THE HEALTH IMPACT OF THE BHOPAL DISASTER AN EPIDEMIOLOGICAL PERSPECTIVE
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THE HEALTH IMPACT OF THE BHOPAL DISASTER i
AN EPIDEMIOLOGICAL PERSPECTIVE
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II
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BY
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THELMA NARAYAN
r
i
Dissertation submitted in partial -fulfillment of the
requirements for the MSc degree in Epidemiology.
London School of Hygiene and Tropical Medicine,
Dept, of Epidemiology,
University of London.
SEPT.1987
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JI
COMMUNITY HEALTH CELl
Ma
Ban*' '
"
Dedicated to the people of Bhopal who have suffered the
consequences of the disaster and to the people from many walks of
life who have responded to this great human tragedy.
" All scientific work is incomplete- whether it be
observational or experimental. All scientific work is liable to
be upset or modified by advancing knowledge. That does not confer
upon us a freedom to ignore the knowledge we already have, or to
postpone the action that it appears to demand at a given time. “
A.B.HILL.
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CONTENTS
Page No.
ACKNOWLEDGEMENTS
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Chap. 1
INTRODUCTION
1
Chap. 2
2. 1
2.2
2.3
OBJECTIVES
Objectives
General comments
Sources of information
4
4
5
5
Chap. 3
3.1
3.2
3.3
3.4
THE DISASTER - A BACKGROUND
The event
The UCIL plant
The manufacturing process
Carbaryl
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6
6
6
7
Chap. 4
4.1
4.2
THE AGENT
Chain of events
Methyl Isocyanate - chemical properties
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8
10
Chap. 5
IMPACT ON THE BIOLOGICAL ENVIRONMENT
12
Chap. 6
6.1
6.2
6.2. 1
6.2.2
6.2.3
6.2.4
THE HEALTH IMPACT OF THE DISASTER
The need for an epidemiological perspective
Descriptive epidemiology
Limitations
Time
Place
Person
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14
15
15
17
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21
Chap. 7
7. 1
7.2
MORTALITY
Exposure related mortality rates
Demographic characteristics of the dead
'icr
Chap. 8
8.1
8.2
8.3
8.4
AUTOPSY FINDINGS
The first week
The second week
The third week
Histopathology
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33
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35
Chap. 9
9. 1
9.2
9.2.1
9.2.2
9.2.3
9.2.4
9.2.5
9.2.6
9.2.7
9.2.8
9.3
9.4
MORBIDITY - CLINICAL FINDINGS
General comments
Acute and subacute phases
The eyes
The respiratory system
The gastrointestinal system
The neurological system
Psychological disorders
Outcome of pregnancy
The reproductive system
Therapeutic trials
Discussion on clinical findings
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Chap. 10
10.1
REVIEW OF EPIDEMIOLOGICAL STUDIES
Eye and general morbidity
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52
Haematology
XU
25
30
Chap.
10.2
10.3
10.4
10.5
General health status
Womens reproductive health
Outcome of pregnancy
Watering of the eyes
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11.1
11.2
REVIEW OF EXPERIMENTAL STUDIES
Pre - disaster
Post - disaster
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DISCUSSION
Summary of findings
Outline of discussion
The exposure variable
The population at risk.
The health outcome - mortality
The health outcome - morbidity
Confounding and interactive variables
Sources of bias
Suggestions for epidemiological studies
in Bhopal
12.9.1 Cross-sectional studies
12.9.2 Longitudinal study
12.9.3 Serial cross-sectional studies
12.9.4 Epidemiological Monitoring Unit
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Chap. 12
12.1
12.2
12.3
12.4
12.5
12.6
12.7
12.8
12.9
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CONCLUSION
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REFERENCES
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TABLES / ILLUSTRATIONS
Map of affected areas
Exposure related mortality rates
Symptom profile
Symptom profile - contd.
Spontaneous abortion rates
Spontaneous abortion rates - contd.
Foetal death ratio
Epidemiological studies - a summary
20
28
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60
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Chap. 13
ACKNOWLEDGEMENTS
Many thanks to :
- the staff of the Dept, of Epidemiology, London School of
Hygiene and Tropical Medicine,for sharing their
epidemiological skills,
- Paul Elliot, my tutor, Neil Andersson and Andy Salmon of the
Dept, of Occupational Health, LSHTM, for useful discussions,
- all my colleagues on the course for very stimulating
interaction,
- members of the Medico Friend Circle, India, for constructive
and critical debate,
- my husband, Ravi, for many discussions and much support,
- and my son, Lalit, for putting up with it all.
CHAPTER 1
INTRODUCTION
I
The world’s most serious disaster in the chemical industry
which occured at Bhopal, is a tragic instance of the adverse impact of
chemical agents on human health. The health profession has
historically more experience and expertise in dealing with biological
and physical agents of disease. Experience with chemical agents was
previously limited to small groups of workers in specialised
occupations. Health problems arising therein were dealt with by
specialised occupational health teams. With rapid growth of the
chemical industry, there has been an increasing use of a variety of
chemicals in activities of daily life as well as in agriculture.
During the past decade there has been a growing realization that the
adverse impact due to human interaction with chemical agents is now
spreading beyond the confines of the workplace, to the environment and
the public in general. Incidents at Bhopal (methyl isocyanate + ?),
Seveso (dioxin), Mexico (butane) and Vietnam (Agent Orange) have
demonstrated dramatic instances of these adverse effects. These
events are often considered unfortunate, uncommon, freak events or
accidents. However, they represent the tail end of the distribution of
the more common, less serious, leaks, injuries and minor health
effects resulting from exposure to chemicals. The long-term effects of
lower dose and/or chronic exposure to several chemicals in use are at
present unknown. However there is
*
*
accumulating evidence of the
adverse effects of some of them eg. the impact of pesticides on the
environment and their effects on animals and man through the food
chain.
1
The increasing use of potentially harmful chemicals, the
conditions in which they are manufactured, the health and safety
regulations adopted and implemented are closely linked to economic and
political factors operating at a national and international level.
People living and working in conditions of material poverty bear the
brunt of the most adverse effects, because for them employment under
any conditions is a necessity for survival. The poor also carry a
double burden - suffering from the diseases of poverty viz.
malnutrition and infections along with the modern diseases of
industrialization. A balance sheet approach of costs and benefits to
people has to be used in evaluating the role of chemicals in this
context. The following quotation by Albert Einstein is relevant and
must be kept in mind,
" 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”.
Responsibility for the safety of workers and communities and
the prevention of technological disasters requires the involvement of
professionals and decision makers from several fields. More
importantly it calls for committment
and political will by wider
forces in society. Public health physicians could contribute by using
epidemiologic skills to study the health effects of these agents. This
would help provide a firm basis of knowledge about possible effects on
health, which could then be used for creating awareness and for policy
making. This has already been recognised and interest in environmental
epidemiology, which includes the above group of agents has been
growing. Being a new area of enquiry, the limitations of the existing
tools of research, have also to be kept in mind.
The chemical accident at Bhopal has been an experience of a
public health emergency caused by a technological disaster. The World
2
Health Organization has defined a disaster as " an event that suddenly
overwhelms the capacity of the normal system to respond" (Wasserman,
1985). Though used to describe natural disasters like earthquakes,
floods and volcanoes the definition could also apply to technological
disasters. In Bhopal, the disaster
overwhelmed the capacity of
individuals, physically and psychologically. And because of the
magnitude of the numbers involved and its complexities it also
overwhelmed the capacity of the macrosystem ie. the social and
administrative structures to respond.
Technological disasters are
very complex and require specialist intervention. Besides the
possibility of causing external bodily harm, they may also act at a
cellular and biochemical level causing a disruption in
physiological
functioning leading to unknown pathological states.
Exposure of the population to toxic chemical vapours during the
Bhopal disaster has resulted broadly in three adverse outcomes :
mortality, morbidity and disability. An epidemiological perspective
and method of study is vital to understanding the pattern and
distribution of the three adverse outcomes in the community.
Epidemiological studies and population profiles can provide data which
could be used for various objectives viz.
a) to substantiate/support, disprove or provide clues for
aetiological hypothesis.
b) following
from the above, to
help indirectly in deciding
upon rational therapeutic interventions and in initiating secondary
and tertiary preventive measures where possible.
c) to plan health services, including rehabilitation, for the
affected people.
d) to provide supportive evidence in court, regarding extent of
injury, in claims of compensation for the victims.
3
CHAPTER 2
OBJECTIVES
2.1
The pbjectivyg o-F this study are :
A)
to review the available literature concerning the health
impact of the Bhopal disaster viz.
a brief review of the event itself,
mortality following the exposure,
morbidity following the exposure.
The latter two would include clinical observations and
findings reported by medical professionals and the findings of a few
epidemiological studies that were conducted.
B)
to use an epidemiological perspective in the appraisal of the
above information.
C)
to review literature regarding the chemistry and toxicology
of the "agent" ie the chemical substances that were released during
the event which produced the adverse health effects.
D)
based on all the above information, to discuss methodological
issues relevant to an epidemiological approach to studying and
understanding the adverse health outcomes following exposure to the
toxic chemicals in Bhopal.
=
4
2.2
general comentu :
In the context of an epidemiological perspective of the health
impact, one must initially consider all available information in broad
categories of the epidemiologic triad of agent, host and environment
and also in terms of time, place and person. In the Bhopal situation,
there were and still are several limitations in attempting this, since
there are big "knowledge gaps" about the chemical agent/s of exposure
and also about the possible outcomes on human health. These will be
considered in greater detail later.
The situation in Bhopal is also complex in other respects. The
incident has enormous medico-legal implications. There has been a
delay in publication of results of ongoing studies. It has therefore
not been easy to get adequate published references from standard
scientific journals. For the purpose of this study a wide variety of
secondary sources of information have been used to build up an
epidemiological profile.
2.3
Sources of information used
These could be broadly classified as follows :
a) Articles published in journals. Many of these are toxicological
studies and a few are reports of epidemiological studies.
b) Reports of the Indian Council of Medical Research (ICMR) that
were available in the first 6 months following the disaster. Some of
these are minutes of meetings at which many of the researchers
presented their interim findings. Furthur reports / results of studies
conducted are not available.
c) Reports of studies and investigations carried out by research
teams not linked with the ICMR.
5
CHAPTER 5
THE DISASTER - A BACKGROUND
3.1
The tvent
The "Bhopal disaster" as it has come to be known, was a major
leakage of toxic chemicals from a pesticide plant in the city of
Bhopal on the night of 2/3 December 1984. The plant, Union Carbide
India Ltd (UCIL), was the Indian subsidiary of a
multinational
chemical company, Union Carbide Corporation Ltd.(UCC), with
headquarters in Danbury, Connecticut, USA. The leak occurred from a
tank containing methyl isocyanate (MIC). It resulted in death and
injury to human, as well as to plant and animal life.
3.2
The UCIL plant
The plant was set up in 1969 and gradually expanded over the
years into a large manufacturing facility for the formulation of
carbaryl, an insecticide, commercially known as Sevin. Till 1979,
methyl isocyanate (MIC) and alpha naphthol, intermediates used in the
manufacture of carbaryl, were imported from the parent company.
Subsequently, from 1980, MIC was manufactured locally with knowhow and
basic design supplied by UCC.
3.3
The manufacturing process
Very briefly the process for the manufacture of carbaryl is as
follows : carbon monoxide is made to react with chlorine to yield
phosgene which is then made to react with monomethylamine to produce
methyl carbamoyl chloride. This is pyrolysed to yield methyl
f
isocyanate and hydrogen chloride. Chloroform is used as a solvent and
caustic lye for the neutralization of any toxic material. Finally MIC
is made to react with alpha naphthol, in the presence of a catalyst
and carbon tetrachloride as a solvent, to produce carbaryl. Different
6
concentrations o-F this are used to -formulate the end products.
3.4
Carbaryl
Chemically known as 1-naphthalenol methyl carbamate, carbaryl
is an insecticide which is " moderately hazardous” according to the
WHO classification o-f pesticides. In 1976, the Environmental
Protection Agency o-f the U.S.A placed it on the list of compounds that
are " hazardous to man and environment". Carbaryl has been found to be
toxic in some animal studies (Phoon,1986).
Alternative processes not requiring MIC, are available for
the manufacture of carbaryl. They are in use by other companies who
wanted to avoid the use of MIC, which was known to be hazardous
chemical. However, they are more expensive and also produce larger
volumes of waste material.
The MIC plant at Bhopal has had a track record of previous
spills and accidents ever since its inception. In late 1981, one
worker was killed and 3 injured from exposure to phosgene. In 1982, 18
workers were exposed to a mixture of three chemicals including MIC
during a leak. The issue regarding inadequate safety measures - both
in design and management practices - had been raised by the workers
union, a local journalist, a safety commission from the US and even in
the local legislative assembly (Agarwal, 1986 and Weir, 1986). However
no action was taken.
*
7
f
CHAPTER 4
THE AGENT
4.1
Chain pf tvgntg
The leakage occurred -from an underground, stainless steel
tank, in which 42 tonnes o-f liquid methyl isocyanate (MIC) had been
stored from Oct 1984. Post disaster, the huge stainless steel tank was
found to have bulged at the end and between the ribs. Part of the tank
had risen out of the ground fracturing the concrete in which it was
embedded. All this is evidence of a tremendous build up of pressure
and temperature inside the tank - with temperatures possibly as high
as 250 to 350oC and pressures upto 11-13 kg/cm2 (Varadarajan,1985).
Knowledge of what triggered the explosive "runaway" reaction,
the type of chemical reaction that occurred and what products were
formed is partly speculative.
The Indian Council of Scientific and Industrial Research
(CSIR) have produced a detailed report about the possible chemical
reactions that could have occurred. This is based on
an analysis of contents of the tank; existing though limited knowledge
of the chemistry of the substances involved and on laboratory
experiments.
Some of the factors that contributed to the chain of events
that took place are as follows (Varadarajan, 1985):
- the inherent chemical properties of MIC, especially its high
reactivity and volatility, which will be described later.
- the storage of large quantities of MIC in very large size
containers for long periods of time.
- insufficient caution in design, choice of materials for
construction, and in the provision of measuring and alarm instruments.
- inadequate controls on systems of storage and on quality of stored
8
materials.
- inadequate guidelines and practices in operations and maintenance.
The probable chain of events that took place was :
- the entry of water and the presence of catalysts initiated an
explosive, runaway, trimerization reaction with a rapid rise of
temperature. A large portion of the stored liquid MIC vapourised with
a rapid rise of pressure.
t
- carbon dioxide produced by the reaction of hydrolysis caused a
mixing of contents in the tank leading to rapid chemical reactions.
- secondary chemical transformations occurred at the high
temperatures reached, leading to the formation of a complex mixture of
chemical substances. The following 12 products were found as residue
in the tank : methyl isocyanate trimer, dimethyl isocyanurate,
dimethyl urea, trimethyl urea, dione, trimethyl biuret,
monomethylamine, di and trimethylamine, chloride and metallic iron.
A description of the properties of MIC only will be given, for
the purposes of this report, to indicate the hazardous nature of the
chemicals involved. MIC was probably present in large quantities in
the cloud of toxic gas and it has also been the focus of most of the
research effort. Hence some information about its chemical properties
and toxicology is available. However it must be kept in mind that
other chemicals could also be playing a causative role in the
morbidity manifesting in the affected population. This could occur due
to:
other chemicals having been formed during the runaway reaction
itself; and/or by the breakdown products of MIC in contact with the
6
atmosphere; and/or
by the reaction/biotransformation products of MIC
in the human system.
i
9
4.2
METHYU ISOCYANATE (MIC),
isocyanic acid-methyl ester, CH3-N=C=0,
Chemical properties :
MIC is mainly used as an intermediate in the production of
Carbamate insecticides and herbicides eg. carbaryl (Sevin), aldicarb
(Temik), carbofuran (Furadan) and propoxur (Baygon). MIC has a known
hazard potential because of its ready volatility, low boiling point,
flammability and high reactivity. Traces of metallic impurities act as
catalysts and stimulate a violent exothermic polymerization. The heat
generated can volatilize a large proportion of MIC. The gas has a very
high inhalation toxicity. Hence extreme precautions are necessary in
the production and
handling of MIC
MIC has a low boiling point of 39.IOC at 760 mm Hg. It is
slightly lighter than water, but the gaseous form is heavier than air.
Its vapour density is 1.97 as compared to 1.0 for air. It has a high
vapour pressure of 348 mm Hg at 20oC. Because of these properties MIC
vapour will be concentrated near ground level and have a greater
impact on people, plants and animals.
The Mol.wt. is 57.05 and Sp.gravity 0.96 at 20oC-
Explosive limits :5.3 7. and 26 7. by volume air.
It is an extremely reactive substance. In the presence of water,
hydrolysis occurs and monomethylamine (MMA) is produced ; one mole of
MMA then reacts with another mole of MIC to form 1,3-dimethyl urea
(DMU) with the generation of heat, or 1,3,5-trimethyl biuret (TMB) if
there is excess MIC. At 73 7. relative humidity MIC can decompose into
monomethylamine.
Isocyanates in general react with carboxylic acid to generate a
peptide bond with the liberation of C02. They are also known for
carbamyl ation at the biochemical level.
MIC reacts with itself and is known to polymerize on storage
10
■For long periods. In the presence o-f a large number o-f metals and other
catalysts a violent exothermic polymerization reaction occurs. It also
reacts with hydroxyl compounds, amines and acids.
On heating and burning it generates several toxic decomposition
products viz. nitrogen oxides, hydrocyanic acid and carbon monoxide.
The ACGIH (American Committee of Government Industrial
Hygienists) have set the Threshold Limit Value (TLV) for MIC to be
0.02 ppm (0.05 mg/m3) for skin. The OSHA (Occupational Safety and
Health Administration) Permissable Exposure Limit (PEL)is 0.02 ppm.
Salmon et al (1985) found that MIC vapour reacts only
slowly with water vapour. Hence substantial amounts of MIC would be
present in a vapour cloud released even into moist air. This would
allow time for MIC to react with its own hydrolysis products.
In air MIC hydrolyses to C02 and a relatively inert amine. It
reacts in sunlight to form alkanes, nitrogen and carbon monoxide. If
moisture is present it converts to MMA, DMU and TMB. With moist soil
it forms methylamine which strongly adsorbs to the soil surface until
degraded.
On contact with plant, animal and human tissues MIC has severe
corrosive or irritant action. It is thought to compete or interfere
with C02 during photosynthesis. In animals and humans it is thought to
transform to methylamine, C02 and other carbamyl derivatives.
Thus, the chemical composition of the agents causing the
adverse health effects in Bhopal are not yet completely known, nor
their mechanism of action fully understood. More work needs to be done
regarding breakdown products of MIC in conditions of high temperature
and pressure and of those formed by hydrolysis. Their properties and
immediate and long term toxic effects need to be studied. Experimental
studies of animal exposure to MIC are described in a later section.
Epidemiologic data could also provide clues regarding etiology.
11
CHAPTER 5
IMPACT ON THE BIOLOGICAL ENVIRONMENT
The toxic gas had an impact on animal and plant life as well as
on soil and water. Most data quoted in this section is from the report
by Agarwal(1986)
Official sources put the number of dead animals - cattle,
goats, sheep etc at 1,047, while about 7,000 received therapeutic
care.
An investigative team from a research institution found that
animals had died within 3 minutes of inhaling the gas. They were
frothing from the mouth, lacrimating and breathless. Many cows
miscarried. In clinically ill animals, there was a drying of milk
after the exposure. Milk production came down from 8-10 kg per day
to 0 - 0.5 kg per day. Poultry were relatively less affected for
unexplained reasons. Many birds escaped death as well.
The effect of MIC on plants and soil was studied by the Central
Board for the Prevention and Control of Water Pollution and the Indian
Council of Agricultural Research. The ’'neem" tree commonly growing in
the area was found to be a sensitive atmospheric indicator. A
vegetation damage contour map was drawn. Vegetation in an area of 3.5
severely affected, 10.5 sq km beyond
sq km around the factory was
that was badly affected, a further 6 sq km moderately and 5 sq km
mildly affected. Leaves bore the brunt of the damage. Scientists found
that there had been instant death in exposed tissues. Another study by
the Benaras Hindu University found genetic defects in locally grown
vegetables. The same species of plants which were otherwise badly
affected were unharmed when found growing near the lake. Plants
submerged in water were also unaffected.
Some clues for human epidemiological research from the above
12
account would be to study the effects on lactation in mothers, as it
is of vital importance to the nutrition and health of infants, and to
check mortality and morbidity near the lakes and beyond. Plant studies
also confirm the gradient in damage at different distances from the
factory, reflecting the gradient in exposure. The area affected, as
given in the contour map, is much wider than the area considered to be
exposed for human health effects.
The Health Dept, even reported a bright side of the disaster.
Gas affected areas have recorded a reduction in the incidence of
malaria. Mosquito breeding has apparantly been
13
affected by MIC.
CHAPTER 6
THE HEALTH IMPACT QF THE DISASTER
6.1
The need for an epidemiological perspectivf i
When studying the health impact of the Bhopal disaster, we are
faced with a situation where the cause of the presenting complex of
symptoms and signs is partially unknown even at present. The long term
effects on human health are also unknown. There is an urgent necessity
to understand the toxicology and pathogenesis of the agent/s involved
so as to be able to provide rational therapeutic care and if possible
to initiate secondary and tertiary preventive measures. Data needed
would include facts about the clinical presentation of the disease
comp1 ex, the pathophysiology of the affected and related organ
systems, the analytical chemistry and toxicology of the agent/s.
The role of the epidemiologist would be to provide information
about:
- the distribution of the new disease complex in the population,
the characteristics
of people who manifest these adverse health
effects,
- the various circumstances which may predispose to the development
of adverse effects,
- the morbidity attributable to the exposure as separate from pre
existing levels of morbidity in the community by comparison with
control groups of similar age / sex structure and socioeconomic
status,
- to provide data relating different symptoms and signs to different
degrees of exposure.
- to understand the natural history of the morbidity over time,
I shall commence by describing available data in the
\
14
epidemiological categories o-F time, place and person recognizing that
the three are intrinsically interrelated.
6.2
Descriptive epidemiology
An attempt has been made to build up a picture of the
descriptive epidemiology of the event and its aftermath from available
sources of information.
6.2.1
At the outset some pf the limitations encountered by groups
involved in carrying out medical work with the victims or in studying
the health impact must be considered viz.
a) There was a lack of authentic informatiom regarding the
chemical composition of the cloud of vapours that escaped that night.
The leak occurred from a tank containing methyl isocyanate following
an explosive runaway reaction. Very little was written (and possibly
known) about MIC, its reactions in different circumstances or its
toxicology, in standard textbooks or journals. The company did not
disclose information that it had accumulated in the process of
registering for the commercial production of MIC. Thus medical
professionals and research workers were handicapped by ignorance about
the identity and properties of the agent whose effects they were
trying to study and treat.
Speculations regarding possible agents ranged from MIC, phosgene,
carbon monoxide, cyanide, cyanogenic substances and a combination of
all the above and/or other unknown chemicals. These drawbacks in
carrying out medical work with the victims have been reflected in the
reporting of the clinical findings and also in the treatment given.
b)
Details of the number of fatalities and of those affected
are not precisely known. Because of the suddeness and magnitude of the
disaster, mass burying/cremation of bodies (human as well as animal)
I
15
was carried out on an emergency footing, to avoid -furthur public
health problems. In the conditions of disaster and panic, with many of
the staff themselves affected, routine administrative structures could
not cope with the need for rigorous documentation vital for future
treatment and compensation of victims and for the understanding of the
epidemiology of the aftermath. Different sources, therefore, give
varying estimates of the numbers who died and who were affected.
c) Because of the medico legal implications of the disaster a
certain degree of administrative overcaution built up in the months
following the exposure and results of studies of morbidity, toxicology
etc. conducted by various research groups of the Government and the
company were not made available to the medical community for
scientific debate.
d) other factors which affected studies in the early phase
were
- mass exodus of people from the affected areas away from Bhopal,
during "operation faith" twelve days following the exposure, when the
remaining MIC in the plant was "neutralised". The people subsequently
returned to Bhopal over a period of time. Hence there is a variability
in the baseline population in the different studies.
- migration outside and into the affected areas altering the
population at risk. Most of the affected areas being shanty towns,
many people had their roots in villages and towns outside Bhopal. A
proportion of people migrated back to their hometowns or villages or
elsewhere for treatment, jobs or for other reasons. Similarly,
relatives of the victims also came into Bhopal to care for their
families. This sort of social support during times of stress is very
common in India. It has been claimed that a large number of unaffected
people migrated into the exposed areas to claim compensation. Studies
have not substantiated this claim. The occasional case reported must
16
be the exception rather than the rule.
- invasion by lawyers and other people created confusion and
distrust among the people. This may affect the reporting of the
history / symptoms to extents that would depend on the degree of trust
I rapport created between the people and the research teams.
6.2.2
Time
The leakage occured on the night of 2/3 December 1984. The leak
was first noticed at 11.30 pm in the MIC production area. Workers
noticed some dirty water spilling from a higher level in the MIC
production structure. They also felt the presence of MIC in the
atmosphere by a sense of irritation in their eyes. Due to experience
with previous minor leaks they were able to recognize the presence of
MIC by its irritant effects. Water was sprayed around the point of
leakage, as in the presence of water MIC converts to less harmful
products. At 12.15 am indicators showed that pressure in MIC tank 610
was shooting up and by 12.30 am it went beyond the maximum on the
scale ie. 55 psig. The temperature indicator was also beyond its range
ie. + 25°C. The safety release valve popped out and a gaseous cloud
was seen coming out of the stack which was 120 feet high. The siren
was sounded around 12.30 am for a short while after which only the
internal factory alarm was continued according to the routine practice
followed in the factory. Water was sprayed to neutralise the MIC but
could not reach the height from where the gas was emanating. Around
03.00 am the safety release valve of the tank is reported to have sat
back and the gas stopped coming out of the tank.
Meanwhile, around 12.45 am people in JayaPrakash Nagar 100
yards south of the plant, woke up choking, coughing and with a burning
sensation in their eyes, nose and throat - reported by the victims
17
"as if chilli powder was in the air".
At Bhopal’s 1,200 bed Hamidia Hospital, about 3 km from the
factory, the first patient reported at 1.15 am and then they came in
thousands. It was around 3.00 am that the first deaths due to the gas
leak were reported. There was a stampede as the populace began fleeing
the city. People died in their homes, in the hospitals, and on the
roads even upto some distance away from Bhopal.
This was the starting point for continuing morbidity and
mortality in the exposed population over the next few days and weeks.
Standard medical therapeutic practices were adopted. However, it was
the experience of local medical practitioners that the exposed people
came repeatedly to the clinics with a variety of symptoms and signs
affecting several organ systems, apparently unrelated to each other.
This continued beyond weeks into months.
Ten days following the disaster it was announced, that as a
safety measure, remaining MIC in the two other tanks 611 and 619 were
to be neutralised by conversion into carbaryl.This created a panic and
?
despite assurances of complete safety, there was an exodus of people
from the vulnerable localities. On December 13, 1984, 100,000 people
left the city. Many took their animals too. By the next day a quarter
of the city’s population had fled. Many hospitalised patients also
left. Cases of injuries and accidents in the virtual stampede during
the fleeing of the city, occurred on both occasions, adding to the
morbidity related to the disaster. The second exodus furthur
aggravated the situation as it interrupted treatment, resulted in
physical and psychological stress in those already affected and was
also an additional financial burden.
Generalizing broadly, the event could be described as an
&
■
exposure of a population to an extremely toxic air borne chemical
agent, with sharp localization in place and time. It resulted in a
18
large excess of deaths and disease frequency in the exposed
population. This is characteristic of an explosive, acute, point
epidemic. However there is evidence of continuing or persistent
morbidity and suggestions of an excess mortality in the exposed
population. Reasons for this are not completely understood. Several
possible mechanisms have been proposed and will be considered later.
6.2.3
Place
Bhopal is the capital of the State of Madhya Pradesh in
central India. The city has a population of about 800,000. The UCIL
plant was located in the northern fringe of the city, adjacent to an
existing residential area and barely 2 kilometers away from the
railway station. Some squatter settlements did grow up around the
Carbide plant after it was opened in the late 1960’s. But some of the
areas worst affected by the gas leak had been inhabited for many years
before the Carbide plant opened.
The high vapour density of MIC along with the conditions of
atmospheric inversion that winter night, caused the cloud of gas to
move down and stay close to the ground. The vapours spread slowly in
the atmosphere due to the low wind velocity. All these factors
resulted in the population being affected greatly. The gas is reported
to have spread over an area of about 40 sq.km and affected people
seriously as far as 5 to 8 km downwind (see map). Classification of
areas into seriously affected and less seriously affected were made on
the basis of crude post exposure death rates in different localities.
J
This was done by the State Govt. The most seriously affected areas
were JayaPrakash Nagar, Kazi Camp, Choi a Road, Chandbad, New Kabbad
Khana, Sindhi Colony and Railway Colony (see map). The two lakes of
Bhopal are said to have averted a larger tragedy as MIC converts to
less harmful substances in contact with water.
19
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II
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would have to be done between relatively small distances away -From the
•factory, t o t e s t a d o s e r e s n o n ae e f f e c t
C ?"
varying degrees o-f exposure
on the ou.tcome. Geograph i ca 1 distance however would be only one among
other indicators of expoWre as
w i 11 b e d i s c u s s e d 1 a t e r
D e s p i t e !<: n o wn 1 i m i t a t i o n s o f a s c e r t a i n m e r 11
and precision, routines sources of data regarding mortality by area
wou 1 d initi a 11 y have to be used« Results of the few population based
e p i d e m i o 1 og i c a 1 s t u d i es w o u 1 d a 1 s o b e ab I e t o p r o v i d e a d d i t i on a 1
i nformat!on. Preparation of mans showing the distribution of deaths
20
t
could be drawn. Relating these numbers to the denominator viz. the
population who were exposed and hence at risk, would give crude death
rates -following the exposure, according to geographical area or
locality. Baseline data o-f the population available -From the census,
electoral rolls or even by the surveys conducted after the disaster by
Governmental agencies, could be used to calculate age and sex
standardised mortality rates -for different areas.
6.2.4
Person
This aspect will be discussed in terms of the population at
risk, its demographic and other characteristics. The picture of
mortality and morbidity will be described in later chapters.
a) Population at risk
Estimates of the total population exposed to the toxic gas or
the "population at risk" for the derivation of mortality and morbidity
rates are 200,000 according to the State Government and UNICEF.
Results from epidemiological, community based studies (Patel et
al,1985 and Nagrik study, 1985) using control groups 10 kms away from
the factory, suggest that even the control groups were mildly affected
by the exposure. This indicates that the basis for defining the
"exposed population" needs furthur substantiation. This will be dealt
with again in the discussion on the exposure variable.
The factor of post exposure migration into and out of the
exposed localities would have also affected the composition of the
population at risk. Andersson et al (1985) observed that the more
seriously affected had gone back to their hometowns or villages.
Sathyamala C (1986), found that in a population of 8159 surveyed in
Sept. 1985, 43 people (0.527.) moved in after the gas leak and 41
(0.507.) had moved out. Both the above movements would result in an
21
overall dilution effect or underestimation of morbidity . Though
quantitatively this may not be of a large order (17. in the above
study) it must be kept in mind that the qualitative difference may be
important if those who were seriously ill had gone away.
New births into the population and deaths (fully, partly or
not attributable to the exposure) would also alter the baseline
population. Since households have been generally used as the sampling
units in the studies conducted so far, this factor has not been
considered at the sampling stage. However it would alter the number
and composition of the baseline population and would affect the
calculation of rates.
Patel et al (1985) extrapolating from prevalence rates of
morbidity have estimated that, of the exposed population about
70,000 would be suffering from serious health effects while 45,000
would be suffering moderate to mild effects.
b) Demographic characteristics
UNICEF officials (Agarwal A 1985) estimate that, of the
affected population :
- 757. are slum dwellers ie. from the lower socioeconomic strata;
- 807. are Muslims;
- 407. are children below the age of 15, 107. are elderly and
- 207. are women in the reproductive age group.
The basis of this analysis is not known. It was probably done as an
estimate for planning and administrative purposes. The demographic
data appear to be direct extrapolations from national figures. This
would be very inadequate data for a thorough understanding of the
aftermath.
Banerji et al (1985) have described the socioeconomic profile
of the study population as follows :
22
Muslims : 307.,
Lower castes : 207.,
Backward castes : 187.
Income of Rs 150/head/month ( ie relatively well off) : 107.
Housing : Kutcha (without brick and cement) : 707.
Pucca (well buiIt/concrete) : 30%
Presence of holes in the structure : 50%
(allowing air entry)
Patel et al (1985) found the population to be predominantly
Muslims and Harijans in JP Nagar and Tamilians and Maharashtrians in
Anna Nagar.They belonged to the lower socio economic class - the
percentage of skilled workers being less than 10 7.. The range of
occupations included daily wage labourers, construction workers, beedi
rol1ers, cobblers, railway and factory employees, domestic workers,
self employed artisans and potters.
The profile is of a population, the majority of whom belong to
the lower socioeconomic class. The poor housing conditions would have
offered no protection from the toxic chemicals in the atmosphere.
c) Community awareness of the hazard potential of the plant
Most people had no idea about the hazardous nature of the
plant operation. Banerji et al (1985) report that the population were
not told earlier of the potential hazard of the plant. Nor were they
aware of preventive measures to be taken in case of a leakage eg. use
of a wet cloth, moving in a direction away from the wind, not running
etc. Unfortunately most of them ran in the direction of the wind
carrying the gas and were furthur exposed. A Patel et al (1985) found
that 8.3% of the population in JP Nagar and 0.08% in AnnaNagar took
safety measures at the time of the disaster. Most of these reported to
having used blankets/wet towels over the face by instinct rather than
I
due to prior knowledge. The workers in the plant knew of these
precautions and all those in the night shift escaped unhurt, except
23
one.
d) Pattern o-f utilization of health services
Banerji et al (1985) found that the utilization of health
services by the study population after the exposure was as follows :
Hospital
40.2 7.
Camps
46 7.
Dispensaries
2.5 7.
General practitioners
25 7.
Registered medical practitioners
2.5 7.
Institutions outside Bhopal
9.1 7.
There is an overlap as some people utilised more than one type of
service. These findings are an indication that when studying the
distribution of disease in the community, data
collection would need
to be population based to get a true picture of morbidity. When using
hospital or clinic based data one would have to keep in mind selection
bias caused by selective attendance of patients. Possible determining
factors for this could be severity of illness, accessibility of
service, social class of the affected persons and so on.
e)
Impact on incpme
Patel et al (1985) found that 65 7. of wage earning individuals
in the exposed group experienced a drop in income ranging from 20 7. to
100 7. with a median of 50 7.. In the controls, only 9 7. reported a drop
in income in the range of 20 - 55 7.. This occurred due to physical ill
health resulting in occupational disability.
24
CHAPTER 7
MORTALITY
7.1
Exposure related mortality r*tes
There is uncertainty as to the exact number of people who
died. In its petition in Court, the Government has claimed 1,700 dead.
This is based on death certificates issued/deaths recorded by
Government authorities.
The Indian Council of Medical Research report (1985) states
that about 1,200 people died in hospital wards. They estimate the
total death figure to be about 2,000. The maximum number of deaths
were recorded in JP Nagar, Kazi Camp, Kenchi Chola and Railway Colony.
These areas accounted for 777 deaths.
They quote a study done soon after the disaster, in which 300
families consisting of 968 males and 863 females were surveyed. 47
deaths in males and 35 deaths in females were recorded ie. the crude
post exposure death rate for this population was 48.55/1000 population
for males and 40.55/1000 population for females. The maximum mortality
was in the 0 to 5 year and above 60 year age group. Most deaths
occurred within 48 to 72 hours of the disaster. No details are given
of exactly how long after the disaster this study was done, from which
population the families were drawn, what the method of sampling was or
details of the age structure of the population or the dead.
Andersson et al (1985), in an epidemiological study, conducted
during the first 10 days after the disaster, found the crude death
rate
derived from households in the worst affected population based
cluster to be 37. or 30/1,000 population, (death rates being calculated
as number deceased/number exposed). They have stated that this data
25
would confirm estimates of a total of 2000 - 2500 exposure related
deaths. Random sampling methods were not used and exact location of
study areas have not been mentioned. However extrapolation of rates
from localised study areas to the total exposed population should be
made with caution. Reasons for this will be apparent when summing up
the results from the various studies conducted.
Patel A et al (1985), in another population based,
cross-sectional study, using statistical methods for sample size
determination and random sampling methods, found that the crude death
rate was 86.6/1,000 population in JayaPrakash Nagar (01) and 7.9/1,000
in the control area of Anna Nagar (15)(refer to the map). The Dept, of
Information and Publicity of the State Govt, had documented the death
rates to be 23.4/1,000 and 3.2/1,000 respectively in the same areas.
It appears that there is a gradient of mortality according to the
degree of exposure. This is another reason why direct extrapolation of
rates from any particular study/area to the total affected population
may be misleading.
Banerji D et al (1985) conducted a survey in the affected
areas, between Jan 6 to 15,1985. Using a sampling frame of 68,000,
they randomly selected a 6.667. sample (1 in 15 households), and
administered a semi structured questionnaire by trained interviewers.
They enumerated 82 dead and 5 missing (presumed dead) in 700
households in the severely and moderately affected areas. The exact
denominator has not been mentioned in their preliminary report, to be
able to calculate rates. They extrapolated the number to their
sampling frame of 68,000 to yield 1305 dead. From this study the crude
death rate for the combined population of severely and moderately
affected communities is 19.19/1,000 population. The exact area covered
by the study has not been mentioned.
Besides the caution mentioned earlier regarding extrapolation
26
of rates, it appears that combining rates from different localities
eg. severely and moderately exposed to give an overall rate may mask
important differences in mortality rates.
Sathyamala C (1986), surveyed 3 exposed localities to study
the impact of the exposure on the outcome of pregnancy. The basis of
selection was the post exposure mortality rates as given in later
unpublished data from the study by Banerji et al.. These were as
follows :
JP Nagar - 65.3/1000, Kazi Camp - 46.7/1000 and Kenchi Choi a 35.7/1000. Their study found the crude post exposure death rate for
the 3 localities together to be 33.19/1000.
A table of postexposure mortality rates as derived from
different studies has been compiled. Relevant aspects of the study
designs have also been given.
£
27
Post exposure mortality rates
A summary from different sources
Study
Population/
sample size
group/
investigator
MP State
Govt.
Sampling
method
Time
of
study
Area
of
study
Crudepost
exposure
deathrate
?
Early
post
disaster
JPNagar
23.4/1000
AnnaNagar
3.2/1000
?
ICMR
300 -families
(968 males +
863 females)
?
shortly
after
disaster
?
48.5/1000
(males)
40.5/1000
(females)
Andersson
et al
? number
in each
cluster
?
10 days
post
exposure
worst
affected
cluster
3 7. or
30/1000
Random
3 months
sampling post
exposure
JPNagar
86.6/1000
AnnaNagar
7.6/1000
Patel A
et al
Banerji
et al
148
exposed
138
controls
700 -families Syste
1 month
post
matic
sampli ng exposure
severely -»
moderatel>
affected
areas
19.2/1000
JPNagar
KaziCamp
K.Choi a
Sathyamala
8165
persons
Random
9 months
sampling post
exposure
28
65.3/1000
46.7/1000
35.7/1000
JPNagar
Kazi Camp
K.Choi a
33.8/1000
together
—
i
There seems to be a wide variation in crude death rates
derived from the various studies as well as in those stated by the
Govt. Possible reasons for this could be ;
a) differences in levels of ascertainment, reporting etc
b) due to factors related to study design - sample size, sampling
methods etc
c) real differences in different localities reflecting varying levels
of exposure to toxic gas.
The methods used in enumerating deaths would also play a role
in accounting for differences between studies in postexposure death
rates. Andersson et al (1984) have mentioned
that they calculated
death rates as the number deceased/number exposed. Other studies have
not stated what they have considered and used in the numerator and
denominator. The different studies were conducted at varying time
intervals following the exposure. We do not know the time period used
in the different studies as cut off points in the enumeration of
deaths attributable to the exposure.
From an aetiological point of view, as well as for the
victims families to receive adequate compensation, it is crucial to
try and achieve greater precision in enumerating deaths. It is
important also to analyse exposure related mortality rates taking into
consideration age, sex, locality in which present at the time of the
disaster and degree of exposure.
29
t
7.2
i
-
Demographic characteristics
Furthur details of the study by Banerji et al (1985) are given
here as it describes the age/ sex and socioeconomic profile of the
dead.
a) Males accounted for 607. of the deaths, which they commented
was an important and unexplained finding. Majority of these were in
the age range of 2 to 20 years. As a first step in interpreting these
differences it is important to take into consideration the sex ratio
and age distribution ie. the population structure, of the
population
at risk. As mentioned before, standardised mortality rates would be
more interpretable.
b) There was one death per household in 49 households, two
deaths/household in 11 households, three deaths/household in 4
households and one household had 4 deaths. There is a need to analyse
these deaths in terms of degree of exposure.
c) In an attempt towards determining the degree of exposure
it was found that:
- 757. of the dead were among those who ran on foot,
- 23.57. among those who remained at home,
- while none who used a vehicle died.
This is related to the finding that 737. ran, 217. stayed in their
house and 6.37. used a vehicle. This is plausible because besides
direct exposure to the toxic chemical laden atmosphere, those who ran
also inhaled deeply and had an increased rate of respiration thus
getting exposed to more of the toxic gas.
d) Among the dead the socio economic profile is as follows :
- 567. lived in houses with large holes,
- the proportion living in kutcha houses was higher,
30
- the proportion belonging to the lower and backward
castes was significantly higher,
- the proportion of Muslims was similiar to that in the
study population
ie. those who died were the poorest of the poor.
The few rich who came within the sweep of the cloud of toxic chemicals
did not suffer as much damage ” because of their well built houses,
healthier bodies and possession of/access to transport."
e) The study hypothesises that there would have been an
underestimation of deaths because of underreporting of deaths among
the homeless and destitute who would have been the most exposed and
vulnerable. An estimate of 3,000 shelterless in Bhopal has been made
(Agarwal 1985). Many of these people used to live around the railway
station which was directly in the line of the cloud of toxic
chemi cals.
The Tata Institute of Social Studies, Bombay,
conducted a
door to door survey regarding exposure, mortality, socioeconomic
status etc the results of which were to become the basis for relief,
compensation and long term treatment. But its total tally of 1021
dead, even less than the officially counted bodies caused it to lose
credibility. The survey failed to cover 600 exposed families in which
deaths could have occurred. It could not enumerate 315 families who
had migrated outside the city after the disaster and 286 families who
had their houses locked. The findings of the study, even with its
limitations, would have provided some information of use. However the
results have not been published or made available.
Many say that the official numbers
are underestimates of the
true figures of mortality. Other estimates have been given ranging
from 5000 - 10,000 (Agarwal,1985). However most of this data is
u
51
OH'WO
COMI / HEAi ru CT- r
Orf-.
fivur;
F
anecdotal and hence difficult to interpret.
Regarding mortality in the months following the disaster,
fI
but attributable to the exposure, a State Govt.official has stated
I
that during the first year on an average 15 such
J
deaths were occuring
per month (Diamond,1985). Whatever the basis and validity of this
statement it raises the important question of the need to evolve a
reliable method to take count of these attributable excess deaths.
The number of excess abortions and stillbirths should also
be added to the death toll.
Tfi summarise? therefore, the main features of mortality in the
data reviewed are :
i
1) Number of deaths :
estimates range from 1,700 - 2,500 - > 5,000.
2) Exposure related death rates :
varies in different studies and in different localities
3) Area distribution
severly affected areas - JR Nagar, Kazi Camp
Kenchi Choi a and
Railway Colony.
4) Sex distribution
apparently an excess in males.
5) Age distribution
excess in under 5 and over 60 age groups
(age / sex estimates based on crude rates)
6) Socio economic class distribution
lower socio economic classes most affected.
7) Excess abortions and still births occurred.
8) Continuing mortality attributable to exposure needs to be
considered.
32
CHAPTER B
AUTOPSIES
Autopsies were conducted at the Medico Legal Institute based
at Mahatma Gandhi Medical College, Bhopal. Findings have been reported
in the ICMR reports (Mar and May 1985) and are described in some
detail here as they are of relevance to understand the pathology
produced in the human system by acute, severe exposure.
8.1
The first week
The usual postmortem lividity or cyanosis was not present, but
there was a pinkish discolouration. Conjunctiva were red. Hypostasis
was present all over the body and was not restricted to the dependant
parts. A common finding was the presence of thick, tenacious , foamy
froth covering the nose and mouth.
Pathological changes were present in the entire respiratory
tract. Lung weight was 2
to 3 times the normal. The lungs were
waterlogged and had a cherry red colour. They showed congestion,
haemorrage and consolidation. The vessels were filled with thick,
viscid, dark cherry red blood. The bronchi and trachea were red in
colour and the lumen was filled with white tenacious material.
Microscopic examination showed severe tracheitis and bronchitis with
denudation of the epithelium in some sections and necrotising
bronchiolitis in some. There was marked congestion and thickening of
the alveolar septa. The alveoli were filled with albuminous fluid.
There was very little evidence of secondary infection.
8.2
The second wetk
While grossly and microscopically the lungs continued to be
the seat of primary change, there was a gradual transition in the
pathological changes. Characteristic cherry red colour of the blood,
33
heavy oedematous darkly reddish lungs and varying degrees of oedema of
■S
$
the brain continued. Acute desquamatous changes in the trachea and
main divisions of the bronchi persisted. There were varying degrees of
3
bronchiolitis, bronchopneumonia and infiltration of the alveolar
spaces by polymorphonuclear cells.
In the acute phase there was oedema of the brain and congestion of the
leptomeninges. In a few cases, the liver showed a mild degree of fatty
change which can be either incidental or secondary to anoxia
consequent to pulmonary changes.
8.3
The third week
The respiratory tract showed the same appearance, though the
lungs were relatively reduced in size and weight. However they were
still reddish and exuded a lot of fluid from cut surfaces.
A striking feature in some cases was that on opening the
thoracic or abdominal cavities, viscera which was normal in colour
rapidly acquired a reddish tinge on coming in contact with
the
atmosphere. There was variable involvement of other viscera. Brains
which were uniformly heavy and oedematous, showed either uncal
grooving or tonsillar herniation with compression of the cerebellum by
the tentorial edge. In a few cases the liver showed severe congestion.
The spleen though markedly congested was shrunken in size and the
capsule was wrinkled. The kidney showed extreme congestion in the
cortex and medulla. The heart contained blood clots which were cherry
red with some chicken fat like material. The liver showed haemorrhage
all over. The capsule of the liver was found to be separated and could
be easily pulled off. The gallbladder was distended. The stomach and
intestines had haemorrhages in the submucosa of the wall. The spleen
was found to be softened. The kidney showed haemorrhages.
■
r
34
8.4
Histopithplggy
The lungs showed congestion and oedema. The bronchial lumen
was full of exudate. The trachea showed superficial ulceration and
i
loss of cilia. Muscle fibres in the bronchial wall showed
fragmentation. The kidneys showed necrosis of the proximal tubules.
Microthrombi were present. The liver showed centrilobular congestion,
patchy necrosis and widening of the central veins. Heart showed
interstitial oedema and necrosis. Atrophy of the malpigian capsule was
a consistent finding in the spleen. The cornea showed denudation of
the epithelium. The thymus ,testis and ovaries showed no changes.
Multiple lesions were common. Sections of the lungs of stillborn
showed no abnormalities.
They quote the case of a woman who had manifested MIC effects
and subsequently recovered. She died of hyperpyrexia following a
Caesarian section in the third week of March 1985. On autopsy (on
29.3.85) lungs showed congestion, oedema and haemorrhage, and the
small bronchioles showed obstruction. There was no pontine
haemorrhage.
Electron microecopic findings from autopsies
Lungs showed loss of lining membrane of the epithelial cells.
Type 11 pneumocytes were present indicating that capacity for
regeneration was not totally lost. Red cells looked different- they
had lost their electron opacity. This could be because haemoglobin is
lost or a change has occurred in the structure of the haemoglobin.
Several areas showed zones of activated fibroblasts. Some lungs showed
secondary bronchopneumonia. The brain showed presence of siderosomes.
I
Neurones showed flocculent opacity indicating necrosis. Examination of
one placenta showed loss of microvilli on the maternal side of the
■
syncitial trophoblast.
35
CHAPTER 9
MORBIDITY - CLINICAL FINDINGS
i
9.1
General comments
A profile of the morbidity caused by the exposure has been
compiled from the following sources of information ;
a) the two reports by the Indian Council of Medical Research
(ICMR) in March and May 1985 describe the clinical picture and results
of laboratory investigations in the acute and subacute phases. These
observations were made by staff of the local Mahatma Gandhi Medical
College at its attached Hamidia Hospital as well as by specialists
sent in from other parts of the country. Several research projects
(22-25) were set up by the two organizations in the initial phase for
long term follow up of the victims. However further reports of their
findings or progress are not available.
b) studies done by non-governmental groups. These include
research teams from academic departments of universities, independent
professional groups and voluntary agencies.
The clinical picture of morbidity is described first followed
by the epidemiologial studies. Comments on the strengths and
limitations of the data are interspersed with the description. There
will be a further discussion of methodological issues later.
The pattern of morbidity varied over time. For the purpose of
this report the acute phase has been considered as the first 2 weeks
post exposure. The subacute phase is from 2 weeks to 4 months and
i
beyond that period is the chronic or long term phase. This
I
classification is arbitrary and partly artificial to help understand
i
i
the clinical picture over time.
The most striking symptoms and signs with which most people
presented immediately after the disaster or in the acute phase were
J
36
related to the eyes and respiratory tract. There were also a wide
variety of clinical symptoms related to different organs and systems.
A description of the clinical findings in the acute and
subacute phases follows.
9.2
ACUTE AND SUBACUTE PHASES
9.2.1
The eyes
Mittal (ICMR, 1985) reported the following eye conditions in
patients from the hospital OPD and wards of Hamidia Hospital.
8,000
patients were seen here in the first 24 hours, and 34,000 patients
were treated in the first few weeks.
Patients initially complained of a severe burning / foreign body
sensation in the eyes, blurring of vision, profuse lacrimation, and
difficulty in opening the eyelids. On examination there was lid
oedema. 60 - 70 7. had superficial keratitis and conjunctivitis.
Superficial ulceration of the cornea in the interpalpebral region was
observed in several cases. Many had punctate keratitis in the lower
sector. Corneal pathology was mainly confined to the epithelial
layers, rarely penetrating the stromal tissues. They observed that
children had fewer ocular problems. Eyes of nearly all the patients
returned to near normal in a weeks time with healing of the lesions.
Detailed investigations did not suggest involvement of the posterior
chamber. There was no evidence of blindness or deterioration in
vision.
Andersson et al (Dec’84) reported findings in 10 hospitalised
patients on the eighth day post exposure. All had discrete superficial
lesions, usually in a band across the interpalpebral region with the
typical whorling pattern of new epithelial growth. No limbal necrosis
or abnormal endothelium was detected. Their findings were in keeping
37
with the report given above.
Andersson et al (Dec’84) also reported -findings -from a study
of community based clusters, 2 weeks post exposure. The exact location
I
and distance of the clusters from the factory were not specified. They
reported that over half the community demonstrated eye signs which
could be attributed to the exposure. These were mainly interpalpebral
injection and signs of healing epithelium. Fundal changes, mostly
venous dilatation were more common in the exposed. There was no
difference in the age standardised visual acuity between exposed and
unexposed groups.
A.Bang (Jan’SS) reported that in the week after the disaster a
quick and crude community survey in JayaPrakash Nagar (100 yards from
the factory) revealed that about 507. of the population had eye
symptoms.
The Nagrik study (1985), found that 807. of people within
km
of the factory had ophthalmic symptoms, as did 607. of those at 2 km
and 40 7. of those at a distance of 8 km. This revealed a gradient of
effect as well as the fact that exposure occurred even upto 8 km away.
9.2.2
The respiratory system
The ICMR report’s (1985) state that people initially
complained of sudden onset of difficulty in breathing, coughing and in
some cases, pain in the chest. On auscultation, many had bilateral
crepitations. Xrays revealed interstitial pulmonary oedema, alveolar
type oedema, pneumonitis, hyperinflation of lungs and collapse of
surrounding area. Rapid deaths following exposure probably resulted
from massive pulmonary oedema and associated hypoxia.
i
I
A.Bang (1985) in the survey mentioned above, found that about
257. of the population in JP Nagar had respiratory symptoms. A large
number, even those with minimal respiratory symptoms had coarse
38
crepitations and rhonchi. Many of the" mild" cases were either not
attending clinics or were not being given a thorough clinical
examination. He pointed out that with inadequately designed studies
and poor documentation the real epidemiology of morbidity may be
missed. He also observed that the expected tide of secondary infection
did not follow the initial period of chemical pneumonitis. Reasons for
this were not understood. At the community level, antibiotic cover was
either not given or was too inadequate for most of the affected
persons and hence could not explain the phenomenon. There are also
anecdotal observations that dead bodies of people / animals discovered
a day or two after the disaster were not decomposing. On experimental
studies (ICMR,1985) MIC was found to have a bactericidal effect.
Andersson et al (1985) observed that respiratory distress was
most marked in the community cluster "second in distance from the
factory", affecting 20 7. of the population. Many were too disabled by
breathlessness to move more than a few steps or even to talk.
S.R.Kamat et al (ICMR,1985) noted on 24 subjects, ( a self
selected group who had gone to Bombay for treatment shortly after the
disaster ), that lung function tests suggested
restriction,
reversible obstruction and defects in oxygen exchange. Blood gas
analysis revealed anoxia, compensatory respiratory alkalosis, raised
carboxyhaemoglobin and methaemoglobin. They reported evidence of
lymphoid granulations in the throat.
They later reported findings from an extensive evaluation of
pulmonary function of 82 patients (also self reporting to Bombay).
Xrays in 78 were suggestive of interstitial pneumonitis. This was
corroborated by blood gas and lung function studies. Methaemoglobin
levels were raised in 63 out of 80 and was stated to be suggestive of
interstitial alveolitis. Pulmonary function tests indicated central
airway obstruction. A large majority of the 82 also showed some
39
restrictive defect. Needle biopsies in 5 cases revealed evidence of
interstitial fibrosis.
i
Later the case group seen at KEN Hospital, Bombay expanded to
113 people. They were people from the middle class, living in well
built houses 2 km away from the factory, who had voluntarily presented
to the hospital 8-53 days post exposure.
Their symptoms were as follows :
- breathlessness on exertion - 957.
- persistent dry cough - 977.
irritation of throat - 667.
- chest pain - 687.
- vomiting - 427.
muscle weakness - 227.
- altered consciousness - 287.
The findings on investigation were :
- low vital capacity of lungs - 277. (< 607. of normal)
- impaired oxygen uptake - 557.
- central airway obstruction - 437.
- respiratory alkalosis - 597.
-low oxygen pressure in the blood - 237.
Though providing good clinical information this is a highly self
selected sample, not representative of the community.
Vijayan (ICMR,1985) in a study of pulmonary function on 129
people carried out in Jan-Feb 1985 noted that 707. of cases had
abnormal ventilatory functions on spirometry. He measured forced vital
capacity, forced expiratory volume at the end of one second and forced
expiratory flow rate at BTPS. He had classified exposure status as
severe, moderate and mild and noted that all those with abnormal
pulmonary function had severe or moderate exposure. Pulmonary function
was studied in 129 cases - approximately 407. of those who complained
b
40
o-F respiratory symptoms had ventilatory impairment, 127. had
restrictive lung disease, 67 obstructive airway disease and 227.
obstructive cum restrictive defect. Ventilatory defects were not
observed in patients with mild exposure to toxic gas.
The ICMR report (1985) states that of 35 patients in whom
blood gas analysis was done, 23 severely exposed patients had arterial
oxygen tension (Pa02) less than 60 mm Hg ie. moderately low levels.
Moderately and mildly exposed patients had normal Pa02. Low arterial
carbon dioxide tension ( less than 35 mm Hg ) was observed in 12
cases. It was stated that these results indicate significant
alteration in blood gases and suggest alteration in oxygen carrying
capacity of the blood.
Narayanan (ICMR,1985) reported, from experience in a 30
bedded, hospital set up adjacent to the factory and hence more
accessible to the affected people. The exposed population were
presenting with recurring respiratory problems. They also complained
of inability to perform accustomed physical activity. They had
tachycardia and severe tachypnoea. The haemoglobin level was normal or
raised. On blood gas analysis, Pa02 and PaC02 were moderately low,
Pv02 was moderately low and PvC02 very high. 2,3 DPG
(diphosphoglycerate) levels were also raised. These findings suggested
a defect in oxygen transport and tissue anoxia.
The ICMR report (1985) states that even two months post
exposure, nearly 407. of patients attending the hospital presented with
respiratory symptoms of breathlessness, cough and in some cases fever.
Persistent tachypnoea was a characteristic feature. In some patients,
symptoms were out of proportion to clinical and radiological
observations.
It has been reported that many of the delayed deaths were
preceded by severe respiratory distress.
41
!
*
I
9.2.3 Haematology
Ram Singh (ICMR,1985) reported initial haematological
findings, 15 days after the exposure. There was haemoconcentration and
leucocytosis. There was no evidence of coagulation disorders.
Approximately 257. of severly exposed cases, reporting to hospital, had
haemoglobin levels above 14 gm’Z and 337. had raised eosinophil counts (
above 207. ).
The ICMR report (1985) describes another series of 237 cases
investigated during the first two weeks. Polymorphonuclear cells were
increased in 35 7. of cases, 527. had raised lymphocyte counts, 197. had
eosinophilia in excess of 207., and 157. had haemoglobin levels above 14
gm 7..
The ICMR report (1985) quotes a study finding of a 20 - 60 7.
reduction of the free amino groups in the haemoglobin of persons
exposed to the toxic gas.
9.2.4
The gastrointestinal system
The ICMR report stated that patients also presented with
nausea, vomiting and burning in the stomach. Endoscopic examination
revealed superficial gastritis and oesophagitis. A small proportion
had hepatomegaly.
9.2.5
The neurological system
ICMR reported that immediately after the disaster severly
affected cases showed varying grades of loss of consciousness ranging
from mild to deep coma. The main presentation in children was coma.
1
I
They report that in a study of neurological disorders in the affected
population , 128 adult subjects were screened and revealed the
following :
t
s
42
neuromuscular weakness- 1,
right hemiplegia - 1,
hearing loss - 2,
tremors and vertigo - 2.
The
method of selection and source of cases has not been mentioned.
nor whether a standardised method of examination was used.
Andersson et al (1984) reported that those who fell
unconscious had few or no eye symptoms or signs on recovery. They also
found that collapse and unconsciousness was noted in the cluster
second in distance from the factory and not in the others. No
quantitative data has been mentioned, to see if the difference is
significant. This observation suggests that different patterns of
morbidity may occur in different clusters.
Bharucha (ICMR,1985) reported initial observations of coma,
tremors and paralysis in some cases soon after the gas leak. No
recognizable patterns of neurological disorders were present 5 months
post exposure, though many people complained of general weakness.
In the 113 affected people seen at the KEM Hospital Bombay
neurological conditions such as sensory motor loss, tremors, loss of
consciousness, irritability and depression were found in a significant
number of cases.
9.2.6
Ptychplogical disorders
Sethi (ICMR,1985), reported that of 168 cases of mental
disorders treated in special clinics, the majority were neurotic
disorders viz. neurotic depression,anxiety neurosis and hysteria.
I
Psychotic disorders were rare. Women under 45 years were predominantly
affected.
S.R.Kamat et al (ICMR,1985) reported on psychometric
evaluations carried out on 68 self reporting cases : 22 showed
I
■
evidence of depression and 19 showed evidence of cognitive defects
with poor memory performance.
43
The team from the National Institute o-F Mental Health and
I
i
!
NeuroSciences (NIMHANS) found a large community load of mental ill
health following the disaster (ICMR,1985). They reported that
approximately 10 - 12 7. of those affected, who visited community based
general practice clinics, were presenting with psychiatric
!
I
manifestations. Symptoms of anxiety and depression were foremost.
r
i
Sleep disturbances, nightmares, gas phobia, feeling of hopelessness
and grief reaction were common. Families of the affected population
were finding it difficult to cope with the stressful situation. This
is an area needing furthur study, as the NIMHANS team noted that long
term after effects have been reported in previous man made disasters.
9.2.7
Outcome of pregnancy
The ICMR report (Mar’1985) reported findings of 97 women who
had delivered. Among them there were 5
stillbirths - 5 (5.157.)
abortions
17 (17.57.) ie. total pregnancy wastage of 22.77.
congenital anomalies (minor) - 3
Most babies were full term but with low birth weight, 2kg. on
average. In terms of development the babies appeared normal. The
!
mothers weight was 40 - 45 kg.
In the ICMR report (May*85)
Dabke described the results of
645 pregnancies : stillbirths - 8
■
abortions
- 67
congenital abnormalies (minor) - 9
i
1
low birth weight - 29.8%
They stated that these were not in excess of those expected in a
normal population. Rates are calculated by relating the numerator to a
given population ie the denominator in a given time period (usually a
year). Hence no comments about normality /abnormality can be made from
44
the above data. Comparison with control groups and if possible with
national and regional rates should also be made.
9.2.8
The reproductive system
R.Bang and M.Sadgopal (1985) studied the impact on women’s
reproductive health 2 months post exposure. 55 women were examined in
Ob/Gynae field clinics in two of the affected slums - 947. of these had
leucorrhoea, 797. pelvic inflammatory disease and 467. had excessive
menstrual bleeding. Women also gave a history of suppression of
lactation,impotence in the husbands, abortions and stillbirths. This
provided a clue that there were adverse effects on reproductive
health, particularly womens health, which needed furthur
investigation. They admitted limitations of the lack of a control
group and small sample size. However there was also the problem of a
self selection in clinic based data.
9.3
THERAPEUTIC TRIALS
Medical management of patients with eye, lung, CNS,
gastrointestinal and other presentations
was symptomatic and followed
standard practice. This approach did prove life saving and offered
some degree of relief to many. However, with the passage of time, it
was observed that patients kept coming repeatedly either with
persistent symptoms or relapses following a remission.
While it was acknowleged that some of the long term,
multisystemic symptoms could be explained as being due to the
aftereffects of severe lung damage, ICMR scientists (ICMR,1985)
suspected the presence of systemic toxicity. Autopsy findings,
laboratory investigations and a rapid literature search lead to the
hypothesis of an enhanced cyanogen pool in the body resulting from the
45
exposure either by direct inhalation of of cyanide or more likely by
5
the breakdown of MIC within the body. The detailed rationale for this
has not been reported.
5
I
Autopsy findings had shown arterialization of venous blood
giving a reddish tinge to internal organs and tissues.
Carboxyhaemoglobin and methaemoglobin were not detected. However,
samples from all victims showed twin bands of oxyhaemoglobin. It was
i
demonstrated that MIC could produce a reddish colour when mixed with
blood.
*■
Urinary thiocyanate levels were found to be higher in the
exposed population.
Smoking and/or exposure to smoke,and the eating of certain
foods eg cabbage, spinach, cassava etc?are known to enhance the
cyanogen pool and result in increased excretion of urinary thiocyanate
V
(which is used as an indicator of cyanide exposure). Rosling (1986)
summarised the mechanism of detoxification of cyanide in the body as
follows - cyanide is trapped in the erythrocyte fraction of the blood
5
and is converted to the less toxic thiocyanate in the presence of
sulfur. This conversion is normally attributed to a reaction with
thiosulfate catalysed by the enzyme rhodanase. Thiocyanate is then
excreted in the urine. Intravenous administration of sodium
I
t-
thiosulfate is known to increase the capacity for detoxification of
cyani de.
The toxic effects of cyanide result from impairment of the
mitochondrial respiratory chain by inhibition of the mitochondrial
enzyme, cytochrome oxidase. Studies (ICMR,1985) have shown that pure
MIC had no effect on cytochrome oxidase, but its degradation products
1
i
I
did. This results in under utilisation or non utilisation of oxygen at
the cellular level.
Based on the hypothesis of an enhanced cyanogen pool resulting
46
from the exposure to toxic gases, sodium thiosulfate was administered
to some patients as an antidote (ICMR,1985). It was stated that this
resulted in marked clinical improvement and a significant increase in
PvC02 in both central and periferal veins indicating better
utilisation of oxygen by the tissues.
A double blind study using sodium thiosulfate and glucose was
conducted. Of 30 patients, 15 each were given 2 injections of sodium
thiosulfate or glucose. Urinary thiocyanate levels were determined at
3 and 5 hourly intervals and compared to the baseline level before the
injection. In patients given sodium thiosulfate there was an 8 to 10
fold increase in excretion of thiocyanate in the urine in a
significantly large number - in 10 out of 15 patients. Only one of the
15 receiving glucose injections showed such an increase. Criteria for
selection into the study have not been stated.
Subsequently, Narayanan (ICMR,1985) reported that of 230 cases
treated, complete records were available for 167 ( 87 men, 69 women
and 11 children). Symptomatology before commencing treatment was
breathlessness and / or general weakness / tiredness. In 29 patients
these symptoms were present at rest. While in 132 they were elicited
by moderate exercise. Following administration of sodium thiosulfate,
9 showed no improvement while there were varying degrees of
improvement in the rest over different periods of time. Details of how
the analysis was done has not been stated. There were 10 cases of
adverse reactions - 5 with feverishness and one each of skin rash,
transient venospasm, a sense of heat over the body, exaggerated
reflexes and loss of memory.
On the basis of these studies, a recommendation to use
thiosulfate as a therapeutic agent for the victims was made.
Indications and contraindications for use, dosages for different age
groups and details regarding administration were spelt out.
47
H.Chandra (ICMR,1985) reporting on the results of sodium
thiosulfate in over 2000 cases stated that it was H found to give
i
J
beneficial results." It is not possible to comment on this. Anecdotal
reports of dramatic cures have also been reported.
N.P.Mishra (ICMR,1985) reported on a trial of sodium
thiosulfate treatment with 120 cases and 100 suitably matched
controls. Only results of clinical observations were recorded as there
were no facilities for blood gas analysis. Urinary and serum
thiocyanate levels were studied. Urinary thiocyanate levels of
controls were in the range of 0.5 to 5.65 mg which is much more than
0.6 to 0.9 mg which has been suggested as the normal range. He
therefore doubted the utility of determining urinary thiocyanate
levels. He studied clinical findings such as dyspnoea, chest pain,
general aches and pains, fatigueability, pain in the abdomen,
appetite, pulse rate, lung signs and subjective feelings. All these
were given an arbitrary score so that in the worst cases the score
totalled to 100. Results showed that in the 100 cases given sodium
thiosulfate :
60 showed a decrease in score,
19 had an increase in score and
21 showed no change
The trial was carried out double blind. An important finding was that
the greater the initial score before therapy, the smaller was the
reduction of the score after therapy. There were very few cases with
side effects. These were feverishness, skin rash, sense of heat all
over the body - all of which were relieved by antihistaminics. Urinary
thiocyanate levels were estimated in 60 cases. The mean value before
therapy was 1.068 +/_ 1.03 and after therapy 1.46 ♦/- 1.113. The basis
for selection of cases and controls has not been specified. No
comparison between cases and controls has been given regarding
48
response to sodium thiosulfate administration or regarding urinary
thiocyanate levels.
I
I
I
I
The data reported regarding all the studies done is inadequate
for a thorough appraisal.
It is also known that levamisole was used in a few patients as
an immunomodulator.
Controlled clinical trials should be performed for treatments
being tried, as only then will a scientific evaluation of their
efficacy be possible.
9.4
DISCUSSION OF CLINICAL FINDINGS
1) From the above account it is apparent that tremendous effort
has gone into the clinical management of the thousands of patients who
poured into the dispensaries and hospitals following the disaster.
Medical staff worked round the clock, many of them suffering from
effects of exposure themselves.
2) The description reveals the involvement of several organ
systems in the body. This occurred even in the acute phase though it
was then masked by the severity of the effects on the eyes and
respiratory system.
The Environmental Health Criteria 27 (1983) states that few of
the non-biologic agents have unique effects on health and conversely
r
?
the effects considered may often be related to a wide range of
factors. Therefore many aspects of the situation should be takn into
f
i
r
i
■
account in trying to understan etiology and mechanism of action.
3) Inspite of receiving medical treatment people kept returning to
the clinics with histories of persistent symptoms or with relapses
following remissions. Recent studies and clinical experience provide
evidence of chronic effects.
i
49
4) It was not possible to fit the apparently unrelated symptoms
and signs with which people were presenting into definate diagnosis.
!*
In the toxic oil syndrome which occurred in Spain clinical
observations in the acute and chronic phase showed features resembling
those of well known disease entities, but the combined clinical
picture and pathology findings were unique and suggested that the
syndrome was new (Grandjean and Tarkowski, 1983). A similar situation
is seen in Bhopal. Here, unlike in Spain the exposure is much more
delineated in time and place. Though the exact composition of the
chemicals causing the morbidity and mortality is not fully known,
there is certainty about it being MIC and its breakdown products or
metabolites. It is the first instance of human exposure to such high
concentrationsof these chemicals. The event has resulted in a pattern
of morbidity which probably comprises a new disease complex.
5) It has been observed that maintenance of records for individual
patients regarding clinical presentation and treatment were a casualty
under the acute emergency conditions. This is a lacunae both for the
future treatment of the individual patient as well as for a thorough
understanding of the pattern of morbidity caused by the disaster.
6) A number of medical professionals and researchers have
documented the general clinical picture with which the affected people
presented to the clinics at varying periods of time after the
disaster. This does provide very valuable qualitative information
about the cases seen and investigated.
7) The approach in the documentation reviewed has been focussed
mainly on the individual" case" and on specific organs and systems.
Some of the limitations of this approach are :
a)
Because only people who voluntarily attended clinics were
considered there is a self selection in the patients seen and
documented. This "selection bias" would result in the picture of
50
morbidity not being representative of the morbidity in the community.
However it would still provide descriptive information about the
morbidity produced in those individuals.
From the estimated 200,000 people exposed or at risk only a
proportion would have utilised the Govt, health services on which
most of the ICMR reports were based. Banerji et al (1985) have
documented his. Other possible health services that people may have
utilised are as follows :
- medical relief camps set up by a variety of volunatary agencies
- local private practitioners or registered medical practitioners special health schemes of which they were members eg ESI
hospitals, Railway health services etc.
- health services outside Bhopal
- other systems of medicine / healing prevalent in India eg ayurveda,
unani, siddha, homepathy etc
- some may have utilised several systems of medicine
or some may not have utilised any service.
Factors affecting utilisation of services would include
accessibility in terms of finance and distance; severity of illness;
tolerance of symptoms; mental health status and the beliefs and
culture of the people.
b)
Cases reported only represent individual patients and cannot
be related to a population to derive rates. Morbidity rates besides
providing an estimate of the magnitude of the problem and its
distribution in the population, could also help one to identify
priority groups for treatment and care.
QH ' \ oo
\'\\
c
i >' .-te-v. th q-’ I
51
Bfica’ore - FPO-ooi.
CHAPTER 10
REVIEW OF EPIDEMIOIOGICAU STUDIES
INTRODUCTION
There have been very Tew epidemiological studies about the
health impact of the disaster. Reports that are available have been of
studies conducted by non governmental groups. They provide important
information about the type and distribution of morbidity in the
community. The methodology and findings of these studies will now be
described in some detail. Findings from the population based, cross
sectional study by Banerji et al have been discussed earlier in the
section on mortality.
REVIEW OF STUDIES
10.1
Epidemiological study of eye and general morbidity
1)
Andersson et al (1984) conducted a survey in the first
fortnight (Dec 11-17,1984) "to assess possible long term visual
disability among survivors". The sample comprised of 8 clusters of
households, selected in different localities which had received
varying degrees of exposure. Two localities of similar socio economic
status, 15 and 17 km away from tha factory, were selected as the
control groups.Detai Is of location of the exposed groups are not
known. The sample size consisted of 261 exposed and 91 unexposed
individuals. The sample size and distribution of the population in
each cluster is not known. It was stated that the sample size was
restricted because of shortage of time before the exodus from Bhopal
during Operation Faith, which disrupted daily life for some weeks.
Assumptions to determine sample size have not been mentioned. It was
observed that the worst afflicted families had left by the time of the
survey leading to an underestimation of effect. Method of sampling has
not been mentioned - it was probably not randomly done. Three
52
ophthalmologists (one with an interpretor) were the interviewers.
An attempt to maintain uniformity was made - standard questions,
!
method of examination and simplified nomenclature was used.
IFindings :
The post exposure death rate (which was specified as the number of
deceased / the number exposed) in the worst affected cluster was 37..
There were differences in symptoms between the various clusters or
exposure groups :
- burning of eyes and throat and coughing were the most
frequently mentioned symptoms.
- vomiting was the third most frequently mentioned symptom in
clusters close to the factory.
- further away choking and shortness of breath was higher.
- collapse and unconsciousness was reported only in the cluster
second in distance from the factory. Among those unconscious,
there were few or no eye symptoms, upon recovery.
- signs of respiratory distress were most marked in this cluster
affecting about 207. of the community.
- over one half of this cluster demonstrated eye signs.
- fundal changes were more common in the exposed group
especially venous dilatation.
- there was no case of blindness, irreversible eye damage or
difference in age standardised visual acuity.
- there was a significantly higher proportion of people with
active eye infection in the unexposed communities ( 57. as
r
compared to 17. ). It was stated that this was possibly due to
widespread use of antibiotics in the week preceding the
[
survey. (Absence of secondary infection was observed by Bang
the respiratory system.)
?
53
in
- there was a similar incidence (this should be prevalence ) o-f
Bitot’s spots in the exposed and control groups reflecting a
1
similar nutritional status in the 2 groups.
- there was evidence of fairly widespread trachoma in all the
groups, though very few active cases were seen.
Andersson et al (1985) reported on a 2 month follow up in the
clusters mentioned above. Among the exposed excluding one cluster to
which they had "no access " the follow up rate was 507.. In both the
exposed and nonexposed groups only 367. (131/360) were located and
reexamined.This is a very high drop out rate. No information has been
given about the baseline or known characteristics or attempts to
follow up the dropouts. The clusters were enlarged and 490 people were
examined. No information is given about the
new examinees viz.
regarding their distribution according to localities, their
demographic structure, method used for their selection etc. Hence data
will have to be interpreted with caution.
Findings :
There were no cases of blindness, decrease in visual acuity or
defect in colour vision. There were no corneal scars in the original
group but 6 scars which could impair vision were detected in the new
examinees. It was not stated whether these were attributable to the
disaster. There was regression of the early healing seen in the first
examination. There was one case of persistant unilateral corneal
oedema and 3 with complaints of persistent excess watering in an
otherwise quiet eye.
•>
10.2 Epidtmioloqic#l wtudy of g»ntr»l health statu*
A.Patel et al (1985) conducted an epidemiological study of the
general health status of the exposed people.
$
54
It was a population based, cross sectional study, using an exposed and
F
a control group. The study was conducted 3 months after the disaster.
Post exposure mortality rates for the different localities, as given
[
■
in publications by the State Govt., were taken as indicators of the
degree of exposure. JayaPrakash (JP) Nagar, 100 yards from the factory
I
in the direction of the wind that fatal night, had an exposure
mortality of 2.347. and was chosen as the study population. Anna Nagar,
10 km from the factory with an exposure mortality of 0.327., was used
as the control group. Both areas were comparable with respect to
housing, sanitation and economic status of the population. Study
results showed that mortality rates were useful indicators of
exposure. However the crude mortality rates found in the study
population were much higher than those reported in the Govt.
publication. The study findings were:
J.P Nagar - 86.6/1000 population,
AnnaNagar -
7.9/1000 population.
Post disaster hospitalisation rates were also found to indicate
differences in exposure : J.P Nagar - 307.
AnnaNagar - 0.727.
Sample size determination was made on the assumption that morbidity
would be 157. in JP Nagar and 57. in AnnaNagar. With a 57. level of
significance and 907. power, a sample of 180 persons in each group
(exposed and control) was chosen. Persons of both sexes, more than 10
years of age were studied.
Numbering of all the households to provide a sampling frame was
already done by the ICMR and the same was utilised in this study. As
random selection of individuals was not possible, a random selection
*
£
of 50 household units was made to yield the required sample size.
A house to house survey was conducted. This consisted of the
following : a) a detailed history on a predesigned questionnaire.
55
Non standardisation or pretesting of the questionnaire has been
accepted as a limitation, and was reported not to have been done
I
5
I
because of shortage of time.
b) general clinical examination of all the systems, the
parameters for which had been defined.
I
c) pulmonary function tests
using Morgans electronic
spirometer set at BTPS. A trained investigator, with experience in
field based studies carried out the tests.
d) estimation of haemoglobin percentage.
e) open ended questions on the people’s perception of the
health services available after the disaster.
Information about training of the interviewers has not been
given. They were not blind to the hypothesis as this was not possible
in any of the studies conducted in that situation. Group meetings were
conducted in the community to obtain consent. The people were informed
about the research group - that they were not related to the Govt.,
nor were they providers of services, nor involved with the claims for
compensation. This would reduce the possibilities for "compensation
malingering" as claimed by some. It was found that members of the
particular sample chosen had not been included in any of the other
studies being conducted, thus ruling out the possibility of the
learning effect or Hawthorne effect.
The two populations were comparable with respect to age and
sex structure, body surface area, history of chronic disease and
smoking. The exposed were slightly better off socio economically than
the controls.
There was a rather high non response rate of 297. in the
£
r
II
>
exposed group and 157. in the control group. However available
information about the non responders was collected. Their age and sex
structure was similar to the responders and 507. or more of them were
56
exposed. 607. and 507. of non responders in the exposed and control
4
groups respectively were out of town, while 257. were away for work.
There were no refusals. Repeated visits were made in the time
available to maximise the response rate (the investigators were a
■
§
group of people who had come from different parts of India and were
not resident in Bhopal). It has been argued that since the actual
difference in morbidity was much greater than the 10 7. assumed in
sample size calculations, a smaller sample size would have
demonstrated a difference and non response may not make such an
impact. Nevertheless the high non response would have altered the
process of random selection
and it must be kept in mind that the
non-responders may differ from the responders with respect to the
outcome following the exposure in unknown and variable ways eg as
stated by Andersson et al if the more seriously ill were among the non
responders there would be an underestimation of effect.
Briefly the study findings are as follows :
Prevalence rates of 26 symptoms were measured in the exposed
and control group at the time of the study. Tests to see if the
differences were statistically significant were done.
The following 15 symptoms were found to be highly
significantly different, being higher in the exposed group : cough
with expectoration, breathlessness on usual exertion, chest pain/
s.
•*
tightness, blurred vision/photophobia, fatigueability, weakness in the
7
extremities, muscle ache, headache, tingling/numbness, loss of memory,
nausea, abdominal pain, flatulence and anxiety/depress!on.
j
The following 6 symptoms were significantly different : dry
*
cough, breathlessness at rest, watering of eyes, skin problems,
I
bleeding tendency and impotence.
-
The following 5 symptoms were not significantly different :
57
fever, blood in sputum, jaundice, vomiting,blood in vomit and malaena.
As many as 637. reported all the important symptoms. Only 2.77.
reported exclusively pulmonary symptoms, while 35.147. did not report
any pulmonary symptoms. Every person in the exposed group reported at
least one serious symptom, but quite a few in the control group did
not report any.
There was a significant difference in the number of attacks of
respiratory infections in the month preceding the study. In the
exposed group it was often described as a continuous respiratory
problem. It was said that this could be a supportive finding to
indicate a state of lowered resistance or immunity.
Exposed women had a significantly higher rate of abnormalities
of menstrual flow, alteration in the length of the cycle,
dysmenorrhoea and leucorrhoea. The sample was too small to report on
abortions and stillbirths. 507. of exposed mothers in the exposed group
reported failure of lactation or a decrease in
milk output post
exposure, compared to 117. in the controls. Impotence in men was
reported by 8.17. in the exposed group and 0.727. in the controls.
On examination:
There was no difference in the resting pulse and respiratory
rates. The mean haemoglobin percent in both males and females was
significantly higher in the exposed group. There was no case of
cyanosis. This was stated to be a significant negative finding in view
of the findings of 877. with breathlessness on exertion, the raised
haemoglobin concentration and that extensive lung damage was expected
to have occurred. 9.47. of the exposed had crepitations and rhonchi in
the chest, as against 2.17. in the controls (P<0.025). This rate was
also stated to be too small to account for the much higher rate of
breathlessness on exertion.
58
Comparison of Symptoms reported by individuals in J.P. Hagar and Anna
Nagar. (Expressed in percentage. Numbers-of cases are shown in brackets.)
bi
J.P. Hagar %
A. Nagar %
P. Value*
27.70 (41)
14 49 (20)
P
2. Cough with Expeatoration
47.29 (70)
23.91 (33)
< 0.001
3.
Breathlessness at rest
10J3 (15)
2^9
(04)
< 0.025
4.
Breathlessness on
usual exertion
87.16 (129)
35 50 (49)
< < 0.001
5.
Chest pain/tightness
50.0
(74)
^6.08 (36)
<< 0.001
6.
Weakness in Extremities
65.54 (97)
36’95 (51)
< < 0.001
7.
Fatigue
81.08 (T20)
39.85 (55)
< < 0.001
3.
Anorexia
-65-2.1 498)
-23^26 439}
9.
Nausea
58. TO (86)
16.66 (23)
< < '0.001
10.
Abdominal pain
53.37 (79)
25.39 (35)
< < 0.001
11.
Flatulence
68.91
(102)
25.36 (35)
< < 0.001
12.
Lacrimation
58.78 (87)
42.62 (58)
<< 0. 01
13.
Bdurred vision/photophobia 77.02 (141)
33*40 (53)
<< 0.001
14.
Loss of memory for
recent events
45.27 (67)
11.59 (16)
< < 0.001
"54772 (81)
^0728 728)
<< 0.001
No.
1.
Symptoms
Dry Cough
T5. Tingling/numbness
<
0.01
•(a) P Values were calculated by X2 method.
Source : Patel A and Patel A, (1985)
The Bhopal disaster aftermath :
an epidemiological and sociomedical survey.
i
59
(3)
Comparison of Symptoms reported by individuals in J.P.Nagar and Anna
Nagar
(Expressed in percentage. Numbers of cases are shown in brackets.)
(Symptoms significantly different but not analysed further)
SI.
No.
Symptoms
J P. Nagar %
A
Nagar %
P. Value
•(a)
0 01
1.
Skin problems
29.05 (43)
11.59 (16)
<
2
Bleeding tendency
9.45 (14)
2.89 (04)
< 0 025
3.
Headache
66.89 (99)
42 02 (58)
<< 0.001
4.
Muscle ache
72.97 (103)
36.23 (50)
< < 0.001
5.
Impotence
8.10 (12)
u 72 (01)
< .05
6.
Anxiety/Depression
43^2 (65)
10.14 (14)
<<0.001
Comparison of Symptoms reported by individuals in J.P Nagar and Anna
Nagar
(Expressed in pe icen rage. Munbers* of oases* are shown in brackets.)
-■
(Symptoms - Non-stgniflcarit)
K
J P. Niger %
A. Nagar %
P. value*
i
-
Si.
Symptoms
No.
1.
Blood in Sputum
10.13 (15)
7-24 (10)
NS.
■?.
Fever
27 70 f41)
• 28.98 (40)
N.S.
3-
Jaundice
0.67 TOT)
00
N.S.
4.
Blood in vornit/stcoF/malena
12.16 (18)
10.14 (14)
N.S.
5
Vomiting
11 48 (17)
5.79 (08)
N.S
(a)
I-
•(a) P Values were calculated by X2rhethdd
Source
: Patel A and Patel A, (1985)
The Bhopal disaster aftermath :
an epidemiological and sociomedical survey.
60
There was a statistically significant difference in pulmonary
function tests in both sexes in the age groups of 15-45 and 45-60
years. The difference in other age/sex categories were not
?
significant. However there were only a small number of observations in
these categories. The mean values of FEV1 and FVC and the FEV1/FVC
ratio in all age/sex categories were diminished in JP Nagar compared
to AnnaNagar. The 15-45 and 46-60 age groups showed a restrictive
pattern while the over 61’s had an obstructive pattern.
It was stated that the control population was also minimally
exposed, thereby diluting or masking the effect of the exposure.
10.3
EpideffHolpqicfrl study of women’s reproductive health
R.Bang (19850 conducted a study of the status of women’s
reproductive health 3 months post exposure. This followed the earlier
survey of a small number of women in the 2 affected slums (refer to
section on morbidity). The sample consisted of 114 women in 2 severely
affected areas and 104 women in a control area. Reasons for selection
of sample size have not been given. Selection of the sample was from
community based Ob/Gynae clinics. This introduces the problem of self
selection as women with Ob/Gynae problems would be expected to attend
these clinics. These cases cannot be related to any population or
denominator. Hence epidemiological extrapolations from these case
studies cannot be made. It is not known if standardised questionnaires
or examination schedules were used.
61
The findings of the study were reported as follows ;
Exposed group
Control group
Total no.studied
114
104
Pelvic exam.done
72 (637.)
52 (507.)
Leucorrhoea
65/72 (907.)
14/52 (277.)
51.67
P.I.D.
57/72 (797.)
14/52 (277.)
34.67
Cerv.erosion/
endocervi ci ti s
54/72 (757.)
23/52 (447.)
11.39
27/87 (317.)
1/81 (1.27.)
26.19
16/27 (597.)
2/16 (127.)
10. 17
Excess menstrual
bleeding since
exposure
Suppression of
lactation
Chi square
The differences are all highly significant (P < 0.001).
The results shown are from a smaller subset of the original
sample, as pelvic examination could not be performed in some women due
to various reasons like pregnancy; not being married; and refusals ie
a selection at this stage has also occurred. However inspite of the
limitations mentioned and also because similar factors of self
selection occurred for both the exposed and control groups the
difference between them is large enough to suggest real differences in
the two groups and point to the need to study this area. Other
studies, subsequently, too have reported similar findings (Patel et
I
al,1985 and Sathyamala,1986).
In the exposed group there was a history of spontaneous
abortion in 7, stillbirth in 4, threatened abortion in 1 and
incomplete abortion in 1 after the gas leak. No women in the
control
group reported any of these adverse outcomes of pregnancy.
Severe pallor was found in 37 (36%) of the control group but
only in 3 (37.) of the exposed group. This corresponds to the finding
of an increase in haemoglobin percentage in the exposed population
62
found in other clinical and epidemiological studies.
10.4
t
3
Epidemiological study of outcome Qf pregnancy
Sathyamala C (1986), conducted a community based study of
pregnancy outcome, 10 months post exposure. A large sample was needed
to detect significant differences in rates of abortion and sti1Ibirth.
The sample size took into account a non response rate of 257. which had
been found in earlier studies. A total population of 8165 people in
1632 households were surveyed. Details regarding assumptions to
determine sample size, power of study etc were not reported. Three
exposed localities (bastis) were selected on the basis of post
exposure morbidity and or mortality rate. These were as follows :
JP Nagar- Mortality rate 65.3/1000, Morbidity rate 667.
Kazi camp Kenchi chola- "
■I
H
ii
46.7/1000,
35.7/1000,
ii
" 54-607.
" 91.97.
These figures were taken from later * unpublished analysis of the
study by Banerji et al. The sampling frame provided by the ICMR was
utilised and random sampling of households done. A” historic control"
was utilised ie history of pregnancy outcome in the year preceding the
disaster, in the same population was used as a comparison. This was
chosen on the basis of studies carried out elsewhere which
demonstrated an abortion recall of 827. accuracy even after a lapse of
10 years. This may have lead to an under reporting in the controls and
an overestimation of the difference between the groups.
A pre-tested questionnaire was used. Methods used to train
interviewers and to avoid interviewer bias have not been mentioned.
The definition of abortion, missed periods and delayed periods used
for the purposes of the study have not been mentioned.
Misclassification between the three could possibly occur
Findings :
The non-response rate was 22 7., within the limits of what had
63
been considered in sample size determination.
There were 275 live births and 13 still births in the
population after the gas leak. The birth rate was stated to be
33.68/1000 population and was said to be comparable with the national
birth rate. However births for only 10 months were taken to calculate
the rate. Normally a period of 12 months is used and hence the rate
calculated would be an underestimation. It is also the crude birth
rate, not being standardised for the age and sex structure of the
population. The stillbirth rate post exposure was found to be
47.27/1000 live births. However live and still births together should
be taken in the denominator. The rate then is 45.25/1000 births. No
comparison with national, regional or study based stillbirth rates has
been made.
The overall spontaneous abortion rate after the gas leak was
370.96 which was statistically very significantly higher than the
spontaneous abortion rate of 32.178 before the gas leak.
Rate Q* spontaneous abortion before and after the gas le»k (GL)
Before GL
After 5L
Total conceptions
404
310
No.of abortions
13
115
Abortion rate
32.178/1000
370.96/1000
conceptions
conceptions
A second important finding is that the rate of spontaneous
abortions in women who conceived after the gas leak is again
statistically highly significantly greater than the abortion rates
before the gas leak. The increase being about 5 times greater than
before the gas leak.
I-
64
Abortion rate in conceptions before GL which aborted before GL
and abortion rate in conceptions after GL
Concep.
Abortion
Abortion
Concep.
Abortion
Abortion
BGL
BGL
rate
AGL
AGL
rate
404
13
32.178/1000
310
45
145.16/1000
conceptions
conceptions
(BGL- before gas leak, AGL- after gas leak)
The overall foetal death ratio was statistically
significantly increased in the year following the gas leak in
comparison to the previous year.
Foetal death ratio before and after gas leak
1985
1984
Quarter
Number
Number
F D
Number
Number
F D
delivered
aborted
ratio
delivered
aborted
ratio
30
2
6.66
76
27
35.52
87
12
13.79
77
24
31.16
56
3
5.35
94
20
21.27
(LB+SB)
Jan-
March
AprilJune
JulySept.
(LB - live births, SB - still births;
FD ratio - foetal death ratio )
The foetal death ratio has not been defined but appears to be the
number of abortions per 100 live and still births.
While past obstetric history, parity, period of gestation at
the time of abortion etc were measured they were not taken into
consideration in the analysis. These are important interactive and
a
confounding variables.
I
65
'<
Changes in regularity of the menstrual cycle, delayed and
missed periods, length of cycle and type of flow, were also found to
be statistically significantly different before and after the gas
leak.
10.5
C»se referent itudy of wateripg o* the tyes
Andersson et al (1986) conducted a case referent study of
persistent eye watering. An eye hospital started in Bhopal in response
to the disaster was used as the source of cases and controls.
Two consecutive retrospective series of clinical records were
drawn, for outpatients on whom exposure data were available. This
would be a source of selection bias as it is probable that exposure
status may not have been recorded equally in the exposed and
non-exposed groups. The method by which exposure was assessed and
recorded has not been mentioned.
Findings :
Gas exposed people were three times more likely to present with
watering eyes ( odds ratio -OR- 2.96, 95 7. confidence interval - CI2.3 - 3.4) and nearly 4 times more likely to present with watering and
at least one other irritant symptom (burning, itching, redness) ( OR
3.8, 95 7. CI 3.12 - 4.4). There was no association between exposure
and refractive errors ( OR 1.16, 95 7. CI 0.83 - 1.9).
There is no explanation for the symptom of persistent
watering of the eyes. The report suggests tear film instability due to
long term effect of exposure on epithelial maturation or abnormality
of the mucus component of the tear film which is derived from the
epithelium itself and from conjunctival goblet cells.
66
In lummary, the epidemiological investigatons conducted have
studied different aspects of the health impact of the disaster at
different points in time. They vary in methodology used and critical
comments regarding this aspect have been given above. They were
conducted in difficult circumstances and despite some methodological
limitations they all record very serious effects on the health of
those exposed. They support clinical findings of multi systemic and
long term effects. However some of the important findings from these
studies, that may provide clues for etiology, if followed up are A) the varying pattern of morbidity in clusters at different distances
away from the factory in the acute phase. This was not just in
magnitude of effect, but there were qualitative differences of
differing symptomatology (Andersson et al) in different clusters. This
points to the possibility of the role played by different chemicals.
Follow up studies should look at different clusters over time.
B) the presence of a percentage or proportion of individuals with
multisystemic symptoms in the absence of lung disease (Patel et al) in
the sub-acute phase. This suggests that severe lung damage may not
account for all the chronic effects.
C)
significantly higher adverse outcome of pregnancy in exposed women
conceiving after the disaster, compared to controls. Congenital
abnormalities also need to be studied. This very serious observation
points to the presence of continuing toxicity.
Infants, preschool and school age children, a vulnerable group
have not been studied. Respiratory disability has not been
studied at
the population level. Natural history of the morbidity and the excess
mortality that continues to occur also remain
i
■I
■
67
to be studied.
Summary t*tolw of epidemiq!pq!c#l studies conducted in Bhppal.
Investigator
Focus
of study
Type of
study
Time
1.Andersson
et al
Eyes, gen
morbidity
Population
based,
clusters +
controls,+
2 month
follow up
2.D Banerji
et al
3.R Bang
Place
Person
Met hpdpl Pfli G ail
Sampling
method
Non
response
Study
instrument
December Severely + General .261
1984,and moderately popula- exposed,
Feb.1985 + mildly
tion
91 un
exposed
exposed
areas
persons
opportunistic
sample ie as
many as could
be examined
64 7. at
followup
3 ophthalmologist
interviewers,
attempts to maintain
uniformity in history
taking and
examination
Mortality, Population
general
based,
features. cross sectional
January
1985
Severely + General .700
Moderately popula- households
exposed
tion
areas
Random
sampling
?
pre-designed
questionnaire,
trained investigator
Womens
Clinic
reproduct based case
ive health series in
exposed +
control
areas
Feb-Mar
1985
Severely
exposed +
control
areas
Womenreprod
uctive
age
group
.114
exposed,
104 un exposed
persons
self selected
sample,women
attending
field based
Ob/Gyn clinics
pelvic
exam.
not done
in 43.27.
1 gynaecologist
investigator,
routine history
taking and
clinical exam.
4.A Patel
et al
General
health
Population
based,cross
sectional,
exposed +
control
areas
March
1985
Severely
exposed +
control
areas
General
popula
tion
>10 yrs
of age
180
persons
in each
group
Random
sampling
29 7. in
exposed,
15 7. in
control
group
Pre-designed
questionnaire
with defined
parameters,
? training of
investigators
5.Sathyamala
Outcome
of
pregnancy
Population
based,
cross sectional,
historic
control
Sept
1985
3severely pregnant
exposed
women
areas
out of
general
popula
tion
8165
persons
in 1632
house
holds
Random
sampling
22 7.
Pre-designed,
pre-tested
questionnaire,
? training
of investigators
6.Andersson
et al
watering
of eyes
case
control,
record
based
Nov’85
-Jan86
eye
hospital
989
those with
recorded
exposure
status
Sample
size
x>
eye
patients
from
gen. pop
-ulation
hospital case
records
I
l
CHAPTER 11
EXPERIMENTAL STUDIES
11.1
Pre- diwasttr
Data on the toxicology of MIC was scarce at the time of the
disaster. Median lethal doses in animals were available eg. it was 5
ppm for 4 hours by inhalation in the rat. In another experiment a dose
of 62.5 ppm for 4 hours killed all the exposed rats. Corneal injury
has been recorded in rabbits.
A dose ranging study in human volunteers has been referred to
by the ACGIH ( American Conference of Governmental Industrial
Hygienists). There were no effects at 0.4 ppm but exposure to 21 ppm
was unbearable.
Mention has been made of the intense irritation caused to
eyes, nose and the throat. Kimmerle and Eben (1964), studying MIC
toxicity by inhalation exposure, observed that it was highly
irritating to skin and mucosa and that it produced pulmonary oedema.
There was little published material on the effects of
sublethal doses, dose response and metabolic/chemical breakdown
products of MIC.
11.2
Post- disaster
Several toxicological studies on different animal models have
been conducted after the disaster. Because of the short life span of
the animals used, each animal year being equivalent to several years
of human life, an estimate of long term effects of exposure can be
made relatively early. Experiments and pathological investigations not
ethical or permissable to be conducted on humans can also be
performed. The main limitation of animal studies however, in general
is that extrapolation of results to humans has to be made with caution
because of the differences in the biological systems. Another limiting
68
factor to be borne in mind in this particular case is that in all the
animal experiments conducted so far, only pure MIC has been used as
the agent of exposure. In Bhopal under the prevalent conditions of
high pressure and temperature and in the presence of catalysts other
chemical reactions could have occurred with the formation of other
chemicals. However the advantage is that these experiments can
indicate lesions attributable to MIC. They can be used to support /
explain epidemiological observations and similarly epidemiological
data can provide clues for experimental work. The objective of both
endeavours together, being to explain mechanisms / pathogenesis to the
extent necessary for rational interventions in the treatment
and /or
rehabilitation of victims and in the prognosis of their condition.
The method of MIC exposure used in animal studies has been by
I
inhalation, with doses varying between experiments. They all tried to
simulate the possible dose range that could have existed during the
Bhopal disaster
Harding et al (1985) reported the development of lens
opacities or cataracts when rat lenses were incubated with MIC.
Salmon et al (1985) reported that at low concentrations in
rats MIC caused severe sensory irritation with slow, irregular
breathing and the production of a sedative effect. At higher
concentrations this was masked by arousal resulting from respiratory
distress. Eye damage was always confined to the epithelial layer with
most severity at intermediate exposures suggesting that at high doses
some protective response was evoked. Urinary thiocyanate levels in the
exposed were lower than in the controls. They observed a dose
dependant response and supported the use of death rates and incidence
of pulmonary damage as a crude index of exposure in epidemiological
studies.
I
Nemery et al (1985) reported that at very
69
high concentrations
(10 mg /L for 15 mins) 50 7. of the rats died. The lungs were enlarged
with air. Gross oedema or haemorrhage
was present only in 2 rats
killed after exposure. The main effects of low concentrations of MIC
on the respiratory tract was to injure the proximal airways with
little alveolar injury. At high concentrations lung parenchyma was
also damaged with resulting interstitial and alveolar oedema,
inflammation and haemorrhage. Though there was complete destruction of
bronchiolar epithelium, repair took place. However despite rapid
resolution, they found isolated foci of more recent injury in animals
killed 2-3 weeks after exposure. They found MIC to be a respiratory
irritant ie both a sensory (stimulation of nerve endings in the nasal
mucosa) and pulmonary irritant (impact on lower respiratory tract ).
Ferguson et al (1986) in mice experiments also found
MIC to be a potent sensory and pulmonary irritant. They have
considerable experience in working with isocyanates and have found MIC
to be the most potent pulmonary irritant they have tested in the
isocyanate series. They found that the RD 50 (the concentration
evoking a 507. decrease in the respiratory rate) and the RD 50 TC (the
RD 50 in tracheally cannulated mice) was seperated only by a factor of
1.5. Thus a concentration capable of evoking intense
sensory
irritation of the eyes ,nose and throat is close to that capable of
inducing pulmonary irritation. MIC is thus classified as a respiratory
irritant. They found it to be 7 times more potent than chlorine.
Luster et al (1986) found a steep dose response for toxicity.
During 90 day recovery studies epithelial injury generally resolved,
but prominent fibrosis developed in the walls of the major bronchi.
They reported no injury to the spleen, liver, kidney, thymus or brain.
Haematological values except for slightly increased haematocrit were
within the normal range. They found humoral immunity to be unaffected.
Inspite of a 307. suppression in T cell lympho-proliferative response
70
I
they found host response resistance not affected.
Fowler and Dodd (1986) studied rats, mice and guinea pigs.
Gassert (1986) observed that this study was the most comprehensive
inalation study of MIC to date. It was produced some years before the
Bhopal disaster under private contract 48 with Union Carbide but was
not published until 1986. It provided evidence of bronchiolitis
obliterans in guinea pigs (only) exposed to 10.5 and 5.4 ppm MIC for 6
hours. They also noted dose related lesions in the respiratory tract.
No deaths occurred in animals exposed to 1 or 2.4 ppm MIC. The
majority of deaths for 10.5 and 20.4 ppm occurred through post
exposure day 3 ; at 5.4 ppm deaths occurred throughout the 14 days.
Deaths were attributed to pulmonary vascular alterations.
ICMR studies (1985) found that the cherry red appearance of
the blood could be due to the direct action of MIC (by carbamylatuon)
and need not necessarily be due to cyanide or carbon monoxide. Carbon
monoxide poisoning was ruled out. Analysis of human tissue by gas
chromatography indicated the presence of monomethylamine. On animal
studies they found that MIC had an LD 50 dose of 85 mg in mice, but
with thiosulfate therapy it shifted to 195 gms. For rats the figures
were 270 and 344 respectively. Normal rabbit lungs weighed 6 gms.
following MIC exposure they weighed 29 gms and had a large number of
haemorrhagic patches. When given sodium thiosulfate immediately after
MIC exposure the lungs weighed 24 gms but the appearance was normal.
With pure MIC they also found a dose dependant response in the
respiratory tract. They found that MIC had bactericidal activity.
Salmon (1986) also reported that MIC could produce a reddish
tinge to blood. However differences could be detected on spectrometric
analysis.
Varma et al reported adverse effects on the oestrus cycle and
fertility in male and female mice
71
I
Gassert et al (1986) reported on a 14 month follow up of rats
[
exposed to MIC. Two exposed rats died at 6 and 8 months following
i
sudden onset of respiratory distress. 6 rats killed at 14 months
•I
revealed a history of mild respiratory infections. Mild interstitial
fibrosis in the peribronchiolar region was present in all exposed
I
rats. A notable finding was that MIC exposed animals had 4 times the
■
amount of lymphoid aggregates found in control animals - adjacent to
the bronchiolar airways. A mild infiltrate of eosinophils was present
§
1
J
Ii
I
!
in the bronchiolar mucosa. Eosinophil and lymphoid infiltrates were
found in the mucosa of the conjunctiva of the eyelids and perilimbal
regions. They state that long term changes in the eyes and lungs may
result from a single 2 hour exposure to acute sublethal doses of MIC
vapours and that the immune system is most probably directly involved.
They suggest that lymphoid hyperplasia may be due to persisting
exposure related antigens or to an increased susceptibility to other
I
immunostimulating agents following MIC exposure.
Thus animal experiments reveal that MIC is extremely toxic on
inhalation - being a potent respiratory irritantft. Chronic morbidity
and a continuing increase in mortality has been reported in the
■s
exposed animals. The studies suggest 3 possible mechanisms by which
1this may occur :
I
a) due to long term sequelae of severe lung damage caused by the
<*■
direct toxic or irritant effects of the chemicals.
b) due to damage to the immunological system.
I
c) due to systemic toxicity caused by mechanisms as yet unknown.
i
i
72
?-
CHAPTER 12
DISCUSSION
I
The main points arising from the description so far are
summarised. This will be followed by a discussion of the main
methodological points pertinent to an epidemiological understanding of
the health impact of the disaster. This will also be relevant to the
conduct of epidemiological studies in the future. Discussion of
methodological issues that have been interspersed in the report will
not be repeated here.
12.1
SUMMARY QF FINDINGS
1) A population of about 200,000 persons were exposed at a
point in time and at a localised place to an airborne toxic chemical
agent.
2) The composition and characteristics of the chemical agent/s
are not fully known. Studies are being conducted to elucidate this.
These include analytical chemical studies, toxicological studies on
animals etc.
3) The exposure resulted in immediate and continuing mortality
and morbidity in the population at risk.
4) The mortality was substantial, though the exact numbers are
not precisely known.
5) Clinical investigations show that the morbidity that has
occurred is complex and affects several systems. It does not fit
easily into previously known disease entities. The combined clinical
and pathological findings probably comprise a new syndrome.
6) Epidemiological studies indicate a large community load of
morbidity. This appears to vary with factors like locality, degree of
exposure and time. Besides manifestations in the acute and subacute
73
phases, long term effects have also been observed. Disease occurrence
and distribution according to characteristics of person need furthur
study.
7) There have been several theories proposed to explain the
mechanisms causing the morbidity viz.
- sequelae of direct damage to lung and eyes which followed exposure
to the toxic chemicals,
- alteration of the immune system following the exposure,
- systemic toxicity caused by the toxic chemicals or their
metabolites in the body,
- psychological trauma caused by the disaster,
- a combination of all the above.
12.2
OUTLINE OF DISCUSSION
The discussion on methodological points will cover the
following areas : a) the exposure variable,
b) the population at risk,
c) the health outcomes,
d) confounding variables and
e) sources of bias.
12.3
THE EXPOSURE VfiRIQPLE
By now, results from the few early studies conducted,
r
together with experience of physicians and social workers in Bhopal
and toxicological studies in animals indicate that the exposure has
f
£
resulted in long term adverse effects on health. These findings point
to the need for long term follow up of the victims. As a first step
valid measurements of exposure need to be evolved.
I
a) Defining exposure
It is necessary in the conduct of epidemiological studies in
■
74
Bhopal to have a working definition of the exposure variable.
Indicators or measures of the degree of exposure are also needed to
estimate possible dose dependant responses in the outcome variables of
mortality, morbidity and disability.
Previous studies have used the following as indicators of
exposure ;
- post exposure mortality rates in defined localities as reported by
the State Govt. Study findings have shown that these did provide a
rough estimate of exposure in different localities. The rates found in
the studies were however much higher than the rates reported by the
Govt. Issues concerning mortality rates have been discussed earlier.
a combination of death in the family or exposure related mortality
rates along with grades of morbidity as a measure of exposure.
- one study found that immediate post exposure hospitalisation rates
were also related to the degree of exposure.
b) Variability in exposure
Epidemiological studies reveal that control areas 10 kms away
from the factory have been mildly exposed. Studies have also shown a
variability in the picture of morbidity in different localities as
well as a variability in individuals or groups of people living in the
same locality. Besides differences in individual susceptibility
accounting for some of the variability, both the above observations
suggest that the factor of "exposure" needs to be considered more
carefully. The two important issues to be considered are :
- the area and hence the population exposed may be larger than
the accepted 200,000,
r
- several variables determine the exposure level for an
individual. Results from the various studies have indicate
that these are :
1) distance from the factory at which the individual was at the
t
75
time of the disaster, taking into consideration the direction
of the wind,
2) type of housing - pucca (well built)
I
i
- kutcha (without brick and cement)
- presence of gaps/holes letting in air,
3) action taken at the time of the disaster viz.
a)
measures of exposure to the atmosphere :
- kept all doors and windows closed and remained indoors
- opened doors and windows, stayed in the house
- went out, remained in the area
b)
measures of exertion :
- left area, walked
- left area , ran
- left area, cycled
- left area , used motorised transport
c)
use of neutralising / protective measures ;
- used a wet cloth over the face
- covered face with a blanket
- went in a direction opposite to that of the wind.
Thus a single parameter by itself eg distance away from the
factory, may not reflect the true exposure status of the individual
which would also depend on other actions that the person took at the
time of the disaster. This could be one of the reasons to explain the
variability in mortality and in the pattern and degree of morbidity in
different individuals even in the same locality. Other factors like
age, level of nutrition and general resistance, presence of other
I
diseases etc would also play a role. All the above will have to be
considered in studies of morbidity as well as in determining priority
groups of people who would need greater care and follow up.
76
c) Exposure at individual and population level
Mortality rates could be a measure of exposure to classify
localities and areas ie. they could be used as indicators of degree of
exposure at the population level. While the other factors outlined
above could be used as measures of the exposure status of individuals.
d) Measurement (assessment) of exposure
History taking is the traditional medical method of
determining the
exposure status of an individual. However in Bhopal a
large population has been affected. Several studies into the health
effects will need to be conducted over a long period of time and
several interviewers will be involved. To ensure comparability between
studies and consistency over a period of time, a standard, repeatable
and valid method of determination of exposure should be used.A
standardised questionnaire, using the factors discussed earlier would
provide a simple, inexpensive, noninvasive tool of investigation.
There have been attempts to develop biological markers of
exposure eg antibodies or enzyme related markers. They are still in
the experimental stage and will have to be field tested. However any
invasive method - in this case blood samples will be needed - have the
drawback of increased nonresponse. Besides this, increased costs, the
need for investigators who have requisite skills, the availability of
laboratory facilities etc
will have to be considered. Studies
carried out so far have shown that the use of crude morbidity and
as markers of degree of exposure. Salmon
mortality rates have served
et al (1985) have confirmed this on the basis of experimental studies.
With a little refining as suggested above, standardisation and
pretesting, questionnaires could continue to be used to measure the
degree of exposure.
77
12.4
I
l
THE POPULATION AT RISK
The population at risk would comprise all those who were
exposed to the agent and who could potentially manifest adverse health
outcomes as a result of the exposure. It would form the denominator in
calculating exposure related rates of morbidity and mortality for the
population. Various subgroups of this population could also be studied
eg according to age. sex, socio-economic status, degree of exposure
etc. Epidemiological profiles for groups broadly classified as
severly, moderately and mildly exposed could be built up. Factors
discussed under exposure variable will have to be considered.
Numbering of all the households to create a sampling
framework was done shortly after the disaster. Since a relatively
small population has been affected and there is a need for long term
follow up, a population register or case registers could be maintained
on computer after a census of the exposed population.
This would provide a good base for follow up studies.
12.5
THE HEALTH OUTCOME - MORTALITY
a) Mortality rates / standardization
The number of deaths following the disaster would have to be
related to the exposed population to derive crude rates. These could
be standardised for age and sex by comparison with a standard
population of similar socioeconomic status, and Standardised Mortality
Ratios (SMR’s) could be calculated. The time period during which
deaths are enumerated, would have to be considered in the calculation
of exposure related mortality rates. As with morbidity this could be
Ii.
calculated for the acute, subacute and long term phases. Rates for
different localities should also be calculated.
These rates could be calculated using routine sources of data.
*
78
However in the longitudinal study, life table analysis could be done.
There should be a good reporting system for deaths in the exposed and
•:£
control populations. Staff and investigators should be trained in the
use of the International Classification of Diseases and if necessary
suitable, standardised criteria could be evolved for the
classification of deaths. Autopsies should be performed in a sample of
deaths among the exposed group, as is the requirement in any medico
legal case.
12-6
THE HEALTH OUTCOME - MORBIDITY
a) Assessment criteria- This has been the first time that a
whole population has been exposed to high concentrations of these
chemical agents. The exposure has therefore resulted in a group of
symptoms and signs which together do not fit easily into established
disease entities. This new disease complex would have to be named
appropriately eg the "Bhopal Toxic Gas Syndrome". For the purpose of
epidemiological studies working case definitions of this disease
complex would have to be developed. This would have to be done based
on the clinical experience of medical professionals treating the
exposed population together with the help of epidemiologists to ensure
simple, standard criteria which can be applied in the field. It would
basically comprise of groupings of characteristic symptoms and signs.
b)
There may be a lag period between the exposure and
some
pathological conditions which have not as yet manifested. Rothman
(1985) states that one must allow for the following
- a biologically appropriate induction time during which a sufficient
cause becomes complete. This may be quicker for heavy exposures and
s.
slower due to interaction with other factors for lower doses of
exposure.
I
- latent period, which is the period after causation before the
■■i
79
disease is detected.
Early studies may thus miss still evolving disease conditions which
could be picked up by prospective longitudinal studies or
epidemiological monitoring systems.
c)
Complementary causes or predisposing factors would play a
role in the development of the disease outcome by increasing the
susceptibility of individuals. People with a larger set of
complementary causes would need a smaller dose of exposure to complete
a sufficient cause and result in a diseased condition (Rothman 1986).
Exposure to the toxic chemicals may unmask or exacerbate existing
disease eg chronic bronchitis, asthma, TB etc. These would be
considered confounding factors in the analysis of studies. But, from
the point of view of the health condition of the people and for the
provision of health care services, their presence would cause the
individual to be placed in a priority group.
12.7
CONFOUNDING AND INTERACTIVE VARIABLES
As discussed previously socioeconomic status is closely
related to exposure and to outcome and would be a confounding factor.
Stratification in design or group matching could be used to account
for this. Age and sex would also have to be considered.
In the Bhopal situation, smoking, exposure to smoke or air
pollution in the home (cooking on smoky fires) or at work, nutritional
status, presence of chronic diseases eg TB, trachoma
asthma ,chronic
bronchitis would be interactive factors which would have to be
measured and allowed for in the analysis.
12.8
SOURCES OF BIAS
Several sources of bias have to be considered :
a) Stewart (1985) has raised the issue ofsurvivor biai*‘in follow up
80
studies of survivors of the atomic bomb explosion in Hiroshima and
Nagasaki. This could occur in any cohort of people surviving a major
catastrophe. The parent population loses a high proportion of
vulnerable individuals - the very young, the old and the sick. Thus
when comparisons of mortality are made with a control group in follow
up studies there will be an underestimation of the effect. One may get
a normal death rate in the survivors, though it may actually be
slightly raised. This is similar to the bias caused by the "healthy
worker effect" in studies of occupational groups. This factor would
have to be kept in mind in long term studies in Bhopal.
T
b) As discussed previously there would be a selection bias in hospital
or clinic based studies due to self selection of people attending
these services. With the plurality of services and factors of
accessibility this would be important in Bhopal.
The utilization of health services in the subacute phase as reported
by Banerji et al (1985) shows that this occurs.
c) Bias due to migration of people into and out of the population 5 new
births and deaths, all of which would affect the baseline population
have been considered earlier in the report.
d) Misclassification of exposure status or of outcome (if the diseased
condition is undiagnosed or misdiagnosed) will enhance or decrease the
association depending on the direction of the misclassification. In
Bhopal this is very likely when using routine sources of data, as many
medical professionals dealing with a previously unknown situation,
have tended to use the nearest known diagnosis to fit the presenting
symptoms and signs. This re-emphasises the need to have a working
h
defination of the outcome for documentation and study.
81
e) The non-response rate has been found to be quite high (20-297.) in
all the studies conducted in Bhopal. Besides altering the sample size
and the power of the studies, this would also affect the composition
|
of the sample, depending on the characteristics of the non responders.
Allowance for non response should be made in determination of sample
size and also in budgeting for time and finances to allow for more
intensive follow up of a percentage of the non-responders.
f) Observer bias leading to a bias in history taking, recording,
interpretation of findings or in diagnosis may occur. The factors that
play a role specifically in Bhopal are
- Those who believe that all is well in Bhopal try to underplay or
explain away the symptoms of the people. This is evident in the
attitude of many who attribute every symptom to the presence of
chronic diseases or as psychosomatic symptoms or as compensation
malingering. On the other hand those who believe that a conscious anti
people crime has been committed in Bhopal may let their beliefs affect
reporting or interpretation of what the people say.
The above factors could be reduced by the training of
interviewers and in the use of blind techniques when possible in
certain investigations eg in reading xray films etc. Keeping
investigators blind to exposure status is not possible.
'i
■
g) Measurement bias would be important to keep in mind especially when
using instrumentation eg spirometers for lung function tests.
Standardised instruments and techniques are available. The instruments
I
1
should be calibrated and maintained to give accurate and reliable
readings over a period of time.
■c
82
12.9
SUGGESTIONS FOR EPIDEMIOLOGICAL STUDIES IN BHOPAL
Several research projects, involving different specialities,
are being undertaken in Bhopal and elsewhere, on various aspects of
the disaster. As outlined earlier there is a need for supportive
epidemiological studies, especially those that are population based. I
have not attempted to design a specific study while based here in
London. More recent information would be available in India,
I
especially regarding the studies set up by ICMR. Also, more details
about the affected population, the numbers in different localities,
their demographic structure etc would be available in Bhopal. By
meeting local medical practitioners and research workers, an
assessment of the present status of morbidity could be made , which
would provide important clues for study. It is hence more appropriate
as well as practical to plan a detailed study design based locally in
India, at Bhopal. However s possible study designs and
methodological
issues concerning longitudinal studies have been delineated.
In Bhopal a cohort of people have been exposed at a point of
time to chemical agents. There is a need to study :
1) the range of health effects stemming from the exposure,
2) the natural history of these health effects.
An epidemiological study is basically an exercise in quantifying
disease occurence and using a logical method in deriving inferences /
explanations to account for variations in disease distribution by
relating them to putative causes. In this particular situation, where
the exposure has defined time and place characteristics, though the
composition may be uncertain, observational follow - up or
longitudinal studies seem logical. Here the study population are
selected with reference to their exposure status.
83
The application of case control studies, where the study
r
'S
population are selected with reference to their disease status, would
be limited. The disease outcome in Bhopal, is not a well defined
entity and is still evolving. The prevalence of what has occurred, is
not rare, but affects 30 - 60 7. of the severely and moderately exposed
I
population. Also, a large proportion of the local population of
similar socioeconomic background have been exposed to the agent, to
some degree.
12.9.1
Cross sectional ytudiey in the sub acute phase have provided
prevalence rates of various symptoms and have also indicated areas of
importance. A repeat cross sectional study
could give prevalence
rates of symptoms and signs 3 years post exposure. It could provide
age, sex and area specific distribution of the" Bhopal toxic gas
syndrome". Relationships with aspects of the exposure variable could
also be tested.
Cross-sectional studies using exposed and control
groups, a variant of case control studies, could be used for
analytical purposes, to study the relationship between symptoms or
groups of symptoms and exposure.
12.9.2
Longitudinal study
A cross sectional study should form the baseline for a
prospective, longitudinal study. Important points in the conduct of a
'•
longitudinal study are now
1)
considered .
Objectives
The hypothesis should be explicitly stated. There is a need to
define the time period of the study. This would be selected based on
biologic assumptions of the disease outcome and its relationship with
a
■
the exposure.
The broad objectives could be :
■
84
a) to study the prevalence / incidence of the "Bhopal toxic gas
syndrome".
b) to relate symptoms / signs observed at the start or appearing
during the course of the study, to various aspects of the exposure.
c) to study the natural history of the condition - its severity,
fatality, the impact of therapy etc.
Other specific areas to be studied are
- a) the percentage of exposed individuals with multisystemic
symptoms and signs in the absence of lung findings.
- b) levels of urinary thiocyanate in the exposed and control
population.
c) prevalence of psychiatric disorders in the two groups.
d) prevalence of respiratory disabilities
- e) outcome of pregnancy in the years following the disaster.
The specific parameters of these outcomes would have to be evolved
locally.
2)
Sample
Small clusters in different localities could be selected to be
able to study the variation in outcome in the different localities.
Other aspects of the exposure variable would also have to be measured
in the individuals in these clusters.
Sample size determination would have to be done locally, with
details of the baseline population. Differences in the prevalence of
symptomatology between the exposed and control groups, as found in
previous studies, should be used for the calculation. The level of
statistical significance and power required for the study should be
decided. The high non response rate as found in previous studies and
possible drop out rates
should be considered .
Method of sampling or sampling procedure - to ensure
85
representativeness and to avoid bias, population based, random
sampling should be used. With this method the probability of selection
Though the
!
into the sample is the same for all individual units.
I
sampling framework has been set up, it could be rechecked keeping in
£
mind the discussion of the population at risk. The method used in the
cross-sectional and longitudinal studies would have to be a house to
house survey.
Community meetings as in the study by Patel et al should be
conducted with the people to inform them of the study, discuss with
them the need for continued study, reasons for random sampling etc.
3)
Ethical aspects
Obtaining consent from study participants and maintenance of
confidentiality of patients records should be planned for.
4)
Study population
Besides the general adult population, infants, preschool and
school age children should also be considered. This group has not been
studied in the studies reviewed. The advantages of this group are that
they would have had no serious exposure to smoke (though passive
smoking would have to be considered) and occupational pollutants.
Chronic disease would also be minimal.
Their respiratory systems are also more sensitive to insults which
makes it easier to detect adverse effects. It has been found that
children can carry out spirometric lung function tests from about 7
v.
Iu
years and can manage a single measurement of PEFR at 5 years (Florey
and Leeder 1982).
5)
•jT
Control population
An unexposed or minimally exposed population is needed for
comparison. It should be comparable in terms of broad socio- economic
characteristics. It would provide an estimate of disease rates
■
I
expected to occur in the absence of exposure.
%
4-
86
6)
Measuring the exposure and outcome variables
The main issues regarding these variables have been discussed.
Working criteria / case definitions for the assessment of exposure and
outcome need to be defined. Several types of outcome can be observed
eg post exposure mortality, specified decrease in lung function, onset
and frequency of respiratory infections in addition to those mentioned
under specific objectives. Sub-classification into definate, probable
and ppossible” cases" could be made.
Criteria and methods of assessing the exposure and outcome
variables should be the same in both the exposed and control groups.
7)
Examination techniques
Simple, valid, repeatable, field tested instruments will have
to be used. These would include :
questionnaires
clinical examination
lung function tests etc
The parameters to be measured at entry and follow up should be
specified. Numerous studies of diseases of the respiratory system and
its risk factors have been conducted. Instruments which are valid and
reliable are available. Three standard questionnaires have been
developed for the study of respiratory epidemiology
by the British
Medical Research Council, U S National Heart and Lung Institute (NHLI)
and the American Thoracic Society. A suitable one could be combined
with general health questionnaires. Standardised methods for
spirometric lung function tests are also available. Random and
systematic sources of error in measurment must be minimised.
8)
Other factors to be considered are
- the training of investigators,
- pilot testing and
- planning for the follow up of a percentage of non-responders.
87
9)
Analysis
In a longitudinal study an unbiased estimate of the relation
between exposure and outcome is obtained. The relative risk (incidence
rate in the exposed/incidence rate in the unexposed) and absolute risk
(incidence rate in the exposed - incidence rate in the unexposed) can
be calculated. It would be more useful to work out person years of
risk and calculate the force of mortality / morbidity or the
instantaneous mortality / morbidity rate. The risk of developing a
particular outcome (death / disease) can be estimated for a variety of
initial characteristics eg distance from factory, action taken at the
time of disaster, main presenting symptom in the acute phase etc.
10) Difficulties
F.
Drop outs causing attrition of the sample are to be expected.
Every effort to get a good follow up should be made.
Substantial loss to follow up may raise doubts the validity of the
results as bias would be introduced if the loss is correlated with
both exposure and disease.
It is important also to maintain consistent criteria and
techniques for measurement throughout the study period. This is in
view of the fact that turnover in staff and availability of newer
instrumentation and techniques will occur over time.
A longitudinal study is also a major undertaking in terms of
resources - personnel, facilities, finances etc. The seriousness of
the situation however demand this effort, which would be best
conducted under the auspices of the State health authorities and the
ICMR.
12.9.3
Multiply qf serial crosi-section*! stpdjrt
Difficulties inherent in the conduct of cohort studies have
led to the use of multiple cross sectional studies. This would be
88
carried out on random samples o-f the population at different points in
time. In Bhopal they would be able to show if there are changes in
prevalence from one survey to another. However, since the same
I
*
individuals would not be followed up, the naturqal history of the
disease will not be studied. Changes in population structure in the
intervening period could cause a change in the measure of outcome. The
sampling method, method of data collection and analysis and response
rate should be comparable at each examination. Comparison of mean
values or frequencies of variables such as age and sex could give an
idea of changes occuring ig the population structure. Sample sizes
will be larger than for cohort studies because the greater power of
tests of difference between paired observations in the same individual
f.
cannot be exploited (Florey and Leeder, 1985). Independent non
governmental groups could probably undertake this study design.
12.9.4
Epidemiological Monitoring Unit
A detailed longitudinal study with intensive efforts to obtain
a good response rate and follow up need be done only for a small
sample of the exposed cohort. The setting up of an epidemiological
monitoring unit should be considered for the entire exposed
population. This would be based on routine records from hospitals and
health centres regarding admissions and deaths. It would necessitate
the building up of an efficient system of recording, reporting and
analysis. A special census of the exposed population could be
conducted and a method of identification of exposed individuals
evolved. The system would be able to pick up important changes in
morbidity or mortality on which appropriate action could be taken.
i
I
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89
CHAPTER 13
CONCLUSION
i
The Bhopal disaster has been a human tragedy of immense
dimensions. The suffering caused is incalculable. Important tasks
remain ahead
for the provision of the best possible care for the
victims and for the prevention of such events in the future.
There is a need, first
for the measurement, understanding and
documentation of the impact of the disaster on the health of those
exposed, so as to be able to provide rational care. It is necessary
also to document the seriousness of the effects so as to prevent an
easy erasure from human memory of the event. Epidemiologic skills
could help in this effort as described in this report.
At the present time it is known that similar small scale
"technological disasters" occur frequently. Larger scale disasters
could also occur. Hence, along with the deeper causes of these
disasters being tackled, there is a need to have a strategy to deal
with such events.
Outlines for this are as follows :
- it is necessary to have epidemiological data for an adequate
understanding of the effects on human health. This would
include data regarding the numbers and demographic structure of
?.
the population at risk, the age / sex / area distribution of
the fatalities if they occur, and similar data regarding
morbidity.
- through collaboration between clinicians and epidemiologists,
it would be necessary to evolve simple, standard criteria for
assessment and documentation of morbidity.
- similarly, a method to assess exposure needs to be evolved.
90
- collaboration and communication between administrators, service
•?
I
j
i
I
?
providers and researchers is important- close contact and communication with the affected people is the
most important factor. In the absence of this, one could easily
slip into esoteric, theoretical exercises, which are
meaningless to the problem at hand.
These efforts have to be seen in the context of the broader
issues raised by such events. In Bhopal, these would include :
- the economic relationship between multinationals and countries
of the Third World which determine factors like technologies
and safety systems used
- the exploitative relationship with the work force and
the local community to maintain high profit margins.
- the siting and safety systems of hazardous chemical plants,
- legislation regarding and implementation of safety controls,
- the workers and communities right to information
- the role of pesticides and
- the acceptable limits to the chemicalization of our world.
The true causes of the disaster and the scope for preventing such
events in the future, lie in the matrix of these issues.
91
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Disaster management - the state of the art, 1984.
Views of an international conference.
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i
F
Agarwal A and Narain S,1986 (Ed’s)
The State of India’s Environment 1984-85. The second citizen’s report.
"The Bhopal disaster" in the Health chapter.
pp 205-233, Centre for Science and Environment N Delhi.
American Thoracic Society, (1979)
ATS statement - Snowbird workshop on standardization of spirometry.
Am.Rev.Resp.Dis.,119,831-838.
American Thoracic Society (1985)
(Andrew C et al)
Guidelines as to what constitutes an adverse respiratory health
effect, with special reference to epidemiologic studies of air
pollution.
Am.Rev.Resp.Dis.,131,666-668.
Andersson N, KerrMuir M, Mehra V,(1984)
Bhopal eye.
Lancet,Dec 22-29,1984, 2;1481
Andersson N et al,(1985)
Bhopal disaster:eye -follow up and analytical chemistry.
Lancet,Mar 30,1985,761-762
Andersson N, KerrMuir M, Ajwani M K< Mahashabde S, Salmon A,
Vaidyanathan K, (1986)
Persistent eye watering among Bhopal survivors.
Lancet, Nov 15, 1986,1152 (letter)
Anon,(1985)
Recent events point to need for health preparedness for technological
disasters.
Disaster preparedness in the America’s, Issue No.22,Jan’85
Anon, (abstract),(1985)
Bhopal methyl isocyanate incident - investigation team report.
Union Carbide Corporation, Danbury,Connecticut, 25 pp.
APPEN (Asia Pacific Peoples Environment Network),1985
APPEN Action alert :Bhopal Anniversary, 23,Nov 1985,
Sahabat Alam, Malaysia.
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Axford A T et al,(1976)
Accidental exposure to isocyanate fumes in a group of firemen.
Br.J.Ind.Med. 33,65-71,1976.
Aydelotte C L,(1986)
Stepped up inspections, laws mark Bhopals legacy in the U.S.
□ccup.Hlth.and Safety, Jan 1986,18-20.
Banerji D and Lakhan Singh,(1985)
Bhopal gas tragedy- an epidemiological and sociological study.
J N U News, April 1985,N Delhi.
92
Bang A, (1985)
Learning from the relief work- a report from Bhopal.
Medico Friends Circle Bulletin, 109,Jan 1985.
Bang R,(1985)
Effects of the Bhopal disaster on women’s health - an epidemic of
gynaecological diseases. Part 1 and 2.
Mimeograph.
Baram S M,(1986)
Chemical industry accidents, liability and community right to know.
Am.J.Pub.Hl th. Vol 76(5),568-572.
Baram S M, 1984
Charting the future course for corporate management of health risks.
Am.J.Pub.Hlth. 74(10),1163-1166.
Barker D J P and Rose G, (1984)
Epidemiology in medical practice,
pp 158,Third edition, Churchill Livingston.
Berardinelli P S and Moyer S E,(1987)
Methyl isocyanate liquid and vapour permeation through selected
respirator diaphragmsand chemical protective clothing.
Am. Ind.Hyg.Assoc.J. 48(4),324-329,Apri1 1987
Bhargava M P,1985
The Bhopal tragedy - a middle word.
Mimeograph
Bhopal disaster Monitoring Group,(1985)
Bhopal never again.
B.D.M.G. Japan, No. 1, Jan 15,1985.
Bhopal Group for information and Action,(1987)
BHOPAL :Issue’s 1,2,3,10,11,Jun’86,Jul’86,Aug’86,Apri1’87,May’87
B G I A, Bhopal, India.
Bhopal Working Group,1987
The public health implications of the Bhopal disaster.
Report to the Program Development Board, Amer.Pub. Hlth.Assoc.
(APHA technical report)
Am.J.Pub.Hlth. 77(2), 230-236, Feb 1987
Bronstein M J,(1984)
The effect of public controversy on occupational health problems:
Byssinosis.
Am. J.Pub.Hl th. 74(10),1133 -1137.
Canas R and Kilbourne E M,1987
Oil ingestion and the toxic oil syndrome :results of a survey of
residents of the Orcasur neighbourhood in Madrid,Spain.
Int.J.Epid. 16,3-6.
Castleman I B, (1979)
The export of hazardous factories to developing nations.
Int.J.Hlth.Services. 9(4),1979.
93
i
5
j
Ibid.,(1983)
The double standard in industrial hazards.
Int.J.Hl th.Services. 13(1),1983
Christoffel T and Swartzman D,(1986)
Nuclear Weapons Testing Fallout ■ Proving causation for exposure
injury.
Am.J.Pub.Hlth. 76(3), 290-292.
Diamond S, (1986)
India Carbide trade charges.
New York Times, 20 June 1985, D5.
Diller W, (1986)
Isocyanate effects.
J.Occup.Med. 28(4),265-266, letter.
I
Documentation for Action Groups in Asia (DAGA)
Asia’s struggle to affirm wholeness of life. Report of a consultation
on TNC’S in Asia :The aftermath of Bhopal.
DAGA,Hong Kong,Nov 1985
Dodd D E et al,(1986)
Acute inhalation studies with methyl isocyanate vapour - 1.
1) Methodology and LC 50 determinations in guinea pigs, rats and mice.
Fund.Appl.Toxicol. 6(4),747-755.
Ibid. (1986)
2) Respiratory tract changes in guinea pigs, rats and mice
Fund.Appl.Toxicol. 6(4),756-771.
Editorial (1966)
Hazards of disocyanates
Lancet,Jan 1,1966, 32-33.
Editorial (1984).
Calamity at Bhopal.
Lancet, Dec 15
Enright P,(1986)
Spirometer use helps detect lung disease in time for treatment.
Occup.Hlth and Safety. 74-77,April 1986.
Environmental Health Criteria, 27 (1983).
Guidelines on studies in Environmental Epidemiology.
IPCS International Programme on Chemical Safety.
UNEP, Geneva,1983.
Ferguson J S et al (1986)
Sensory and pulmonary irritation with exposure to methyl isocyanate
Toxicol.and Appl.Pharmacol. 82(2), 329-335.
I
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r
r
Fienberg S E et al, (1985)
Longitudinal analysis of categorical epidemiological data :
A study of Three Mile Island.
Envir.Hlth.Persp. 63,241-148.
Florey C du V and Leeder S R (1982)
Methods for cohort studies of chronic airflow limitation,
pp 134, WHO Regional Publications, European Series No. 12.
94
Gassert T, (1986)
Toxicology o-f methyl isocyanate - a lesson -from Bhopal -for disaster
prevention.
Dissertation -for MSc in Occupational Hygiene, LSHTM,
University o-f London, Sept. 1986.
Gassert T, Mackenzie C, KerrMuir M, Andersson N, Salmon AG,(1986)
Long term pathology o-f lung, eye, and other organs -following acute
exposure o-f rats to methyl isocyanate.
Lancet, Dec 13, 1986, 1403 (letter)
Goldsmith J R et al, (1986).
Pulmonary function screening and monitoring in occupational health.
J.Occup.Med. 28(8), 656-663.
Grandjean P and Tarkowski S (eds), (1983)
Toxic oil syndrome : Mass food poisoning in Spain.
Report on a WHO meeting, pp82,
WHO Regional office for Europe, Copenhagen.
Haastrup P, (1984)
Indoor fatal effects of outdoor toxic gas clouds.
J.Occup.Accidents. 5,279-290.
Harding J J and Rixon C K, (1985)
Lens opacities induced in rat lenses by methyl isocyanate.
Lancet, 30 Mar’85,762.
Higgins M W and Keller J B, (1970)
Predictors o-f mortality in the adult population o-f Tecumsehrespiratory symptoms, chronic respiratory disease and ventilatory lung
•function.
Arch. Environ. Health Vol 21,418-424.
Indian Council of Medical Research, (1985)
Health effects of exposure to toxic gas at Bhopal.
An update on ICMR sponsored researches. 10,Mar,1985.
Ibid (1985)
Minutes of the third meeting of the working group on thiosulfate
therapy of the MIC exposed population. 4,April, 1985.
Ibid (1985)
Minutes o-f the review meeting o-f ICMR sponsored researches on health
effects of exposure to toxic gas at Bhopal.
May 3-4,1985, Bhopal.
Jo-f-fe M, (1985)
Biases in research on reproduction and women’s work
Int.J.Epid. 14(1),118-123.
Kapila M,(1986)
An epidemiological report on the health consequences o-f the Lake Nyos
disaster.(Volcano)
Mimeograph, Yaounde and Cambridge, Min. o-f Pub. Hl th. and ODA, UK.
Kimmel C A and Kimmel G L (1986)
Interagency regulatory liaison group workshop on reproductive toxicity
risk assessment.
Envir.Hlth.Persp.66, 193-221.
95
■
Kimmerle 6 and Eben, (1964) Abstract
Toxicity of methyl isocyanate and its quantitative determination in
the air.
Archiv.Fuer.Toxicologie. 20, 235-241,(German)
Kreiss K, (1986)
Approaches to assessing pulmonary dysfunction and susceptiblity in
workers.
J.Occup.Med. 28(8),664-669.
Luster M I et al, (1986)
Immunotoxicity studies on mice exposed to methyl isocyanate.
Toxicol.Appl.Pharmacol.86,140-144.
MacMahon B and Pugh T F,(1970)
Epidemiology - principles and methods,
pp 376, Little Brown and Company.
Mac Sheoin T, (1986)
Bhopal :a bibliography.
Int.J.Hlth.Services. 16(3), 441-468.
Mcdonald A D et al, (1986)
Spontaneous abortion and occupation.
J.Occup.Med. 28(12), 1232-1238.
Me Farlane A C et al, (1985)
Australian research into the psychological aspects of disasters.
Disasters, 9(l),32-34.
Medico Friend Circle, (1985)
Medical research in Bhopal : the realities and recommendations.
Ibid. (1985)
Medical research in Bhopal - are we forgetting the people?
MFC Bulletin, 109,April 1985.
Merchant J A,(1986)
Preparing for disaster. (editorial)
Am.J.Pub.Hlth. 233-235, Mar’86
Mileti S D et al, (1975)
Human systems in extreme environments :a sociological perspective.
Monograph 21, Institute of Behavioral Science, University of Colorado.
Morehouse W and Subramaniam M A, (1986)
The Bhopal Tragedy : What really happened and what it means for
American workers and communities at risk.
A report for the Citizens Commission on Bhopal.
Council on International and Public Affairs, USA
Moyer S E and Berardinelli P S, (1987)
Penetration of methyl isocyanate through organic vapour and acid gas
respirator cartridges.
Am.Ind.Hyg.Assoc.J. 48(4), 315-323.
96
t
Nagrik Rabat aur Punarvas Committee (Nagrik study)(1985)
Medical survey on Bhopal gas victims.
In association with the Voluntary Health Association of India, Delhi
and The Bhopal Relief Trust, Bombay, Mar 1985.
Nemery B et al, (1985)
Effects of methyl isocyanate on the respiratory tract of rats.
Br.J.Ind.Med. 42,799-805.
4
I
NIOSH (abstract), (1977)
Organoisocyanates in "Information profiles on potential occupational
hazards.", NIOSH contract No. 210-77-0120,
265-275, Oct 1977.
Parnell H A, (1986)
Perspectives in the development of asbestos litigation and its future
implications.
Am.Ind.Hyg.Assoc.J. 47(11), 708-711.
Patel A and Patel A,(1985)
The Bhopal disaster aftermath :an epidemiological and socio- medical
survey.
Medico Friend Circle,
PP, 1985
Peto R et al (1983)
The relevance in adults of air flow obstruction, but not of mucus
hypersecretion to mortality from chronic lung disease.- Results from
20 years of prospective observation.
Am.Rev.Resp.Dis., 128, 491-500.
Phoon W 0 et al (WHO task force),
-force), (1986)
Carbamate pesticides : a general introduction.
Environmental Health Criteria 64, pp 137.
International Programme on Chemical Safety (IPCS).
WHO, Geneva.
Rinsky et al, (1986)
A mortality evaluation of employees with potential exposure to MIC.
J.Occup.Med. (letter), 28(3), 243.
Rosling H, (1986)
Cassava, cyanide and epidemic spastic paraparesis- a study in
Mozambique on dietary cyanide exposure.
pp 52, Uppsala University, Sweden.
Rothman K J, (1986)
Modern Epidemiology,
pp 358, Little Brown and Company.
Rye A W, (1973)
Human responses to isocyanate exposure.
J.Occup.Med. 15(3), 306-307.
Salmon A G et al, (1985)
Acute toxicity of methyl isocyanate : a preliminary study of the dose
response for eye and other effects.
Br.J.Ind.Med. 42, 795-798.
97
Salmon A G ,(1985)
Does acute toxicity testing tell us anything useful?
Methyl isocyanate as a test case.
Br.J.Ind.Med. 42,577-578
Sangster B and Cohen H, (1985)
Medical aspects of environmental pollution - environmental incidents
in the Netherlands 1980- 84.
Clinical. Toxicol. 23 (4-6), 365-380.
Sango C R L and Sharping G, (1986)
Determination of isocyanate and aromatic amine emissions from
thermally degraded polyurethanes in foundries.
Am.Ind.Hyg.Ass.J. 47(10), 621-628.
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Siesjo B K, (1985)
Oxygen deficiency and brain damage: localization, evolution in time
and mechanisms of damage.
Clin.Toxicol. 23(#_$), 267-280.
Simmonds J, (1987)
Europe calculates the health risk.
New Scientist, 23 April, 1987.
Special Supplement (1986)
Health effects of volcanoes : an approach to evaluating the health
effects of an environmental hazard.
Am.J.Pub.Hl th., supplement,76, pp 90.
Stewart A, (1985)
Detection of late effects of ionizing radiation : why deaths of A-bomb
survivors are so misleading.
Int.J Epid. 14 (1), 52-56.
Tamashiro H et al, (1985)
Mortality and survival for Minamata disease.
Int.J.Epidem. 14(#0, 582-588.
Teague H J (1985)
Cyanide poisoning of Bhopal victims (?) - a hypothesis.
Unpublished article.
5
Traver G A, Cline MG, and Burrows B, (1979)
Predictors of mortality in chronic obstructive pulmonary diseasea 15 year follow up study
Am.Rev.Resp.Dis., 119, 895-902.
i
t
Varadarajan et al (1985)
Report on scientific studies on the factors related to the Bhopal
toxic gas leakage.
Council for Scientific and Industrial Research (CSIR), India.
81 pp, Dec 1985
i
Vincent W J, Ketcham N H, (1980)
A new fluorescence procedure for the determination of MIC in the
occupational environment.
Analy.Tech.in Occup.Hl th.Chemistry. ACS symposium series No. 120,
121-147.
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