

References

Ray P K Edi Immunobiology of transoiuraation. . oncer ond
prtgnancyby (Pergatnon Press..New Yrrt: I9S3. :-24.

194

2 Ray P K. Dohadwala M & Bandyopadhyay S, Cmr«
mo Pharmacol. 4 (1985) 59.
3 Dohadwala M & Ray P K. Cancer Chemo PhamuaA
(1985) 135.
“3
4 Snvastava S P. Singh K P. Saxena A K. Serb P K Sc rCv
Biochem Phamacol. 36 (1987) 4055
5 Singh K P, Saxena A K. Zaidi S I A. Dwivedi P D, Sriva,
S P. Seth P K & Ray P K. J Appl Toxicol, (1987) C<x
mealed.
-nwi
6 Ray P K & Singh K P. in Research in industry, edited by
ky M J, Snvastava H C, Varsya Bhanendu (Oxford
IBH PublishingCo Pvt Ltd), 1987. 168-178.
-“jl
7 Axford A T, Me Kerrow C B. Parry Jones A & Le Quemj5
M. Br J Indust,Med. 33 (1976) 65.
8 Le Quene P M. Axford A T. Me Kerrow C B & Perry JoZt
A. Br J Indus Med. 331197^)72.
9 Thruman G B. Suntms B G. Goldstein A L & Killian DU
Toxicol Appl Pharmacol. 44 (1976)617.
10 Sagha G K & Alarie Y, Toxicol Appl Pharmacol, 50 (197gp
II Tse C S & Pesce A J. Toxicol Appl Pharmacol. 51 (1979)jj.
12
Charles J. Bernstein A. Jones B. Jones D J. Edwards J IV
Seal RME & Seaton A. Thorax. 31 (1976) 127.
Saxena A K. Singh K P. NagaJe S L. Gupta B N. Ray P
vastava R K. Tewari S P & Sineh Randhir. Indian J Exift
BtoZ. 26 (1988) 173.
14
Koller L D. Roan J G & Brouner J A. J Environ Pathol 7atfg2&
co4 3(1980)407
! 5 Bobak D & Whisler R. J Immunol 125(1980) 2764.
16 Hocking W G & Golde D W. N Engl J Med, 301 (1979) 580®
17 White W G, Morris M J. Sugden E & Zapata E, LanceFSgR
(1980)756.
JMH
’.8 Howard R J. Curr Prob Surg. 17(1980)275.
: 9 Saxena A K. Singh K P. Dutta K K. Gupta G S D. Nagale S
Misra A. Zaidi S I A & Rav P K, Indian J Exp Biol, 26«y*'
(1988)195.
1 I Crowle A J. Ad Immunol. 20 (1975) 197.

13

f

'

L-lJlnq JZnch-ix
J

1/S'- no# .

r-tc^ i<t %-/
f V-6r

59

METHYL ISOCYANATE SURVIVORS OF BHOPAL —
SEQUENTIAL FLOW VOLUME LOOP CHANGES OBSERVED
IN EIGHTEEN MONTHS FOLLOW-UP
*
PATEL, M. H„ KOLHATKAR, V. P„ POTDAR, V. P., SHEKHAVAT, K. L.,
SHAH, H. N. AND KAMAT, S. R.
E.
'Department of Respiratory Medicine, King Edward Memorial Hospital, Parel, Bombay-400 012.
(Received original. August 1986; revised version February 1987)

ABSTRACT

One hundred and thirteen symptomatic victims of methyl isocyanate (MIC) toxicity were
investigated by peforming maximal expiratory flow volume measurement sequentially for 18
mor^K Expiratory flows remained low and inspiratory flows declined. (Abnormalities of the
flow volume loop included saw tooth (12.3%), doming (16.5%), hesitation (25.8%) in inspiration
and doming (30%) and concavity (53.6%) during expiration. The changes persisted despite
■ improved spirometric values.

Introduction

Deadly methyl isocyanate gas spewed forth on
Second December 1984. from the Union Carbide
'.factory at Bhopal.
Pulmonary function assessment
Kwas carried out on 113 subjects who were victims of
‘•Bhopal gas tragedy and these have been reported2 3.
..Many of these victims were assessed with careful
,-flow volume loop measurements at intervals of three.
jsix. 12 and 18 months, in order to elucidate more
-fully the ventilatory and small airway abnormalities.
jToluene diisocyanate has been documented to
induce occupational asthma1. Oxygen exchange,
blood gases and immunoglobulin changes were also
^studied in the methyl isocyanate victims. A group of
£160 normals were assessed for flow volume to esta­
blish our laboratory normal standards. Flow rates
.wera^raluated for. evidence of airway obstruction4.
'Flo^t and lung volumes have been correlated5.
^Extensive data are available for flow volume abnor|Tnalities in chronic obstructive pulmonary disease6.
^Expiratory flow volume curves have been worked out
..for South Indian men’.

Material and Methods

■'•The victims who presented to our hospital in
Bombay from the first week onward from Bhopal
formed the material for the study.
h All persistently symptomatic subjects underwent a
detailed questionnaire (British Medical Research

rPUncil Respiratory Questionnaire. 1976 edition)
and had detailed physical examination, chest radio­
graphy spirometry (Stead-Wells. W.E. Collins), bron­

chodilator assessment with nebulised salbutamol.
minute ventilation, arterial blood gases at rest and on
exercise. CoHb and MetHb (co-oximeter. Instru­
mentation Laboratories Inc.)
In relevant patients, electrocardiography (number
52). mechanics of breathing (48). bronchoalveolar
lavage (12). rheumatoid and antinuclear factor (32).
lung biopsy (8) and immunological antibody studies
(93) in association with Dr. M.H. Karol. University of
Pittsburgh were also carried out.
* Flow volume norms were derived with Fleisch
No. 3 Pneumotachograph and Hewlett Packard
X-Y Recorder in 160 normals. The latter recorded
a maximal flow volume loop after a calibration
with H.P. calibration set up (No. 09911) and
oscilloscope. Typical two loops were measured
after 10 records were faithfully reproduced. The
volumes were derived by integration. All nor­
mals were healthy nonsmokers belonging to ages
17-60 years and had normal spirometric values by
Indian standards reported earlier8.
For comparing our standards. 25 chronic obstructive
pulmonary disease and 12 interstitial fibrosing alveo­
litis patients were also studied similarly. Manual cal­
culations from the loop were carried out for expira­
tory and inspiratory flow rates at Peak V25. V50. V75 and
related ratios. Multiple regression analyses for age.
sex. height and weight were undertaken to derive
prediction equation in normals. For comparison, the
data on MIC exposed subjects has been also presented

* Based on Preliminary report presented at the Fifth National Con­
gress on Respiratory Diseases at Jaipur. December 1985.

LUNG INDIA (1987). V. No. 2. (P

60

as real and standardised (for age 30 and Height
cm in males and 160 cm in females) values.
1

TABLE—1

RESPIRATORY FLOW RATES IN NORMAL INDIANS

Results

(a) Expiratory flow rates:
PEFR

NIo.

Age

VE25

VE50

The flow volume loops for males (Fig.
females (Fig. 2) are similar to those of North Ai
subjects, but lower in absolute values.

VE75

group/yrs.

MALE
-- AMERICAN N
INDIAN NORMAL

Male:
17-20 20
21-30 40
31-40 20
>40 10
Total 90

8.02 ±2.29 7.38 ±2.05 4.67 ±1.42 2.37 ±0.92
8.03 ±1 22 7.42 ±1.27 4.69 ±0.92 2.18 ±0.56
7.93 ±1.36 7.37 ±1.30 4.68±0.86 1.99 ±0.34
6.79 ±0.70 6.42 ±0.66 4.04 ±0.46 1.72 ±0.28
7.33 ±1.54 6.84 ±1.48 4.32 ±0.99 1.96 ±0.53

Female:

17-20
21-30
31-40
>40
Total

17
26
15
12
70

Age

h10.

5.13 ±0.61 4.68 ±0.65 3.55 ±0.43 2 04 ±0.47
6.01 ±1.05 5.66 ±1.04 3.97 ±0.90 2.19 ±0.57
5.49 ±0.85 5.13 ±0.76 3.46 ±0.85 1 83±0.46
5.12 ±0.98 4.73 ±0.89 2.96±0.59 1.56 ±0.41
5.55 ±0.92 5.16±0.97 3.61 ±0.84 1.99 ±0.54

PIFR

Vl25

Vi so

Vi75

group/yrs
Male:

17-20
21-30
31-40
>40
Total

20
40
20
10
90

5.29 ±1.51 4.34 ±1.32 5.17 ±1.40 4.62 ±1.36
5.19 ±1.05 4.28 ±0.92 5.05 ±1.05 4.48 ±0.96
4.99 ±0.98 4.07 ±0.80 4.86 ±0.88 4.29 ±0.79
4.26±0.51 3.57 ±0.54 4.17 ±0.59 3.68 ±0.52
4.70 ±1.13 3.88 ±0.97 4.59 ±1.09 4.03 ±1.01

Female:

17-20
3.48±0.51
21-30 26 3.90 ±0.80
31-40 15 3.72 ±0.97
>40
3.13±0.65
Total 70 3.58 ±0.80

3.04 ±0.50
3.90 ±0.80
3.32 ±0.89
2.74 ±0.53
3.16 ±0.80

3.47 ±0.40 2.91 ±0.54
3.86 ±0.78 3.25 ±0.77
3.56±0.91 2.93 ±0.84
3.05 ±0.58 2.33 ±0.52
3.55 ±0.79 2.95 ±0.79

Mean Flow Volume loops in Normals—Male.
Flow rates at 50% on the expiratory slope.

eg

TABLE—2
PREDICTION FORMULAE FOR NORMALS

PEF
VE25
VE50
VE75
PIF
Vl2S
Viso
V175

Male

Female

2.024—0.025 Age 4- 0.043 Ht. —0.010 Wt.
3.612—0.021 Age 4- 0.027 Ht.
3.085—0.013 Age 4- 0.010 Ht
—0.332—0.016 Age 4- 0.017 Ht.X
0.014—0.021 Age 4- 0.034 Ht.
—1.91 —0.01 Age + 0.041 Ht
0.061—0.019 Age 4- 0.033 Ht.
—0.733—0.020 Age 4- 0.032 Ht.

5.964__0.028 Age + 0.010 HL +0.038 Wt.
4.525—0.024 Age + 0.036 WL
2.204—0.031 Age + 0.020 Wt
0.975—0.019 Ago + 0.011 Ht.X
1.341—0.020 Aga + 0.027 Wt
1.720—0.016 Age + 0.024 Wt.
2.128—0.023 Age + 0.024 Wt
2.55 —0.029 Age + 0.021 Wt

X Unreliable prediction formula. Prediction by Weight (kg) has large errors in males lor all parameters:
for all parameters in females except PEF. has large errors.

J

61
chest pain (69%). muscle weakness (32%). poor
memory (29%) and poor concentration. (11%). Later
dyspnoea (mainly on exertion), cough, chest pain.
muscle weakness, poor concentration, and body pains
persisted as prominent symptoms. The mean res­
piratory symptom score in 113 subjects initially studied
was 2.92+1.55. it was 2.08+1.25 at six months
and 2.8 + 1.2 at 18 months.

Radiologically at initial stage. 36% showed 1-2
zone. 24% 5-6 zone involvement. Mainly linear (82%),
punctate (37%) and reticulonodular (27%) interstitial
deposits were seen. In 15 to 19% changes consistent
with those due to emphysema, and cardiac enlarge­
ment were seen while pleural scars (21%) and patchy
consolidations (4%) were other findings. After three
months 38% showed improvement and 16% showed
worsening. At 18 months. 97% still showed linear.
23% punctate and 22% reticulonodular deposits.
Initially carboxyhaemoglobin was raised (mean.
5.97%) in 94.3% of 70 subjects tested and methaemo­
globin was (in 111 subjects), mean 1.76% high (over
1%) in 83% subjects. After three months, (but not
when studied in few days) both the CoHb and MetHb
values came down (P< 0.05 and P<0.01 for res­
pective two parameters).
Oxygen uptake values at rest were low initially but
continued to improve significantly later. FVC and
PEF showed significant improvement but not
MEFRo.2s-o.7j.
The radiographic extent of zone in­
volvement initially was related to methaemoglobin
reading (P< 0.05). Also initially clinical respiratory
score showed a relation to FVC (P<0.05) and FEV1
(P<0.01).

E'of 113 subjects 23% were females, 33% smokers

and 10 below 20 years and 41 between 21-30
{years.^Qie distance from the Union Carbide factory
at ihs^Be of exposure was upto one kilometre in 16
,-subjects and beyond two kilometres in nine subjects.
Severity of immediate clinical illness was derived by
Lnumber and severity of respiratory, eye. abdominal and
{neurologic symptoms, duration of hospitalisation, his| lory and duraton of complications (e.g.unconsciousL’ess). Thus 30 had initially mild. 57 moderate and
{26 severe illness. This showed a significant relation­
pop to distance from the factory (P <0.05). By the
Itime we studied these subjects. 69% had improved.

had worsened and 27% had unchanged disability.

J As shown in Table. 3. the initial (first assessment)
Bnnptomatology was: eye congestion
(43%).
Burred vision (29%).
abdominal pain
(30%).
jf°u9h (98%). sputum (42%). dyspnoea (97%).

Flow rates in MIC exposed subjects

Generally, the values are lower than for normals.
particularly for inspiratory flow rates (Table 4). Over
next three to six months most flow rates improved
significantly (except VE75 which showed only in­
significant changes).
The improvement in flow rates continues over the
follow up for PEF and V,2j (18 months). After
an initial improvement for PIF. V130 and VI23 (after
12 months). VE30
(after three months). VI73
(after six months) all the flow rates decreased at
18 months. In contrast, forced vital capacity has
improved steadily after six months significantly
(P<0.05 for all differences).

The trends for males (nonsmokers and smokers)’
and females are shown graphically in Fig. 3-5. For

62

LUNG INDIA (1987). V. No. 2. (P. 59S

TABLE—3
SEQUENTIAL SUMMARY OF CLINICAL AND FUNCTIONAL BACKGROUND OF MIC EXPOSED SUBJECTS (n:113).

(a)

Clinical:
Cough
Sputum
Dyspnoea
Chest pain
Muscle weakness
Poor memory

Initial
(*)

At 12 months
(«)

98
42
97
69
32
29

69
58
93
48
53
20

Initial
(«)
(b)

Poor concentration
Eye congestion
Blurred vission
Abdominal pain
Abnormal lung signs

11
43
29
30
51
Initial (70)
Mean ±SD
5.97<± 11.1
(C) Carboxyhaemoglobin %
Methaemoglobin (111) % 1.76<± 0.74
(d) Oxygen uptake resting:
Mean±SD
197.5 ±58.5
Initial
3 months
222.5 ±51.0
246.6±91.4
12 months
Initial
(e) Blood gases and PH
100.8 ±12.1
PO,
33.3 ±3.7
PCO,
7.49 ±0.04
pH
(0 Spirometric indices:
Period (month) (No.)
0(113)
3(80)

50
3
9
15
—

Chest radiograph:
Normal
Cardiac enlargement
Emphysema. Pulm.
hypertension
Pleural scar
Consolidation
Interstitial Deposits:

2
19
15
21
4

Linear
Punctate
Micronodular/Nodular
Reticular
After 3 months (73)

82
37
27
27

2.26 ± 1.42 P<0.05
0.89 ± 0.73 P<0.01

0^1
2 ’3
og|
.'9
4?
65
4Q
12 £
g*
X
X
<
JSs
-3

12 months
94.2±11.9
33.5±3.1
7.43±0.03

6(76)

Standardised to age 30 and ht (167cm.M; x—P<0.05. 160 cm :F).
FVCxLiL
2.31 ±
2.384
2.40 ±
0.59
0.53
0.58
95.9 ±
95.5 ±
FEVj/FVC %
96.7 ±
3.9
4.1
8.9
PEFxLit/min.
389±123
448±107
448±103
MEFR (0.25-0.75)
200.8 ±
213.8 ±
212.9 ±
81.5
94.5
93.6

a®
S
S

12(94)

18(74)

3.10x4
0.77
86.24
9.0
487±105
185.4±
117.3

3.17 x±
0.56
81.4 ±
8.5
610±240
173.6±
56.3

TABLE—4
SEQUENTIAL CHANGES IN RESPIRATORY FLOWRATES IN MIC EXPOSED SUBJECTS

Standardised® Values
Period (months), (number of subject)
PEF Lit/Sec.
PIF Lit/Sec.
L/Sec.
Vbjs
Vbso L/Sec.
L/Sec.
VE75
L/Sec.
V1M
L/Sec.
VlSO
L/Sec.
Vns
FVC liL

®

At12monL
(%)T

0(52)
5.71+ ±1.79
3.40® ±1.08
5.47* ±1.64
3.48® ±1.13
1.90 ±0.67
2.47"±0.94
3.23'±1.04
2.85 ±0.93
2.30 X ±0.70

3(79)
6.69+ ±1.86
3.60 ±1.20
6.12*± 1.83
3.86 + +±1.42
2.10±0.93
2.83 ±1.01
3.48 ±1.18
3.05 ±1.01
2.19 ±0.56

6(70)
.6.75+ ±1.71
3.67 ±1.32
6.08 ±1.80
3.72 ±1.22
1.99 ±0.74
2.98 ±1.10
3.45 ±1.25
3.25 ±1.20
2.20 ±0.55

• to height 167 cm (M) and 160 cm(F) and age 30 years.
X. *.+:P<0.05 4—{-Significant increase upto 3 months and then decline upto 18 months:P<0.05
t NS P<0.05 for females only.
f : P<0.05
':NS
S Significant increase upto 6 months and then dedine at 18 months:Pz0.05

12(73)
6.88 ±2.20
3.92®±1.62
6.13 ±2.24
3.62 ±1.49
1.90 ±0.88
3.47° ±1.45
3.77'±1.56
3.14 ±1.39
2.48 ±0.75

'.1SK
■WM
W

-JE

+£

i

18(64)
6.95+41.M
3.2941.1lf|
6.06 ±1.95*^|
3.46®±1.32y
1.78 ±0.79 <
3.02° ±1.0<
3.17'± 1.01^.2.77 ±1.0#
2.68 X ±0J^‘

ptel efs/:

63

Me,hyl Isocyanate Survivors of Bhopal

' a|e smokers (in six. 15. 14. 11 and nine subjects on
JJe respective occasions Fig. 3) the initial pattern

Fig. 5. Flow volume loops in MIC exposed subjects-Nonsmokers. Female (see text!

smoker {see text)

shows low flow rates particularly on inspiration.
There is inspiratory hesitation developing at 18 months
and obstructive small airway pattern on expiration
at six to 12 months. Some improvement seen at
three to six months declined later.

TABLE—5
SEQUENTIAL PATTERN OF ABNORMALITIES FOR FLOW
VOLUME LOOP IN MIC EXPOSED SUBJECTS
18

Period (months)

0

3

6

12

No.

52

79

70

73

64

45.4

44.3

42.8

30.1

59.7

(a) Inspiration:
Normal

Sawtooth

123*

18.7

30.0

15.0

0*

Doming

16.5*

12.5

35.7*

21.8

83*

Hesitation

25.8

313

42 8

32.8

34.7

(b) Expiration:
Normal

19.6

15.6

50.0

10.9

12.5

Doming

30.0

31J

35.7

53.4

48.6

53.6

59.8

143

43.8

41.6

Concavity

• P<0.05

Fig. 4. MIC exposed sub/ecrs male non-smoker (see text)

Fig. 4 shows the results in male non-smokers (in
34. 50, 43. 46 and 41 subjects respectively). This
flroup has higher flow rates. There is no evidence of
Inspiratory hesitation but concavity on descending
expiratory limb is seen at 12 and 18 month stage.
fig. 5 shows the results in females all non-smokers
-On 12.14.13.16, and 14 subjects respectively). This
.flroup has lower readings generally while expiratory
■dows show some improvement, inspiratory flows do
[not improve to that degree. However there is no
jpridence of concavity on the expiratory curve.

Table. 5 shows the nature of abnormalities in flow
volume loop in MIC exposed subjects. These abnor­
malities were categorised as hesitation (poor starting
of inspiration with fluctuations due to incoordination).
sawtooth (indicating incoordination of inspiratory
movement due to variable intra or extrathoracic cen­
tral airway obstruction)*, doming (inability to sustain
peak flow indicating fixed central airway obstruction)’
and expiratory concavity (indicating small airway
disease)6. We did not find any correlation between'
clinical symptoms, spirometric values and flow rate
restriction in MIC exposed subjects.

At the initial stage 45.4% inspiratory and 19.6%
expiratory loops were normal (Table 5). While
this proportion did not improve for expiration, there

64

LUNG INDIA (1987). V. No. 2. (P.

59-E

I

is insignificant increase of normal pattern (59.7%) for
inspiratory loop at 18 months. Similarly frequency
of sawtooth and doming abnormalities significantly
reduced at 18 months. However proportions showing
hesitation on inspiration (suggestive of mild airway
incoordination) did not change. The expiratory
abnormalities continued unchanged but there was
transistory improvement at six month stage.

to MIC. This group also found that abnon^
flow patterns persisting beyond six weeks upto eigj,
months. We have not found overt evidence of pi*H
obstructive lung disease and large reversibility l
contrast to reported occupational asthma in expose
to toluene diisocyanate3.
>

It is true that lower FVC values may account for
lower flow rates, in our population (in comparison to
the U.S. subjects6) we do not think this is the whole
explanation. The inspiratory and expiratory flow
patterns could be considered related to mechanical
properties of lung (mainly elastic recoil): but these
are also effort dependent.5

The pattern of chronic respiratory disability showing
flow volume reductions alongwith restrictive lung.
damage with alveolitis on acute exposure to M|(
observed by our group with improvement in son*
aspects suggest the need for more extensive and
long term studies amongst the survivors.
ife

Conclusion

Acknowledgement
Discussion
We have found larger S.E. (by two to three
times) for prediction formulae than those by
Bass, possibly indicating that in comparison
to spirometry, the utility of F-V loop for flow
rates is lower in our population. The limitations
in using such prediction norms for flow rates
viz. population selection, technical limitation, coope­
ration. and standardisation of methods have been
stressed by Knudson et al13 earlier. Perhaps the
pattern of flow volume loop may indicate airway
abnormalities more definitively. While expiratory
flow rates would reduce earlier in obstructive airway
disease, inspiratory flow rates would decrease as the
disease progresses. Jordanoglou and Pride10 and
Kryger9 have analysed causes of abnormal pattern
particularly on inspiration. Variable intra and extrathoracic airway changes, airway distortion, laryngeal
or upper airway obstruction and small airway disease
have been implicated for various abnormalities obser­
ved. However the actual proof for any of the causes is
I still not available.

Significant restrictive functional changes (oxygen
exchange studies), airway inflammation and distor­
tion (bronchoscopy) increased cellular exudation
(broncho-alveolar lavage) as well as bronchiolitis and
alveolitis (biopsy) have been documented3. While
we have observed some improvement in spirometry.
oxygen exchange and blood gases, the decreases in
flow rates seem to be progressive. This has been
marked in 11 of 99 subjects studied showing
positive immunologic (RAST. IgE and ELISA. IgM.
IgA) antibodies specific to MIC (being reported
seperately; Karol M. H.. et al 1986). The changes
in our flow volume studies have been similar to those
observed by Alarie et al’4 in guinea pigs after exposure

We thank Dr. G. B. Parulkar. Dean for permitting
this study and Indian Council of Medical Research
for financial support. We are grateful to Dr. R.fc
Agarwal. Chief Medical Officer and Dr. A. K. Sarkar
of Central Railway for patient referrals. We acknow­
ledge the secretarial assistance of Gracy G. Andrade.^;
REFERENCES

Kamat. S.R.. Mahashur. A.A.. Tiwari. A.K.8. at al. (1985).
Early observations on pulmonary changes and clinical morbidity
due to the isocyanate gas leak at Bhopal. J. Postgrad. M«L
31. 63-72.

Kamat. S.R.. Patel. M.H.. Kolhatkar, V.P.. Dave. AA and
Mahashur. A.A. (1986). Sequential respiratory changes?1n
those exposed to the gas leak at Bhopal. Ind. J. Med. ^esr
83. (to be published).
3.

White. W.G.. Sugden. E.. Morris. M.J. and Eapata. E. (1980)?
Isocyanate induced asthma in a car factory. Lancet.
756-760.

4.

Morrie. J.F.. Koski. A. and Breese. J.D.. Normal values and
evaluation of forced expiratory flow. (1975). Arne. Rev. RespC
Dis. 111.755-762.

5.

Hyatt. R.E.. Schilder. O.P. and Fry. D.L (1958). Relationship
between maximum expiratory flow and degrees of lung inflation. J. Appt. Physiol. 13. 331-336.

6.

Bass. R. (1973). The flow volume loop: normal standards
aad abnormalities in chronic obstructive pulmonary disea»
Chest 63.171-176.
&

Singh. H.D. (1984). Mean Expiratoy flow volume curve fa?
South Indian men. Lung India 2. 293-296.
Kamat S.R.. Sarma. B.S.. Raju. V.R.K. et al. Indian norms W
Pulmonary Functions (1977). J. Assoc. Phys. India.
631-540.
W

Krygor. N.. Bode. P.. Antia R.. and Anthonisan. N. (1975
Diagnosis of the upper and central airways obstruction. Am
J. Med. 61. 85-93.

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65

jordanogiou. J. and Pride. N.B. (1968). A comparison of
maximum inspiratory and expiratory flow in health and in lung.
disease. Thorax. 23. 38-45.

volume curve with growth and aging. Arne. Rev. Respir. Dis
127.725-734.

pjtel et a/:

Kamau S.R.. Tyagi. N.K.. Rashid. S.SA (1982). Lung func­
tion in Indian adult subjects. Lung India. 7.11-21.
Jain, S.. Pande. R.S.. Ahuja. S.K. (1984). Pulmonary studies
in Myasthenia Gravis. Indian J. Med. Rsearch. 79. 806-812.

Knudson. R.J.. Lebowitz. R.D.. Heiberg. C.J. and Burrows. B.
(1983). Changes in the normal maximal expiratory flow

Alarie, Y„ Ferguson. J.S.. Stock, H.P.. Weyel. D.A. and
Schaper. M. (1986). Sensory and pulmonary irritation of
methyl isocyanate in mice and pulmonary irritation and possible
cyanide like effects of methyl isocyanate in guinea pigs. En­
viron. Hlth. Persp. (In press).

Correspondence/Request for reprints to: Dr. S. R. Kamat. Respiratory
Medicine Department. K.E.M. Hospital. Bombay-400 012.

•ects of Inhaled Sublethal Concentration of Me±yl Isocyanate on Lung
Mechanics in Rats
R K SR1VASTAVA. R VUAYARAGHAVAN, PRAVTN KUMAR. S C PANT, S K SHARMA.
A S SACHAN & M P KAUSHIK
Defence Research & Development Establishment, Gwalior 474 002, India
Received 15 September 1986; revised 22 May 1987
& ' Rats exposed for 30 min to a concentration of 137 ppm (1/3 LCS0) of methyl isocyanate (MIC) showed respiratory
IT distress. After 24 hr of exposure the animals were free from distress. There was no external haemorrhage and the lung
£ body weight index did not show presence of pulmonary edema in these rats. Characteristics of pressure-volume curves
£ drawn from the excised air filled lungs, phospholipids content of the lung lavage, minimum dynamic surface tension
Jg-ynri histomorphologicai studies showed that the lung surfactant was not affected. However, the lungs of these rats deve■Kped emphysema as was evident by decreased maximum dynamic surface tension, increased total lung capacity, greaquantity of air trapped in the lungs at the end of deflation process and significant increase in the compliance and
specific compliance. Lung emphysema was further confirmed by histophatological studies. Besides, there was very
parked inflammatory reaction in the alveolar septa and the walls of capillaries were damaged. Red blood cells were
i-?. spilled in the interstitial and alveolar air spaces. The results show that sublethal concentration of inhaled MIC damage
jg lung parenchyma and produce emphysema. These seem to be lingering effects of MIC independent of its pulomonary
r? edema inducing capability.

Ethyl isocyanate (MIC) a highly reactive, volatile,
mmahle and toxic liquid causes corrosive damage
tissues exposed by inhalation and topical applicai1. Intoxication by inhalation produces pulmonedema, mottled red lungs, dyspnea and respirai failure associated with inflammation and squais metaplasia of respiratory epithelium2. Expoto sublethdl concentrations of MIC may proe increased secretion, cough, pain in breathing
obstruction in airspaces causing temporary re­
ttery distress. However, no attempt has been
' to study the effect of inhaled sublethal conrtions of MIC on the morphology and lung me3 in experimental animals. Being an industrial
ical, most of the studies have been confined to
Me data on perceptible and irritant concentr. for human subjects3 and the lethal concentr: by systemic and inhalation routes of adminis®on in experimental animals43.
The present study has been designed to find the
fan of inhaled MIC on the lung mechanics of rats
dependent of pulmonary edema and haemor-

Aerials and Methods
Male Wistar rats weighing 85-100 g raised in the
•tnal House of the Establishment and fed on
»dard Hind Lever Feed were used in the present
<ty. Ten animals were used in each treated and
ttrol group, except for histomorphologicai stud*here lungs of three rats were processed.

Methyl isocyanate (MIC) was synthesized in the
Chemical Laboratories of this Establishment by
reaction of acetylchloride with sodium azide in the
presence of phase transfer catalyst.

With a view to minimising the risk of exposure of
the investigators, the rats were exposed to MIC in a
specially designed static exposure chamber6. Two
rats at a time with loading complement of less than
1.0% were exposed for 30 min to vapours of MIC.
Seven pl of MIC was spontaneously evaporated in a
small glass test tube attached to the inhalation
chamber and the monitored concentration of MIC
was 0.32 mg/1 (137 ppm). This is slightly less than
1/3 LC50. Calculated LC<0 (using the static chamber
for 30 min exposure) was 1.08 mg/1 (95% of confid­
ence limit 0.89-1.3 mg/1 which is equal to 465 ppm.
The control rats were also confined for the same du­
ration to the environment of the exposure chamber
but without MIC.

After 24 hr of exposure, the rats were bled to
death through a cut in the abdominal aorta under
pentobarbital sodium anaesthesia.
Lung body-weight index (LBI)—The lungs were
removed, freed from adhering tissues, blood and
weighed. The LBI was calculated by the formula:
LB! = Lung weight xl0()

Body weight

Dynamic surface tension—Dynamic surface ten­
535

sion, maximum (y max) and minimum (y min) of
lung homogenates was determined ’. Lungs freed
from adhering tissues and blood were homogenised
in cold normal saline. The homogenate was filtered
through cotton, diluted with normal saline to 100
ml/g lung tissue, poured in the trough of the Wilhelmy Assembly and allowed to age for 40-50 min at
27’C. Thereafter the surface film was tompressed
cyclically from a maximum of 55 cm2 to a minimum
of 19 cm2 at the rate of 4 cycles/min for about 30
min. The surface tension area loops were recorded
onaX-Y recorder.

Pressure-volume curves (P-V curves)—Excised rat
lungs were cannulated through the trachea and de­
gassed under vacuum. Subsequently, they were in­
flated with air at the rate of 1 ml/nun to a maximum
pressure of 40 cm H?O and then deflated (1 ml/nun)
to 0 cm H,0 intrapulmonary pressure. The lung vo­
lumes at each measured pressure point were used to
construct P-V curves. The stability index (SI), expan­
sion index (El), total lung capacity (TLC or V„„)
and the volume of air at 0 cm H,O pressure (Vo) and
5 cm H.O pressure (V;) were compiled from the P-V
curves3-’. The slope of the deflation curve between
55 to 80% of TLC was taken as the specific compli­
ance and from that compliance was calculated (com­
pliance = specific compliance x TLC/100 )10.

breathing). After 24 hr, the animals were antn^SH
normal with no symptom of respiratory distrZ^SM
Lung body weight index—LBI of expeii^SB
and control rats (10 animals in each grounV^’Mi
0.59 ±0.02 and 0.69 + 0.03 respectively.
ference was marginally significant (P< 0.05).
Dynamic surface tension—Significant decrease®!
y max (PCO.Ol), y min and stability ratio (P<nj^B
was observed in MIC exposed rats (Table 1)
Pressure volume curves—The mean of 'ttffjSM
curves is shown in Fig. 1. Summary of resultsnfe3
tained from the analysis of P-V curves is preserii4t3
in Table 2.
In MIC exposed rats, the total lung capacity
the volume of air trapped in the lungs at the endof'3
deflation process were markedly increased*!

(P< 0.001).
The stability index, expansion, index, the voiu^S
of air retained during deflation (% TLC) compliance—
and specific compliance were significantly increased «
from the control values.
yaSUM

Table 1 —Pulmonary Dynamic Surface Tension and!
bility Rauo of Control and MIC Exposed Rats/
[Values are mean ± SE of 10 animals m each group] /
Surface tension (dynes/cmf

Lung phospholipids—The lungs in situ were per­
fused with cold normal saline through the pulmon­
ary circulation to remove the blood from the pul­
monary capillary bed. Thereafter, the trachea was
cannulated and the lungs were lavaged with 5 ml
cold normal saline. The process was repeated 5
times. The lipids, in the pooled lavage, were extract­
ed and fractionated for phosphatidylcholine and
phosphatidylethanoiamine by Thin Layer Chroma­
tography11-12. Total phospholipids (TPL). phosphati­
dylcholine (PC) and phosphatidylethanoiamine (PE)
were estimated spectrophotometrically 13.

Control
23.0 ±1.00
MIC exposed 20,7 ±0.36*
P value; ‘ <0.05: “ < 0.01. SR - 2 (y max -y min)/y max*i

Histomorphological studies—Excised lungs of
rats were inflated with air to an intrapulmonary
pressure of 10 cm H;O. The trachea was ligated and
the whole lung was fixed in the buffered formaline.
Representative samples of tissue from various lobes
of the lungs were cut into small pieces and pro­
cessed for routine histological examination.
Mean values for each group of animals were test­
ed for significance by Student's t test. A level of sig­
nificance of P< 0.05 (two tailed) was chosen.
Results
Gross effects—AU the MIC exposed rats deve­
loped temporary respiratory distress (mouth

536

Fig. 1-Pressure-volume curves of control and expose*^
(Lower panel: inflauon limb ( — ) and the deflation 11,11
control (—) and exposed (—) rats. The upper panel: do**
limbs of control (—) and exposed (—) rats taking TLC as

SRIVASTAVA et au EFFECT OF INHALED MIC ON RAT LUNG

Total lung
capacity
(CC/100 g
body wt;
TLC)
6.00 ±0.25

Table 2—Results Computed from P-V Curves of Lungs of Rats
[Values arc mean±SE of 10 animals in each group]
Compliance
Expansion
%Air
Stability
Volume of air
index t El)
evacuated
index (SI)
(CC/lOOg

1.00 ±0.02

0.57 ±0.01
0.68 ± 0.01b

0.348 ±0.031
0.762 ±0.045b

Specific
compliance

3.90 ±0.19
7.68 ± 0.4 lb

»values:’<'0.01:b<0.°01;SIT
u m - V • VH = 11

g : Lung phospholipids—Extractable TPL, PC and
tp^id not show statistically significant deviation
IfiUlhe control values (Table 3). However, TPL
'and PC tended to be low and percent of PC in TPL
iras marginally increased.

B Histomorphological studies—In Fig. 2 are shown
the histomorpjrological features of a lung from a
control rat observed under light microscope. The
airways, air sacs and the alveolar septa are normal.
The lining of the respiratory bronchioles is intact.
On exposure to MIC epithelial cell lining of respira­
tory bronchioles and the walls of the finer capillaries
in the alveolar septa were degenerated (Fig. 3).
Alveolar atelectasis was seen only in the peripheral
alveoli. Larger blood vessels were clogged with
blood. However, the most significant finding was
that red blood corpuscles were seen scattered in the
alveolar septa and alveolar spaces (Fig. 4).
Discussion
j Pulmonary edema and haemorrhage are com­
monly occurring gross effects induced by agents ing MIC, which have profound irritant effect on
spiratory tract1,14,16. The presence of edema­
tous fluid and blood in the air spaces of the lung may
mask the underlying mechanisms involved in caus­
ing changes in the lung mechanics by such agents.

«

-Unlike lethal exposure to MJC where LBI in^eases due to pulmonary edema and haemorrhage,
lungs of rats in the present study (1/3 LC7o)
*»e free from these effects as is evident by no infrtase in LBI. The reduced LBI observed here may
*due to lesser intake of water (including food) as
”le'e animals were under acute respiratory distress
“fa few hours after exposure to MIC. Hence, it is
easonable to assume that the findings on P-V
51rves, dynamic surface tension and TPL were pri­
ority due to the effects of MIC on the lungs inde-

Table 3—Phospholipids Contents (mg/g) of Lung La­
vage of Control and MJC Exposed Rats
[Values are mean ± SE of 10 animals in each group}
Group
Total phos­ PhosphaPhospha­
pholipids tidylcholine lidylelhanol(TPL)
amine (PE)
(PC)
Control
1.79
1.35
0.21
73.7
±0.13
±0.13
±0.03
±4.05
MIC
1.55
1.26
0.22
77.8
exposed
±0.13NS
±0.26NS ± 0.03 NS
±2.52N
NS: not significant

pendent of the influence of accumulated edematous
fluid and blood. The marginal decrease in LBI of
MIC exposed rats was possibly due to the trauma as
these rats did not take food and water during the 24
hr post exposure period.
It is evident that MIC, in the concentration and
duration of exposure used, had no destabilizing ef­
fect on the alveoli, mediated through the lung sur­
factant system since the TPL. PC were not dec­
reased significantly. Furthermore, y min was not in­
creased. The histomorphological studies also did
hot reveal alveolar atelectasis.

Significant increase in TLC, Vo, sp. compl. and SI
computed from P-V curves of lungs of rats exposed
to MIC indicated presence to emphysema. This
contention is further substantiated by the finding
that dynamic maximum surface tension (y max) was
appreciably lowered in the homogenates prepared
from these lungs. Emphysematic lungs have been
reported to retain large volumed of air (increased
Vo) and had relatively lower maximum dynamic sur­
face tension15. Emphysema was also seen in the his­
tomorphological studies carried out in the MIC ex­
posed lungs.
The most striking finding of the histomorphologi­
cal studies under light microscopy was the presence

537

INDIAN J EXP BIOL, VOL. 25, AUGUST 1987
Fig. 2—Normal lung from a control rat showing fi«l|
alveolar pattern with normal alveolar septa, ducts^flB
oles with intact epithelial lining H & E X280. Fig. 3^^^
ed epithelial lining of bronchiole has undergone exien^sl
mage. H & Ex 300. Infiltration of inflammatory cellr^
spaces (arrow) seen. Fig. 4—Infiltration of large numb^—
blood cells in the alveolar spaces is seen. H & E x 38q
septa are inflammed. There is no evidence of oedemat**®
The emphysema is also very marked) 1&||S

of randomly distributed red blood cells in the aS
lar airspaces. Other histomorphological findia
were inflammatory response with severe intenSj
pneumonia and disintegrated walls of finer nulmnj
ary capillaries in the lungs of rats which had*8
covered from initial respiratory distress. Rutlg
more, there was no externally visible haemonhai
in these lungs. Pulmonary' injury induced by sub!
thal concentration of MIC appears to have adyen
effects on the lung mechanics independent of itspn
monary edema inducing effect.
Acknowledgement
The authors arc indebted to Dr P.K. Ramachai
dran. Director, for keen interest and guidanc
Thanks are due to Mr Hari Afley for secretarjaTj

sistance.
References
I Kimmeric G & Eben A. Arch ToxicoL 20 (1964) 23j
2 Fowler E H & Dodd D E. Fundam Appl Toxicol#
756.
3
Rve W A. J Occup Med, 15 1973) 306.
4
Smvth H F Jr. Carpenter C P. Weil CS. Pozzani UC,Sti|
J /\ & Nycum J S. Am Ind Hyg Ass J, 30 (!1969fgM
5
Vernot E H. Macewen J D. haun C C & Kinkead E
colAppl Pharmacol. 42 (1977) 417.
6
Vijayaraghavan R & Kaushik M P. Indian J Exp
(’1987)531.
7 Mendenhall R M. RevSci Instrum, 42 (1971) 878.,
8
Gruenwald P. JAppl Physiol. 18(1963) 665.
9
Srivastava R K. Sachan A S & Sharma S K. Indian J
0414(1976)428.
10
Szapiel S V. Fulmer J D. Hunninghake G W, EBoeffi
Kawanami O. Aerrans V J & Crystal R C.
spir Dis. 123-1981- 680.
. ,
11
Folch J. Lees M <fc Sloane-Stanley G H. J Biol c
(1957)497.
12
Abramson D & Blecher M. J Lipid Res. 5 (1964)
13
Bartlett G R. J Biol Client. 234.1959) 466.
14
Nemery B. Dinsdale D. Sparrow S & Ray D E. BrJ
42(1985)799.
•. jWB
15
Clements J A. Hustead R F. Johnson R P &
Physiol. 16(1961)444.
16
Ferguson J S. Schaper M. Stock M F. Weyel D A
ToxicolApplPharmacol. 82 (1986) 329.

jgMM

Gri^.5«S

538

British Journal of Industrial Medicine 1988:45:269-274

fleets of methyl isocyanate on rat muscle cells in
' ;ulture
►Una ANDERSON.' SHOBHA GOYLE.-’ B J PHILLIPS.' A TEE.' LINDA BEECH.1
«H BUTLER'
1
the British Industrial Biological Research Association.’ Carshahon, Surrey SMS 4DS. UK, and School of
MtSct nces.' Jawaharlal Nehru University. New Delhi. India

i
JigTRACT Since the Bhopal disaster, in which the causal agent was methyl isocyanate (MIC).
fjposed^kple have complained of various disorders including neuromuscular dysfunction. In an
Attempt ^rgain some information about the response of muscle tissue to MIC its effects were
Krestigated in cells in culture isolated from muscle of 2 day old rats. After treatment with a range of
KlC concentrations (0025-0-5 /d/5 mi culture) the total number of nuclei of the two main cell types
Bibroblasts and myoblasts) and the number of nuclei in muscle fibres (myotubes) were recorded. At
■wer doses which had little effect on the total number of nuclei, the formation of muscle fibres—that
Ifusion of muscle cells—was prevented as the proportion of nuclei in myotubes was decreased. At
Jigher >ses both cell types were killed. This would suggest cither an effect on muscle differentiation
Ira selective toxicity towards myoblasts. The observations were supported by light and electron
■aicroscopy.

nhe industrial disaster in Bhopal. India, tn 1984 the
akage of 40 tons of methyl isocyanate (MIC) gas

leslim. ied 15 000 people sutfering from a variety of
ibnent- Three months later 50 000 of the people
tntinueu to have disorders of the lungs and eyes and
deration of the gastrointestinal tract and many
anplained of kidney, liver, and neuromuscular dys»ction.; Since then, various researchers have been
tillering tmticological information.
Kimme^Bnd Ebcn showed that MIC was highly
riant to slun and mucosae and produced pulmonary
ulema.-’ Nemery er al suggested that MIC at high
trcentrations probably caused peracutc death
iroug'■ -.-tlcx inhibition of breathing and rats surviv'8ex, sure exhibited narrowing of the airways and
“morrnagic pulmonary oedema.' The lesions were
Paired rapidly but renewed inliammation and peri’°nchial fibrosis were apparent. Nemery et al also
J°*ed that cyanide intoxication is not concerned in
'clinical syndrome seen after exposure to M1C nor
'“sodium thiosulphate protect rats from the acute
subacute effects of MIC/ Cellular immunity has
’’tpk

April I9K7

been shown to be slightly compromised by exposure to
MIC.'
In investigations of the genotoxic potential of MIC
it has been reported to be non-mulagcnic in the
^standard Ames1’and prcincubation assay, and Ander­
son et a! showed that negative results were also
obtained in the Ames lest when urine from animals
treated with MIC was tested.'' Shelby et al have also
reported a negative sex linked recessive lethal test
in Drosophila.’ Positive results have been shown.
however, for point mutation tn the mouse lymphoma
assay and in Chinese hamster ovary cells in culture for
chromosome aberrations and sister chromatid ex­
change in the absence of rat liver S9.' In vivo there was
marginal evidence of an effect for chromosome aber­
rations and sister chromatid exchanges in the B6C3F,
hybrid mouse but results were not reproducible. The
results from the bioassay using the same strain are
eagerly awaited since they would give an indication of
the potential carcinogenicity of MIC in man.
In man there have been complaints of neuro­
muscular dysfunction1 but little or nothing is known
about the toxicology of such effects. In an attempt to
gain some information on muscular function we
examined the effect of MIC administered to rat muscle
cells in culture.

269

,... . u. oeech

Materials and methods
ISOLATION OF MUSCLE CELLS CULTURE
TECHNIQUES
Cells were isolated from muscle of 2 day old rats by
treatment with dispase solution. Cells were cultured in
Dulbecco s medium with 10% fetal calf serum in 25
em: flasks and placed in a CO; gassing incubator at
37'C until treatment.

Table 2 Study 2: the effect of MIC treatment at vart
times after culture establishment (day 0) on the growth*
fusion of rat muscle cells

TREATMENT REGIMEN
MIC was added directly to the flasks and left for two
hours and then replaced by fresh medium. Flasks were
then incubated until fixation.

EXPERIMENTAL APPROACHES
Various experimental protocols were used. The first
study with treatments on days I and 2 was to
determine a suitable range of doses for the final study­
in which the compound was administered at days 2. 4.
and 6 in culture in order to treat the myoblasts at
different stages of development.

CELL FUSION COl NTS ON STANDARD
CULTURES
Counts were made on It) fields lor each culture. The
total number of nuclei of all cell typesand the number
of nuclei in myolubes was recorded.

Results
s runr i

In those cultures treated on day 2 with lower dose
treatments and fixed at day 9 there was little effect on
total nuclei but myotube formation w as much reduced
at tl-25 and mi'.'al (table I).

' Fixed on day <
J Fixed on day <<
Footnotes as tor study I

STUDY 2
The results for control cultures were similar to those;.
the first study with mean values of 2-76 x 10*nud<
I 13-0% fused) on day 5 and 2X9 x 10" (17-6% fusee
on day X (table 2). Because of the larger number«
control cultures in this study it was possible toobsen
the variation obtained w ith this counting method. Th<
total nuclei were relatively consistent (a range of 2-2'
to 3 4X x |o”) but fusion was more variable (8-1 tc
25 6%).
With treatment on day I. nuclear counts were
significantly reduced al 0-25 pl (more than two stan­
dard deviations below the control mean) and fusion
was significantly lower at both 0-25 and 0-125 pl in
cultures fixed on day 5. No cells were present after
treatment with 0-5 /al.
.After treatment on day 4 and lixation on day 8 total
counts were similar to controls at doses up to 0-25pl
but fusion was inhibited at 0-125 and 0-25 pl. There
were no cells present after treatment with 0-5 pk
Treatment on day 6 resulted in a decrease in nuclear
counts and fusion at a dose of 0 05 pl and cells were
destroyed at higher concentrations.
microscopy
.
On days 4 and 6 al the light microscope level IJ
control cultures consisted of a mixed population
long strap-like multinucleate muscle cells and mon
nucleated spindle cells resembling fibroblasts (ng .
The fibroblasts showed many fatty cytop..il^J
vacuoles while both fibroblasts and muscle ceUs
dense cytoplasmic inclusions. At the c*cctron.!Tij fcv
scope level two cell types could be readily identmeo . ,

271

*^eech,

■

pojmetnyi isocyanate on rat muscle cells in culture

' 15 nw""" ",iCrO!!raphCU"Ure ,rea,ej

WC ‘0 :51‘‘/" '•<> culture) showinf. residual necrotic cell.

Anderson. Goyle. Phillips. Tee. Beech
the characteristic fibres of the muscle cells and the
form of the endoplasmic reticulum of the fibroblasts
(fig 2).
Cultures receiving 005 tzl MIC on day 4 were
essentially the same as the controls at both the light
and electron microscope level. At a treatment level of
0125 ul MIC changes were observed. The syncytial
muscle cells were much less abundant and necrotic
cells were scattered throughout the culture (fig 3). At
the electron microscope level the mononuclear cells
could be identified as both myoblasts and fibroblasts.
The myoblasts were less abundant than the fibroblasts
and often had a simplified profile (fig 4). The fibro­
blasts were similar to the controls.
At the treatment level of 0-25 zd MIC all the cells of
the culture were necrotic and there was no evidence of
the syncytial muscle cells (figs 5 & 6).

Discussion

The results suggest that MIC is toxic for a mixed
culture of fibroblasts and muscle cells but that the
m>oblasts appear io be more susceptible to the acute
toxic action ol MIC. Even at relatively low concentra­
tion u was toxic. Lower doses tended to prevent
mxotube formation since the proportion of nuclei in
m\<nubes was decreased at concentrations which had
little effect on total numhero! nuclei as shown at doses
of HI 25 /zl and 0-25 /zl after treatment on day I and
fixation on day 5 and at a dose of 0 125 zzl and 0 25 /zl
after treatment on day 4 and fixation on day <S. Al
higher doses (he total number of nuclei were reduced.
These findings would suggest either an effect on muscle

differentiation or selective toxicity to myoblasts Af
treatment on day 6 effects were more severe because
this stage cells were detaching as monolayer sheets
the hieher doses and both cell types appeared tn i
killed?
The importance of the findings for muscle tissue
the intact animal is not clear where muscle cells a.
under the control of the nervous system. It ma.. j
speculated that MIC would directly affect muse
tissue and prevent differentiation as shown in the >
vitro situation. If MIC were also to directly attack if
nervous tissue this might superimpose a lack $
coordination in addition to a lack of differentiation
References

I Zaidi M. Bhopal and alter. .4 m J Ind Med 1986:9:215-6.
- Kimmerie R. Eben A Zur Toxicitat von Methylisocyanat m*
dessen quantitatwer Bestimmung m der Luft. Arch Toxu
1964:20:235-41.
3
Nemery B. Dinsdale D Sparrow S. Ras DE. Effects of mcih
isocyanate on the respiratory tract of rats. Br J Ind \f(.
19X5:42:799-805
4
Nemery B. Sparrow S. Dinsd.de I). Methyl isocyanate: ibiosw
phatedoes not protect Lancet I9X5;:i:I245.
5
Silver M. Gcrmalcc I). Vorc S. fucker A Luster M. Immunotox
cology ol'methyl isocyanatein mice. The Toxicologist 1986:6:7$
iAbstract No Ml i
6
National Toxicology Programme. Research Triangle Park. Nort
Carolina: Department ot Health Human Services. 1983:5-6
(Tech bulletin No '• i
’ Shelby Ml). Zeigcr It. Caspary W. Mason J. Tice R. Genet*
toxicity of methyl isocyanate t.MICi. The Toxicologist 1986.6
78 t Abstract No M2.1
X Anderson I). Blowers SD. Nemery B Investigation of the Ama
test oi urine samples irom rats exposed to methyl isocyanate.
J Ind \frd-19X6:43 '66-7

Effect of Exposure to Toxic Gas on the Population of Bhopal:
S- part I—Epidemiological, Clinical, Radiological & Behavioral Studies
B N GUPTA. S K RASTOGI, H CHANDRA, A K MATHUR, N MATHUR, P N MAHENDRA, B S PANGTEY,
S KUMAR, P KUMAR. R K SETH, R S DWTVEDI & P K RAY*
Industrial Toxicology Research Centre, Lucknow 226 001, India

Received 30 December 1987

Systematic follow-up studies were conducted to obtain information on after effects of exposure to the toxic gas on
fcn/ [fog population of Bhopal A total of 1109 subjects were studied on location in Bhopal. This paper deals with the general
demographic data and the findings of clinical radiological and behavioral studies. The majority of the subjects had
symptoms pertaining to respiratory, cardiovascular, gastrointestinal and musculoskeletal systems. The prevalence of
• symptoms pertaining to respiratory and gastrointestinal system was significantly higher in population residing within 4
. Vm than among those residing beyond that distance from the factory. A number of clinical signs in regard to various sys­
tems were observed. 739 Subjects (81.8%) out of a total of 903 subjects studied radiologically showed no abnormality
in their chest X-rays, whereas 91 subjects (10.1%) showed radiological changes suggestive of definite pathology like
hulmonary tuberculosis, pneumonitis, emphysema, etc. Specific radiological changes were observed in 73 subjects
*.1%) and out of these, in 48 subjects the abnormal findings on X-ray was because of exposure to the toxic gas. In 17
subjects radiological changes suggestive of old disease were observed. Since the symptoms appeared only after expo­
sure to the toxic gas it was presumed that in those cases the old pathology was aggravated because of the exposure to the
gas Pneumonitis was commonly seen in the right zone. There was no correlation between the radiological picture andt
the clinical presentation. The cases with clear-cut pneumonitis had no evidence of toxaemia. The results of behavioral
studies revealed that memory mainly visual perceptual and attention/response speed alongwith attention/vigilance
were severely affected in the exposed population.

Background Information
Bhopal (Lat. 23.16N, Long. 77.24’E). the capital
of Madhya Pradesh, having a population of approxi' mately 9 lakhs and located 568 km south of Delhi.
^ fmet with the world’s worst chemical disaster on the
<night of Sunday, 2 December 1984, and early hours
SjA of Monday, 3 December 1984. The storage tanks in
gfei-Union Carbide Plant which were storing methyl
isocyanate (MIC) leaked leading to a variety of
health problems in the population of Bhopal.
g®. Henceforth. we will mention in all our subsequent
PaPers this exposed population as the population
I ^-exposed to toxic gas released from the Union CarF
bide Plant This is a local pesticide plant situated at
easI and about 2 km from the Bhopal railstation. The escaping gas quickly spread as a
wgged cloud over a large and thickly populated
•"-TS areas of about 7-8 km mostly to the south and east
HK of the plant (Map 1).
The effect on the people, living in the shanty setf-Sc KJn’ent^ iust over the plant fence, was immediate.
■4-T i,an^
t^le’r beds>never knowing what killed
t™n- Others staggered out of their homes, blinded
ggpf y c**°hing to die on the street within minutes.
Ofe-hTh' m°re succumbed later on- some after reach.hospitals and emergency aid centres. The worst
IT’■-s.

jj|ft^orr<spondeni author

affected areas of the city are situated 1 -3 km from
the factory (Map 2).
The early acute effects beside the heavy death toll
were frightening particularly of long term prognosis.
As the cloud of gas swept over parts of the city,
stfickcn residents experienced a burning sensation
in the eyes, nose and throat. Many ran out of their
homes, coughing and gasping for a breath. Some
had begun uncontrolable vomiting. Others col­
lapsed right away whereas ulcers formed on the cor­
nea of some victims leading to blindness.
Most deaths have been attributed to various
forms of respiratory distress. In some people, the
toxic gas caused such massive internal secretions
that their lungs became clogged with fluids, while in
others, spasmodic constrictions of bronchial tubes
led to suffocation.
Many of those who survived the first day were
found to have impaired lung function. Their breath­
ing was shallow, making it difficult for them to get
enough oxygen. The tragic occurrence gave rise to
certain important questions like what are the long
term effects with regard to the physiological func­
tioning of various systems and the severity of the da­
mage caused to the population exposed to the gas.
Introduction
<
The systematic studies were carried out to obtain

149

INDIAN J EXP BIOL. '•’OL. 25. \LA3eCS

information on after effects of exposure to the toxic
gas on the population of Bhopal. The scientific in­
formation on toxicity of the gas and related com­
pounds is available to some extent1 “7. Some studies
have been reported on the toxic effects of toluene
di-isocyanate and diphenyl methane di-isocyanate
in the literature15'11. The present study was underr
taken to note clinical, radiological and behavioural
changes in the population exposed to the toxic gas.

toxtc gas. . res seam comp nsec specialists hfW
meriir-rnf: pesmooary physiology, radiology C*
tology. demasaourai tc-axology, biochemistry—-"

dy centre was started;

forward v/-.»irrmTty for getting thetnse
2985' 68"

Materials and Methods
A team of scientists/technicians from ITRC
reached Bhopal on 11 February, 1985 to conduct
follow-up studies of the population exposed to the

affected
-ike Caeca Road, Kazi Camp,
Railway Sctoco. Cbamdbagh, etc. were exaji.

Map 1—Map of Bhopal ary snowuM gas arfecred areas
150

■' GlH’TA eraL EFFECT OF EDXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL-I

2r-Location of UCIL factory m Bhopal Maximum number of study subjects were drawn from the areas in the circle

1^592. persons were covered. The following
rs were studied in each case—History
ng, clinical examination, chest X-ray and behavi~"es.
firory taking—A complete history including bioand occupational background of each subject
recorded on the basis of a questionnaire pre­
according to WHO epidemiological-study
linical examination—A complete clinical examinon that covered general physical examination.
on of respiratory, cardiovascular, gastromusculoskeletal and central nervous sysMof the subjects was done.
Radiological
examinarion-A
full
sized
£525 cm) plate was used for chest X-ray pos­
er view in 903 exposed persons using a
X-ray machine International General
Company IGE). The X-ray films were read
«panel of experts including a radiologist, a chest
specialist and an industrial medicine special-

ural studies—Psychological tests were
>n 350 random subjects of either sex repJgdifferent socio-economic groups and

.oi;t

drawn from different age groups. Children were ex­
cluded from this study. The following tests were
.conducted.
Digit Span Test: This is a subtask of Wechsler
Adult Intelligence Scale (WAIS) and Wechsler
Memory Scale (WMS) used for testing immediate
auditory memory.
Benton Visual Retention Test: This is a visual
memory test and also measures attention and visual
ability.
Digit Symbol Test (DST): This is also a substask
of Adult Intelligence test and is used to measure
perceptual motor speed. This is considered as the
most valid detector of cerebral dysfunction.
Bourdon Wiersma Vigilance Test: This also mea­
sures perceptual motor speed. The score represents
perceptual accuracy as percentage.
Simple Reaction Time (SRT): It is the length of
time between the onset of a stimulus and execution
of motor response. This is a sensitive indicator of
toxic effects.
Santa Ana Test: This is used for measuring per­
ceptual motor coordination in terms of manual dex­
terity.
Personality tests like Rorschach Inkblot and Ey151

I

INDIAN J EXP BIOL, VOL. 26, MARCH 1988
senck Personality Inventory (EPI): These are used to
detect non intellectual personality disturbances,
changes in mood, readiness for affective reactions,
neuroticism and the dimension of extroversion/introversion, etc. The above tests were also conducted
in control subjects which were equally distributed
according to age, sex and socio-economic status,
comparable to the exposed population, the only dif­
ference being that the subjects of this group were
not exposed to any toxic or irritant gas.
Statistical analysis—The following statistical tools
were used for the analysis of data pertaining to
memory, perceptual motor speed, attention/response speed and manual dexterity.
Analysis of variance: In order to test the signific­
ance of the variations among three different groups,
viz. control, exposed male and exposed female, the
analysis of variance as suggested by R.A. Fischer,
was worked out.
Student’s t test: This test is applied to find out the
significance between two groups. The expression
standard error (SE) of the difference between two
groups is represented by:

SE(Diff) = EMS
where EMS = mean square within groups
n, and n, denote the sizes of the two groups.

Observations
General profile of the study population—Out of
1109 persons studied 202 (18.2%) were Hindus.
894 (80.6%) were Muslims and 13 (1.2%) belonged
to other religions. This high proportion of Muslims
in the population under study is because of the fact
that most of the residents in the areas worst affected
by the gas exposure were Muslims.
Among the population studied. 32.6% were un­
married and 67.4% married. In the age group < 15
years 100%. in 16-25 years 54%, in 26-35 years 2%,
in 46-55 years 3% and in the age group above 56
years 3% were unmarried. The rest were married.
As regards food habits 134 subjects (12.1%) were
vegetarian while 975 subjects (87.9%) were non­
vegetarian.
Out of 1109 subjects, 259 (23.4%) belonged to
the nuclear type of family while 850 (76.6%) be­
longed to the joint type. 29% in age group of < 15
years. 24% in 16-25 years, 25% in 26-35 years, 19%
in 36-45 years. 17% in 46-55 years and 20% in
more than 56 years age group respectively belonged
to the nuclear type. The remaining persons be­
longed to joint families.
Out of the total population studied (1109 subjects,
671 subjects (60.5%) lived within a distance of 2 km
152

«|

from UCIL factory at the time of accident. Thj,
population was worst affected by exposure to the
gas. 345 subjects (31.1%), 63 subjects (5.7%) and 3q
subjects (2.7%) lived at a distance of 2-4, 4-6 and
more than 6 km respectively from UCIL factory
(Table 1).
£
Out of 1109 subjects studied, 386 (34.8%) had
fewer than 5 members in the family, while 57j(51.7%) and 150 (13.5%) had 6 to 10 members and
more than 11 members in the family respectively'
Six to ten members or more than 11 members reflex
crowding in the family.
..jg'
As regards the level of literacy among the study
population 32.4% were illiterate, 21.6% had re­
ceived only primary education, 10.3% were educat­
ed up to Junior High School, or Middle, 8.7% up to'
High School, 11.4% up to Intermediate and 15.6%.
were degree holders.
In the study population of 1109 subejcts 438
(39.5%) slept in the open while 671 (60.5%) lived in
closed (covered) houses.
Out of 1109 cases studied, 993 (89.5%) had a per
capita income of Rs 300 or less. 78 (7.0%) had aper
capita income of Rs 301-500, 24 (2.2%) had a per
capita income of Rs 501-800 and 14 (1.3%) had a-,
per capita income of Rs 801 or more per month)
(Table 2).
Symptomatology—Of the overall complaints, the.
majority, i.e. 22.1 and 20.2% respectively were reg

_______________________________ 9
Table 1 — Agewise Distribution of Population Livingatft
Various Distances from Union Carbide Factory
Age group
years

<15
16-25
26-35
36-45
46-55
>56
Total

•

Distance (km)

2

2-4

4-6

112
170
152
102
70
65
671
(60.5%)

53
86
95
68
22

10
20
18
9
3
3
63
(5.7%)

345
(31.1%)

6
1
14

~

8
1

V

-

a

30
(2.7%) &

Table 2—Agewise Distribution of Population on the
Basis of Per Capita Income
Age groups

Per capita income (Rs per month)

300
<15
16-25
26-35
36-45
46-55
>56
Total

162
260
247
161
84
79
993
(89.5%)

301-500
9
17
18

501-800
□
10
4

5
8
78
(7.0%)

3
1
(22%)

801
3
3
*7
1
4
1
14

3

fn
V
J

(1.3%) 1

GUPTA el al: EFFECT OF EDXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL-I

hied to respiratory and ocular system, followed by
.* e reiated to gastrointestinal system (16.4%) and

(51.9%) while jaundice noted in 15 subjects (1.4%)
and congestion in 338 subjects (16.4%).

the musculoskeletal system (12.3%). Psychogenic
jjomplaints constituted 11% of the overall symp-

During the examination of oral cavity, the teeth
and gums were found normal in 790 subjects
(71.2%) and 1039 subjects (93.6%) respectively.
The incidence of caries was found in 195 subjects
(17.6%) and the teeth were missing in 124 subjects
(11.2%). Bleeding, hypertrophy and infection of
gums were noted in 42 subjects (3.8%), 26 subjects
(2.3%) and 2 subjects (0.2%) respectively.

"^L^Complaints related to cardiovascular system,

urinary system, genital system and CNS were
’’ oily 3.L 1.2, 0-8. 0-2 and 0.1% respectively. Head­
raj?'' jejre, ear or dental problems and thirst, included in
ijS^snellaneous group, formed 10.4% of the total
Stcomplaints.
'> Cnmnlaints and systems involved were also analysed according to distance from the factory (Tables
.. 3 & 4). The average number of complaints per person showed a decline with the increase of distance
t■*’ from the factory. The prevalence of symptoms per~ ■ raining to respiratory and gastrointestinal system
,aefwas significantly higher in the population residing
... .' 4^ than 4 km than in population living beyond 4
I < _ SBrom UCIL factory.

f
Sleep was normal in 69.8% subjects while 31.2%
I J ■ complained of insomnia.

l
Clinical findings—The majority of subjects
k * (66.0%) was of average built whereas 17.5% popula1 Li tion had a good physique. 12.5% had a poor general
t £.;r£_appearance and 4.0% were obese.
,■
gr- Examination of the tongue showed a normal clean
'..'S.ittongue in 735 subjects (66.3%) while 309 subjects
EsSI»(27.9%) had a coated tongue. Furring, ulceration,
’;
>7 dryness and cyanosis was observed in 0.8%, 0.5%,
M8s£-4.2% and 0.3% cases respectively.

||2Ei'.-The conjunctivae were normal in 574 subjects

Tanle 3 :

Lymphadenopathy was seen in 95 subjects
(8.5%).
Tachycardia (pulse rate of more than 80 beats/
min) was found in 67.8% subjects while the remain­
ing 322% had a pulse rate of less than 80/min.

163 (14.7%) out of 1109 subjects examined had
systolic blood pressure of more than 140 mm Hg
and 141 subjects (12.7%) had a high diastolic pres­
sure of more than 90 mm Hg.
Abnormal breath sounds on auscultation were
heard in 131 subjects (11.8%). Out of this 5.8% had
rhonchi. 3.4% crepts and 2.6% diminished breath
sounds. In the rest (88.2%) of the population normal

bronchovascular breath sounds were heard in all
areas of chest.
Clinical examination of heart and blood vessels
did not reveal any significant abnormality in the ma­
jority of subjects examined.
Out of the total persons examined, 895 (80.5%)
had no abnormality in the abdomen on palpation,
,while 211 (19.9%) subjects showed mild, tender and

Agewise Njmber of Complaints and systems Involved

Involved*

fotal x

26-35

281(20.1)
280(20.1)
171(12.2)
10(0.7)

68 (2.9)
549 (23.8)
316(13.7)
35X1513)
14(0.6)
X0.2)

322(23.0)

238( 10.0)

149(10.6)
Total complaints
1399
Total population studied 182

6(0.3)
268(11.6)
2298
284 282

48X20.7)
40X17.4)
330(14.1)
14(0.6)
X0.1)
460(19.7)
31X13.3)
20(0.8)
01(0.4)
249(10.6)

317 (22.0)
23X16.2)

19(1.3)
6(0.4)
270(18.8)
150(10.4)
14(0.9)
137(9.54)
1435
83
8.2

191(23.5) 142(22.9) 1964(22.1)
12X15.0) 10106.3) I460O6.4)
20904.5) 640 5.1) 129504.5)
1X1.5) 1 (0.6) M 10.8)
XCL6)
>(0L2)
20 (0.2)
16009.6) 144(23.2; 1000(20.2)
9X11.0) 52(8.4) 1800(20.2)
X0.6)
10(1.6) 10X1.2)
2(0.2)
mn
66(8.0)
928(10.1)
619
8899
1097
82

Figures in parenthesis are the percentage of total complaints
A = C anno vascular; 9= Respiratory; C= Gastrointestinal; 0= Musculoskeletal; E= urinary; 1 > Genital;
Psychological; 1» Dermatological ; J- Genual Nervous system; k - misceiianeous.

153

INDIAN J EXP BIOL..VOL. 26,’MARCH 1988

paipacie liver. Spleen was found palpable in 5
zO.4% subjects.
Radiological findings—Radiological findings of
903 X-rays of chest are given below:
Normal
739
Abnormal
164
Group A
48
Group B
17
Group C
8
Pneumonitis
7
Pulmonary tuberculosis
55
Primary complex
7
Chronic bronchitis
4
Emphysema
2
Bronchiectasis
2
Cardiac abnormalities
11
Collapse
2
Effusion
1
Tension bullae
1
Total
903

"39 Subjects i81.8%)outof a total of 903 studied
raoioiogically showed no abnormality in their
X-rays. X-ray picture of 91 subjects (10.1%) showed
radiological changes suggestive of definite disease
condincns like pulmonary tuberculosis, pneumoni­
as. chronic bronchitis, emphysema, etc. Specific ra­
diological changes were observed in 73 subjects
8.1% . These subjects have been classified as fol­
lows:
Group A. X-ray showing radiological abnormalities
because of exposure to the toxic gas
48 subjects
Group B: Radiological changes suggestive of old
puimonry disease, but symptoms appear­
ing only after exposure to the toxic gas 17 subjects

5-Respiratory
C-Gastrointestinal
□-Musculoskeletal
E-urinaryF-Genital
h-Psychological

J-Central Nervous System
/-Miscellaneous

(In this category old pulmonary disease is Ja
aggravated by exposure to the toxic gas)
Group C: Radiological findings not definitely relat­
ed to exposure to the toxic gas
Total
73?S

The subjects have been divided according3
positive findings in respect of symptoniav
X-ray findings, PFT values, and findings on tlfc
ical examination (Table 5).
sgttH
To screen out malingerers the findings <jf3|
tomatology, clinical examination. X-ray an3
monary function tests were correlated. Thn^jM
jects whose chest X-ray did not show any abrriS|

ity and whose lung function values were normal '
where no abnormality was detected on clinirjj a
aminatioin were very strongly suspected to be'
lingers giving a false statement of suffering frogA
spiratory symptoms like cough, brcaihlessnessjsj
and/or tightness in chest, etc. for the lure of #M
compensation or otherwise, their symptomqM

Table 5—Distribution of 48 Radiologically HxSi
Cases with Respect to Symptomatology, Clinical?
Pulmonary Function Examination

SI No.

3
4
5
6

Sympto- Clinical
matology

—
+
—
+

+
+
+
+

207 (3.5)
1311 (22.2)
957 (16.2)
872 (64.8)
49 (0.8)
11 (0.2)
1175(19.9)
609 (10.3)
65 (1.1)
03 (0.1)
646 (10.9)
■5905
655

Average no. com plaints/person

LFT

N
N
Impaired
Impaired

60 (2.4)
551(22.3)
446 (18.1)
329(13.3)
20 (0.8)
05(0.2)
516(20.9)
286 (20.9)
24 01.0)
06(0.2)
226(9.1)
2469
351

7.0

Figures in parenthesis are the percentage from total complaints
No/)f subjects in over 6 km distance was small hence it was pooled with 4-6 kms category.

154

Total '“B
cases

20
6
13
3

KW
.jM

>4 K «S 1
7(1.3) J
102(19.4) ]

57 (10.8) 1
94(12.9) j
2(0.4) J

4(0.8) 1
108(20.8) :
80 (15-2) j
14(2.7) 1
56 (10.7) j
525
91
5.8

4J
1

I^UFTArt^ effect of edxposure to toxic gas on population of bhopal-i

v! JBgSrr -jure consequent on the severe tra■■Bp*7® L, them. Such cases need to be studEjggggyXttail during follow-up studies.

K®^iSibiects showed definite radiological
f ^^.tocular infection. Of these 55 subjects
findings of pulmonary tuberculosis
of
complex;rhe incidcnTf
^Sfection (6.8%) is much more than NaBHRwierculosis Survey-7 findings of 1.8/o.
Of X-rays where findings were sugl*£Srfbulmonary tuberculosis showed that they
There is a strong possibility that
HBEBtiberculosis cases could not survive the
'
of the gas and those with healed tuberIJfiMtgEher pulmonary and cardiac abnormalities
\sSed in the population exposed to the toxic gas
rSefemlar to such abnormalities in any group of
HSgiKopulation. Seven cases showed presence of
HBQ^is in their X-rays. Out of these cases inliJjJEit of the right lower zone was seen in 5 subEjEgfgt lower zone in 1 subject, and of both lowISgies in 1 subject, while left-sided pleural effuBjSgBobserved in 1 subject only. Tension bullae
right lower zone in one subject and lung coltfro cases—one on the right lower lobe and
i»»<r rhe middle lobe-were observed. 73 subjects
®Bffiidiowed radiological abnormalities which
^HjjGspected to be related to the exposure to the
IK^tnxr.Out of these in 48 subjects the radiological
SSEjgjes observed appeared to have been caused by
■■Miirdno the toxic gas. The radiological findings
SBMbk;oases are given in Table 6. The radiological
SHijjlBsebserved in these X-rays are definitely abMMmmI but they do not confirm any definite diagnoThese findings were haziness seen in different
MK^the lungs, hilar prominence, fine mottling,
IgPyyton. etc. The chahges are more marked in
right than in the left lung. Haziness was more
B^nonfy seen in the lower zone (40 X-rays out of
^.riiowing haziness in the right lower zone whereas
Hfe4|ri»*ng haziness in the left lower zone). One case
Egflp haziness in the right upper zone whereas, no
Bgemowed haziness in the left upper zone. ComgR^gthe middle zone on right and left sides, it was
t*'at 3 03565 sf|owc|f haziness in the right
gg^?one where 6 cases showed haziness in the
gF^'dle zone. Preponderance of abnormalities.

prominence-etc- on lhe rig11' s‘dc
v °ecause °f the anatomical configuration
WBr srid1
'eb bronchus. The right bronchus
?robabl>r permitted more of the gas to
lung and hen-.e more abnormalities
BEtZ’6™”1.0’1 the right side. Although haziness

feS|v'Served bl almost all X-rays in this group it

was surprising to note that hardly a few subjects pre­
sented with fever also.
Hilar shadows were prominent in 47 out of 48
cases in this group. Prominence of the right hilum
was more common (in 47 out of 48 cases) whereas
left hilum was prominent in 41 out of 47 cases. Cos­
tophrenic angle, heart size and trachea did not re­
veal any significant abnormality. There was no
correlation between radiological picture and clinical
presentation. The cases with clearcut pneumonitis
had no evidence of toxaemia.
Out of these 48 cases, 37 subjects were within 2
km distance from UCIL factory at the time of expo­
sure and 10 were at distance of 2-4 km, while only
one person was at a distance of more than 4 km. As
37 out of 48 subjects were within 2 km from the fac­
tory they are likely to have been exposed to a signifi­
cant amount of gas. and the resultant radiological
changes in their X-rays are due to high exposure.
Group B: Cases showing radiological changes suggestive of old
disease which was aggravated by exposure to toxic gas.
Tuberculosis
7
Chronic bronchitis
6
Pneumonitis
4
Total
17

The radiological findings of 17 subjects revealed
the old diseases as tuberculosis, chronic bronchitis
and pneumonitis. These old diseases seem to be ag­
gravated by exposure to the toxic gas as the symp­
toms in these subjects appeared only after the gas
exposure.
Pneumonitis was more commonly seen in the
right lower zone similar to the observation in group
A subjects.

Behavioralfindings
(1) Memory
(a) Auditory memory (immediate)—The exposed
group particularly the females were significantly in­
ferior to control group. This showed that the effect
of exposure in reducing the auditory memory was
more in case of females than in males. Exposure to
toxic gas significantly reduced the auditory memory
of the individuals.
(b) Visual memory—The exposed male group
showed statistically significant (P< 0.001) differ­
ences with the control group (Table 7a, b). Further
the immediate memory was below in males as com­
pared to females. Group results showed that imme­
diate visual memory of the subjects was affected be­
cause of exposure to toxic gas.
There was significant (P< 0.01) difference in del­
ayed visual memory among the three groups. It was

155

GUPTA et aL: EFFECT OF EDXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL-1

Er attered calcified
attered calcified
shadows C fine mottling
Scattered calcified
shadows C mottling

Central

Clear
Clear
Clear

Scattered calcification
Fine mottling C old

cular marking C fine
mottling ano scattered
calcification
Scattered calcification

Fine mottling
calcification
fine mottling

Analysis of variance
Source of variation Immediate Memory (Auditory)! m mediate Memory (Visual) Delayed Memory for 10 Sec.
OF
OF
MS
F
OF
MS
Between group
within group

15.045
3.265

453

368

Significant at p = 0.05
• Significant at p = 0.001.

176.80
3.98

(visual)
F

362

Significant at p =.0.01

(0) Mean Memory Scores and Test of Significance of Different Comparison

Comparisons

Control vs Exposed
Control vs Male

control
Exposed
Male
Control
Exposed
Male
Female

0.2044
0.2232
0.2287
0.1920
0.2335
0.2546
0.2745
0.2461

Control vs Female

100
2t»>
156
109

5.35
3.55
3.51
3.61

1AM Immediate auditory memory

Dnm Delayed visual memory for '.0 seconds

1.93
2.25
2.29
2.20

Control vs Exposed
Control vs Male
Control vs Female
Male vs Female

1.80
1.84
1.74
0.10

Very highly significant
Highly significant
Significant

P = 0.001 —

0.2547
0.2780
0.3005
0.2709

1.120
2.886

NS
p - 0.01

9.122
9.309

p - 0.001

7.067
6.619
5.790
0.369

P - 0.001
P - 0.001
P = 0.001
NS

P - 0.001
P = 0.05

p = n.oi*«
p = U.05*

157

...o, MARCH 1988
found that the exposed group as such was signifi­
cantly inferior (P<0.01) to control group whereas
there was no difference between exposed male and
female indicating that both were equally affected by
exposure to toxic gas. It was thus concluded that vis­
ual memory was more affected than auditory memo­
ry by the exposure.

Taole 9: (oh Mean and

Test of Significance ot Different Comparisons

K;

Character

Group

size
(n)

Mean

SO

Comparisons

DlfT. of
mean

SE (0)

Simple
reaction
time (SRI)
Qignt)

Control
Exposed
Male
Female

70
357
190
167

027
0.31
030
0.31

0.05

Control vs Exposed
Control vs Male
Control vs Female
Male vs Female

aO35
aoso
0040
0.010

00128
00137
00139
00104

2.190
2.878
0962

Simple

Control

(SOLMYl)

Female

70
357
190
167

0.18
022
0.21
0.22

Control vs Exposed
Control- vs Male
Control vs Female
Male vd Female

a035
0030
0040
0.010

00098
00105
00107
00079

’•57’ ~
2-857 ••
3.738 •••
1.266 (NS)

• Significant at p
•• Significant at p
••• Significant at p
NS Non Significant

158

Perceptual motor speed: Both Digit SyjjSIS
and Bourdon-Wiersma test measure the
motor speed the second test includes attend?,
gilance as an additional parameter (Table 8) SsJ
changes were significant (P< 0.001) while
git Symbol Test such a level of significance
observed. The analysis of questionaire and r&j?

005
0.01
0.001

an

0.10
0.11

ao4

008
0.08
0.08

significance

••

•
••
(NS)

jRH

WW
W B9
W
» KB

»

CUFTA « “L: EFFECT OF EDXPOSURE TO TOXIC GAS ON POPULATION OF BHOPAL-1
ity was
observed
in 57.1% cases. Only 4.5% cases
had
neurotic
tendencies.
withWnatic
complaints. Lack of extroversive activ­
r- It was concluded that the highest percentage of
witMBpr
scores
had was
a tendency
to fatigue
general
fatigue
E cases
with poor
score
in general
soFemalewith
Male
n > 135
n «followed
154
g-.matic complaints (88.6%),
by general labiltjty symptoms (72.5%) and neuroticism found only
113
or
scores
on
general
lability
items,
whereas
88.6%
k tn/
4.5% of230
the population.
(75.97)
(83.70) 2.645
f When the data of the exposed population for
123
135
I males
and 256
females were separately compared the rc■
(86.36)
(91.11) 1.603
j srnts
the questionnaire
indicated thatrevealed
formally
the79.6%
females
cases
had
more
po­
72 vere
93 that
^affected than the males. The distribution
of 1.462
cases
(53.33)
(609)
(57429)

si-BT

13 .
(6^7) 1.907*
(2.60)
S
(»J0)
intellectual personality disturbances. The analysis of
X2 5X ■ - 3JM1
U07
K, U81

,1s.

fer—---------------(Sfctefviews with the exposed subjects revealed that

’?,>pie
these subjects
were having
a lackfor
ofdetecting
concentration
questionnaire
is a method
non­
aiid j^poor attention. The study also revealed that
■
vigilance was significantly impaired in the
■population affected by the toxic gas.
■kgAitention response speed: This was studied by us®ing the Reaction Time Test. It was tested by both
gjfaht and sound stimuli. It was observed that the exlation. group had a significantly delayed response as
•. .■■posed
^compared to that of the control group. The expoJg-sure to the toxic gas equally affected the reaction
Emine(attention-response speed) for both the stimuli
Hgji the exposed population (Table 9).
■KgManual dexterity—To see the effect of exposure
Bairn manual dexterity in comparison groups namely.
control, exposed male and exposed female groups.
riot analysis
affect theofmanual
dexterity
of the
exposed
ithe
variance
of the data
was
made. popu
The F­

I

’value was found to be less than one. It was, there­
fore, concluded that exposure to the toxic gas did

with poor scores is given in Table 10. Statistically
significant differences were observed between the
control and exposed groups of all parameters used.
It was observed (Table 10) that the majority of
cases with poor scores were in the second category.
i.e. general fatigue with somatic complaints (88.6%)
followed by 79.6% cases in the first category, i.e.
general lability items.
The effects of toxic gas on the population was
mainly on ocular, gastrointestinal and musculos­
keletal systems. Radiologically 48 cases showed
specific changes because of exposure to the toxic
gas, out of these 37 were staying within 2 km of the
factory. The results of behavioral tests revealed that
memory, mainly visual perceptual and attention/response speed alongwith anennon/vigilance were se­
verely affected in the exposed population.
A majority of exposed subjects staying within a
distance of 6 km were affected by one or the other
health problems. Besides clinical and radiological
morbidity changes in behaviour were objectively
measured in a large number of subjects. TTius the
gas manifested its effect in various systems of body
depending on exposure, dose and individual suscep­
tibility.
References
I IPCS-1RPTC Information sheet on Methyl Isocyanate, In­
ternational Programme on Chemical Safety—Interna­
tional Registry of Ftotenoally Toxic Chemicals. Geneva.
1985,7 Jan.
2 Kumar C D & Mukhcrii S K. Set Today. 19 (1985) 11.
3 Editorial. Calamity at Bhopal Lancet. 11 (1984) 1378.
4 <Rye W A.. J Occup Med. 15i1973) 306.
5 Munn A. Ann Occup Hyg, 8(1965) 163.
6 B R M A. British Rubber Manufacture Association Limited,
Birmingham, 1977.
7 Berstein L, Aller Clin ImmunoL 70 (1982) 24.
8 Fuchs S & Valadc P. TDI Arch Mai Prog. 12(1951)191.
9 Reinl W. Sickness caused by working with plastics and lac­
quers on polyurethanes. For be and Lack. 60 (1954) 69.
10 Walworth H T & Virchow W E. Am Ind Hxg Ass J. 20
(1959)205.
11 Williamson K S. Trans Ass Ind Med Off. 15 (1965) 29.
12 Hanninen H & Lindstrom K. Behavioral test battery for toxtcopsychological studies Instr. Occup. Health. Helsinki),
1979.
13 Benton A L. The visual retention test—Clinical ^experimen­
tal (Psychological Corp- New York), 1972.92.
14 Eysenck H & Eysenck S. Manual of eyesenck personality in­
ventory. Repr Hodder and Stonghton. Dunton Green
Sevenoaks. Kent, 1976.24.
15 Devos G A. J Proj Tech. Rbruary 28.1951.
16 Hanninen H. BrJ Industr Med. 28 (1971)374.
17 Hanninen H. in Behavioral toxicology, edited by C. Xintaras,
B.L. Johnson and L De Groot (US Department of
Health. Education and Welfare, Washington. DC). 1974.

18 Hanninen H, Eskelinen L. Huszan K & Jurminen M. ScandJ
Work Environ Health. 2 (1976)240.

159

INDIAN J EXP BIOL, VOL. 26. MARCH 1988
19 Klopper B & Davidson H H, The Rorschach technique: An
introductory manual (Harcourt, Brace and World Inc.,
New York) 1962,245.

20 Lindstrom K, Work Environ Health, 10 (1973) 151.
21 Lindstrom K, Harkonen H & Hemberg S D. Scand J Work
Environ Health. 2 (1976) 129.
22 Mira Y & Lopez E. Hans Huber Berne, 1965,164.

160

23 Rorschach H, Psychodiagnostik, Hans Huber,
277.
24 Takala MI, Ann Sci Fenn Ser 81(1953) 132.5
25 Wechsler D The measurement and appraisal ofadt^t'
ence (The Williams and Wilkins Co.). 1958,297'
26 Wechsler D, J Psychol. 19(1945)87.
’
27 Tuberculosis in India: A sample survey, 1955-58 1
Council of Medical Research, New Delhi) 1959 -

<■■***'*’
Editorial

On the Bioavailability of Methyl Isocyanate in the Bhopal Gas Leak

Methyl isocyanate (MIC), the toxin that escaped from the
Union Carbide plant at Bhopal, India, in December, 1984, is
now well known for its highly irritant properties.' This toxin
manifested its primary acute effects on the lungs and eyes of
the victims who came in contact with the gas. More than
3 000 lives were claimed, and the toxin is responsible for
chronic health effects in an additional 50 000 survivors.
Chronic lung effects, i.e., pulmonary fibrosis, currently appear
to be the main cause of morbidity and mortality among the
surviving population.2 Clearly, the varying exposure of victims
to MIC was a major factor in determining toxicity. Singh and
Ghosh computed exposure estimates from an analytic disper­
sion model, which incorporated meteorological and topo­
graphical factors around the Union Carbide plant.3 These
estimates ranged from 0.12 ppm to 85 ppm and are higher
than the workplace threshold limit value (TLV) of 0.02 ppm.
Proximity of residence to the Union Carbide plant and activity
(e.g., running versus remaining at home) are variables that
determine the total dose of MIC experienced by the victims.
Was methyl isocyanate bioavailable in Bhopal? On contact
with water, MIC decomposes to methylamine and dimethyl­
urea.4 For this reason, systemic absorption into the blood­
stream through the respiratory tract was not initially seriously
considered because MIC was expected to decompose on con­
tact with fluids in the respiratory tissues.
The question of whether MIC became a systemic poison
after environmental exposure was debated subsequent to ear­
ly studies, which reported that multiple systems were involved
in the Bhopal victims.5 Clinical manifestations of toxicity were
observed in the gastrointestinal, reproductive, and central and
peripheral nervous systems. Gastrointestinal symptoms in­
cluded anorexia, nausea, vomiting, and abdominal pain. En­
doscopic examination of patients revealed congestion and
hemorrhages in the lower esophagus and stomach. Reproduc­
tive manifestations included an increased incidence of spon­
taneous abortions and stillbirths. Neurological problems in­
cluded coma, tremors, vertigo, hearing loss, muscle weak­
ness, and peripheral neuropathy.
It can be argued that some of these manifestations could be
explained by the effects of hypoxia and acidosis, which were
secondary to suffocation and respiratory damage.6 This view
was supported by results from a study done by Fedde et al.,7
which demonstrated that a drop in blood PaO2 and pH and a
rise in pCO2 occurs following exposure of mice to MIC. The
most likely mechanism that would produce altered ventila­
tion-perfusion relationships and impaired gas exchange in this
study was thought to be obstruction of small airways from
sloughing of epithelium into the bronchioles. Undoubtedly,
hypoxia secondary to respiratory damage must have occurred
in many gas-exposed victims. However, clinical studies con­

September/October 1992 [Vol. 47 (No. 5)]

ducted by the Industrial Toxicology Research Centre at
Lucknow, India, revealed that some multi-systemic com­
plaints were persistent and occurred even in those patients
who did not have significant respiratory damage.8 In a sample
from a gas-exposed population studied 3 mo after the acci­
dent, biochemical indicators of stress response were observ­
ed: blood ceruloplasmin levels were increased 200% over
control values in more than 45% of those tested.9 In these
studies, urinary creatinine was significantly higher in study
subjects (2.95-3.3 g/24 h • 1.5 I of urine) than in controls (1.71
g/24 h • 1.5 I of urine). Blood glutathione was significantly
depressed in approximately 40% of the population examined.
In some animal studies, systemic toxicity has been found in
target organs other than the lung.10'13
Bucher,14 in his review of the health effects research done
on MIC, states that if MIC is shown to bind to normal hemo­
globin (carbamoylation), this would provide evidence that the
chemical crosses the alveolar barrier, and would, therefore,
support MIC's potential for systemic exposure. Cyanates can
be absorbed from the gastrointestinal tract, and they exert an­
tisickling properties when administered orally. In patients with
sickle-cell disease, the cyanate anion (NCO‘) produces ir­
reversible inhibition of red blood cell sickling via carbamoyla­
tion of the amino-terminal valine residue of sickle-cell hemo­
globin.'5 The life span of the erythrocyte is increased, and im­
provement of hemolytic anemia is seen.16 Though once con­
sidered as potential therapeutic agents in the long-term man­
agement of sickle-cell anemia, cyanates have not been used
for this purpose because of their toxicity.
At the University of Pittsburgh, Ferguson et al.17 studied the
uptake and distribution of radiolabeled (,4C) MIC in guinea
pigs. The animals were exposed to concentrations of 0.5-15
ppm for periods of 1-6 h. Their findings showed that the
radiolabel was rapidly absorbed and distributed in all tissues
of the body, including the uterus, placenta, and fetus.
Clearance of the radiolabel was gradual for 3 d. A significant
amount of this absorption occurred in the nasal mucosa and
upper-respiratory tract. Less absorption occurred in the
tracheal route than in the upper-respiratory passages. The
authors concluded that "these findings may help to explain
the toxicity of MIC or MIC reaction products on organs other
than the respiratory tract."17
Bhattacharya et al.,18 who are at the Defence Research and
Development Establishment, Gwalior, India, studied distribu­
tion and binding of MIC to tissue proteins throughout the
body. They used radiolabeled MIC (label on isocyanate frac­
tion, CHj—N-HC-O) and dosed female Wistar rats by in­
halation and intraperitoneal (i.p.) routes. Their results in­
dicated that MIC carbamoylates globin, total blood proteins,
and liver proteins. The radiolabel was also distributed in its ac-

385

eru
r-u

Indian J Med Res [B], February 1990. pp 28-33

BHANDARI et al : PREGNANCY OUTCOME IN BHOPAL GAS DISASTER

(ii) Those who delivered within this period (934).
(in) Those who were found to be pregnant at the
time of survey (1251). ■

Pregnancy outcome in women exposed to toxic gas at Bhopal
N.R. Bhandari, A.K. Syal, I.Kambo*, A. Nair*, V. Beohar, N.C. Saxena*, A.T. Dabke, S.S. Agarwal** &

f

B.N. Saxena*
Department of Paediatrics, Gandhi Medical College, Bhopal, * Division of Human Resource Development
Research, Indian Council of Medical Research, New Delhi & ** Department of Genetics, Sanjay GandhlPost

'

Graduate Institute of Medical Sciences, Lucknow

Accepted October 19, 1989

A study was undertaken to compare the effects of exposure to the toxic gas in pregnant women in Bhopal
with pregnant women in a similar, unexposed area. A high incidence of spontaneous abortions (24.2%) in
the pregnant women exposed to the toxic gas was observed as compared to those in the control area
(5.6%). Other indices of adverse reproductive outcome, such as the rate of still birth and congenital
malformation were not found to be different. The perinatal and neonatal mortalities were significantly
higher in the affected area (6.9 and 6J% respectively), as compared to the control area (5.0 and 4.5%
respectively).

Bhopal gas disaster known as one of the worst
industrial accidents in history, has left several
unanswered questions regarding long term sequelae
including potential genotoxic/teratogenic effects of
the toxic gas that leaked out on the fateful night of

December 2, 1984.
In utero exposure of embryo / foetus to a
chemical can produce a variety of toxic effects. In.
severe circumstances, the embryo/foetus may die
leading to spontaneous abortion or still birth
depending upon the period of gestation at which
the exposure has occurred. Interaction with DNA
can produce genetic -diseases and congenital
malformation. In less severe cases, a toxic agent
may interfere with processes of intrauterine growth
leading to intrauterine growth retardation. In utero
exposure may also lead to effects on growth and
development in later life causing physical and/or
mental retardation.

A study was carried out to monitor the adverse
effects in pregnant women who were exposed to
toxic gas at Bhopal, in comparison to the data
collected on pregnant women in a similar, but

unexposed area. The outcome of pregnancy and
neonatal status are reported here.
Material & Methods

The study was carried out in 10 severely affected areas of Bhopal city, around the Union Carbide ■
Factory identified on the basis of records of ;
■ casualities. The following localities from gas
! exposed areas were included: J.P. Nagar, Kazi
Camp, Tila. Jamalpura, Shahjanabad, Straw •
Product, Bus Stand- Ibrahimganj, Kenchi Chhola, ‘
Railway Colony, Station Bazaria and Chandbarh. ;
A door-to-door population survey was carried out
during April-May, 1985 to identify women who
were pregnant at the time of exposure (as assessed by .
recording those with the last menstural period
before 18th November, 1984).
As this made the study partly retrospective and
partly prospective, the identified study population '
were classified into the following three groups:i.
(i) Those who aborted between December 3,1
1984 and the date of the commencement ofX
survey (381).

■

:____ _____ J

Information in abortions and on women who
had delivered before the commencement of survey
was obtained on the basis of-history given by the
woman and confirmed by interview of neighbours
and a review of the records of the nursing home
and hospitals wherever possible (125 cases).
Spontaneous abortions were reconfirmed through
a quick survey (as suggested by the concerned
Project Advisory Committee held in December,
1985). The women who were pregnant at the time
of survey were prospectively followed till delivery.
All the babies born since December 3, 1984 and
who were alive were examined to detect congenital
malformations (both major and minor malforma­
tions), if any. In cases where the child had died or
there was a still birth, a' set of photographs of
common congenital malformations were shown to
either parents or others who had seen the child, to
verify the presence or absence of congenital
malformations.

A control area of similar socio-economic status
was selected including the following localities of
Bhopal: Anna Nagar, Vishwakarma Nagar,
Habibganj, Janta Colony (near Arera Colony),
Panchsheel.Nagar, Harshvardhan Nagar, Ambedkar
Nagar, Banganga and Roshanpura. Study of
women in the control area could not be done
simultaneously as it was more important and
urgent to the pregnant women in the-affected area.
Thus, study in the control area was started a year
later, taking 3rd Dec., 1985 as the cut-off point; all

women pregnant on this date were registered to
obtain a cohort of similar type in respect of period
of gestation.
The study on the control area was thus totally
prospective. A door to door survey was carried out
to identify the pregnant women, who were carefully
followed for outcome of pregnancy. Statistical
analysis was done using the Student’s ‘t’ test and
proponion test for testing the difference between
•stages and rates respectively.

Results
18^78 ,Olal number of households surveyed was
covering a population of approximately'
in affected area and 13,539 househoids-

29

covering a population of approximately 60.000 in
control area. Of these. 2566 women from the
affected area and 1218 women from the control
area were identified as pregnant on December. 3rd
1984 and 1985 respectively, and the outcome of
pregnancy was studied. There were 2153 deliveries
in the affected area, of which 1071 (49.7%)
deliveries were conducted in hospitals and 39
(1.8%) were conducted in MCH Centres and
Nursing-Homes, the rest, 1043 (48.4%) having been
conducted at home. There were 1180 deliveries in
control area, 627 (53.1%) women having delivered
in Hospitals, one (0.08%) delivery being conducted
in a nursing home and 552 (46.8%) deliveries
having been conducted in home.

Socio-economic profile : Most of the women were
from the low socio-economic group. The mean per
capita income was Rs. 122 ± 69 in control area and
Rs.96 ± 87 in affected area. Though the per capita
income was slightly higher, the literacy rate was
found to be lower in the control area (32.5%) than
in the affected area (39.4%).

Religion
The proportion of Muslims was
considerably higher in the affected area (40.3%), as
compared to the control area (14.4%). This was
mainly because no other area of similar socio­
economic status with such high proportion of
Muslims could be found within the unexposed
areas of Bhopal.
Consanguinity: Consanguinity was observed to be
15.6 per cent in the affected area as compared to
6.7 per cent in control area. This difference in
consanguinity rate was probably due to higher
proportion of Muslims in the affected area.
Age : The mean age of the women in affected and
control areas was 24.9 and 24.4 yr respectively. In
the affected area, 21.6 per cent (341) women were
aged 30 yr or above, as compared to 15.7 per cent
(74) in the control area, the difference being
statistically significant (P< 0.01).

Previous obstetric history : Previous obstetric
history was taken for all the women included in the
study. Average parity of the overall sample in
affected area was 2.8 of which 2.5 were live births,
0.04 were still births, 0.23 were spontaneous
abortions and 0.02 were induced abortions. In the
control area the average parity was 2.1, of which 1.9
were live births,-0.03 were still births,. 0.17 were.

INDIAN.) MED RES[B], FEBRUARY 1990

30

abortions. The average number of living male and
female children was 1.2 each in the affected area
and 0.7 and 0.9 in the control area respectively.
Gestation period (as on December 3) : The period
of gestation at which women enter the cohort was
considered important, as the outcome of pregnancy
is associated with this factor. There was
considerable variation in the distribution of women
according to gestation on 3rd December in the
affected and control area. There was 57.3 per cent
pregnancies with period of gestation up to 20 wk
on 3rd December, 1984 in affected area. The
corresponding figure for control area was 39.9 per
cent. Percentage of women with gestation 21-27 wk
was 15.7 and 22.2 in affected and control area
respectively. The remaining 27.0 per cent pregnan­
cies in affected area and 37.9 per cent pregnancies
in control area were of gestation 28 wk or more.
This difference may be due to the fact that those
women (from the affected area) who were in the
third trimester of pregnancy perhaps went
elsewhere for their delivery recognizing that
pregnancy constituted increased risk particularly in
the wake of the general atmosphere of shock, fear
and controversies prevalent at the time of the
disaster. These women obviously could not be
included in the study as they were not present at the
time of survey (Table I).
Outcome of pregnancy :
Abortion - Abortion having been defined as
termination of pregnancy before 20 wk of
gestation, only those women who were up to 20
wk of gestation on 3rd December 1984/1985 were
considered to be at the risk of abortion. These
including 1468 women in the affected area as
Table I. Period of gestation of studied women as on 3rd

BHANDARI et al : PREGNANCY OUTCOME IN BHOPAL GAS DISASTER

against 485 women in the control area. Among
these, 355 (24.2%) pregnancies from the affected
area and 27 (5.6%) pregnancies from the control
area ended in spontaneous abortions. A diagnosis
of abortion was recorded only when the women
gave history of amenorrhoea of -at least 8 wk

•
■
■
,
*
|

and/or had actually observed expulsion of
products of conception. All spontaneous abortions
were confirmed through a re-survey done by
doctors, using a detailed information check list; in

j
I
I
I

125 cases of spontaneous abortions, records were
available from hospital or doctors. The history of D
& C was confirmed from hospital records (43
cases). The abortion rate was significantly higher in

|
|
j
!

affected area (P< 0.001; Table II).
In the affected area, the abortion rate was 32.5
per cent in women (341) of age 30 yr or above
compared to 22.1 per cent in women below 30 yr.
This difference was statistically significant. Whereas
no case of spontaneous abortion was reported from
control area in women (74) 30 yr or above.

i

Religion and consanguinity were not found to
have any association with the abortion rate. In the
Table II. Outcome of pregnancy

Affected area

Control area

Total number of pregnancies

2566

1218

Number of women at risk of
abortion

1468

485

Number of spontaneous
abortions

Abortion rate (%)

355

27

24.2*

5.6‘

Number of induced abortions

26

3

Intermediate foetal death

32

8

2153

1180

December, 1984/1985

•P<.001

Affected area
No.

Control area
No.

<12
13-20
21-27
28-36
>37

934 (36.4)
534 (20.9)
401 (15.7)
450(17.6)
242 (9.4)

250 (20.6)
235 (19.3)
270 (22.2)
307 (25.2)
154(12.7)

1216

Hindu

832

26.3

402

20

2561

219

Total

'607
29

133
3

21.9
10.3

77
6

7

z

Muslim
Others

Total

1468

355

24.2

485

27.

Period of
gestation (wk)

Gestation period
not known

5

Figures in parentheses are the percentages

Table III. Spontaneous abortions in relation to religion

Religion

Affected area

Control Area

Number of
At risk of Sponl. Rate
abortion abor.
100

Number of
At risk of Spont. Rate
abortions abor.
100

j-

Affected area
Consanguinity
Number
At risk of Spont.
abortion abort.

5.0
9.1

I
i

—
5.6

1
‘|

Table V. Neonatal outcome

Control Area
Rate

ioo

Number
At risk of Spont. Rate
abortion, abort. /ioo

Yes

248

66

26.6

33

2

6.6

No
Not
known

1208

289

23.9

448

25

5.6

12

—

—

4

—

—

Total

1468

355

24.2

485

27

5.6

affected area, abortion rate was 26.3 per cent
among Hindus and 21.9 per cent among Muslims.

In the control area, the abortion rate which
slightly higher among the Muslims (9.1%), was not
significant as compared to 5.0 per cent in the
Hindus (Table III). Among consanguinous and
non-consanguinous marriages abortion rates were
26.6 and 23.9 per cent respectively in affected area
and 6.6 and 5.6 per cent respectively in control area
(Table IV). Abortion rates were significantly higher
in affected area irrespective of religion or
consanguinity.

Intermediate foetal deaths - In the affected area,
32 (1.2%) intermediate foetal deaths (pregnancy
termination between 21-27 wk of pregnancy) were
recorded, as compared to 8 (0.7%) cases of
intermediate foetal deaths in the control area
(Table II).

(21-27 wk of gestation)
Number of deliveries

Table IV- Spontaneous abortions in relation to consanguinity

Still births — Taking into consideration the
pregnancies which terminated at 28 wk of gestation
and above, there were 2153 deliveries in affected
area, qf which 56 were stillbirths and 2117 live
births as 20 deliveries had resulted in twin births.
This gave a stillbirth rate of 2.57 per cent. In the
control area, the total number of deliveries at or
after.28 wk of gestation was 1180. Of these, 27 were
stillbirths and 1160 live births giving a still birth
rate of 2.27 per cent. No difference was observed in
thc.stillbirth rates from affected and control area.
*n c°ntrol area 7 deliveries (0.59%) resulted in twin
births as compared to 20 (0.93%) in the affected
arca’ lhe difference being not significant (Table V).
Congenita malformations : There were 31 congenital
“^formations in the affected area out of 21-73
In the control area 15 of a total of 1187
showed congenital malformations, giving a

31

No. of deliveries
No. of twin births
No. of live births
No. of still births
Still birth rate/1000
deliveries
No. of early neonatal deaths
(0-7 days)
Total perinatal loss
PMR/1000 births
No. neonatal deaths
(0-28 days)
NMR/1000 livebirths
No. of congenital
malformations
Rate/1000 births

Affected area

Control area

2153
20
2117
56

1180
7
1160
27

26.0
95

’

22.9
33_

151
69.48*
129

60
50.54*
52

60.9**

14.8**

31

15

14.2

12.6

P values, *< .001; ** < .001

rate of 14.2 per 1000 births and 12.6 per 100.0 births
.in the affected and control areas respectively (Table
V). Details of the nature of congenital malforma­
tions observed in the two areas are depicted in
Table VI. As in case of abortions, religion did not_
show any relationship with the congenital
malformations. The latter were found to be slightly
higher in consanguinous as compared to nonconsanguinous marriages in both the affected and
the control areas. It was 1.9 and 2.5 per 1000 births
for consanguinous marriages and 1.4 and 1.2 per
1000 births in non-consanguinous marriages in
affected and control areas respectively. These
differences were statistically significant.
Perinatal and neonatal mortality : Of the 2153
deliveries in the affected area, 2117 were live births
(including 20 twin deliveries). Of these, 95 babies
died within 7 days of birth and 34 between 8-28
days of birth, giving a perinatal mortality rate of
69.48 per 1000 births and a neonatal mortality rate
of 60.9 per 1000 live births. In the control area, of
the 1160 live births (including 7 twin deliveries) out
of 1180 deliveries, 33 babies died within 7 days of
birth while another 19 died between 8-28 days,
giving a perinatal mortality rate of 50.54 per-1000
births and neonatal mortality of 44.8 per 1000 live
births. Both perinatal and neonatal mortality were
significantly lower in the control area than in the
affected area (Table V).
Babies who survived beyond 28 days i.e., (1988

INDIAN J MED RES [B], FEBRUARY 1990

BHANDARI et al : PREGNANCY OUTCOME IN BHOPAL GAS DISASTER

33

32

Table VI. Congenital malformations

Exposed area

Control area

Congenital talipes
cquinovarus

13

02

Congenital heart disease

07

03

Meningo myelocoel
Exomphalus

02
01

—

Type of malformation

Micro opthalmaia with
lenticular opacity

Imperforate anus

—

01

—

01*

02

Congenital aplasia of
both eyes

01

—

Haemangioma scalp

01

—

Hirschsprung disease

01

—

Hypospadius

01 +

01

Cleft lip with cleft palate

01

—

~ or

—

—

02

Anencephaly

—

02

Microcephaly

—

01

Polydactyly

—

01

Foetal ascitis

—

01

Total

31

15

Rocker bottom foot
Multiple congenital anamolies

•With recto-vaginal fistula.
+ With absence of external ear

babies from the affected area and 1108 babies from
the control area) are being followed up for
morbidity and mortality during infancy.

Discussion
In this study, those women who were pregnant at;
the time of gas exposure from moderate to severely
affected areas were studied for adverse pregnancy
outcome in order to determine possible embryo­
toxic effects of MIC. Control area of similar socio­
economic status from unexposed area of Bhopal
was selected and pregnant women were registered.
Women were followed till outcome of pregnancy to
obtain comparative data. Although both the
affected and the control areas fall in the low socio­
economic group, there was a slight increase in per
capita income in control area. The difference in the
income in the control area could be due to the fact
that the study in the control area started one year
after the exposure. The proportion of Muslims was
also higher in affected area (40.3%) as compared to

control area (14.4%), as there was no other area in
Bhopal of similar socio-economic status with such
a high proportion of Muslims. These factors were
taken into account while comparing indicators of
pregnancy outcome.
The variation in the distribution of period of
gestation seen in affected area as compared to
control area may perhaps be due to the fact that
women from affected area nearing term went
elsewhere for their delivery and could not be
registered for the study.
The abortion rate was more than four times in
the affected area as compared to control area.
Religion and consanguinity did not show
association with abortion rate. Abortion rate in
affected area was significantly higher in women 30
yr of age or above (32.5%) as compared to women
below 30 yr of age (22.1%). There was no case of
abortion in women 30 vr or above in control area.
Abortion rate in the affected area after standar­
dizing for age according to the control area was
found to be 23.6 per cent as compared to 5.6 per
cent in control area, which was still very high.

Stillbirth rate was found to be similar in the
affected and control areas, but both perinatal and
neonatal mortality rates were observed to be higher
in the exposed area. Though per capita income was
slightly higher in the control area, it cannot
account for higher mortality rates in the affected
area, as none of the mortality rates were associated
with income. Further, both the control and affected
areas belonged to the low income groups. The
difference in religion could not also account for
this as perinatal and neonatal mortality were not
different among Hindus and Muslims. As the study
was partly retrospective, information on birth
weight was not available for the total study sample ‘
and there were differences in methodology for
recording birth weights. Hence, frequency distri­
bution of birth weight could not be related to ;
perinatal and neonatal mortality in affected and
control area. In relation to age perinatal mortality
was higher in women of 30 yr or above and there
were 20.4 per cent women in that age group in
affected area as compared to 16.4 per cent in
control area. Standardized perinatal mortality in t
exposed area considering control area as standard ‘
was seen to be still higher. In the control area, the ;
perinatal mortality was not higher in the older ag^I

group. After standardization the neonatal mortality
in the exposed area of 60.6 from 60.9 per 1000 live
births was still significantly higher than 44.8 in
control area. The only factor that could not be
studied in relation to these rates was the time
factor, as the study in the control area Was started
a year later.
When compared to the national averages, the
perinatal mortality is higher in affected area than
the national average of 53.6 per 1000 deliveries but
neonatal mortality although higher than in control
area is below the national average of 67.2 per 1000'
live births1.

Any exposure to a genotoxic gas can produce
damage to DNA in somatic and/or in germ cells.
Direct consequences of mutations include both
alteration of chromosomes and if severe it may lead
to obvious adverse reproductive outcome such as
increased rate of abortion, still births, congenital
malformations and perinatal mortality in exposed
population. The congenital malformation rate did
not show any significant difference in both areas
(14.2 per 1000 births in affected area and 12.6 per
1000 births in control area). These rates are also
not significantly different from several hospital
based studies reported in Indian literature2.
Our study showed a marked increase in the
spontaneous abortion rate.but how much of it is
due to genetic damage caused by MIC could not be
assessed from this study as no cytogenetic studies
were carried out on abortuses. Considerable
proporation of the abortions may be due to the
stress and trauma associated with the disaster itself.
Although the possibility of possible genetic damage

cannot be ruled out, the highlights of this study was
an increase in abortion rate, perinatal mortality
and neonatal mortality in the areas exposed to the
gas leak as compared to the unexposed areas.

In women exposed to toxic gas, the lungs were
one of the target organs and the respiratory tract
showed series of pathological changes. The
deffusion of gases was affected and many pregnant
women, who were exposed had respiratory
problem, which could affect the foetus. Although
the present study does not show any alarming
incidence of acute toxicity, the long term genetic
effects revealing subsequently cannot be ruled out.

Acknowledgment
The authors are thankful to the Director-General, Indian
Council of Medical Research, New Delhi, for funding the
study and to the Dean, Gandhi Medical College, Bhopal, for
permission to carry out the Project. We are specially thankful
to members of the Project Advisory Committee Drs V.L.
Ramachandran, Narain Choudhary and Vijay Kumar, for
their suggestions and constant guidance in the conduct of the
study. We also thank the R.Os and A.R.Os. Drs Alka Jain.
S.N. Dwivedi, S.S. Velury, N. Siddiqui, P. Pathak,
Manorama Dubey and D.Kaur. for assistance in carrying out
this work.

References
1.

Family Welfare Programme in India-Year Book 1985-86
(Figures quoted are for the year 1983) (Ministry of Health
and Family Welfare, Govt, of India, New Delhi). 1987 p
100.

2.

Verma. l.C. and Mathews, A.R. Congenital malformation
in India.In: Peoples of India - Some genetical aspects,
G.V. Satyavati, Ed. Proc. XV. Int.Cong. of Genetics,
New Delhi, India (Indian Council of Medical Research,
New Delhi) 1983 p 70.

Reprint requests: Dr N.R. Bhandari, Professor of Paediatrics., Gandhi Medical College, Bhopal 462001

RASSEGNE

Health effects
of the Bhopal
gas leak:
a review
Ramana Dhara
Dept, of Environmental & Community
Medicine Umdnj - Robert Wood
Johnson Medical School - Piscataway,
NJ 08854

Introduction
The world’s worst industrial disaster
occurred in India on the night of Decem­
ber 2-3, 1984. The accident took place at
the Union Carbide plant situated in Bhopal,
(pop..900,000) the capital city of Madhya
Pradesh, one of the largest states in India.
The accident was apparently initiated
by the introduction of water into the met­
hyl isocyanate (MIC) storage tank resul­
ting in an uncontrollable reaction with
liberation of heat and escape of MIC in
the form of a gas. Safety systems like the
flare tower (to burn excess gas), caustic
soda scrubber (for neutralization) and the
refrigeration unit were either not functio­
ning or inadequate to deal with the large
volume of escaping chemical [1],
This paper reviews health effects of gas
exposures from published human studies
and discusses some of the clinical and epi­
demiological issues being debated. Because
of the relative paucity of information, the
author has also reviewed unpublished
data from studies conducted by local phy­
sician groups. Some of these studies have
helped to highlight specific health pro­
blems from the disaster and initiate more
organized research to address these pro­
blems. The reader may also wish to con­
sult articles by John Bucher [2] and Mehta
et al. [3] for reviews on human and animal
toxicology.
Manufacturing Process

Methyl isocyanate (CH3-N=C=O) is an
intermediate product in the manufacture
of carbaryl (Sevin), a carbamate pesticide.
The process begins with a mixture of car­
bon monoxide and chlorine to form pho­
sgene. Phosgene is then combined with
monomethylamine to form methyl iso­
cyanate. Methyl isocyanate is further
mixed with naphthol to produce the end­
product, carbaryl.
Chemical and Physical Properties
Ricevuto: febbraio 1992
Versions definiliva accellata: ottobre 1992

22

Epiderniologia e prevenzione n. 52. 1992

MIC is a clear, colorless liquid with a
pungent odor (b.p.: 39°C, f.p.: -80’C, s.g.:

0.96, m.w.: 57.1, vapor pressure of348 mm
Hg at 20°C). It is moderately soluble in
water and hydrolyses on contact to form
carbon dioxide and methylamine. When
MIC is pyrolyzed in the temperature
range of 427-548°C, decomposition pro­
ducts like hydrogen cyanide and carbon
dioxide are formed [4].

Toxicological Properties
MIC is highly irritant to the skin, eyes
and mucus membranes of the respiratory
tract. This irritant property is based on its
reactivity with water which enables it to
penetrate tissues and interact with pro­
tein. Absorption through the skin is
known to occur [5]. Because the ACGIH
TLV of 0.02 ppm is less than the mucus
membrane irritation threshold, (> 0.4
ppm), and the odor threshold (> 2 ppm),
the compound is considered to have poor
warning properties [6].
Exposure Conditions
It is estimated that about 27 tons of
methyl isocyanate escaped from the two
tanks in the plant during a period of one to
two hours [1]. The release occurred
around midnight with adverse prevailing
atmospheric conditions (inversion and a
low wind speed) which prevented disper­
sion of the gas [7]. Eyewitness accounts
report that a cloud of gas enveloped the
area and moved slowly along.
Because of the unexpectedness, time
and brief period of release of the gas, air
monitoring was not possible nor was it
subsequently attempt ed.
Based on quantity of the chemical
released and area of spread, (40 sq. km)
the Central Water & Air Pollution Con­
trol Board estimated MIC concentration
to be about 27 ppm [7], a figure which is
about 1400 times that of the OSHA work­
place standard of 0.02 ppm for 8 hrs. This
calculation, however, assumes equal con­
centration over the whole area of conta­
mination and does not account for varia­
bility of concentration with distance.
Using an analytic dispersion model, Singh

RASSEGNE

and Ghosh have provided simulations of
exposure concentrations at various distan­
ces downwind of the plant [8]. Twenty
seven sites were identified with ground
level concentrations ranging from 85.6 ppm
to 0.12 ppm with a median of 1.8 ppm.
Factors contributing to variability in
human exposure include distance of resi­
dence from the plant, duration of expo­
sure and activity during exposure. No
systematic attempts have been made to
reconstruct individual exposure based on
these criteria. In the actual incident, acti­
vity during exposure to the gas was cer­
tainly a major dose-regulating factor. The
acute irritant effects of MIC created panic,
great anxiety and disorientation, resulting
in people running out of their homes. The
running resulted in increased ventilatory
rates in these people, thereby increasing
the dose of the chemical delivered to the
respiratory system. The Medico Friend
Circle study reports exposure history and
safety measures taken by people at the
time of the gas leak [9]. In a study sample
of 158 persons, 124 ran out of their homes.
Only 12 persons used a wet towel or blan­
ket as a safety measure.
Major organs of exposure to the gas
were the eyes and respiratory tract. Signi­
ficant amounts of MIC were also, most
probably, dissolved in saliva and swallo­
wed into the gastro-intestinal tract. Skin
exposure certainly took place but was less
clinically important than the respiratory
tract.
A cohort of 80,021 has been registered
from the population residing around the
Union Carbide plant and classified as
mild, moderate and severely exposed
based on mortality rates in each area [10].
An unexposed population in Bhopal was
used to select the control group of 15,931
individuals.

Characteristics of the exposed population
In the exposed areas, about 53% of the
population comprise of Hindus, 45.6% are
Muslims and the rest are Christians and
Sikhs. In 1985, the monthly income of
80% of the population was below Rs 145/
month ($6) and only 1.25% earned over

Rs 465/month ($18). By 1988, 65% of the
population was earning below Rs 145/
month, indicating some improvement in
economic level. However, the above figu­
res indicate that most of the exposed
people are close to the government-defi­
ned poverty level of Rs 300/month (S12).
Ten percent of the population are smo­
kers, 1.4% alcoholics and 5.5% chew
tobacco. Only 34% of the population live
in a ‘pacca’ (permanent) house [10].
Mortality
Of the more than 200,000 persons expo­
sed to the gas, the initial death toll within
a week following the accident was over
2,500. In Nov. 1989, the Dept, of Relief &
Rehabilitation, Govt, of Madhya Pradesh,
placed the toll at 3598 [11], Dr. SR Kamat,
a pulmonary physician who has conduc­
ted studies on a large number of gas vic­
tims, states that most of the later deaths
appear to be occurring from respiratory
complications (personal communication,
1990). Mortality rates are declined but
were still slightly higher in the severely
exposed area (8.75/1000) in comparison
with the control area (7.5/1000) during the
period May 1989-Mar 90 [10],
Overall Morbidity

Symptom prevalence surveys conduc­
ted by the Indian Council of Medical
Research (ICMR) indicate that morbidity
was higher in the exposed areas (26%) as
compared with the control area (18%)
during the period Nov 1988-Mar 90.
About 11% of people experienced 2 or
more spells of illness in a 1-year period.
Respiratory, ocular and gastro-intestinal
symptoms account for most of this morbi­
dity. This trend appears to be persistent in
the survey conducted in the latter part of
1990 [12],

Ocular Problems
The intensely irritating effect of MIC
on the cornea resulted in severe ocular

burning, watering, pain and photophobia
[13], Examination of the eye showed
involvement of the corneal and conjuncti­
val epithelium with redness of the eye,
corneal ulceration and lid swelling. Fortu­
nately, the comeal ulceration in most
cases turned out to be limited to the
superficial layers of the cornea. Slit lamp
examination showed discrete lesions in a
band across the interpalpebral area, punc­
tate keratopathy, conjunctival chemosis
and some pigmentary deposition on the
cornea [14]. Relatively few cases of iritis
were seen [15]. Treatment at the initial
stage consisted ofsaline eyewashes, pupil­
lary dilatation and topical antibiotics.
Andersson and others performed a fol­
low-up study on the eyes of survivors 9
months after the accident and reported
that no case of blindness could be found
that could be attributed to gas exposure
among the nearly 20,000 persons atten­
ding the Bhopal Eye Hospital [16]. Howe­
ver, they did find persistent eye watering
and other chronic irritant symptoms like
burning, itching and redness. Raizada and
Dwiwedi [17] studied eye pathology
among 1140 exposed persons and found
that the main chronic lesions were chro­
nic conjunctivitis, deficiency of tear
secretion and persistent corneal opacities.
Animal experiments conducted by Sal­
mon [18] on male Lister hooded rats indi­
cate that the most severe effects on the
eye occur at exposure levels of 65 ppm.
Andersson et al. [19] performed a fol­
low-up of 93% of exposed and unexposed
Bhopal residents 3 years after exposure.
Their findings indicated an increased risk
of eye infections, hyperresponsive pheno­
mena, (watering, irritation, phlyctens),
excess cataracts and resolution of the cor­
neal erosions in exposed persons. These
phenomena have been characterized as
the ‘Bhopal eye syndrome’. The authors
state “in its response to MIC, the eye
should be considered a ‘sentinel organ’
for more general phenomena in the
body”.
Though there is no evidence that severe
damage to the eye's external and internal
structures has occurred, the single acute
exposure seems to have resulted in a chro­
nic inflammatory process. The problems
Epidemiologia e preventions n. 52. 1992

23

RASSEGNE

of persistent eye watering in some cases
and tear secretion deficiency in others
coupled with chronic conjunctivitis indi­
cate that there is some damage to the eye
epithelium. It is conceivable that housing
conditions in the Bhopal slum areas like
overcrowding, poor ventilation and expo­
sure to dust and smoke may exacerbate
the ocular effects causing irritation and
infections.

Respiratory Toxicity

Acute symptoms of the respiratory tract
were mainly due to the irritant action of
MIC on tissues. Because MIC is modera­
tely soluble in water, lesions were seen in
both the upper and lower respiratory tract.
Predominant symptoms were cough
accompanied by frothy expectoration, a
feeling of suffocation, chest pain and
breathlessness [20]. Other symptoms
included dryness and irritation of the
throat and rhinorrhea.
Autopsies on 300 victims revealed
severe necrotizing lesions in the lining of
the upper respiratory tract as well as in the
bronchioles, alveoli and lung capillaries.
Enlarged and edematous lungs, con­
solidation, hemorrhage, bronchopneu.monia and acute bronchiolitis were seen
hij.
Follow-up studies were conducted 2.53 months after the accident by a team
from the Industrial Toxicology Research
Centre (ITRC) at Lucknow, India [22].
Exposed persons were contacted and
requested to come forward voluntarily to
be examined. A total of 1279 men, women
and children were examined. In these
studies, radiological examination of the
lungs was carried out on 903 subjects to
assess damage to the respiratory tract.
Out of 164 abnormal X-rays, 65 were
determined to have specific radiological
changes which were considered to have
occurred or aggravated as a result of gas
exposure. These were classified into two
groups:
Group A (48 subjects) were those with
radiological abnormalities thought to
have occurred as a result of gas exposure.
These changes were haziness in different
24

Epidemiologia e preventions n. 52. 1992

zones of the lung, hilar prominence, fine
mottling and reticulation. 16 of the 48 sub­
jects had respiratory symptoms (cough,
chest pain/tightness, breathlessness) cli­
nical signs (adventitious sounds) and
abnormal lung function. Twenty subjects
had respiratory symptoms but clinical
examination and lung function were nor­
mal.
Group B (17 subjects) showed abnor­
malities suggestive of old disease which
was aggravated (symptoms appearing
after exposure) by exposure to the gas.
These abnormalities were tuberculosis,
chronic bronchitis and pneumonitis.
Spirometry was carried out on 783 sub­
jects from the above sample to determine
respiratory impairment [23]. Vital capacity
(VC), forced vital capacity (FVC) and for­
ced expiratory volume in 1 sec (FEV0„,
FEV,) were the main parameters recor­
ded. Impairment was classified as restric­
tive (VC or FVC < 80% of predicted),
obstructive (FEV,/FVC < 70%) and a
combined pattern (FVC < 80% of predic­
ted and FEV,/FVC ratio < 70%).
The results showed that 39% of the
sample was found to have some form of
respiratory impairment. The combined
pattern of impairment (obstructive and
restrictive disease) had the highest preva­
lence in the sample (22%). Smoking had
no effect on the prevalence of this impair­
ment. Females suffered more mild and
moderate impairment. Severe impair­
ment was equally distributed (2.4%)
among the two sexes.
Broncho-alveolar lavage fluid was ana­
lyzed in 36 mild, moderate and severely
exposed persons and 12 unexposed nor­
mal controls 1-2.5 years after exposure
[24], The results indicated that severely
exposed smokers and non-smokers sho­
wed a significant increase in alveolar
macrophages. Based on these results, the
authors concluded that an inflammatory
alveolitis may be present in severely
exposed subjects and that long-term
follow-up must be done to determine if
further impairment of lung function
occurs.
Sharma et al. [26] report the interesting
case of a resident of the gas-exposed area
who, in his professional capacity, conti­

nued to be exposed for a few days to trap­
ped gases in victims. This 60-yr old nonsmoker had no respiratory symptoms
(other than bouts of cough) till the begin­
ning of 1989 when he started complaining
of severe cough and breathlessness on
exertion. Pulmonary function showed a
mild obstructive ventilatory defect and
CT scan revealed subpleural thickening,
punctate lesions and bilateral septal scars,
suggesting that extensive pulmonary
fibrosis had occurred.
Though isocyanates are known to be
allergenic in the lung [26] the respiratory
toxicity of MIC appears to be primarily
due to its irritant nature. Follow-up stu­
dies with lung biopsies done six months
after exposure showed evidence of inter­
stitial fibrosis and bronchiolitis oblite­
rans. These findings were similar to those
found in several animal studies [27,28]
thus revealing the close association bet­
ween animal data and clinical findings in
Bhopal victims.

Reproductive Toxicity
Concerns that the gas leak had effects
on reproductive health were raised early
in 1985 when reports indicated that men­
strual cycle disruption, leucorrhea and
dysmenorrhea had occurred in gas-expo­
sed women [29]. Risk to the fetus was con­
sidered because of exposure to the gas and
factors like stress, anoxia and ingestion of
various prescribed drugs like antibiotics,
bronchodilators, and analgesics.
An epidemiological survey by Varma
[30] showed pregnancy loss and infant
mortality to be high in gas-exposed
women. In a sample of 865 women who
lived within 1 km of the plant and who
were pregnant at the time of the gas leak,
43% of the pregnancies did not result in
live births. Of the 486 live births, 14% of
babies died in the first 30 days as compa­
red to a death rate of 2.6% to 3% for
previous deliveries in the 2 years prece­
ding the accident in the same group of
women.
A pregnancy outcome survey of gasexposed women [31] using historic con­
trols, demonstrated a four-fold increase in

RASSEGNE

spontaneous abortion rate. Alteration in
menstrual cycle lenght was also observed.
Animal experiments conducted by Schwetz [32] and Varma [33] exposing pre­
gnant mice to MIC by inhalation showed
that this exposure does indeed have a fetotoxic effect. Varma observed a concentra­
tion-dependant increase in embryo loss,
decrease in fetal and placental weights
and a 20% reduction in length of mandible
and bones of the extremities.
Varma et al. [34] studied the contribu­
tion of maternal hormonal changes and
pulmonary damage to fetal toxicity of
MIC in rats and mice. Their findings sho­
wed that fetal toxicity of MIC was partly
independent of maternal pulmonary
damage and that MIC could be directly
fetotoxic. In the Bhopal situation, results
from the animal studies, when considered
with the findings from human epidemio­
logy, suggest that exposure to MIC is feto­
toxic and that this is probably the result of
a direct effect on the fetus.
Genotoxicity and Carcinogenicity

Chromosomal studies were done two
and a half months after the gas leak to eva­
luate genetic damage among the sample
of gas-exposed survivors studied by the
ITRC [35]. Blood was collected from 31
exposed adults and a similar number of
age and sex-matched unexposed controls
to assess the occurrence of chromosomal
aberrations (breaks and gaps) in lympho­
cytes. The results show a significantly
increased (p < 0.001) number of breaks
and gaps in the exposed subjects. No fol­
low-up studies were done to see if this
effect was persistent.
Cytogenetic studies were done 3 years
after exposure on a sample of 40 male and
43 female exposed persons [36]. Results
from this study showed statistically higher
frequencies of chromosomal aberrations
in the exposed group as compared to 46
age and sex-matched unexposed controls.
The aberrations were in the form of
breaks, gaps, dicentrics, rings, tri and quadri-radial configurations and were more
pronunced in female subjects. Sister chro­
matid exchanges were not significantly

different. The authors concluded that
though the results may indicate a residual
effect on T-cell precursors, further studies
are required to demonstrate an exposure­
effect relationship.
Short-term tests using Chinese hamster
ovary cells showed induction of SCEs and
chromosomal aberrations both without
and with activation by S-9 mix from Aroclor-induced rat liver [37]. Sex-linked
recessive tests in Drosophila and the
Ames test were negative. The Ames test
was also found to be negative by Shelby
[38]. Meshram and Rao [39] using a diffe­
rent pre-incubation procedure for the
Ames test (10’C for 60 min instead of the
standard 37°C) found MIC to be weakly
mutagenic.
Shelby et al. [38] performed genetic
toxicity testing on B6C3F1 mice exposed
to MIC by inhalation. Analyses on lymp­
hocytes, bone marrow and lung cells were
done using single and multiple exposures.
Multiple exposure experiments in the
mice showed increased frequencies of
SCEs and chromosomal aberrations which
were not seen in 2 hr exposures. Delay of
cell-cycle time was also reported [40,41],
While animal and in vitro studies
demonstrate MIC’s potential for genoto­
xicity, it is not clear that such toxicity has
actually occurred in exposed humans.
To assess carcinogenic potential, rats
and mice were exposed to MIC for 2 hrs
by inhalation. Marginal increases of
pheochromocytomas of the adrenal
medulla and adenomas of the pancreas
were seen but these tumors were not consi­
dered clearly related to the exposure [42].
A population-based cancer registry has
been established in Bhopal in 1986 to
study possible carcinogenic effects of the
gas leak. All cases of cancer are being regi­
stered and categorised by exposure area
[10], Though it has been predicted that
MIC has a significant potential for cancer
induction [43], it is not expected that the
onset of gas leak-related cancers, if any,
will occur before the 30-40 yr lag period.
Immunotoxicity

Following exposure to the gas in Bho­

pal, there was concern amongst the health
authorities that the population might
experience an increased rate of infections.
Possible reasons for this increased suscep­
tibility included depressed immune func­
tion from chemical effects, psychological
and physical stress, disruption of normal
life (particularly during the 2 mass migra­
tions out of Bhopal), and pulmonary
injury.
Immune function was studied [35] in
exposed subjects from the ITRC sample
two and a half months after exposure to
ascertain whether any change had occur­
red in the immune status. Humoral
immunity was assessed by quantitation of
immunoglobulins (IgG, IgM, IgA) in over
300 exposed and 10 non-exposed persons.
Cell-mediated immunity (CM1) was
assessed by phagocytic activity of lympho­
cytes and quantitation of T-cell rosettes in
19 exposed and 8 non-exposed persons.
Results from this study showed that no
difference in mean immunoglobulin
levels was found when compared to con­
trols. The T-cell population (28%) was
found to be less than half that found nor­
mally in the Indian population (65%).
Significant depression of phagocytic acti­
vity of lymphocytes was found as compa­
red to controls.
Concurrent with the human studies,
immunotoxicological evaluation of rats
exposed to MIC showed a number of posi­
tive results (44). Alveolar and peritoneal
macrophage function was depressed and
exposed rats were susceptible to E. coli
endotoxin. Delayed type hypersensitivity
was assessed by injecting sheep RBC’s
into the foot pads and was found to be
impaired. Based on these results, the
researchers concluded that the gas had a
suppressive effect on cell-mediated
immunity.
Karol and Kamat [26] found MlC-specific antibodies in guinea-pigs injected with
MIC as well as in 12 of 144 human survi­
vors. This showed that MIC was capable
of eliciting an immunogenic response.
The antibody titers in the human studies
were low and transient suggesting a weak
response.
Limitations of the human studies
include the relatively small sample sizes.
Epidemiologia e preventions n. 52, 1992

25

RASSEGNE

choice of control groups and unclear
exposure ascertainment. The above limi­
tations make it difficult to arrive at defini­
tive conclusions regarding immunotoxi­
city from MIC exposure for the gas vic­
tims.
Psychological and Neuro-behavioral Toxi­
city

numbness, a sensation of pins and needles
in the extremities and muscle aches.
To assess whether MIC was toxic to
muscle, Anderson et al. [47] evaluated the
effects of MIC on rat muscle cells in cul­
ture. At lower doses, the formation of
muscle fibers was prevented. At higher
doses, death of fibroblasts and myoblasts
was seen. The findings suggested either
an effect on muscle differentiation or
selective toxicity to myoblasts.

Srinivasamurthy and Isaac [45] noted
that psychological problems of Bhopal
Clinical Problems
survivors fell into four major categories.
1. Post-traumatic stress disorders
Paucity of information on the toxico­
which occurred as a result of the tremen­
dous emotional stress of the disaster. logy of MIC had created a great deal of
Symptoms were anxiety, emotional recall confusion and debate about the manage­
of the event, restlessness, sleep disturban­ ment of the gas victims. The medical
ces and generalised weakness and fatigua­ system in Bhopal was severely tested by
the twin factors of large numbers of inju­
bility.
2. Pathological grief reactions charac­ red people streaming into hospitals and
terised by intense grief, depression, suici­ the absence ofa definite protocol for treat­
dal ideation and guilt feelings arising out a ment of the poisoning. Patients were trea­
ted on a symptomatic basis. For ocular
sense of failure to protect their family.
3. Emotional reactions to physical pro­ problems, atropinization of the eye, local
blems: victims with ocular, lung and other antibiotics and padding were used [14],
problems developed feelings of depres­ Respiratory problems were treated with
sion, hostility, insecurity and helpless­ bronchodilators, steroids, diuretics, anti­
biotics and oxygen administration.
ness.
Questions of clinical importance, some
. 4. Exacerbation of pre-existing psy­
of which still persist to this day, are:
chiatric problems.
- Were there toxins other than MIC
In a psychiatric out-patient serrvice pro­
gram set up specifically for gas victims, released in the accident?
- What were the specific antidotes?
Sethi et al. [46] detected 208 persons suffe­
- Did cyanide poisoning occur in the
ring from mental problems. Of these, 45%
were suffering from neuroses, 35% from victims and, if so, how was it manifest and
anxiety states and 9% from adjustment what was the source of the cyanide?
- Does MIC enter the blood-stream and
reactions.
Neuro-behavioral tests were conducted cause multi-systemic disease?
- What were the risks to exposed pre­
on 350 exposed subjects two and a half
months after the accident [22], Auditory gnant women and the unborn child?
- There is no doubt that MIC was
and visual memory, attention response
speed, and vigilance were found to be clearly the major toxin released in the
significantly impaired in this group as accident. However, the circumstances lea­
compared to controls. No effect was seen ding to the release (hydrolytic and exot­
hermic reaction of water with MIC) raised
on manual dexterity.
the possibility of impurities (phosgene) or
decomposition products (hydrogen cya­
nide, nitrogen oxides, carbon monoxide)
Neuromuscular Toxicity
being present in the gas cloud.
Suspicion that some of the early deaths
Neuromuscular symptoms in Bhopal
survivors have persisted since the gas leak were due to cyanide poisoning arose from
the reporting of rapid fatalities and acute
[10]. These symptoms are mainly tingling.
26

Epidemnlogia e prevenzione n. 52. 1992

symptoms of syncope, and extreme weak­
ness. Autopsy studies done by Dr. Heeresh Chandra at the local medical college
showed two features considered to be cha­
racteristic of cyanide poisoning. These
were cherry-red discoloration of the blood
and other organs, and the unpleasant odor
of “bitter almonds” when the lungs were
opened [48].
A double-blind clinical trial was perfor­
med by the ICMR 2 months after expo­
sure to determine the efficacy of sodium
thiosulfate as an antidote to the poisoning
[12]. The trial was done on 30 gas-exposed
symptomatic patients who were admini­
stered sodium thiosulfate, a cyanide anti­
dote, intravenously. The results showed
alleviation of symptoms with an 8-10 fold
increase in thiocyanate excretion in the
urine for 10 out of 15 patients and served
to fuel suspicion that cyanide poisoning
was involved. (Thiocyanate is the water­
soluble detoxification product of cya­
nide).
On the basis of this study, the ICMR in
February 1985 recommended the use of
sodium thiosulfate on a mass scale for
detoxification of symptomatic gas-expo­
sed persons. Union Carbide denied the
possibility of cyanide poisoning and toxi­
cological experts around the world were
either unsure or skeptical about cyanide
[1].
In this atmosphere of confusion, the
local health authorities in Bhopal failed to
carry out the recommendations of the
ICMR on a widespread and systematic
basis.
The scientific hyphoteses seeking to
explain the source of the cyanide poiso­
ning and the apparent effectiveness of
sodium thiosulfate fell into three catego­
ries:
1.
Cyanidefrom an external source: That
the entry and mixing of water with MIC in
the storage tank resulted in a violent exot­
hermic reaction at high temperatures (>
420°C)) which led to the decomposition of
MIC to hydrogen cyanide, carbon mono­
xide and nitrogen oxides. This reaction
was first discovered by Blake and Maghsoodi in 1982 and was documented in the
NIOSH Occupational health guidelines
for MIC [49].

RASSEGNE

2. Cyanidefrom an internal source: That cyanide may result in an underestimation
the MIC was being converted to some of the long-term effects of MIC.
Persistent multi-systemic symptoms
form of cyanide after being absorbed into
the body resulting in enlargement of the have been reported by Bhopal survivors.
That exposure to MIC can produce repro­
body’s cyanogen pool.
3. Thiosulfate effective against MIC: ductive health problems has been shown
That sodium thiosulfate was alleviating in human and animal studies [55]. Fergu­
the symptoms caused by MIC toxicity. son and Alarie [56] have demonstrated
(Sodium thiosulfate was hitherto unk­ that there may be a physiopathological
basis for the persistence of multi-systemic
nown as an MIC antidote).
Investigators from India [50] investiga­ symptoms in Bhopal survivors. Their stu­
ted the first of the three hypotheses by dies on experimental animals have shown
pyrolysing MIC at 350°C and found that that radio-labeled MIC is capable of being
cyanide was produced even at this lower absorbed and distributed throughtout the
temperature as a decomposition product. body. These findings have been confir­
They further injected the decomposition med by Bhattacharya et al. [57] who have
products into rats and found that brain shown that MIC binds covalently to tissue
cytochrome oxidase activity (the bioche­ proteins in its active form and not as its
mical basis for cyanide toxicity) was signi­ breakdown product, methylamine.
There is no known antidote for MIC
ficantly depressed.
There has been no evidence to date to toxicity. If further studies confirm that
support the second hypothesis that MIC is MIC is indeed distributed in the body,
converted to a form of cyanide in the there is a need to develop a method of
body. Animals exposed to MIC by inhala­ treatment for MIC poisoning.
tion have not shown any evidence of cya­
Epidemiologic Considerations
nide in the blood [51].
Animal studies testing the third specu­
In the early period following the acci­
lation have not shown that sodium thio­
sulfate has any protective effect against dent, clinical treatment of the injured
took priority over the planning and con­
direct MIC toxicity [52,53].
If one accepts the possible efficacy of duct of epidemiological studies. This was
thiosulfate in alleviating symptoms of gas- particularly true given the limited health
exposed persons, it must be in the light care resources available for a large num­
of the first hypothesis that the cya­ ber of affected people and the general lack
nide poisoning came from an external of experience in dealing with a disaster of
this nature.
source.
Studies to determine chemical compo­
A few cross-sectional studies (Table 1)
sition of the MIC tank residues are cur­ were done during the early recovery
rently being undertaken by the ICMR and period (6 months) for various systemic
may shed some light on the toxins relea­ health end-points. Virtually all of the epi­
sed in the accident [10]. Whether cyanide demiology for the late recovery period is
was actually released may never be known being conducted by the Bhopal Gas Disa­
with absolute certainty as it involves re­ ster Research Centre, a branch of the
creation of the actual conditions leading Indian Council of Medical Research.
to the accident.
About 10 different epidemiological stu­
In the Bhopal situation, administration dies were initiated to monitor long-term
of an essentially harmless drug like trends in morbidity and mortality. Results
sodium thiosulfate on a mass scale, with from these studies are currently being
adequate follow-up, would have enabled awaited. As Bertazzi [58] notes, the selec­
gathering data which would confirm or tion ofa cohort rather than using a popula­
reject the usefulness of the drug.
tion registry for epidemiological studies
Andersson [54], however, points out avoids two major biases: dilution of expo­
that acute MIC exposure is more toxic sure prevalence and selective migration of
than cyanide and an undue emphasis on people out of the disaster area.

The early cross-sectional studies suffer
from a number of defects in study design,
resulting in bias and consequent difficulty
in clearly establishing causal relations­
hips. In one follow-up study performed 3
months after the accident, exposed per­
sons were contacted and requested to
come forward voluntarily for examination
[22], This method ofsubject selection may
have resulted in severely exposed/affected subjects being examined and a conse­
quent over-estimation of health effects. If,
however, the severely affected victims
were unable to present themselves for
examination due to illness, an under-esti­
mation of health effects may have occurred.
Relatively crude methods like mortality
rates or distance of residence from the fac­
tory have been used in defining commu­
nity exposures. Koplan et al. [59] stated
that epidemiologic studies following disa­
sters should accurately estimate exposure
to enable correct dose-response relations­
hip modeling. These data are useful fora)
identifying exposed and ill persons, b)
determine long-term effects and c) link
exposure and effects for litigation and
compensation.
For the Bhopal gas victims, there is a
need to do epidemiological studies to
determine morbidity prevalence in the
population stratified by estimated pulmo­
nary dose. Such an approach will allow
scientifically valid and detailed studies of
different health end-points to be perfor­
med on relatively small sample sizes [60],
Exposure-based stratified random sam­
pling will also reduce bias due to self­
selection and exposure misclassification,
as well as permit dose-response and inte­
raction relationships to be understood.
Conclusions

Clinical and toxicological studies have
shown that MIC is a potent toxin. Chronic
inflammation of the eye and respiratory
tract account for a major portion of the
morbidity. Certainly the potential exists
for these damaged organs to be more
susceptible to other environmental insults
like infections, irritants, and allergens.
For e.g., a person with airway damage
Epidemiologia e preventions n. 52. 1992

27

RASSEGNE

may be more prone to infections or
respond adversely to smoke and dust. Pul­
monary function limitation may preclude
survivors from working on jobs which
require moderate or strenuous activity.
Progressive pulmonary fibrosis and
restrictive lung disease appear to be a
major cause for concern among the gasexposed. Given the completely unexpec­
ted and devastating nature of the disaster
. and the resultant stress, it is expected that
a number of survivors will suffer from
post-traumatic stress disorders for many
years. Establishment of a specialised
medical center for dealing with health
problems from the gas leak will permit a
co-ordinated method of investigation and
treatment for the injured.
It is a striking fact that much of the mor­
tality and morbidity could have been aver­
ted by the simple expedient of covering
the face with a wet cloth. MIC would have
been decomposed on contact with the
water. Unfortunately, the community was
never informed of the existence of such a
potent chemical in the factory and contin­
gency measures to be taken in the event of
a leak.
Fora disaster of this magnitude, there is
a relative paucity of knowledge based on
epidemiological and clinical investiga, tion. Some of the medical studies done on
the survivors suffer from unscientific
design and it is difficult to utilise informa­
tion from these studies with confidence.
Stratified sampling techniques using iso­
pleths of exposure from dispersion
models may be one way of conducting an
epidemiological study without including
the total exposed population.
It is imperative that long-term monito­
ring of the affected community be done
for at least the next fifty years. Formal stu­
dies of ocular, respiratory, reproductive,
immunological, genetic and psychologi­
cal health must be continued to under­
stand the extent and severity of long-term
effects of the disaster.

Acknowledgements

The author wishes to thank the following persons
for their helpful comments and criticisms: Carol and

28

Epidemiologia e preventtone n. 52. 1992

Table 1 - Human health effects studies on the Bhopal Gas Leak
Tabella 1 • Studi degli effetti sulla salute umana dell'incidente di Bhopal

Author

Design

(cases/controls)

Study Period
(time after
gas leak)

8000 exposed

8 days

chemosis, corneal ulcers,
watering photophobia.
no blindness

photophobia
corneal erosions

Major findings

Ocular Studies

Andersson et al.,
1984, (4)

Case-series

Andersson et al.,
1988, (13)

Crosssectional

261/ 99

2 weeks

Dwivedi et al.,
1985, (15)

case-series

232

a few weeks

Andersson et al.,
1985, (69)

case-series

490

2 months

corneal scars
no blindness

Maskati,
1986, (61)

Crosssectional

261/106

104 days

conjunctivitis
corneal opacities
persistent watering

chemosis, redness
watering, corneal ulcers

Andersson et al.,
1986, (10)

Case-series

989

9-12 months

Raizada,
& Dwiwedi
1987, (17)

Case-series

1140

2 years

corneal opacities, chronic
conjunctivitis

Respiratory Studies
Mishra et al.,
1987, (70)

Case-series

978

2 days

resp. distress, pulm,
edema, pneumonitis

Sharma & Gaur,
1987, (62)

Case-series

500 X-rays

> 72 hrs

pulm. edema, emphysema,
pneumothorax

Misra & Nag
1988, (20)

Case-series

33

1 week

Dyspnea, upper and lower
respiratory tract irritation,
pulm. edema, pneumonia

Bhargava et al.,
1987, (63)

Case-series

224

1 -4

Gupta et al.,
1988, (22)

Crosssectional -

1109

2.5 months

65 subjects with
+ve X-ray changes

Kamat et al.,
1985, (64)

Case-series

113

3 & 6 months

Emphysema, pulm.
hypertension
pleural scars,
interstitial depositis

Medico Friend
Circle
1986, (9)

Cross­
sectional

136/137

4 months

Obstructive &
restrictive lung disease

Increased pregnancy
loss,
increased infant mortality

months

Obstructive &
restrictive lung disease

Reproductive Studies
Varma,
1987, (30)

Medico Friend
Circle
1986, (31)

Survey

Survey

865

9 months

486 live/births/
historic controls

9 months

381/historic
controls

9 months

Increased spont.
abortion rate,
alteration of
menstrual cycle

RASSEGNE

Table 1 - Human health effects studies on the Bhopal Gas Leak
Tabella 1 - Studi degii effetti sulla salute umana dell’incidente di Bhopal

Design

(cases/controls)

Study Period
(time after
gas leak)

Kanhere et al.,
1987, (66)

Crosssectional

134/24

9 months

Decreased placental
& fetal weight

Daniel et al.,
1987 - (67)

Crosssectional

18/10

6 months

No effect on
spermatogenic function

Cell cycle delay

Author

Major findings

Genetic Studies
Deo et al., 1987
(68)

Crosssectional

22/13

11 days

Saxena et al.,
1988, (35)

Crosssectional

31/31

2.5 months

Increased chromosomal
aberrations

Ghosh et al.,
1990, (36)

Crosssectional

83/46

3 years

Increased chromosomal
aberrations

Immune Function
Deo et al.,
1987, (68)

Crosssectional

67/15

4-8 weeks

Decreased response
to T & B cell mitogens

Saxena et al.
1988, (35)

Crosssectional

44
19/8

2.5 months
' 2-5 months

Decreased T-cell
population, decreased
phagocytic activity

Karol et al.
1987, (26)

Case-series

144

1-12 months

Transient MIC
antibodies in
12 subjects

208

2-6 months

Neuroses, anxiety
states & adjustment
reactions

350/100

2.5 months

Impaired auditory
& visual memory,
vigilance & attention
response speed

Psychological Studies

Sethi et al.
1987, (46)

Case-series

Neurobehavioral Studies
Gupta et al,
1988, (22)

Crosssectional

Gerard Nalarelli. Rosaline Dhara, Drs. Steven Marko­
witz, Rashid Sheikh, David Kriebe! and David Wegman.
Drs. Michael Gochfeld and Meredeth Turshen pro­
vided support and guidance during the writing of this
paper.
Riassunto
II peggior disastro industriale della storia si verified
in India la nolle tra il 2 e ii 3 dicembre 1984 a Bhopal.
cilia di 900000 abitanti e capitale dello stato di Madhya
Pradesh. L’incidente fu probabilmente iniziato dalI’introduzione di acqua nelle cisteme deposito di Metilisocianato (MIC) e dalla conseguente reazione in-

controllata con liberazione di calore e di MIC sotto
forma di gas. I sistemi di sicurezza o non funzionarono o furono inadeguati per il grande volume di sostanza chimica coinvolta nella reazione.
Queslo lavoro passa in rassegna gli effetti dell’esposizione al MIC cosi come sono conosciuti da studi
umani e discute alcuni degii aspetti clinici ed epide­
miologic! dibattuti.
Per quanto riguarda I’esposizione della popolazione si stima che circa 27 tonnellate di MIC fuoriuscirono dalle cisteme in un arco di 1-2 ore [1]. L’incidente
awenne intomo a mezzanotte in condizioni metereologiche avverse che prevenirono la dispersione del gas
e fecero ristagnare sulla zona una nube tossica [7].
Stime basate sulla quantita di sostanza fuoriuscita e
sull’area interessata (40 miglia quadrate) pongono la

concentrazione di MIC nell’area a 27ppm, circa 1400
volte Io standard OSHA per i luoghi di lavoro di 0.02
ppm durante le 8 ore [7]. Simulazioni che tenessero
conto della variability di concentrazione di MIC identificano 27 aree con concentrazioni varianti da 85.6
ppm a 0.12 ppm con una mediana di 1.8 ppm (8]. La
dose assunta dipese anche dai comportamenti indivi­
dual! al momento dell’incidente. In uno studio su un
campione di 158 persone, ad esempio. 124 fuggirono
dalle case (aumentando quindi con la ventilazione
polmonare la quantita di sostanza assunta) e solo 12
utilizzarono stoffa umida davanti alia bocca come for­
ma di protezione [9].
Una coorte di 80021 soggetti fu iden tificata nella popolazione residente intorno allo stabilimento della
Union Carbide e classificata come esposta in modo |
lieve, moderate e severo sulla base dei dati di monalita
delle diverse aree. Un gruppo di popolazione di Bho­
pal non esposta (15931 soggetti) venne identificato co­
me controllo. Nelle aree esposte rispettivamente il
53%, 46% e 1% erano di religione indu, musulmana,
cristiana o sikh. L’80% della popolazione aveva un reddito inferiore a 6 dollar! al mese e solo IT% superiore a
18 dollari. La soglia di poverta e stabilita dal governo in
12 dollari al mese. Solo il 34% della popolazione viveva
in una casa stabile (“pacca” house) [10].
Delle 200000 persone esposte 2500 morirono nella
settimana successiva all’incidente. Al novembre 1989
risultava un totale di 3598 vittime decedute prevalentemente per complicazioni respiratorie. Nel periodo
maggio 1989-marzo 1990 la mortality generale risulta­
va essere piu elevata nelle aree esposte (8.75/1000) relativamente alle aree di controllo (7.5/1000) [10].
Surveys sulla prevalenza di sintomi indicano una
morbidita piu elevata nelle zone esposte (26%) rispetto alle aree di controllo (18%).
L’articolo e la tabella 1 passano in rassegna i lavori
condotti sulla patologiaoculare, respiratoria, riproduttiva, sulla genotossicita, carcinogenicita e immunotossicita del MIC suite popolazioni esposte ed i problemi
psicologici e di tossicita neuroambientale e neuromuscolare. Vengono infine valutati i problemi chimici
collegati ad una possibile tossicita di altri prodotti pre­
sent! nella nube tossica e potenzialmente formalist.
duranie la reazione di idrolilica ed esotermica.
I
Considerazioni generali riguardanti gli studi epide­
miologic! condotti nell’area di Bhopal sono:
1.
Nel periodo immediatamente seguenie l’incidente
la totality degii sforzi medici si concenlrarono sulla cu­
re del numero elevatissimo di intossicati e solo in un
secondo periodo vennero pianificati studi al fine di valutare gli effetti cronici ed acuti dell’esposizione alia
nube tossica.
2.
Gli studi trasversali, i primi ad essere disegnati.soffrirono di numerosi problemi nel disegno dello stu­
dio. Gli studi prospettici vennero disegnati con maggiore attenzione agli aspetti delle distorsioni di selezione.
3.
E importante ricordare che larga parte della morta­
lity e morbidity avrebbe potuto essere evitata con misure di protezione individuate molto semplici, quale il
coprirsi il viso con un panno bagnato. Purtroppo lacomunita non era mai stata informata ne dalla presenza
di tossici cosi potenii nello stabilimento. ne di forme
di protezione individuate da applicare in caso di inci-

Summary

The methyl isocyanate (MIC) gas leak from the
Union Carbide plant at Bhopal, India in 1984 was the
worst industrial disaster in history. Exposure estimaEpidemiologia e prevenzione n. 52. 1992

29

RASSEGNE

(es of gas concentrations in the area range from 85 to
0.12 ppm. Of the approximately 200.000 persons expo­
sed. 3598 deaths have resulted as of November 1989.
Chronic inflammatory damage to the eyes and lungs
appears to be the main cause of morbidity. Reproduc­
tive health problems in the form of increased sponta­
neous abortions and psychological problems have
been reported. Questions about the nature of .MIC to­
xicity have been raised by the persistence of multi-sy­
stemic symptoms in survivors. Animal studies using
radio-labeled MIC given by the inhalation route have
shown that the radio-label is capable of crossing the
lung membranes and being distributed to many or­
gans of the body. This paper reviews health effects of
gas exposure from published studies and discusses so­
me of the clinical and epidemiological issues being de­
bated.

17. Raizada JK. Dwiwedi PC. Chronic ocular le­
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ANDERSSON N. KERR MUIR M. MEHRA V. Padma Prakash on behalf of Medico Friend Circle at
Health. Occupational health Guidelines for Chemical
SALMON AG. Exposure and response to methyl iso­
1BCS. Bombay. India. 1986.
cyanate: results of community-based survey in Bho­
32.
SCHWETZ BA. ADKINS B Jr. HARRIS M. Hazards: Methyl Isocyanate. Us. Dept, of Health Hu­
man Services. Washington. D.C.. 1978.
pal. BrJInd Med 1988; 45: 469-475.
MOORMAN M. Sloan R. Methyl Isocyanate: Repro­
50. Bhatt acharya BK. Malhotra RC. Chat14.
ANDERSSON N. MUIR MK. MEHRA V. Bhopal ductive and developmental toxicology studies in
Eye. Lancet 1984: 2: 1481.
TOPADHYAY DP. Inhibition of rat cytochrome oxida­
Swiss mice. Environ Hlth Perspect 1987; 72: 147-150.
15. Dwiwedi PC. Raizada JK. Saini vk. Mit­
33.
Varma DR, FERGUSON J. ALARIE Y. Repro­ se activity by pyrrolysed products of methyl isocyana­
te. Toxicol Lett 1987; 37: 131-134.
ductive toxicity of methyl isocyanate in mice. J Toxicol
tal PC. Ocular Lesions following methyl isocyanate
51. Bucher JR. Gupta BN, adkins b Jr. Thomp­
Env Hlth 1987; 21: 265-275.
contamination: the Bhopal experience. Arch Ophthal­
34.
Varma DR. GUEST I. SMITH S. MULAY S. Dis­ son m. Jameson cw. thigpen je. schwetz
mol 1985; 103: 1627.
sociation between maternal and fetal toxicity of met­
BA. Toxicity of Inhaled Methyl Isocyanate in F344/N
16. ANDERSSON N. KERR MUIR M. AJWaNI MK.
hyl isocyanate in mice and rats. J Toxicol Env Hlth
Rats and B6C3FI Mice. 1. Acute Exposure and Reco­
Mahashabde S. Salmon a. vaidyanathan K.
1990: 30: 1-14.
very Studies. Environ Health Perspect 1987; 72:53-61.
Persistent eye watering among Bhopal survivors. Lan­
35. Saxena ak. Singh kp. Nagle SL. Gupta
52.
NEMERY B. SPARROW S. DlNSDALE D. Methyl
cet 1986; 2: 1151
30

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Isocyanate: Thiosulphate does not protect. Lancet
1985; 2: 1245-1246.
53.
VUAYRAGHAVAN R. KaUSHIK MP. Acute to­
xicity of methyl isocyanate and ineffectiveness of so­
dium thiosulphate in preventing its toxicity. Ind J Exp
Bi0l\us 1987: 25: 531-534.
54.
ANDERSSON N. Long term effects ofmethyl iso­
cyanate. Lancet 1989; 1: 1259.
55.
DHARA VR. On the bioavailability of methyl
isocyanate in the Bhopal gas leak. Editorial. Arch Env
Health 1992:; 47: 385-386.
56.
FERGUSON JS. KENNEDY AL. STOCK MF.
BROWN WE. ALaRIE Y. Uptake and distribution of
,4C during and following exposure to [ IJCj methyl iso­
cyanate. Toxicol Appl Pharmacol 1988; 94: 104-117.
57. Bhattacharya BK. Sharma SK. Jaiswal
DK. In vivo binding of [l4C] methylisocyanate to va­
rious tissue proteins. Biocheni Pharmacol 1988; 37:
2489-2493.
58.
BERTA7.ZI PA. Industrial disasters and epide­
miology: a review of recent experiences. Scant! J Work
Environ Health 1989; 15: 85-100.
59.
KOREAN JP. Falk H. GREEN G. Public Health
Lessons from the Bhopal Chemical Disaster. JAMA
1990; 264: 2795-2796.
60.
DHARA VR. KRIEBEL D. The long-term health
consequences of the Bhopal gas disaster: dose-re­
sponse studies. Apha 120th Annual Meeting Exhibi­
tion Abstracts. Washington, D.C.. 1992; 130.
61.
MASKATI QB. Ophthalmic survey of Bhopal vic­
tims 104 days after the tragedy. J Postgrad Med 1986;
32: 199-202.
62.
SHARMA PN. GaUR KJBS. Radiological spec­
trum of lung changes in gas exposed victims. Ind J
Med Res 1987; 86 (Suppl): 39-44.
63. Bhargava DK, Varma a, Batni G. Misra
NP. TIWaRI UC, VIJAYAN VK. Jain SK. Early obser­
vations on lung function studies in symptomatic ‘gas’exposed populations of Bhopal. Ind J Med Res 1987; 86
(Suppl): 1-10.
64. KaMaT SR. MaHASHUR AA. TIWaRI AK,
POTDAR PV. Early observations on pulmonary chan­
ges and clinical morbidity due to the isocyanate gas
leak at Bhopal. J Postgrad Med 1985: 31: 63-72.
65. KAMAT SR. PATEL MH. KOLHATKAR VP. DA­
VE AA. MAHASHUR AA. Sequential respiratory
changes in those exposed to the gas leak at Bhopal. Ind
J Med Res 1987; 86 (Suppl): 20-38.
66. Kanhere S. Darbari BS. SHR1VASTAVA AK.
Morphological study of expectant mothers exposed to
gas leak at Bhopal. Ind J Med Res 1987; 86 (Suppl): 7782.
67. Daniel CS. Singh ak. siddiqui P. Mathur
BBL. Das SK. AGARWAL SS. Preliminary report on
spermatogenic function of mate subjects exposed to
gas at Bhopal. Ind J Med Res 1987; 86 (Suppl): 83-86.
68. DEO MG. G ANGAL S. BHISEY AN. SOMASUNdaram R, Balsara B. Gulwani B. Darbari BS.
BHIDE S. MaRU GB. ImmunologicaL mutagenic and
genotoxic investigations in gas exposed population of
Bhopal. Ind J Med Res 1987; 86 (Suppl): 63-76.
69. Andersson N. Kerr Muir M. Salmon AG.
Wells CJ. Brown RB, et al. Bhopal Disaster: Eye fol­
low-up and analytical chemistry. Lancet 1985: 1: 761762.
70. MISRA NP. PATHAK R. GAUR KJBS. JAIN
SC. YES1KAR SS. MANORIA PC. el al. Clinical pro­
file ofgas leak victims in acute phase after Bhopal epi­
sode. Ind J Med Res 1987: 86 (Suppl): 11-19.

La Cooperativa Epidemiologia e Prevenzione annuncia il

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Epidemiologia e prevenzione n. 52, 1992

31

©HI :

PS

People's right to information --- Interview with Dr. Thelma Narayan
I did my schooling in Bhopal and
we used to stay in the Polo Bun­
galow (which is now a thirty-bed
Community Hospital). The Union
Carbide Factory came up in the
seventies just opposite where we
stayed.
I belong to a group called
Medico Friend Circle, a group of
doctors and other people who are
involved in Health issues. It is
All India group. Dr. Ravi
Narayan, my hunsband, is the con­
venor of this group and the. orga­
nisational office of this group is
here in Bangalore. Other volun­
tary groups, who knew about MFC
needed an objective assessment
of the situation, and requested our
group to send a team to Bhopal.
About eleven MFC members
along with three friends from
Baroda Medical College had gone
to make a study. What we learned
was that on day one, on the 3rd
day of December itself the Pro­
fessor of Forensic Medicine, Dr.
Heeresh Chandra who conducted
s^^he autopsies on the bodies felt
^that the picture he saw was some­
thing like Cyanide poisoning. The
blood was cherry red in appear­
ance whereas normally it would
be bluish. He suggested that the
antidote to Cyanide poisoning,
namely Sodium Thiosulfate be
given. The local medical com­
munity scoffed at him and said
that he was a doctor of the dead
and that he shouldn’t be talking
about the living.
At the same time there was a
telex message from the medical
director of Union Carbide from

America, Dr. Bipin Avashia, saying
that the treatment
should be
symptomatic. He also happened to
mention that if Cyanide poisoning
was suspected to give Sodium
Thiosulfate. But a few days later
when he did come to Bhopal he
withdrew the statement.

A German toxicologist was in-.
vited to come to Bhopal . by ’ the
Government of India. . He arrived
about four or five days after the
disaster, Dr. Mar Daunderer. He
brought with him various tools of
investigation. Based on that he
also felt that it was some
Cyanide-like poisoning and he
suggested that Sodium Thiosulfate
be given to the patient. Anyway
there was a lot of opposition to
this and he was soon packed off
to Germany.-'
ICMR carried out a very detailed
study on the efficacy of Sodium
Thiosulfate, the study, called a dou­
ble blind study is one of the scien­
tific method of studies. On the
analysis of the data ICMR found
that when given Sodium Thio­
sulfate the patients had very signi­
ficant symptomatic relief On the
basis of this study they made
certain recommendations to the
Government of India that the
affected victims should be given
Sodium Thiosulfate. They gave
certain criteria to select the pati­
ents. This was at the end of
January and a press release was
given in the first week of Feb­
ruary to the same effect. The
Central Government obviously ac­
cepted this. But there was a hitch
at the State level because ulti­

mately health is a State subject
and the State Health authorities
have to take action on any recom­
mendations given by either ICMR
or the Central Government. No
action was taken on this recom­
mendation.
The local voluntary groups who
had a scientific background kept
raising this Issue of Thiosulfate.
Despite all their protests Thio­
sulfate was not given. The State
health
authorities had another
meeting with ICMR. They took
action In May and made Thio­
sulfate available through their
clinics and dispensaries.
The
doctors In these clinics were
totally unconvinced about its effi­
cacy. We made a short survey
and found that the drug was being
given so slowly that it would take
about seven years to cover the
affected population. This was a
totally ridiculous situation.

In June four groups of activists
formed Jan Swasthya Samiti in- • ~ ,
volving the bast! people and volun­
teers from different sections. The
West Bengal Drug Action Forum
sent doctors on a voluntary basis
to run clinics. Volunteers from
MFC, and from Delhi and Bombay
also helped. This group of doctors
and other health workers devised
a questionaire by which patients
were monitored before and after
the injections to see whether there
would be a significant improve­
ment.
In Bhopal one of the most active
groups was Zahreeli Gas Kand
Sangharsh Morcha with Dr. Anil
Sadgopal and a band of volunteers.

OH 1

"RATIONALE
AS

FOR

THE

USE

IN

THE

TREATMENT

BHOPAL

GAS

DISASTER

AH

ANTIDOTE

OF

THE

OF

THIOSULPHATE

SODIUM

-

2°\

VICTIMS

OF

THE

A

REVIEW"

June 1, 1985

b y
Thelma Narayan,

C. Sathyamala,

Mira Sadgopal
*

Members, Medico Friend Circle,
326 V Main
I
Block, Koramangala,
Bangalore 560 034

and
Vijaya Shankar Varma

Department of Physics, Delhi University, Delhi 110 007
Consultant, Technical Cell, Zahreeli Gas Kand Sangharsh
*
Morcha

Multisystemic involvement, persistence of
symptoms, continued alteration of blood gas
percentages indicative of poor oxygen carry­
ing capacity of blood with resultant tissue
anoxia, suggest that some toxin still exists
in the body (the cyanogenic pool) and needs
to be eliminated^
Significant symptomatic relief, increased
excretion of urinary thiocyanates and improve­
ment in the blood gas picture after administ­
ration of sodium thiosulphate indicates that
it is an effective antidote in the, treatment
of the victims of the Bhopal gas disaster.

*Contact address: Gandhi Bhavan, near Polytechnic College,
Shyamala Hills, Bhopal 462 002.

CONTENTS
Part - I

1.

Introduction

2.

Clinical picture in the sub-acute phase

3.

A flashback Autopsy findings
Haemoglobin Examination

Urine thiocyanates
The initial double blind study with thiosulphate
and subsequent developments
Blood gas analysis

Animal experiments
Cyanogenic pool
Guidelines for the use of sodium thiosulphate (ICMR)

4.

Conclusion

5.

References

6.

Appendix

I

-

proforma for the clinical monitoring

of patients on thiosulphate therapy.
Part - II

Review of literature on cyanide poisoning

1.

Symptoms

2.

Lethal dosage

3.

Toxic action

4.

Detoxification - Antidotes

a)

Sodium nitrite

b)

Sodium thiosulphate

c)

Oxygen

d)

Hydroxocobalamin

e)

Cobalt edetate

5.

Fate of cyanide ion in the body

6.

References

par t - I

1.

Introduction

Since the gas disaster in December, 1984, at Bhopal which
killed thousands of people and left approximately 70,000

seriously injured and 45,000 with mild to moderate disability

controversy has surrounded the issue of an effective form

of therapy for the affected population.

This has led to

the withholding of sodium thiosulphate (NaTS - an antidote,
recommended by ICMR in February, 1935)

end hence to the

prolonged and unnecessary suffering of people.

After months of uncertainty the Madhya Pradesh Government
Health Services officially sanctioned the use of sodium

thiosulphate in April, 1985, and it reached the peripheral
dispensaries and health centres only in May.

To cover the

affected population, at the rate set by the M.P. Government,

e.
i.

13 centres giving approximately 300 injections a day,

complete detoxification will take years, by which time it
may just be too late.

If the majority of victims are to receive this specific
therapy in time it is essential to pressurize the government

to tackle the problem on a war footing.

There is a need

to utilize all available resources in as efficient a manner
as possible.

Dispensaries and health centres run by non­

governmental agencies too, need to be involved.
To undertake this task, medical personnel from the govern­

ment and voluntary sector need to understand the rationale
behind the use of sodium thiosulphate as one of the specific
therapies for the gas affected victims.

This paper is intended to sort out some of the confusion
that has

arisen from the controversy regarding the use

of sodium thiosulphate and hopefully to clarify some of

the questions.

2.

Clinical picture in the sub-acute phas

2.1

A common picture has emerged from observations by
three independant studies, viz.

a)
"Health
effects of exposure to toxic gas at
Bhopal. An update on ICMR sponsored researches",
10th March, 1985.
"Medical
b)
survey on Bhopal gas victims" (March 1985),
conducted by Nagrik Rahat aur Punarvas Committee,
Bhopal, in collaboration with Voluntary Health
Association of India, Delhi and Bhopal Relief Trust,
Bombay.2

c)

2.2

"The Bhopal disaster aftermath - a socio-medical
and epidemiological survey" (March, 1985) Medico Friend Circle.3 (unpublished data)

In the affected areas, most persons had more than one
symptom -or group of symptoms.

These have been grouped

according to the body systems they belong to, with

some inevitable overlap.

a)

Respiratory system - Breathlessness on rest and
on accustomed exertion, dry cough, cough with
expectoration, pain/tightness in the chest.

Persistent tachypnoea is a common feature.
Rales and rhonchi are present in 9.4%.3 In
some patients symptoms were out of proportion to
the physical and radiological observations.
40% of those who complained of respiratory symp­
toms had ventilatory impairment, 12% had restr­
ictive lung disease, 6% obstructive airway
disease, 22% obstructive-cum-restrictive defect.
Ventilatory defects were not observed in patients
with mild exposure to toxic gas.1
Blood gas analysis in 35 patients indicates
abnormality in the oxygen carrying capacity of
haemoglobin.
23 patients with severe exposure
had PaO2 60 mm Hg. Arterial CO2 tension 35 mm
Hg. was observed in 12.1

b)

Gastro-intestinal system - Loss of appetite,
nausea, vomiting, abdominal pain ard burning,
flatulence, diarrhoea.

Endoscopic examination has revealed superficial
gastritis and oesophagitis.
c)

Eye - Blurring of vision, irritation and burning
of eyes, redness, difficulty in See:.ng bright
light.
80% of people within
krn lad ophthalmic
symptoms, as did 60% of those at 2 ]m and 40% of
those at 8 km distance.2

d)

Reproductive system ; Women - Frequent menstrual
periods, polymenorrhoea, abnormalities of menstr­
ual flow - scanty or heavy, blackish in colour,
excessive vaginal discharge, suppression of lacta­
tion.
Men - loss of libido.

2.3

e)

Neuromuscular - Muscle weakness, sensation of
pins and needles, tingling and numbness.

f)

Mental - Headache, anxiety, apprehension,
confusion, irritability, forgetfulness, grief,
guilt or apathy, disturbed sleep, depression.

The picture which emerges is one of multisystemic
involvement.

2.4

Present explanations for the cause of the above
picture are:

3
a)

after-effects of lung damage.

b)

increase in the cyanogenic pool in the body.

c)

psychosomatic manifestations as a result of the
severe trauma experienced.

In each individual there is possibly an overlap and

2.5

interplay of the three causative factors which result
from variations in parameters such as distance from
disaster site, type of house, action taken at the time
of disaster, degree of breavement, etc.

The percent­

ages of patients with symptoms predominantly due to any
one of the above factors is not known.

3.

A Flashback

3.1 Autopsy Findings
To begin with, there was a great deal of uncertainty
as to the nature and composition of the gas that

Initial autopsy findings showed a cyanide-

escaped.

like poisoning as the cause of death.

Instead of the

normal postmortem lividity and cyanosis,

there was

a pinkish discolouration of the organs.

The arterial

and venous blood and the organs had a characteristic

bright "cherry-red11 colour.
3

Lung weight was 2.5 to

times the normal, heavily water-Logged by oedema.

There was also a varying degree of oeder.i i of the

brain.

Autopsy findings even up to the 21st of

December, 1984, remained similar.
3•2 Haemoglobin Examination
Spectroscopic and spectrophotometric studies of haemo­

globin were carried out from the 14th to 21st of
December.

Control blood samples, samples of blood

preserved in the deep freeze and fresh samples from
subsequent autopsies were analysed.

The samples did

not show any evidence of the presence of carboxyhaemo ­
globin or cyanomethaemoglobin.I Further, samples from

the victims showed the presence of the characteristic
twin bands of.oxyhaemoglobin.1 This ruled out carbon
monoxide poisoning which is also characterised by a

cherry red appearance of the blood.

Arterialization

of venous blood as seen here is a characteristic of

4

cyanide poisoning also.

Later, experimental studies

in all animal species carried out so far have shown
that MIC also produces a cherry-red appearance of the

blood.

A recent study also indicates a 26-60% reduc­

tion of the free amino groups in the haemoglobin of

persons exposed to the toxic gas.
On estimating 2-3 DPG (diphosphoglycerate)

in blood,

levels- were found to be raised in the gas-exposed

population — thereby indicating ancxia.

Haemoglobin percentage was found to be significantly

higher among the affected population in Anna Hagar

indicating compensatory polycythemia (to anoxia)

3.3 Urinary Thiocyanates -

Thiocyanates are normally

present in urine and smokers show levels 50% higher

than non-smokers.
The presence of increased levels of urinary thiocyanates

(the form in which cyanide is excreted) „n the affected
victims also seemed to indicate a cyanide like poison­
ing.

Taking 20 Delhi-based urine samples as a control, ■

a base-line of 0.5 mg/100 ml of thiocyanate in urine

was set as the upper limit of normal.'

In persons who

were exposed to the toxic gas the urinary thiocyanate
levels estimated were always greater than 2 mg/100 ml.

In a study at Bhopal, it was observed that over 65% of
the samples from the gas affected population and 70% of
samples from hospital workers

(indirect exposure) showed

urinary thiocyanate levels greater than 1 mg/100 ml,

while only 33% of samples from the non-exposed popula­

tion had similar levels.

After administration of NaTS,

the level of thiocyanate in urine increased several

folds initially and then showed a dip.

On the basis

of the experiments it is felt that urine thiocyanate
level is a reasonably good indicator that will corro­

borate the other clinical manifestations of the toxic

exposure and in such cases, administration of NaTS
will produce significant increase in -che the thiocya­
nate excretion in urine. 4

5

3.4

The initial Double Blind Study with Thiosulphate
Thirty patients were selected.

They were given two

injections of either sodium thiosulphate or glucose.

Urinary thiocyanate levels were determined at 3 and

5

hour intervals and compared to the baseline level

before the injection.

In patients given sodium thio­

sulphate there was an 8-10 fold'increase in excretion

of thiocyanate in a significantly large number (10 out

of 15). Only one of 15 receiving the:glucose injection
,
.
, .
1
i
showed such increase.
j
Subsequently 230 cases were treated with NaTS with over
Of these complete records are avail­

1,000 injections.

able for 167

(87 men, 69 women and 11 '.children) .

The

symptomatology at the time of inclusion of therapy was
weakness and breathlessness.

This was present at rest

in 29 cases and in another 132 cases moderate exercise
elicited the symptoms.

Following NaTS administration,

there was no effect in 9 cases.

The remaining 158

persons showed varying grades of improvement for variable
periods of time.
were:

There were no deaths.

Adverse reactions

5 cases of feverishness, 1 case each of transient

loss of memory, exaggerated reflexes, sense of 'heat'
4

over the body, skin rash and transient venospasm.

. In another study various clinical symptoms were scored

on an arbitrary scale so that in the worst case the
score totalled 100.

Of the 100 patients given NaTS

therapy, 60 showed a decrease in score, 19 showed an
increase, while 21 showed no change.

/The worse the

initial symptoms the smaller the improvement after the­
rapy.

8

Of another 10 patients given intravenous glucose

showed reduction in score, but nocchange in their

lung function.

Another 10 were given intravenous amino­

phylline, all of whom claimed they felt better with
their FVC, FEV^, MEFR all showing improvement.

However,

the scoring system adopted needs improvement as differ­
ent symptoms should not be given equal weightage nor
should the scores be just added linearly.

The question

also arises as to why the results of lung function tests

•■on the persons given NaTS were not reported.

The find4
ings of this study are, therefore, not conclusive.’

6
3.5

Blood gas analysis

In the initial study, blood gas was analyzed in 20
patients, using ABL gas analyzer and an oxymeter.
PaO2 was lower than normal with a range of 47.3 to

85.6 mm Hg.

Those showing higher values had a history

of treatment with sodium thiosulphate.

8 out of 14

untreated patients had arterial PaC02 of 35 mm Hg or

less, which is below normal.

The venous sample showed

a normal or low Pv02 value but an elevated PvC02 in 9

of 13 cases.

The level of PvC02 after treatment with

sodium thiosulphate was increased markedly in comparison

to pre-treatment levels.

The increase in PvC02 was pro­

portional to improvement in clinical symptoms.

The

inference from the above is that oxygon transport was
found to be affected leading to tissue anoxia which

eventually produced less carbon dioxide in the peripheral
„

veins.

0n; treatment with NaTS, the increase in PvC02

occurred with predictable reproducibility.

It was

thought that owing to the inability of haemoglobin to
take up carbon dioxide it was carried' in solution in
the blood with the partial pressure going up to 70 mm Hg.

On cardiac catheterisation the difference in levels of
PvC02 between central and peripheral venous samples was

negligible.

Serial data showed that after administration

of NaTS!, PvC02 in both central and peripheral veins

showed;a significant rise indicating better uptake and

utilisation of oxygen by the tissues.

Studies have

shown;that pure MIG had no effect on cytochrome oxidase,
but its degradation products did
. .
4 '
uptake.
3.6

thus affecting oxygen

Animal Experiments ■
MIC has an LD 50 dose of 85 mg in mice, but with thio­
sulphate therapy it is shifted to'195 mg.

For rats,

the figures are 270 and 344 respectively.

Normal rabbit

lungs weighed 6 gms, with MIC they weighed 29 gms and

had a large number of haemorrhagic patches.

When given

NaTS immediately after MIC, lungs weighed 24 gms and

appearance was near normal.

Generally longer the dura­

tion after exposure, greater was the lung oedema observ­
ed.

Salbutamol had no blocking effect on the action
4
Haematocrit increased to a high level.

of MIC.

3.7

Cyanogenic Pool

The continued presence of the cyanide radical in the

body of the gas affected victims increases the cyano­
genic pool in the body.

This was responsible for the

multisystonic symptoms.

An improvement in symptoms

could occur only if the cyanogenic pool was depleted.

(Refer to Part-II for greater details).

ICMR studies show that NaTS therapy gives significant

symptomatic relief to people suffering after-effects of
exposure to toxic gas. This relief can be objectively
quantified by appropriate investigations.
In general

NaTS therapy has also been found to be harmless, although
allergic reactions may occur in 1 out iof 1,000 or 10,000
cases arising from imprities in the N^TS. Hence it has

been recommended for use, besides other therapeutic

measures, in selected patients.

[

Guidelines for the use of sodium thiosulphate (ICMR)
Criteria for selection of Patients - -

1.

Patients suffering from acute and/or chronic symptoms

relating to the respiratory, gastro-intestinal and

neuromuscular systems presumably related to possible
exposure to MIC gas.

2.

Patients presenting with recurrence of symptoms after

having obtained some measure of relief from the acute

phase.
3.

Recorded cases of acute pulmonary oedema and/or coma
occuring immediately following the ppisode and those
who are currently symptomatic.

Contradictions

1.

Pregnancy - routine use not advised, decision depends

on severity of symptoms.
2.

Renal disease.

Procedure

1.
2.

Record name, address.
Detailed record of symptoms and clinical findings

should be made with special, reference to a tendency

8

for early fatigue, exhaustion, respiratory signs

and symptoms. This information should be recorded
before and afcter treatment.
(Refer Appendix-I for a sample proforma)

3,

Check urine for albumin.

4.

Dose :

5.

a)

Adults - 1 gm (10 cc of 10% NaTS or 4 cc of
25% NaTS) given intravenously, daily for a
maximum of 5-6 days.

b)

Children - less than 2 years : 3,' cc of 10% NaTS.
2-8 years
s 5 cc of 10% NaTS.
more than 8 years : Adult dose.

Disposable syringes and needles are to be used for

this purpose.
6.

Alkaline mixture diuretic

with soda um chloride should

be administered to the patients to facilitate increased
excretion of thiocyanate for the duration of therapy.

7.

The patient should be kept under observation for at
least one hour after the injection.

8.

Pulse rate, respiratory rate, response to exercise

and level of physical activity should be recorded

during therapy and afterwards in order to assess

the progress/improvement.
Side-effects/Precautions

1.

It is a safe drug.

Minor side-effects - feverishness,

bodyache etc. respond to symptomatic treatmeht .and

antihistaminics.

2.

Adverse reactions, if any, should be brought to the

notice of local senior physicians for prompt manage­
ment, and also to the health authorities.

3.

Routine precautionary measures to manage anaphylactic
reactions which are kept as stand-by's when giving

any I.V. injections should be available in the dis­
pensary, eg. I.V. fluids, steroids and antihistamine

inj ections.

4.

If extravascation of the drug occurs, the patient

wild have intense burning locally which is transitory

and needs reassurance.

9
Drug Interactions

-

Nil.

Availability

1.

The following are available with Dr. Tandon, Medical

Superintendent, JP Hospital, 1250, South TT Nagar,
Bhopal

:

Inj. Sodium Thiosulphate,

b)

Disposable syringes and needles.

c)

Alkaline mixture.

d)

Printed forms for recording and.monitoring
patients' symptoms and signs.
Cotton, spirit, steroids, antihistaminies etc.

e)

2.

(Timings : 9 am - 1 pm and 4 pm - 6 pm)

a)

Presently NaTS stocks have been given to peripheral
government dispensaries and polyclj.nics, Red Cross

and a couple of voluntary agencies.

3.

There is an urgent need for government and voluntary
agencies to work in a coordinated manner and cover

the affected population within 3-6 months.
4.

OXFAM has also made an offer to help voluntary agenc­
ies interested in using thiosulphate for the affected

population.

Contact Nagpur office •• Field Director,

OXFAM (India) Trust, P.O. Box 71, Nagpur

4.

440 001.

Conclusions

Scientific investigations show the continued presence of an
increase in the cyanogenic pool in persons exposed to the

toxic gas, even months after the disaster.

This is one of the factors responsible for continued morbidity
among the affected population.

The other known causative

factors are structural lung damage and manifestations follow­

ing severe psychic trauma.

Many areas, even regarding existing theories, are yet unknown
—and there is an urgent need for further study.

When on the basis of experiments and investigations therapeutic
interventions are suggested it is essential that the logic

for such measures is made open for scientific scrutiny. This
information should also be made available to the treating
medical personnel since it is irrational to expect physicians

to prescribe drugs without being aware of the rationale for
their use.

10

This is perhaps one of the many reasons why NaTS is at
present being given half-heartedly at the cost of much ill-

health, suffering and economic loss for thousands of helpless

victims.
After the draft of this paper was ready, we came across a

report of the Pollution Control Board giving the chemical

analysis of samples of air collected on the 5th and 6th
December, 1984.

Despite the fact that these samples had been

collected in the open air 3 to 4 days after the gas leak,
these measurements show that the air near the MIC storage

tank of the Union Carbide factory contained cyanide at a con­
centration of 4,533 mg/m3 (4.5 ppm). This is nearly half the'

Maximal Allowed Concentration (MAC)

and about l/50th of the

Lethal Concentration (LC) set for hydrogen cyanide.

The

cyanide level reduced to half this value 50 metres away from
the tank and cyanide was not detected in samples collected

from three other localities further away from the factory -

the clear inference being that cyanide was still leaking from
the MIC storage tank even on the 5th and 6th of December.

The most probable origin of the cyanide must have been the
thermal decomposition of the MIC stored in the ill-fated tank.

When one ties up the above mentioned evidence with the reports
that cyanide was detected by the German toxicologist Dr. Max
Daunderer in the blood of the gas victims and also by the

CBI team in the ambient air using chemical spot tests, a few
days after the tragedy, the case of NaTS therapy for the
surviving gas-affected population becomes almost irrefutable.

11

5.

1.

References for Part-I

"Health effects of exposure to toxic gas at Bhopal",
An update on ICMR sponsored researches,

10th March,

1985.

2.

"Medical survey on Bhopal gas victims", conducted by

Nagrik Ra’nat aur Punarvas Committee, Bhopal, in
collaboration with Voluntary Health Association of

India, Delhi and Bhopal Relief Trust, Bombay,
March, 1985.
3.

"The Bhopal disaster aftermath - a sociomedical and
epidemiological survey", Medico Friend Circle,
March, 1985.(unpublished)

4.

Minutes of the third meeting of the Working Group

on Thiosulphate Therapy of the MIC exposed population
4th April, 1985.

Appendix, - I

PROFORMA FOR THE CLINICAL MONITORING OF SODIUM THIOSULPHATE
ADMINISTRATION

PEOPLE'S

HEALTH

PROGRAMME

Sl.No.

Date of Registration—

Name

Sex Age

Smoking ; Yes/lJo

Tobacco chewing ; Yes/No

Where were you when the Gas leaked
Where did you run and how
Were you admitted to Hospital?

If yes, which hospital?

Did any family member die?
Treatment

:

Government

Private

Fees

Expenses

Drug
Others

C omp en s ati on ______________________________ i__________ ____
What have you heard about proper treatment for the gas?

What have you heard about sodium thiosulphate?

SUMMARY TREATMENT AND INVESTIGATION

Previous Complaints

Yes

No

What

Nervous System

—

—

—

Eyes

—

—

—

Nose and Throat

—

—

—

Chest

—

—

—

G.I.T.

—

—

—

Skin

—

—

—

Genito Urinary

—

—

—

Musculo-skeletal

—

—

—

Treatment

Date

Details

Investigation

Date

Details

PRESENT SYMPTOMS/CHECK■LIST

I.

Nervous System
HEADACHE/HEAVINESS

:

DIZZINESS

;

ANXIETY

:

POOR MEMORY

:

LOSS OF SLEEP

:

TINGLING AND NUMBNESS

:

II. Eyes

BURNING OF EYES

:

WATERING OF EYES

:

DIMNESS/BLURRING OF VISION:

III.

IV.

Nose and Throat

RUNNING NOSE/SNEEZING

:

SORE THROAT

:

Chest and Cardiovascular system

PALPITATION

:

BREATHLESSNESS

:

CHEST PAIN

;

DRY COUGH

:

COUGH WITH EXPECTORATION

:

HAEMOPTYSIS

V.

VI.

Gastrointestinal System

ULCERS IN MOUTH

:

LOSS OF APPETITE

:

NAUSEA

;

DISTENSION OF ABDOMEN

:

PAIN ABDOMEN

;

DIARRHOEA

;

CONSTIPATION

:

HAEMATEMESIS

;

Skin
ITCHING

VII.

Urogenital System
BURNING CN PASSING URINE :

VIII.

IX.

LEUCORRHOEA

:

IMPOTENCE

:

PAIN ON INTERCOURSE

:

SCANTY/HEAVY BLEEDING

:

SHORTENED/LENGTHENED
CYCLES

?

Musculoskeletal System
TIREDNESS/VrEAKNESS

:

FEVER

:

PAIN IN THE CALF MUSCLES :

BACK PAIN/BODYACHE

;

PAIN IN THE EXTREMITES
X.

;

Any others

PRESENT SIGNS-CHECK LIST
ANAEMIA

;

PULSE RATE

:

RES .’IRATORY RATE

:

CYANOSIS

:

CORNEA AND CONJUNCTIVA

ACUITY OF VISION

:

SKIN INFECTION

:

SKIN RASH

|

SHIFT OF MEDIASTINUM

:

NATURE AND CHARACTER
OF BREATH SOUND

:

ADDED SOUNDS

OHI • 2>l .

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
K-14 (FF) Green Park Extn., New Delhi -110016
Tel: 6196640, 6163830, Fax: 6198042. Email: admin@tom.unv.ernet.in

44 Sant Kanwar Ram Nagar, Berasla Road, Bhopal - 462001
Tel: 0755 - 730914. Email: sathyu@.unv.ernet.ln

Madhukar Pai
Department of Community Medicine
Sundaram Medical Foundation
4lh Avenue, Shanti Colony
Ana Nagar West
Chennai, Madras, 600 040

S1*1 November 1998

Dear Madhukar Pai, Anand Zakharia and Prabir Chaterjee
Re: Invitation to Coordinate the Fact Finding Team on Medical Research in Bhopal - 15
Years on.
It is now almost fourteen years since the Union Carbide Bhopal gas disaster. Yet the medical,
legal, environmental, social and economic condition of the survivors is no better. In fact in many
ways, it is much worse than it was in the immediate aftermath of the disaster in December 1984.
Institutional indifference, apathy and corruption has compounded the difficulties faced by the
survivors in their everyday struggle for justice and a dignified life. The inability of institutions to
effectively respond to the world’s worst industrial disaster and the resilient struggles of the
survivors since 1984, has made it imperative that creative initiatives are taken to ensure that the
people and lessons of the world’s worst industrial disaster are not forgotten.

In the last fourteen years a number of groups have actively worked on the issues facing survivors.
As you may know, a number of independent actions have also been taken to look at specific
issues facing those affected. For instance, the Permanent Peoples’ Tribunal on Industrial Hazards
and the Environment (1990-94) gave survivors of Bhopal and other industrial disasters an
international forum to testify on the continuing impact on their lives; and the International
Medical Commission on Bhopal (1994) in which international experts assessed the ongoing
health effects and state of medical care in Bhopal. Those working consistently in Bhopal,
however, now feel that it is time to take stock of these and other issues^and explore new
directions for future long term work with and for the people of Bhopal.

Thus, in an attempt to go beyond previous studies, we propose an independent Fact Finding
Mission, with specific teams to examine the current status of the issues faced by the survivors of
the disaster; as well identify areas where critical interventions can be made. We hope that several
teams comprised of experts, researchers and volunteers will come together to conduct studies and
collate information over a period of six months. It is envisaged that a final report will be
presented by July 1999 as a precursor to organizing working groups on specific project areas.
This is the first opportunity in 14 years that such a comprehensive initiative has been proposed. It
is clear that the issues of Bhopal are very complicated and the reports of each team will have
implications on other areas. The studies, highlighting the most effective ways forward will give
those working on Bhopal fresh direction and support. The overall initiative, and the subsequent
commissioning of working groups will be an effective tool in compelling an otherwise indifferent
Organizing Committee
Rashida Bi, Bhopal Gas Peedit Mahila Stationary Karamchari Sangh
Jabbar Khan, Bhopal Gas Peedit Mahila Udyog Sangathan
Balakrishna Namdeo, Bhopal Gas Peedit Nirashrit Pension Bhogi Sangharsh Morcha
Satinath Sarangi, Tamjit Bird!, Bhopal Group for Information and Action
S. Muralldhar, Advocate, Supreme Court of India
E. Deenadsyaian, The Other Media

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
K-14 (FF) Green Park Extn., New Delhi -110016
Tel: 6196640, 6163830, Fax: 6198042. Email: admin@tom.unv.ernet.in

44 Sant Kanwar Ram Nagar, Berasla Road, Bhopal - 462001
Tel; 0755-730914. Email: sathyu@.unv.ernet.in

government to remain accountable to the continuing suffering of the people of Bhopal. We intend
that results from the working groups be presented in time for the fifteenth anniversary of the
disaster next year.
We would like to invite you to participate in this independent initiative as a joint coordinator of
the Fact Finding team on Medical Research in Bhopal, as well as taking responsibility for the
completion of the final report. We have outlined, in consultation with those already working in
Bhopal and survivors organizations, the issues which we feel are most pertinent and will need to
be examined:
Medical Research
□ Consolidation of studies carried out by government, private and other agencies and a
reassessment of their major findings
□ Analysis of the design and implementation of government studies
□ Analysis of various studies conducted by Central Govt institutions for rehabilitation
□ Outline of studies required for long term monitoring of health effects
□ Assessment of the health status of gas affected persons, and their continuing exposure to
hazards at both, the occupational and domestic levels
□ What are the existing public health initiatives, and what is required?
We have requested Padma Prakash of the Economic and Political Weekly to assist in the
coordination of this team.
We undertake to provide resources in terms of office-cum-accommodation and food in Bhopal.
Whilst we expect to provide volunteers locally, we will need your assistance in identifying
trained volunteers, specific logistics needed for the work, and whether it will be possible for the
institution that you represent to offer any support. Any other suggestions on the parameters
outlined would also be appreciated.
You will find enclosed a Backgrounder summarizing the issues facing those in Bhopal, the
Parameters of the Fact Finding teams and Terms of Reference and a list of all those we are
requesting to be part of this venture.

We will be launching the Mission on 30lh Novemvber 1998, in Delhi. We very much hope it will
be possible for you to attend. We would be extremely grateful if you could confirm your
involvement as soon as possible.We look forward to your participation as a joint coordinator of
the Fact Finding Team and thank you in advance for your co-operation and support.
With warm regards

-. rx__________
E. Deenadayalan & Tarnjit Birdi
On behalf of the Organizing Committee
Organizing Committee
Rashida Bi, Bhopal Gas Peedit Mahila Stationary Karamchari Sangh
Jabbar Khan, Bhopal Gas Peedit Mahila Udyog Sangathan
Balakrishna Namdeo, Bhopal Gas Peedit Nirashrit Pension Bhogi Sangharsh Morcha
Satinath Sarangi, Tarnjit Birdi, Bhopal Group for Information and Action
S. Muralidhar, Advocate, Supreme Court of India
E. Deenadayalan, The Other Media

SURVIVING BHOPAL: 15 YEARS OH
A FACT FINDING MISSION

Backgrounder
Introduction :
On the midnight of 2nd - 3rd December 1984, the worst industrial disaster of this century was
caused by Union Carbide Corporation, USA in the capital city of Bhopal, Madhya Pradesh, a
city with about one million people. Over 40 tonnes of Methyl Isocyanate and other lethal gases
including Hydrogen Cyanide, leaked from Carbide's pesticide factory in the northern end of the
city killing over 8,000 people in its immediate aftermath, causing multisystemic injuries to over
500,000 people. The number of deaths has risen to over 16,000 in the subsequent years and there
appears no end to the physical and mental suffering caused by exposure to the poisonous gases.
Breathlessness, diminished vision , loss of appetite, pain, menstrual irregularities, recurrent fever,
0 persistent cough, neurological disorders, fatigue, weakness, anxiety and depression are the most
common symptoms. Research findings on chromosomal aberrations suggest that the future
generations of the survivors will possibly carry ravages of the industrial toxins. Union Carbide
continues to withhold toxicological information on the leaked gases thereby impeding medical
treatment. The majority of those affected by the gases are people who earned, their livelihood
through hard physical labour and today their economic condition forces them to continue with
their jobs, thus exposing themselves to further health risks. Little has changed in the living
environment of the survivors, most of whom live in congested slums without facilities for safe
drinking water, sanitation and clean air. Judicial systems in both USA and India have failed to
ensure adequate compensation and justice for the survivors. The settlement amount, an average
of US $ 940 for each survivor, paid by Union Carbide resulted in a nominal loss to its
shareholders of merely 50 cents per share. Compensation sums awarded for personal injury' have
been unjust and inadequate and in over 90% of cases the victims have received only about
Rs 15,000/- (or about $430). Nearly two hundred thousand persons directly affected by Union
Carbides gases remain to be compensated. For a large number of the victims the sums received as
a compensation have been spent in repaying debts incurred in medical treatment in the last several
years. Officials of Union Carbide who have been charged with manslaughter and other criminal
offences are absconding from Indian courts where criminal proceedings against them been
pending for the last six years. Every week in a public park in the city , hundreds of gas-affected
women hold public meetings calling for the trial of the prime-accused Warren Anderson, former
Chairman of the corporation, who is known to be on vacation at Vero Beach, Florida, USA.
Medical impact of the disaster:
Most of the information on the medical consequences of the Union Carbide disaster in Bhopal has
been generated by the Indian Council of Medical Research (ICMR), an agency of the Indian
government that carried out 25 research studies from 1985 to 1994. All ICMR studies in Bhopal
were prematurely terminated by December 1994.

The ICMR established that the toxins from Carbide's factory have crossed into the blood stream
of those exposed and have caused damage to the lungs, brain, kidneys, muscles as well as
gastro- intestinal, reproductive, immunological and other systems.

Six monthly morbidity surveys by ICMR from 1987 to 1991, show that the number, of people with
exposure-related symptoms actually increased in that period. According to one study, there
were three times more persons with respiratory symptoms in 1991 as compared to. 1987. The
damage to the respiratory system and particularly the lungs comprises, t.he, most obvious and very
significant part of the overall health damage. Bronchial asthma. Chronic Obstructive Airways
Disease, recurrent chest infections, and fibrosis of the lungs are the prinpipal effects of exposure
induced lung injury. The prevalence of pulmonary tuberculosis among the exposed population has
been found to be more than three times that of the national average.
Damage caused to the eyes of the survivors have led to early-age cataracts found to be three
times more prevalent among the exposed population compared to an unexpqsed population at the
far end of the city. Pregnancy outcome studies on women who were pregnant at the time of the
disaster have shown that the spontaneous abortion rate was almost:'.three, times that of.the
national average. In
the exposed population the stillbirth rate was three times, perinatal
mortality was two times and neonatal mortality was one and a halftimes more than the
comparative national figures. Study on growth and development of the,children whose mothers
were exposed to the toxic gases during pregnancy revealed that majority of children had
delayed gross motor and language sector development. Studies have also presented evidence of
chromosomal aberrations of gaps and breaks in the chromosomal material as well as increased
sisterchromatid exchange indicating likelihood of congenital abnormalities among future
generations of the exposed persons.

Toxic gas exposure was found by ICMR researchers to have had a detrimental effect on the
immune system. Immunoglobulin levels were significantly raised , T-cells were reduced in number
and there was a tendency towards the reversal of T4/T8 ratio indicative of immuno-suppression.
Various studies conducted by non-government organizations have pointed out that the medical
consequences of the Union Carbide disaster have been under-assessed by the ICMR and certain
exposure related injuries have been overlooked.
The pregnancy outcome survey referred to above was carried out by Medico Friend Circle in
September '85 and showed that the spontaneous abortion rate among gas exposed women
was several times higher than that reported by ICMR. A survey of psychiatric morbidity carried
out by a group of independent doctors from Bombay found that nearly 40% of those exposed
suffered from post-traumatic stress disorder, a condition not studied by ICMR.

SOBVMNG BHOPAL: 15 YEABS ON
A FACT FINDING MISSION

An epidemiological survey coupled with clinical investigation carried out by the International
Medical Commission on Bhopal, composed of 14 medical specialists from 11 different
countries, reported in January 1994 significant multi-organ symptoms persistent among the
exposed population. Clinical examinations have shown significant lung impairment, marked
reduction in control over limb movements and reduced memory function caused due to exposure.
Their findings include evidence of a range of neurotoxic injuries in the exposed population.

State of Medical Care and Monitoring :
The medical care of the survivors has largely remained symptomatic since the time of the disaster
and continues to be ineffective in providing sustained relief. Union Carbide continues to withhold
information on the composition of the leaked gases and their long term effects on the human
body. In the absence of such information, doctors in Bhopal indiscriminately prescribe antibiotics,
steroids and psychotropic medicines causing more harm than good. A study undertaken by the
International Medical Commission on Bhopal confirmed that therapies prescribed for the ailing
survivors are aimed at temporary symptomatic relief rather than long term amelioration of chronic
disease processes. The major emphasis of the medical relief programmes of the Madhya Pradesh
government has been :o build hospitals so much so that Bhopal now has more per capita hospital
beds than is recommended by the World Health Organization. Yet as per the reports of the 1CMR
the number of diseased persons has gone up with the years. For the last several months almost no
medicines are available to the gas victims at any of the hospitals and clinics meant for them.
People who do not have sufficient means for their basic needs are asked to buy medicines and
even syringes and IV sets by doctors at these institutions that are supposed to provide free
medical care. There has been hardly any government initiative in providing community based
medical care to chronically ill survivors. Also lacking are initiatives for provision of medical care
through systems of medicine such as Ayurveda, Unani and Yoga that have demonstrated their
superior efficacy in the treatment of exposure related illnesses. The growing inadequacies of
government medical care has led to unregulated proliferation of private and expensive medical
clinics. With the termination of 25 medical research projects of the ICMR in.December 1994, long
term monitoring of the health condition of the survivors has been abandoned. The Centre for
Rehabilitation Studies funded by the state government since March 1995 is yet to initiate any
research work. The official agency for monitoring exposure related deaths has been wound up in
December 1992 and there is no official record of deaths that continue to occur. With the
premature termination of research and monitoring there is almost no current data on the
prevalence of tuberculosis, cancers and infertility among the exposed population al! of which are
reported to be on the rise by doctors involved with the treatment of the survivors.
A recent issue of major concern is the proposed handing over of the health infrastructure set up
the government to the so called Bhopal Hospital Trust set up by Union Carbide. Despite vigorous
opposition by the survivors, the state government has begun handing over the eight community
clinics to the Bhopal Hospital Trust (BHT) set up by Union Carbide Corporation. Preparations for
transfer of the

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION

four Red Cross clinics are also on. Ironically, one of the main factors impeding appropriate
medical treatment at these government clinics has been withholding of medical information by
Carbide and the closure of the Red Cross clinics followed from withdrawal of financial support by
the corporation. The source of funds'of the BHT is the value of shares of Union Carbide that had
been judicially attached to ensure that the representatives of the corporation face criminal charges
related to the disaster. By means of interventions in the Supreme Court through the sole trustee
of BHT, Sir Ian Percival (an attorney working for Union Carbide from 1984 to '92) the
corporation has been able to get the shares dis-attached and continues to abscond justice. In the
last two years Percival has spent Rs. 7 crores on the construction of a 260-bed hospital ,which
happens to be 8 kms away from the gas affected area, and Rs. 5 crores on his own fees, travel and
office expenses. Quite clearly providing medical care to the survivors is not among the priorities
of BHT. Its sole purpose is to build a humane image for the corporation while helping it to
abscond criminal justice on the massacre. Percival's plans of health care administration have been
severely criticized by national and international professional groups including the IMCB. Among
other misgivings, concerns have been expressed regarding transparency of activities at the
proposed medical research centre to be set up by the BHT.
Economic and Social Impact :
There has hardly been any systematic effort to document the social and economic impacts of the
disaster. Official information on orphaned children and families that lost their breadwinners in the
immediate or long aftermath is scanty, if available at all. Over 70% of the exposed population has
been in the unorganized sector, with people earning subsistence wages through day labour or
petty trade. A large number of men and women who pushed hand carts, carried loads, dug soil,
repaired cars and did other jobs can no longer pursue their trades after being exposed to Carbide's
gases. Gas exposed factory workers in textile and paper mills are more sensitive to occupational
hazards and are absent from work due to illness as much as 15 days in a month. Over 90 % of the
survivors have received a compensation of Rs 15,000 which is just enough for the cost of
medicines for five years, and many of these people will be in need of medical care till the end of
their lives. Given the complete inadequacy of official rehabilitation efforts the loss of regular
income has driven tens of thousands of families to chronic starvation conditions. Loss of income
also makes people borrow money from local money lenders who charge upto 200% interest so
that chances of paying back are low and debts keep growing. Gas exposed women's inability to
carry out reproductive functions have led to their desertion by their husbands and gas exposed
young women continue to suffer social discrimination in marriage.

Environmental problems:
Thirteen years after the disaster, Union Carbide's toxic legacy continues to harm people in more
ways than one. Communities in the vicinity of the Carbide factory continue to be exposed to toxic
chemicals that are injurious to the lungs, liver and kidneys and can cause cancer. Water in over
200 wells around f '’-■rbide factory have been declared unfit for human consumption by the
municipal authoriti
'his is a result of routine dumping of hazardous chemicals during the
operation of the fac.
thus

SURVIVING BHOPAL: 15 YEARS ON

A FACT FINDING MISSION
contaminating soil and groundwater in and around the factory premises. Analysis carried out by
the Citizens Environmental Laboratory (CEL), Boston in 1991 show presence of toxic chemicals
in the community wells around the factory.
This report presented at the company's annual
shareholders meeting drew the attention of the senior officials to the problem. The Corporation
gave the job to Arthur D. Little Inc. who sponsored a collaborative investigation with an Indian
government agency in 1994 in to the matter of contamination caused by dumping chemicals inside
the factory premises.
This study done without public knowledge recommends a fuller
investigation for better assessment of the environmental contamination. The findings of this study
confirm the worst apprehensions of activists and people in the community. Meanwhile, in 1996
the company management has dug up bottom soil from the "Solar Evaporation Ponds" and buried
the heavily contaminated sludge under three metres of farm soil in a bid to cover up evidence of
environmental damage. Survivors' organizations have been calling for an official assessment of the
damage wrought by Union Carbide so that the corporation could be asked to pay the costs of
environmental rehabilitation and supply of safe drinking water for the affected communities.
Economic Social and Environmental Rehabilitation :
The government programmes for economic rehabilitation have been badly designed and only few
have been implemented. While an estimated population of 50,000 is in need of alternate jobs
currently less than 100 gas victims have found employment under the government's scheme. 42
worksheds that had been built between 1985 to 1987 were allotted to so called NGOs between
1994 to 1996. However, apart from two worksheds employing about 50 women, none of them
have ever been made available for employment of the survivors. Official promises have been on
record that 50 % jobs in the Railway Coach Repair Factory would be reserved for gas affected
people. However, only 205 of the 1000 employees of this factory are gas affected persons. In
1987 a special industrial area for training and employment of over 10,000 survivors was
inaugurated and 152 worksheds were constructed at a cost of Rs.8 crores. However, till date not
a single survivor has found any employment. A programme offering women survivors tailoring
jobs ran successfully from 1986 to 1992 employing 2300 women and making an yearly profit of
Rs. 1 crore. The rehabilitation centres where these jobs were offered were also places where
women survivors could gather, share their concerns and organize themselves. However, this
programme was terminated without any reason in July 1992.

Till date the government has no record of the social condition of the persons who have been
widowed, orphaned, or have been permanently disabled as a result of the gas disaster. The state
government has deemed its work of social rehabilitation to be over by constructing 2500 houses
and a few schools. There has been no official attention towards the urgent need of life long
pension for widows, orphans, chronically ill and disabled survivors. The Supreme Court's final
order with regard to provision of insurance coverage to about one lakh children likely to suffer
delayed effects of the lethal gases is also being ignored by the Central government.

Despite the expenditure of over Rs. 70 crores in environmental rehabilitation basic necessities
such as clean drinking water and sanitary facilities remain unavailable to majority of the gas
affected communities.
Legal Aspects:
Subsequent to the disaster the Indian government through the Bhopal Gas Leak Disaster
(Processing of Claims) Act in March 1985 arrogated to itself, sole powers to represent the
victims in the civil litigation against Union Carbide. On behalf of the victims the Indian
government filed a suit for compensation of more than 3 billion US $ in the Federal Court of the
Southern District of New York. However, in May 1986 the case was sent to the Indian courts on
grounds of forum non-convenience, under the condition that Union Carbide would submit to their
jurisdiction. During the proceedings at the Bhopal District Court, Union Carbide was directed to
pay an interim relief sum of Rs.35O crores so that the delay in the adjudication of the case does
not adversely affect the claimants. However, Union Carbide refused to pay interim relief and its
appeal against this decision reached the Supreme Court. On Feb 14,1989 in a sudden departure
from the matter of interim relief, the Supreme Court passed an order approving the settlement
that had been reached between the government of India and Union Carbide without the
knowledge of the claimants in Bhopal. According to the terms of the settlement, in exchange of
payment of US S 470 million the Corporation was to be absolved of all liabilities, criminal cases
against the company and its officials were to be extinguished and the Indian government was to
defend the Corporation in the event of future suits. The settlement sum, nearly one-seventh of the
damages initially claimed by the government, while being far below international standards is also
lower than the standards set by the Indian Railways for railway accidents. There were widespread
protests by the Bhopal victims against the betrayal by the government and many organizations and
individuals including prominent members of the parliament supported the call to oppose the
infamous settlement. Several petitions seeking review of the order on settlement were filed and
the Supreme Court announced its revised judgement on October 3,1991. This final judgement
upheld the settlement amount paid by Carbide but directed the Indian government to make good
any shortfall during the distribution of compensation. Also the criminal cases against the
Corporation and its officials were reinstated in the final judgement. The Supreme Court also
directed Union Carbide to finance a 500-bed hospital for the medical care of the victims.

Compensation:
The amount paid as compensation (Rs. 715 crores) has multiplied as a result of the increase in the
value of the dollar and the accruing interest. Out of this amount, about Rs. 850 crores have been
paid to nearly 3.2 lakh claimants and a balance of about Rs. 1100 crores remains to be disbursed.
The procedures for compensation disbursement have been tortuous and thoroughly unjust. More
than 90% of the claimants have been paid a sum less than Rs. 25,000 as compensation for
personal injuries out of which nearly Rs. 10,000 have been routinely deducted against interim
monetary relief paid by. the government from 1990. The remaining money does not half cover the
medical expenses borne by the

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION

claimants in the last several years let alone provide for future expenses. Out of the 15,168 death
claims adjudicated 65% have been rejected or converted into personal injury cases where
compensation sums are lower. Judges at the claim courts are completely ignorant of the medical
consequences of the toxic exposure and the administration of compensation is riddled with
corruption so that claimants inability to pay bribes often results in denial of compensation. In
response to an official announcement for fresh registration of claims in December 1996 over 4
lakhs claims have been filed. Majority of these claims have been filed by persons residing outside
the gas affected area including elite neighbourhoods and it is most likely that genuine victims will
be the ultimate loser in the disbursement of compensation.

A

Criminal Case
A First Information Report for causing death by negligence and a number of other serious
offences was registered on December 3,1984 at the local police station. On December 1,1987 the
government's prosecution agency the Central Bureau of Investigation (CB1) pressed charges in
the Bhopal District Court against UCC and its Asian and Indian subsidiaries namely Union
Carbide Eastern (UCE), Hong Kong and Union Carbide India Limited (UCIL) respectively as
well as nine officials including the then Chairman, Warren Anderson The twelve accused were
charged under sections 304 (Part IF), 326, 324 and 429 of the Indian Penal Code, with culpable
homicide, causing grievous hurt, causing death of and poisoning animals and other serious
offences punishable by imprisonment upto ten years and fines. The Corporation blamed a
fictitious saboteur and lat^r a disgruntled worker for causing the disaster and organized public
relations campaign to distance itself from criminal liability. The CBI with the cooperation of the
workers in the factory presented a strong case linking key managerial decisions to the disaster. As
the proceedings in the Bhopal District Court began, Union Carbide and its officials chose to
ignore the Court's summons claiming that Indian courts had no jurisdiction over them. Finally
Anderson was served summons through the Interpol and on his repeated refusal to obey them, the
Chief Judicial Magistrate (CJM),Bhopal proclaimed him an absconder. After the criminal
immunity granted under the settlement was revoked by the October 1991 final judgement of the
Supreme Court a non-bailable arrest warrant was issued against Anderson and the shares of
Union Carbide in its Indian subsidiary were attached by the CJM, Bhopal. Five years have passed
since the issuance of arrest warrants against the accused Corporation and its officials, yet the
Indian government has not taken any steps towards seeking the extradition of the foreign accused.
Union Carbide deregistered UCE, Hong Kong in 1992 and now operates in Asia through Union
Carbide Asia Ltd. and Union Carbide Asia Pacific Inc.(UCAP) both wholly owned subsidiaries of
the parent US based Corporation. Ramasami Natarajan the former CEO of UCE is now the
President of UCAP, Hong Kong. The CBI has expressed , in Court, its inability to proceed
against UCE as it has deregistered itself. On Sep. 13, 1996, in response to an appeal moved by
Keshub Mahindra and other accused officials of Union Carbide India Ltd. (UCIL), the Supreme
Court passed an order diluting the charges of culpable homicide to death caused by negligence
(Sec. 304A of the I P C), thereby reducing the maximum sentence from 10 years to 2 years. Trial
of the Indian accused are currently going on before the CJM, Bhopal, and only five of the over
two hundred witnesses for the prosecution have testified in the last four

SURVIVING BHOPAL: 15 YEARS ON

A FACT FINDING MISSION
months. Meanwhile, the managers of Eveready Industries India Limited (new name of Union
Carbide India Ltd.) have dismantled most of the Bhopal factory that is supposed to be under the
custody of the CBI as evidence in the criminal case. In the absence of any preemptive action by
the CBI, survivors organizations sought judicial and executive intervention into the erasure of the
memory of the disaster as well as destruction of evidence. However, these attempts were
unsuccessful.
Memorial
In a meeting of the state cabinet in end June 1988, the government decided to take back the 60
acre stretch of land in Bhopal on which the Union Carbide pesticide factory had been built. In
July, the Madhya Pradesh state government committed itself to constructing a memorial at the site
of the Union Carbide factory in Bhopal. The shape or content of this memorial remains to be
decided.

SURVIVING BHOPAL: 15 YEARS ON
a FACT FINDING MISSION
Unresolved Issues of the Union Carbide Disaster in Bhopal
Medical :

1.
i.
ii.
iii.

2.
i.
ii.

Research and Monitoring
Lack of research on continuing gynaecological, neurological, endocrinal,
chromosomal and mental health impacts of the disaster.
Lack of administrative set up for carrying out long term, and possibly trans
generational research activities in Bhopal.
Absence of monitoring of continuing exposure related mortality and morbidity.

Information
Lack of information on health impacts available with government and private
doctors involved with the medical care of the survivors.
No official initiative towards disseminating information on health impacts and
preventive and ameliorative measures to the survivors.

Health care
Absence of perspective and administrative set up to respond to the chronic nature of
exposure related diseases.
ii.
Absence of protocols for the proper treatment of exposure induced illness
iii.
Absence of a system of recording health status and efficacy of medical
interventions.
iv.
Absence of a community based health care approach and overwhelming emphasis
on hospital based treatment.
v.
Negligence of Indigenous systems of medicine.
vi.
Unavailability of medicines and facilities for investigations at government hospitals
and clinics.
vii.
Indiscriminate use of Steroids, Antibiotics, Psychotropic and symptomatic drugs.
viii.
Absence of drug- free therapies such as Yoga.

3.
i.

4.
i.
ii.

Health Education and Public Health improvement
Absence of official initiatives towards health education among survivors.
Lack of official initiatives towards provision of clean air, water and sanitation
facilities to the survivors.

SURVIVING BHOPAL: 15 YEARS ON
iii.

iv.

2.
i.
ii.
iii.
iv.
v.
vi.
vii.

viii.

Absence of criminal case against Union Carbide for contamination of ground water
and soil.
Absence of criminal case against Eveready Industries India Limited for dismantling
and demolition of the factory.
Civil
,
Inadequate amount of compensation
Wrongful rejection of claims
:
Wrongful denial of registration of claims
Lack of fora for review and redress
Utilization of over Rs 1000 crore expected to be left over after disbursal of
compensation to all claimants
Continuing legal liability of Union Carbide Corporation, USA and Government of
India for medical, economic and social rehabilitation of survivors.
Legal liability of Union Carbide Corporation, USA for. contamination ..of
groundwater and soil in the vicinity of its factory.
Ensuring democratic control over the funds currently held by Bhopal Hospital
Trust

fl FACT FINDING MISSION

A FACT FINDING MISSION
Economic, Social and Environmental Rehabilitation :

1. Information
i.
No identification of individuals, families and communities most in need of
economic and social rehabilitation .
ii.
No information on production and training skills available locally
iii.
No information on locations requiring environmental rehabilitation.
iv.
No information on technologies for decontaminating soil and groundwater poisoned
by Union Carbide
2.
i.
ii.
iii.

iv.

v.

3.
i.
ii.
iii.
iv.

Programmes
Absence of long term perspective and administrative structure to carry out long
term programmes of economic and social rehabilitation.
. Absence of integration of economic and social rehabilitation programmes with
programmes of medical care and monitoring.
Lack of innovation and imagination in the design of economic and social
rehabilitation programmes.
No scope for participation of survivors in design and implementation of
rehabilitation programmes.
Absence of an ecological perspective in planning and implementation of
environmental rehabilitation programmes.
Administration
Absence of a well defined coordinating agency
Absence of community based organization
Absence of a mechanism for feed back and review
Gross mis- utilization and mis- appropriation of funds Legal :

Legal Issues

I. Criminal
i.
Revision of charges against accused Union Carbide India Limited and its officials
including Keshub Mahindra and others pending since September 1996
ii.
Slow pace of trial of Indian accused

SURVIVING BHOPAL 15 YEARS ON

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION

Terms of Reference
Towards developing a comprehensive overview of the current issues faced by those affected by
the Bhopal gas disaster, it is envisaged that the fact finding mission will.
I.

Analyze the continuing impact of the disaster on different areas of the lives of survixors of
the disaster.

2.

Identify specific failures, including policy and institutional, in the last fourteen years and their
subsequent repercussions on the people of Bhopal.

3.

Compile documentation on all the various aspects related to the Bhopal gas disaster.

4.

Outline larger policy changes as a result of the disaster.

5.

Provide concrete suggestions for effective democratic interventions.

mv f

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION

Parameters of the Fact Finding Mission
In a meeting of the Organizing Committee we identified the following 14 aspects of Surviving
Bhopal that we feel that the Fact Finding Mission must address. We have also arrived at broad
parameters for each Fact Finding Team which are briefly outlined below. We would appreciate
your response to these outlines and any suggestions you have to make, either on expanding the
scope of the Fact Finding Teams' study and analysis, or the inclusion of any other aspect that we
may have overlooked.

I.
□
□
□
□

□
□
□

2.
□
□
□
□
□
□

Medical Care
Estimated figures of exposure-related deaths per month, persons chronically ill. persons
acutely ill and persons with exposure-related injuries
The extent and nature of knowledge on treatment and treatment efficacy available with
doctors. RMPs etc
The most commonly prescribed dings and lines of treatment
Available facilities for medical care in different systems of medicine: No. of beds, doctors.
specialists, equipments, investigation facilities, availability of medicines and attendance per
day and utilisation of beds in government, private and other hospital/clinics.
Systems of registration and medical record keeping
Issues confronting employees of various hospitals and clinics, especially in gas affected areas
Possibilities of improvement in health care

Medical Research
Consolidation of studies carried out by government, private and other agencies and a
reassessment of their major findings
Analysis of the design and implementation of government studies
Analysis of various studies conducted by Central Govt institutions for rehabilitation
Outline of studies required for long term monitoring of health effects
Assessment of the health status of gas affected persons, and their continuing exposure to
hazards at both, the occupational and domestic levels
What arc the existing public health initiatives, and what is required?

J. Legal Issues
□ The current status of legal actions pending before different courts
□ The situation with respect to compensation distribution
□ An investigation of the systematic institutional corruption forced on the survivors
□ The policy and legal fall outs of the disaster
□ The possibilities rtf further legal action
□ The status of survivors' access to justice in terms of legal aid and counselling
□ Compilation of a list of documents available with the CBI

4.
□
□
□
□
□

Economic Rehabilitation
Outline of existing government and non-govemment rehabilitation programmes
The estimated figure of persons unemployed due to exposure related ill health
Profile of the range of occupations in different sections of the gas affected population and the
estimated per capita income.
Outline of the skills available for income generation
List of the potential markets for goods produced through income generating projects

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
12.
Memorial on the Disaster and its People
□ To present the current status of the State government plans to build a memorial
□ To highlight future possibilities
□ To outline how peoples’ participation in constructing and managing the memorial can be
ensured
13.
Disaster Management
□ To assess the disaster management policies and programmes, implemented by the state bodies
in the immediate aftermath of the disaster
□ To examine whether Union Carbide Corporation and Union Carbide India Limited had any
strategics for management of a possible disaster at the Bhopal factory',, whether they were
implemented and their effectiveness
□ Based on the Bhopal experience, what would be the proposed ■ disaster management
programme in the event of an industrial tragedy?

14.
Media’s Response
□ To present a critique of national and international media response in the last fifteen years
□ Compilation of media articles, reports etc....

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
Proposed List of Participants
Proposed Members of Fact Finding Mission:

Justice Bhagwati, Dr PM Bhargava, Mahashweta Devi, Prof. Satish Dhawan Sayeda Hamid,
Dr L.C Jain, Girish Kamad, Sugatha Kumari, Arundhati Roy
Proposed Coordinators of Fact Finding Teams:

Medical Care:

Medical Research '.

Law.
Economic Rehabilitation:

Labour:
Social Rehabilitation:

Environment:

Union Carbide:

Scientific Institutions:
Role ofState and Central:
Governments:
NG0 ’s and Peoples ’
Organisations:

Memorial:
Disaster Management:
Media’s Response:

Dr C.K Jacob , Medical Superintendent, Christian Medical
College Hospital, Velore
Satinath Sarangi, Sambhavna Trust, Bhopal
Dr Mohan Rao, School of Community Health and Social
Medicine, JNU, New Delhi.
Dr Padma Prakash, Economic and Political Weekly, Mumbai.
S. Muralidhar, Advocate Supreme Court, New Delhi.
Sandeep Sharma, Advocate, Bhopal.
David Selvraj, VISTHAR, Bangalore
Jabbar Khan, Bhopal Gas Peedit Mahila Udyog Sangathan,
Bhopal.
Sujata Goteshkar, Workers Solidarity Centre, Mumbai.
Ashim Roy, Hind Mazdoor Kisan Panchayat, Ahmedabad.
Shiv Vishwanathan, Centre for the Study of Developing
Societies, Delhi.
Dr Veena Das, Department of Sociology, Delhi University (**)
Ravi Aggrewal, Shrishti, New Delhi
Ashish Kothari, Kalpavriksh, Pune
Ward Morehouse, Council on International and Public Affairs,
New York, USA.
Raghunandan, Delhi Science Forum.
Babu Matthew, National Law School, Bangalore
Mohan Mani, Centre for Workers’ Management,Bangalore.
C.R Bijoy, PUCL, Coimbatore
Kalpana Kanabiran, Asmita Resource Centre for Women
Sheba Chachi, New Delhi
K.T Ravindran, Architect, New Delhi
To be decided
Prafi.il Bidwai, Columnist, New Delhi.

twenty months after the disaster wreaked
by Union Carbide.
Poisoned by a killer
multinational, neglected by the government,
ignored by the media,
the gas victims
continue to suffer from illnesses that are
yet to be properly diagnosed,
let alone
cured. And they continue to die.
Like
Moolchand of Patel Nagar, Bhopal.

On 2 September 1985, in a last desperate
bid to save his life, a pale and emaciated
Moolchand went, once again, to the govern­
ment polyclinic at Bharat Talkies. He
shuttled for days between the clinic and
Hamidia Hospital. Until, on 9 September
1985, he was admitted to the MIC ward.
He still complained of breathlessness,
cough with expectoration, muscular weak­
ness in the legs and generalised weakness.
Clinical and pathological examinations
ruled out tuberculosis but pointed to
bilateral crepitation. The diagnosis:
"MIC-induced lung diseases"!

The

Story of

Moolahand
J"une.

Moolchand died at 5.15 p.m. on 14
1986, on bed No. 17 of the MIC Ward, nine
months after admission to the Hamidia
Hospital. His tragic tale is the tale of
many many more who wait, spent and dispi­
rited, for a slow, troubled death.
Moolchand came to Bhopal in 1950 in the
tumultuous aftermath of the partition of
the country. A Sindhi migrant from Paki­
stan, Moolchand had little to survive on
when he started life anew at Bhopal. He
eked out a living as a scrap merchant,
carrying his load of waste around the city
on a bicycle. The only one to help him
was his son,. Vasudev. And they did manage
to survive and sustain their small family
through the years. Until, the night of
2nd December, 1984.

That fateful night, Moolchand awoke with
a start to find his room thick with acrid,
irritating fumes of gas. He was afraid,
and alone, for his family had fled. So he
too ran, like thousands of others, to save
his life. And he survived. But just.
The toxins had ravaged his body, so much he
was unable to work. His business suffered.
He could not breathe properly, his body
was wracked by coughing, he lost his appe­
tite, he couldn't see well. And then be­
gan his frustrating search for a cure, or
even for seme relief from suffering.

Each morning he joined the queues at the
government clinics with his wife Premvati,
who was similarly affected. He took drugs
and drugs and more drugs. But to little
avail. There was little respite from his
painful condition. In despair he went to
private doctors. His savings were all
gone. He had to sell off his wife's
jewels to pay for the expensive medicines
the doctors prescribed. Again, to little
effect, because he continued to suffer and
his condition deteriorated.

TWO

His wife, herself suffering, was his
constant companion at the hospital. She
made the daily four-kilometre trip from
their home in Patel Nagar to the hospital
with their son. Moolchand was prescribed
pain-killers, broncho-dilators, steroids..
... "He used to take almost half a kilot
gram of medicines everyday", reminisces
another patient in the ward.
Then one day Moolchand slipped and fell
in the bathroom. (This is not uncommon
in government hospitals where reeking
toilets and bathrooms are covered with
the slippery slime of dirt and excreta) .
He fractured his thigh bone. The fract­
ure was improperly Set. As a result,
one leg was an inch shorter than the
other when the cast was removed. Already
weak, Moolchand was now further immobil­
ised , confined to his hospital bed. He
lay gasping for six months, his family
driven to the brink of deprivation. Till
he finally lost the will to live. As a
final act of resignation and despair, he
stopped eating just prior to his death.
He died in the evening of 14 iSoSy, 1986.

Many, like Moolchand, continue to die.
In the absence of a meaningful and ade­
quate system for monitoring the condi­
tions of victims, many of these deaths
go unreported. Says Professor Heeresh
Chandra, Director of the Medico-legal
Institute, under whose charge the autopsy
of Moolchand's body was carried out,
"Many of the gas victims are dying, yet
very few dead bodies are brought in for
autopsy." Despite many suggestions, the
government has not made autopsy compul­
sory. Such an emission attains crucial
significance in the context of the opin­
ion expressed by Michael Ciresi, the
lawyer retained by the Government of
India, that the nexus between exposure
to gas and subsequent deaths has to be
established beyond reasonable doubt if
damages for death are to be claimed
from Union Carbide Corporation.

The complete absence of such initiative was
blatantly made clear in an interview with
the Director of Claims, Mr. Khare. We
asked how Moolchand's family could file a
claim for compensation. Sitting in his
office tucked away in a maze of government
buildings, seven kilometres away from
Patel Nagar, Mr. Khare confessed, "We do
not make any attempts to inform people
that they can still file claims." When
pressed, he tried to justify this glari _
omission by saying - "somehow seme people
do come!"

Such wilful neglect condemns the gas
victims to prolonged suffering and death,
even as the death dealing multinational
goes unscathed.
TOXIC

EMISSICNS

CCXiTINUE

Shortly before noon on 19th -jiine. ;9U6,
clouds of black smoke ware visible at
the UC plant in Bhopal. In', er cigat
by BGIA revealed a raging fire next tc
the administrative building inside
plant. On enquiry, security guards said
that plastic cans containing toxic chemi­
cals were being destroyed. The fire
continued for almost an hour.
This is not the first time since the
December, 1984, gas leak that toxic mat­
erials have been disposed off in this
manner by Union Carbide without informing
the public. In February last year, toxic
fumes from the incinerator inside the
plant entered a double storied school
building near the eastern wall of the
plant while the school was in session.
About 50 children, all below twelve years,
started coughing violently and some
started vomiting. A number of children
complained of giddiness and nausea. The
teacher, not knowing how to respond to
such a situation, declared the school
closed for the day and the children were
asked to go hone. The matter was taken
up with the authorities but no action was
forthcoming. The emissions frem the
incinerator continued unabated. It was
only after a group of young people from
Shaktinagar, where the school is located,
went up to the gate and hurled stones
that the authorities got the message and
the emissions stopped.

Incidents such as these aggravate the
panic-bound psyche of the gas victims,
besides causing injury to their already
damaged bodies. Many of the victims
continue to talk about the poison clouds
of the December leak and visions of that
catastrophe recur, in their dreams.
Mention is often made, sometimes in hush­
ed tones and semetimes in anger, that

is still going on in the plant.
But who is bothered about the gas victims
anyway?

WITHOUT COMMENT

Last month,< the UCO bank in Bhopal was :
robbed in broad daylight; by a .band: of
:
yet unidentified persons. They.are ■
reported to: have introduced themselves'
as "Hum log gas.peedit.:haih, : bank ::16otne
aye hein" (We are gaa victims, we)have •;
come to loot the bank). Reading the
report, an old gas,; victim commented, ' •
"Gas peediton ke haam se kitnon ne loot
liya, yeh ok aur sahi" (So many have ;
:looted in the name of gas victims, this
•is just, one more instance)...

STREET VS STAGE

Rangmandal, the theatre group of Bharat
Bhavan, the elite cultural centre of Bhopal
staged a play early this month based upon
the Bhopal gas disaster. •Banjh Ghati*
(Barren Valley), staged twenty months after
the disaster, was, however, eclipsed by the
forceful 'Dastan-e-Gas Khand1 (Tale of the
gas disaster) enacted at the same time on
the streets opposite the Bhavan by 'Shuruat*
a group of amateur artistes. This group
has been performing the play since early
last year in many parts of Bhopal and else­
where, including the gas affected slums.
Among the crowd which preferred to watch
the street theatre were many young artistes
of Bharat Bhayan. itself.

THREE

SURAKSHA

^8
A new project, involving the gas affected
children in painting, music, story telling,
poetry and drama, has started in the Jayaprakash Nagar Basti of Bhopal. It has been
organised by David Bergman, a young British­
er who has been in Bhopal for the past three
months.
(David and a friend undertook a
cycle tour from England to Bhopal to raise
funds for the gas victims of the Bhopal dis­
aster.) The group which has been set up for
the purpose is called SURAKSHA.

At present, five teams of local artists (of
2/3 individuals per team), each conduct a
workshop in the basti once a week. A large
covered area is used for these activities.
The project is now in its third week, and
30-50 children are regularly involved.
Suraksha feels that although there is an
obvious need for such opportunities to be
given to basti children everywhere, there
is a special need for them in Bhopal today.
Apart from the physical disabilities the
children are still suffering from, many of
them have also gone through extreme mental
anguish and stress during and after the gas
disaster. Emphasis is, therefore, being
placed in these workshops on psychological
therapy.

For the next few months, Suraksha plans to
limit itself to working in this basti with
these five teams of artists. Indeed, much
needs to be done just to make these activ­
ities with the children successful. Rela­
tionships of friendship and trust need to
be built up between the artists and the
permanent workers of Suraksha, on the one
hand, and between Suraksha and the children,
on the other. The children must be involved
in all aspects of the project. ' Attempts
must also be made to get the general accep­
tance of the project within the basti com­
munity. Only then can they become involved
in the general organisation of Suraksha and
in the supervising of the activities. Fin­
ally, much discussion needs to be done with
the artists themselves to work out coherent,
structured activities which have an overall
aim behind them. Such activities can then
continue over a number of weeks and months,
with new teams of artists joining in at
different points.

FOUR

“The gas leak is okay. What we’ve got to
guard against is the leaks to the press. ”

We have

the right to know
From September/October onwards, it is
hoped that Suraksha will be working in
two or three independent "activity huts"
structures of timber and bamboo - around
JP Nagar and Shakti Nagar. Apart from
the core of activities being carried out
by local artists and others frcrn the
basti, individuals and groups working
with children from other parts of the
country are also being invited to cane
to Bhopal to work intensively for two or
three weeks. Such groups could exchange
ideas with local teams so that their work
and methods could be continued in their
absence.

Once a good understanding and friendship
has been built up with the children,
Suraksha is interested in organising a
nutritional study of the children. Such
a survey is especially important now
because of the large amounts of drugs
that their bodies are being subjected to.
The success of all this is very much dep­
endant on two to three more permanent
workers committing themselves for at least
three months to this project. So the
group requests interested people to come
and work with them. The group also in­
vites ideas and suggestions from interest­
ed people. If interested, write to:

SURAKSHA
A—73 SANT KANWAR RAM NAGAR
BHOPAL 462 018.

■e

I

Support the call by KSSP for a
Global boycott of all products of Union Carbide
by Environment and Consumer Groups
with immediate effect.
For more information and details on campaign, please write to:
KSSP -

AIRPLAN

In May, 1985, representatives from
environment groups fran across the world,
including India, met at Eerbeek, a village
in Holland. The subjects of concern were
the growing menace of AIR POLLUTION,
particularly Acid Rain and the issues
raised by Bhopal.
Out of this meeting grew a new global
network linking environmental groups
concerned about these issues. AIRPLAN,
as this network is called, coordinates
international campaigns and is a forum
for exchange of information and action
plans <
AIRPLAN has been around tor a very short
while but has already demonstrated the
potertial of such a network. Recently,
an appeal sent out by it resulted in
international pressure being applied on
the government of an East European couhtxy
to free two environmentalists who had been
jailed for raising ecological issues. In
order to maintain a regular channel for
communication and information exchange,
AIRPLAN publishes a bimonthly newsletter,
two issues of which have already cane out.
AIRPLAN welcomes interested groups to
join and strengthen its network.
Their address:
PO BOX 5627
1007 AP. Amsterdam
The Netherlands.

AIR POLLUTION ACTION NETWORK

A writ petition on the issue of the
right to know has Deen filed recently in
the Supreme Court of India by the environ­
mental action group, Kalpavriksh. This
petition is an intervention in the ongo­
ing case against the Sriram Foods and
Fertilizers Company which was responsible
for the Oleum gas leak in Delhi, on the
first anniversary of Bhopal, which
resulted in the death of one person and
injuries to many others.
Kalpavriksh had earlier intervened in
the case, pleading that the plant be shut
down and relocated. As readers might
recall, the Supreme Court had then ruled
that the plant could reopen subject to
its management meeting certain conditions,
prominent amor
which is the one which
holds the top management personally res­
ponsible for
in th-?
jev^nt qf future accidents.
Hie right to knot
ion argues tnat
Citizens have the right to be informed
about the nature of the dangers posed
to them by hazardous ndustries. The
petition is due for hearing later this
year.

Kerala Sastra Sahitya Parishad,
Parishad Bahvan,
Trivandrum 695037
Kerala, South India.

•3

'FAITH WITHOUT FOUNDATION

the Union Carbide factory in Bhopal
collapsed recently. The works
manager, Mr. Mukund; and the supervisor of the MIC plant,
S*P.
Choudhary, were heard to comment
during their spot visit
"Apparen­
tly, the wall haa no foundation.
Incidentally, this wall was part of
safety system No.5 during ‘Operation
Faith1.

FIVE

Quacks have a field day
Every gas affected person in Bhopal must have
visited a private medical practitioner at
some point in time over the past year and a
half. Every private medical practitioner
must have treated anywhere between 2,000 and
10,000
gas affected patients during this
period. Indeed,this group of "businessmen"
could not have had things better - the boom
in their trade stands in stark contrast to
the gloom and depression pervading every
other economic activity in the area.
In normal times, the present period of the
year is referred to as the "slack season"
by these private practitioners. But these
are not normal times - the stream of patients
does not end, the ‘shops* stay open till late
in the night. Clearly, the potential of
these private doctors to do .good or cause
harm to their patients is phenomena?.., The
question is - how safe are the lives of the
thousands of gas affected people in the
hands of these 200 odd self-professed medicos?

The first thing one notices while visiting
a private doctor in the gas affected areas
of Bhopal is his sign board. Often oversized,
it proclaims the doctor to be a specialist
in a variety of areas of medical knowledge.
One sign board, for instance, advertises its
owner as a specialist in medicine, surgery,
gynaecology, paediatrics and sex ■problems.
Seme sign boards mention the degrees the
"doctor" has acquired. These are usually
a curious mixture of unevenly spaced letters
amenable to a variety of interpretation U.V.P., V.V.P., M.I.A.M.S., M.A.M.S. etc.
On a rough estimate, eight out of every ten
private doctors have received no formal train­
ing in medicine. Their medical qualifications
usually comprise an apprenticeship with an­
other private doctor, coupled with lessons
received from correspondence courses offered
by ubiquitous "institutes" characterised by
their anonymity and dubious reputations.
Many doctors take such correspondence courses
simultaneously in more than one system of
medicine. Thus, it is not rare to meet a
private doctor who claims to treat his pa­
tients by the allopathic, homoeopathic, ayur­
vedic and Unani systems. As one doctor
interviewed put it, "We try different systems
and see which one fits - my patient must find
relief." The treatment is, by and large,
oriented to provide instant relief. "People
are workers here", one doctor explained,"they
have to be fit for work, so they want quick
relief lest they lose their wages."

SIX

Talking to seme of these private doctors,
one picks up very interesting bits of
information. One learns, for instance,
that Sodium Thiosulphate is a drug from .
the U.S. and is not of much use in India
because the blood circulation, the pulse
rate and breathing rates of Indians are
different from those of people in the U.S.
One also learns that the outermost layer
of the eye, contrary to what class nine
biology students are taught in schools,
is called the Retina. One also encounters
a host of very interesting theories which
attempt to explain the effect of the tox­
ins in the body. One such theory is,that
the gas has produced"heat in the body"
I
which cannot btackled by ordinary medi­
cines,. since the gas has interfered with
the formation of pancreatic juices and
saliva, causing problems of digestion.

.ptjivatfe-.doctors' per tir.ont :■
:s±itiuat±on.

the.: total liealUr:-bascis.:They:-:are in:- a

:pdsitloA- to do :so: since :many :h'av* :b6eh::in::::::<
;some:of:fcbRi!a::obS0rv^tions:::-:->::-::-::.:.:.-.-.-.:@:Wh.iie.:..the:ncimber:Eif:petlEntA:<is<etil:i:::::$:
:
consider,thio, there has ■ been- a 50 ' per
< cent: fall: in. :the: past year. ::-0na<-reasbn< \ :
: :is.:.tb.at :Jnany.-:ga&: vic;tiros:-:bAVe .:resiq»ied.
to their suffering / : ■

patient J who Visited, their clinics only
i ... once: a-month ^before: the ,ghb :<Hsaster-now
•••■■■■■- do :ea :oncE-:-oir >qven<twiee: everyzweek <
A., large iiurnber:o£ patients have-be.cn.'--.: ^-i
• p?: :&uf f Bring without: respite::evdr:-:sloiie the.:
::::::q«::leak::and-:despite:tbe:treet»eht:::-::::::'
: desplte:;.thB<;treatment- -rece±yed::f rcmthe:rirb.priyathfmedioaspaDdrgOVernitent/aJ-inics.: :

Moro:-tban: half:-.tbe patlentsr-wha :come to -• •
:their-: clinic?: have. symptams:-:directiy •
related to gas exposure
:::A:DiseaseBiwhlcb:-.were: :prev!eilent::eai?j.:ier<now
:.”..qccur: more: frequentl'y. ahd- «ith-.':intensxtY.

The-: variety ::.and :natui:e-' Of: symntems : is <
.baffling.; They, include breatblaSrSnt?^;
gastric disorders,loss of appetite,
^rr/fatigue^weakness^bodyi^ehes^diz-zihess-,
abdominal pain /headache,menstrual
irregularities ,lmpotsocy,losa <?£ vision^buming senSatlort in- the eyes,
: : :-: :p:aln :dwlng :dnterco.urse, aiixiety ,:. : : :
>inaqmhia,headache 'and chest-pain-'

According to another theory, "MIC affected
patients need hard drugs, potent drugs,
drugs which are costly. Only then can they
get better."
These beliefs, coupled with the hard-sell
tactics of big drug companies (smooth
talking medical representatives and styl­
ishly printed literature which invariably
adorns the walls of the clinics) have re­
sulted in utter irrational and dangerous
"therapy". Antibiotics are prescribed
at the first signs of cough, fever or
boils. Rarely are patients prescribed
the full course? where they are., patients
discontinue use half way through the
course, rendering themselves more vulner­
able to f< ~ther infection's, Injections,
the ultimate panacea in the eyes of many
patients, are re:-.?ily given by the doctors
st® patients
money to spend on these
.'"miracle" drugs. Ar other f r/ourite is
steroids (which rovide a 'sense of wellbeing" though they impair the natural
immunity system of the body). Tonics,
which, according to one doctor, are pres­
cribed "to give energy to the gas victims",
formulations such as "Protinules",
"Protinex", "Sharkaferrol" and "Ferradol"
and useless drugs such as Kaolin-Pectin
mixture for children with diarrhoea are
also routinely prescribed. Moreover,
drugs such as Phenylbutazone and Oxyphenabu^azone preparations (e.g. Actigesic, Bestophen, Suganril and Reducin)
which have been categorised by the drug
controller of India, as restricted for
use in the treatment of ankylosing spondy­
litis and gouty arthritis (and whose
potent toxic after effects have been
demonstrated by the fact that Ciba Geigy
the principal manufacturers of these drugs is
reported to have recorded 1674 deaths due
to these drugs) are routinely given for
(ibody aches.
The private medical practitioners charge
between Rs. 5/- and Rs. 25/- per patient per
visit. An average household in the gas
affected area would have spent at least
Rs .2,000/- in the last eighteen months on
medicines and consultation fees of these
private doctors. There are many who have
borrowed money for this purpose at rates
of interest sometimes as high as 120%.*
The goverrment run hospitals, on the cont­
rary, charge nothing. The obvious question
is - why do the victims prefer these priv­
ate .doctors to the hospitals run by the
government. There are several reasons,...

(These figures give lie tothe ill^conceived
notions of most goverrment doctors who
maintain that the gas victims are pretending
to be sick as they want compensation).

The government run hospitals and clinics
are open only during the day and in the
early evening, times when people are out
working, while private clinics are open
till late in the night.

The attitudes of the doctors towards
their patients is an impressive blend
of smart salesmanship and a veneer of
professionalism cultivated over several
years of experience and practice. In
sharp contrast, the government doctors
who are too pressed for time do not
spend enough time or give personal att­
ention to their patients. The private
medicos give a patient hearing to each
person and spend considerable time in
clinical examinations. Indeed, the
private doctors score over even the
ICMR researchers and senior government
doctors when asked to provide an oral
list of symptoms presently displayed
by the gas affected people.
The shortage of government doctors means
long queues at the clinics. There are
several other inadequacies in the gov­
ernmental medicare system. As one pri­
vate doctor stated very candidly "The government doctors prescribe
the same medicines as we do, they have
much greater facilities, if they happen
to improve their services, we will be
out of business."

That doctor, like most others operating
in the gas affected bastis of Bhopal,
does not lose sleep over this possibility,
fully aware that such a change in the
governmental attitude is extremely impro­
bable.

SEVEN

In the first issue of 'BHOPAL' which we mailed to you a month
ago, we laid out the objectives of the Bhopal Group for Infor­
mation and Action. We have received a positive response
to
that issue and to the idea of BGIA. Our thanks to all those
who've responded.
In the last month, we've begun the task of collecting material
on Bhopal and setting up the documentation centre. We've also
found a place near the Union Carbide factory to house the cen-

As we mentioned, last time, we see our small group here as a
mere extension ‘of a shared desire of. a' vast community to sus­
tain work on Bhopal and related issues. Moreover, the
task
of documentation, bringing out the newsletter and running and
information service can be sustained only with your
active
support.
At the moment, BGIA requires the fcilowii";. assistance from you?
and we trust you will try your best ■ o help:

■ e

- We need a list of all documents concerning Bhopal which youW
may possess or have access to. This list is vital for the\
building up of the documentation centre.

- We need some equipment and financial assistance. Equipment
includes a typewriter, storage cabinets, stationery and pa­
per.

- We need contributions to keep the newsletter going. We urge
you to
— contribute a minimun of Rs. 24/- a year in advance (Rs 30/for institutions and $ 30/- for foreign groups)j and
— undertake to sell a minimum of five copies of the newsletter on a regular basis at Rs. 2/- a copy.
More than anything else, we value your comments,
and advice.

criticisms

HI5T INDIA^^Q

'BHOPAL* is brought out
by the Bhopal Croup for
Information and Action .

<8 <3 OX. PqS i

d-42 piro'os nagar

BHOPAL

452 018

Articles in this news­
letter may be freely
reproduced»
This issue was produced
by Satinath Sarangi, S,
Ravi. Rajan and Vinod
Raina, with assistance
from NR Mohandas,

c> HA.U V
C/W<OZ)/

MA

77^LD/<.J»,

/V/ Pfi

I

5^/ 2.-37

ISSUE 3

AUGUST 1986

Contributory Price

Rs 2

And now the.rain is after them

A flooded basti in one of the gas-affected areas (left); People crowd
into the only shelter avail able - the front yard of a vegetable
storage depot (Right) courtesy "Nai Dunia" and "Free Press Journal'

The nightmare continues.First the gas,
then an indifferent response from a
corrupt adminJ stration and now
the
worsts rains in this century.Will Bho­
pal’s hibakushas ever live in peace?

On the night of the disaster (December 2/3
1984), KR Deshmukh and YN Singh, security
guards, were on duty inside the UCIL Bhopal
plant. This is how they narrate their
experience.
“Both of us were on night duty from 10 p.m.
to 6 a.m. At 12.30 a.m., during the tea
break, we were in the canteen when gas
started leaking. Some of the people fran
the- MIC Plant were also at the canteen.
Soon the gas started coming out more viol­
ently and the workers tried to control it
by spraying water but when it got out of
control they ran for their lives. The nine
security guards on duty, three of whom were
quite badly exposed by now, were asked by
Mr. Chouhan, the Asstt. Security Officer,
to stay on and do their duty. We were
never told about the toxic materials inside
the plant nor were we given any safety app­
liances like masks. So, not knowing what
to do, we stayed on in a state of helpless­
ness and panic. Around 3.30 a.m., people
frcm Dai Prakash Nagar started caning inside

This account of the disaster and its imm@ci—
iate aftermath was given to us by the two
secuiity guards in the course of a detailed
interview we had with them. Further dis­
cussions with them as well as other security
guards brought out the insecure state of
the security guards of the UCIL Bhopal
plant.
Deshmukh (33) and Singh (32) are two of the
forty-three security guards employed by the
Star Security and Emergency Services (SSES) and
posted at the UCIL Bhopal Plant. The SSES,
owned by Mr. RN Nagu, an ex-inspector Gen­
eral of Police, is an agency that is con.tracted by
several industries in Madhya
Pradesh and is managed from the office in
Mr. Nagu's posh house atop Shyamla Hills
beside the lake.

While the plant was in operation, the
security guards had to work under hazardou^S
conditions. "Since most of us have had our
posts near the plants we have inhaled a lot
of those poisons which used to emit fran

THE INSECURE
SECURITY STAFF
the plant - they were coughing, cooking,
blinded, stumbling, groping and all crying
out for help. We took them to the plant
dispensary, sprinkled water on their faces
and gave them water to drink. Major Mehra,
our Security Officer, told us to mind our
posts and said that one person was enough
to attend to the people who were streaming
in. We refused to go by his orders and
continued helping the people who were now
coming in large numbers and in more acute.
conditions. Some were dying inside the
plant. By 8 O'clock in the morning more
than a thousand people must have come inside’
the plant. We were all very worried about
the welfare of our family members but to
our relief we found when we rushed heme in
the morning that none of our family members
was dead. They were suffering quite badly
and so were we. We were getting breathless
and our eyes were swollen and for the next
two days we just could not report for our
duties at the plant."

TWO

them", they said, "and pain in the chest
was an ailment common to us. Apart fran
small emissions, massive leaks were also
not uncommon SIX MONTHS PRIOR TO THE
DISASTER", said Deshmukh, "While I was on
night duty, gas had leaked around midnight.
There was almost no wind so very little
spread outside the plant but the whole
plant was engulfed in it. Workers fled
fran the plant and people fran Jai Prakash
Nagar came enquiring about the reasons for
the irritating 'mirchi ki dhans’ (smell of
burnt chillies) they were getting. Condi­
tions became better after two hours and
workers returned at 4 O'clock." while all
this was happening, Deshmukh and his co’.leagues PL Gopalan and MC Tiwari, not know­
ing how to respond, hid themselves in the
bathroom behind the security office. Acc­
ording to the security guards, even today
hazardous practices are followed. Last
month, according to the orders of the man­
agement, daily wage labourers were employed
to bum waste napthal lying in the plant.

This went on from 8.30 a.m. to 5 p.m. for
about 10 days till some passengers of a
train passing near the plant who were ex­
posed to the nauseating fumes reported to
Hanumanganj police station about it. Sulphonic acid tanks are kept open leading
to the formation of acrid fumes that aff­
ected the people of Jai Prakash Naaar.
While such hazardous practices were being
carried out almost routinely in this plant,
the security guards were not informed about
the barest essentials of safety practices.
"Only after the gas disaster, the Carbide
management
told us that we should
have put wet clothes over our faces." They
did not have access to any safety equipment
like gas masks and goggles and in the event
of disaster were left to find their own
means of survival.
With such hazardous conditions of work for
the security guards, attention was never
paid towards their medical care either by
^^.he Carbide management or by Mr. Nagu.
"ven basic human considerations were absent
in their attitudes towards the workers.
The salaries of the security workers, who •
could not report for duty because they were
affected by the toxic gases on the night of
the disaster, were deducted for the number
of days they were absent. The three secur­
ity guards who were severely affected while
on duty lost 15 days" salary. Even now
Deshmukh remains absent for 8—10 days in a
month because of the ailments he suffers
due to exposure to the toxic gases and
loses his salary.
The security workers are paid low salaries
and the rise in their pay has not been
commensurate with the rise in prices.
"Since 1975 prices of things have gone up
5 to 6 times, our salaries have gone up
by 2 times only", says Deshmukh who gets
Rs. 600/- (less when there are deductions)
and has to pay Rs. 150/- as rent for his
one-room family accommodation. "And Nagu
Sahab says", adds Singh,"if you can't sup^port your family with the salary we give
you, you are free to leave". Since 1975,
about 60 of the workers have left their
jobs, some who could not support their
families left quietly while others, who
were bold enough to ask for a raise of
salaries, were dismissed. Dismissals have
almost always been without notice and on
the basis of trumped-up charges. Prior to
the gas disaster, SR Sakalya and Shiv Dhyan
Singh,who were identified as "leaders" by
the Carbide management, were dismissed on
concocted charges of "sleeping during duty
hours”. After the gas disaster, three
security guards who were quite vocal,
MP Pathak, Padam Singh and Govind Kurosia
have been dismissed on charges of theft.
Both Deshmukh and Singh were quite sure
that these were just the manageeent's way
of suppressing dissent.

Since the gas disaster, the condition of
the security workers has become much more
precarious. They have had to spend large
sums of money on the medical care of their
family members as well as themselves.

The majority of them have not received
the ex-gratia relief of Rs. 1,500/-'distri­
buted by the MP Government. Absenteeism
due to poor health conditions lead to cuts
in the salary and requests for a sympath­
etic consideration from both the officials
of SSFS as well as- fran the Carbide manage­
ment met with callousness. While employees
of the plant, and contract employees in the
plant canteen have received compensation,
the security workers have not received any.
They are unsure how long they will continue
to be employed - as Mr. Nagu has pointed
out to them, their future was linked to the
future of the UCIL plant, and the UCIL management has 'informed* them that they ar®
not responsible for 'contract workers'.
Almost all of them come from places distant
from Bhopal like Kerala, Bihar, Uttar Prad­
esh and some districts of Madhya Pradesh.
' They have no land to go
back to, , so the
options before them are limited. "We are
never sure-it is possible that tomorrow we
get a letter saying our services are not
required. Where can we go? We have spent
the best years of our life and our bodies
have taken in all these poisons-who will
give us jobs now?" - asked some of the worK >rs.
Tn their desperation the security workers
have tried several means to have their
grievances heard but their experience so
far has been rather disappointing. Ini­
tially they had joined hands with the
Union Carbide Karmachari Sangh (UCKS)
(the recognised trade union of the UCIL
Bhopal employees) and contributed to their
funds, but in the matter of obtaining com­
pensation from the company and getting
alternative jobs from the government, the
UCKS leadership did not take into account
the problems of the security workers. They
have met the Chief Minister and submitted
their grievances at least ten times, only
to be given empty assurances. For the
last two months, they have been members
of the AITUC (the workers* trade union of
CPI) whose leadership has made promises
to them of obtaining permanent government
jobs. While the promises are yet to be
fulfilled some of the workers are consi­
dering militant action to press their
demands.
With their low number, poor economic con­
ditions and faced with a repressive man­
agement, the security workers at UCIL,
Bhopal, have a limited possibility of
overcoming their present state of conti­
nued insecurity.

THREE

Carbide's Fraud
Why is Union Carbide
spending $2 million on a
^rehabilitation project for
twelve people ?

The Bhopal Technical and Vocational Train­
ing Centre stands by the Upper Lake in a
remote part of the town, Lal Ghati, amidst
a mango orchard, surrounded by rich farm­
land. With a large and spacious mansion
as its nucleus - an old country home now
converted to its present use, the Centre
comprises four acres of most beautiful
aspect with a view of the lake that only
the richest homes in Bhopal can command.
Workers and staff dart about the place
looking efficient, in the process of est­
ablishing a yet larger and more efficient
Technical and Vocational Training Centre.

The
Director of the Centre says she
would like the Centre to be like Tagore's
Shantiniketan - a laudable sentiment. But
the more one finds out about the Bhopal
Technical and Vocational Training Centre,
the more intriguing its operation and
activities - and indeed, its very exist­
ence, become. For the financier of this
enterprise is none other than the Union
Carbide Corporation.
Despite its name, the Centre offers nei­
ther technical nor vocational training at
present. Everyday, twelve students are
brought in, six blind and six deaf, to
attend classes in Braille and in sign
language respectively. Their instructors
have been brought in from the Arizona
State University (ASU) which operates
the Centre; every two months new instruc­
tors from ASU fly in as replacement (and
stay at the exclusive Jehan Uuma Palace
Hotel). Training in welding and sewing
will commence at some point for a similar
number of people. The 'latest equipment'
and expertise are being imported, and
everything used at the Centre, down to
the wall charts, is from the US. Experts
and officials frcm ASU fly in and out
constantly; there can be few groups of
twelve students who are pampered quite as
much.

FOUR

"The technology and know-how for training
in these areas (i.e.
Braille, sign
language, welding) is inadequate in India",
said an ASU professor, a liaison officer
in the project. "This is a giant leap for
Bhopal into the 20th century", he proclaim­
ed. When asked to explain the strikingly
modest number of participants, he became
defensive - "This is only a prototype",
he said, “it represents a beginning."

Admitting that Carbide was financing the
$ 2 million project, he said that Carbide
and ASU both were anxious to avoid public­
ity.
One instructor frcm ASU candidly
told us -"We have been asked to keep a low
profile." That Union Carbide, hardly a
spendthrift on public welfare, should sudd­
enly be coy and furtive about its philanthropy is strange enough. But more intri­
guing still is the fact that hardly any of
the twelve trainees are. gas victims. If
Carbide was funding this, surely they would
admit only those injured in the gas leak
"But how can you tell who is a gas victim?"
responded the Director, who narrowly missed
Congress(I) nomination to the Rajya Sabha
this year -"everybody is claiming to be a
gas vic tim."
The mystery was cleared’up when highly placed
sources informea us that Union Carbide was
reportedly trumpeting its munificence to
the Bhopal public in corporate journals in
the US. If brought under public scrutiny
here, the farcical nature of its relief '
scheme would become apparent. The story of
a $ 2 million charitable project would pre­
sumably do much to appease corporate liber­
als in the US, and would improve Carbide’s
reputation there - "there", of course,being
the only place it matters.

What is disturbing is the high-level co­
operation this project has obtained frcm
the Central Government. "Ay. their papers,
including their foreign exchange remittance
permits, were in order - we couldn’t touch
them”, said one state administrative officer.
It is imperative that Union Carbide is not
permitted to make capital of this masquerade.

—wwf——i
In the din following the judgement of John Keenan
returning the case to India,many of the several
manoeuvers in the US courts since then have
escaped public notice.Following,in chronological
order,are some of the more important events.
May 12, 1986; Judge John F. Keenan of the
Federal District Court for the Southern
District of New York finally ruled on the
forum non-conveniens motion made by Union
Carbide Corporation in July 1985. Keenan's
decision was to return the case to India,
^with three important conditions:

"1. Union Carbide shall consent to sub­
mit to the jurisdiction of the
courts of India, and shall continue
to waive defenses based upon the
statute of limitations;
"2. Union Carbide shall agree to satisfy
any judgment rendered by an Indian
court, and if applicable, upheld by
an appellate court in that country,
where such judgment and affirmance
comport with the minimal requirements
of due process;

"3. Union Carbide shall be subject to
discovery under the model of the
United States Federal Rules of
Civil Procedure after appropriate
demand by plaintiffs."

May 20, 1986: Hearing in Chambers. Keenan
entertained oral arguments and notions re­
lating to his May 12th forum ruling.

Attempts at reaching on out-of-court set­
tlement did not end with the rejection in
March by the Indian government of a $350
million settlement offer. In fact, with
the Keenan decision on forum, it became
even more important for the .individual
plaintiff attorneys to attempt such a
settlement, as they stand to lose both
.their clients and their contingency fees
if the case moves to India. On May 20th
Stanley Chesley and F. Lee Bailey (indivi­
dual members of the Plaintiffs’ Executive
Committee) made oral arguments requesting
that the Court "conduct a hearing to de­
termine whether the settlement proposed
for these plaintiffs is fair and reason­
able."

At this hearing. Carbide's attorney.
Bud Holman, raised three issues. He
requested that the period for Carbide
to respond to the conditions in Keenan's
May 12th Order be extended to as many as
60 days, only after which the appeal
period would begin. Holman also asked
that two changes be made in the condi­
tions; that the words "against it" be
inserted in the second condition so that
it would read "Union Carbide shall agree
to satisfy any judgement rendered against
it by an Indian court..." to insure that
it refers to Union Carbide and not to
Union Carbide India Limited.

Holman in addition requested Keenan to
amend the third condition which requires
Carbide to "be subject to discovery under
the model of the United States Federal
Rules of Civil Procedure..." Holman
argued that Keenan has authority to dem­
and from the Indian Government that it
submit to similar rules of discovery—
an argument that Keenan had already add­
ressed in his May 12th ruling in these
words: "While the Court feels that it
would be fair to bind the plaintiffs to
American discovery rules, too, it has no
authority to do so." (emphasis added).

May 21, 1986: The individual plaintiff
attorneys entered a Motion for a Fair­
ness Hearing requesting in written form
that the court consider the following
questions in determining whether the
settlement proposed is "fair and reason­
able:"

"A. To what extent have the victims
been informed as to what amounts
of money they would receive indi­
vidually if the present offer
were accepted?
"B. Do these victims wish to renounce
the retainers they have signed
with their American counsel, or
do they wish American counsel to
continue to negotiate on their
behalf even if the case is trans­
ferredi to India?

FIVE

MEETING

Yet Another Survey
A state cabinet sub-committee of the
MP government decided recently to
conduct a medical check-up for each of
the five lakh odd people who have filed
compensation claims.According to "The
Hindustan Times" which reported this on
July 26,the chief minister has said that
such a medical record (which would include
X-rays and blood and other tests) would
be necessary for determning the amount
of compensation to be paid to each gas
victim.
The proposal,however,is shrouded with
controversy.The Claims-and Compensation
Secretariat is reportedly insisting
that the previous surveys be studied
in
order to avoid the mistakes that
were committed while concieving and
conducting them.The Chief Medical Officer
feels that such an exercise would be a
wasLp of '.time.
The survey form is believed to be over
eleven pages long,of which nine are to
be filled inby the examining doctor
and the rest by a CCS surveyer.Civen
the government's track record in
implementing projects and the logistical
enormity of the present enterprise,the
survey might be the major preoccupation
of government departments for a long time.
Meanwhile,one wonders what happened
to the previous
surveys,including
the much talked about ICMR epidemiological
survey.If they are
as bad as to
neccessiate another major survey,what is
the guarantee that the present one,
more ambitious than its predecessors,
would be successful?

Carbide to shift
Bombay unit

BOMBAY, Aug 4 (UNI):
Giving in to mounting public
pressure after the Bhopal dis­
aster, the Union Carbide com­
pany has expressed willingness
to shift its chemical plant else­
where from Chembur In north­
east Bombay.

^BHoEAETTT’brought out
by the Bhopal Group for
Information: .and. : .Action
'• d-42 F1RDOS ' NAGAR v

, BHOPAL. : 462 018.

Article? in this news-.
.letter-..'roay' be: • freely •

reproduced.
ithi’s -iss.ue • was/.prbduced
by- Arvirid Rajgopal; • .
Satinath Sarangi, Vinod
Raina.arid S. Ravi Rajan
with assistance from.
NR Mohandas .ShM*

AT

WARDHA

==--=-.=
A meeting was held at Sevagram, Wardha,
fretn July 27 to July 29, to consider
the need and feasibility of carrying
out a comprehensive epidemiological
(nature and extent of disease) surveyof the gas affected areas of Bhopal,

The participants included members from
Drug Action Forum (West Bengal), Lav yers
Collective (Bombay), Medico Friend
Circle, Bhopal Group for Information
and Action and many individuals.

A tentative evaluation of existing sur­
veys suggested that there was need f sr
a more thorough study of the gas-aff:cted
population to provide a basis for ccnpensation, .medical relief and rehabilit­
ation. It was decided that, after a
rigorous critique of all previous surve-^k
and a review of existing literature on ”
MIC and its break-down products, a study
design should be prepared in consultatinn
with all known experts in the field. The
Government of India would then be urged to
carry out such a survey with the parti­
cipation of non—governmental organisa­
tions. To demonstrate the feasibility
of the
design, a pilot study would be
conducted in one of the gas affected
areas.
The meeting also arrived at the consensus
that a National Convention of activists,
environmentalists and scientists should
be held to mobilize action on the larger
issues thrown up by the Bhopal disaster.
In view of the announced (see page )
medical survey by the Government, the
proposed design for an epidemiological
survey assumes added urgency.

NOV/DEC 1986

ISSUE

6 6: 7

Contributory Price Rs 5/-

SAZDABAOT'T^rC^j'W^i^rSre
UCIL worker killed by Phosegene in .981;
Umrao Dulha Bagh)
On December 3, ’84 I arrived at Bhopal by
the Lucknow-Bombay Express from Kanpur.
The train stopped at the platform at 1.30
m.
a.
I started coughing, as soon as I got
off the train. The platform was deserted.
My two children were with me. One was 5
and the other 4. The elder was called
Arshad Mohammed Khan and the younger one
Shoeb Mohammed Khan. We were all coughing,
after which I doA't remember anything.
Someone carried me to the hospital from
where I was later dropped at my brother's house. My children were
abandoned at the piatfom,, At 7 a.mr
askad for my children. Then my
brother went to the station to look tor thpm and brought them back.
At
9
a.m. my elder son Arshad Mohammed Khan expired. After my husband died
I
got no compensation. My in-laws have filed ft court case and they are
asking for the money. I have got nothing.
I. still have not got the
1
1500 rupees. My in-laws sent me out of the house after my husband died.
My husband died on December 25, '81. This also happened because of the
manager's mistake. His duty time was over and he was asked to open a
valve. The valve had not been opened or even touched for three years,
and there was phosegene gas inside. My husband asked him three times
if there was gas inside. Three times -the manager said, No. After the
valve leaked, my husband was kept in the factory dispensary, and later
I have nbt got anything yet.
taken to the hospital.

GAURI SHANKAR (23, Unemployed; Indira Nagar)
lEver since I was hit by the gas I have had breathing trouble
'all the time. I can't ride my cycle.
I used to earn 50 rupees
daily but now even a cup of tea is a problem.
Before the gas
i
I had some tools with me and I was thinking of opening a work'shop. But after the gas I was forced to sell some and mortgage
'the rest to get medicines.
I am not very old, I am a youth.
I
think that.if I get a good .doctor, I will get better. Carbide
should be punished. Carbide is a mass-murderer, which has takeiw)
thousands of lives, thousands of women, thousands of cattle and
birds. Birds no longer flew in the sky. In my heart I feel, like setting
Carbide on fire, blowing it up. When I was admitted in the Indore hospi­
tal, I used to read poems about Union Carbide and wrote some myself.
RADHA BAI (50, Beedi-making/housework; Jaiprakash Nagar)

My husband is dead.. He died in the month of 'Chait' on poornira.
He was then under treatment at the DIG Bungalow hospital, he
got some medicines fran there and took them and then he said,
It is Chaiti Punno* so I will take a bath. He pulled up one
bucket of water (from the well) and while pulling the second,
he fell into the well, he had become giddy. Now I make bidis.
The government people said, I could not get relief for his
death was not due to the gas.

*• Festival on the full moon night of the Chait month (March-April) .
TWO

THREE

JAGADISH (35, Worker in Straw Products; Shaktinagar)
The government doctors, they just chased me out of there. When I was
admitted to Hamidia hospital, I asked the doctor to.keep me there. My
I ,
condition was very bad. The'doctor
The doctor said, You get out right now.
In the afternoon the doctor said,
thought I would wait and try again
I don't want to talk to you.
Go now, you have been discharged.

ABID ALI RIZWI (32, Union Official; Chandbad)
I am the Vice-president of the Textile Mill
’ '
The main problem of the. workers
Workers Union.
after the gas incident is lack of stamina. They
have to stand at_ she machines for eight hours
non-stop,>. Now their capacity to do so is fin­
ished. :In one or two hours, they are done for.
If they work for two to four
They need rest
Absenteeism
days, they have to go on leave
has greatly increased now, and no division has
all its workers present.

e
NARAIN I BAI (35, Housework; Shaktinagar)
Before the
We have no money and no job to earn our livelihood.
Bow I can't do that. After-;,.
leak, I used to work as a labourer.
I
get’rt
leak,
I
have
worked
only
for
eight
or
ten
days
the gas
I feel, *
I feel dizzy, my head aches. When I rest.
breathless
When
I
get
back
to
work,
I
feel
sick
again.
slightly better,

— MAHESH (10, class 3 student; JP Nagar)

I lost many of my friends during the gas leak
My friend Goonja died. Most of my playmates
are no more.
I get out of breath and cannot
run when I play.

RAJESH TIWARI (28, Unemployed; Kainchi Chhola)
Instead of helping the people, the government
is putting people on the dole.
But people have
■ their rights. After the gas I could see that
no political party supports the people,
I took
part in processions and sit-ins, r:
so that gas
victims should get what they are entitled^to.
But they have not got anything. Carbide should
-^definitely be punished because the dreadful in<cident that occurred here should
‘
not happen
again elsewhere.
KANTH BAHADUR (35, Unemployed; Shaktinagar)
I came here from Nepal and immediately after that the gas
leak occurred. The gas had a very adverse effect on meo
I was in the Hamidia Hospital for eight days and in the
TB Hospital for a full month. I lost my job after that,

*

GAFOORAN BEE

(60, Housework; Indira Nagar)

I feel as if there is a fire in my head and it
, seems as though the same gas is leaking.
®
/ I cough it feels as though it is the gas again.
/ What do I know about the case?
I can neither
■>
read nor write. I have got my claim form filled.
But I don't know how much it asks for. who . news
when we will get the compensation?

KAMLA BAI (35, Bidimaking/Houseworl
Indira Nagar)

I
don't feel as hungry as I used tc
before the gas.
I can't eat more
than two rotis. Many things don’t
taste good now. My mouth tastes
bad.
dARl SHANKAR (40, Street Magician; Vijay Nagar)
Before the gas leak I used to perform magic on the streets. Now
I
can't do it. I get breathless. I speak for some time and
leaves me breathless and my ’chest pains.
I went to find work
at the Chandbad Rehabilitation Centre but they told me that 7.
was 'overage'.

/
f
'

1
A

SHANKAR LAL (45, Ex-UCIL employee; Kainchi Chhola)
I
used to work at the incinerator in Carbide.
I used to
get about 1200 rupees a month. After being laid off from
Carbide, I got a job a year later (January '86) in the
Irrigation Department. I now get 430 rupees a month.
This does not meet my household expenses.
Because of
illness I often go late to my new job, and I get shouted
at. I have to go to the hospital often. At the most I can work for 10
or 15 days a month. Then I fall sick and I go without pay.
TULSA BAI

(55, Housework; Vijaynagar)

After the gas leak, when I went to the village, people
said, How dark you have become, and how weak. Even now
I
remember the gas leak. Sometimes I completely forget
about it. And sometimes. it comes back to my heart.
I
had been on a procession We went to break the gates of Carbide
break the gates and voice our demands - to ask. Why have you caused the
gas leak and brought us pain? But the police did not let us go. The
police beat us up.

-------------- !RAMESH (24, Cycle Mechanic; JP Nagar)
I
Five to six months after the leak, government officials
came and collected applications for loans,
in March '86
Wv/te
they told me that my loan had been sanctioned. Then thev
I ■
'asked me to get a photograph of myself and a'no dues'
I
aS' ~ i | certificate..
.1 got. no dues certificates fran 22 banks
Day after day, hungry and thirsty, I went fran bank to bank. For thra/
months I did only this.
unree
SIX

SEVEN

___

__ .

, ........ .

TU^SH~(87nasT“Tistudent; Shaktinagar)
There is very little to eat. Very little
to wear.
Papa just doesn’t get a ion he has no permanent job.
Before tne leak,
he used to work on a boring machine. Now
he cannot work on that machine.
Carbide .must be punished. Take them to
the police station, then hit them, and
then jail them - those Carbide fellows.

I can’t play like X used to before the gas
leak. Now X am weak. My hands and legs
ache when I run.
I get breathless soon.
’If I run I fall down immediately.

JAMEEL KHAN (35, Saw Mill Worker; Rajgarh Colony)
I work as a helper at the Saw Machine.
I have been doing
since childhood. After the leak I find it difficult to work
mid
stand
the
saw
dust,
but
now it has become
Previously I c<
unbearable and it makes me cough. I get 400 rupees a month.
;
I
earned
600
rupees
including.
overtime.
Before the lea)
SUMATI BAI (50, Assistant in Aanganwadi*; Shaktinagar)
I participated in a number of protest marches. We had
gone on a procession to Kamala Park and there the police
beat us all up badly. They hit me on my hand, and till
today, a full year later, I feel the pain - I can't even
lift my hand. I can’t do any work with this hand.
I
can't lift any loads.
I can't fill vessels with water and carry them.

We felt we ought to punish Carbide by ourselves, that is why I partici­
pated in the procession - otherwise why should we go? We benefitted
from the protest. We got grain.
* Child-care centre.

SAYEEDAN BEE (60, Housework; Indira Nagar)
After the gas everything has been razed to the ground.
If we had stayed
for two more minutes (during the gas) we would all have been wiped out.
I escaped death, but what am I good for new? I have become half-dead.
compensation from Carbide? I know nothing about it.

GOPI LAL (40, Cartpuller; Rajnagar Colony)
I push loaded carts.
I am breathless most of the time.
I go to far off places pushing my cart-loads. My
earnings have been reduced by half. There are lots of
carts these days. Everyone seems to own a cart bought
through bank loan. There weren't so many carts in the
days before the leak and business used to be good. Now
I can't find any work.

EIGHT

JjKANTI BAI (30, Housework; Vijay Nagar)
yl have five children. All of them suffer from ailments.
?related to the gas leak. The youngest, Somnath, is
.^suffering the most. He is two years old. He was born
3 two days before the gas leak. He is always out of breath.
—The medicines just ease his pain for two days after which
it comes back again. I admitted him in Hamidia Hospital. There the
doctors said he had TB. He was given three injections a day for eight
days and then he was discharged. After some time he became just as
sick again. Before the gas no one in my family had suffered ;frcm TB.
BARJOR SINGH (45, Blacksmith; Kabad Khana)

At the time of the gas I was at home. All at once
it hit us. We looked outside. Everything was
We stayed home out of fear.
If we had
dark.
stayed outside for two or three minutes, we would
I
have
trouble,
working.
My
all have died. Now
hands and legs have no life in them. My hands
I experience numbness and
\have become scaly.
singling. My hands and legs have become black
I have no property. What I get is what I beat

BHANWAR LAL (46, Worker at Straw
Products; JP Nagar)
The amount of work I used to do
before the leak I can never do
again. Now I have reached such astate that I feel like
I have six
But I am helpless
giving it all up and sitting at home.
children, and I am the only earner.
SHAMMU KHAN (50, Cycle shop owner; Indira Nagar)

People are still going around in circles for their 1500
Y'ij rupees relief money. The assets of Carbide are still
tact. Neither is the government taking it over, nor
it using Carbide’s assets to help the poor victims.
The people are not quiet, it’s just that they are
being lulled. Like when a child cries, one soothes
it by diverting its attention saying a tiger is
coming or a goat is coming. Neither does the tiger
come nor does the goat. And the child eventually
sleeps. The government is working in a similar
fashion. We will have to cry out all over again.
RAEESA BEE (35, Housework/knitting machine work; Bapna Colony)
I used to go to the rehabilitation centre to do work. After
three months of work in the.centre, they said, You people
will have to repay in in­
will get loans for machines. You
1
stalments.
Because of the gas,
gas my condition is bad, I cannot
make 350 ruoees a month to pay the instalments. They had
taken the responsibility of sending somebody to teach me, but
nobody came.
In 3 months, I could not learn properly at the
centre with 12 women working on one machine.

TEN

SAGEERA BEE

•

(30, Housework; Rajgarh Colony)

? have spent nearly 8000 rupees on private treatment.
I
' na<^ tO Dorrow this money at 25% a month interest. I have
'3 sold my goats. Our son has become very weak. Day by day
his condition bee ernes worse. He is 14 months old.
SHANTI SAI (26, employed in rehabilitation centre; Shaktinagar)

I work at a sewing centre. In a month, we get jobs for 20 days,
sometimes for 15 days and at other times for 12; never do we get
employed for a full month. My monthly wages are 250 rupees sometimes,
200
pees at others and at times 275 rupees. Never do we get more
than
If I work for a full day, I experience pain in the hands
axid legs, and a burning sensation in the throat and chest pain.

MAMTA (6, Housework; Shaktinagar)
They distribute bread at the aangai
us go.
I like bread. We don’t ge
■ ~j’ith at the aanganwadi. We are tai
i RAMCHARAN

(20, class 11 student; Indira Nagar)

! My health was good before the leak. Ever since the leak,
I feel giddy, my eyes have become weak and I can't read
,
well. This year 50% of my class has failed. Before the
gas leak we had an 80% pass percentage and our school
had a good record. My condition worsens day by day. Pre■>'..viously we never realised that this factory would be so
i
. A
—- lethal and dangerous. After the leak everyone knows. We
have seen this factory around for ages but we were never told what
it manufactured.

■

<

PRADEEP (12, class 6 student; Kainchi Chhola)
It is Carbide's fault that the poison escaped. The
big-big officers in Carbide should be punished. They,
should be hung.

SUNIL KUMAR (14, class 9' student; JP Nagar)

Just as people were killed by the gas, something
similar should be done to punish Carbide.
This punishment cannot be given by the Bhopal Court
Two
years have passed and Carbide and the Government are
still arguing, but they are doing nothing.
I think if the owner
(of Carbide) were here, I would slay him - and it is not just me
but the whole colony that thinks so. Carbide has destroyed my family­
seven people, my mother, father, three sisters and two. brothers died.
Many of my friends also died.

ELEVEN

TWO

YEARS

AFTER

Two years ago, the whole world held its breath at the horror that Union Carbide's
satanic factory had caused, through UC's merciless and hell-bent quest for pro­
fits. For years, people had warned of the madness' of pouring poisons into our
environment in the name of prosperity. Carbide, through its relentless cost­
cutting and its systematically hazardous management of ultra-hazardous materials,
has taken a short-cut to the devastation that we dreaded. Two years have passed.
Neither the death of thousands nor the misery and suffering of lakhs has made
Carbide flinch from its attitude to ■’business as usual'. On the contrary, it
has done everything to impede justice to the people of Bhopal. But Carbide will
not go unpunished.
The dimensions of the tragedy are heightened by the scandals that surround every
aspect of it. The government’s relief and rehabilitation plans still remain so
many castles in the air. Fully two years after the event the government has
become, if possible, even more fanatical about secrecy than it ever was. Com­
pounded with Carbide’s criminal refusal to divulge any information on the nature
of the gases, the victims are again the same. With all the. medical studies com­
missioned into effects of the gas (nearly 2'0 by the ICMR alone) , the treatment
remains practically the same as it was in the first week of the disaster. The»
ICMR studies including the epidemiological survey are still ,’Confidential'.

We wanted to review all aspects of the disaster in this issue. The question
was - how? With unmitigated hostility and suspicion from government officials
towards BGIA, collecting information continues to be hazardous. We wrote let­
ters to all the chief officials in charge of gas relief with a detailed"list
of questions on government action and planning. Not one responded. We decided
therefore, to let the gas victims speak for themselves - this would be the-.b^st
way of conveying the nature of their suffering, the most revealing and compre­
hensive means of understanding their condition,.
’ /*■?■
Physical suffering is unabated-,.- the medical treatment, such as it is, has had
little effect.' Perhaps rj^tSqfe^tating is their anguish at their helplessness.
Their chief source of piadjeC.work, their ability to provide for themsel­
ves, has been taken away^rortr^tB®4. But their voices are as eloquent as ever.
Any hope for proper and
relief and compensation seems possible only
as a result of such eloquew^glfruggle. But how long can a deprived and debilitated
community struggle? Gradually, hope is likely to give way to despair. When
that happens, the industry, government and the general public shall- write 'finiX^
to Bhopal and march on relentlessly till another one is let loose. We must not’
let that happen.

•BHOPAL' is brought out
by the Bhopal Group for
Information and Action.
D-42 FIRDOS NAGAR
BHOPAL 462 018
This issue was produced
by Goutam Banerjee,Vinod
Raina, S Ravi Rajan,
Arvind Rajagopal, Satinath Sarangi, and MK
Srinivasan with assist­
ance from NR Mohandas.

BOOK-POST

Kw AUj
(577 TrtV;

For private circulation

only

ISSUE 2
JULY 1986
-sContributary Price. Rs 2

The

Deaths

Continue
Death still stalks the shanties ox
:bpal
twenty months after the disaster wreaked
by Union Carbide.
Poisoned by a killer
multinational, neglected by the government,
ignored by the media,
the gas victims
continue to suffer from illnesses that are
yet to be properly diagnosed,
let alone
cured. And they continue to die.
Like
Moolchand of Patel Nagar, Bhopal.

On 2 September 1985, in a last desperate
bid to save his life, a pale and emaciated
Moolchand went, once again, to the govern­

The
Story ■

Moolchand
Moolchand died at 5.15 p.m. on -14 fesgs
1986, on bed No. 17 of the MIC Ward, nine
months after admission to the Hamidia
Hospital. His tragic tale is the tale of
many many more who wait, spent and dispi­
rited, for a slow, troubled death.
Moolchand came to Bhopal in 1950 in the
tumultuous aftermath of the partition of
the country. A Sindhi migrant from Paki­
stan, Moolchand had little to survive on
when he started life anew at Bhopal. He
eked out a living as a scrap merchant,
carrying his load of waste around the city
on a bicycle. The only one to help him
was his son,. Vasudev. And they did manage
to survive and sustain their small family
through the years. Until, the night of
2nd December, 1984.

That fateful night, Moolchand awoke with
a start to find his room thick with acrid,
irritating fumes of gas. He .was afraid,
and alone, for his family had fled. So he
too ran, like thousands of others, to save
his life. And he survived. But just.
The toxins had ravaged his body, so much he
was unable to work. His business suffered.
He could not breathe properly, his body
was wracked by coughing, he lost his appe­
tite, he couldn't see well. And then be­
gan his frustrating search for a cure, or
even for seme relief frem suffering.
Each morning he joined the queues at the
government clinics with his wife Premvati,
who was similarly affected. He took drugs
and drugs and more drugs. But to little
avail. There was little respite frem his
painful condition. In despair he went to
private doctors. His savings were all
gone. He had to sell off his wife's
jewels to pay for the expensive medicines
the doctors prescribed. Again, to little
effect, because he continued to suffer and
his condition deteriorated.

TWO

ment polyclinic at Bharat Talkies.

He

shuttled for days between the clinic and
Hamidia Hospital. Until, on 9 September
1985, he was admitted to the MIC ward.
He still complained of breathlessness,
cough with expectoration, muscular weak­
ness in the legs and generalised weakness.
Clinical and pathological examinations
ruled out tuberculosis but pointed to
bilateral crepitation. The diagnosis:
"MIC-induced lung diseases”I
His wife, herself suffering, was his
constant companion at the hospital. She
made the daily four-kilometre trip from
their home in' Patel Nagar to the hospital
with their son. Moolchand was prescribed
pain-killers, broncho-dilators, steroids..
... "He used to take almost half a kilo­
gram of medicines everyday", reminisces
another patient in the ward.

Then one day Moolchand slipped and fell
in the bathroom. (This is not uncommon
in government hospitals where reeking
toilets and bathrooms are covered with
the slippery slime of dirt and excreta) .
He fractured his thigh bone. The fract­
ure was improperly set. As a result,
one leg was an inch shorter than the
other when the cast was removed. Already
weak, Moolchand was now further immobil­
ised , confined to his hospital bed. He
lay gasping for six months, his family
driven to the brink of deprivation. Till
he finally lost the will to live. As a
final act of resignation and despair, he
stopped eating just prior to his death.
He died in the evening of 14 July, 1986.
Many, like Moolchand, continue to die.
In the absence of a meaningful and ade­
quate system for monitoring the condi­
tions of victims, many of these deaths
go unreported. Says Professor Heeresh
Chandra, Director of the Medico-legal
Institute, under whose charge the autopsy
of Moolchand's body was carried out,
"Many of the gas victims are dying, yet
very few dead bodies are brought in for
autopsy." Despite many suggestions, the
government has not made autopsy compul­
sory . Such an emission attains crucial
significance in the context of the opin­
ion expressed by Michael Ciresi, the
lawyer retained by the Government of
India, that the nexus between exposure
to gas and subsequent deaths has to be
established beyond reasonable doubt if
damages for death are to be claimed
from Union Carbide Corporation.

The complete absence of such initiative was
,made ,clear in an interview with
the Director of Claims, Mr. Khare. We
asked how Moolchand's family could file a
claun for compensation. Sitting in his
?
tucked away in a maze of government
buildings, seven kilometres away from
Patel Nagar, Mr. Khare confessed, "We
not make any attempts to inform neople
tliat they can still file claims." When
pressed, he tried to justify this glaring
omission"by saying — "somehow seme people
Such wilful neglect condemns the gas
victims to prolonged suffering and death,
even as the death dealing, multinational
goes unscathed.

TOXIC

EMISSIONS

CONTINUE

Shortly before noon on 19th June, 1986,
clouds of black smoke were visible at
the UC plant in Bhopal. Investigations
by BGIA revealed a raging fire next to
the administrative building inside the
plant. On enquiry, security guards said
that plastic cans containing toxic chemi­
cals were being destroyed. The fire
continued for almost an hour.

This is not the first time since the
December, 1984, gas leak that toxic mat­
erials have been disposed off in this
manner by Union Carbide without informing
the public. In February last year, toxic
fumes frem the incinerator inside the
plant entered a double storied school
building near the eastern wall of the
plant while the school was in session.
About 50 children, all below twelve years,
started coughing violently and some
started vomiting. A number of children
complained of giddiness and nausea. The
teacher, not knowing how to respond to
such a situation, declared the school
closed for the day and the children were
asked to go home. The matter was taken
up with the authorities but no action was
forthcoming. The emissions frem the
incinerator continued unabated. It was
only after a group of young people from
Shaktinagar, where the school is located,
went up to the gate and hurled stones
that the authorities got the message and
the emissions stopped.
incidents such as these aggravate the
panic-bound psyche of the gas victims,
besides causing injury to their already
damaged bodies. Many of the victims
continue to talk about the poison clouds
of the December leak and visions of that
catastrophe recur, in their dreams.
Mention is often made, sometimes in hush­
ed tones and sonetimes in anger, that

But who
anyway?

still going on in the plant.
bothered about the gas victims

WITHOUT' COMMENT

Last. month, the :.UCO. bank in Bhopal: was
robbed in broad' daylight;.by a band - of ..J
;yet unidentified persons. . They, are
reported to have ; introduced themselves■'■.
as."Hum log gas-:<peedlt >hain/<bank::?lbotne:
aye hain" (We are gas victims, we have
come to loot the bank).Reading the
report, an old gas victim commented,.
"Gas peediton ke naam sekitnon ne loot
liya, yeh- ek aur sahi1'. (So. many have <
looted in the name of ga$ victims, this
is., just one. more •••instance) .;

STREET VS STAGE
Rangmandal, the theatre group of Bharat
Bhavan, the elite cultural centre of Bhopal
staged a play early this month based upon
the Bhopal gas disaster. ‘Banjh Ghati'
(Barren Valley), staged twenty months after
the disaster, was, however, eclipsed by the
forceful 'Dastan-e-Gas Khand' (Tale of the
gas disaster) enacted at the same time on
the streets opposite the Bhavan by 1Shuruat*
a group of amateur artistes. This group
has been performing the play since early
last year in many parts of Bhopal and else­
where, including the gas affected slums.
Among the crowd which preferred to watch
the street theatre were many young artistes
of Bharat Bhavan. itself.

THREE

<KS H A

<0131
A new project, involving the gas affected
children in painting, music, story telling,
poetry and drama, has started in the Javaprakash Nagar Basti of Bhopal . It has been
organised by David Bergman, a young British­
er who has been in Bhopal for the past three
months.
(David and a friend undertook a
cycle tour from England to Bhopal to raise
funds for the gas victims of the Bhopal dis­
aster.) The group which has been set up for
the purpose is called SURAKSHA.

At present, five teams of local artists (of
2/3 individuals per team', each conduct a
workshop in the basti once a week. A large
covered area is used for these activities.
The project is now in its third week, and
30-50 children are regularly involved.

Suraksha feels that although there is an
obvious need for such opportunities to be
given to basti children everywhere, there
is a special need for them in Bhopal today.
Apart from the physical disabilities the
children are still suffering fron, many of
them have also gone through extreme mental
anguish and stress during and after the gas
disaster. Emphasis is, therefore, being
placed in these workshops on psychological
therapy.
For the next few months, Suraksha plans to
limit itself to working in this basti with
these five teams of artists. Indeed, much
needs to be done just to make these activ­
ities with the children successful. Rela­
tionships of friendship and trust need to
be built up between the artists and the
permanent workers of Suraksha, on the one
hand, and between Suraksha and the children,
on the other. The children must be involved
in all aspects of the project. ‘ Attempts
roust also be made to get the general accep­
tance of the project within the basti com­
munity. Only then can they becane involved
in the general organisation of Suraksha and
in the supervising of the activities. Fin­
ally, much discussion needs to be done with
the artists themselves to work out coherent,
structured activities which have an overall
aim behind them. Such activities can then
continue over a number of weeks and months,
with new teams of artists joining in at
different points.

FOUR

"The gas leak is okay. What we've got to
guard against is the leaks to the press."

We have

the right to know
From Septeinber/October onwards, it is
hoped that Suraksha will be working in
two or three independent "activity huts"
structures of timber and bamboo - around
JP Nagar and Shakti Nagar. Apart from
the core of activities being carried out
by local artists and others from the
basti, individuals and groups working
with children from other parts of the
country are also being invited to come
to Bhopal to work intensively for two or
three weeks. Such groups could exchange
ideas with local teams so that their work
and methods could be continued in their
absence.
Once a good understanding and friendship
has been built up with the children,
Suraksha is interested in organising a
nutritional study of the children. Such
a survey is especially important now
because of the large amounts.of drugs
that their bodies are being subjected to.

The success of all this is very much dep­
endant on two to three more permanent
workers committing themselves for at least
three months to this project. So the
group requests interested people to come
vites°idpa«th ^hern* The 9rouP also inZd nennf!
suggestions from interest­
ed people. If interested, write to:
SURAKSHA
sant kanwar ram nagar

BHOPAL

462 018.

Support the call by KSSP for a
Global boycott of all products of Union Carbide
by Environment and Consumer Groups
with immediate effect.
For more information and details on campaign, please write to:
KSSP -

AIRP LAM

In May, 1985, representatives from
environment groups frem across the world,
including India, met at Eerbeek, a village
in Holland. The subjects of concern were
the growing menace of AIR POLLUTION,
particularly Acid Rain and the issues
raised by Bhopal.
Out of this meeting grew a new global
network linking environmental groups
concerned about these issues. AIRPLAN,
as this network is called, coordinates
international campaigns and is a forum
for exchange of information and action
plans.

AIRPLAN has been around tor a very short
while but has already demonstrated the
potential of such a network. Recently,
an appeal sent out by it resulted in
international pressure being applied on
the government of an East European country
to free two environmentalists who had been
jailed for raising ecological issues. In
order to maintain a regular channel for
communication and information exchange,
AIRPLAN publishes a bimonthly newsletter,
two issues of which have already cane out.
AIRPLAN welcomes interested groups to
join and strengthen its network.
Their address:
PO BOX 5627
1007 AP Amsterdam
The Netherlands.

AIR POLLUTION ACTION. NETWORK

A writ petition on the issue of the
right to know has Deen filed recently in
the Supreme Court of India by the environm“^LnC^°n gf°UP' KalP^riksh. This
petition is an intervention in the ongoing case against the Sriram Foods and
GomPany which was responsible
for the Oleum gas leak in Delhi, on the
first anniversary of Bhopal, which
resulted in the death of one person and
injuries to many others.
Kalpavriksh had earlier intervened in
the case, pleading that the plant be shut
down and relocated. As readers might
recall, the Supreme Court had then ruled
that the plant could reopen subject to
j.r ? management meeting certain conditions,
p:-eminent among which is the one which
holds the top management personally res­
ponsible for paying conpensation in the
event of future accidents.
Tne right to know petition argues tnat
A™ citizens have the right to be informed
about the nature of the dangers posed
to them by hazardous industries. The
r petition is due for hearing later this
I year.

Kerala Sastra Sahitya Parishad,
Parishad Bahvan,
Trivandrum 695037
Kerala, South India.

• FAITH WITHOUT FOUNDATION

'

A portion of the wall surrounding
ithe. Union Carbide factory-inBhopal.
col laps ed recently. The. works
.
manager, Mr. Mukund, 2nd • • e-:pP •
visor of the- MIC plant,
.
Choudhary, were heard,to
'
during their spot
•
tly, the wall hes no tonnd^tlon..
incidentally, this wal1^^^
safety’’system N0.5 ,ourj. y .... p
Fai.th1 ,

FIVE

Quacks have a field day
Every gas affected person in Bhopal must have
visited a private medical practitioner at
some point in time over the past year and a
half. Every private medical practitioner
must have treated anywhere between 2,000 and
10,000
gas affected patients during this
period. Indeed,this group of "businessmen"
could not have had things better - the boom
in their trade stands in stark contrast to
the gloom ana depression pervading every
other economic activity in the area.

In normal times, the present period of the
year is referred to as the "slack season"
by these private practitioners. But these
are not normal times - the stream of patients
does not end, the ‘shops1’ stay open till late
in the night. Clearly, the potential of
these private doctors to do good or cause
harm to their patients is phenomenal. The
question is - how safe are the lives of the
thousands of gas affected people in the
hands of these 200 odd self-professed medicos?
The first thing one notices while visiting
a private doctor in the gas affected areas
of Bhopal is his sign board. Often oversized,
it proclaims the doctor to be a specialist
in a variety of areas of medical knowledge.
One sign board, for instance, advertises its
owner as a specialist in medicine, surgery,
gynaecology, paediatrics and sex-problems.
Some sign boards mention the degrees the
"doctor" has acquired. These are usually
a curious mixture of unevenly spaced letters
amenable to a variety of interpretation U.V.P., V.V.P., M.I.A.M.S., M.A.M.S. etc.

On a rough estimate, eight out of every ten
private doctors have received no formal train­
ing in medicine. Their medical qualifications
usually comprise an apprenticeship with an­
other private doctor, coupled with lessons
received from correspondence courses offered
by ubiquitous "institutes" characterised by
their anonymity and dubious reputations.
Many doctors take such correspondence courses
simultaneously in more than one system of
medicine. Thus, it is not rare to meet a
private doctor who claims to treat his pa­
tients by the allopathic, homoeopathic, ayur­
vedic and Unani systems. As one doctor
interviewed put it, "We try different systems
and see which one fits - my patient must find
relief." The treatment is, by and large,
oriented to provide instant relief. "People
are workers here", one doctor explained,"they
have to be fit for work, so they want quick
relief lest they lose their wages."

SIX

Talking to some of these private doctors,
one picks up very interesting bits of
information. One learns, for instance,
that Sodium Thiosulphate is a drug from
the U.S. and is not of much use in India
because the blood circulation, the pulse
rate and breathing rates of Indians are
different fran those of people in the U.S.
One also learns that the outermost layer
of the eye, contrary to what class nine
biology students are taught in schools,
is called the Retina. One also encounters
a host of very interesting theories which
attempt to explain the effect of the tox­
ins in the body. One such theory is that
the gas has produced"heat in the body"
which cannot be tackled by ordinary medi­
cines,. since the gas has interfered with
the formation of pancreatic juices and
saliva, causing problems of digestion.

hrti-aso- ciao tors ::have. several: pertinent/:’: '////'
■
co ci-11---: : axout: the. :tot:al .health.-/
•^situation:-: in:-tho.’toast£s;:-They.:af.e<iovii::::::::<:’.:::
position: to do so since many, hove- been -in///:
hthe/^ea/fpr/.l^qf
csomaidfc-tbete.-'obb^rwatioris:/-?//-!:.---:.:::.:.-:?-:-:;:;:-:.:-!/:■':(■ 1 whiieithe: number at: patients; is still/ '
cocmsiderabiei-tbere< has:::been’:a.:50’per<<::-:::::::
- cent: fall/ib- 'che-past year.. Oocr reason. 1
: i- that’ many: :gac : v.Lc-timo,:beve rc.'sicticd' :
to their: suf feting/ /.- /I:/// //:■?

O P^ticbts W|-:Q visited, their clinics only
:o.:-::.bhoe:::a/.manffi: :bqfpre/:tbe/g4k/.<H.oastkr>now:/
do: :sa :onae : or /6V6:h-:twi<ie: every:- week: :■
large: numberl’b£/patients: have/ been : ::: 1
:/.:./::sxif:fBrdhg/wl-i#gut.:.r^pit<i/dvdxt/dibu.h::tbe:jO^
• qhd leak ..ahdidespite the' treatment
.
/://< despite/ths ?fcreatmw.t . received..::rora/tbs :
/:::.::’::priy-3.bet:.®ediocisb.and:goyeirnment;:diin’ics.> /•:
^M^praf^han.j.haif/.-tbecp'atientsisiha .fcomeoVo:-:-:/ : :.::their:/clinici<:h’fiyd.: symptenm; :dirc>ctly ::'
:-::;::relate(J-.-to.gas lexpasuxe:-.-:: I:-:;?:-:-??:-:-.:?. .
Di9^eK: ^loh:..were:.p’re>?!<il0n.t ::e'brller'-:how
. /occur more frequently:and with hintensity.
Tha-. variety hmd
: symptoms is. . •

fatlgue#.weakness,body' aehes^dizziness

^“■'kurning senlatloh itf €he •ey’e&;
pain during intercourse,anxiety,
•inspmftia,headache and' cbesp pain-

’

According to another theory, "MIC affected
patients need hard drugs, potent drugs,
drugs which are costly. Only then can they
get better."

These beliefs', coupled with the hard-sell
tactics of big drug companies (smooth
talking medical representatives and styl­
ishly printed literature which invariably
adorns the walls of the clinics) have re­
sulted in utter irrational and dangerous
"therapy". Antibiotics are prescribed
at the first signs of cough, fever or
boils. Rarely are patients prescribed
the full course; where they are, patients
discontinue use half way through the
course, rendering themselves more vulner­
able to further infections. Injections,
the ultimate panacea in the eyes of many
patients, are readily given by the doctors
to patients with money to spend on these
"miracle" drugs. Another favourite is
steroids (which provide a "sense of wellbeing" though they impair the natural
immunity system of the body) . Tonics,
which, according to one doctor, are pres­
cribed "to give energy to the gas victims",
formulations such as "Protinules",
"Protinex", "Sharkaferrol" and "Ferradol"
and useless drugs such as Kaoldn-Pectin
mixture for children with diarrhoea are
also routinely prescribed. Moreover,
drugs such as Phenylbutazone and Oxyphenabu^azone preparations (e.g. Actigesic, Bestophen, Suganril and Reducin)
which have been categorised by the drug
controller of India, as restricted for
use in the treatment of ankylosing spondy­
litis and gouty arthritis (and whose
potent toxic after effects have been
demonstrated by the fact that Ciba Geigy
the principal manufacturers of these drugs is
reported to have recorded 1674 deaths due
to these drugs) are routinely given for
body aches.
/

The private medical practitioners charge
.between
F
/ ’and De
c;/- ner
Rs. e5/Rs*. 925/per natient
patient D<
per
visit. An average household in the gas
affected area would have spent at least
Rs .2,000/- in the last eighteen months on
medicines and consultation fees of these
private doctors. There are many who have
borrowed money for this Purpose at rates
of interest sometimes as high as 120a.
The goverrment run hospitals, on the cont­
rary charge nothing. The obvious question
is - why do the victims prefer these priv­
ate doctors to the hospitals run by the
government. There are several reasons....

(Th:r r^s^v^^^
no<i2=in Lat the gas victims are pretending
to^beaslc?as they want canpens ation).

The government run hospitals and clinics
are open only during the day and in the
early evening, times when people are out
working, while private clinics are open
till late in the night.

The attitudes of the doctors towards
their patients is an impressive blend
of smart salesmanship and a veneer of
professionalism cultivated over several
years of experience and practice. In
sharp contrast, the government doctors
who are too pressed for time do not
spend enough time or give personal att­
ention to their patients. The private
medicos give a patient hearing to each
person and spend considerable time in
clinical examinations. Indeed, the
private doctors score over even the
ICMR researchers and senior government
doctors when asked to provide an oral
list of symptoms presently displayed
by the gas affected people.
The shortage of government doctors means
zjgjfe long queues at the clinics. There are
several other inadequacies in the ggvwij ernmental medicare system. As one private doctor stated very candidly "The government doctors prescribe
&&£ the same medic,ines as we do, they have
much greater facilities, if they happen
to improve their services, we will be
gjijj out of business."

That doctor, like most others operating
in the gas affected bastis of Bhopal,
does not lose sleep over this possibility,
fully aware that such a change in the
governmental attitude is extremely improbable©

SEVEN

i

AN

A P' PEAL

In the first issue of 'BHOPAL' which we mailed to you a month
ago., we laid out the objectives of the Bhopal Group for Infor­
mation and Action, We have received a positive response
to
that issue and to the idea of BGIA. Our thanks to all those
who've responded.

In the last month, we've begun the task of collecting material
on Bhopal and setting up the documentation centre. We've also
found a place near the Union Carbide factory to house the cen­
tre.
As we mentioned last time, we see our small group here as a
mere extension of a shared desire of a vast community to sus­
tain work on Bhopal and related issues. Moreover, the
task
of documentation, bringing out the newsletter and running and
information service can be sustained only with your
active
support.

At the moment, BGIA requires the following, assistance from you
and we trust you will try your best to help:
- We need a list of all documents concerning Bhopal which you
may possess or have access to. This list is vital for the
building up of the documentation centre.
- We need some equipment and financial assistance. Equipment
includes a typewriter, storage cabinets, stationery and pa­
per.

- We need contributions to keep the newsletter going. We urge
you to
— contribute a minimun of Rs. 24/- a year in advance (Rs 30/for institutions and $ 30/- for foreign groups)? and
— undertake to sell a minimum of five copies of the news­
letter on a regular basis at Rs. 2/- a copy.
More than anything else, we value your comments,
and advice.

•BHOPAL’ is brought out
by the Bhopal Group for
Information and Action,
D-42 pirdos nagar
BHOPAL 462 018

Article# Au this news­
letter may be freely
reproduced♦ : .
This issue was produced
by Satinath Sarangi, S.
Ravi Rajan and Vinod
Raina, with assistance
from N R Mohandas»

criticisms

oH 1 *3®
PC-SPIRS 3.40

MEDLINE

(R)

10/97-12/97

MEDLINE (R) 10/97-12/97 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

,TI:

1 of 2
Marked Record
A study of cognitive functions in methy1-iso-cyanate victims one year after

•bhopal accident.
AU: Misra-UK; Kalita-J
AD: Department of Neurology,

Sanjay Gandhi Postgraduate Institute of Medical

Sciences, Lucknow, India.
SO: Neurotoxicology. 1997; 18(2): 381-6
this source is not Available in S■J.M.C■Library
LA: ENGLISH
AB: There is a paucity of information regarding the late effects of
methyl-iso-cyanate (MIC) poisoning. In this study, the clinical and cognitive
functions of 52 MIC victims were evaluated one year after the Bhopal gas
accident. There were 15 severely, 14 moderately, and 23 mildly affected
patients. Their mean age was 38.2 (range 15-651 years and 30 patients were
males. Their clinical picture was dominated by^espiratory symptoms in 36
patients, of which 17 had abnormal chest radiographs. Neurological examination
of these patients was normal. Rsychometry in 33 patients revea1ed-significant
impairment of standard progressive matrices (SPM), associate learning and motor
speed and precision tests (p < 0.01) in severely exposed MIC patients. In the
moderately affected group associate learning and motor speed and precision were
significantly impaired. Motor speed and precisian tests had significant
positive correlation with eye signs, (r = 0.42) and disability score (r = 0.68).
Our results suggest significant cognitive impairment in severely exposed MIC
victims.

2
of 2
Marked Record
PC-SPIRS 3.40

MEDLINE

(R)

1/96-1/97

MEDLINE ,(R) 1/96-1/97. usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 1
.
Marked Record
II: Long term morbidity in survivors of the 1984 Bhopal gas leak.
AU: Cullinan-P; Acquilla-SD; Dhara-9R
AD: National Heart and Lung Institute, London, UK.
SO: Natl-Med-J-India. 1996 Jan-Feb; 9(1): 5-10
____ This source is Available in S.j.M.C Library
____ Call Number: From: 1988+
LA: ENGLISH
AB: BACKGROUND: The extent and nature of long term health sequelae among
survivors of the Bhopal gas disaster are not known. In 1994 an International
Medical Commission was set up with the aim of assessing respiratory?
neurological and other health effects attributable to gas exposure. METHODS: An
epidemiological survey of a representative sample of gas-exposed inhabitants of
Bhopal, was conducted in January 1994; for reference, a group of unexposed
persons in the same city were surveyed. Questionnaires regarding’health and
exposure were administered to 474 persons, and a random sample (n=76) were
subjected to respiratory and neurological testing. Responses to the "
questionnaire and the results of clinical testing were analysed according to a
measure of individual gas exposure. RESULTS: A large number of subjects
reported general health .probl_ems (exposed v. unexposed; 947. v. 527.) and
episodes of fever (7.5/year v. 2.5/year); adverse- outcome of pregnancy (e.g.
still-births, 97. v. 47.) and respiratory symptoms (817. _v._ 387.) , 'with ~a strong
gradient by exposjire category. This was not accounted for by differences in
smoking, and was consistent with the results of spirometric testing.

testing tiSrtoC™?i™eLmdfthrr"5Ult* °f "'^oKgL.lltT^TJ.t^in’anJ'"’
resting tended to confirm this finding. Ophthalmic symptoms demon--tratori imilat pattern. Although a number of other symptoms were’reported1(with the
FC^PJLRS 3.40
MEDLINE (R) l/97r.9/4 there was n> ^ar eJiSencI of
MEDLINE (R) 1/97-9/97 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 5
Marked Record
TI: Respiratory morbidity 10 years after the Union Carbide gas leak at Bhopal:
a cross sectional survey. The International Medical Commission on Bhopal [see
comments]
AU: Cullinan-P; Acquilla-S; Dhara-VR
AD: Department of Occupational and Environmental Medicine, Imperial College
(National Heart and Lung Institute), London.
SO: BMJ. 1997 Feb 1; 314(7077): 338-42
____ This source is Available in S.J.M.C Library
____ Call Number: From 1914+
LA: ENGLISH
AB: OBJECTIVE: To examine the role of exposure to the 1984 Bhopal gas leak in
the development of persistent obstructive airways disease. DESIGN: Cross
sectional survey. SETTING: Bhopal, India. SUBJECTS: Random sample of 454 adults
stratified by distance of residence from the Union Carbide plant. MAIN OUTCOME
MEASURES: Self reported respiratory symptoms; indices of lung function measured
by simple spirometry and adjusted for age, sex, and height according to Indian
derived regression equations. RESULTS: Respiratory symptoms were significantly
more common and lung function (percentage predicted farced expiratory volume in
one second (FEV1), forced vital capacity (FVC), forced expiratory flow between
257. and 757. of vital capacity (FEF25-75), and FEV1/FVC ratio) was reduced among
those reporting exposure to the gas leak. The frequency of symptoms fell as
exposure decreased (as estimated by distance lived from the plant), and lung
function measurements displayed similar trends. These findings were not wholly
accounted for by confounding by smoking or literacy, a measure of socioeconomic
status. Lung function measurements were consistently lower in those reporting
symptoms. CONCLUSION: Our results suggest that persistent small airways
obstruction among survivors of the 1984 disaster may be attributed to gas
exposure.
2
of 5
Marked Record
TI: Relationship between lung inflammation, changes in lung function and
severity of exposure in victims of the Bhopal tragedy [see comments]
AU: Vijayan-VK; Sankaran-K
AD: Cardiopulmonary Medicine Unit, Indian Council of Medical Research, Madras,
India.
SO: Eur-Respir-J. 1996 Oct; 9(10): 1977-82
____ this source is not Available in S■J„M.C.Library
LA: ENGLISH
AB: The world's worst chemical industrial disaster, which occurred at Bhopal on
2-3 December, 1984, resulted in considerable respiratory morbidity in the
exposed population. Therefore, a study was planned to evaluate the relationship
between lower respiratory tract inflammation, lung function and severity of
exposure. Sixty patients exposed to methyl isocyanate and presenting with
respiratory symptoms were studied using bronchoalveolar lavage (BAL) 1-7 yrs
after the accident. Pulmonary function tests included farced vital capacity
(FVC) and forced expiratory volume in one second (FEV1). An index of severity
of exposure was derived retrospectively on the basis of the acute symptoms in
the victims themselves or the occurrence of death among their family members.
Total lung inflammatory cells (p < 0.01) and absolute numbers of macrophages (p
= 0.01) and lymphocytes (p < 0.05) increased as severity of exposure increased.

PC-SPIRS 3.40

MEDLINE (R)

1998/01-1998/10

MEDLINE (R) 1998/01-1998/10 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 1
Marked Record
TI: Improving the U.S. EPA Toxic Release Inventory database for environmental
health research.
AU: Neumann-CM
AD: Department of Public Health, Oregon State University, Corvallis 97331-6406,
USA. neumannc@ccmail.orst.edu
SO: J-Toxicol-Environ-Health-B-Crit-Rev. 1998 Jul-Sep; 1(3): 259-70
LA: ENGLISH
AB: In 1986, Congress passed the Emergency Planning and Community Right-to-Know
Act (EPCRA) in response to the tragic death of thousands of people in Bhopal,
India, following the accidental release of the toxic gas methyl isocyanate
(MIC) from a Union Carbide facility. As a component of EPCRA, certain
manufacturers are required to report annually the total mass (pounds per year,
Ib/yr) of toxic chemicals released into the environment (air, water, land, or
underground injection), treated on-site, or shipped off—site for further waste
treatment. This information is compiled by the U.S. Environmental Protection
Agency (EPA) into a publicly accessible database known as the Toxic Release
Inventory (TRI). The TRI database is designed to encourage pollution prevention
and waste reduction by increasing public access to and knowledge of
environmental chemical releases. EPCRA has been generally considered by
industry, government, and community representatives as one of the most
successful environmental laws in U.S. history. Over the past few years, EPA has
initiated a three-phased expansion to EPCRA reporting requirements that will
enhance the overall usefulness of the TRI database. The focus of this article
is to discuss these changes and highlight several current uses of the TRI
database in environmental health research.
PC-SPIRS 3.40

MEDLINE (R)

1/97-9/97

MEDLINE (R) 1/97-9/97 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 1
TI: The lessons of Bhopal Etoxic] MIC gas disaster scope for expanding global
biomonitoring and environmental specimen banking.
AU: Sriramachari-S ; Chandra-H
AD: Institute of Pathology (ICMR), Safdarjang Hospital Campus, New Delhi,
India.
SO: Chemosphere. 1997 May; 34(9-10): 2237-50
____ this source is not Available in S.J.M■C.Library
LA: ENGLISH
AB: Bhopal Toxic gas tragedy represents one of the worst chemical accidents of
the world. Autopsy and toxicological studies, apart from presenting evidence of
acute and even chronic cyanide toxicity, provided a unique example of the
incriminated chemical being traced to the bodies of the victims. The entry of
methyl isocyanate (MIC) into the blood stream was established by the presence
of carbamoylated end-terminal amino acids of haemoglobin and other tissue
proteins. The presence of MIC trimer and a few other identified as well as
unidentified tank residue constituents in the blood and viscera further
established a close nexus of the products of pyrolysis of MIC in the aerosol
inhaled by the victims. The Bhopal studies exemplify the scope for biological
monitoring (BM) and environmental specimen banking (ESB) in chemical accidents
as part of the global efforts.

FEV1/FVC 7. (p = 0.05) was also significantly lower as severity of exposure
increased. Moderately exposed subjects had significantly lower FEV1/FVC 7. (p <
0.05) compared to those mildly exposed. In nonsmokers, BAL neutrophils, both
percentage and absolute numbers, showed significant negative correlations with
FEV1 7. predicted (rs = -0.350, p < 0.05; and rs = -0.374, p < 0.01,
respectively). Neutrophil percentage was negatively correlated with FEV1/FVC 7.
(rs = -0.378; p < 0.01). Absolute lymphocytes had significant negative
correlations with FVC 7. pred (rs = -0.318; p < 0.05). Macrophages had
significant positive correlations with FVC 7. pred (rs = 0.322; p < 0.05) and
FEV1 7. pred (rs = 0.433; p < 0.01). Radiographic abnormalities (International
Labour Organization (ILO) classification) were associated with decline in FEV1
7.
pred (p < 0.05). This study suggests that pulmonary function abnormalities
occur in gas-exposed subjects as a consequence of an abnormal accumulation of
lung inflammatory cells (lymphocytes and neutrophils), and that the intensity
of lung inflammation and reduction in pulmonary function are greater in
severely exposed subjects. As it has been observed that decline in pulmonary
function is associated with radiographic abnormalities, there is a suggestion
that injury following toxic gas exposure can lead to irreversible lung damage.
3
of 5
Marked Record
TI: Late consequences of accidental exposure to inhaled irritants: RADS and the
Bhopal disaster [editorial; comment]
AU: Nemery-B
SO: Eur-Respir-J. 1996 Oct; 9(10): 1973-6
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
4
of 5
Marked Record
TI: International Medical Commission, Bhopal : a model for the future.
AU: Bertell-R; Tognoni-G
AD: International Institute of Concern for Public Health, Toronto, Ontario,
Canada.
SO: Natl-Med-J-India. 1996 Mar-Apr; 9(2): 86-91
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1988+
LA: ENGLISH

5
of 5
Marked Record
TI: Major chemical accidents in industrializing countries: the socio-political
amplification of risk.
AU: de-Souza-Porto-MF; de-Freitas-CM
AD: Study Center of Workers' Health and Human Ecology, National School of
Public Health, Rio de Janeiro, Brazil.
SO: Risk-Anal. 1996 Feb; 16(1): 19-29
____ this source is not Available in S■J.M■C.Library
LA: ENGLISH
AB: Accidents in the chemical industry, such as those that took place in Seveso
(1976) and Bhopal (1984), may kill or injure thousands of people, cause serious
health hazards and irreversible environmental damage. The aim of this paper is
to examine the ever—increasing risk of similar accidents becoming a frequent
ocurrence in the so-called industrializing countries. Using figures from some
of the worst chemical accidents in the last decades, data on the Bhopal
disaster, and Brazil's social and institutional characteristics, we put
forward the hypothesis that present social, political and economic structures
in industrializing countries make these countries much more vulnerable to such
accidents and create the type of setting where—if and when these accidents
occut-- they will have even more catastrophic consequences. The authors argue
that only the transformation of local structures, and stronger technical

cooperation between international organizations, industrialized and
industrializing countries could reduce this vulnerability.

PC-SFIRS 3.40

MEDLINE (R)

1/95-1/96

MEDLINE (R) 1/95-1/96 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 5
Marked Record
TI: Persistently toxic. The Union Carbide accident in Bhopal continues to harm
[news]
AU: Mukerjee-M
SO: Sci-Am. 1995 Jun; 272(6): 16, 18
____ This source is Available in S.J.M.C Library
Call Number: From: 1949+
LA: ENGLISH
2
of 5
Marked Record
: Comparative toxicity of methyl isocyanate and its hydrolytic derivatives in
^pits. II. Pulmonary histopathology in the subacute and chronic phases.
AU: Sriramachari-S ; Jeevaratnam-K
AD: Institute of Pathology, New Delhi, India.
SO: Arch-Toxicol. 1994; 69(1): 45-51
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: This paper describes the long-term (subacute and chronic) histopathological
effects in the lungs of rats subjected to a single exposure to methyl
isocyanate (MIC) by both the inhalation and subcutaneous (s.c.) routes as well
as the role of methylamine (MA) and N,N'—dimethyl—urea (DMU), the hydrolytic
derivatives of MIC in eliciting the observed changes. At the subacute phase,
the intraalveolar and interstitial edema were prominent only in the inhalation
group as against the more pronounced inflammatory response in the s.c. route.
With the progress of time the evolution of lesions appeared to be similar,
culminating in the development of significant interstitial pneumonitis.and
fibrosis. MA, one of the hydrolytic derivatives of MIC, also caused
interstitial pneumonitis progressing to fibrosis, albeit to a lesser extent
than MIC, indicating its contribution to the long-term pulmonary damage. The
cLiffuse interstitial pulmonary fibrosis observed at 10 weeks after a single
^Pposure to MIC by either route is of greater significance in the context of
the occurrence of pulmonary fibrosis in the late autopsies of Bhopal gas
victims and also clinical sequelae in some of the survivors.
3
of 5
Marked Record
TI: Comparative toxicity of methyl isocyanate and its hydrolytic derivatives in
rats. I. Pulmonary histopathology in the acute phase.
AU: Jeevaratnam-K; Sriramachari-S
AD: Defence Research and Development Establishment, Gwalior, India.
SO: Arch-Toxicol. 1994; 69(1): 39-44
_____this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: The present study describes the acute histopathological changes induced by
methyl isocyanate (MIC) in the lungs of rats at 24 h after a single exposure to
varied concentrations/doses of MIC by inhalation and subcutaneous (s.c.) routes
and also delineates the effects due to the hydrolytic derivatives of MIC, viz.,
methylamine (MA) and N,N'-dimethyl urea (DMU). MIC, either inhaled or
administered s.c., resulted in a wide range and extent of histopathological
changes in the lungs, proportional to the exposure concentration/dose. The
salient, effects of inhaled MIC are acute necrotizing bronchitis of the entire

respiratory tract accompanied by varying degrees of confluent, congestion,
hyperemia and interstitial and intra-alveolar edema, while MIC administered
s.c. led to prominent vascular endothelial damage, congestion and severe
interstitial pneumonitis with apparently normal bronchial epithelium; and
intra—alveolar edema only with the high dose. The only noteworthy lesion
produced by MA and DMU (to some extent) was interstitial pneumonitis,
suggesting their possible involvement in the subsequent inflammatory response
of MIC. Except, for the endothelial changes, the overall spectrum of the
histopathological lesions is quite comparable to those observed in the lungs of
Bhopal victims during the acute phase.
4
of 5
Marked Record
TI: Chronic lung inflammation in victims of toxic gas leak at Bhopal.
AUs Vijayan—VK; Sankaran—K; Sharma—SK; Misra-NP
ADs Cardio—Pulmonary Medicine Unit, Indian Council of Medical Research, Madras.
SO: Respir-Med. 1995 Feb; 89(2)s 105-11
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: Bronchoalveolar lavage (BAL) studies in 20 patients at Bhopal, 1.3 +/- 0.4
yr and 2.7 +/- 0.6 yr after toxic gas exposure had revealed that the lower
respiratory tract inflammation had progressed from initial macrophage
ajVeolitis to macrophage-neutrophi1ic alveolitis. The interval between the two
lavages was 1.4 +/- 0.6 yr. BAL studies in a new group of 24 patients 5.1 +/1.0 yr after exposure had confirmed chronic inflammation of the lower
respiratory tract as evidenced by macrophage-neutrophi1ic alveolitis in these
subjects as well. Clinical, radiographic and pulmonary function abnormalities
were persistent in a proportion of subjects in both groups. Fibronectin (FN)
levels were estimated in BAL fluid in 41 patients. Elevated FN levels were seen
in 12 (29.37.) subjects and nine of these 12 had radiographic abnormalities.
Severely exposed subjects (n = 30) had significantly higher BAL fibronectin
levels compared to normal subjects and mi Id/moderately exposed subjects. Repeat
FN estimations in BAL samples from 10 patients had revealed that five had
abnormally high FN including three who had high FN on both occasions. The
number of patients showing abnormal decline in pulmonary function was higher in
patients with elevated FN than in patients with normal FN. Thus, persisting
clinical, roentgenographic and ventilatory abnormalities, as well as
macrophage—neutrophi1ic alveolitis along with abnormally elevated FN levels in
a proportion of subjects, suggest the possibility that lung fibrosis can occur
in subjects exposed to toxic gas at Bhopal.

5
of 5
Marked Record
TI: The ultimate poison center call—Bhopal [editorial]
AU: Wax—PM
SO: J—Toxicol—Clin—Toxicol. 1995; 33(1): 18
____ This source is Available only few issues in S.J.M.C.
LA: ENGLISH

Library

PC-SPXRS 3.40

MEDLIME

(R)

1994

MEDLINE (R) 1994 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 2
Marked Record

TI: The Bhopal tragedy [letter]
AUs Murlidhar-V
SO: Natl—Med-J—India. 1994 May-Jun; 7(3): 150-1
____ This source is Available in S.J.M.C Library
____ Call Number: From; 1988+
LA: ENGLISH
2 of 2
Marked Record
TI: Isolation of an unknown compound, from both blood of Bhopal aerosol
disaster victims and residue of tank E-610 of Union Carbide India
Limited—chemical characterization of the structure.
^)U: Chandra-H; Saraf-AK; Jadhav-RK; Rao-GJ; Sharma-VK; Sriramachari-S;
^airamani-M
AD: Medicolegal Institute, Gandhi Medical College Building, Bhopal, India.
SO: Med-Sci-Law. 1994 Apr; 34(2): 106-10
_____this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: A total of more than 28 chemical entities/reaction products in the form of
gases, vapour and particulate matter were reported from the tank E-610 of
methyl isocyanate (MIC) storage tank of Union Carbide India Limited on the
night of 2/3 December 1984 in Bhopal■ In earlier studies, methyl isocyanate and
its trimer, with a few other compounds, were reported in the human victims
preserved in deep freeze. Randomly selected samples were analysed by gas
chromatograph coupled with mass spectrometer (ITD-800, Finnigan MAT, UK). Four
of the cases showed the peaks and fragmentation pattern identified with one of
the unidentified compound of molecular weight 269 amu in the Tank Residue,
which constituted about 0.2 area per cent on GC-ITD. After isolation by column
chromatography and being exposed to characterization, it was identified as a
Spiro compound. It was possibly formed by the polymerization of five molecules
of methyl isocyanate.

PC-SPIRS 3.40

MEDLINE (R)

1993

MEDLINE (R) 1993 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 5
Marked Record
II: The public health physician's role in chemical incidents.
AU: Gunnell-DJ
AD: Somerset Health Authority, Taunton.
SO: J-Public-Health-Med . 1993 Dec; 15(4): 352-7
this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: Chemical incidents such as the methyl isocyanate release at Bhopal and the
aluminium sulphate incident in Lowermoor, Cornwall, are uncommon. However, five
chemical incidents occurred in Somerset in 12 months between 1990 and 1991, and
District Health Authorities are required to have plans to deal with such
events. A survey of the plans held by the Consultants in Communicable Disease
Control in South Western and Wessex Regional Health Authorities is discussed
=<□■1 the roles of public health physicians and emergency organizations are
olVl ined.
2
of 5
Marked Record
TI : The Bhopal accident and methyl isocyanate toxicity.
AU: Varma-DR; Guest-I
AD: Department of Pharmacology and Therapeutics, McGill University, Montreal,
Canada.
SO: J-Toxicol—Environ—Health. 1993 Dec; 40(4): 513-29
____ This source is Available only few issues in S.J.M.C. Library
LA: ENGLISH
AB: The Bhopal accident, the world's worst industrial disaster, in which nearly
40 metric tons of methyl isocyanate (MIC) was released from the Union Carbide
pesticide plant, occurred nearly 10 yr ago during the night of December 2 and
3,
1984. Over 3000 people residing in areas adjacent to the plant died of
pulmonary edema within 3 d of the accident. Follow-up studies revealed
pulmonary, ophthalmic, reproductive , immunologic, neurological, and hematologic
toxicity among the survivors. Despite high reactivity, MIC can traverse cell
iHMbranes and reach distant organs, perhaps as a reversible conjugate with
gSRathione, which may explain some of the systemic effects of MIC. MIC can be

degraded as a result of pyrolysis and interaction with water, but none of the
breakdown products can duplicate the toxicity observed in Bhopal and in animal
models. MIC may be the most toxic of all isocyanates because of its very high
vapor pressure relative to other isocyanates and because of its ability to
exert toxic effects on numerous organ systems.
3
of 5
Marked Record
TI: The Bhopal gas disaster: it's not too late for sound epidemiology
[editorial]
AU: Dhara-VR; Kriebel-D
SO: Arch-Environ-Health. 1993 Nov-Dec; 48(6): 436-7
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1960+
LA: ENGLISH
4
of 5
Marked Record

fl: The epidemiology of disasters and adverse reproductive outcomes: lessons
learned.
AU: Cordero-JF
AD: Division of Birth Defects and Developmental Disabilities, Centers for
Disease Control, Atlanta, GA 30333.
SO: Environ-Health-Perspect. 1993 Jul; 101 Suppl 2: 131-6
____ this source is not Available in S. J .M.C.Library
LA: ENGLISH
AB: A disaster has been defined as a disruption of human ecology that exceeds
the capacity of the community to function normally. Little is known about the
adverse effects of natural disasters on reproductive outcomes. Important
lessons can be derived from several disasters caused by human factors, such as
the Minamata Bay disaster. Adverse reproductive outcomes include infertility,
early pregnancy loss, stillbirths, congenital malformations, and serious
developmental disabilities such as cerebral palsy and mental retardation.
Recent disasters like the Chernobyl and Bhopal explosions have provided
important lessons on the need for accurate and sound information about the risk
of prenatal exposures for adverse reproductive outcomes. To study questions of
adverse reproductive outcomes and disasters requires a well-planned approach.
It should include early development of surveillance for adverse reproductive
outcomes, analytic studies on the risk of disasters from direct and indirect
effects, sensitive methods to measure early pregnancy loss, and long-term
f(^ow-up programs to assess outcomes such as developmental disabilities.
5
of 5
Marked Record
TI: Environmental release of chemicals and reproductive ecology.
AL): Bajaj-JS; Misra-A; Raj alakshmi-M; Madan-R
AD: Department of Medicine, All India Institute of Medical Sciences, New Delhi.
SO: Environ-Health-Perspect. 1993 Jul; 101 Suppl 2: 125-30
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: Reproductive ecology is defined as "the study of causes and mechanisms of
the effects of environmental risk factors on reproductive health and the
methods of their prevention and management." Major areas of concern, within the
purview of this paper, relate to adverse pregnancy outcomes, effects on target
tissues in the male and the female, and alterations in the control and
regulatory mechanisms of reproductive processes. Teratogenic potential of
chemicals, released as a result of accidents and catastrophes, is of critical
significance. Congenital Minamata disease is due to transplacental fetal
toxicity caused by accidental ingestion of methyl mercury. Generalized
djgKirders of ectodermal tissue following prenatal exposure to polychlorinated
b^P'ienyls have been reported in Taiwan and Japan. The Bhopal gas disaster, a
catastrophic industrial accident, was due to a leak of toxic gas, methyl
isocyanate (MIC), in the pesticide manufacturing process. The outcome of
pregnancy was studied in female survivors of MIC exposure. The spontaneous
abortion rate was nearly four times more common in the affected areas as
compared to the control area (24.27. versus 5.67.; p < 0.0001). Furthermore,
while stillbirth rate was found to be similar in the affected and control
areas, the perinatal and neonatal mortality rates were observed to be higher in
the affected area. The rate of congenital malformations in the affected and
control areas did not show any significant difference. Chromosomal aberrations
and sister chromatid exchange (SCE) frequencies were investigated in human
survivors of exposure. The observed SCE frequencies in control and exposed
groups indicated that mutagenesis has been induced. Strategies for the
management, prediction, and preventability of such disasters are outlined.

PC-SPIRS 3.40

MEDLINE (R)

1992

MEDLINE (R) 1992 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 9
Marked Record
TI: Critical appraisal of entomological data of Madhya Pradesh for 1991 and its
relevance to the National Malaria Eradication Programme.
AU: Saxena-VK; Narasimham-MV; Kalra-NL
AD: National Malaria Eradication Programme, Bhopal.
SO: J—Commun-Dis. 1992 Jun; 24(2): 97-108
,This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1978-1992
LA: ENGLISH
AB: Entomological data generated in five entomological zones, of Madhya Pradesh
State during 1991 including, Bhopal, Bilaspur, Gwalior, Indore and Raipur were
analyzed. The entomological parameters that were studied included per man hour
(pmh) density, abdominal physiology and parity status. The inferences were
related to i) resting behaviour (exophily/endophily) ii) duration of indoor
i^^ting period of mosquitoes iii) man-vector contact iv) efficacy of residual
insecticide and v) vulnerability of the area to focal malaria outbreaks. The
data chiefly pertains to the putative malaria vector Anopheles culicifacies in
all the five zones under study. The studies have brought out that A.
culicifacies, traditionally endophilic and endophagic, has demonstrated radical
departure in its resting and feeding behaviour. In Gwalior zone the species
shows high preference for exophily. In Bhopal and Indore zones there is
differential resting behaviour with respect to season. The species shows, for
most part of the year exophily but is also endophilic during post monsoon
period. In Bilaspur zone the species shows marked exophily and endophagy.
Irrigation practices seem to have affected the mosquito population density
patterns in these regions as brought out in Indore and Bilaspur zone, where
high density pattern is observed between November and February. These findings
have obvious implications in selecting the appropriate intervention methods and
the period of spray in areas where residual spray is the method of choice for
interruption of transmission.
2 of 9
Marked Record
Health effects of the Bhopal gas leak: a review [published erratum appears
in Epidemiol Prev 1992 Dec;14(53):48]
AU: Dhara-R
AD: Dept, of Environmental & Community Medicine UMDNJ, Robert Wood Johnson
Medical School, Piscataway 08854.
SO: Epidemiol-Prev. 1992 Sep; 14(52): 22-31
____ this source is not Available in S.J,M.C.Library
LA: ENGLISH
AB: The methyl isocyanate (MIC) gas leak from the Union Carbide plant at
Bhopal, India in 1984 was the worst industrial disaster in history. Exposure
estimates of gas concentrations in the area range from 85 to 0.12 ppm. Of the
approximately 200,000 persons exposed, 3598 deaths have resulted as of November
1989. Chronic inflammatory damage to the eyes and lungs appears to be the main
cause of morbidity. Reproductive health problems in the form of increased
spontaneous abortions and psychological problems have been reported. Questions
about the nature of MIC toxicity have been raised by the persistence of
multi-systemic symptoms in survivors. Animal studies using radio-labeled MIC
given by the inhalation route have shown that the radio-label is capable of
crossing the lung membranes and being distributed to many organs of the body.

This paper reviews health effects of gas exposure from published studies and
discusses some of the clinical and epidemiological issues being debated.
3 of 9
Marked Record
TI: On the bioavailability of methyl isocyanate in the Bhopal gas leak
[editorial]
AU: Dhara-VR
SO: Arch-Environ-Health. 1992 Sep-Oct; 47(5): ,385-6
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1960+
LA: ENGLISH

4 of 9
Marked Record
TI: Global estimates of acute pesticide morbidity and mortality.
AU: Levine-RS; Doull-J
AD: Department of Family and Preventive Medicine, Meharry Medical College,
Nashville, TN 37208.
SO: Rev-Environ-Contam-Toxicol. 1992; 129: 29-50
____ this source is not Available in S.J■M.C.Library
LA: ENGLISH
AB: Mathematical models have projected increasing numbers of pesticide
kisoning throughout the world, rising from 500,000 cases/yr in 1972 to
25,000,000 cases/yr in a 1990 estimate. Among 148 outbreaks (excluding Bhopal
and three probable epidemics of pesticide-related suicide) reported between
1951-90, the known number of cases was 24,731 with 1065 deaths (4.3Z case
fatality); these are probably underestimates. Among the known outbreaks, the
most commonly identified agents were organophosphates (58), carbamates (23),
chlorinated hydrocarbons (23), and organic mercurials (11). Food was the most
common vehicle of exposure in these epidemics (83 outbreaks), followed by skin
contact (26), multiple types of exposure (22), and respiratory exposure (16).
Two countries, the United States and Thailand, accounted for more than half the
reports. Both the mathematical models and the outbreak investigations support
the need for continuing investigation and improved surveillance throughout the
world.

5 of 9
Marked Record
TI: The industrial safety professionals: a comparative analysis from World War
I until the 1980s.
AU: Dwyer-T
feD: IFCH/DCS, Universidade Estadual de Campinas, Sao Paulo, Brazil.
SO: Int—J—Health-Serv. 1992; 22(4): 705-27
____ this source is not Available in S.J.M■C■Library
LA: ENGLISH
AB: The birth of industrial society produced demand for the services of
professionals specialized in matters related to industrial safety. Three
professions —safety engineering, industrial medicine, and ergonomics—are
examined. These professions are observed to either submit to single sets of
demands, to integrate contradictory demands, or to experience scission. Until
the late 1960s their growth appears to have been relatively peaceful and
uncontroversial. From this period onward, controversy breaks out over questions
related to industrial safety, and professions and government administrations
grow. Increasingly, the traditional approach of safety professionals is called
into question, and they adopt new orientations. These changes are mapped
through the examination of data drawn principally from the United States,
France, Great Britain, and to a lesser extent Brazil. The traditional standards
approach competes with cost-benefit analysis and with systemic safety for
influence; in addition, an emergent approach that analyzes accident causes in
terms of social relations of work is detected. From Bhopal to Chernobyl, new

technologies subject civilian populations to risks of catastrophic accidents,
and the action of safety professionals comes under the spotlight. The analysis
constructed permits new understandings of the past and the future of these
professions.
6 of 9
Marked Record
TI: Sequential respiratory, psychologic, and immunologic studies in relation to
methyl isocyanate exposure over two years with model development.
AU: Kamat-SR; Patel-MH; Pradhan-PV; Taskar-SP; Vaidya-PR; Kolhatkar-VP;
Gopalani-JP; Chandarana-JP; Dalal-N; Naik-M
AD: Department of Respiratory Medicine and Psychiatry, Seth G. S. Medical
College, Bombay, India.
SO: Environ-Health —Perspect. 1992 Jul; 97: 241-53
_____this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: Of 113 methyl isocyanate (MlC)-exposed subjects studied initially at
Bhopal, India, 79, 56, 68, and 87 were followed with clinical, lung function,
radiographic, and immunologic tests at 3, 6, 12, 18, and 24 months. Though our
cohort consisted of subjects at all ages showing a varied severity of initial
illness, fewer females and young subjects were seen. Initially all had eye
problems, but dominant symptoms were exertional dyspnea, cough, chest pain,
sputum, and muscle weakness. A large number showed persistent depression mixed
(With anxiety, with disturbances of personality parameters. The early
radiographic changes were lung edema, overinflation, enlarged heart, pleural
scars, and consolidation. The persistent changes seen were interstitial
deposits. Lung functions showed mainly restrictive changes with small airway
obstruction; there was impairment of oxygen exchange. Oxygen exchange improved
at 3-6 months, and spirometry improved at 12 months, only to decline later. The
expiratory flow rates pertaining to large and medium airway function improved,
but those for small airways remained low. There were changes of alveolitis in
bronchoalveolar lavage fluid on fiber optic bronchoscopy, and in 11 cases
positive MIC-specific antibodies to IgM, IgG, and IgE were demonstrated. On
follow up, only 487. of the subjects were clinically stable, while 507. showed
fluctuations. Thirty-two percent of the subjects had lung function
fluctuations. Detailed sequential behavior over 2-4 years was predicted for
dyspnea, forced vital capacity, maximum expiratory flow rate (0.25-0.75), peak
expiratory flow rate, V02, and depression score. A model for clinical behavior
explained a total variance of 52.47. by using the factors of cough, PC02 and
X-ray zones in addition to above five parameters. The behavior of the railway
colony group (1640 patients) revealed a similar pattern of illness. When this
observed pattern of changes was transferred to the affected Bhopal city
sections (with an equitable age-sex distribution), our model results were again
validated. Thus the picture of MIC-induced disease seems similar despite the
differences for age-sex and initial severity of illness in our cohort and in
the population of Bhopal city as predicted by our model.
7 of 9
Marked Record
TI: Toxicity of the methyl isocyanate metabolite S—(N—methylcarbamoyl)GSH on
mouse embryos in culture.
AU: Guest-I; Baillie-TA; Varma-DR
AD: Department of Pharmacology and Therapeutics, McGill University, Montreal,
Quebec, Canada.
SO: Teratology. 1992 Jul; 46(1): 61-7
____ this source is not Available in 8.J.M■C.Library
LA: ENGLISH
AB: Methyl isocyanate, the chemical involved in the 1984 accident at Bhopal.
India, forms a labile conjugate, S-(N-methylcarbamoyl)GSH (SMG), by way of a
reversible reaction with GSH. We studied the toxicity of SMG on mouse embryos
explanted on day 8 of gestation and cultured in rat serum for 42 hr. SMG caused

concentration-dependent decreases in growth and development over the range
0.1-2 mN, without causing significant mortality. At a concentration of 2 mN,
SMG completely arrested embryo development, but heartbeat was absent in only
one of nine embryos at 42 hr. At a concentration of 0.25 mH, SMG reduced embryo
size to 757. and protein content to 637. of the control; 187. of embryos failed to
rotate. At this concentration (0.25 mH), which was selected for all other
studies, spinal kinks and somite pair distortion in the region of the forelimb
were evident in 387. of embryos; no other abnormalities were noted. DNA content
of and thymidine incorporation by embryos and yolk sacs was reduced by SMG,
although this was more pronounced in the yolk sac than in embryos. At subtoxic
concentrations, the L-cysteine precursor (-)-2-oxo-4-thiazolidine-carboxy 1ic
acid did not, but GSH did, inhibit embryotoxicity of SMG. It is concluded that
SMG exerts embryotoxic and dysmorphogenic effects and may contribute to
systemic toxicity of methyl isocyanate.

TI: Trojan horse. Did a protective peptide exacerbate Bhopal
AUs Rennie—J
SO: Sci-Am. 1992 Mar; 266(3): 15-6
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1949+
LA: ENGLISH

8
of 9
Marked Record
injuries? [news]

9
of 9
Marked Record
TI: Accident analysis of large-scale technological disasters applied to an
anaesthetic complication [see comments]
AU: Eagle-CJ; Davies-JM; Reason-J
AD: Department of Anaesthesia, Foothills Hospital, University of Calgary,
Alberta, Canada.
SO: Can—J—Anaesth. 1992 Feb; 39(2): 118-22
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1966+
LA: ENGLISH
AB: The occurrence of serious accidents in complex industrial systems such as
at Three Mile Island and Bhopal has prompted development of new models of
causation and investigation of disasters. These analytical models have
potential relevance in anaesthesia. We therefore applied one of the previously
described systems to the investigation of an anaesthetic accident. The model
chosen describes two kinds of failures, both of which must be sought. The first
group, active failures, consists of mistakes made by practitioners in the
provision of care. The second group, latent failures, represents flaws in the
administrative and productive system. The model emphasizes the search for
latent failures and shows that prevention of active failures alone is
insufficient to avoid further accidents if latent failures persist unchanged.
These key features and the utility of this model are illustrated by application
to a case of aspiration of gastric contents. While four active failures were
recognized, an equal number of latent failures also became apparent. The
identification of both types of failures permitted the formulation of
recommendations to avoid further occurrences. Thus this model of accident
causation can provide a useful mechanism to investigate and possibly prevent
anaesthetic accidents.

PC-SPIRS 3.40

MEDLINE (R)

1991

MEDLINE (R) 1991 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 10
TI: Fetal loss and contraceptive acceptance among the Bhopal gas victims.
AU: Kapoor-R
AD: International Institute for Population Sciences, Bombay, India.
SO: Soc-Biol. 1991 Fall-Winter; 38(3-4): 242-8
_____this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: The rates of fetal loss and family planning acceptance among Bhopal gas
victims from 1984 to 1989 were compared to those of a control group. In all,
136 eligible women in the affected area and 139 women in the control area were
interviewed. Care was taken to ensure that these women had conceived at least
once during the previous five years. The The fetal loss rate among the
gas-affected women was abnormally high (26.3 per cent) compared to that of
women in the control area (7.8 per cent). Family planning acceptance in both
areas was similar, with most women using permanent methods. In the case of
temporary methods, the percentage of use was higher in the gas-affected area.
2
of 10
TI: GC-MS identification of MIC trimer: a constituent of tank residue in
preserved autopsy blood of Bhopal gas victims.
AU: Chandra-H; Rao-GJ; Saraf-AK; Sharma-VK; Jadhav-RK; Sriramachari-S
AD: Medicoleqal Institute, Bhopal, India.
SO: Med-Sci-Law. 1991 Oct; 31(4): 294-8
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: Based on the external and internal findings of Bhopal gas disaster victims,
it was apparent that the gases and particulate matter came out as an aerosol.
This was possibly the pyrolysed, reformulated, reconjugated suspension of
constituents of the tank E-610 of Union Carbide India Limited, Bhopal, while it
was claimed to be methyl isocyanate (MIC) only. It was postulated by the
manufacturer of MIC, that the material inhaled by the victims of the Bhopal gas
disaster does not cross the lung barrier (UCC press conference on 14th December
1984). It was observed that the more the victims ran, the more aerosol they
inhaled and the fatalities were observed in such victims. The tissues', which
were preserved in the deep freeze, were randomly selected and analysed by GC
coupled with MS (ITD) Finnigan MAT, UK. 14 out of 34 autopsy cases showed MIC
trimer peak in extracts of blood. This was one of the constituents of the
aerosol and was also located in the tank residue, thereby proving that the
trimer had passed the lung barrier.
3
of 10
TI: GC-NPD and GC-MS analysis of preserved tissue of Bhopal gas disaster:
evidence of methyl carbamylation in post-mortem blood.
AU: Sriramachari-S ; Rao-GJ; Sharma-VK; Jadhav-RK; Saraf-AK; Chandra-H
AD: Institute of Pathology (Indian Council of Medical Research), Safdarjung
Hospital, New Delhi.
SO: Med-Sci-Law. 1991 Oct; 31(4): 289-93
____ this source is not Available in S.J■M.C.Library
LA: ENGLISH
AB: Twenty-five preserved autopsy blood samples of Bhopal toxic gas exposed
victims were analysed by gas chromatography (GC) coupled with either
Nitrogen-Phosphorous detector (NPD) or mass spectrometer (MS) for the presence
of methyl carbamyl valine in terms of valine methyl hydantoin (VMH). 847. of

these samples showed a positive test for VMH on GC-NF'D and the identity of the
peaks were further confirmed on GC-MS. The concentration of VMH in the
gas-affected positive blood samples ranged from 2.56 to 51.28 nanomoles. These
results indicate entry of methyl isocyanate (MIC), one of the constituents of
the toxic cloud caused by the disaster, into the blood stream of victims who
had inhaled gas.

TI: Industrialization and emerging environmental health issues:
the Bhopal disaster.
AU: Murti-CR
AD: Madras Science Foundation, India.
SO: Toxicol-Ind-Health. 1991 Sep-Nov; 7(5-6): 153-64
_____this source is not Available in S.J,M■C.Library
LA: ENGLISH

4
of 10
lessons from

5 of 10
TI: Objective thoracic CT scan findings in a Bhopal gas disaster victim.
AU: Sharma-S; Narayanan-PS; Sriramachari-S; Vijayan-VK; Kamat-SR; Chandra-H
AD: Department of Radiology, G.B. Pant Hospital, New Delhi, India.
SO: Respir-Med. 1991 Nov; 85(6): 539-41
____ this source is not Available in S■J,M.C■Library
LA: ENGLISH
6
of 10
TI: Mass deaths by gas or chemical poisoning. A historical perspective.
AU: Eckert-WG
AD: Milton Helpern International Center of Forensic Sciences, Wichita State
University, Kansas.
SO: Am—J-Forensic-Med-Pathol. 1991 Jun; 12(2): 119-25
____ this source is not Available in S.J,M,C.Library
____ Call Number: From 1980+
LA: ENGLISH
AB: This review chronicles the characteristics of deliberate and accidental
mass poisonings that occurred in World Wars I and II, in Bhopal. and in other
historical cases up to and including modern wars. It also considers approaches
to the investigation of such cases from the medicolegal as well as general
standpoints.
7
of 10
TI: Technological disasters—towards a preventive strategy: a review.
AU: Andersson-N
AD: Centre for Tropical Disease Research (CIET), Faculty of Medicine,
Universidad Autonoma de Guerrero, Acapulco, Mexico.
SO: Trop-Doct. 1991; 21 Suppl 1: 70-81
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1971-1992
LA: ENGLISH
AB: Technological or man-made disasters are a growth industry. Widely
publicized industrial disasters like those in Bhopal and Chernobyl are only the
tip of the iceberg of human and environmental risk from technological
development. Other less well publicized disasters, including the contamination
of food, water and air, have affected millions of people. The 'slow'
technological disasters - like air pollution, pesticides, radiation, lead,
asbestos and other industrial hazards - also compromise human intellectual,
behavioural and physical development. Although it can be argued that there are
hazards attached to virtually every industrial activity and that it is almost
impossible to remove completely the risk of technological disasters, it is
possible to reduce this risk by decentralizing or deconcentrating knowledge on
technological processes. Global recommendations may provide a framework for
priority action, but they are obviously not applicable everywhere with the same

intensity. A measurement-based approach is described that is beginning to have
an effect in several developing countries.

TIs Cytogenetic studies on MIC gas-exposed persons in Bhopal
AU: Das-BC
SO: Hum-Genet. 1991 Aug; 87(4): 513-5
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH

8
of 10
[letter; comment]

9
of 10
TI: An overview of process hazard evaluation techniques.
AU: Gressel-MG; Gideon-JA
AD: National Institute for Occupational Safety and Health, Division of Physical
Sciences and Engineering, Cincinnati, OH 45226.
SO: Am-Ind-Hyg-Assoc-J. 1991 Apr; 52(4): 158-63
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1970-1975
LA: ENGLISH
AB: Since the 1985 release of methyl isocyanate in Bhopal, India, which killed
thousands, the chemical industry has begun to use process hazard analysis
techniques more widely to protect the public from catastrophic chemical
releases. These techniques can provide a systematic method for evaluating a
system design to ensure that it operates as intended, help identify process
areas that may result in the release of a hazardous chemical, and help suggest
modifications to improve process safety. Eight different techniques are
discussed, with some simple examples of how they might be applied. These
techniques include checklists, "what if" analysis, safety audits and reviews,
preliminary hazard analysis (PHA), failure modes and effect analysis (FMEA),
fault tree analysis (FTA), event tree analysis (ETA), and hazard and
operability studies (HAZOP). The techniques vary in sophistication and scope,
and no single one will always be the best. These techniques can also provide
the industrial hygienist with the tools needed to protect both workers and the
community from both major and small-scale chemical releases. A typical
industrial hygiene evaluation of a facility would normally include air
sampling. If the air sampling does detect a specific hazardous substance, the
source will probably be a routine or continuous emission. However, air sampling
will not be able to identify or predict the location of a nonroutine emission
reliably. By incorporating these techniques with typical evaluations, however,
industrial hygienists can proactively help reduce the hazards to the workers
they serve.
10 of 10
TI: Developmental toxicity of methylamines in mice.
AU: Guest-I; Varma-DR
AD: Department of Pharmacology and Therapeutics, McGill University, Montreal,
Canada.
SO: J-Toxicol-Environ-Health. 1991 Mar; 32(3): 319-30
____ This source is Available only few issues in S.J.M.C. Library
LA: ENGLISH
AB: Monomethylamine (MMA), dimethylamine (DMA), and trimethylamine (TMA) are
endogenous substances as well as metabolites of methyl isocyanate, the chemical
involved in the 1984 accident at Bhopal, India. Although methylamines exert
several toxic effects including inhibition of protein turnover and oocyte RNA
synthesis, their reproductive toxicity has not been investigated. We therefore
studied the possible developmental toxicity of these amines using pregnant CD—1
mice and mouse embryo culture as experimental models. Intraperitoneal
injections (daily from d 1 to 17 of gestation) of TMA at 2.5 and 5 mmol/kg/d
significantly (p less than .001) decreased fetal body weight but not the
placental weight or maternal body weight gain; however, 5 of 11 mice treated
with 5 mmol/kg TMA died. Similar treatment with DMA and MMA did not exert any

obvious maternal or fetal effects. All three methylamines, when added to
embryos in culture, caused dose-dependent decreases in size, DNA, RNA, and
protein content as well as embryo survival; the order of toxicity was TMA
greater than DMA greater than MMA. The ability of methylamines to adversely
affect fetal development suggests that these amines, especially trimethylamine,
may act as endogenous teratogens under certain conditions.

FC-SPIRS 3-40

MEDLINE (R)

1990

MEDLINE (R) 1990 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 12
Marked Record
TI: Industry's voluntary program: Community Awareness and Emergency Response
Program and the Emergency Planning and Community Right-to-Know Act.
AU: Cooper-JS
AD: Environmental Policy Group, Hill and Knowlton Public Affairs Worldwide,
Washington, D.C. 20007.
SO: Toxicol-Ind-Health. 1990 Oct; 6(5): 13-21
____ this source is not Available in S.J.M,C.Library
LA: ENGLISH
AB: This paper describes the chemical industry's Community Awareness and
Emergency Response (CAER) Program, and voluntary and mandatory actions by the
chemical industry to comply with the major environmental legislation. The
chemical industry started the voluntary CAER Program soon after the Bhopal
Disaster in 1984; it is coordinated through the Chemical Manufacturer's
Association. This program, which began in March 1985, is a long-term industry
commitment to develop a community outreach program and to improve local
emergency response planning. The Congress of the United States began, in 1985,
to consider proposals for mandatory programs. This led to enactment of the
Superfund Amendments and Reauthorization Act of 1986, known as SARA. A portion
of this Act, entitled Title III is also known as the Emergency Planning and
Community Right-to-Know Act. Although this legislation has many mandatory
requirements, it should be emphasized that a significant degree of voluntary
industrial participation is needed if the purposes of the statute are to be
achieved. Title III has created an intricate and still evolving system that
ties together the EPA, industrial plant managers, state emergency response
commissions, local emergency planning committees and fire departments with
jurisdiction over the facility. Each of these groups has a different role and
responsibilities but must work cooperatively with other participants. Because
of the intricate network of participants, the magnitude of the information
flow, and the continuing evolution of the system, unique public relations
problems exist in order to comply with Title 111.(ABSTRACT TRUNCATED AT 250
WORDS)
2
of 12
Marked Record
TI: Air toxics in the U.S.: magnitude of the problem and strategy for control.
AU: Berry—DK
AD: Air Quality Management Division, U.S. Environmental Protection Agency,
Research Triangle Park, North Carolina 27711.
SO: Toxicol-Ind-Health. 1990 Oct; 6(5): 1-12
____ this source is not Available in 5■J■M.C.Library
LA: ENGLISH
AB: Over the past several years, substantial concern has been expressed by some
in Congress, environmental groups, and members of the public concerning the
lack of progress in regulating toxic air pollutants by the U.S. Environmental
Protection Agency (EPA). As a result, a number of amendments to the Federal
Clean Air Act have been introduced to require EPA to regulate in a relatively
rapid timeframe, a large number of potentially toxic pollutants that are
released to the ambient air. This paper discusses EPA's current understanding
of the magnitude and nature of the air toxics problem in the U.S., and the
pollutants and source categories that pose the most significant risk to the
public. The focus of the discussion is on routine releases, as opposed to

catastrophic, accidental releases such as the one in Bhopal. India. The paper
then discusses the strategy that ERA has put in place to "deal with the problem
and presents the status of a number of regulatory and non-regulatory activities
under way to better understand the problem and to mitigate it. The strategy
involves important roles for: (1) ERA to regulate national problems using a
variety of Federal authorities in addition to the Clean Air Act, and (2) States
to develop their own air toxic control programs to deal with unique local
problems involving • high risk point sources and multipollutant, multisource
problems in large urban or industrialized areas.

•
3 of 12
Marked Record
TI: The current practice of health risk assessment: potential impact on
standards for toxic air contaminants.
AU: Paustenbach-DJ; Jernigan-JD; Finley-BL; Ripple-SR; Keenan-RE
AD: ChemRisk, Division of McLaren/Hart Environmental Engineering Corp.,
Alameda, California.
SO: J-Air-Waste-Manage-Assoc. 1990 Dec; 40(12): 1620-30
this source is not Available in S■J■M.C.Library
LA: ENGLISH
AB: Since the Bhopal incident, the public has placed pressure on regulatory
agencies to set community exposure limits for the dozens of chemicals that may
be released by manufacturing facilities. More or less objective limits can be
established for the vast majority of these chemicals through the use of risk
assessment. However, each step of the risk assessment process (i.e., hazard
identification, dose-response assessment, exposure assessment, and risk.
characterization ) contains a number of pitfalls that scientists need to avoid
to ensure that valid limits are established. For example, in the hazard
identification step there has been little discrimination among animal
carcinogens with respect to mechanism of action or the epidemiology experience.
In the dose-response portion, rarely is the range of "plausible" estimated
risks presented. Physiologically based pharmacokinetic (PB-PIC) models should be
used to understand the difference between the tissue doses and the administered
dose, as well as the difference in target tissue concentrations of the toxicant
between rodents and humans. Biologically-based models like the
Moolgavkar-Knudson-Venzon (MKV) should be developed and used, when appropriate.
The exposure assessment step can be significantly improved by using more
sensitive and specific sampling and analytical methods, more accurate exposure
parameters, and computer models that can account for complex environmental
factors. Whenever possible, model predictions of exposure and uptake should be
validated by biological monitoring of exposed persons (urine, blood, adipose)
or by field measurements of plants, soil, fish, air, or water. In each portion
of an assessment, the weight of evidence approach should be used to identify
the most defensible value. In the risk characterization, the best estimate of
the potential risk as well as the highest plausible risk should be presented.
Future assessments would be much improved if quantitative uncertainty analyses
were conducted. Procedures are currently available for making future
assessments. By correcting some of these shortcomings in how health risk
assessments have been conducted, scientists and risk managers should be better
able to identify scientifically appropriate ambient air standards and emission
1imits.
4
of 12
Marked Record
TI: Industry's voluntary program: Community Awareness and Emergency Response
Program and the Emergency Planning and Community Right-to-Know Act.
AU: Cooper—JS
AD: Environmental Policy Group, Hill and Knowlton Public Affairs Worldwide,
Washington, D.C. 20007.
SO: Toxicol-Ind-Health. 1990 Oct; 6(5): 13-21
this source is not Available in S.J.M.C.Library

LA: ENGLISH
AB: This paper describes the chemical industry's Community Awareness and
Emergency Response (CAER) Program, and voluntary and mandatory actions by the
chemical industry to comply with the major environmental legislation. The
chemical industry started the voluntary CAER Program soon after the Bhopal
Disaster in 1984; it is coordinated through the Chemical Manufacturer's
Association. This program, which began in March 1985, is a long-term industry
commitment to develop a community outreach program and to improve local
emergency response planning. The Congress of the United States began, in 1985,
to consider proposals for mandatory programs. This led to enactment of the
Superfund Amendments and Reauthorization Act of 1986, known as SARA. A portion
of this Act, entitled Title III is also known as the Emergency Planning and
Community Right-to—Know Act. Although this legislation has many mandatory
requirements, it should be emphasized that a significant degree of voluntary
industrial participation is needed if the purposes of the statute are to be
achieved. Title III has created an intricate and still evolving system that
ties together the EPA, industrial plant managers, state emergency response
commissions, local emergency planning committees and fire departments with
Jurisdiction over the facility. Each of these groups has a different role and
responsibilities but must work cooperatively with other participants. Because
of the intricate network of participants , the magnitude of the information
flow, and the continuing evolution of the system, unique public relations
problems exist in order to comply with Title 111.(ABSTRACT TRUNCATED AT 250
WORDS)

5
of 12
Marked Record
TI: Public health lessons from the Bhopal chemical disaster [published erratum
appears in JAMA 1991 Feb 20;265(7):869] [comment]
AU: Koplan-JP; Falk-H; Green-G
AD: Centers for Disease Control, Center for Chronic Disease Prevention and
Health Promotion, Atlanta, GA 30333.
SO: JAMA. 1990 Dec 5; 264(21): 2795-6
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1918+
LA: ENGLISH

TI: Bhopal tragedy's health effects. A review of methyl
[see comments]
AU: Mehta-PS; Mehta-AS; Mehta-SJ; Makhijani-AB
AD: Humana Hospital, Aurora, Colo.
SO: JAMA. 1990 Dec 5; 264(21): 2781-7
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1918+
LA: ENGLISH

6 of 12
Marked Record
isocyanate toxicity

7
of 12
Marked Record
TI: Effects of methyl isocyanate on rat brain cells in culture.
AU: Anderson-D; Goyle-S; Phillips-BJ; Tee-A; Beech-L; Butlet—WH
AD: British Industrial Biological Research Association, Carshalton, Surrey.
SO: Br-J-Ind-Med. 1990 Sep; 47(9): 596-601
____ This source is Available only few issues in S.J.M.C. Library
____ Call Number: From: 1956-1991
LA: ENGLISH
AB: Since the disaster in Bhopal, India, people exposed to methyl isocyanate
(MIC) have complained of various disorders including neuromuscular dysfunction.
In an attempt to get information about such dysfunction we have previously
shown that MIC can affect muscle cells in culture. The present communication

reports investigations into the effect of MIC on brain cells in culture. MIC
was toxic to brain cells and the response was dose related. The observations
were supported by light and electron microscopy.
a of 12
Marked Record
TIs Cytogenetic studies in human populations exposed to gas leak at Bhopal .
India.
AU: Ghosh-BB; Sengupta-S; Roy-A; Maity-S; Ghosh-S; Talukder-G; Sharma-A
AD: Human Genetics Unit, Center for Advanced Study in Cell and Chromosome
Research, Calcutta, India.
SO: Environ-He'alth-Perspect. 1990 Jun; 86: 323-6
____ this source is not Available in S.J■M.C.Library
LA: ENGLISH
AB: Frequencies of chromosomal abnormalities, sister chromatid exchanges, and
replicative index were assessed following peripheral lymphocyte culture in 129
individuals from Bhopal. India. Of these, S3 persons (40 male and 43 female)
had been exposed directly to the methyl isocyanate (MIC) gas after the accident
at the Union Carbide plant on December 2 and 3, 1984. The remaining 46 samples
were taken from age-matched unexposed persons in the same city. Chromosome
aberrations were recorded at first cycle metaphase (Ml) and sister chromatid
exchanges, at second cycle metaphase (M2), following standard schedule. The
frequency of chromosomal aberrations was, in general, higher in individuals
from the exposed populations, with the females showing a higher incidence.
Nondisjunction of chromosomes or laggard was rare. The frequencies of sister
chromatid exchanges and depression in mitotic and replicative indices could not
be related to exposure or sex. The persistence of chromosomal abnormalities in
the form of replicating minutes and exchange configurations, even 1114 days
after exposure to the gas, may indicate a residual effect on T—cell precursors.

9 of 12
Marked Record
TI: Delayed eye and other consequences from exposure to methyl isocyanate: 937.
follow up of exposed and unexposed cohorts in Bhopal.
AU: Andersson-N; Ajwani-MK; Mahashabde-S; Tiwari-MK; Muir-MK} Mehra-V;
Ashiru-K; Mackenzie—CD
AD: TUC Centenary Institute of Tropical Medicine, London School of Hygiene &
Tropical Medicine.
SO: Br-J-Ind-Med. 1990 Aug; 47(8): 553-8
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: .1956-1991
LA: ENGLISH
AB: A follow up study three years after exposure to methyl isocyanate in 937. of
exposed survivors and "control" residents in 10 Bhopali communities showed an
excess of eye irritation, eyelid infection, cataract, and a decrease in visual
acuity among the exposed people. Breathlessness was twice as common in the
heavily exposed clusters as those with lower exposure, a trend that could not
be explained by different age or smoking patterns (OR 2.05, 957. CI 1.36—3.08).
Case referent analysis of outpatient attendances at Bhopal Eye Hospital,
considering patients with severe refractive errors and astigmatism as
"controls," showed a 407. increased risk of trachoma, 367. increased risk of
other lid infections, and 457. increased risk of irritant symptoms among
previously exposed people. "Bhopal eye syndrome" may thus include full
resolution of the initial interpalpebral superficial erosion, a subsequent
increased risk of eye infections, hyperresponsive phenomena (irritation,
watering, and phlyctens), and possibly cataracts. It remains to be confirmed
whether this reflects a more generalised disease as a consequence of previous
exposure to methyl isocyanate or whether it is only the eye that is affected.
10 of 12
Marked Record

Marked Record
TI: Early observations on pulmonary changes and clinical morbidity due to the
isocyanate gas leak at Bhopal.
AU: Kamat-SR; Mahashur-AA; Tiwari-AK; Potdar-PV; Gaur-M; Kolhatkar-VP;
Vaidya—P; Parmar-D; Rupwate—R; Chatterjee—TS; et—al
SO: J-Postgrad-Med. 1985 Apr; 31(2): 63-72
____ This source is Available only few issues in S.J.M.C. Library
Call Number: from 1955-1985
LA: ENGLISH
8 of 11
Marked Record

TI: The Bhopal tragedy.
AU: Das-JJ
SO: J-Indian-Med-Assoc. 1985 Feb; 83(2): 72-4
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
9 of 11
Marked Record
TI: American personal-injury lawyers at Bhopal . Ethics and public policy in
mass disaster.
AU: Curran-WJ
SO: N-Eng1—J-Med. 1985 Oct 24; 313(17): 1068-70
This source is Available in S.J.M.C Library
Call Number: From: 1945+
LA: ENGLISH

10 of 11
Marked Record

TI: Bhopal tragedy focuses on changes in chemical industry.
AU: Aydelotte-C
SO: Occup-Health—Saf. 1985 Mar; 54(3): 33-5, 50, 59
____ this source is not Available in S.J■M,C.Library
LA: ENGLISH
11 of 11
Marked Record
TI: Bhopal tragedy's repercussions may reach American physicians [news]
AU: Marwick-C
SO: JAMA. 1985 Apr 12; 253(14): 2001-3
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1918+
LA: ENGLISH

PC-SPIRS 3.40

MEDLINE (R)

1984

MEDLINE (R) 1984 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.
1 of 1
Marked Record

TI: Calamity at Bhopal [editorial]
SO: Lancet. 1984 Dec 15; 2(8416): 1378-9
____ This source is.Available in S.J.M.C Library
Call Number: From: 1930+
LA: ENGLISH

PC-SPIRS 3.40

MEDLINE (R)

1985

MEDLINE (R) 1985 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 11
Marked Record
TI: Bhopal disaster: eye follow-up and analytical chemistry [letter]
AU: Andersson-N; K.err-Muir-M ; Salmon-AG; Wells-CJ; Brown-RB; F'urnell-CJ;
Mittal-PC; Mehra-V
SO: Lancet. 1985 Mar 30; 1(8431): 761-2
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1930+
LA: ENGLISH
2
of 11
Marked Record

TI: An eyewitness in Bhopal.
AU: Sutcliffe-M
SO: Br-Med-J-Clin-Res-Ed. 1985 Jun 22; 290(6485): 1883-4
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH

TI: Chronobiologic considerations of the Bhopal methyl
[letter]
AU: Reinberg-A; Smolensky-MH
SO: Chronobiol—Int. 1985; 2(1): 61-2
this source is not Available in S.J.M■C.Library
LA: ENGLISH

3
of 11
Marked Record
isocyanate disaster

4 of 11
Marked Record

TI: Bhopal tragedy—a year later [editorial]
AU: Sainani-GS; Joshi-VR; Mehta-PJ; Abraham-F'
SO: J-Assoc-Physicians-India. 1985 Dec; 33(12): 755-6
____ this source is not Available in S■J.M.C.Library
LA: ENGLISH

5 of 11
Marked Record
TI: Aftermath of Bhopal tragedy [editorial]
AU: Das—JJ
SO: J-Indian-Med-Assoc . 1985 Oct; 83(10): 361-2
____ this source is not Available in S.J.M■C.Library
LA: ENGLISH

TI: Ocular lesions following methyl isocyanate contamination:
experience [letter]
AU: Dwivedi-PC; Raizada-JK; Saini-VK; Mittal-PC
SO: Arch-Ophthalmol . 1985 Nov; 103(11): 1627
____ This source is Available in S.J.M.C Library
Call Number: From: 1943+
LA: ENGLISH

6 of 11
Marked Record
the Bhopal

LA:

This source is Available only few issues in S.J.M.C. Library
Call Number: from 1955-1985
ENGLISH

13 of 17
Marked Record
TIs The Bhopal tragedy—what has Swedish disaster medicine planning learned
from it?
AU: Lorin-HG; Kulling-PE
SO: J-Emerg-Med. 1986; 4(4): 311-6
_____this source is not Available in S.J.M.C■Library
LA: ENGLISH
AB: On December 3, 1984, a leak of methyl isocyanate (MIC) from a chemical plan
in Bhopal, India, affected 150,000 to 200,000 people. More than 10,000 people
were severely injured and approximately 2,500 died. In this article a survey o
symptoms, treatment, and rescue work is given. On the basis of this, we discus
ways to help reduce the effects of a major release of an irritant gas. People
living in the vicinity of potential health hazards need information on how to
behave in case of accidents. Rescue workers and medical personnel must be
trained to operate under "toxic conditions." There must be planning for
treatment of thousands of patients at the same time, a circumstance that will
often require temporary "satellite hospitals" to be opened. As symptoms and
injuries are of the same kind, even if the magnitude and the effect may differ
treatment can, in many ways, be standardized. Therefore members of the health
care team, irrespective of their daily different specialty fields, can work
with the most urgent missions.

14 of 17
Marked Record

TI: Bhopal tragedy—a year later [letter]
AU: Misra-NP
SO: J-Assoc-Physicians-India. 1986 Apr; 34(4): 307
this source is not Available in S.J.M.C.Library
LA: ENGLISH
15 of 17
Marked Record

TI: Bright red blood of Bhopal victims: cyanide or MIC? [letter]
AU: Salmon—AG
SO: Br-J-Ind-Med. 1986 Jul; 43(7): 502
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1956-1991
LA: ENGLISH
16 of 17
Marked Record

TI: Bhopal and after [editorial]
AU: Zaidi-SH
SO: Am-J-Ind-Med. 1986; 9(3): 215-6
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
17 of 17
Marked Record
TI: From Flixborough to Bhopal: is legislation enough? [editorial]
AU: Baxter-PJ
SO: Br-J-Ind-Med. 1986 Jan; 43(1): 1-3
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1956-1991
LA: ENGLISH

AU: Maskati-QB
SO: J-Postgrad-Med. 1986 Oct; 32(4): 199-202
____ This source is Available only few issues in S.J.M.C. Library
Call Number: from 1955-1985
LA: ENGLISH
7 of 1.7
Marked Record
TI: Sequential study of thiocyanate levels in Bhopal water following methyl
isocyanate gas leakage.
AU: Acharya-VN; Naik-SR; Potnis-AV; Bhalerao-RA
SO: J-Postgrad-Med. 1986 Oct; 32(4): 192-4
____ This source is Available only few issues in S.J.M.C. Library
Call Numbers from 1955-1985
LA: ENGLISH
8 of 17
Marked Record

TI: Medico-legal aspects of the Bhopal tragedy.
AU: Parikh—CK
SO: Leg-Med. 1986: 28-39
____ this source is not Available in S.J.M.C.Librarv
LA: ENGLISH
9 of 17
Marked Record
TI: Gynaecological and obstetrical survey of Bhopal women following exposure to
methyl isocyanate.
AU: Shilotri-NP; Raval-MY; Hinduja-IN
SO: J-Postgrad-Med. 1986 Oct; 32(4): 203-5
____ This source is Available only few issues in S.J.M.C. Library
____ Call Number: from 1955-1985
LA: ENGLISH

10 of 17
Marked Record
TI: A survey of Bhopal children affected by methyl isocyanate gas.
AU: Irani-SF; Mahashur-AA
SO: J-Postgrad-Med. 1986 Oct; 32(4): 195-8
____ This source is Available only few issues in S.J.M.C. Library
____ Call Number: from 1955-1985
LA: ENGLISH

11 of 17
Marked Record
TI: Medical survey of methyl isocyanate gas affected population of Bhopal ■ Part
II. Pulmonary effects in Bhopal victims as seen 15 weeks after M.I.C. exposure.
AU: Naik-SR; Acharya-VN; Bhalerao-RA; Kowli-SS; Nazareth-H; Mahashur-AA;
Shah-S; Potnis-AV; Mehta-AC
SO: J-Postgrad-Med. 1986 Oct; 32(4): 185-91
____ This source is Available only few issues in S.J.M.C. Library
Call Number: from 1955-1985
LA: ENGLISH
12 of 17
Marked Record
TI: Medical survey of methyl isocyanate gas affected population of Bhopal ■ Part
I.
General medical observations 15 weeks following exposure.
AU: Naik-SR; Acharya-VN; Bhalerao-RA; Kowli-SS; Nazareth-H; Mahashur-AA;
Shah-S; Potnis-AV; Mehta-AC
SO: J-Postgrad-Med. 1986 Oct; 32(4): 175-84

PC-SPIRS 3.40

MEDLIME (R)

1986

MEDLINE (R) 1986 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.
1 of 17
Marked Record
TI: Persistent eye watering among Bhopal survivors [letter]
AU: Andersson-N; Kerr-Muir-M; Ajwani-MK; Mahashabde-S; Salmon-A; Vaidyanathan-K
SO: Lancet. 1986 Nov 15; 2(8516): 1152
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1930+
LA: ENGLISH

2 of 17
Marked Record
TI: Ophthalmic survey of Bhopal victims—100 days after the tragedy.
AU: Maskati-QB
SO: Indian-J-Ophthalmol. 1986; 34: 328-31
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1973+
LA: ENGLISH
3 of 17
Marked Record

TI : Acute ocular lesions in Bhopal gas tragedy.
AU: Raizada-JK; Dwivedi-PC
SO: Indian-J-Ophthalmol . 1986; 34: 324-7
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1973+
LA: ENGLISH
4 of 17
Marked Record

TI: Bhopal: a bibliography.
AU: Mac-Sheoin-T
SO: Int-J-Health-Serv. 1986; 16(3): 441-68
____ this source is not Available in S.J.M.C,Library
LA: ENGLISH
5 of 17
Marked Record
TI : Toxic chemical disasters and the implications of Bhopal for technology
transfer.
AU: Weiss-B; Clarkson-TW
SO: Milbank-Q. 1986; 64(2): 216-40
_____this source is not Available in S.J.M.C.Library
LA: ENGL ISH
AB: The dramatic disaster in 1984 at Bhopal , India, may be overshadowed in
total impact by less immediate health effects characterized by long latency,
cumulative damage, and subtle impairments. Transfer of chemical technology must
be accompanied by transfer of the corresponding infratechnology, toxicology,
only then can the process of technology transfer be managed with fewer risks,
fewer costs, and fewer tragic surprises.
6 of 17
Marked Record
TI: Ophthalmic survey of Bhopal victims 104 days after the tragedy.

TIs Penetration of methyl isocyanate through organic vapor and acid gas
respirator cartridges.
AU: Moyer-ES; Berardinel1i-SP
SO: Am-Ind-Hyg-Assoc-J. 1987 Apr; 48(4): 315-23
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1970-1975
LA: ENGLISH
AB: Methyl isocyanate (MIC) is a volatile., toxic chemical [Threshold Limit
Value (TLV) = 0.02 ppm] used to manufacture carbamate pesticides. The principal
manufacturer of MIC is Union Carbide, and the site of production is Institute,
West Virginia. In light of the December 1984 Bhopal, India disaster and
possible safety problems at the Institute facility, NIOSH conducted this
research as a basis upon which to recommend protective equipment that might be
used in an emergency situation where extremely high MIC concentrations might be
encountered. Both protective clothing and respirators were evaluated. In
particular, NIOSH studied air-purifying respirators in order to assess their
effectiveness against MIC vapor penetration. NIOSH does not recommend any air
purifying respirator for MIC because of its high toxicity and lack of warning
properties and because no effective end of service life indicator currently is
available for MIC. This report addresses only MIC penetration through
air—purifying cartridges at challenge concentrations designed to simulate
emergency escape conditions. Another report addresses the protective clothing
issue. The results presented are for two different manufacturers' organic vapor
(OV) and acid gas cartridges. Penetration tests were conducted at three or four
MIC challenge concentrations and at three different humidity conditions. In
general, breakthrough times (17. of challenge concentration) were very short
(less than 20 min). Also, high relative humidity was found to decrease the
breakthrough time of MIC.
29 of 29
Marked Record

TI: Bright red blood of Bhopal victims? [letter!
AU: Nemery-B
SO: Br—J-Ind-Med. 1987 Apr; 44(4): 287
____ This source is Available only few issues in S.J.M.C. Library
____ Call Number: From: 1956-1991
LA: ENGLISH

stillbirths, infant mortality, and fetal abnormalities, no clinical or
experimental studies on the reproductive toxicity of MIC were reported in
scientific journals for several months after the accident. We therefore
conducted, 9 months after the accident, a preliminary survey of 3270 families
in Bhopal and experimental studies on the effects of MIC in pregnant mice. It
was found that 437. of pregnancies in women residing near the Union Carbide
pesticide plant did not result in the birth of a live child. Likewise, exposure
of mice to relatively low concentrations of MIC (9 and 15 ppm) for 3 hr caused
complete resorption in more than 757. of animals. A decrease in fetal and
placental weights was observed at 2 to 15 ppm MIC. In general, the experimental
findings in mice corroborate the epidemiological data from Bhopal■ The
mechanism of the fetal toxicity of MIC remains to be established.

25
of 29
Marked Record
TI: Biological effects of short-term, high-concentration exposure to methyl
isocyanate. I. Study objectives and inhalation exposure design.
AU: Dodd-DE; Frank-FR; Fowler-EH; Troup-CM; Milton-RM
SO: Environ-Heal th-F'erspect. 1987 Jun; 72: 13-9
____ this source is not Available in S■J.M.C.Library
LA: ENGLISH
AB: Early reports from India indicated that humans were dying within minutes to
a few hours from exposure to methyl isocyanate (MIC). Attempts to explain the
cause(s) of these rapid mortalities is where Union Carbide Corporation
concentrated its post-Bhopal toxicologic investigations. The MIC studies
involving rats and guinea pigs focused primarily on the consequences of acute
pulmonary damage. All MIC inhalation exposures were acute, of short duration
(mainly 15 min), and high in concentration (ranging from 25-3506 ppm). MIC
vapors were statically generated in a double chamber exposure design.
Precautionary measures taken during exposures are discussed. Guinea pigs were
more susceptible than rats to MIC exposure-related early mortality. A greater
than one order of magnitude difference was observed between an MIC
concentration that caused no early mortality in rats (3506 ppm) and an MIC
concentration that caused partial (6%) early mortality in guinea pigs (225 ppm)
for exposures of 10 to 15 min duration. For both species, the most noteworthy
clinical signs during exposure were lacrimation, blepharospasm, and mouth
breathing. Fifteen minute LC50 tests with 14-day postexposure follow-up were
conducted, and the LC50 (957. confidence limit) values were 171 (114—256) ppm
for rats and 112 (61-204) ppm for guinea pigs. Target exposure concentrations
for the toxicologic investigations of MIC—induced early mortality were
established. A short summary of pertinent results of Union Carbide
Corporation's post-Bhopal toxicologic investigations is presented.
26
of 29
Marked Record

TI: The Bhopal tragedy.
AU: Srivatsa-LP
SO: J—Toxicol-Clin-Exp . 1987 Jan-Feb; 7(1): 47-9
____ this source is not Available in S.J■M.C.Library
LA: ENGLISH

27-of 29
Marked Record
TI: Spectre of the Bhopal disaster [letterj
SO: Am-J-Public—Heal th. 1987 Jul; 77(7): 878-9
____ This source is Available only few issues in S.J.M.C.
Call Number: From: 1942-1991
LA: ENGLISH

Library

28 of 29
Marked Record

21
of 29
Marked Record
TI: K.A.P. survey of contraception in Bhopal and surrounding villages.
AU: Ranganekar-G; Sapre-S; Singh-H
SO: Indian-J-Med-Sci. 1987 Jun; 41(6): 119-23
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1947+
LA: ENGLISH

22
of 29
Marked Record

TI: Bhopal aftermath re-assessed [news]
AU: Jayaraman-KS
SO: Nature. 1987 Oct 29-Nov 4; 329(6142): 752
This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1956-1993
LA: ENGLISH
23
of 29
Marked Record
TI: The antibody response to methyl isocyanate: experimental and clinical
findings.
AU: Karol-MH; Taskar-S; Gangal-S; Rubanoff-BF; Kamat-SR
SO: Environ-Health-Perspect. 1987 Jun; 72: 169-75
____ this source is not Available in S■J■M■C.Library
LA: ENGLISH
AB: As a result of the industrial accident in Bhopal, India (December 1984) in
which thousands of people were exposed to methyl isocyanate (MIC), concern was
raised for possible long-term health effects. The well-recognized immunologic
consequences of exposure to other industrial isocyanates prompted investigation
of an antibody response to MIC. Using procedures which had been developed in
this laboratory to evaluate isocyanate immunotoxicity, animal studies were
undertaken to develop and test reagents which could be used to detect
antibodies to MIC in the exposed population. Guinea pigs were injected with MIC
in its reactive isocyanate form. Three weeks later, blood was drawn and serum
evaluated using ELISA. To detect antibodies, an antigen was prepared by
reaction of MIC with guinea pig serum albumin. Antibodies were detected in each
of the four animals injected with MIC. Titers achieved were 1:5120 to 1:10,240.
Inhibition assays revealed antibody specificity directed toward the MIC hapten.
Analogous antigens prepared by reaction of MIC with human serum albumin were
used to evaluate sera from individuals exposed in Bhopa1 to MIC. Antibodies
were detected in 12 of 144 exposed persons. Antibodies were specific for MIC,
as evidenced by inhibition assays, and belonged to the IgG, IgM and IgE
classes. However, titers were generally low and transient and were found in
persons having had the highest MIC exposures. Total IgE values of sera were not
significantly different from those of control sera obtained from Bombay
residents. The results indicate that exposure to methyl isocyanate resulted in
production of specific antibodies. However, the low titers observed and the
transient nature of the response suggest little health consequence should
result form the antibody response.
24
of 29
Marked Record
TI: Epidemiological and experimental studies on the effects of methyl
isocyanate on the course of pregnancy.
AU: Varma-DR
SO: Environ-Health-Perspect. 1987 Jun; 72: 153-7
____ this source is not Available in S■J.M.C.Library
LA: ENGLISH
AB: Although press reports indicate that the leakage of methyl isocyanate (MIC)
on December 3, 1984, in Bhopal has led to an increase in spontaneous abortions,

This source is Available in S.J.M.C Library
____ Call Number: From; 1943+
LA: ENGLISH
15 of 29
Marked Record
TI: Mental health needs of Bhopal disaster victims & training of medical
officers in mental health aspects.
AU: Murthy—RS; Isaac-MK
SO: Indian-J-Med-Res. 1987; 86 Suppl: 51-8
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1943+
LA: ENGLISH

16 of 29
Marked Record
TI: Psychiatric morbidity in patients attending clinics in gas affected areas
in Bhopal.
AU: Sethi-BB; Sharma-M; Trivedi-JK; Singh-H
SO: Indian-J-Med-Res. 1987; 86 Suppl: 45-50
____ This source is Available in S.J.M.C Library
Call Number: From: 1943+
LA: ENGLISH

17 of 29
Marked Record
TI: Sequential respiratory changes in those exposed to the gas leak at Bhopal.
AU: Kamat-SR; Patel-MH; Kolhatkar-VP; Dave-AA; Mahashur-AA
SO: Indian-J-Med-Res. 1987; 86 Suppl: 20-38
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1943+
LA: ENGLISH
18 of 29
Marked Record
TI: Clinical profile of gas leak victims in acute phase after Bhopal episode.
AU: Misra-NP; F'athak-R; Gaur-KJ; Jain-SC; Yesikar-SS; Manoria-PC; Sharma-KN;
Tripathi-BM; Asthana-BS; Trivedi-HH; et-al
SO: Indian-J-Med-Res. 1987; 86 Suppls 11-9
____ This source is Available in S.J.M.C Library
____ Call Number: From; 1943+
LA; ENGLISH

19 of 29
Marked Record

TI: Scientific studies on Bhopal gas victims. Part-A.
SO: Indian-J—Med-Res. 1987; 86 Suppl: 1-86
____ This source is Available in S.J.M.C Library
____ Call Number; From: 1943+
LA: ENGLISH
20 of 29
Marked Record
TI: Early observations on lung function studies in symptomatic "gas" exposed
population of Bhopal.
AU: Bhargava-DK; Verma-A; Batni-G; Misra-NP; Tiwari-UC; Vijayan-VK; Jain-SK
SO: Indian-J-Med-Res. 1987; 86 Suppl: 1-10
____ This source is Available in S.J.M.C Library
Call Number: From; 1943+
LA: ENGLISH

survivors. Available evidence, which is limited, suggests that chronic damage,
when present, is, or resembles, fibrosing bronchiolitis obliterans, the
expected consequence when permanent injury results from acute, high-level
irritant gas exposure. Definition of the follow-up population is uncertain, and
exposure information is lacking. Dose-response relationships are not likely to
emerge from follow-up studies.
9 of 29
Marked Record
TI: The public health implications of the Bhopal disaster. Report to the
Program Development Board, American Public Health Association. Bhopal Working
Group.
SO: Am-J-Public-Health. 1987 Feb; 77(2): 230-6
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1942-1991
LA: ENGLISH
10 of 29
Marked Record

TX: Bhopal—what is their suffering?
AU: Srivatsa-LP
SO: J—Toxicol-Clin-Exp. 1987 Sep-Oct; 7(5): 323-9
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
11 of 29
Marked Record
TI : Preliminary report on the spermatogenic function of male subjects exposed
to gas at Bhopal.
AU: Daniel—OS; Singh-AK; Siddiqui—P; Mathur—BB; Das—SK; Agarwal—SS
SO: Indian-J-Med-Res. 1987; 86 Suppl: 83-6
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1943+
LA: ENGLISH
12 of 29
Marked Record
TI: Morphological study of placentae of expectant mothers exposed to gas leak
at Bhopal.
AU: Kanhere-S; Darbari-BS; Shrivastava-AK
SO: Indian-J-Med-Res. 1987; 86 Suppl: 77-82
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1943+
LA: ENGLISH
13 of 29
Marked Record
TI: Immunological, mutagenic & genotoxic investigations in gas exposed
population of Bhopal.
AU: Deo-MG; Gangal-S; Bhisey-AN; Somasundaram-R ; Balsara-B; Gulwani-B;
Darbari-BS; Bhide-S; Maru-GB
SO: Indian-J-Med-Res. 1987; 86 Suppl: 63—76
____ This source is Available in S.J.M.C Library
Call Number: From: 1943+
LA: ENGLISH
14 of 29
Marked Record
TI: Neurological manifestations among those exposed to toxic gas at Bhopal .
AU: Bharucha-EP; Bharucha-NE
SO: Indian-J-Med-Res. 1987; 86 Suppl: 59-62

with standard control group of same socioeconomic status in a non-gas affected
slum area of Bhopal. The main chronic lesions noticed were chronic
conjunctivitis, refractive changes, deficiency of tear secretion and persistent
corneal opacities of various forms.
6
of 29
Marked Record
TIs Long term follow up of ocular lesion of methyl-isocyanate gas disaster in
Bhopal.
AU: Khurrum—MA; Ahmad-SH
SO: Indian-J-Ophthalmol. 1987 May-Jun; 35(3): 136-7
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1973+
LA: ENGLISH
7
of 29
Marked Record
TI: The antibody response to methyl isocyanate: experimental and clinical
findings.
AU: Karol-MH; Kamat-SR
AD: Department of Industrial Environmental Health Sciences, Graduate School of
Public Health, University of Pittsburgh, PA 15261.
SO: Bui 1—Eur-Physiopathol-Respir. 1987 Nov-Dec; 23(6): 591-7 .
this source is not Available in S.J■M.C.Library
LA: ENGLISH
AB: Sera from 99 subjects exposed to the industrial gas leak in Bhopal on
December 2, 1984 were studied along with sera from guinea pigs exposed to
methyl isocyanate (MIC) to determine the production of antibodies specific to
(MIC). Each of the four guinea pigs injected with the reactive isocyanate
produced MIC-specific antibodies in titres of 1:5120 to 1:10240, when tested
with MIC-guinea pig albumin antigen conjugate. Analogous antigens prepared by
reaction of MIC with human serum albumin were used to probe production of
antibodies in 264 serially obtained human sera from 99 subjects from Bhopal■
MIC-specific antibodies belonging to IgG, IgM and IgE classes were detected in
eleven subjects. Though titres were low and transient (declining after several
months) these findings indicate that the single large exposure to MIC resulted
in an immunologic response. This finding was concomitant with chronic
respiratory effects following MIC exposure.

8
of 29
Marked Record
TI: Disaster at Bhopal : the accident, early findings and respiratory health
outlook in those injured.
AU: Weill—H
AD: Tulane University School of Medicine, Department of Medicine, New Orleans,
Louisiana 70112.
SO: Bui1-Eur-Physiopathol-Respir. 1987 Nov-Dec; 23(6): 587-90
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: In December, 1984, in Bhopal, India, a massive leak of methyl isocyanate
(MIC) resulted from operational and equipment malfunctions in a pesticide
plant. Many thousands of residents of the city, most in proximity to the plant,
suffered sublethal and lethal respiratory injuries, the expected consequences
of high-level exposure to this type of potent irritant chemical vapour. Animal
toxicologic information was limited prior to the accident, but has since
confirmed that the lung is the major target of these lethal injuries,
invariably with pulmonary oedema. Early concerns regarding acute cyanide
intoxication were not supported by subsequent scientific inquiry. Superficial
corneal erosions did not result in permanent eye injury. The primary medical
(and, presumably, legal) issue which is unresolved, and perhaps unresolvable,
is the incidence and determinants of long-term respiratory injury in the

PC-SPIRS 3.4a

MEDLINE (R)

1987

MEDLINE (R) 1987 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 29
Marked Record
TI: The Bhopal disaster.
AU: Tachakra-SS
SO: J-R—Soc-Health. 1987 Feb; 107(1): 1-2
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
2 of 29
Marked Record
TI: Methyl isocyanate: a review of health effects research since Bhopal■
AU: Bucher-JR
AD: National Toxicology Program, National Institute of Environmental Health
Sciences, Research Triangle Park, North Carolina 27709.
SO: Fundam-Appl-Toxicol . 1987 Oct; 9(3): 367-79
____ this source is not Available in S.J■M.C.Library
LA: ENGLISH
3 of 29
Marked Record
TI: Toxicity of inhaled methyl isocyanate in experimental animals—a review of
studies published less than two years after the BhopaJL. disaster [published
erratum appears in Bull Eur Physiopathol Respir 1987 Nov-Dec;23(6):667]
AU: Nemery—B; Dinsdale—D; Sparrow-S
AD: Toxicologie Industrielle et Medecine du Travail, Universite Catholique de
Louvain, Bruxelles, Belgique.
SO: Bui 1—Eur-F'hysiopathol-Respir. 1987 Jul-Aug; 23(4): 315-22
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH; FRENCH

4 of 29
Marked Record
TI: Acute inhalational injury.
AU: Schwartz-DA
SO: Occup-Med. 1987 Apr-Jun; 2(2): 297-318
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: Recent events, such as the Bhopal, India tragedy, dramatically illustrate
the potential consequences of acute exposure to toxic inhalants. This article
covers problems in clinical management of the toxic gases, mists and fumes that
are capable of inducing acute lung injury or systemic toxicity.

5 of 29
Marked Record
TI: Chronic ocular lesions in Bhopal gas tragedy.
AU: Raizada-JK; Dwivedi—PC
SO: Indian-J-Ophthalmol . 1987; 35(5-6): 453-4
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1975+
LA: ENGLISH
AB: A comprehensive eye checkup programme was carried out in 1140 cases of
affected community to evaluate the exposure response and exposure effect with
Methyl Isocynate on human eyes. The final evaluation of these cases was made

response of muscle tissue to MIC its effects were investigated in cells in
culture isolated from muscle of 2 day old rats. After treatment with a range of
MIC concentrations (0.025-0.5 microliter/5 ml culture) the total number of
nuclei of the two main cell types (fibroblasts and myoblasts) and the number of
nuclei in muscle fibres (myotubes) were recorded. At lower doses which had
little effect on the total number of nuclei, the formation of muscle
fibres—that is, fusion of muscle cells—was prevented as the proportion of
nuclei in myotubes was decreased. At higher doses both cell types were killed.
This would suggest either an effect on muscle differentiation or a selective
toxicity towards myoblasts. The observations were supported by light and
electron microscopy.

12
of 12
Marked Record
TIs Inhibition of methyl isocyanate toxicity in mice by starvation and
dexamethasone but not by sodium thiosulfate, atropine, and ethanol.
AU: Varma-DR; Ferguson-JS; Alarie-Y
AD: Department of Pharmacology and Therapeutics, McGill University, Montreal,
Quebec, Canada.
SO: J-Toxicol-Environ-Health. 1988; 24(1): 93-101
This source is Available only few issues in S.J.M..C. Library
LA: ENGLISH
AB: Effects of starvation (24 and 48 h), dexamethasone, sodium thiosulfate,
atropine, and ethanol on the toxicity of methyl isocyanate (MIC) vapor, which
escaped during the Bhopal accident of December 3, 1984, were studied in male
Swiss-Webster mice. Toxicity to MIC appeared to be biphasic; majority of
animals died between 1 and 2 d or between 7 and 21 d after exposure to 40 ppm
MIC. Starvation.(24 or 48 h) or an injection of 2 mg dexamethasone/kg prior to
exposure inhibited the toxicity of MIC, especially during the first 6-7 d;
administrations of sodium thiosulfate, alcohol, and atropine before or of
dexamethasone after the exposure to MIC were ineffective. Starvation increased
serum corticosterone levels. The antidotal effects of both starvation and
dexamethasone might be due to suppression of the inflammatory response to MIC.

____ Call Number;
LA: ENGLISH

From:

1972+

8 of 12
Marked Record
TI: Effect of exposure to toxic gas on the population of Bhopal: Part
I—Epidemiological, clinical, radiological & behavioral studies.
AU: Gupta-BN; Rastogi-SK; Chandra-H; Mathur-AK; Mathur-N; Mahendra-PN;
Pangtey-BS; Kumar-S; Kumar—P; Seth-RK; et-al
SO: Indian-J-Exp-Biol. 1988 Mar; 26(3): 149-60
____ This source is Available in S.J.M.C Library
Call Number: From: 1972+
LA: ENGLISH
9 of 12
Marked Record

TI: Bhopal gas disaster: clinical & experimental studies.
SO: Indian-J-Exp-Biol . 1988 Mar; 26(3): 149-204
____ This source is Available in S.J.M.C Library
I
Call Number: From: 1972+
LA: ENGLISH
10 of 12
Marked Record
TI: Exposure and response to methyl isocyanate: results of a community based
survey in Bhopal.
AU: Andersson-N; Kerr-Muir-M; Mehra-V; Salmon-AG
AD: Department of Occupational Health, London School of Hygiene and Tropical
Medicine, UK.
SO: Br-J-Ind-Med. 1988 Jul; 45(7): 469-75
____ This source is Available only few issues in S.J.M.C. Library
Call Number: From: 1956-1991
LA: ENGLISH
AB: In the two weeks immediately after the Bhopal disaster a community based
survey was carried out in a series of eight exposed and two non-exposed
clusters of households. The primary concern was the effect of the gas
(subsequently identified as methyl isocyanate) on the eyes of the victims but
data were also sought on respiratory status and the first symptoms of the
^exposure. No case of blindness was encountered that could be attributed to the
gas. The most frequent symptoms reported were burning of the eyes, coughing,
watering of the eyes, and vomiting. Among these, the frequency of cough most
closely followed the rate of death in the different clusters. Although much
rarer overall, the frequency of reported diarrhoea appeared to bear a stronger
relation to death rates. Reports of photophobia and the clinical finding of
superficial interpalpebral erosion of the cornea were more frequent where the
death rates were lower. This clinical and epidemiological picture is consistent
with different effects of the gas at different doses (as estimated from
distance from the factory).

11 of 12
Marked Record
TI: Effects of methyl isocyanate on rat muscle cells in culture.
AU: Anderson—D; Goyle-S; Phi 11ips-BJ; Tee-A; Beech-L; Butler-WH
AD: British Industrial Biological Research Association, Carshalton, Surrey, UK.
SO: Br-J-Ind-Med. 1988 Apr; 45(4): 269-74
____ This source is Available only few issues in S.J.M.C. Library
____ Call Number: From: 1956—1991
LA: ENGLISH
AB: Since the Bhopal disaster, in which the causal agent was methyl isocyanate
(MIC), exposed people have complained of various disorders including
neuromuscular dysfunction. In an attempt to gain some information about the

determining the liability of the Union Carbide Company (U. S. A.) for the
Bhopal disaster; the criteria for determining compensation; and the
international remedies available to the Indian government in the event that
Bhopal victims fail to get justice within the Indian court system. The article
discusses two applicable sets of proposed international standards—the U. N.
Draft Code of Conduct on Transnational Corporations, and the U. IM.
International Law Commission's Draft on International Liability for Injurious
Consequences Arising out of Acts Not Prohibited by International Law. The
scattered 'hard' and 'soft' jurisprudence of international environmental law
establishes liability and accountability for environmental hazards. It makes
both state and non-state entities liable to pay compensation to the victims of
environmental pollution. This jurisprudence, in addition to domestic law
analogies, can influence Indian courts in determining the amount of damages
payable to the victims of the Bhopal disaster. The authors conclude that the
Bhopal disaster has demonstrated that enforceable international standards are
clearly and urgently needed for hazardous industries, especially those
operating in developing countries. Such standards would eliminate, or at least
narrow, the gap between standards prevailing in the developed countries and
those in the Third World. Even without enforcement, international standards
could provide norms for measuring the performance of individual companies
engaged in hazardous activities such as the manufacture of MIC at Bhopal■
4 of 12
Marked Record

TI: A clinical study of toxic gas. poisoning in Bhopal . India.
AU: Misra-UK; Nag-D; Nath-P; Khan-WA; Gupta-BN; Ray-PK
SO: Indian—J—Exp—Biol. 1988 Mar; 26(3): 201-4
This source is Available in S.J.M.C Library
____ Call Number: From: 1972+
LA: ENGLISH
5 of 12
Marked Record
TI: Effect of exposure to toxic gas on the population of Bhopal: Part
IV—Immunological and chromosomal studies.
AU: Saxena-AK; Singh-KP; Nagle-SL; Gupta-BN; Ray-PK; Srivastav-RK; Tewari-SP;
Singh-R
SO: Indian-J-Exp-Biol,, 1988 Mar; 26(3): 173-6
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1972+
LA: ENGLISH
6 of 12
Marked Record
TI: Effect of exposure to toxic gas on the population of Bhopal: Part
III—Assessment of toxic manifestations in humans—haematological and
biochemical studies.
AU: Srivastava-RC ; Gupta-BN; Athar-M; Behari-JR; Dwivedi-RS; Hasan-SK;
Bharti-RS; Singh-A; Misra-M; Ray-PK
SO: Indian-J-Exp-Biol . 1988 Mar; 26(3): 165-72
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1972+
LA: ENGLISH
7 of 12
Marked Record
TI: Effect of exposure to toxic gas on the population of Bhopal: Part
II—Respiratory impairment.
AU: Rastoqi-SK; Gupta-BN; Husain-T; Kumar-A; Chandra-S; Ray-PK
SO: Indian-J-Exp-Biol. 1988 Mar; 26(3): 161-4
This source is Available in S.J.M.C Library

PC-SPIRS 3.40

MEDLINE

(R)

1988

MEDLINE (R) 1988 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 12
Marked Record

TI: Aluminium phosphide: worse than Bhopal [letter]
AU: Kabra-SG; Narayanan-R
SO: Lancet. 1988 Jun 11; 1(8598): 1333
This source is Available in S.J.M.C Library
____ Call Number: From: 1930+
LA: ENGLISH
2 of 12
Marked Record
TI: The Bhopal disaster and the right to know.
AU: Jasanoff-S
AD: Program on Science, Technology and Society, Cornell University, Ithaca, NY
14853.
SO: Soc-Sci-Med. 1988; 27(10): 1113-23
____ this source is not Available in S.J.M.C.Library
LA: ENGLISH
AB: The chemical disaster in Bhopa1 jolted activist groups around the world
into renewing their demands for right-to-know legislation granting them broader
access to information about hazardous technologies. This article explores the
obstacles to creating effective right-to-know policies when technology is
transferred across national boundaries. The events leading to the Bhopal
accident are first examined in order to assess how far the tragedy can be
attributed to gaps in knowledge or to breakdowns in communication. Using Bhopal
as a case study, the article then considers three issues that are central to
the design of right-to—know policies: who has a right to receive information
about hazards; who has the duty to disclose such information, and, where
necessary, to produce missing information; what information should be available
for disclosure? This inquiry suggests that the circles of those with a right to
know and those with a duty to disclose should both be larger than under
existing right-to-know laws. More systematic risk information should also be
generated, including probabilistic estimates of risk and environmental impact
analyses. Finally, the article asks whether such improvements in knowledge and
communication would prevent disasters of the kind that occurred in Bhopal. It
concludes that for knowledge to be meaningful it must be correlated with the
power to act preventively. This implies, in turn, that those with a right to
know have to be given an opportunity to participate in technology transfer
decisions before it is too late to choose a technology that is well adapted to
the technical and cultural circumstances of the importing country.
3 of 12
Marked Record
TI: Some international law aspects of the Bhopal disaster.
AU: Tyagi-YK; Rosencranz-A
AD: International Law & Economics, School of International Studies, Jawaharlal
Nehru University, New Delhi, India.
SD: Soc-Sci-Med. 1988; 27(10): 1105-12
this source is not Available in S■J■M■C■Library
LA: ENGLISH
AB: This article explores certain international law aspects of the Bhopal
disaster, namely the principles and rules of international law establishing
international accountability for environmental damage; the criteria for

PC-SPIRS 3.40

MEDLINE (R)

1989

MEDLINE(R)1989 usage is subject to the terms and conditions of the
Subscription and License Agreement and the applicable Copyright and
intellectual property protection as dictated by the appropriate laws of your
country and/or by International Convention.

1 of 2.
Marked Record
TIs Hydrogen cyanide and Bhopal [letter; comment]
AU: Varma-DR
SO: Lancet. 1989 Sep 2; 2(8662): 567-8
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1930+
LA: ENGLISH
2 of 2
Marked Record
TI: Bronchoalveolar lavage study in victims of toxic gas leak at Bhopal .
AU: Vijayan—VK; Pandey-VP; Sankaran-K; Mehrotra-Y; Darbari-BS; Misra-NP
SO: Indian—J—Med-Res. 1989 Dec; 90: 407-14
____ This source is Available in S.J.M.C Library
____ Call Number: From: 1943+
LA: ENGLISH
AB: Bronchoalveolar lavage using flexible fibreoptic bronchoscope was carried
out in 50 patients 1-2 1/2 yr after exposure to the 'toxic gas' at Bhopal .
Thirty six patients in the analysis were categorised into 3 groups (via., mild,
moderate and severe), depending upon the severity of exposure. There was an
increase in cellularity in the lower respiratory tract (alveolitis) of the
severely exposed patients (in both smokers and non-smokers), compared to
normals (P less than 0.05). The increase in cellularity in severely exposed
non-smokers was due to abnormal accumulation of macrophages (P less than 0.01),
and in severely exposed smokers, to macrophages (P less than 0.01) and
neutrophils (P less than 0.05). Mild and moderately exposed patients did not
show significant change in cellularity in lower respiratory tract, compared to
normal individuals (P greater than 0.2). There was a trend towards increasing
cellularity, as the severity increased (P less than 0.0001) and higher numbers
of total cells were seen in severely exposed smokers, suggesting that smoking
is a risk factor. It appears, therefore, that subjects severely exposed to the
toxic gas at Bhopal may have a subclinical alveolitis characterised by
accumulation and possibly activation of macrophages in the lower respiratory
tract. Smokers, who were exposed to the gas had in addition, accumulation of
neutrophils.

TI: Bhopal : deal is less than -final [news]
AU; Jayaraman-KS
SO: Nature. 1990 Aug 9; 346(6284): 503
____ This source is Available only few issues in S.J.M.C.
Call Number: From: 1956-1993
LA: ENGLISH

Library

11 of 12
Marked Record
TI: Pregnancy outcome in women exposed to toxic gas at Bhopal.
AU: Bhandari-NR; Syal-AK; Kambo-I; Naif—A; Beohar-V; Sexena-NC; Dabke-AT;
Agarwal-SS; Saxena-BN
AD: Department of Paediatrics, Gandhi Medical College, Bhopal.
SO: Indian-J-Med-Res. 1990 Feb; 92: 28-33
____ This source is Available in S.J.M.C Library
____ Call Number: From; 1943+
LA: ENGLISH
AB: A study was undertaken to compare the effects of exposure to the toxic gas
in pregnant women in Bhopal with pregnant women in a similar, unexposed area. A
high incidence of spontaneous abortions (24.27.) in the pregnant women exposed
to the toxic gas was observed as compared to those in the control area (5.67.).
Other indices of adverse reproductive outcome, such as the rate of still birth
and congenital malformation were not found to be different. The perinatal and
neonatal mortalities were significantly higher in the affected area (6.9 and
6.17. respectively), as compared to the control area (5.0 and 4.57.
respectively) .
12 of 12
Marked Record
TI: Search for chromosomal variations among gas—exposed persons'in Bhopal [see
comments]
AU: Goswami-HK; Chandorkar-M; Bhattacharya-K; Vaidyanath-G; Parmar-D;
Sengupta-S; Patidar-SL; Sengupta-LK; Goswami—R; Sharma-PN
AD: Department of Genetics, Bhopal University, India.
SO: Hum-Genet. 1990 Jan; 84(2): 172-6
_____this source is not Available in S■J.M.C■Library
LA: ENGLISH
AB: A chromosomal survey using standard lymphocyte cultures employing different
media and G-banding techniques was initiated in 1984. This study became
particularly important following the tragic gaseous exposure of the population
in Bhopal at midnight on 2 December 1984. We have been able to formulate a
chromosomal profile for each person whom we have studied; during 1986-1988, 154
persons were examined twice. Among seemingly normal individuals, as many as 207.
might possess some chromosomal abnormality; of these, 507. may develop, at a
later date, some kind of pathological complication (such as tumours, recurrent
abortion or transmission of defects to their offspring). The people exposed to
methyl isocyanate have repeatedly shown Robertsonian translocations, mostly in
acrocentric chromosomes 13 and 21. Other types of translocations have been
studied among all exposed (53) and normal (101) persons; the involvement of
chromosomes 5, 9, 11, 14 and 16 is statistically significant (P = less than
0.001). One of the major clinical symptoms is dyspnoea; we have estimated that
almost all seriously dyspnoeic patients have developed at least two categories
of chromosomal aberrations, one of which is Robertsonian translocation, in at
least 107. metaphases. Our chromosomal survey will be of significance because we
are able to identify people with chromosomal aberrations that might be
correlated with future pathological consequences of the accident. The
"chromosomal load" that can be sustained with an apparently normal phenotype
can also be measured.

SURMNGRH0PAL:15YEARS0N
A FACT FINDING MISSION

Terms of Reference
Towards developing a comprehensive overview of the current issues faced by those affected by
the Bhopal gas disaster, it is envisaged that the fact finding mission will

I.

Analyze the continuing impact of the disaster on different areas of the lives of survivors of
the disaster

2.

Identify specific failures, including policy and institutional, in the last fourteen \ cars and their
subsequent repercussions on the people of Bhopal.

3.

Compile documentation on all the various aspects related to the Bhopal gas disaster.

4.

Outline larger policy changes as a result of the disaster.

5.

Provide concrete suggestions for effective democratic interventions.

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
Parameters of the Fact Finding Mission
In a meeting of the Organizing Committee we identified the following 14 aspects of Surviving
Bhopal that we feel that the Fact Finding Mission must address. We have also arrived at broad
parameters for each Fact Finding Team which are briefly outlined below. We would appreciate
jour response to these outlines and any suggestions you have to make, either on expanding the
scope of the Fact Finding Teams’ study and analysis, or the inclusion of any other aspect that we
may have overlooked.
1.
□

□
□
□

3
□
3

2.
□

Medical Care
Estimated figures of exposure-related deaths per month, persons chronically ill. persons
acutely ill and persons with exposure-related injuries
The extent and nature of knowledge on treatment and treatment efficacy available with
doctors. RMPs etc
The most commonly prescribed drugs and lines of treatment
Available facilities for medical care in different systems of medicine: No. of beds, doctors.
specialists, equipments, investigation facilities, availability of medicines and attendance per
day and utilisation of beds in government, private and other hospital/clinics.
Systems of registration and medical record keeping
Issues confronting employees of various hospitals and clinics, especially in gas affected areas
Possibilities of improvement in health care

□

Medical Research
Consolidation of studies carried out by government, private and other agencies and a
reassessment of their major findings
Analysis of the design and implementation of government studies
Analysis of various studies conducted by Central Govt institutions for rehabilitation
Outline of studies required for long term monitoring of health effects
Assessment of the health status of gas affected persons, and their continuing exposure to
hazards at both, the occupational and domestic levels
What are the existing public health initiatives, and what is required?

3.
□
□
□
□
□
□
□

Legal Issues
The current status of legal actions pending before different courts
The situation with respect to compensation distribution
An investigation of the systematic institutional corruption forced on the survivors
Tlie policy and legal fall outs of the disaster
The possibilities of further legal action
The status of survivors' access to justice in terms of legal aid and counselling
Compilation of a list of documents available with the CBI

4.
□
□
□

Economic Rehabilitation
Outline of existing government and non-govemment rehabilitation programmes
The estimated figure of persons unemployed due to exposure related ill health
Profile of the range of occupations in different sections of the gas affected population and the
estimated per capita income.
Outline of the skills available for income generation
List of the potential markets for goods produced through income generating projects

□
□
□
□

□
□

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
5.
□
□
□
□

Labour
The status of Carbide workers and their families today
Outline of how labour unions have responded to the disaster
The impact of exposure on survivors' capacity to work
Effect on their opportunities of livelihood in the job market e.g special covenants

6.
□
□
□

Social Rehabilitation
Estimated figures of those needing social support as a consequence of the disaster
The social impact of the disaster (qualitative study of 50 families?)
Outline of the specific impact of the gas disaster on women in terms of economic, social
status etc.
How the gas disaster has impacted children in terms their of childhood, education, health and
livelihood
Other possibilities of social rehabilitation

□
□

7.
□
□
□

Environment
The environmental impact of the factory and toxic contamination
Assessment of government and non-governmental studies related to environmental impact of
the disaster
The pattern of industrial development in and around Bhopal since the disaster

8.
□

Union Carbide
An overview of Union Carbide Corporation. Union Carbide Eastern and Union Carbide India
Limited and their assets, annual profits, facilities, products, board of directors, number of
employees, number of countries, new projects, rating as a corporation, other disasters, health
and safety records

9.
□
□

Scientific Institutions
Assessment of studies conducted by different scientific institutions and their major findings
Possibilities of further involvement from scientific institutions

10.
Role of State and Central Governments
□ Outline of the government bodies and their responsibilities
□ To provide details of programmes, policies and their analysis
□ Analysis of expenditure and accounts
□ Outline of the infrastructure, of government departments meant for the welfare of gas
survivors, e.g, number of personnel
□ Outline the database available with state and central governments
11.
Non-Governmental Organizations and Peoples’ Organizations
□ To provide a list of NGOs and Peoples' organizations
□ To outline major demands, objectives and activities
□ To identify their sources of funding and other support
□ Strengths and weaknesses, achievements and failures
□ To list national and international support
□ Suggestions for improved functioning

SRRTONG BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
12.
Memorial on the Disaster and its People
□ To present the current status of the State government plans to build a memorial
□ To highlight future possibilities
□ To outline how peoples' participation in constructing and managing the memorial can be
ensured

13.
Disaster Management
□ To assess the disaster management policies and programmes, implemented by the state bodies
in the immediate aftermath of the disaster
□ To examine whether Union Carbide Corporation and Union Carbide India Limited had any
strategies for management of a possible disaster at the Bhopal factory, whether they were
implemented and their effectiveness
□ Based on the Bhopal experience, what would be the proposed disaster management
programme in the event of an industrial tragedy?

14.
Media’s Response
□ To present a critique of national and international media response in the last fifteen years
□ Compilation of media articles, reports etc. ...

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION
Backgrounder
Introduction :
On the midnight of 2nd - 3rd December 1984. the worst industrial disaster of this century was
caused by Union Carbide Corporation, USA in the capital city of Bhopal, Madhya Pradesh, a
city with about one million people. Over 40 tonnes of Methyl Isocyanate and other lethal gases
including Hydrogen Cyanide, leaked from Carbide's pesticide factory in the northern end of the
city killing over 8,000 people in its immediate aftermath, causing multisystemic injuries to over
500,000 people. The number of deaths has risen to over 16,000 in the subsequent years and there
appears no end to the physical and mental suffering caused by exposure to the poisonous gases.
Breathlessness, diminished vision , loss of appetite, pain, menstrual irregularities, recurrent fever,
persistent cough, neurological disorders, fatigue, weakness, anxiety and depression are the most
common symptoms. Research findings on chromosomal aberrations suggest that the future
generations of the survivors will possibly carry ravages of the industrial toxins. Union Carbide
continues to withhold toxicological information on the leaked gases thereby impeding medical
treatment. The majority of those affected by the gases are people who earned their livelihood
through hard physical labour and today their economic condition forces them to continue with
their jobs, thus exposing themselves to further health risks. Little has changed in the living
environment of the survivors, most of whom live in congested slums without facilities for safe
drinking water, sanitation and clean air. Judicial systems in both USA and India have failed to
ensure adequate compensation and justice for the survivors. The settlement amount, an average
of US S 940 for each survivor, paid by Union Carbide resulted in a nominal loss to its
shareholders of merely 50 cents per share. Compensation sums awarded for personal injur.' have
been unjust and inadequate and in over 90% of cases the victims have received only about
Rs 15,000/- (or about $430). Nearly two hundred thousand persons directly affected by Union
Carbides gases remain to be compensated. For a large number of the victims the sums received as
compensation have been spent in repaying debts incurred in medical treatment in the last several
years. Officials of Union Carbide who have been charged with manslaughter and other criminal
offences are absconding from Indian courts where criminal proceedings against them been
pending for the last six years. Every' week in a public park in the city , hundreds of gas-affected
women hold public meetings calling for the trial of the prime-accused Warren Anderson, former
Chairman of the corporation, who is known to be on vacation at Vero Beach. Florida, USA.
Medical impact of the disaster:
Most of the information on the medical consequences of the Union Carbide disaster in Bhopal has
been generated by the Indian Council of Medical Research (ICMR), an agency of the Indian
government that carried out 25 research studies from 1985 to 1994. All ICMR studies in Bhopal
were prematurely terminated by December 1994,

The ICMR established that the toxins from Carbide's factory have crossed into the blood stream
of those exposed and have caused damage to the lungs, brain, kidneys, muscles as well as
gastro- intestinal, reproductive, immunological and other systems.
Six monthly morbidity surveys by ICMR from 1987 to 1991, show that the number of people with
exposure-related symptoms actually increased in that period. According to one study, there
were three times more persons with respiratory symptoms in 1991 as compared to 1987. The
damage to the respiratoiy system and particularly the lungs comprises the most obvious and very
significant part of the overall health damage. Bronchial asthma, Chronic Obstructive Airways
Disease, recurrent chest infections, and fibrosis of the lungs are the principal effects of exposure
induced lung injury. The prevalence of pulmonary tuberculosis among the exposed population has
been found to be more than three times that of the national average.

Damage caused to the eyes of the survivors have led to early-age cataracts found to be three
times more prevalent among the exposed population compared to an unexposed population at the
far end of the city. Pregnancy outcome studies on women who were pregnant at the time of the
disaster have shown that the spontaneous abortion rate was almost three times that of the
national average. In
the exposed population the stillbirth rate was three times, perinatal
mortality was two times and neonatal mortality was one and a half times more than the
comparative national figures. Study on growth and development of the children whose mothers
were exposed to the toxic gases during pregnancy revealed that majority of children had
delayed gross motor and language sector development. Studies have also presented evidence of
chromosomal aberrations of gaps and breaks in the chromosomal material as well as increased
sisterchromatid exchange indicating likelihood of congenital abnormalities among future
generations of the exposed persons.
Toxic gas exposure was found by ICMR researchers to have had a detrimental effect on the
immune system. Immunoglobulin levels were significantly raised , T-cells were reduced in number
and there was a tendency towards the reversal of T4/T8 ratio indicative of immuno-suppression.

Various studies conducted by non-government organizations have pointed out that the medical
consequences of the Union Carbide disaster have been under-assessed by the ICMR and certain
exposure related injuries have been overlooked.
The pregnancy outcome survey referred to above was carried out by Medico Friend Circle in
September '85 and showed that the spontaneous abortion rate among gas exposed women
was several times higher than that reported by ICMR. A survey of psychiatric morbidity carried
out by a group of independent doctors from Bombay found that nearly 40% of those exposed
suffered from post-traumatic stress disorder, a condition not studied by ICMR.

SURWtfiNC BHOPAL: 15 YtflBS ON
A FACT FINDING MISSION

An epidemiological survey coupled with clinical investigation carried out by the International
Medical Commission on Bhopal, composed of 14 medical specialists from 11 different
countries, reported in January 1994 significant multi-organ symptoms persistent among the
exposed population. Clinical examinations have shown significant lung impairment, marked
reduction in control over limb movements and reduced memory function caused due to exposure.
Their findings include evidence of a range of neurotoxic injuries in the exposed population.
State of Medical Care and Monitoring:
The medical care of the survivors has largely remained symptomatic since the time of the disaster
and continues to be ineffective in providing sustained relief. Union Carbide continues to withhold
information on the composition of the leaked gases and their long term effects on the human
body. In the absence of such information, doctors in Bhopal indiscriminately prescribe antibiotics,
steroids and psychotropic medicines causing more harm than good. A study undertaken by the
International Medical Commission on Bhopal confirmed that therapies prescribed for the ailing
survivors are aimed at temporary symptomatic relief rather than long term amelioration of chronic
disease processes. The major emphasis of the medical relief programmes of the Madhya Pradesh
government has been to build hospitals so much so that Bhopal now has more per capita hospital
beds than is recommended by the World Health Organization. Yet as per the reports of the ICMR
the number of diseased persons has gone up with the years. For the last several months almost no
medicines are available to the gas victims at any of the hospitals and clinics meant for them.
People who do not have sufficient means for their basic needs are asked to buy medicines and
even syringes and IV sets by doctors at these institutions that are supposed to provide free
medical care. There has been hardly any government initiative in providing community based
medical care to chronically ill survivors. Also lacking are initiatives for provision of medical care
through systems of medicine such as Ayurveda, Unani and Yoga that have demonstrated their
superior efficacy in the treatment of exposure related illnesses. The growing inadequacies of
government medical care has led to unregulated proliferation of private and expensive medical
clinics. With the termination of 25 medical research projects of the ICMR in December 1994, long
term monitoring of the health condition of the survivors has been abandoned. The Centre for
Rehabilitation Studies funded by the state government since March 1995 is yet to initiate any
research work. The official agency for monitoring exposure related deaths has been wound up in
December 1992 and there is no official record of deaths that continue to occur. With the
premature termination of research and monitoring there is almost no current data on the
prevalence of tuberculosis, cancers and infertility among the exposed population all of which are
reported to be on the rise by doctors involved with the treatment of the survivors.
A recent issue of major concern is the proposed handing over of the health infrastructure set up
the government to the so called Bhopal Hospital Trust set up by Union Carbide. Despite vigorous
opposition by the survivors, the state government has begun handing over the eight community
clinics to the Bhopal Hospital Trust (BHT) set up by Union Carbide Corporation. Preparations for
transfer of the

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION

four Red Cross clinics are also on. Ironically, one of the main factors impeding appropriate
medical treatment at these government clinics has been withholding of medical information by
Carbide and the closure of the Red Cross clinics followed from withdrawal of financial support by
the corporation. The source of funds of the BHT is the value of shares of Union Carbide that had
been judicially attached to ensure that the representatives of the corporation face criminal charges
related to the disaster. By means of interventions in the Supreme Court through the sole trustee
of BHT, Sir lan Percival (an attorney working for Union Carbide from 1984 to ’92) the
corporation has been able to get the shares dis-attached and continues to abscond justice. In the
last two years Percival has spent Rs. 7 crores on the construction of a 260-bed hospital ,which
happens to be 8 kms away from the gas affected area, and Rs. 5 crores on his own fees, travel and
office expenses. Quite clearly providing medical care to the survivors is not among the priorities
of BHT. Its sole purpose is to build a humane image for the corporation while helping it to
abscond criminal justice on the massacre. Percival's plans of health care administration have been
severely criticized by national and international professional groups including the IMCB. Among
other misgivings, concerns have been expressed regarding transparency of activities at the
proposed medical research centre to be set up by the BHT.

Economic and Social Impact:
There has hardly been any systematic effort to document the social and economic impacts of the
disaster. Official information on orphaned children and families that lost their breadwinners in the
immediate or long aftermath is scanty, if available at all. Over 70% of the exposed population has
been in the unorganized sector, with people earning subsistence wages through day labour or
petty trade. A large number of men and women who pushed hand carts, carried loads, dug soil,
repaired cars and did other jobs can no longer pursue their trades after being exposed to Carbide's
gases. Gas exposed factory workers in textile and paper mills are more sensitive to occupational
hazards and are absent from work due to illness as much as 15 days in a month. Over 90 % of the
survivors have received a compensation of Rs 15,000 which is just enough for the cost of
medicines for five years, and many of these people will be in need of medical care till the end of
their lives. Given the complete inadequacy of official rehabilitation efforts the loss of regular
income has driven tens of thousands of families to chronic starvation conditions. Loss of income
also makes people borrow money from local money lenders who charge upto 200% interest so
that chances of paying back are low and debts keep growing. Gas exposed women's inability to
carry out reproductive functions have led to their desertion by their husbands and gas exposed
young women continue to suffer social discrimination in marriage.

Environmental problems:
Thirteen years after the disaster, Union Carbide's toxic legacy continues to harm people in more
ways than one. Communities in the vicinity of the Carbide factory continue to be exposed to toxic
chemicals that are injurious to the lungs, liver and kidneys and can cause cancer. Water in over
200 wells around the Carbide factory have been declared unfit for human consumption by the
municipal authorities. This is a result of routine dumping of hazardous chemicals during the
operation of the factory thus

SURVIVING BHOPAL: 15 YEARS ON

A FACT FINDING MISSION
contaminating soil and groundwater in and around the factory premises. Analysis carried out by
the Citizens Environmental Laboratory (CEL), Boston in 1991 show presence of toxic chemicals
in the community wells around the factory. This report presented at the company's annual
shareholders meeting drew the attention of the senior officials to the problem. The Corporation
gave the job to Arthur D. Little Inc. who sponsored a collaborative investigation with an Indian
government agency in 1994 in to the matter of contamination caused by dumping chemicals inside
the factory premises. This study done without public knowledge recommends a fuller
investigation for better assessment of the environmental contamination. The findings of this study
confirm the worst apprehensions of activists and people in the community. Meanwhile, in 1996
the company management has dug up bottom soil from the "Solar Evaporation Ponds" and buried
the heavily contaminated sludge under three metres of farm soil in a bid to cover up evidence of
environmental damage. Survivors' organizations have been calling for an official assessment of the
damage wrought by Union Carbide so that the corporation could be asked to pay the costs of
environmental rehabilitation and supply of safe drinking water for the affected communities.

Economic Social and Environmental Rehabilitation :
The government programmes for economic rehabilitation have been badly designed and only few
have been implemented. While an estimated population of 50,000 is in need of alternate jobs
currently less than 100 gas victims have found employment under the government's scheme. 42
worksheds that had been built between 1985 to 1987 were allotted to so called NGOs between
1994 to 1996. However, apart from two worksheds employing about 50 women, none of them
have ever been made available for employment of the survivors. Official promises have been on
record that 50 % jobs in the Railway Coach Repair Factory would be reserved for gas affected
people. However, only 205 of the 1000 employees of this factory are gas affected persons. In
1987 a special industrial area for training and employment of over 10,000 survivors was
inaugurated and 152 worksheds were constructed at a cost of Rs. 8 crores. However, till date not
a single survivor has found any employment. A programme offering women survivors tailoring
jobs ran successfully from 1986 to 1992 employing 2300 women and making an yearly profit of
Rs. 1 crore. The rehabilitation centres where these jobs were offered were also places where
women survivors could gather, share their concerns and organize themselves. However, this
programme was terminated without any reason in July 1992.
Till date the government has no record of the social condition of the persons who have been
widowed, orphaned, or have been permanently disabled as a result of the gas disaster. The state
government has deemed its work of social rehabilitation to be over by constructing 2500 houses
and a few schools. There has been no official attention towards the urgent need of life long
pension for widows, orphans, chronically ill and disabled survivors. The Supreme Court's final
order with regard to provision of insurance coverage to about one lakh children likely to suffer
delayed effects of the lethal gases is also being ignored by the Central government.

Despite the expenditure of over Rs. 70 crores in environmental rehabilitation basic necessities
such as clean drinking water and sanitary facilities remain unavailable to majority of the gas
affected communities.

Legal Aspects :
Subsequent to the disaster the Indian government through the Bhopal Gas Leak Disaster
(Processing of Claims) Act in March 1985 arrogated to itself, sole powers to represent the
victims in the civil litigation against Union Carbide. On behalf of the victims the Indian
government filed a suit for compensation of more than 3 billion US $ in the Federal Court of the
Southern District of New York. However, in May 1986 the case was sent to the Indian courts on
grounds of forum non-convenience, under the condition that Union Carbide would submit to their
jurisdiction. During the proceedings at the Bhopal District Court, Union Carbide was directed to
pay an interim relief sum of Rs.350 crores so that the delay in the adjudication of the case does
not adversely affect the claimants. However, Union Carbide refused to pay interim relief and its
appeal against this decision reached the Supreme Court. On Feb 14,1989 in a sudden departure
from the matter of interim relief, the Supreme Court passed an order approving the settlement
that had been reached between the government of India and Union Carbide without the
knowledge of the claimants in Bhopal. According to the terms of the settlement, in exchange of
payment of US S 470 million the Corporation was to be absolved of all liabilities, criminal cases
against the company and its officials were to be extinguished and the Indian government was to
defend the Corporation in the event of future suits. The settlement sum, nearly one-seventh of the
damages initially claimed by the government, while being far below international standards is also
lower than the standards set by the Indian Railways for railway accidents. There were widespread
protests by the Bhopal victims against the betrayal by the government and many organizations and
individuals including prominent members of the parliament supported the call to oppose the
infamous settlement. Several petitions seeking review of the order on settlement were filed and
the Supreme Court announced its revised judgement on October 3,1991. This final judgement
upheld the settlement amount paid by Carbide but directed the Indian government to make good
any shortfall during the distribution of compensation. Also the criminal cases against the
Corporation and its officials were reinstated in the final judgement. The Supreme Court also
directed Union Carbide to finance a 500-bed hospital for the medical care of the victims.

Compensation:
The amount paid as compensation (Rs. 715 crores) has multiplied as a result of the increase in the
value of the dollar and the accruing interest. Out of this amount, about Rs. 850 crores have been
paid to nearly 3.2 lakh claimants and a balance of about Rs. 1100 crores remains to be disbursed.
The procedures for compensation disbursement have been tortuous and thoroughly unjust. More
than 90% of the claimants have been paid a sum less than Rs. 25,000 as compensation for
personal injuries out of which nearly Rs. 10,000 have been routinely deducted against interim
monetary relief paid by the government from 1990. The remaining money does not half cover the
medical expenses borne by the

SUBtfIVIHC BHOPAL 15 YEABS OH
A FACT FINDING MISSION

claimants in the last several years let alone provide for future expenses. Out of the 15,168 death
claims adjudicated 65% have been rejected or converted into personal injury cases where
compensation sums are lower. Judges at the claim courts are completely ignorant of the medical
consequences of the toxic exposure and the administration of compensation is riddled with
corruption so that claimants inability to pay bribes often results in denial of compensation. In
response to an official announcement for fresh registration of claims in December 1996 over 4
lakhs claims have been filed. Majority of these claims have been filed by persons residing outside
the gas affected area including elite neighbourhoods and it is most likely that genuine victims will
be the ultimate loser in the disbursement of compensation.
Criminal Case
A First Information Report for causing death by negligence and a number of other serious
offences was registered on December 3,1984 at the local police station. On December 1,1987 the
government's prosecution agency the Central Bureau of Investigation (CBI) pressed charges in
the Bhopal District Court against UCC and its Asian and Indian subsidiaries namely Union
Carbide Eastern (UCE), Hong Kong and Union Carbide India Limited (UCIL) respectively as
well as nine officials including the then Chairman, Warren Anderson. The twelve accused were
charged under sections 304 (Part IF), 326, 324 and 429 of the Indian Penal Code, with culpable
homicide, causing grievous hurt, causing death of and poisoning animals and other serious
offences punishable by imprisonment upto ten years and fines. The Corporation blamed a
fictitious saboteur and later a disgruntled worker for causing the disaster and organized public
relations campaign to distance itself from criminal liability. The CBI with the cooperation of the
workers in the factory presented a strong case linking key managerial decisions to the disaster. As
the proceedings in the Bhopal District Court began. Union Carbide and its officials chose to
ignore the Court's summons claiming that Indian courts had no jurisdiction over them. Finally
Anderson was served summons through the Interpol and on his repeated refusal to obey them, the
Chief Judicial Magistrate (CJM),Bhopal proclaimed him an absconder. After the criminal
immunity granted under the settlement was revoked by the October 1991 final judgement of the
Supreme Court a non-bailable arrest warrant was issued against Anderson and the shares of
Union Carbide in its Indian subsidiary were attached by the CJM, Bhopal. Five years have passed
since the issuance of arrest warrants against the accused Corporation and its officials, yet the
Indian government has not taken any steps towards seeking the extradition of the foreign accused.
Union Carbide deregistered UCE, Hong Kong in 1992 and now operates in Asia through Union
Carbide Asia Ltd. and Union Carbide Asia Pacific Inc.(UCAP) both wholly owned subsidiaries of
the parent US based Corporation. Ramasami Natarajan the former CEO of UCE is now the
President of UCAP, Hong Kong. The CBI has expressed , in Court, its inability to proceed
against UCE as it has deregistered itself. On Sep. 13, 1996, in response to an appeal moved by
Keshub Mahindra and other accused officials of Union Carbide India Ltd. (UCIL), the Supreme
Court passed an order diluting the charges of culpable homicide to death caused by negligence
(Sec. 3 04A of the I P C), thereby reducing the maximum sentence from 10 years to 2 years. Trial
of the Indian accused are currently going on before the CJM, Bhopal, and only five of the over
two hundred witnesses for the prosecution have testified in the last four

SURVIVING BHOPAL: 15 YEARS ON

A FACT FINDING MISSION
months. Meanwhile, the managers of Eveready Industries India Limited (new name of Union
Carbide India Ltd.) have dismantled most of the Bhopal factory that is supposed to be under the
custody of the CBI as evidence in the criminal case. In the absence of any preemptive action by
the CBI, survivors organizations sought judicial and executive intervention into the erasure of the
memory of the disaster as well as destruction of evidence. However, these attempts were
unsuccessful.
Memorial
In a meeting of the state cabinet in end June 1988, the government decided to take back the 60
acre stretch of land in Bhopal on which the Union Carbide pesticide factory had been built. In
July, the Madhya Pradesh state government committed itself to constructing a memorial at the site
of the Union Carbide factory in Bhopal. The shape or content of this memorial remains to be
decided.

SURVIVING BHOPAL: 15 YEARS ON
A FACT FINDING MISSION

Unresolved Issues of the Union Carbide Disaster in Bhopal
Medical :
1. Research andMonitoring
i.
Lack of research on continuing gynaecological, neurological, endocrinal,
chromosomal and mental health impacts of the disaster.
ii
Lack of administrative set up for carrying out long term, and possibly trans
generational research activities in Bhopal.
iii.
Absence of monitoring of continuing exposure related mortality and morbidity.

2.
i.
ii.

Information
Lack of information on health impacts available with government and private
doctors involved with the medical care of the survivors.
No official initiative towards disseminating information on health impacts and
preventive and ameliorative measures to the survivors.

3.
i.

Health care
Absence of perspective and administrative set up to respond to the chronic nature of
exposure related diseases.
ii.
Absence of protocols for the proper treatment of exposure induced illness
iii.
Absence of a system of recording health status and efficacy of medical
interventions.
iv.
Absence of a community based health care approach and overwhelming emphasis
on hospital based treatment.
v.
Negligence of Indigenous systems of medicine.
vi.
Unavailability of medicines and facilities for investigations at government hospitals
and clinics.
vii.
Indiscriminate use of Steroids, Antibiotics, Psychotropic and symptomatic drugs.
viii.
Absence of drug- free therapies such as Yoga.

4.
i.
ii.

Health Education and Public Health improvement
Absence of official initiatives towards health education among survivors.
Lack of official initiatives towards provision of clean air, water and sanitation
facilities to the survivors.

A FACT FINDING MISSION
Economic, Social and Environmental Rehabilitation :
1. Information
i.
No identification of individuals, families and communities most in need of
economic and social rehabilitation .
ii.
No information on production and training skills available locally
iii.
No information on locations requiring environmental rehabilitation.
iv.
No information on technologies for decontaminating soil and groundwater poisoned
by Union Carbide

2.
i.
ii.

iii.
iv.

v.

3.
i.
ii.
iii.
iv.

Programmes
Absence of long term perspective and administrative structure to carry out long
term programmes of economic and social rehabilitation.
Absence of integration of economic and social rehabilitat