MERCURY
Item
- Title
- MERCURY
- extracted text
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file:///C|/Lever docs/Hgdocs/merckaren.
MercGr.' Poisoning
RF_E_A_5_SUDHA
Universitat Erlangen-Nurnberg, Institut fur Organische Chemie
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Mercury Poisoning
Everyone working with organomercury compounds should read this!
The following article is found in Main Group Chemistry News 1998, 6, 29
Mercury Poisoning
Karen E Wetterhahn, Professor of Chemistry and Albert Bradley Third Century Professor in the
Sciences at Dartmouth College, died June 8, 1997 at the age of 48 from mercury poisoning.
Wetterhahn's research work involved understanding how elevated levels of heavy metals interfere with
such processes as cell metabolism and the transfer of genetic information. That work was the direct
cause of her death.
"Karen was the acknowledged international expert in chromium carcinogenicity," noted John S. Winn,
chairman of the Dartmouth chemis try department. She began a sabbatical at Harvard in the fall of'95.
The work involved doing some model compound studies involving mercury chemistry with Steve
Lippard's group at MIT.
That work led to mercury NMR characterization of the model compounds with the use of
dimethylmercury as this element's NMR standard. Winn relates that while preparing the mercury NMR
standard in a fume hood on August 14,1996, Dr. Wetterhahn spilled one to a few drops of
dimethylmercury onto her latex glove near her thumb. Knowing that dimethylmercury was very toxic,
she'quickly cleaned it up. What she did not know was that dimethylemercury was so soluble that it
permeated the glove instantly and penetrated her skin and was absorbed into the blood- stream. It took
five months until her gait began to falter and her words slur. By the time Dr. Wetterhahn connected
that laboratory spill with the damage spreading in her brain, nothing could help her. Tests showed that
her body contained more than 80 times the lethal dose of mercury. Her vision narrowed to a pencil's
thinness and winked out. She lost her hearing and speech and she faded into a long coma.
Dr. Wetterhahn was a most meticulous scientist, her colleagues said, taking what would have seemed
to be appropriate precautions. It is an accident that could occur to any experienced chemist. This,
however, is not the first fatality from work with dimethylmercury. Documented cases extend back to
the early 1940's. See C & E News, June 16, 1997, page 6.
Dartmouth suggests that when handling dimethylmercury, a combination of gloves, a highly resistant
laminate underneath a heavy duty, chemically resistant outer glove, should be used. Dr. Wetterhahn
was the first tenured female professor at Dartmouth. She received the largest single grant to a faculty
member at the college. It amounted to a seven million dollar grant to work on toxic heavy metals.
A related article (in German) may be found in the September issue, 1998, of Nachrichten aus Chemie,
1 of 2
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file:///C|/Leverdocs/Hgdocs/merckaren.hu
Mercury Poisoning
Universitat Erlangen-Nurnberg, Institut fur Organische Chemie
Mercury Poisoning
Everyone working with organomercury compounds should read this!
The following article is found in Main Group Chemistry News 1998, 6, 29
Mercury Poisoning
Karen E. Wetterhahn, Professor of Chemistry and Albert Bradley Third Century Professor in the
Sciences at Dartmouth College, died June 8, 1997 at the age of 48 from mercury poisoning.
Wetterhahn's research work involved understanding how elevated levels of heavy metals interfere with
such processes as cell metabolism and the transfer of genetic information. That work was the direct
cause of her death.
"Karen was the acknowledged international expert in chromium carcinogenicity," noted John S. Winn,
chainnan of the Dartmouth chemis try department. She began a sabbatical at Harvard in the fall of'95.
The work involved doing some model compound studies involving mercury chemistry with Steve
Lippard's group at MIT.
That work led to mercury NMR characterization of the model compounds with the use of
dimethylmercury as this element's NMR standard. Winn relates that while preparing the mercury NMR
standard in a fume hood on August 14, 1996, Dr. Wetterhahn spilled one to a few drops of
dimethylmercury onto her latex glove near her thumb. Knowing that dimethylmercury was very toxic,
she quickly cleaned it up. What she did not know was that dimethylemercury was so soluble that it
permeated the glove instantly and penetrated her skin and was absorbed into the blood- stream. It took
five months until her gait began to falter and her words slur. By the time Dr. Wetterhahn connected
that laboratory spill with the damage spreading in her brain, nothing could help her. Tests showed that “
her body contained more than 80 times the lethal dose of mercury. Her vision narrowed to a pencil's >
thinness and winked out. She lost her hearing and speech and she faded into a long coma.
Dr. Wetterhahn was a most meticulous scientist, her colleagues said, taking what would have seemed
to be appropriate precautions. It is an accident that could occur to any experienced chemist. This,
however, is not the first fatality from work with dimethylmercury. Documented cases extend back to
the early 1940's. See C & E News, June 16, 1997, page 6.
Dartmouth suggests that when handling dimethylmercury, a combination of gloves, a highly resistant
laminate underneath a heavy duty, chemically resistant outer glove, should be used. Dr. Wetterhahn
was the first tenured female professor at Dartmouth. She received the largest single grant to a faculty
member at the college. It amounted to a seven million dollar grant to work on toxic heavy metals.
A related article (in German) may be found in the September issue, 1998, of Nachrichten aus Chemie,
1 of 2
7/06/01 6:38
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file:///C|/Lever docs/Ugdocs/tcstin^
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Testing for Mercury Exposure
' There are ways to monitor amounts of mercury in the human body. One should only worry about these
tests if they have been exposed to large amounts of mercury (such as a large spill), or if they work
around mercury often and are concerned about exposure. Small amounts of mercury in fish or in water
are not large enough to warrant any kind of medical attention.
The mercury blood test measures exposure to all three types of mercury (mercury-zero,
mercury-twoTand organic mercury compounds). However, mercury remains in the blood
stream only a few days after exposure so the test must be done soon after exposure. Most
non-exposed people have mercury levels of 0 to 2 (all blood measurements are in
micrograms of mercury per deciliter of blood, or ug/dL). Levels above 2.8 ug/dL are
required to be reported to the Health Department. This test can be influenced by eating
fish that contain methylmercury.
The urine mercury test only measures exposure to elemental and inorganic mercury.
Organic mercury is not passed out the body in the urine so it cannot be measured this way.
A person with no exposure to mercury would probably have a urine mercury level between
0 and 20 ug/dL. The Health Department requires reporting levels above 20.
There are also medical tests that should be administered if one thinks he/she may have
mercury poisoning. These tests are given by a doctor and usually will start with a medical
history. The doctor will then usually then target the nervous system, kidneys, oral cavity,
lungs, eyes and skin. These organs will usually show chronic or acute mercury exposure if
there has been any. Then the doctor will look for symptoms of mercury poisoning which
include personality changes, weight loss, irratability, fatigue, nervousness, loss of
memory, indecision, and intellectual deterioration. A basic handwriting sample will be
taken to compare to later samples to see if a tremor is developing. Tremors are common to
people who suffer from mercury poisoning. This medical exam is usually repeated once a
year to people who are at risk to mercury exposure.
To Mercury Exposure Menu
1 of i
© Copyright
7/06/01 6:50 P
wysiwyg://l/file:/C|/Leverdocs/Hgdocs/merctest.htm
1CURY POISONING. The Columbia Encyclopedia: Sixth Edition. 2000
The Columbia Encyclopedia: Sixth Edition. 2000.
%
mercury poisoning
tissue damage resulting from exposure to more than trace amounts of the element mercury 1
or its compounds. Elemental mercury (the silver liquid familiar from thermometers) is the
most common occupational source. Exposure typically comes from inhaling mercury
vapors. Inorganic salts of mercury (e.g., mercurous chloride, or calomel) are used in some
products to inhibit the growth of fungi and bacteria. Organic mercury compounds,
especially methylmercury, are more toxic than other forms because they easily cross cell
membranes. They are most often ingested in contaminated fish.
Mercury poisoning can cause severe neurological and kidney damage. Acute exposure can 2
affect the respiratory and gastrointestinal systems. Organic mercury can cross the
blood-brain barrier and cause irreversible nervous system and brain damage, e.g., loss of
motor control, numbness in limbs, blindness, and inability to speak. Some studies have
connected maternal mercury exposure to fetal damage. Mercury poisoning can be
confirmed by urine tests. Chelation therapy is used for poisoning with elemental mercury
and mercury salts; there is no treatment for organic mercury poisoning.
Mercury has become an environmental pollutant in areas where eroding mercury-bearing 3
rock or agricultural and industrial wastes containing the metal escape or are discharged
into waterways. Elemental mercury and mercury salts, although fairly inert when
posited on the bottom of waterways, are converted into organic mercury, typically
methylmercury, by microorganisms. This compound then enters the food chain where it is
biomagnified up to 100,0(i0 times in predacious fish. Consumption of toxic fish and of
game birds and mammals that feed on fish is the main risk to humans. Minamata disease
was named after the occurrence, in the 1950s and 1960s in Minamata, Japan, of many
cases of severe mercury poisoning. It was found that a chemicals factory was discharging
mercury-containing wastes into the local waters, contaminating fish that residents caught
for food.
4
Mercury has long been known to be toxic; the phrase “mad as a hatter” refers to the
19th-century occupational disease that resulted from prolonged contact with the mercury
used in the manufacture of felt hats. Some workers today, especially laboratory
technicians, nurses, and machine operators, continue to be exposed to mercury on the job.
Most mercury pesticides have been withdrawn from the U.S. market, and many countries
banned ocean dumping of mercury and other pollutants in 1972. Production of
mercury-containing interior and exterior paints in the United States was phased out in
1991. Mercury, which has been used in medicines for hundreds of years, continues to be
~d in dental amalgams and various medicaments that deliver minimal exposures. Most
Gv»er medical uses have been banned or are being phased out, but mercury use in industry
is increasing.
5
See also water pollution.
See L. Elbert, Mercury Poisoning in Man (1978); P. A. and F. M. D’itri, Mercury
Contamination: A Human Tragedy (1988).
V5
6
The Columbia Encyclopedia, Sixth Edition. Copyright © 2000 Columbia University Press.
CONTENTS • GUIDE • BIBLIOGRAPHIC RECORD
7/06/01 6:19 PM
i
Hudson P J, Vogt R L, Brondum J, Witherell L, Myers G & Paschal D C.
Elemental Mercury Exposure Among
Children of Thermometer Plant
Workers.
/
Pediatrics 79:935-938 (1987)
ABSTRACT: "Because evidence of mercury exposure was found among workers of a
mercury thermometer-manufacturing plant in March 1984, the Vermont Department
of Health studied the workers’ children for both exposure to mercury and evidence of
mercury toxicity. The median urine mercury level of 23 workers' children was 25
ug/L. This was significantly higher than the level (5 ug/L) among 39 children
randomly selected from nonworkers’ households in the same community (=<.001).
Mercury-in-air levels measured in workers' homes were higher than those measured
in control homes. A significant correlation was found between the urine mercury
levels of their working parents. No child had frank mercury toxicity. No evidence of
neurologic toxicity among exposed children was discovered by a pedriatric
neurologist who examined these and unexposed children without knowledge of their
exposure status. This is the first report demonstrating mercury exposure in children of
mercury workers. Although toxic effects of mercury were not demonstrated at these
levels of exposure, children of mercury workers are at risk for mercury exposure and
potential mercury toxicity."
Bo Walhjalt 95-09-11 e-mail: bosse&yes(.gu.se
(Abstracts from a database maintained by Leif Hedegdrd
)
F
Queiroz MLS, Perlingeiro R C R, Dantas D C M, Annichino Bizzacchi J M &
De Captani E M
Immunoglobulin Levels in Workers
Exposed to Inorganic Mercury.
Pharmacol Toxicol 74:72-75 (1994)
ABSTRACT: "The serum immunoglobulin (IgG, IgM and IgA) concentrations of 44
mercury-exposed workers were examined and compared with those of non-exposed,
age- and sex-matched individuals. At the time of testing, the exposed population had
a mean (+-S.D.) mercury urinary concentration of 24.7+-19.1 and in 40 of them
urinary mercury levels were below the currently accepted limit of 50 ug/g creatinine.
Increased IgG, IgA and IgM levels were found in the mercury-exposed individuals
and in 16, a second evaluation was performed six months later. During the
intervening six months, the level of hygiene was improved was improved throughout
the plant, and urinary mercury concentrations were determined monthly in each
worker. Despite a significant reduction in mercury urinary concentration, serum
immunoglobulin levels did not return to the normal range. There was no correlation
between the length or level of exposure and the immunoglobulin levels. Liver protein
synthesis, as studied by factor V, prothrombin time and transaminase activity, was
normal and liver injury, as evaluated by serum aspartate and alanine aminotransferase
activities (AST and ALT, respectively), was not observed. No haematological
abnormalities were noted. These results indicate that ’’safe” levels of mercury
exposure may lead to humoral immunological stimulation."
Bo Walhjalt 95-09-11 e-mail: bosse&yest. gu. se
(Abstractsfrom a database maintained by Leif Hedegard
)
FR0I1 : I'iJFIIII JI TOUPS & TRAUELS KODAI
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Dr. Joshi
Original Message---- From: "Nityanand Jayaraman”
<nity_@del3.Ysnl.net.in To: <jo_shjtk@ysnl.com Cc:
<navrozmo@vsnl.net; <md_utta@ysnl.net; <tj_d_el_hi@vs_nl._c_o_m;
<n_ian^oforu@hotmaij.com Sent: Monday, April 16, 2001 10:38 AM
Subject: Confidential: Lever mercury exposure
)
■4
Hello Dr. Joshi:
It was good talking to you yesterday. I’m putting down a short synopsis of
what we know about workers and the environmental/worker safety practices at
the mercury thermometer factory.
I
1. The mercury thermometer factory is a 2nd hand factory that was relocated
from the United States to Kodaikanal between 1977-1983. The factory began
production in 1983. It is a 100% export-oriented unit. It imports all the
mercury (primarily from the United States) and glass and exports all
I .
thermometers to United States. From the US, the thermometers find their way
to Canada, Spain, Australia, UK and Germany.
*
2. The factory was owned/operated by Cheseborough Ponds and Ponds India Ltd
until 1997 at which time Hindustan Lever acquired Ponds India Ltd.
Hindustan Lever is 51% owned by Anglodutch multinational Unilever which has
its headquarters in London.
3. In 2000, the company imported about 4.5 tonnes of mercury, which is
likely to be their annual consumption.
4. ENVIRONMENT: On 7 March, 2001, residents of Kodaikanal, ex?workers and
community groups along with environmental NGQs from India and abroad
protested against HLL after uncovering a 5.3 ton dump of broken
*
mercury-containing thermometers in a scrapyard in a Crowded part of the
hillstation. The mercury-glass wastes were stored in open and torn,sacks
with their contents spilled onto the shopfloor which was frequented by
5
people and children, some of whom are barefoot The scrapyard dealer said
1
the scrap has lain there for mroe than 6 months. His boys had recovered
nearly half a litre of mercury from the scrap last year, but he was unable .,
to trace the bottle.
The scrapyard lies midway on a slope below which lie houses on a terraced
land with some agriculture (vegetables) and mostly habitation. Most of the
people downslope from the yard depend on sub-surface spring water.
5. ENVIRONMENT: We also found mercury wastes dumped behind the factory in
the forests that form part of the watershed for the Pambar River which runs
down to the plains towards Madurai.
4
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6. ENVIRONMENT: It is now known that the company has in the past buried much
of its mercury-containing wastes within the factory premises. These wastes
have now been exhumed in a clandestine operation over the last few weeks by
unprotected
workers.
4
7. ENVIRONMENT: Shipments of mercury-containing glass wastes are reported to
have left the factor/ for unknown locations outside the factory in different
parts of the state ofTamilnadu.
8. WORKERS: Workers at the factory work with barehands, a cloth cap and some
• of the workers are provided with cloth half-face-masks. The workers leave
their clothes behind at work. However, they are not required to shower
before they leave for home. Many of the workers are contract labourers who
are not "confirmed." Occupational safety aside, there is a high level of
. dissatisfaction even among the senior supervisory staff about the
administration and their treatment of the workers.* ~
9. WORKERS: The company is divided into two sections: the noil- mercury area ■and the mercury area Workers from the mercury sections report that mercury
spillage is common. That it is commonplace for mercury to be handled. There
is a high rate of breakage of thermometers.
■
.
...
Mercury spilled on the floor is washed with water into a ditch alongside the
shopfloor and channeled to a settlement pond. Large spills are/were
<
recovered by vacuuming (a practice that is potentially dangerous). The
sediment is reportedly conveyed to a mercury vaporiser to recover mercury. The resultant
ash is disposed of We don’t know how.
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--------
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10. In the mercury section, filled thermometers are kept in an oven
overnight. Workers are exposed to gusts of mercury vapour wtfen the oven door
is opened in the daytime.
11. WORKER COMPLAINTS: Workers have complained of general malaise, loss of
appetite, infertility, skin discoloration. Most common complaints have to do ' ’f
with the stomach and kidneys. Irritation while passing urine, stomach pains,
ulcers etc. Workers also report heart disorders among relatively young
workers, tumours (brain tumour — one case), vomitting blood (because of
ulcers) etc.
.j
12. URINE ANALYSIS: Urine analyses are conducted infrequently. However,
these results are not made available to the workers. The company admits that
urine is analysed and workers who are found to have higher than acceptable
*
levels are relocated to other work areas. We do not have an indication of
what the "acceptable levels" are.
■ t
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13. Kindly visit www.greenpeaceindia.org website for more information.
ciao, nity Nityanand Jayaraman
4
r
It would be great if a note is circulated on Unilever and Kasaragod prior to
the meeting. I will send a note on Unilever. SRlDHARlISHA: Can you put
something brief out to the rest of the above list on Kasaragod - Shree's
email is not working.
ciao, nity
hello dr. ravi:
4
below is an email that i received from dr. t.k.joshi in response to my email
’ .......................... .................................... ...
’
I *
note detailing the Kodaikanal problem, this along with the two attached
files should give you some idea of the nature of the beast we are dealing
%
with.
ciao,nity
>
-Froni;
1
”T.K. Joshi” ^iQshitki@ysn_Lcom
To:
<nity68 @vsnl, com
Subject:
Re: Confidential: Lever mercury exposure
Date sent: Mon, 16 Apr 2001 12:20:25 +0530
Thanks for such detailed information which does not surprise me. This is the
way the big companies operate. How is your equation with factoiy inspector
»
of the area as they wield much power. The union should ask, or on behalf of
workers some one has to ascertain; Is there a health safety policy? Is there
a safety committee? Arc the
meetings of the committee held, if yes how frequently? Are the minutes
I
recorded? Are workers properly informed of hazards of mercury exposure?
this will include aMSDS duly translated into the local language and
communicated to the workers. Are pre placement health check ups done? Is a
j
periodic health check up done? Are records available to the worker( he has
right to demand his records and all the tests/investigation reports Is the
physician doing the check ups, a qualified occupational health
hysicianChaving attended the three months course at CLI Mumbai, if he does
not hold a diploma) The ambient monitoring frequency and the results The
urinary mercuiy levels Work practices Ventilation standards Waste
disposal practices. As little as 4 gms of mercy can destroy a midsize lake.
If you can get even few workers together let them submit a PIL on a plane
paper addressed to the chiefjustice of India You will see the results. The
signs and symptoms that you have mentioned may be due to mercury as well as
due to other factors. Do workers suffer ’gum problems, specially loosening
of teeth and bleeding”? do they suffer tremors, do they have any personality
changes like they become shv. and secluded?
1
s
I
■
■
The one key question is, the difference or the change in the health status
compared io the day they started the work, and the day they left the work.
Only those need be asked who had exposure to mercury. What main change did
they notice in their health which was not there before after they started the work? Did all the
exposed workers had some what similar picture or it varied from person to
1
person? Did they smoke, take food at the workplace?
It will not be a bad idea to have a neuropsychiatric and neurological
evaluation of the few of the worst victims. You have to be sure not to tell
the physicians that the workers were exposed to mercury as this may inject
an element of bias. Even if three or four worst affected workers undergo
t • such evaluation and some positive findings emerge, it will be extremely
favorable for filing aPIL.
4"
I
*
i
Fw Methods for monitoring mercury exposure
"A
Subject: Fw: Methods for monitoring mercury exposure
Date: Thu, 28 Jun 2001 08:56:05 +0530
From: "Thelma & Ravi Narayan" <tnarayan@vsnl.com>
To: <sochara@vsnl.com>
----- Original Message-----From nity68@vsnl.co m
T o:navrozmo@vsnl.nplnaravan@vsnl.com
Cc: manqoforu@vsnl .npdevika@xlweb .com
SentWednesday, June 27, 2001 2:17 PM
SubjectFwd: Methods for monitoring mercury exposure
hello navroz:
here's some very useful information about mercury in urine, our guess was right and the 20 micrograms/liter
figure is meaningless, perhaps, we can hang the bastards on that one.
‘ao, nity
The attached information addresses your second question as to whether
there are documented health affects of persons with urine mercury levels
above 20 ug/1. Mercury harms the kidneys and the nervous system. In
fact, it is possible to detect sub-clinical changes in a person’s
kidneys even when a person has urine mercury levels BELOW 20 ug/1.
You might be interested to know that: 1) measuring urine mercury levels
is not considered as accurate aguage of mercury exposure as measuring
blood mercury levels because you fail to detect organic forms of mercury
in urine; 2) when measuring urine mercury levels, it is afar more
useful indicator of toxicity to express urine mercury levels as
micrograms of mercury per microgram of creatine (a common substance
found in urine) rather than as micrograms of mercury per liter.
Expressing urine mercury levels this way (ug/gram of creatine) controls
for the dilution of mercury in urine -- it is becoming the standard
method of medical researchers and doctors for expressing urine mercury
, levels.
See below.
More next week.
Warmly,
Mark
http: //www. pp. okstate. e du/ehs/training/mercury. him
New Jersey State Department of Health
Division of Occupational and Environmental Health
THE HEALTH EFFECTS OF MERCURY
i
'■
■■
Mohan Issac's visit
Subject: Re: Dr.Mohan Issac's visit
- •-.
Date: Mon. 9 Jul 2001 01:50:36 +0530
From: "Navroz Mo" <'navTozmo@vsn!.net>
To: "Community Health Ceil" <^ochara(ajvsni.com> s
CC: <ps5'chhto,@nnnhans.k3r.nic.m>
Dear Ravi, Dr Isaacs, 21st will be fine. We will have a local doctor
■j
available. I£ Lhere is any speuixxc piepaxatioxi to be (lone, pleast; let Ute
know. Regards Navroz
•’
?
---- Original Message--- *—
From: Community Health Cell <sochara@vsnl.cam>
To: <navrozmo@vsnl.net>
: Monday, July 02, 2001 4:59 PM
3
abject: Dr.Kohan Isaac’s visit
> Dear Navroz,
> i'
■
> Greetirigs from Community Health Celli
'
4
> Thl's Is in reference to Kodi visit between 6-eth July. Presently Dr. % A
> Mohan Issac has some unexpected new committment on the above dates. So
> it is unlikely that he shall make it in this weekend. Hcwabput 21st £ /
> 22nd of July. Is it convenient for you? Hereby enclosing Dr. liohan
> Issac's email id for further communication.
>
> psychiatryQn1mhans.kar.nlc.In
> ne^L winlitiS r
>
> Dr.Praveen
rpr
/7
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;
No. 54782
-.Regd
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Subject:
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CC:
Re: Dr. Mohan Issac visit
Thu, 28 Jun 2001 01:26:45 +0530
"Navroz Mo” <navrozmo@vsnl.net>
’’Community Health Cell” <sochara@vsnl.com>
<nity@del3. vsni. net in>, <mangoforu@hotmai1. com>, <kanan@vsni. com>
Dear Ravi,
this is good news, Sixth to eighth will be very good for Dr Issac
and team to visit as I shall be in Kodi at the time . I will arrange a place
for their stay. Pl give them my no in Kodi: 04542-40286.
There is some very interesting new info on mercury testing in urine as well
as on the process of methylysation which I will email you tomorrow.
Regards Navroz
i
pLeonO
£4
•)f 1
6/2.8/01 1:54 PM
$
4
£
/)S-|
• NN 67. Ana. 25.2001: Mercury and Mercun7 Thermometers
Subject: NN 67, Aug. 25, 2001: Meremy and Mercury Thermometers
Date: Sat, 25 Aug 2001 08:51:25 -0700
From: "Nanny’s Notes’" <nannynote@moonlily.com>
To: djz@efii.org
notes
<><><><><><><><><><><><>
issue 67, Aug. 25, 2001
Mercury and Mercury Thermometers
A nublication of Nanny's Place
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CONTENTS
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Advertisement: Children's Book-of-the-Month Club
News: Mercury News Notes
Advertisement: Country Homes i Gardens
Tips and Tidbits
What is Mercury and why is It Dangerous?
Mercury Thermometers
If a Mercury Thermometer Breaks
Sources for all Mercury Items
Advs rt i s er.er.t: He rb s
er Healthcare
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Mercury News Notes
1 of6
2x71
NN 67. Aug. 25. 2001: Mercury and Mercury Thermometers
8/27/
’Earlier this month, Maine passed a bill that will require
dentists to inform their patients about the use of mercury.
A waiting-room sign and patient brochure will explain that
dental amalgams (alloys) contain mercury, and point cut the
health risks of this element. Maine is the first state to,
have passed this kind of bill.
»In July, the American Academy of Pediatrics (AAP) published
a technical report urging pediatricians to reduce children’s
exoosure to mercurv and in oarticular, to stoo using all
mercury-containing devices, including mercury thermometers.
The AAP also recommended that doctors should advise parents
to do the same.
’Some hospitals and cities, including Duluth and San
Francisco, have bannea mercury thermometers and some chain
stores have stopped sellina them.
*The AAP has joined with the Public Health Service, to reduce
+-hA ucjp
3 'Y’o-KT,-!**y-conbaip.ing p^esenative, thimero.sal,
vaccines. ,'Xone of the vaccines currently in the recommended
childhood iirnuunizatlon schedule cGntain thimerooal./
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What is Mercury and Why is It Dangerous?
Mercury is a shiny, silver-white metallic element that is
liquid and slight1 y vo1 at-41 e at room temperatures. This
means that any liquid mercury exposed to the air will
eventually evaporate to form mercury vapor.
Mercury is usea in thermometers because its change in volume
tor each degree of change in temperature is the same, which
allows accurate readings. It is also used in other types of
scientific apparatus such as barometers and electric
switches, and
id. is
i s ^ound iin- mercury-vapor ultraviolet lamps.
Mercury can form several compounds; for example, the red
form of mercuric sulfide (vermilion) is used as a coloring
material, and mereurochrome is an organic mercury compound
that is used as an antibacterial agent.
2 of 6
8/27/(-
’ NN 67 Aug. 25. 2001: Mercury and Mercury Thermometers
4$
Mercury is toxic and sianificant exposure can produce a
and
broad range of effects on the kidneys, lungs, skin
skinand
.
a
.. . In children, this car result in
central nervous
system.
nervous system effects ranging from learning disabilities
serious problems such as mental retardation and blindness.
Mercury vapor is acutely hazardous and if it is aspirated
into the lungs can cause severe pneumonia and even death.
Mercurv can also form toxic water-soluble and fat-soluble
salts. The most toxic are the fat-soluable, including the
highly dangerous methylmercury compounds, such as dimethyl
mercury.
If a product containing liquid iiiercury breaks, the jaercury
becomes exposed to the air and can evaporate, possibly
resulting in dangerous levels of mercury vator m a small,
*
enclosed soace. Even if the area'is large and ventilated and
there is no danger fr m the mercury vapor, the mercurymay
pventup.? ]y find ;i"s way into stroams and lakes, whore it can.
be transformed into the highly toxic methylmercury- All it.
takes is one gram of mercury per year to contaminate all of
the fish in a lake with a surface area or 2*0 ^acres, Since
the developing fetal nervous system is particularity
sensitive to mercury, if you dre pregnant or nursing you
M
should not eat mercury-contaminated fish such as tuna and
*
fish
caught
from
mercury-contaminated
water.
swordfish, or
You should also lim''t the amount o^ this kind of fish that
('
’■
Mercury can also be released into the enviruiHUent when
chermomecers or other mercury-containing products are burned
or otherwise inadequately disposed of. In fact, one of,the
main ways mercury enters the atmosohere is through burning
of garbage that includes mercury-containing products.
*0* 0*0* 0* 0* 0*
Mercury Thermometers
* a mercury fever thermometer is a glass tube that contains
silvery liquid mercury. If the substance inside your
thermometer is red or blue it is an alcohol thermometer.
* Elemental mercury should never he used where children 2iva
and play, P.eplace your mercury thermometer with an
alternative, such as a digital, glass alcohol, or glass
gallluiii-lndluiu-Gln (galinstan) cheriuometer. You can also get
ear canal thermometers and flexible forehead thermometers.
Currently, digital thermometers seem to be the most
accurate. Forehead thermometers are convenient and
comfortable, but not very accurate.
* When, you replace your mer ury thermometer, be sure to take
it to a hazardous waste col action center. Do not just throw
it in the trash oi burn it.
* One thermometer manufacturer estimates that the
thermometers sold in the United States each year contain 4.3
tons of mercury. A typical mercury thermometer contains
mercury and larger models
about 700 milligrams (.7 grams}
car. contain up to three grams.
* There are no known or anticipated health risks froiu other
kinds of thermometers.
3 of 6
NN 67. Aug. 25.2001: Mercury and Mercury Thermometers
8/27/(-
* Known environmental hazards from other kinds of
thermometers are significantly less than those of mercury
thermometers,
ma’.r concern, is from the mercury in the
button cell batteries used in the digital or ear canal
models, rlowever, those batteries contain only 3.5 to 11
milligrams or mercury compared to cue 7GG milligrams round
in uhe smaller mercury cnermomeLers, so rhe amount released
into the environment is much less.
*n*n*0*o*O*O*
t-f
g Mercury mh?=>
o +- n ** B r 9
If you do break a mercury thermometer, it’s unlikely to
cause health problems if you clean it up immeaiacely and
venrilane rhe area. The greacesr danger of significant
exposure is in a small, poorly-ventilated room, where the
mercurv vanor is able to build un into danaerous levels.
However, you may not be aware that the thermometer broke or
the mercury may seep 4nto an area that’s difficult to clean,
so the best thing to do is to play it safe and not use
mercury thermometers at all.
If your child breaks a mercury fever rhermomerer in his
mouth, the mercury he swallows is a low risk in comparison
with breathing the vapor, as the mercury just passes through
his body without being absorbed. However, it then enters the
waste water system and through that, the environment. (And.
personally, I wouldn’t want my child swallowing any kind of
toxic substance.)
what lo do if a thermometer breaks:
* If possible, close off the room from the rest of the
house.
* Increase ventilation with o;
fans for at least one hour.
air; if possible, use
x Pick up the mercury with an eyearopper or scoop it up with
heavy caper such as an index card. Be sure to use something
that can be discarded.
* Dlacp everyth4^hef’s been co^ta**14rated (paper,
eyedropper, broken glass, and so on,' into a plastic zip bag.
Place this bag into a second bag and then into a third,
making sure earn bag is tightly sealed. Then place the
triple bag into a wide-mouth, sealable plastic container.
* Call vour local health department to find out the nearest
place to dispose of the contaminated material. If there is
no such location, dispose of the piastre container according
to state and local requirements.
5r Weather permitting, leave your windows open for about two
days.
★ When you are cleanino up the mercury spill
- Do NOT use household cleaning products, especially ones
that contain, ammonia or chlorine which will react violently
with the mercury and release a toxic gas.
- Do NOT use a broom or paint brush. This will break the
mercury into smaller beads and spread them around.
- Do NOT use a regular or shop vacuum cleaner. This will
4 of 6
8/27/
NN 67. Aug. 25,2001: Mercury and Mercury Thermometers
put the mercury vapor into the air and increase your chances
of exposure.
*0*0*0*0*0*0*
Sources for all Mercury I tens
» Press Release about the Mercury bill in Maine, This was
emailed to me, so i have no uRL, but two people who worked
on the bill are Pam Anderson <dranderson0ainop.com> and
Marnorie Monteleon <orestonbrian0acadia.net>.
* RAD SUPPORTS PT TMTyn'nTfiv nir MPPCTTP.v-CONTAIhTIN'G
THZPMOMETEP.S
http: //;vww. aap. org/advGcacy/rGleaocs/j ulymsrc. hem
M fAQ about Mercury Fever Thermometers
http://www.epa.gov/glnDo/bnsdocs/hg/thermfaq.html
* The entry on mercury from the InfoPedia 2 Encyclopedia
* The entry or. mercury from the 1995
Zncyclopodla
Grolier Multimedia
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*0*0*G*0*0*0*
Nanny’s Notes is published every Saturday (with special
editions as necessary) oy Donna Dolezal Zelzer. if you have
not received your issue by Sunday evening, please contact
nannvnote@moonlilv.com.
Please invite your friends to subscribe!
Send them a copy with your recommendation.
To leave the list, send your email address to
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For Questions, comments or other matters, write to
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*o*o*o*o*c*o*
Copyright 2001 by Donna Zelzer, all rights reserved.
The individual writers hold copyright to the individual
articles.
5 of 6
NN 67. Aug. 25. 2001: Mercury and Mercury Thermometers
8/27
Copies may be freely distributed electronically, as long as
1. This oermission and the authorship of the articles are
retained in any additional publication of the article.
2. The content of the article is not changed in any way.
3. You do not charge for the article, other than the cost of
download and/or connect time, or photocopying costs, in the
case of a printed version.
4. subscription information is included.
6 of 6
8/27
G- - A S- 7-
EVER, CLEAN UP,
DON'T COVER UP
'July 2001
Incredible as it may sound, the lush, green hill resort of
Newsletter
.. '-
Kodaikanal in the Western Ghats has been contaminated by deadly
mercury wastes emanating from a thermometer factory owned
by corporate giant Hindustan Lever.
Greenpeace activists and a local conservation group recently
joined hands to expose this threat to Kodaikanal’s environment.
exercise”. Comments Navroz Mody, Greenpeace
Campaigns Director, “We are not interested in a Bhopal
style cover up. If Hindustan Lever doesn’t know how
much mercury contaminated waste has left its factory,
it’s irresponsible and insensitive to say that what left
On March 7, community groups of Kodaikanal alongwith, the factory was only ‘some glass with mercury waste’.”
activists of Greenpeace and the Palni Hills Conservation Council
(PHCC), former workers of the factory and women’s groups Tamil Nadu Alliance Against Mercury
cordoned off a local scrap yard containing several tons of mercury- Greenpeace encouraged local groups totally against the
contaminated broken thermometers. The thermometers were mercury menace. On March 12, over 30 groups formed
spilling out of tom sacks onto open ground where workers walk the Tamil Nadu Alliance against Mercury and decided
about barefeet. The scrap yard is located in a crowded part of the to provide support to HLL workers who complain of
town, adjacent to two schools.
health problems that may be related to mercury
About 400 people marched to the factory site and found that poisoning. The Alliance also strategised on how to deal
mercury contaminated wastes were also dumped behind the with the pollution. Consignments of contaminated glass
factory wall onto the slopes leading to Pambar Shola, a rich have reportedly been sent to various parts of the state
tropical forest Watershed designated as a sanctuary area. The Shola and could affect many unknowing victims,
is one of the last remaining pockets of mega biodiversity in the
js behaving like any multinational by covering
region. The Pambar stream drains the forests behind the factory up, |yjng, anc| hoping that this will die down. We’re
and runs down to the Kumbhakarai waterfalls,
c_n_ a- *tourist♦ bathing surprised how the individuals in Lever can live this
site.
down, that their inaction may cause the poisoning of
Both the past and present factory workers have complained of unknown masses,” says R. Kannan of the Palni Hills
several health problems that they say are caused by handling Conservation Council. The Council fears that 18
varieties of rare plants and trees in the Pambar Shola
mercury at the plant.
are also at risk.
U/
Hindustan Lever’s Reaction
After initially denying responsibility for pollution, Hindustan
Lever Ltd’s (HLL) Mangement subsequently admitted that there
was a “remote chance” that mercury contained in broken
thermometers may have left the factory and attributed it to possible
“human error.’*
On April 22, ex-workers of HLL went on a day-long
hunger strike, protesting that the company was
unrepentant and was resorting to lies and threats to cover
up polluting practices.
Meanwhile, the Tamil Nadu government has set up a
committee on hazardous wastes and has invited
On March 8, the company announced that, “HLL has decided to
Greenpeace to be a member.
carry out a comprehensive audit of the operation of the factory
including a review of disposal of glass as scrap. Pending this Qur Demands The community groups and Greenpeace
audit and the review, as a matter of abundant caution, the company demand that: HLL should immediately end the use of
:ury in the factory and ensure that the livelihoods
has decided to suspend thermometer production at the factory.” mercury
of workers are not jeopardised by their decision to
It is obvious that the mercury plant was sited in India to take
suspend operations. A full investigation should be
advantage of lax environment and safety laws and low labour
conducted into the extent and nature of mercury
I costs.
pollution caused by the factory within its premises, at
The thermometer plant’s entire production is exported to the
scrap yarj an(] jn the surrounding environment. HLL
United States. The mercury for the plant is imported, mainly from must, uncjer striGt supervision, clean up the mercury
USA. The plant was itself imported from USA by Ponds India scrap yard in Moojikal as it poses a threat to children at
Ltd and set up on the Pambar Shola ridge after securing special the adjacent schools and to a densely populated
exemption on the grounds that it was non-polluting. In 1977, it communjty. HLL must account for all past waste
was bought by (HLL), a 51 percent-owned subsidiary of Anglo- shipments to other parts of Tamilnadu. HLL should pay
Dutch multinational Unilever.
|for a full medical investigation of all its ex and current
workers and affected community members, pay the costs
Mercury Hazards
of restoration of their health and compensate them for
Far from being non-polluting, mercury is highly toxic. Methyl the loss of quahty of life. HLL must be held criminally
mercury affects the human central nervous system, kidneys and and financially liable for the damage done to workers,
liver through air, water or skin contact. Greenpeace calls for a community and environment of Kodaikanal and the
worldwide phase out of mercury as it is a dangerous, non- Palni Hills.
biodegradable substance. Cleaner alternatives to mercury-based
What you can do
i instruments exists. Where they don’t, alternatives need to be
I
SREENPEACE ENVIRONMENT | developed urgently.
Log on to www.greeenpeaceindia.org and send a petition
TRUST
to officials of Hindustan Lever who continue to ignore
Meanwhile, activists and community members have dismissed
15, SAKET, NEW DELHI-110017
their ongoing poisoning of Kodaikanal.
Hindustan Lever’s official response as an “insensitive PR
•HONE: 011-6962932, 6862679
or
Email :
ia.orc
■
5co
u
Topical
CAPTURING
the^S
Toxte
Shipbreaking
Campaign
Notqffes Up
Victories
Toxic
Stop Polluting Our
Water.Our Land.
Genetic
Engineering
Does India Need
Monsanto's Bt
■tttonW
Ghl^l^ews
^l?aiTan®Says
NO to GMOs
WE’RE
The Workers’ Story
HLL Worker Vijayalaxmi
If conservationists are concerned with the fallout of mercury
contamination on Kodaikanal’s
flora and fauna, the workers of
Hindustan Lever Limited (HLL)
are worried sick about the
effects on their health.
HLL is quite aware that
mercury is a hazardous
chemical. The company
admits that it conducts
occasional urine tests to
analyse whether workers are
contaminated, and relocates
to the non-mercury area of
the plant, those who have
higher than “acceptable
levels” of exposure to
mercury. It has not disclosed what these “acceptable levels”
are.
HLL workers wear practically no protective clothing. They
use their bare hands. Some are provided with cloth caps and
cloth half-face masks.
In the mercury area of the plant, spillage is common.
Thermometers break frequently. Mercury spilled on the floor
is washed with water into a ditch alongside the shop floor
and channeled to a settlement pond. Large spills are
reportedly recovered by vacuuming (a dangerous practice).
The sediment is conveyed to a mercury vapouriser tore cover
mercury.
Workers complain of loss of appetite, infertility, skin
discolouration, irritation while passing urine, stomach aches,
ulcers and various stomach and kidney problems besides
cardiac problems, and neurological disorder.
OUTRAGED BY
US REFUSAL TO
CURB
GREENHOUSE
GASES
Greenpeace Logs A
Victory for the
Rainforest
OJ
co
|
z
e
c-3
Thermometer
If you are feeling feverish, stop, don’t reach out for a mercury
thermometer. Production of these thermometers is a cause of
mercury contamination of people and the earth.
Mercury is a very toxic metal. It poisons the environment through
air, water or soil wherever it is disposed of. That is the reason why
mercury must be phased out of industrial use worldwide. In India,
there is no regulation on the use of mercury, or standards on its
discharge.
Although hazardous, mercury is used in various industrial processes
and in a variety of instruments in the healthcare sector.
US Firm Recalls
Mercury
Shipment
to
India
An
international
coalition
of ci
is,
environmental and labour organizations declared an
initial victory in their effort to prevent a 118-ton
stockpile of hazardous mercury from being exported
to India. The mercury belongs to the defunct Holtra
Chem chlorine manufacturing plant in Maine, USA.
Greenpeace USA played an active role in the
campaign against mercury export.
Indian Dockworkers Refuse to
Unload Mercury
The owner of the waste, Don Goldsmith of D. F
Goldsmith Inc., decided to recall the first 20-toi
consignment of the material, already on its way to
India, after protests began in India. Alerted by
Greenpeace and Toxics Link, in January 2001 the
All India Port and Dockworkers’ Federation
President S.R.Kulkami directed all affiliated unions
at major ports in the country not to unload the
consignment.
Likewise the Indian goverment expressec
,ve
doubts about the shipment. The Goldsmith decision
was influenced by the fact that the States of New
York and Maine declared the material a hazardous,
waste. This declaration would have made its entry
into India illegal under the Indian hazardous waste
import ban and under the Basel Convention — an’
international accord designed to minimize trade in
hazardous waste.
“The people of India were absolutely justified in
rejecting this toxic shipment,” said Michael Belliveau
of the Natural Resources Council of Maine. “The
mercury from the HoltraChem plant has already
despoiled enough of our environment in Maine. We
cannot let the same toxic nightmare cause even more
grief abroad.”
The mercury discharged by the Holtra Chem plant
has resulted in the highest levels of mercurycontaminated sediment possibly ever recorded in the
world.
I
>
David Fraser McTaggart
1932 - 2001
Founder, Greenpeace International
A Tribute by Steve Sawyer,
. friend and colleague
W hen the history of these times comes to be
written, David McTaggart will emerge as far more
significant than most politicians. Certainly he
achieved more for the environment than any politician
alive or dead.
McTaggart lived his life at a time when the human
world was destroying its home, the natural world at
y "nprecedented rate and to a suicidal degree. Many
s also saw the need for action but nobody took
action like McTaggart. Some politicians denounced
him, others admired him but far more were influenced
by his creation - the first global environmental
organisation which was effective as a movement, as
a name and as a catalyst to achieve change for the
good, while opposed by big business and big politics.
He coverted Greenpeace from a disparate fleet of local
organisations into an international entity with a
culture, public proposition, and capabilities that
enabled it to act globally, proactively, effectively and
with public support.
Greenpeace has been a phenomenal success as a
communicator because it has been able to express
widely shared values and feelings, in concrete visible
actions. It has been able to convey emotion and to
connect with people’s instincts as well as their
rationality, about big issues, through small moving
acts of human endeavour. McTaggart was one of
tb^ce who inspired this in Greenpeace by his personal
a
is, such as sailing on his little ship the Vega to
oppose the last atmospheric nuclear test in the world,
in the Pacific. But McTaggart went further. He
applied his personal charisma, charm, and energy to
engineering and sustaining an organisation that was
able to take the core values of non-violence and
• internationalism and use them to moral effect.
Phenomenal Achievements
McTaggart’s tally of environmental achievements is
impressive in a conventional sense.
Nuclear testing: facing the French State in their
Courts after they rammed his ship, beat him up and
almost blinded him in the Pacific.
Whales: adding twenty countries to the alliance to
protect whales while working at the International
Whaling Commission with the British conservationist
Sir Peter Scott.
Pushing for World Park Antarctica, with a
combination of challenging world powers on the spot
on the continent, and working ‘behind the scenes’ with a host of
world leaders to get the job done.
Setting up Greenpeace in Moscow: the first international Non
Governmental Organisation in Cold War Russia.
Conducting Televisual Political Opera
McTaggart brought a style and system to Greenpeace which enabled
it to conduct televisual political opera that again and again, forced
Governments and corporations to uphold the public interest rather
than private gain through planetary damage. His real genius was in
creating a Greenpeace that others could support, lead and find their
own rewards from, while doing good.
A journalist wrote of the Greenpeace struggle to prevent Shell
dumping its redundant Brent Spar oil installation in 1995 that it
was “an incident crammed with dramatic polarities and symbolism
of the most unsubtle kind, it seemed a small but perfectly formed
victory for sanity, for people against machines and moguls”. What
he described was a result of the campaign machinery, strategy and
logistics inspired and founded by McTaggart. It is typical of the
man that in that summer of 1995 he was himself about to undertake
yet another trip into the French nuclear test zone, where he spent
his 63rd birthday hiding out from the French and delaying their last
nuclear explosions.
The Empire Builder
McTaggart was as an empire builder, though he disdained all of its
trappings for himself: And not a military or criminal or business
empire but an empire of the soul, of devotion to nature above
nationalism or material greed. McTaggart inspired his followers to
follow Greenpeace, not himself. He was above all a strategist,
described by one former Greenpeace Director as ‘cold but majestic’;
but at the same time is remembered by close friends as having an
incredible capacity for personal compassion.
Many who met David remarked on his piercing blue eyes which
were unnervingly laser like rather than twinkling.
As a former successful businessman and sportsman, McTaggart
was intelligent and worldly enough to realise that one cannot inspire
change through intellectual argument but through action and
symbols. He deployed science and ethics like an intelligencer and
an alchemist - the result was loved by the public and hated by
Greenpeace’s critics.
All empires wax and wane and Greenpeace already operates in a
changed world from the days when McTaggart first sailed his yacht
against French warships. It has played a big role in convincing
most people that humanity must transform its ways. The attitude of
America to climate change shows, however, that there are still
dramatic polarities, and need for sanity and new victories in people’s
fight against moguls and machines.
If anyone deserves to rest in peace it is David McTaggart but if one
thing is certain, his spirit will be out there, wandering the seas and
looking over the forests, urging more action until the world is
genuinely both peaceful and green. McTaggart could say “I told
you so” but he ought better io say, “I showed you so”.
£
^3
Can we
save the
Earth?
11 makes patent good sense to
protect the environment. Not
only does this result in better
health, it also ends up boosting
the economy.
Time and time again, across
the world, events have proven
that shortcuts taken that harm
the environment in the short
run turn out to be extremely
expensive in the long run.
Predictably, people who
taught such lessons, such as
Rachel Carson, were first
ridiculed, then fought by the
powers that be in the industrial
countries when they were
forced to deal with substances
like DDT, PCB and heavy
metals in the human food
chain. In the case of nuclear
radiation, the situation was
even worse and we have Three
Mile Island and Chernobyl as
proof.
Thousands of deaths and
billions of dollars later,
most
G-7 countries are now
extremely reluctant to allow
toxic industries to come up
near human habitations.
This, however, does not
prevent G-7 governments
from exporting such toxic
processes, wastes and
industries to Third World
countries, like India. And it is
to prevent precisely such acts
of chemical aggression that
Greenpeace International
decided to set up a liaison
office in India.
Hopefully, working together,
Indian and overseas environ
mental groups will be able to
defend innocent Indians from
such threats in the years to
come. Towards this end, YOU
can play a vital role by joining
or supporting Greenpeace
India. Together we can, and —
will, save the world!
czj
- -s
Bittu Sahgal
<u
Editor,
Sanctuary Magazine
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o
CAPTURING THE SUN:
Earthquake Hit Villages Go Solar
A.t dusk in Naredi, a hamlet in Kutch, began preparing to plunge
Hazardous
■BM
Shipbreaking at Alang
Until Greenpeace led a
campaign in Alang, 30,000
workers worked at the yard
without any protective gear. In
June 2000 Greenpeace
undertook an extensive
scientific environ-mental
investigation of the Alang
yards. We found that in less
than two decades of operation,
the contamination levels in the
Alang shipbreaking yard had
reached levels found in parts of
Europe that had experienced
industrial activity for over 50
years. Levels of the deadly
poison tributyl tin in Alang soil
and sediments were so high that
they would classify as
hazardous wastes in Europe.
We found asbestos fibre even
in the living quarters of the
workers.
According to Dr. Frank
Hittmann, an occupational
physician from Germany, every
fourth worker at Alang could
contract cancer due to
workplace exposure to toxic
and cancer causing substances.
Greenpeace’s exposes have
forced the Gujarat Maritime
Board to take action. In April
2001 path breaking regulations
were adopted like regular
working hours, compulsory
insurance for workers and
monitoring of safety standards.
Land is to be acquired for waste
disposal and a hospital is to be
set up in Alang.
The Greenpeace toxics trade
campaign demands that the
shipping industry dispose off
ships in an environmentally
sound manner. Persistent
campaigning has begun to pay
off internationally. The
International
Maritime
Organisation is discussing
regulation of the global
shipbreaking industry. The
International
Labour
^Organisations are developing
— programmes of safe work for
=sthe shipbreaking industry.
^Finally shipbreakers are
beginning to realise that ships
?jhave to be decontaminated
prior to export to Asia.
into darkness. A young Rabari woman in black was in a hurry to
cook dinner before it grew dark. The kerosene lantern hanging in
the porch was nearly empty. At nightfall the village would be dark
and dreary. In its 45 years of existence Naredi had not experienced
‘modem amenities’ like electricity. However, when over 30 solar
lanterns lit up the night in Naredi, it stirred wonder and excitement
in the villagers’ lives.
Naredi is one of two villages that Greenpeace chose for solar
electrification, in the wake of the devastating earthquake that struck
the Kutch region of Gujarat in January this year. In just two months,
Greenpeace provided solar power to every household in two quakeravaged villages, Naredi and Umarsar. Greenpeace also helped
restart three schools. This was done in collaboration with Medecins
Sans Frontieres and the NGO Saraswatam.
The multi-million dollar lignite-based power plant located in the
region had been unable to provide electricity to the villages for the
past two decades. As the people of Naredi learnt to tap power from
the Sun, the massive power plant that belches out fly ash over their
fields appeared in a different light.
Gujarat’s centralised, conventional energy system has failed to
provide basic energy services and power supply is erratic in Kutch.
Particularly ironic is the plight of Umarsar which is located against
the backdrop of the Akrimota power plant. Umarsar does not receive
electricity but bears the repercussions of lignite mining for the plant.
Umarsar’s 32 families were traditionally agriculturists but have
become labourers since mining rendered agriculture unsustainable.
The earthquake destroyed most houses in Umarsar. Miraculously,
a community structure survived and that is where Greenpeace
installed 32 solar panels to charge lamps. Every morning the villagers
come to the community centre to plug in their lamps for recharge
and take them home at dusk.
J,.
«
Ministry for the Environment detained it due to
concerns that it contained asbestos, heavy metals and
hazardous waste.
The export of hazardous waste is illegal under the
1995 Basel Ban that prevents Organisation for
Economic Corporation and Development countries
from exporting it to non-OECD countries, such as
India. The European Union ratified the ban in 1997.
Greenpeace was invited by the Dutch Environmental
Inspectorate to testify that the ship was destine
scrapping in India. Alang in Gujarat was till recently
the world’s largest ship breaking yard where 400 ships
were scrapped annually.
Worldwide many ships are now reaching the end of
their useful lives, making safe disposal a major
concern. Ships exported for scrapping are made of
materials like cancer-causing asbestos that is used for
insulation, paints that contain heavy metals and
explosive gases and oils. Workers and the
environment are exposed to these substances when
the ships are broken. For instance, when asbestos is
handled, minute particles settle in workers’ lungs and
cause breathing complications that could eventually
lead to death.
■
Umarsar’s residents blame the power plant and mining for creating
environmental, human and animal health problems. They complain
of smog and destruction of vegetation that has caused changes in
monsoon patterns. Children are prone to respiratory illness due to
fly ash and mining residues. In adults the incidence of TB and cancer
has gone up. Many women suffer increased spontaneous abortions.
Before it begins to reconstruct the devastated Kutch region, the
Gujarat government needs to re-examine its whole approach to
power generation. Most villages in Kutch are connected to the
power grid but there is no power to supply these lines. Greenpeace
believes that instead of re-laying electicity cables, funds should be
diverted to develop sustainable energy technologies.
We need your support:
“The decentralised nature of the communities in the region means
that renewable energy systems are highly appropriate,” says Karl
Mallon, a climate change campaigner with Greenpeace International,
who visited Kutch recently.
tear08
entotced
Toxic Shipbreaking
Campaign Notches Up
Victories
The Sandrien, a 34-tonne Mauritian owned vessel, was recently
detained in the Netherlands before it could leave for the Alang ship
breaking yard in India. The vessel was to be scrapped. The Dutch
occupy
ovetsee u
sate?/
steps
I
Is
Stop Polluting Our
Water, Our Lana
Gujarat Villagers & Greenpeace take
on Industry & World Bank
Clean Production is
the Solution
Industrial pollution is a huge environment issue in
the heavily industrialized state of Gujarat today.
Hundreds of illegal toxic waste dumpsites dot the
land, the groundwater has been contaminated in 74
talukas (sub-districts), and the streams are foamy red
and foul smelling. The industries have attracted a
large migrant workforce and these workers drink
water from polluted wells and hand pumps, unaware
of the risks to their health. Their children play on the
dumpsites, unmindful of the hazards they contain.
Pollution control authorities have in recent years
been pushing the Common Effluent Treatment Plant
FP) strategy to treat these industrial wastes.
Vvastes from different factories are channelised to
CETPs. This is a dubious strategy because instead
of controlling pollution it concentrates it in one place
into a deadly cocktail of toxins.
To spotlight the issue, on October 19, 2000 over 60
Greenpeace activists occupied a CETP at Vapi that
discharges toxic wastes into the Damanganga River.
The protest was joined by over 100 people from local
communities affected by the pollution. Four
Greenpeace activists chained themselves to the valves
controlling the discharge of the poisonous water.
“This effluent treatment plant is a farce. It spews out
disgusting water into our river and we believe that
the poisons in the waste water are the reason behind
our declining fish stocks and health "problems,” said
Devjibhai Tandel, former Member of Parliament.
Tandel lives in Daman, a fishing community
downstream of the CETP.
?mical Dreams
The World Bank funded CETP serves the Vapi
Industrial Estate, part of Gujarat’s ‘Golden Corridor’
• that houses 17 major industrial estates.
The state of Gujarat has launched an ambitious and
* ill-considered programme to attract US$ 12 billion
worth of investment in the chemical sector alone. A
matching amount is being sought from the World
Bank and the Asian Development Bank for
supporting infrastructure including superhighways,
ports and power projects.
Gujarat’s industrialists and politicians dream of
making the state India’s leading chemical
manufacturer. They boast about competing with the
Asian Tigers. Considering the environmental
consequences of industrial expansion is not on their
agenda.
Global Toxic Hotspot
In 1999 Greenpeace declared South Gujarat’s industrial corridor a
Global Toxic Hotspot. Greenpeace’s scientific investigations
confirmed that industrial pollution has poisoned the groundwater,
rivers and lands with life-threatening substances, including highly
toxic chlorine-containing pollutants. Vapi waste water contained
toxic metals such as lead, cadmium, chromium, copper and mercury
and highly poisonous hexachlorobenzene and polychlorinated
biphenyls.
Over the last decade, government agencies, goaded by institutions
such as the World Bank, have pushed CETPs as a magic solution
to pollution, with disastrous consequences.
On November 6, Greenpeace activists and members of the
Sarvodaya Society, the Paryavaran Suraksha Samiti and the Matsya
Udyog and Agricultural Sahkari Mandali met officials of Gujarat’s
Pollution Board and Ministry of Environment to protest the
pollution.
The Pollution Control Board agreed to examine the evidence against
CETPs and said it would stop new CETPs from coming up, if its
reassessment indicated that they were polluting.
What’s Wrong with Effluent Plants?
It is ironic that plants set up to treat pollution should increase it but
infact, Greenpeace believes, CETPs lead to concentrated pollution.
Factories send wastewater to the CETP via pipelines, open channels
or tanker trucks. At the CETP the wastewater goes through processes
such as filtration, settlement, aeration and microbial and chemical
treatment ponds, before it is discharged.
Industrial wastewaters are a mixture of poisons, each of which
require different methods for removal or destruction. For a CETP
to function optimally, the influent flow needs to be controlled and
the effluent characteristics need to be consistent. In practice, this
does not happen.
CETPs merely convert the poisons from liquid to solid sludge. This
reduces contamination of surface waters, but creates an additional
problem of poisonous sludge that must be disposed off. There is
also substantial air pollution.
CETPs can fix simple parameters such as Total Dissolved and
Suspended Solids, BOD, COD and pH and meet the discharge
standards for these parameters. But CETPs cannot get rid of many
of the persistent organic poisons. They cannot destroy the heavy
metals. They do not even address the volatile organic compounds.
Greenpeace believes that the
key to less pollution is not
CETPs but Clean
Production. Elimination of
pollutants needs to begin at the
factory level by substituting the
poisonous chemicals with less
Mttank
Responds to
Greenpeace Protest
In the 1990s the World Bank
began lending money to the
Indian government to set up
CETPs when polluting
industries faced a series of
public interest litigations and
court verdicts.
The Vapi CETP was set up
with a loan from the Industrial
Development Bank of India
drawn from World Bank funds.
World Bank funding of
polluting
technologies
includes loans under the
project Industrial Pollution
Control, 1991 (IBRD $124
million/IDA $ 31.6 million)
and under the Industrial
Pollution Prevention Project,
1994 ($250 million).
The World Bank now admits
that it is reconsidering the
CETP strategy. On November
1, 2000 World Bank President
Janies D. Wolfensohn wrote to
Greenpeace, “I appreciate the
detailed analysis Greenpeace
has provided on the question
of
Common
Effluent
Treatment Plants. We agree
with your assessment, which
reflects our own thinking, and
have taken significant
corrective action for the past
three years now.... We have
moved away from investments
in pollution control hardware
towards an emphasis on
creating clear accountability
for industrial pollution,
monitoring and compliance.”
However, at least seven new
CETPs are under finalisation ~v.
in Gujarat, reportedly with
World Bank funding. The 4J
Bank has stopped short of zr.
declaring that they will <L>
suspend all funding.
Does India Need
Monsanto's Bt Cotton?
Bt Cotton^ Some Facts
Bt cotton is a genetically
altered crop. It is created by
inserting a synthetic version
of a gene from the naturally
occurring soil bacterium,
Bacillus thuringiensis (Bt).
This genetic alteration
enables the cotton plant to
produce its own Bt toxins to
destroy pests.
The European Union has
rejected market approval of
the same variety of Bt cotton
on grounds of environ
mental and health safety.
A major hazard of insect
resistant crops such as Bt
cotton is that targeted pests
could develop resistance to
the effects of Bt. In some
regions of the United States,
between 1996 and 1998 the
cotton bollworm acquired a
tenfold increased tolerance to
the toxin found in Bt cotton.
BREAKING NEWS
June 20,h, 2001
INDIA REMAINS GMO
FREE!
The first genetically
modified crop MonsantoMahyco’s Bt Cotton, is not
given
approval
for
commercialisation, by the
Committee set up by the
Ministry of Environment and
Forests.
After an open dialogue held
with scientists, farmers,
Greenpeace and Government
representatives- the Genetic
Engineering
Approval
Committee
(GEAC),
expressed dissatisfaction
with the data presented and
have demanded another year
of field trials.
« This is a big victory for
Greenpeace in its campaign
against the release of
z Genetically
Modified
Organisms (GMOs) into the
« environment.
i/
Greenpeace Exposes Sham Field Trials
There were other irregularities. Bt cotton in all seven
plots was planted much after the sowing season. It is
ironical that a trial intended to establish resistance to
the bollworm pest, actually missed the main period
of pest attack due to late sowing. Inferences made
about the efficacy of Bt can thereby be invalidated.
India is the third largest cotton producer in the world and cotton
production plays a major role in the Indian economy, providing
employment to a million farmers.
But the cotton crop in India is in a crisis. One major cause is
cultivation of hybrid varieties and heavy use of expensive pesticides.
Cotton is grown on only 5 percent of India’s land but consumes 5259 percent of pesticides. There have been increasing reports of crop
failures and of pest resistance to pesticides.
In 1997-98, approximately 300 farmers in the southern state of
Andhra Pradesh committed suicide when the cotton crop failed and
they were unable to pay back loans taken mainly to purchase
pesticides.
At this juncture, when cotton farmers in India are desperate for an
alternative, genetically modified cotton (Bt cotton) is being offered
as a solution.
Monsanto’s Bt Cotton in India
The agribusiness multinational Monsanto-Mahycl^fst attempted
to field test its Bt cotton, claimed to be resistant to the bollworm
pest Helicoverpa Armigera, in India in 1998. The company said
that it would increase yields and reduce pesticide consumption
drastically.
Monsanto’s attempts at field testing were controversial. Flouting
all norms and rules, Monsanto applied to the wrong Government
committee for permission. Bt cotton was planted even before
permission had been granted. In 1998, farmers and local activists
launched ‘Operation Cremation Monsanto’ bringing the field trials
to a halt. A court case challenging the trials was filed in the Supreme
Court. Although the case is ongoing, permission was again granted
to Monsanto to conduct large scale field trials in July 2000.
This could signal the beginning of the end of India’s small farmer
owned, biodiversity based agriculture. No genetically engineered
crop has been grown commercially in India so far. Bt cotton, if
commercialised, would be India’s entry into the genetically modified
market.
Greenpeace Investigates Field Trials
Greenpeace located seven ongoing Bt field trials in five districts of
Andhra Pradesh and found that even basic scientific practices are
flouted. The trials are being conducted unscientifically,
undemocratically and pose a danger to the environment. Farmers
are given no information on the nature of Genetically Modified
Organisms (GMOs) or the precautions to be taken.
For instance, company personnel tried to persuade Komarareddy
Pratap Reddy of Mahbubnagar district to sow Bt cotton. He got the
impression that Bt cotton requires no pesticide at all and said he
would incur the wrath of the local pesticide agent if he bought no
pesticide. In response, the company staff brought along the retired
circle inspector of the village to ‘assure’ the farmer of protection!
Dr. Ramanjaneyulu of Science for People,
Hyderabad, points out that three years ago when
scientists raised questions about the unsafe trials, the
Government assured them that the tests would be
done under the ‘protection’ of the agricultural
universities. “But evidence clearly shows that even
the universities have not followed any procedures. *
Besides the potential dangers this poses, any decision
based on the data collected would be unscientific,”
he says.
A serious cause for concern is the danger of genetic
contamination of nearby cotton crops. Normally, trial
crops are isolated from regular crops to prevent cr""s
pollination. Yet in Kanchanapally villag
Warangal, farmer Chandraiah Konkati cultivated
hybrid cotton 10-12 metres away from the Bt test
site. Such tests could affect human and animal health
because cottonseed oil is used for human consumption
while the seed cake is used for animal feed.
Supervision and monitoring on the sites was carried
out by uninformed personnel. No measures for
containment (not even a fence) to prevent grazing of
animals or picking by others were taken. All the plots
visited showed visible signs of pest attack and damage
from whitefly, cotton bollworm and pink bollworm.
Plant production has been sparse and yields
negligible.
A Bizarre Situation
“The entire episode with Monsanto is bizarre. Who
is supervising these trials? Are the people involved
aware of the dangers of GMOs? It is apparent
irresponsible private enterprise colludes with con«pt
governments to form a nexus which has devastating
consequences. Any scientist is aware of the potential
dangers from the release of genetically engineered •
organisms into the environment. This simply cannot
be permitted,” comments Dr. P.M Bhargava, founder
of the Centre for Cellular and Molecular Biology,
Hyderabad. He suggests that all information
regarding field trials be made public and an inquiry
committee of scientists be set up.
“It is shocking to see the manner in which a potentially
dangerous gene-altered crop is being tested. This is
no way of testing and very simply is un scientific,”
says Michelle Chawla, Genetic Engineering
Campaigner with Greenpeace. “The field trials are a
farce under the guise of ‘scientific research’. The
primary aim is commercialization,” she adds.
I
I
|v<erimehts
GMOs Hurt Your Health
<
»«•>•»
I
I
J
i
I
Greenpeace Alerts
People on Dangers
of GMOs
1
,
Wearing death masks and carrying placards.
Greenpeace activists demonstrated outside the British
Council’s offices in Connaught Place, the heart of
New Delhi to protest a biotechnology tour that
promoted Genetically Modified Organisms (GMOs)
in India.
Greenpeace pointed out that the advocates of genetic
engineering were using the British Council as a tool
to build a false image of this technology and to create
—w market opportunities for themselves. The Bright
iks Biotechnology tour by six scientists, several
of them proponents of Genetic Engineering (GE),
included many closed sessions with invited audiences
of biotech professionals and scientists.
“It’s alarming to see the manner in which many
institutions and forums are being indiscriminately
used to promote GMOs. Simultaneously, due to very
little public awareness on the issue, there is no real
debate,” says Michelle Chawla, Greenpeace’s Genetic
Engineering Campaigner in India
Cautioning urban Indians that GMOs would soon hit their markets,
Greenpeace activists warned that, besides damaging the
environment, GMOs also pose a serious risk to human and animal
health.
For instance, introducing untried, untested and foreign material into
food (scientists are introducing genes from bacteria, scorpions and
jellyfish) increases the risk of allergic reactions in humans. Many
genetically engineered crops also contain an antibiotic resistant
‘marker’ gene that could spread to harmful bacteria and render them
immune to the effects of the antibiotic. This could add to the already
alarming medical problem of antibiotic resistant bacteria.
It is ironical that in the UK these health impacts have been
acknowledged. In fact the British Medical Association (comprising
119,000 members) has demanded a moratorium on the commercial
planting of GM crops, specifically asking for a ban on the use of
antibiotic resistant marker genes in GM food.
Global Resistance to GMOs
"c
•a
.2
^5
Thailand Says NO
to GMOs
Thailand became the
first Asian nation to
disapprove genetically
engineered (GE) crops
in April when the Thai
cabinet decided to halt
all approvals for field
trials of these crops.
The decision should
GE foods are not favoured by consumers in the US either. Last
year the Starlink scandal broke out when a GE maize variety that
was by law restricted to use only as animal feed (since it could
cause allergic reactions in human beings) was detected in hundreds
of consumer products. Over a billion dollars were spent trying to
recall Starlink com that contaminated 430 million bushels of harvest.
There has been a string of such scandals in the UK and Europe
where GE contamination has been found in cotton, rapeseed,
soybeans, maize and sugar beets. Since 1998 as many as 28
countries, including Japan, Korea and countries of the European
Union, have introduced regulations that require labelling of GE
products. Canada and the US are resisting labelling.
Greenpeace Global News
mark an end to
ongoing field trials on
GE cotton and GE
com, being conducted
by agribusiness giant
Monsanto, the
country’s second
largest seed provider.
Thailand has already
banned all commercial
growing of GE crops
\Ne're OUTRAGED by US Refusal to curb Greenhouse Gases
on its territory.
Monsanto is currently
Environmentalists worldwide are outraged by US President Bush’s rejection of the Kyoto Protocol, an international
agreement to prevent global warming. Climate Negotiations are scheduled in Bonn in July and Greenpeace urges the
European Union, Japan, Russia, India. China and other countries to ensure that the US does not wreck these negotiations.
The international community can ratify the Protocol without the US, if necessary.
conducting field trials
The US houses 5% of the world's population but emits 25% of the world’s carbon dioxide. Burning of coal, gas and
other fossil fuels contributes enormously to global warming. Bush broke his election promise to regulate greenhouse gas
emissions from power plants and opposed the Protocol within weeks of becoming President. It is obvious that the oil
and gas companies have huge influence in the White House. After all. Esso and BP were two of the biggest donors to the
Republican Party during the Bush election campaign.
society organizations
Greenpeace urges governments and corporations to switch to green fuels like bio-diesel and hydrogen. Renewable
energy sources, such as the wind and the sun, must be explored and tapped.
ment and Forests
demanding banning
Greenpeace Logs A Victory for the Rainforest
GE seeds and crops.
Canada’s Great Bear Rainforest will be saved from massive deforestation by logging companies because of an intense
global campaign by Greenpeace. An agreement between Greenpeace and two logging companies, Interfor and West
Fraser, allows for permanent protection of 20 rainforest valleys, deferrals of logging in another 68 valleys and an
ongoing process to protect the ecology of the rainforest.
For months, Greenpeace targetted the trade and investments of companies involved with logging the Rainforest. Protests
were carried out in Europe, North America, China and Japan, with blockades of wood shipments and protests at embassies,
retail outlets and lumber yards. In March the Canadian Embassy at the Hague was showered with woodchip to protest
Canada’s logging practices. In January a Canadian court freed a 72-year old grandmother, who was sentenced to a year
in jail for trying to save the forest, after massive public opposition to her arrest. British and Canadian fund managers
were persuaded to divest shares in logging companies and many firms including pulp buyers, timber importers and
furniture manufacturers in Europe, Japan, Australia and other countries boycotted the logging companies’ products.
The relentless global campaign paid off.
of GE cotton in India.
A petition by civil
and scientists has been
submitted to the
Ministry of Environ
<u
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is
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z
oin
Voice...
2
Now!
Greenpeace is a global
environmental campaigning
organisation.
We organise public campaigns
for the protection of oceans and
ancient forests, for the phasing
out of fossil fuels and the pro
motion of renewable energies in
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Credit Card No.
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Valid till
□□□□□□□□□□□□□□□□
Visa
Diners Card
Cardholders Signature
a s-3
VAIGAI
Scan : 74088
Resi : 25088
c Oi.OR SCAN
S. ENI-625 551.
D1‘. T. PAMDIXRAJ
D..M.R :
•Sonoloaist
PATIENT'S NAME
2
MR.
-.LPFERED BY DR
JEYAPAL
PREMABHAT B„s„M„S,
THAME YOU FOR YOUR REFERRAL.
Rea 1
t i m e E< n j o d e? w 11 r a o u. n ci e>: ami n a t .1 on o f
ss h c:« w s Liver n o r m a 1
esi on &eeri.
Ga 11
d u c L1
i n <=> i z e „ H a m o g e? n e o u s e c h o g e n i c i t y B
Intra he pa tic:
bi 1i ary
U o m tna n
No mass
radicles are not dilated.
b 1 a d d c? r s h c w s s m o a t. h w a 1 1 s „
q r d w t j •) p r e b e n t.
t he? a bdDinen
b i ]. e d u c: t
N cj q a 11 s t o n e s o r
is normal
in diameter.
j a .1 c u 11p r &? s &n t. B
E' ISHT
Oor Lira
rDIME- ’>
ec t a .Qeriir i ty
.. SYSTEM .....Dn^rgg,
URETER VISUALISED
norrnal .
.yPE£R.. SPINDLE DP.THE. DILATED
A-£ALCULUS_SEEN.IN. J HE UPPER URETER SIZE
1.—.ffi-- --li^i5ARWal_.calc^^^
LliE.ABOUT.7..,^^.
L.EFT KIDNEY NORMAL
is nDrmal.
IN SIZE..
N o d i 1 a t a t i cn a f
p e J.
Cor t. i c a 1
i c: a 1 y c t? a 1
er. hogen i c i t y
s y s t & / n p r e? s e n t.
.lNTRARENAL.CALgyiTIS SEEN IN. THE LOWER POLE.
P a n <j r e a e i ,■ d r m a 1
LJ
;! j a r- e
i n s i. z C1.
H o m o q e? n e o u e e c h o q e n i c: i t y u
lesion seen. M a i n p a n c r e? a t. i c: d l< c t. i s
Spleen norma1
No
No
in si ze
d o r in a 1 .
Homogeneousi echogenicity„
mass 1esion seen » Splenic vein normal.
«*
(PTO)
Aortax, IVC normal.
Urinary bladder capacity normal.
smooth.
I
Internal surface
No calculus or growth present.
Prostate Normal in size. Capsule regular.
Homogeneous
!
ec hog en i c i ty.
I
IMPRESSION s.
I’
I
;
WITH HYDROURETER.
* RIGHT SIDE HYDRONEPHROSIS
;,7.i
■ • - i- (
t
_ ..lAcic*
r.-..V-... H
Upper ureteric Partial calculus obstruction.
*
''
LIVER, GALL BLADDER, PANCREAS, SPLEEN,
URINARY BLADDER AND PROSTATE ARE
-■ SONOGRAPHICALLY NORMAL.
7
DATE : 03.02.200-1.
DR. T. PAND3 RAJ M^
^S. , D.M.R.D.
SONOLOGIST.
i
I
Scan : 74088
Resi : 75088
V
/\ 15
vA
I
OP
-
K>’ .i V
SCAN
1-625 .37) >.
■>> .
PANDI3.RAJ M.B.B.S. D.M.Fi
’ ’ •' n o i n (; • <j t
i . iT .TENT - S NAME
:
MR .
— H LFi) H¥ DR
J EV Al”'AL
PREMABHA•
R . S . M .. h .
THANK YOU FOR YOOR REF-ERRhL .
Real time? E< mijcic”1 ultrasound examination of
I-, r-, u.) ■
[. i v o r
seen .
n q r )T|J
in s i e » H cj m o q e n e o u s e? c. hi c:» q e n i c i t y K
I n tr a he pa tic I::.' I.
i
'■ ■
d u <: t I
C o m in o n b i 1 e d 1 < c: t
No maiss
ad i c 1 es a re n ot d i 1 a ted .
Ga 11 b 1 a d d e r s h o w s s m o 0 h t i w a 1 1 s ..
0 r o w t h p r e s e n t.
the abdomen
No q a 1 1 s t o n e s o r
.1 s norma 1 in diameter.
No
a 1 c u 1 u s p r e s e n t.
Cor Lit.. a 1. ei i .<( :«qen ic i. ty
RIGHT KIDNEY
normal .
j.
i1h.l;...dilat.ed
..SYSTEM...DILAIED.
C.B.ETCR..y.ISUALlSE.D
A.. CAi.CUL.US.. SE;tLN.....lN.JJHOJEEE
ABOU!...1.2...mm..,.... AN J. NTg.ARENA L.. C/AdlULUS _SEEN„.T N... J.HE.. UPPER..POLE
■<L11:...ABDUI..
LEFT KIDNEY NORMAL
normal.
IN SIZE.. Cortic a 1 g'C hogen ic i Ly
No dilatation of pelvicalyceal system present.
'IN. INTijARENAL CALCULUS SEEN IN.THE LOWER POLE
F a n (_■ r e et s i ■.• o r m a 1
i»’i
i e.
H o m o q en e o c e c: h o g e r i i c: i t y .
na "-SH. 1 ee . l on seen . M a i n p a n c: r e a t. i t:: d u c: t
Spleen normal i n
s 17. e r
is
normal.
H o m o gene o u s e hi o q e n i c: i t y .
No fi a s s 1esion seen . S p ?i en i c vein normal.
(F'TO)
Aorta 9 IVC normal.
Urinary bladder capacity normal.
smooth.
InternaU surface
No calculus or growth present.
Prostate Normal in size. Capsule regular.
Homogeneous
echogenicity.
I IMPRESSION :
*
RIGHT SIDE HYDRONEPHROSIS WITH HYDROURETER.
nHisafe. h-l :ip-7:
Upper ureteric Partial calculus obstruction.
-p.,
* LIVER, GALL BLADDER, PANCREAS9 SPLEEN,
URINARY BLADDER AND PROSTATE ARE
-SONOGRAPHICALLY NORMAL.
DATE : 03.02.2001.
DR. T. PAND
RAJ
J. , D.M.R.D.
SONOLOGIST.
4
JEYAPAL
3.5CA/5.0/A
PPT 150 .2 «■
W
VQIGAI COLOR SCANS
1
I
p.-.
5
f
;
'?, ■...-.
'
THENI
ABDOMINAL
03 FEB Bl
■qyWg*^
•■'if
^VAIGAI
Lt ;ki^(|ev'
.'.^■
iv
6*
-r.
■Swsssj
FR
3i?
PplViS ;TS
;
Bladder (
>
-'-Ljl
■■
■
L22'WBf
9
HINDUSTAN LEVER LIMITED
Thermometer Factory
St. Mary’s Road. Kodaikanal - 624 101. India.
Phone No.:(91)-4542- 40520 Fax No: (91)-4542-41288
June 23, 1999
‘•..'r R..S. Jaypal Joseph,
Kodaikanal 624101
Dear Mr. R.S. Jayapal Joseph,
This has reference to our training letter dated June 26, 1998
As you are aware, for the past fortnight there is no adequate work for
continuing your training programme, which is of a hands-on-natui e. We
are therefore, forced to terminate your training programme,accordingly
you will be paid one month’s stipend as notice and your training will
cease effective 23.06.1999.
Should the condition improve$,we shall let you know.
Yours faithfully
For HinuusianLever Limited
Authorised Signatoiy
f
Rsgisteied OIHce: Hindustan Lever House, 165/166, Backbay Reclamation, Mumbai-400 020, India.
L-i 2 -J;
Ponds (India) Limited
THERMOMETER DIVISION
Mount St. Mary, St. Mary's Road, Kodaikanal
Phone : (91 j-4542-40520 ❖ Fax : (91J-4542-41288
- 624 1 01, India
June 26,1998
MR.R.S.Jayapal Joseph
Kodaikanal
Dear Sir,
With reference to your application dated 25.06.98, we are
pleased to advise you that you are selected for the General
Training Programme for a period from 01.07.98 to 30 06 99
on the following terms and conditions:
1 . You will undergo the
general Teaming Programme for a
period from 01.07.98 to 30 06 99"
. ,-----During the training
period you
will be paid
paid ALL
ALL INCLUSIVE STIPEND of
Rs . 750/-(Rupees Seven i:Hundred and Fifty Only), per month.
and Rs.7/-(Rupees
Seven■\°'
only)
You win
(?1y)lper day of your attendance as
conveyance. You WTll not be eligible for any other allowance
or benefits applicable to regular employee of the company.
2. On successful completion of the General ”
‘ '
Training
Programme,
you may be short
listed for consideration against
'
regular
vacancies that r
may arise from time to time, provided you make
an application to the
i---• after
—j management
successful
completion
Of the General Training proRramme?
- You may be considered for
employment as a regular employe.,
if you are found suitable
for a part-icular job 1o: which a
vacancy
the company has no obligation whatsoever may exist. However,
to provide you
employment even at that time.
fe
During the General Training Programme
in ON THE JOB tr aining in all departments you will be involved
and in various jobs
■hat will be assigned to •
_u you from time to time.
t:- You wi11 be
assessed fur the quality and
—I quantum of work entrusted
---- 1 to you.
4. The place/department i.,
in which training is to be imparted
and the timing and duration of the f
' “
training
programme are
lable to be followed at the discretion
<_
of
the
management, and
.
>cu will devote your whole time attention
— . -.i to 1 earn the
work ent rust ed to you. The
company shall be the sole judge in
dec i d »•ng_ the
‘ 1
completion of your training programme and you
shall abide by- theJ di cision of the
... j company .
T. You will rabide
* * ‘ by all instructions
and carry out ail
assignments given
- . to
.o you by your superjors from time to time.
You -ill he
responsible and accountable- for f
the quality and
quantum ul work
-tR as assigned to you by your
superiors.
•Dage 1 of 2
I WM
L_S
c* cuni;<CArw*»
toots
ISO9002 CERTIFIED FACTORY
CERTIFICATE NO FM 30872
ERED_^TCE • 26' -THlRAJ SALAI, CHENNAI 600 i
105/MAIL P.O. BOX No. 6809, CHENNAI-600 105
+
■^FAX : (44) 8268581 4- TELEPHONE : 8277533
CABLE : VASOPONDS CHENNAI
...................................
I * TELEX : 41-7382
Ponds (India) Limited
THERMOMETER DMS!ON
Mount St. Mary, St. Mary's Road, Kodaikanai - 624 101, India
Phone : (91J-4542-40520 ❖ Fax : (91 )-45^-41288
6- In the event of your committing any act of indiscioline or
showing negligence or disinterest in your training programme
per;orX.o.ns^:.spt,joy:t]:
.<,,
y,fd.;:%
a,''1n9
adjustments if any against the dues you are liable to nav tn
a
7. You will be governed by the standing orders applicable
to
the factory.
2
ou are also hereby informed that your selection for the
General Training Programme does not automatically
give you the
•9ht to claim for the permanent employment
--- : in the company
’«pi?ysotrr?Ln,;.sr?;s9so“j,^:o"Si:vaiJy :s.rm’n*u m
.5 days stfp^d
or
15
Please confirm ;your
--- acceptance
of the above t
by signing and
returning the duplicatej copy of this letter terms
havingj junderstood and
accept with the terms and conditions mentioned above.
Be t
i 3hes >
Very truly yours
FOi ^pond’s [[India] limi D
/rvAz^
x
-- 1
h.raghupathI
VICE-PRESIDENT—IR
Signature.
fgnitying my acceptance.
IS09002 CERTIFIED FACTORY
CERTIFICATE NO FM 30872_
c!TFTEVAD<=npnMEr>: 26' ETHIRAJ SALAI' CHENNAI 600 105/MAIL P.O. BOX No. 6809, CHENNAI-600 105
*
TELEX: 41-7382
<■
FAX : (44) 8268581
+ TELEPHONE : 8277533
■Pond's (India) Limited
THBflMOMETER DIVISION
Mount St. Mary, St. Mary’s Road, Kodaikanal-624 101
Phone : (4542) 40520
LRTTC-
•
Fax : (4542) 41288
on oftet
workmen
n - F . “ , .jay A PAL
DATE: C-1 . 10.96
• "-i are hereby offered employment i n
Factory as a temporary
- a •- k me n t a ccarry
a i’ r y out
ou t L am p r,a r
i t e m 5 o r work and also such worksr
no
rma111y be .y ? .5 pp r man a n t nature? due to temporary
-■ ’= j c h
may n
o rma
orr pas a in
those
wor.-.:.
t h o s e ar*?o=.
temporary employment will commence fOctober 1r 1996 and
employment will automatically cease s= at close of work on
L-camber 31? 1996.
o«i ;•
employment in the ractory w x. 1 o e- t. $ r m i n a t e d o n the expiry
periods nr on completion nF the itsms oF work for which
s pe c i-f i ca 11 y employed; wn :. c c e e r is earlier. You will
right
'/ o u a r e
b
to
CGntiriue
required t. □ car r y
and the wc- k- t h a t
you i-
1 r.
Er’r p j
OUt
=^';j
ay
£.‘ i
a-Fter
above
period.
assigned in the department/
to you From time to time
squired to work in shifts as
V n u may also
Gti i
the
ed .
or ti-a uAy-s you actually ^ort m tns Tsclcry ( For a period of 8
h c-d ■ = pe r day i you w i 11 be pa i d R s-. 25 - ' <upeeE Thirty five only)
;.-r. day. / c u wil] not be entitled to any o t h e r pa ym e n t and
p i < i ] ege s nhenr-Fits enjoyed by
e p e■man ent w o rkmen of the
d.'mpany- You w i 11. he paid weekly.
■- G
1 . • ■ c- p>a j u wagc- s
.> ?■ t,
provtuu- work due to an
■' mack i nary.
; e
e •. ''ease*ns what sof v a c
5
-
1
which- the company is
C’ f raw ma te rials?
- • t o c k s t power cuts?
- “• 1
GO^y an c. i /ar c. F tempor,a.‘y employment and can not
’-i' • r ide
offer of permanent acrp 1 oyment under any
cc- c-<mstariras whatsoever.
REGISTERED OFFICE: 26, ETHIRAJ SALAI, MADRAS 600105/MAIL: P.O. BOX No. 6809, MADRAS-600105
CABLE : VASOPONDS MADRAS
TELEX: 41-7382 « FAX: (44) 8268581 « TELEPHONE : 8277533
be
7i
•Pond’s (India) Limited
■
DIVISION
■
■-
Mount St. Mary, St. Mary's Road, Kodaikanal-624101
Phone: (4542) 40521 • Fax: (4542) 41288
: 2 :
e.
You will also have no claim for any other privileges or
benefits whatsoever that exists or may be extended to a permanent
workmen in the factory- For the days you actually work you will be
j=liqible only for such facilities that may be extended to temporary
workmen in the factory as per company rules- The management reserve
the rights to introduce or withdraw these facilities at any time
not withstanding anything stated above.
Your temporary empolyment is liable to be terminated without
notice, if in the opinion of the company you are found guilty of
any misconduct as defined in our standing orders.
10, Xf you are agreeable to the above terms and conditions, you are
hereby required to signify your acceptance to the above by signing
your name in the space provided hereunder -
PGR POND’S EINHIA1 LIMITED
R RASHUPATHYl
VK C PRESIDE!
HRD
I hereby agree to the terms, which I have fully understood,
and the same has been read over and explained to me in Tamil.
I sign in acceptance of the above terms.
Signature1
-« -ax
1
____ tL..i :/
l
POND’S (INDIA) LTD, KODAIKANAL
PAYSLIP FOR THE MONTHI OF JUL 1993
6
: JAYAPAL JOSEPH R S
NA HI
I GNAT 1 ON
i l„ I . BAS IC
LI. ! . DA
I O I AL WAGE S
; SAGA YAM P
:
:
r
:
I#
Cl.
AMOUNT (Rs.)
MONTHLY WAGE RATE
CONVEYANCE ALLOWANCE
GRO'JC SALARY
MO : A 30
3®
DOJ : 01/07/1998
PF A/C NO. : TN/17287/855
' ’
DAYS PAID : 31.0
1
Trainee
0.00
0.00
0.00
i MINNINGS
EMI-' M
SciW/v.
;
ll’w
rf
Bo
Sw®
0-00 EL :
DEDUCTIONS
645.00
189.00
PF
EMPLOYEES CONT.
CANTEEN DEDUCTION
834.00
TOTAL DEDUCTIONS
NET SALARY
FACTORY LICENCE N0.DA94
- fS!
L t-
HINDUSTAN LEVER LTD. f HERMOMETER F actory
PAYSLIP FOR THE MONTH OF MAP
i. IB'
■>
10
NAME
F/H NAME
DESIGNATION
ELI. BASIC
ELI. DA
tota i
wages
■ IAYAPAL’ JOSEPH R 3
SABATIAN
Trainee
0.00
0.00
0.00
EARNF NGS
monthly wage rate
CONVEYANCE ALLOWANCE
GROSS SAI,ARY
1
FACTORY LICENCE NO.DA94
WELCOME TO HLL
AMOUNT (Rs.)
L ; „;i! I
EMP. NO . 395 '
DOJ : 01/07/1993
PF A/C NO. : TN/17287/855
DAYS PAID r-■ 31.0
CL :
0-00 EL :
DEDUCTIONS
0-00 SL r
- -
j
...
0.00
I; '
.
AMOUNT (Rs.)
750.00
109.00
PF
939.00
TOTAL DEDUCTIONS
NET SALARY
- EMPLOYEES CONT.
90.00
I:
I cl
90.00
349.00
SIGNATURE OF EMPLOYEE
T
I
-- •...
• -j*..
-■■9
-
•J
A
>
■>
L
’£
PIONEER DIAGNOSTIC
19:56
22/06/92
PNR 32dB o
SC 150mm
PPI FRL
DRH EEL LIVER
TOF
3.5
KIDNEY
19:54
27/06/92
PWR 32dB o
SC 150mm
PPI FPL
DRH EEL
TOFF
3. 5L
Jonsultan! Scnologis!
Age/ Sex :
NAME:
Ref. by :
i
PIONEER
DIAGNOSTIC ULTRASOUND
Dr. R. Suresh Mohan
<2Gy
C.K. (b y Md
Date: 2.
Ofo/)
nl
<<
I
W
PealTime (B Mode Ultrasonography of Aldomen :
/
Liver shows homogenous /-&wKe parenchymal echoes.
There is e^/ no hepatomegaly.
IHl'B'RjindC'B'D af&/ not dilated.
(fall ‘Bladder is normal / shorvs calculi
Spleen is
^VU-vtAAa/1
Tancreas appears
‘Botfi f^idneys sfww a normal/ increased echo texture
‘With no evidence / eyidf^ec of calculus
Telvicalycealsystem appears normal/ dilttzd
ProohM' c
/b'b
cy
IMPRESS I (MC.
LKi '
^ S'
(Dr. R. SURESH MOHAN)
72-A3, Mathura Terrace
New Avudi Road
•
Madras - 600 010
•
Phone : 614278
© 6426922, 6426667, 6424710
IT 6426922, 6426667, 6424710
V.K. HOSPITAL
V. K. HOSPITAL
77, Dr. Alagappa Road, Madras - 600 084.
X-Ray, E.C.G. Lab, I.C.C.U., Maternity and Day & Night Emergency Service
77, Dr. ALAGAPPA ROAD, MADRAS-600 084.
/M#<’ pom'nJL
Pfs Name ^r>Paner,rSelvani Age : 24 Sex :
Male
pef.byDr C .Vi^ iKumar, M.lT;,No-; no Date: 27.6.97
arT)
uJK
X - RAY REPORT
CHEST PA VIEW
Heart shows unfolded aorta with L.V.
configuration.
h'
7-
Lung fields appear normal.
1 ■
Bony cage, softtissue and both domed of
diaphragm appear normal.
Radinlnni^t
7 d.rw'rm^130 (^So)
b''
/a^f
PHONE : 6426922
NK V.K. HOSPITAL
6426667
6424710
X-RAY, E.C.G. LAB, I.C.C.U., MATERNITY AND DAY & NIGHT EMERGENCY SERVICES
77, Dr. ALAGAPPA ROAD, CHENNAI - 600 084.
Patient's Name :
Mr. Panner Selvam.
Da,e '■ 27.6.97.
Referred by Dr
C. Vijai Kumar. M.D.,
R. No. :
110
BIO - CHEMISTRY
Blood sugar
Alkaline phosphatase
KA units
KA units
Random
mgms%
Acid phosphatase
Fasting
mgms%
Amylase
Post Prandial
mgms%
Lipase
S.U.
Units / ml
Units /100 ml
jlood Urea
99
mgms%
CPK
Serum Creatinine
9.6
mgms%
Total Bilirubin
mgms%
Serum Uric Acid
mgms%
Direct Bilirubin
mgms%
Serum Cholesterol
mgms%
Indirect BiNrubin
mgms%
Serum Triglycerides
mgms%
Thymol Turbidity
units
Total Proteins
mgms°/o
Icteric Index
units
Albumin / Globulin ratio
mgms%
Prothrombin time
Secs
SCOT
IU
SGPT
IU
Medi^Q^W
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K.S. Hospital, 748, Poonamallee High Road, Kilpauk, Chennai - 10
Phone: 641 2960 / 641 2326
ECHO CARDIOGRAPH'
* :k
** * ********
2«--0b-97
Da re :
Mr«Panner Sei vam»
Name
26 Years.
i!
Ace
M ale.
Sex
ReT :b Y D r C« V i .i a i Kumar.
M.D.
Consultant Physician
Measurements
——■ ~
~ — •—
\
mm
)
” — --
• —•
~
2D
LV
F a r' a s t e r n a 1 S h □ r t axis :
AORTA
Ad i c a 1 F:ou.r- Chamber :
LA
27
RO
35
F' a r a =• t e r- n a J. L o n □ a x i •=■
ROOT
a—
40
25
MFA
RA
45
c:' us*
LA
AU'ATA
43
a.- X-
32
42
M-Fl ODE
AT MV
Mid LV
Th
I VS
11
amp
5
LVd
Th
53
LVs
36
IV S
12
amp
6
LV El-
48
" "'FPLER
_~
~
MITRAL VELOCITY
E/A
PULMONARY FLOW
AORTIC
Th
LPW
=
FLOW
RVd
Th
LPW
0. 85
Fl/SEC.
0.99
M/SEC.
1.29
M/SEC.
10
a mo
11
amp
6
y- Z.
10
COLOR FLOW MAPPING
VIEW
CHAMBER
JET AREA
LESION
sq . cm
M I TRAL REGL1RGI TAT I ON
1.30
so. cm
LA
16.90
MITRAL REGURGITATION
3.30 sa.cm
LA
29.60 so.cm
PSLAX.
A4C.
< P. T. 0)
DIAGNOSTIC RADIOLOGY
ECHOCARDIOGRAPHY
Dr. S. Shanmugasundaram MD., DM
PERIPHERAL DOPPLER
Dr. A. Ramalingam.
MD DMRD DCH
Dr. R. Barath Kumar MD.. DM.
Dr. K.S. Vijayaraghavan
MS . FRCS -ICS
Dr. A. Balaguru MD
DM
nn ERF RE I AT I ON
M-ffiode„
Dod p j. e r
3. nd
Co i o r
11 ow
inane i nu
done.
wore?
M i 1 □ o o n c e? n b r i c I e t t v e? n t r i c u 1 a r h y p e r t r- o p h y +.
Le f t ven t r i c:u 1 a r er 11 a rqernen t +,
Left atrial en 1 arqernen t-f-.
R i p h t v e n t r i c. 1 e a n cl R i n h t a t r i u.m are of normal ditensions.
I n ter
*•
a t r • i a 1 s e o t u. rn a n ci Inter ventricu. 1 ar septu.m are intact.
y s? n t r i c u. 1 a r
i n£ e f t
i n f c? r .1. □ r a n d p os t e r o 1 a t e r a 1 wa 1 1
e x h i b i t rn i 1 ci to inoderate hypok i nes i a at m i ci ven t r i u.c 1 ar reci i ori „
Rest of 1 e f t v e n t r i c i e a n d i n t e r ven t r i c u. 1 a r sep t nm ap p ea rs t e
have normal C £) n t r a c 111 i t y a n d w a J. J. in o v e rn e n t •==■.
M i t r a I va a ve 1 s norma1 i n s t r u c t u r e B
m :i. t • ■ • a 1 y a. 1 y e is normal.
with
-«■
Ao i-1 i c
D :l as to 11 c maYements of
Systol ic: coaptation point appear
.1 eft ven trie le .
1 I"!
/a 1 ve? 5
are norma 1
T r i c u s p j. d y a 1 v e a n d F’ u. 1 m o n a r y •.' a j. y e
in structure and f u.n c: 11 on .
No e ■■■/ i d en c e o f thrombus or per?cardial e f f usion o r' v eo eta11ons-
IMPRESSION
-.x: ™~ “if zr
2
x: ±::
LEFT VENTRICULAR HYF'ERTRDFHV
( HILD )
♦
CONCENTRIC'
*
HYPOKINETIC INFERIOR AND POSTERO LATERAL WALL.
«■
IMPAIRED LEFT VENTRICULAR FUNCTION.
*•
PAP ILLARY MUSCLE DYSFUNCT I ON.
*
MITRAL RECURSI TA TION (MILD
DR.A.DALASURU >
Uma Ciinical Laboraion/ and Endocrinology,/ Cent re
S72. POONAMAILEE HIGH ROAD. MADRAS
PANNEER
MR
ID NUMBER
f.V.l ■'
SEL..VAM
805080
600 Ox 1
£8/06/9'7
Dr C ..VIJA J IUJMAR MD
V..K .. HOSP'I T AL
DESCRI PT’ I ON OF’ TEST
NORMAL
s RESULTS
...
:■ BLOOD BIOCHEMISTRY
CHOLESTEROL
TRIGLYCERIDES
HDL CHOLESTEROL
LDI... CHOLESTEROL
VLDL CHOLESTEROL
■ URINE ANALYSIS
2TT HOURS URINE ANALYSIS
:
;;
::
s
s
150-250 ®g=7.
60 - 160 =115 =-S
806
180
58
130 mgs%
86 mg
NOT GIVEN
TIMINGS . Week Days 7.45 A M. to 8.30 P.M. Sundays 7.45 A M *
’ 2 00 NOON
Uma < luacai Laboratory and Endocrinology Centre
872 POOE’.AMAU IT IIIGH ROAD. MADRAS (x'<)
I -’A MME EF:' SI-J. ./.’AM
RUMEEF ;; SOSMSS
!.;■ n ’•z T /T A i
;
-Tl
I
|
I
30/06/97
KUMAR MD
: r '• r /AL
RESULTS
| lijR! ‘Al.
■I, VC?.4'■ 1 Dt S
I S06 m -sX
; 13B mgs%
150-850 jfiqsK
60 - ‘60 SiC=’-
i ■: //. / • • ' E! "jl.
;■
30
CHEH 1:9 i LEHI
SHU!. ESTEROL
j
130 mqs/'
r/UTUM
SF
TEST
BLOOD BIOCHEMISTRY
■ ! !:
ML0!
?iT
Higs/
:: S6 mgs/
URINE ANALYSIS
84 HOURS UR]ME ANALYSIS
•TH UME
..•'■lA
P8A
DONI
CVERYDAY
s 600 ml/84 hrs
", 4 3 m g s / B 4 h r s
8-7 sqR84 hrs
BLOOD AMMONIA
DONE
everyday
TIMINGS : Week Days 7.45 A.M. to 8.30 P.M. Sundays 7.45 A M
12.00 NTOON
PHONE : 6426922
'XK V.K. HOSPITAL
6426667
6424710
X-RAY, E.C.G. LAB, I.C.C.U., MATERNITY AND DAY & NIGHT EMERGENCY SERVICES
77, Dr. ALAGAPPA ROAD, CHENNAI - 600 084.
Patient's Name :
r.r.
Referred by Dr
Date: 2 j. 0.37
annc' r ■—•C 1 7 .diit
71 j ciy d
R. No. :
ii'i d27/ i• D • t
110
BIO - CHEMISTRY
Alkaline phosphatase
KA units
mgms%
Acid phosphatase
KA units
mgms%
Amylase
mgms%
Lipase
olood Urea
mgms%
CPK
Serum Creatinine
mgms%
Total Bilirubin
mgms%
Serum Uric Acid
mgms%
Direct Bilirubin
mgms%
Serum Cholesterol
mgms%
Indirect BiNrubin
mgms%
Serum Triglycerides
mgms%
Thymol Turbidity
units
Total Proteins
mgms°/o
Icteric Index
units
Albumin / Globulin ratio
mgms%
Prothrombin time
Secs
Blood sugar
Random
Fasting
Post Prandial
120
15 5
SCOT
IU
SGPT
IU
S.U.
Units / ml
Units /100 ml
Medical Officer
© 6426922, 6426667, 6424710
0 6426922, 6426667, 6424710
V. K. HOSPITAL
V. K. HOSPITAL
77, Dr. Alagappa Road, Madras - 600 084.
77, Dr. Alagappa Road, Madras - 600 084.
Date :
Date :
■r^
O)
■ WK
'CUnA-d^
of-t- p __
£
/
C
cWuX __ /
4
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Apollo Hospitals
MICROBIOLOGY
— Towards greater strides In modern medicare
21, Greams Lane, Off. Greams Road, Chennai - 600 006. Phone : 8277447, 8274749
Mr.Panneerselvam
NAME
Age:
26
Sex:
Source of Specimen:
DM31283
Received on:
347
Reported on:
Unit No.
M
Micro No.
Referred by:
Blood
1/7/97
3/7/97
Cl 332
SEROLOGY/IMMUNOLOGY REPORT II
Result
Test
ASO (Anti-Streptolysin-O)
CRP (C-Reoctive Protein)
Latex
RHEUMATOID FACTOR
Rose-Waaler (DAT)
Anti Thyroglobulin
Anti Microsomal
AUTO ANTIBODIES
Anti Sperm
lg A_______
IMMUNOGLOBULINS
IgG
lg rn______
Patient
Total
(Haemolytic)
Control
sc4___
COMPLEMENT
102mg%(Normal:80^180mg%y
7 90»6mg%(Normal:22-80mg%)
VDRL_______________________________
PREGNANCY TEST (Beta-HCG in urine)
TOXOPLASMA
Ab
RUBELLA
CMV_______
Ab____________________
Ab (Cytomegalo Virus)
________________
HSV_______________ Ab (Herpes Simplex Virus)
IgA____________
Ab
TUBERCULOSIS
IgG___________
IgM
Dr. M.A. THIRUNARAYj
Comments
7 Q
—___ ;_____ '___ :____ --
.D.
*1
'
•d
j
■■
■
.
■■
ife 11111
■
5'
•o
\
\
Apollo Hospitals
TRANSPLANTATION
IMMUNOLOGY
- towO'Os gieo'ef strides m modern medicare
21, Greams Lane, Off. Creams Road, Chennai - 600 006. Phone : 8277447/8277059/8277052 Extn. : 2479
NAME :
Age :
Mr Panneer Selvam
26
yrs
Source of Specimen :
Sex :
Male
Blood
Received on : 1/7/97
Unit No.
WatX/'OP
Reported on ;4/7/97
347
m
u
V K Hospital
Referred by :
Lab. No.
1215/97
SCREENING FOR AUTO ANTIBODIES BY INDIRECT IMMUNOFLUORESCENCE
RESULT
TEST
ANTI NUCLEAR ANTIBODY
Hep 2
TISSUE SUBSTRATE
ANTI n DNA
JTI NEUTROPHIL CYTOPLASMATIC ANTIBODY
C - ANCA -
P - ANCA -
ANTI MITOCHONDRIAL ANTIBODY
ANTI SMOOTH MUSCLE ANTIBODY
NEGATIVE
ANTI GBM ANTIBODY
ANTI PARIETAL CELL ANTIBODY
ANF, BY THIS SENSITIVE METHOD IS DITECTED IN A SMALL
PERCENTAGE OF NORMAL ELDERLY INDIVIDUALS, IN NON - IMMUNE DISORDERS
LIKE DIABETES GOUT etc AND IN AUTOIMMUNE DISEASES
Dr. RAMA MANI, M.D.
''K V.K. HOSPITAL
X-RAY, E.C.G., LAB, I.C.C.U., MATERNITY AND DAY & NIGHT EMERGENCY SERVICES
DISCHARGE SUMMARY
SEX: MALE
PATIENT'S NAME: MR.PANNEERSELVAM
AGE:26
DATE OF ADMISSI0N:27.6.97
DATE OF DISCHARGE:1-7.97
DIAGNOSIS
: ACCELERATED HBP / LVF
DYSLIPIDEMIA
ADMITTING DOCTOR:DR.C.VIJAIKUMAR„M.D.,
Patient admitted with C/o. Breathlessness since 3 months.
H/o. Headache +, H/o. Vomiting
H/o. Cough +, H/o- Bilateral
lower limb swelling + H/o. Palpitation+„ H/o. Blurred vision
H/o.
urinary output +.Patient known HT since last September
and was on irregular treatment. Patient in the months o-F
April was Found to have
lipid proFile. Patient has H/o.
acid peptic disease. Not a known DM.
0/E: Patient conscious, G.C.Fair, aFebr ile, No pedal edema.
BP: 250/170mmHg, CVS: S1S2 +, RS: NVBS, Abd: SoFt <,
Epigastric tenderness +.
TREATED WITH:
I.V.FLUIDS:
Inj. Lasix 1 amp iv bd
Tab. Enam lOmg od
Cap. Calcigard 5mg sos
USG ABDOMEN DONE REPORTS ARE
WITH THE PATIENT.
ECHO DONE REPORTS ARE WITH THE PATIENT.
ADDED: Liq. Aludrox 2tsp tds
Stopped. T<.En.am . . q
.
Tab. Calcigard Retard Ibd
Tab. Tenormin 50mg od
77, Dr. Alagappa Road, Madras - 600 084. Phone : 6426922, 6426667, 6424710
28.6.97: Dry cout#?, Strahan’s Road, Madras - 600 012. Phone : 6421451
1
Added:
Stopped plain calcigard
Syp. Linctus codine 3tsp tds
Tab. Askamin H 1 bd
Inj. Ranitidine 1 amp i v st.
30/7/97: Mild Haemoptysis ++.
Antibodies at Apollo.
Suggested: C3C4 ?< Anti &BM
Nephrologist opinion.
SEEN BY DR.M.VIJAIKUMAR.M.D., D.M. ,
HT/Renal Parenchymal1 accelerated.
??AC in ct.,
RF ? CHRONIC
I--severe.
Urine routine , HbsAg,
Suggested: S.Ca,
S . Ca , S.ph.
S.ph..
s.Cr-eatinine ?< Electrolytes.
Repeat Bl.Urea
1/7/97
_______Serum Ca +P04, e
creatinine, at Osker labs
protein, creatinine clearance Hbs g.
INVESTIGATIONS
DONE REPORTS ARE WITH THE PATIENT.
„ A-Febrile, Mild cough
ON DISCHARGE: Patient Conscious
150/120mmHg J.CVS/RS: NADj, Abd: so-Ft .
BP:
THE PRESCRIPTION GIVEN SEPERATELY.
ADVICE: TO FOLLOW
M.D. , AS SUGGESTED.
review
with
dr
.
c
.
vijaikumar
,
TO
*******************
******************
OSLER DIAGNOSTICS PRIVATE LTD
No. 34 Hindi Prachor Sabha Street. T Nagar. Chennai-600 017
Phone
434 6424.
434 5881.
434 7093
Fax 434 5883.
SEX
AGE s 26
NAME. s MR PANEER SELVAN
: M
1675
LAS MO :
REF . BY : DR R VIJAYAKUMAR MD DM
REPORTED ON : 07/07/97
RECEIVED ON : 07/07/97
£< t ocne:M :e s t
v
Normal Values
Findings
320
mg /d 1
15 - 40
: 22.6
mg / d 1
0.6
SODIUM
117
mEq /L
135 -• 148
POTASSIUM
5.4
rnEq /L.
3.5
5.3
S3
rnEq /L
95
105
BICARBONATE
16
mEq /L
22
28
CALCIUM
7.9
mg / d 1
8.1
10.4
PHOSPHORUS
13.1
mg/d 1
2.7
4.5
UREA
CREATININE
CHLORIDE
2
.1.3
S EE FC O L_ O (S V
HBsAg
; NEGATIVE
SxgX<at.ure
OSLER DIAGNOSTICS PRIVATE LTD
No 34 Hindi Prachar Sabha Street. T Nagar Chennai-600 017
Phone
434 6424.
434 5881.
434 7093
Fax 434 5883.
4.
AGE : 26
NAME : MR PANEER SELVAM
SEX : M
1675
REF. BY : DR VIJAYAKUMAR
LAB NO :
RECEIVED ON : 09/07/97
REPORTED ON : 09/07/97
CL I N I CAL.
24 Hours URINE for:-
VOLUME
230
ml/day
PROTEIN
253
mg/day
(NR : 40
150 mg/day)
Signature
&
DETAILS OF TREATMENT AND EXPENSES
HOSPITAL CHARGES :
ROOM 8 BOARD
Name of Patient PuJZdtkZLiO
o
Admitted to hospital on------ lU
_ _ Total Rs__ L^L-Oj?
_2jL—- Days at Rs
__.. -
__ at A
P.M.
Dr,
at A.M.
P.M.
Discharged on-------
_iy__......
OTHER CHARGES
Diagnosis from Records (if injury, give date and place of accident) : ■
Fees of Anaesthalist
j
... and/or Anaesthesia
; Rs_____
x Operating or Delivery Room!
Charges
JRs----------
Laboratory
Rs------
X Ray
Rs------
Operation or obsterical Procedure performed :
Dressing
Rs-----
(Nature and Date describe fully)
Drugs
Rs------
^5.^
a.4i=®)
Rs~...
,_zz&
Rs-----
ECG
Rs_„.
7W4t
TOTAL Rs.
VAN ALLEN
Hospital:
---------Taken from records on----------------------------------------
VAN ALtFN HOSPITAL
______________________ KDOA-heAnAt?96.............. .
SURGEON'S FEES
Patient’s Name: —
Nature of Surgical or obsterical
Procedure (describe) fully.
Charge for this procedure Rs--------Where performed--------- - ----------------
Dated :---- - ----- - -19
_____ 19__
.Date performed------Signed-----
Address------
7 r-Ti;oP^ienL_a^^r^Lwan..
2)
(Operating Surgeon)
...........
__Age
lotal Rs.....
Diagnosis:...................
°n.... «’.............. . ..........10131 Rs... ..... sc"
Consultation on
’ 0 fl
(5 Rs
Total Rs
Consultation on...................................... e
-t................ ’ “Siane*d..............................................................................
Dated :
..................... 19
Address-
^rSStScal if tL^ent is to be ^nJ^T^r dischauje fro^: hospital
D
ote :
2)
i/iISC 176
The form must be completed in every respect.
•AttTty•Trr’g’:PTT,At" •
KDDAIKaN/X
[Vl. U
1>L. «' 1
1.
■
For oihr.o Uh'> only
THE ORIENTAL INSURANCE COMPANY LIMITED
S *
P BEV‘OUS ULA^-’
(Inc or porn tod in Irdia)
{(Viqi-jturotl O«h«:o ■
| CLAIM NO.
PtiPOB* N°-
Employee's Codo
P-yiicv N-.v
Statement of Claim
....
b)
Salary Group
Staff No. I Dept
d)
Covered from..
Employct)'s Nunrra...
I.
b)
Claim made for Husband/wfe/son/daughter/
a)
FatherJmother/brother/Sister
d)
Date of Birth :
c)
[month]
[day]
Yes/No.
Whether employed :
e)
[month]
[day]
Residential Address:
C)
i / H ,• »h ;
Name : .
(in case of child Whether married :
Yes/No.
[year]
If so by whom ?
lf an ACCIDENT involved answer the following :
3.
[ycnrj
AM/PM.
« *;==n.PP.~a r . V.S/NO
a)
b)
Give brief description of the accident..............-..---
_
0)
4.
a)
tvean
[month]
• -'[dayT
b)
additional' medical expense'.
d)
Charges .
.......... ............ ..
a)
as necessary by him.
mRdical benefits or services' provided under am
Did Youor are you
6.
Yes/No.
If "YES" give details of :
a.)
-
s ;. f'o
•
b)
I
••
............. ......................I ;
’
cijimHo
b)
Total Amount of this claim
'
.... -.....
Dated :
-----
19
\
Date..
;l;i.
•Lrs.. ••••.... ■—
”
"•
• XC.Ev .........
. v t .
;
•'
-
,E,.by«... .w.p.
8.
••• v..............
«wi................... ............. .
•
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<
Amount received or due
.
-..........
.
:
. .-t-.o.-.
sl ned......................
w
rue:t -■
' / —
made without any reservatior
Employee)
... , .
Important:
•i-
DETAILS OF TREATMENT AND expenses
HOSPITAL CHARGES :
ROOM Er BOARD
Total Rs—
__.J?C..Days at Rs
Age JIS'—
Name of Patient A...
7.0’q-
Admitted to Hospital on------
Discharged on—1-------
_____ at A,M_
P.M.~
OTHER CHARGES
Diagnosis from Records (if injury, give date and place of accident) :
Operating or Delivery Rooml
Charges
f Rs--------------------------------------
___________ _ _ __________________________
____ ___ /-----
Laboratory _
...
Operation or obsterical Procedure performed :
(Nature and Date describe fully)
-
-
X Ray _ . .
________
:
___
Rs__________ _______ _____
Dressing
Drugs;-. •
Oxygen
ECG
BMR
. .-.rs_.A^A_j_S-C__
Rs______________________
Rs J_______________ ___
Rs______________________
TOTAL Rs.
------ Address.
Takerufa^ records on---------------------------------- U_U*-O >• — IS^'i
.^BUg^bNTs FEES
"Patient's Name:1--
7T
---------------- -*■-- ------- --
Sjgned by_V^^akg
Signed
___ oa-os
...Signed---------
19
Address—
X
(Operating Surgeon)
_ Age—2LSZ----
CONSULTATION
Name of Patient----Diagnosis :
/
Consultation on
'
.
r................................... RS....3Q.........................
@ Rs
Signed
. fl. J.
3
D.,.d ,...->./a.o
........ »
.Total Rs...^£l.;..Q0.............
Total Rs
........
.Total Rs
@ Rs
.................................................................
Consultation on........
;
:teodi
.............
-
ry^ian)
-
Patient has been found fit on
.................. ...................... .............. ....................... (VIC~~ASSIb! ANT
-- ------ 1} p|ease indicate if treatment is to be continued after discharge from the hospital
2)
5C 176
'• T
______ 19—
Date performed----------
Charge for this procedure Rs_
Where performed--------------------
•
.• (HospifaVAupa^mes;
__ _ _ _ ___ _—7r-1p*rTHJCR
Nature of Surgical or obsterical
Procedure (describe) fully.
Consultation on
--------- Rs -
- - - ■ - Rs _
....------------------- -
Dated :--------------
?
) Rs.
Fees of Anaesthalist
and/or Anaesthesia
________ ____________ ________ —_________
The form'must be completed in every respect.
MADURA
-
s» •
Phone
55 49 12 to 16
522 52 3S
522 52 55
Fax No. :
• tDUCaro iJJ
91-44-55 49 is
DIABETES RESEARCH CENTRE
AND
M. V. HOSPITAL FOR DIABETES
4, Main Road, (West Mada Church Street)
ROYAPURAM, MADRAS-600013. /
I
L '.'ecicf
Pref. M. VISWANATHAN,
Dale
M.D., Fjk.M.S.
Deputy Dirt etc rs ;
Dr. A. RAMACHANDRAN,
Ph.D.
M.D.,
Dr. VIJAY VISWANATHAN,
M.D.,
Secretary ;
Mr. ARUN VISWANATHAN
Department of Biocfiemrstry ;
Dr. Mrr. C. SNEHALATHA?
M.Sc., C.Sc. J
r /-I ved of :f,C
T/>»»v.T‘t.7r/'
;
Mr. A. PANOiAN, B.Sc.
Mr. R
StKh'AR. E.Sc.
V
*1r. J. VENUGCPAL, B.Sc.
//
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Pott-Doctoral Reiserch Associate:
)7 L SUSHEELA. M?Scm Ph.D.
Of>ertrr
of Diabetes Education ;
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1
« R. w.OBHAnX'mLa.
(Head of the Dept. & Asst. Director)
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Av42i
Dept, of Dlefietic Kidney Disene :
t F Al ROZA BA..U, B.Sc.,
'
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Dept, of Medtcef Records ; j
«. NIRMALA
. MEENA
^•pt. of Prevention :
P. SHYAMALA. B.Sc., D.N.D.
T. ANNIE JOSEPH. B.Sc., D.N.D.
SEENA VERGHESE. 8.A.
A. SAOHANA. B.Sc., D.N.D.M.
M. PADMAVATHY. B.Sc..
artment of Dietetics & Nutrftion ; J
INDIRA PADMALAYAM, M.Sc.,
feed of the Dept. & Asst. Director)
SHEELA PAUL B Sc.. D.N.D.
VANAJA VIJAYAKUMAR. B.Sq.,
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522 52 55
91-44-55 49 19
DIABETES RESEARCH CENTRE
REStARCH /ztS EDUCATION IE
AND
M. V. HOSPITAL FOR DIABETES
4, Main Road, (West Mada Church Street)
ROYAPURAM, MADRAS-600 013.
| Director ;
Prof. M. VISWANATHAN,
i
Deputy Directors :
Daie.^'^r^.
£' -•. / 7 3.
M.D., F.A.M.S.
’
Dr. A. RAMACHANDRAN,
f) Pr
M.D., M.NJX.M.S., Ph D.
4^. 73
<c<.
. Co /"/
Dr. VIJAY VISWANATHAN,
M.D.,
Secretary :
cL( S
■
^Ir. ARUN VISWANATHAN
CCK'V/'i
; Department of Biochemistry :
Dr. Mrs. C. SNEHALATHA.
M.Sc., D.Sc.
(Head of the Department)
Mr. A. PANDIAN, B.Sc.
4g,—</k.
Mr. R. SEKHAR, B.Sc.
Mr* J. VENUGOPAL. B.Sc.
! Post-Doctoral Research Associate:
$ 6W
Dr? L. SUSHEELA, M.Sc., Ph.D.
Department of Diabetes Education : :
J
U/
Mrs. R. SHOBHANA, M.A.
(Head of the Dept. & Asst. Director)
I Dept, of Diabetic Kidney Disease : I
44
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Mrs. FAIROZA BANU, B.Sc.,
.4X0
ept. of Medical Records : |
I_________ ____
Mrs. NIRMALA
B l Q^.
C'\
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Ms. MEENA
.
Dept, of Prevention :
Ms. P. SHYAMALA, B.Sc., D.N.D.
Ms. T. ANNIE JOSEPH, B.Sc., D.N.D.
Ms. SEENA VERGHESE, B.A.
Ms. A. SADHANA, B.Sc., D.N.D.M.
Ms. M. PADMAVATHY, B.Sc.,
[ Department of Dietetics & Nutrition :
Mrs. INDIRA PADMALAYAM, M.Sc.,
(Head of the Dept. & Asst, Director)
Mrs. SHEELA PAUL B.Sc., D.N.D.
Mrs. VANAJA VIJAYAKUMAR, B.Sc.,
Mrs. PRABHA J. RATCHAGAN, M.Sc.,
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MEDICAL OFFICER'S
RESIDENCE 4254
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VAN ALLEN HOSPITAL
KODAIK ANAL
-f --jZ.'
KODAIKA»AL
28.02.94
From
A, RATHMARAJIASEELAS,
S/0. S.l. A.ANDARAJ,
AATTUVAM IATTI COLONY,
ATTUVAH PATTI,
KODAIKANAL.
T»: TiD? MANAGER,
.PONDS (INDIA) LT ITED,
THERMO METER DIVISION,
ST.MARY'S RC-.D,
KODAIKL.AL.
Respected Sir,
medical treatment.
I an taking
As my health conditio;) is not well.
Sir, I a>a anable to coot! .ue my service in your company,
So I am resi :gning my Job effected from 28.02.94.
Kindly accent >«y resinpuation and
Sir,j 1 request y u te
realive me from u*y Service, (From 28.02.94) as iOt early as
possible.
Tn««king you.
Yours faithful.y
(A o RATrUA ;<AtaASj^sLA^ )
■Pond's (India) Limited
THERMOMETER DIVISION
Mount St. Mary, St. Mary’s Road, Kodaikanal-624 101
Phone : (4542) 40520/40521
•
Fax : (4542) 41288
March 1 ,
7o
■1994
Mr.A.Rathnar.-ijascelan
T.No. 164
KODAIKANAL.
Dear Sir,
With reference to your le.tter of resignation dated E8.0P.94
we accept your letter of resignation with regret and relieve
you from our s e r v i c e s with immediate effect.
Your accounts will be settled separately.
With best wishes.
Very truly yours
FOR POND’S EIND1A3 LIMITED
R .GOPALAKF.’ JSHNAN
OPERATIONS MANAGER
THERMOMETER DIVISION
MN:
REGISTERED OFFICE: 26, C-IN-C ROAD, MADRAS 600 105/MAIL: P.O. BOX NO. 6809, MADRAS-600 105
CABLE : VASOPONDS MADRAS ■ TELEX : 41-7382 ■ FAX : (44) 6266551
• TEL EPHON E : 6277533
Pond’s (India) Limited
THERMOMETER DIVISION
Mount St. Mary, St. Mary's Road, Kodaikanal-624 101
Phone : (4542) 40520/40521
•
Fax : (4542) 41288
APRIL 12, •1994
SERVICE CERTIFICATE
:
Name
Date
of
01.07.85
, i! ■ i 11 j n g
:
Designation
Mr . A.Ralhnara j a.see lan
Production Operator
Date of leaving
: 01.03.94
Reason for leaving
: RESIGNED
Last drawn wages
: Rs. 1490.50 (Including allowances)
Conduct and
:
character
Satisfactory
R .GOPALAKRISI !NAN
OPERATIONS MANAGER
/'iR
REGISTERED OFFICE : 26. C-IN-C ROAD. MADRAS 600 105/MAIL: P.O. BOX MO. 6809, MADRAS-600 105
CABLE : VASOPONDS MADRAS ■ TELEX : 41-7382 • FAX : (44) 8268581 ■ TELEPHONE : 8277533
7/2/01 10:19 AM
1 of 6
FXv Methods for monitoring mercury exposure
TYPES OF MERCURY
There are three important types ofmercuty:
1. The pure element,
2. Inorganic compounds (such as mercuric chloride) and
3. Organic mercury compounds (such as phenyl mercuric propionate).
Each type poses a different health hazard.
Elemental mercury is a liquid and gives off mercury vapor at room temperature. This vapor can be inhaled
into the lungs and passed into the blood stream. Elemental mercuiy can also pass through the skin and into the
blood stream. If swallowed, however, this form of mercury is not absorbed out of the stomach, and usually
passes out of the body without harm.
Inorganic mercury compounds can also be inhaled and absorbed through the lungs, and may pass through the
skin. But the compounds can also be absorbed through the stomach if swallowed. Many inorganic mercury
compounds are irritating or corrosive to the skin, eyes and mucus membranes as well.
Organic mercury compounds can enter the body readily through all three routes-lungs, skin and stomach.
ACUTE HEALTH EFFECTS
Veiy high exposures to mercuiy vapor in the air can cause acute poisoning. Symptoms usually begin with
cough, chest tightness, trouble breathing and upset stomach. This may go on to pneumonia, which can be fatal.
If tlie inorganic mercuiy compounds are swallowed, nausea, vomiting diarrhea and severe kidney damage can
occur.
CHRONIC HEALTH EFFECTS
Exposure to any form of mercury on a repeated basis, or even from a single, very high exposure can lead to the
disease of chronic mercuiy poisoning. There are three main symptoms:
1. Gum problems. The gums become soft and spongy, the teeth get loose, sores may develop, and there may
be increased saliva.
2. Mood and mental changes. People with chronic mercury poisoning often have wide swings of mood,
becoming irritable, frightened, depressed or excited very7 quickly for no apparent reason. Such people
may become extremely upset at any criticism, lose all self-confidence, and become apathetic.
Hallucinations, memory loss and inability to concentrate can occur.
3. Nervous system. The earliest and most frequent symptom is a fine tremor (shaking) of the hand. A
tremor may also occur in the tongue and eyelids. Eventually this can progress to trouble balancing and
walking.
OTHER HEALTH EFFECTS
There are a number of other symptoms that may be caused by exposure to mercury7 and mercuiy-containing
compounds.
* A skin allergy may develop. If this happens, repeated exposure causes rash and itching.
• Exposure to mercury vapor can cause the lens of the eye to discolor.
2 of 6
7/2/01 10:19 AM-
Fw: Methods for monitoring mercury exposure
• Some of the inorganic mercury compounds can cause bums or severe irritation of the skin and eyes on
contact.
EFFECTS ON THE REPRODUCTIVE SYSTEM
Some organic mercuiy compounds (methylmercury) are known to cause birth defects in children bom of
exposed mothers. It is not known whether inorganic compounds or elemental mercury have this effect.
TESTS FOR MERCURY EXPOSURE
There are two tests available to measure mercury in the body:
The Mercury Blood Test measures exposure to all three types of mercury, but because mercury remains in tlie
bloodstream for only a few days after exposure, the test must be done soon after exposure. Most non-exposed
people have mercury levels of 0 to 2 (all blood measurements are in micrograms of mercury per deciliter of
blood, or ug/dl). Levels above 2.8 ug^dl are required to be reported to the Health Department. This test can be
influenced by eating fish, because fish (particularly certain deep sea fish) may contain mercury.
The Urine Mercury Test only measures exposure to elemental and inorganic mercuiy. Organic mercury is not
passed out the body in the urine and thus cannot be measured this way. A person with no exposure to mercury
would probably have a urine mercury level of 0 to 20 ug/L. The Health Department requires reporting of
levels above 20.
APPENDIX
RECOMMENDED MEDICAL MONITORING FOR WORKERS EXPOSED TO METALLIC AND
INORGANIC MERCURY
Medical monitoring is the periodic evaluation of exposed workers to insure that they are experiencing no
adverse effects of potentially hazardous workplace exposures. It serves as back- up for a program of routine
air and biologic monitoring, which are the primary means for insuring that exposure levels are below those
associated with adverse health effects. A medical monitoring program should be designed to detect adverse
effects of exposure as early as possible, at a stage where they are still reversible, so that exposures can be
controlled and serious permanent adverse effects prevented.
Baseline and periodic examinations
.An initial medical examination should be performed on all employees exposed to potentially hazardous levels
of mercury. The purpose of this examination is to provide a baseline for future health monitoring.
The examination should include a complete medical history' and symptom questionnaire, with emphasis on the
nervous system (target organ for chronic exposure), the kidneys (target organ for acute and chronic exposure),
the oral cavity (target organ for chronic exposure), the lungs (target organ for acute exposure), the eyes
(affected by chronic exposure), and the skin (since mercuiy is a known skin sensitizer). Signs and symptoms of
file earliest signs of mercury intoxication should be elicited; these include personality changes, weight loss,
irritability, fatigue, nervousness, loss of memory, indecision, and intellectual deterioration. Complaints of
tremor and loss of coordination should also be sought. Physical examination should focus on the target organs
described above. A baseline handwriting sample should be obtained. Laboratory evaluation should include at
minimum a complete urinalysis (see below).
This examination should be repeated annually. ‘Results should be compared with the findings on the baseline
examination for changes suggestive of mercuiy toxicity. Handwriting samples should be compar ed to the
baseline sample for evidence of tremor. Interim evaluations should be conducted if symptoms suggestive of
mercury intoxication are occurring.
3 of 6
7/2/01 10:25 AM
Fw: Methods for monitoring mercury exposure
Confidentiality of Medical Information
Questionnaire and physical examination results for periodic examination should be compared to the baseline
examination to detect any change which might be attributed to mercury intoxication. The results should be
conveyed in detail to the worker, fhe employer should be informed by the examining physician if mercury
intoxication is suspected on the basis of symptoms or results of the physical examination or laboratory tests. If
intoxication is suspected, the worker should be removed from exposure and expert medical consultation
should be sought. Otherwise, the results of the physical exam should be kept confidential, and no management
personnel other than health professionals should have access to the medical records.
Importance of evaluating group results
The results of the questionnaire and physical examination should also be evaluated on a group basis. This is
important because early mercury poisoning might cause only very mild, clinically insignificant increases in
symptomatology in each individual which, when seen in the aggi egate, might provide an important clue that
toxic exposure to mercury is taking place.
Who should perform the medical examinations
All medical monitoring of exposed employees should be conducted by a physician knowledgeable in
occupational medicine. In particular, interpretation of the group data should be undertaken only by a trained
occupational health physician or other physician with expertise in performing such analyses.
Using more sensitive medical tests
Several studies have shown that some special tests may be useful in detecting early signs of mercury toxicity.
Neurobehavioral tests, designed to detect early changes in concentration, response time, memory, and
hand-eye coordination, can be usefill on both an individual and a group basis in detecting early nervous system
effects of mercury exposure.
Early kidney damage may be detected by looking for the presence of low molecular weight proteins in the
urine. The presence of these proteins in the urine indicates that kidney damage has occurred long before a
routine urinalysis indicates an abnormality. Beta2 microglobulin and N-acetyl-B-D glucosaminidase (NAG)
are two of the proteins which can be measured in the urine. The tests are useful on both an individual and
group basis.
These special tests should be arranged and interpreted by a trained occupational physician or other physician
with special expertise in these areas.
BIOLOGIC MONITORING
Biologic monitoring is the measurement of an chemical agents in the blood, urine, or other body tissue of
exposed individuals to determine how much of the chemical has been absorbed into the body. It selves as a
back-up to environmental exposure measurements, since air measurements cannot assess skin exposure or the
effects of protective equipment and work practices. Since it measures the amount of an agent actually absorbed
into the body, it is usually a better estimate of risk for adverse health effect than air monitoring.
Tliere is no ideal biologic monitor for evaluating the risks of mercury intoxication from metallic or inorganic
mercury. Mercury can be measured in both blood and urine. Individual levels may vary greatly from day to
day and even within a given day. While proper interpretation of the results can be difficult, the measurements
can nevertheless provide information on potential overexposure. Measurements should be carried out
regularly (several times per year) in chronically exposed workers, and individual as well as group results
should be evaluated. Baseline levels should be obtained before exposure begins for comparison purposes.
Mercury in Urine
of 6
7/2/01 10:25 AM
Fw Methods for monitoring mercury exposure
Measurement of mercury’ in urine is the recommended biologic monitor for workers exposed to metallic and
inorganic mercury. Ideally, the collection should be over 24-hours, but this is seldom feasible. Spot urine
samples may also be taken, but care must be taken to always collect them at the same time of day near the end
of the work week after several montlis of steady exposure. Overnight samples may also be collected; this
collection extends from the time the employee goes to bed through the first urination of the morning.
Samples must be collected in containers provided by the laboratory, since a preservative must be added. At
least 25 cc of urine must be collected. Great care must be taken to prevent contamination of the sample
containers or the urine with mercury1 from the skin or workplace air.
When results are interpreted, the urine values should be corrected for grams of creatinine in the sample, and
should be expressed as ug Hg/gram creatinine. In persons not occupationally exposed to mercury, urine levels
rarely exceed 5 ug/g creatinine.
Vvliile many laboratories indicate that only levels above 150 ug/L should be considered toxic, there is strong
vidence that early signs ot mercury intoxication can be seen in workers excreting more than 50 ug Hg/L of
urine (standardized for a urinary’ creatinine of 1 gram/L). This value of 50 ug/g creatinine is proposed by many
experts as a biological threshold limit value for chronic exposure to mercury vapor, and in 1980 this was
endorsed by a World Health Organization study group.
Exposed individuals with levels above 50 ug/g creatinine should be placed in anon-exposed job until the
reason for their overexposure has been identified and corrected and their urine levels have fallen below the
biologic threshold limit value.
Mercury in blood
The concentration of mercury in blood reflects exposure to organic mercury as well as metallic and inorganic
mercury; thus it can be influenced by the consumption offish containing methylmercury.
Samples should always be taken at the same time of day near the end of the work week after several months of
steady exposui e. The blood should be collected in mercury-free heparinized tubes after cai eful skin cleansing.
In unexposed individuals, the amount of mercury in blood is usually less than 2 ug/100 ml. According to some
experts, an average airborne concentration of 50 ug/m3 corresponds to a mercury concentration in blood of
about 3-3.5 mg/100 ml. Early effects of mercury toxicity have been found when the blood concentration
exceeds 3 ug/100 ml. Any worker exceeding this level should be placed in anon-exposed job until dietary’ and
workplace exposures have been evaluated and blood levels have relumed to baseline.
Removing Employees fi om Exposui e
An individual who must be removed from mercury exposure because of elevated blood or urine mercury'
levels or physical examination results suggesting early mercury' intoxication should be given alternative work
with no exposure. His or her wages, benefits and seniority should be maintained. No employee should be
terminated or otherwise punished because of overexposure to mercuiy.
In the event that no job without mercury exposure is available, tl]e employee may continue to work using a
supplied air respirator, provided that biological monitoring results and/or symptoms display a satisfactory
decline over time:
New Jersey State Department of Health
Division of Occupational and Environmental Health
ON 360. Room 706
Trenton NJ 08625-9972
(609) 984-1863
7/2/01 12:03 PM
5 of 6
* ‘
V
Fw Methods for monitoring mercury exposure
to
Safety Trnivmg Hor^p. Page
Name: mercury.htm
Type: Hypertext Markup Language (text/html)
; PHmercinyhtm
Encoding: quoted-printabk
•' of 6
7/2/01 12:03 PM
7/2/01 11:44 AM
’ rf
Mercury
OTHER HEMTH EFFECTS
There are a number of other symptoms that may be caused by exposure to mercury and mercury-containing
compounds.
• A skin allergy' may develop. If this happens, repeated exposure causes rash and itching.
• Exposure to mercury vapor can cause the lens of the eye to discolor
• Some of the inorganic mercury' compounds can cause bums or severe irritation of the skin and eyes on
contact.
EFFECTS ON THE REPRODUCTIVE SYSTEM
Some organic mercurv compounds (methylmercury') are known to cause birth defects in children bom of
exposed mothers. It is not known whether inorganic compounds or elemental mercury' have this effect.
'ESTS FOR. MER.CURY EXPOSURE
There are two tests available to measure mercury in the body:
t he Mercury Blood l est measures exposure to all three types of mercury', but because mercury remains in the
bloodstream for only a few days after exposure, the test must be done soon after exposure. Most non-exposed
people have mercury levels of 0 to 2 (all blood measurements arc in micrograms of mercury per deciliter of
blood, or ug/dl). Levels above 2.8 ug/dl are required to be reported to the Health Department. This test can be
influenced by eating fish, because fish (particularly certain deep sea fish) may contain mercury.
The Urine Mercury Test only measures exposure to elemental and inorganic mercury. Organic mercury is not
passed out die body in the urine and thus cannot be measured this way. A person with no exposure to mercury
would probably have a urine mercury level of 0 to 20 ug/L. The Health Department requires reporting of
levels above 20.
APPENDIX
RECOMMENDED MEDICAL MONITORING FOR WORKERS EXPOSED TO METALLIC .AND
INORGANIC MERCURY
Medical monitoring is the periodic evaluation of exposed workers to insure that they are experiencing no
adverse effects of potentially hazardous workplace exposures, ft serves as back- up tor a program of routine
air and biologic monitoring, which are the primary means for insuring that exposure levels are below those
associated with adverse health effects. A medical monitoring progi am should be designed to delect adverse
effects of exposure as early as possible, at a stage where they are still reversible, so that exposures can be
controlled and serious permanent adverse effects prevented.
Baseline and periodic examinations
An initial medical examination should be performed on all employees exposed to potentially hazardous levels
of mercury. The purpose of this examination is to provide a baseline for future health monitoring.
The examination should include a complete medical history and symptom questionnaire, with emphasis on the
nervous system (target organ for chronic exposure), the kidneys (target organ for acute and chronic exposure),
the oral cavity (target organ for chronic exposure), the lungs (target organ for acute exposure), the eyes
(affected by chronic exposure), and the skin (since mercury is a known skin sensitizer). Signs and symptoms of
the earliest signs of mercury intoxication should be elicited; these include personality changes, weight loss,
2 sfS
7/2/01 11:44 AM
Merciirv
irritability, fatigue, nervousness, loss of memory, indecision, and intellectual deterioration. Complaints of
ti'emor and loss" of coordination should also be sought. Physical examination should focus on the target organs
described above. A baseline handwriting sample should be obtained. Laboratory evaluation should include at
minimum a complete urinalysis (see below)
t his examination should be repeated annually. Results should be compared with the findings on the baseline
examination for changes suggestive of mercury toxicity. Handwriting samples should be compared to the
baseline sample fur evidence of tremor. Interim evaluations should be conducted ii symptoms suggestive of
mercury intoxication are occurring.
Confidentiality of Medical Information
Questionnaire and physical examination results for periodic examination should be compared to the baseline
examination to detect any change which might be attributed to mercuiy intoxication. The results should be
conveyed in detail to tlie worker. The employer should be informed by the examining physician if mercuiy
intoxication is suspected on the basis of symptoms or results of the physical examination or laboratory tests. If
toxication is suspected, the worker should be removed from exposure and expert medical consultation
should be sought. Otherwise, the results of the physical exam should be kept confidential, and no management
personnel other than health professionals should have access to the medical records.
Importance of evaluating gi oup results
The results of the questionnaire and physical examination should also be evaluated on a group basis. This is
impoitant because early mercury poisoning might cause only very mild, clinically insignincant increases in
symptomatology in each individual which, when seen in the aggregate, might provide an important clue that
toxic exposure to mercuiy is taking place.
Who should perform the medico! examinations
All medical monitoring ot exposed employees should be conducted by a physician knowledgeable in
occupational medicine' In particular, interpretation oftlie group data should be undertaken only by a trained
occupational health physician or oilier physician with expertise in performing such analyses.
Using more sensitive medical tests
Several studies have shown that some special tests may be useful in detecting early signs of mercury toxicity.
Neurobehavioral tests, designed to detect early changes in concentration, response time, memory, and
hand-eye coordination, can be useful on both an individual and a group basis in detecting early nervous system
effects of mercury exposure.
Early kidney damage may be detected by looking for the presence of low molecular weight proteins in the
urine. The presence of these proteins in the urine indicates that kidney damage has occurred long before a
routine urinalysis indicates an abnormality Beta? microglobulin and N-acetyl-B-D glucosaminidase (NAG)
arc two of the proteins which caii be measured in the urine. The tests are useful on both an individual and
group basis.
These special tests should be an tinged and imci pi cted by a trained occupational physician or other physician
with special expertise in these areas.
BIOLOGIC MONI i ORiNG
Biologic monitoring is the measurement of an chemical agents in the blood, urine, or other body tissue of
exposed individuals to determine how much of the chemical has been absorbed into the body. It serves as a
back-up to environmental exposure measurements, since air measurements cannot assess skin exposure or the
effects of protective equipment and work practices. Since it measures the amount of an agent actually absorbed
7/2/01 11:41 AM
! of 2
•i
Mercury
New Jersey State Department of Health
Division of Occupational and Environmental Health
THE HEALTH EFFECTS OF MERCURY
TYPES OF MERCURY
There are three important types of mercury7:
1. The pure element.
2. Inorganic compounds (such as mercuric chloride) and
3. Organic mercury compounds (such as phenyl mercuric propionate).
Each type poses a different health hazard.
Elemental mercuiy is a liquid and gives off mercury vapor at room temperature. This vapor can be inhaled
into the lungs and passed into the blood stream. Elemental mercury can also pass through the skin and into the
blood stream. If swallowed, however, this form of mercury is not absorbed out of the stomach, and usually
passes out of the body without harm.
Inorganic mercury compounds can also be inhaled and absorbed through the lungs, and may pass through the
skin. But the compounds can also be absorbed through tlic stomach if swallowed. Many inorganic mercury
compounds are irritating or corrosive to the skin, eyes and mucus membranes as well.
Organic mei ciuy compounds can enter the body l eadily through all tlu ee routes-lungs, skin and stomach.
ACUTE HEALTH EFFECTS
7eiy high exposures io meiuuiy vapor in the air can cause acute poisoning. Symptoms usually begin with
cough, chest tightness, trouble breathing and upset stomach. This may go on to pneumonia, which can be fatal.
if the inorganic mercury compounds are swallowed, nausea, vomiting diarrhea and severe kidney damage can
occur.
CHRONIC HEALTH EFFECTS
Exposure to any form of mercury on a repeated basis, or even from a single, very high exposure can lead to the
disease of chronic mercury poisoning. There are three main symptoms:
1. Gum problems. The gums become soft and spongy, the teeth get loose, sores may develop, and there may
be increased saliva.
2. Mood and mental changes. People with chronic mercury poisoning often have wide swings of mood,
becoming irritable, frightened, depressed or excited very quickly for no apparent reason. Such people
may become extremely upset at any criticism, lose all self-confidence, and become apathetic.
Hallucinations, memory loss and inability to concentrate can occur.
3. Nervous system. The earliest and most frequent symptom is a fine tremor (shaking) of the hand. A
tremor may also occur in the tongue and eyelids. Eventually this can progress to trouble balancing and
walking.
7/2/01 11:47 AM
of 5
Mercury
into the body , it is usually a better estimate of risk for adverse health effect than air monitoring.
There is no ideal biologic monitor for evaluating the risks of mercury intoxication from metallic or inorganic
mercnrv Mercutv can be measured in both blood and urine. Individual levels may vary greatly from day to
day and even within a given day. V?nilc proper interpretation of the results can be difficult, the measurements
can nevertheless provide information on potential overexposure. Measurements should be carried out
rA<mlarly (several times per year) in chronically exposed workers, and individual as well as group results
'should be evaluated. Baseline levels should be obtained before exposure begins for comparison purposes.
Mercury in LTine
^Measurement of mercurv in urine is the recommended biologic monitor for workers exposed to metallic and
inorganic mercury. Ideally, the collection should be over 24-hours, but this is seldom feasible. Spot urine
samples mav also be taken, but care must be taken to always collect them at the same time of day near the end
erf the work week after several months of steady exposure. Overnight samples may also be collected; this
collection extends horn the time ilie employee goes to bed through Hie first urination of the morning.
Samples must be collected in containers provided by the laboratory7, since a preservative must be added. At
ast 25 cc of urine must be collected. Great care must be taken to prevent contamination of the sample
containers or the urine with mercury from the skin or workplace air.
When results are interpreted, the urine values should be corrected for grams of creatinine in the sample, and
should be expressed as ug Hgzgram creatinine. In persons not occupationally7 exposed to mercury7, mine levels
rarely exceed 5 ug/g creatinine.
VtTiile many laboratories indicate that only7 levels above 150 ug/L should be considered toxic, there is stiong
evidence that early signs of mercurv intoxication can be seen in workers excreting more than 50 ug Hg/L of
urine (standardized for a urinary7 creatinine of 1 gram/L). This value of 50 ug/g creatinine is proposed by mdny
experts as a biological threshold limit value for chronic exposure to mercury vapor, and in 1980 this was
endorsed by a World Health Organization study eroup.
Exposed individuals with levels above 50 ug/g creatinine should be placed in anon-exposed job until the
reason for their overexposure has been identified and corrected and their urine levels have fallen below the
biologic threshold limit value.
/Ter'cury m b!«n<!
The concentration oi mercurv in blood reflects exposure to organic mercury as well as metallic and inorganic
mercuiy; thus it can be influenced by the consumption offish containing methylmercury.
Samples should alwavs be taken at the same time of day near the end of the work week afler several months of
steady exposure. The blood should be collected in mercuiy-free heparinized tubes after careful skin cleansing.
Tn unexposed individuals, the amount of mercury in blood is usually less than 2 ug/100 ml. According to some
experts, an average airborne concentration of 50 ug/m3 corresponds to a mercury concentration in blood of
about 3-3.5 mg/100 ml. Early effects of mercury toxicity have been found when the blood concentration
exceeds 3 ug/100 ml. .Any worker exceeding this level should be placed in a non-exposed job until dietary and
workplace exposures have been evaluated and blood levels have rctunicd io baseline.
Removing Employees from Exposure
An individual who must be removed from mercury’ exposure because of elevated blood or urine mercury
levels or physical examination results suggesting early mercury intoxication should be given alternative work
with no exposure. His or her wages, benefits and seniority should be maintained. No employee should be
terminated or otherwise punished because of overexposure to mercury7.
■. 5,f «
7/2/01 11:47AM
Mercury
In the event that no job without mercury exposure is available, the employee may continue to work using a
supplied air respirator, provided that biological monitoring results and/or symptoms display a satisfactory
decline over time.
New Jersey State Department of Health
Division of Occupational and Environmental Health
CN 360, Room 706
Trenton NJ 08625-9972
(609) 984-1863
pgj
EIIS
Page
£-
Mercurv
New Jersey State Department of Health
Division of Occupational and Environmental Health
THE HEALTH EFFECTS OF MERCURY
MI-
TYPES OF MERCURY
There are three important types of mercury:
1. The pure element,
2. Inorganic compounds (such as mercuric chloride) and
3. Organic mercury compounds (such as phenyl mercuric propionate).
Each type poses a different health hazard.
Elemental mercury is a liquid and gives off mercury vapor at room temperature. This vapor can be inhaled into
the lungs and passed into the blood stream. Elemental mercury can also pass through the skin and into the blood
stream. If swallowed, however, this form of mercury is not absorbed out of the stomach, and usually passes out
of the body without harm.
Inorganic mercury compounds can also be inhaled and absorbed through the lungs, and may pass through the
skin. But the compounds can also be absorbed through the stomach if swallowed. Many inorganic mercury’
compounds are irritating or corrosive to the skin, eyes and mucus membranes as well.
Organic mercury compounds can enter the body readily through all three routes-lungs, skin and stomach.
ACUTE HEALTH EFFECTS
Very high exposures to mercury vapor in the air can cause acute poisoning. Symptoms usually begin with cough,
chest tightness, trouble breathing and upset stomach. This may go on to pneumonia, which can be fatal.
If the inorganic mercury compounds are swallowed, nausea, vomiting diarrhea and severe kidney damage can
occur.
CHRONIC HEALTH EFFECTS
Exposure to any form of mercury on a repeated basis, or even from a single, very high exposure can lead to the
disease of chronic mercury poisoning. There are three main symptoms:
1. Gum problems. The gums become soft and spongy, the teeth get loose, sores may develop, and there may
be increased saliva.
2, Mood and mental changes. People with chronic mercury poisoning often have wide swings of mood,
becoming irritable, frightened, depressed or excited very quickly for no apparent reason. Such people may
become extremely upset at any criticism, lose all self-confidence, and become apathetic. Hallucinations,
memory loss and inability to concentrate can occur.
3. Nervous system. The earliest and most frequent symptom is a fine tremor (shaking) of the hand. A tremor
may also occur in the tongue and eyelids. Eventually this can progress to trouble balancing and walking.
s
Mercury
OTHER HEALTH EFFECTS
There are a number of other symptoms that may be caused by exposure to mercury and mercury-containing
compounds.
• A skin allergy may develop. If this happens, repeated exposure causes rash and itching.
• Exposure to mercury vapor can cause the lens of the eye to discolor.
• Some of the inorganic mercury compounds can cause bums or severe irritation of the skin and eyes on
contact.
EFFECTS ON THE REPRODUCTIVE SYSTEM
Some organic mercury compounds (methylmercury) are known to cause birth defects in children bom of exposed
mothers. It is not known whether inorganic compounds or elemental mercury7 have this effect.
TESTS FOR MERCURY EXPOSURE
There are two tests available to measure mercury in the body:
The Mercury Blood l est measures exposure to all three types of mercury, but because mercury remains in the
bloodstream for only a few days after exposure, the test must be done soon after exposure. Most non-exposed
people have mercury levels of 0 to 2 (all blood measurements are in micrograms of mercury per deciliter of
blood, or ug/dl). Levels above 2 .8 ug/dl are required to be reported to the Health Department. This test can be
influenced by eating fish, because fish (particularly certain deep sea fish) may contain mercury7.
The Urine Mercury Test only measures exposure to elemental and inorganic mercury. Organic mercury is not
passed out the body in the urine and thus cannot be measured this way. A person with no exposure to mercury
would probably have a urine mercury level of 0 to 20 ug/L. The Health Department requires reporting of levels
above 20.
APPENDIX
RECOMMENDED MEDICAL MONITORING FOR WORKERS EXPOSED TO METALLIC AND
INORGANIC MERCURY
Medical monitoring is the periodic evaluation of exposed workers to insure that they are experiencing no adverse
effects of potentially hazardous workplace exposures. It serves as back- up for a program of routine air and
biologic monitoring, which are the primary7 means for insuring that exposure levels are below those associated
with adverse health effects. A medical monitoring program should be designed to detect adverse effects of
exposure as earlv as possible, at a stage where thev are still reversible, so that exposures can be controlled and
serious permanent adverse effects prevented.
Baseline and periodic examinations
An initial medical examination should be performed on all employees exposed to potentially hazardous levels of
mercury. The purpose of this examination is to provide a baseline for future health monitoring.
The examination should include a complete medical history and symptom questionnaire, with emphasis on the
nervous system (target organ for chronic exposure), the kidneys (target organ for acute and chronic exposure),
the oral cavity (target organ for chronic exposure), the lungs (target organ for acute exposure), the eyes (affected
by chronic exposure), and the skin (since mercury is a known skin sensitizer). Signs and symptoms of the earhest
signs of mercury intoxication should be eficited; these include personality changes, weight loss, irritability7.
Merciirv
fatigue, nervousness, loss of memory, indecision, and intellectual deterioration. Complaints of tremor and loss of
coordination should also be sought. Physical examination should focus on the target organs described above. A
baseline handwriting sample should be obtained. Laboratory evaluation should include at minimum a complete
urinalysis (see below).
This examination should be repeated annually. Results should be compared with the findings on the baseline
examination for changes suggestive of mercury toxicity. Handwriting samples should be compared to the baseline
sample for evidence of tremor. Interim evaluations should be conducted if symptoms suggestive of mercury
intoxication are occurring.
Confidentiality of Medical Information
Questionnaire and physical examination results for periodic examination should be compared to the baseline
examination to detect any change which might be attributed to mercury intoxication. The results should be
conveyed in detail to the worker. The employer should be informed by the examining physician if mercury
intoxication is suspected on the basis of symptoms or results of the physical examination or laboratory tests. If
intoxication is suspected, the worker should be removed from exposure and expert medical consultation should
be sought. Otherwise, the results of the physical exam should be kept confidential, and no management personnel
other than health professionals should have access to the medical records.
Importance of evaluating group results
The results of the questionnaire and physical examination should also be evaluated on a group basis. This is
important because early mercury’ poisoning might cause only very mild, clinically insignificant increases in
symptomatology in each individual which, when seen in the aggregate, might provide an important clue that toxic
exposure to mercury is taking place.
Who should perform the medical examinations
All medical monitoring of exposed employees should be conducted by a physician knowledgeable in
occupational medicine. In particular, interpretation of the group data should be undertaken only by a trained
occupational health physician or other physician with expertise in performing such analyses.
Using more sensitive medical tests
Several studies have shown that some special tests may be useful in detecting early signs of mercury toxicity.
Neurobehavioral tests, designed to detect early changes in concentration, response time, memory, and hand-eye
coordination, can be useful on both an individual and a group basis in detecting early nervous system effects of
mercury exposure.
Early kidney damage may be detected by looking for the presence of low molecular weight proteins in the urine.
The presence of these proteins in the urine indicates that kidney damage has occurred long before a routine
urinalysis indicates an abnormality. Beta2 microglobulin and N-acetyl-B-D glucosaminidase (NAG) are two of
the proteins which can be measured in the urine. The tests are useful on both an individual and group basis.
lltese special tests should be arranged and interpreted by a trained occupational physician or other physician
with special expertise in these areas.
BIOLOGIC MONITORING
Biologic monitoring is the measurement of an chemical agents in the blood, urine, or other body tissue of
exposed individuals to determine how much of the chemical has been absorbed into the body. It serves as a
back-up to environmental exposure measurements, since air measurements cannot assess skin exposure or the
effects of protective equipment and work practices. Since it measures the amount of an agent actually absorbed
into the body, it is usually a better estimate of risk for adverse health effect than air monitoring.
3 of 5
6/28/01 1:5
Mercurv
There is no ideal biologic monitor for evaluating the risks of mercury7 intoxication from metallic or inorganic
mercury7. Mercurv can be measured in both blood and urine. Individual levels may vary greatly from day to day
and even within a given day While proper interpretation of the results can be difficult, the measurements can
nevertheless provide information on potential overexposure. Measurements should be carried out regularly
(several times per year) in chronically exposed workers, and individual as well as group results should be
evaluated. Baseline levels should be obtained before exposure begins for comparison purposes.
Mercury in Urine
Measurement of mercury in urine is the recommended biologic monitor for workers exposed to metallic and
inorganic mercury . Ideally, the collection should be over 24-hours, but this is seldom feasible. Spot urine samples
may also be taken, but care must be taken to always collect them at the same time of day near the end of the
work week after several months of steady exposure. Overnight samples may also be collected; this collection
extends from the time the employee goes to bed through the first urination of the morning.
Samples must be collected in containers provided by the laboratory^, since a preservative must be added. At least
25 cc of urine must be collected. Great care must be taken to prevent contamination of the sample containers or
the urine with mercury from the skin or workplace air.
When results are interpreted, the urine values should be corrected for grams of creatinine in the sample, and
should be expressed as ug Hg/gram creatinine. In persons not occupationally exposed to mercury, urine levels
rarely exceed 5 ug/g creatinine.
While many7 laboratories indicate that onlv levels above 150 ug/L should be considered toxic, there is strong
evidence that early’ signs of mercury intoxication can be seen in w orkers excreting more than 50 ug Hg/L of urine
(standardized for a urinary creatinine of 1 gram/L). This value of 50 ug/g creatinine is proposed by many experts
as a biological threshold limit value for chronic exposure to mercury vapor, and in 1980 this was endorsed by a
World Health Organization study group.
Exposed individuals with levels above 50 ug/g creatinine should be placed in a non-exposed job until the reason
for their overexposure has been identified and corrected and their urine levels have fallen below’ the biologic
threshold limit value.
Mercury in blood
The concentration of mercury7 in blood reflects exposure to organic mercury7 as well as metallic and inorganic
mercury; thus it can be influenced by the consumption of fish containing methylmercury.
Samples should always be taken at the same time of day near the end of the work w eek after several months of
steady exposure. The blood should be collected in mercury-free heparinized tubes after careful skin cleansing.
In unexposed individuals, the amount of mercury in blood is usually less than 2 ug/100 ml. According to some
experts, an average airborne concentration of 50 ug/m3 corresponds to a mercury7 concentration in blood of about
3-3.5 mg/100 ml. Early effects of mercury’ toxicity' have been found when the blood concentration exceeds 3
ug/100 ml. Any worker exceeding this level should be placed in a non-exposed job until dietary and w orkplace
exposures have been evaluated and blood levels have returned to baseline.
Removing Employees from Exposure
An individual who must be removed from mercury exposure because of elevated blood or urine mercury levels or
physical examination results suggesting early mercury intoxication should be given alternative work with no
exposure. His or her w7ages, benefits and seniority7 should be maintained. No employee should be terminated or
otherwise punished because of overexposure to mercury.
In the event that no job without mercury exposure is available, the employee may continue to work using a
6/28/01 2:04 PM
4 of 5
Mercury
supplied air respirator, provided that biological monitoring results and/or symptoms display a satisfactory decline
over time.
New Jersey State Department of Health
Division of Occupational and Environmental Health
CN 360, Room 706
Trenton NJ 08625-9972
(609) 984-1863
\etum to EHS Safety Training Home Page
5 of 5
6/28/01 2:04
soitk time. Under other condtions, it nia\T well ibrmjMeHg. Perhaps the
simplest way to demonstrate tins is to make some measurements. All you
need to cb is collect some samples, freeze them in containers which we
would provide and slip them back to us in coolers.
Normally we would charge about $100 per sample but if you are working on
a tight budget the first few sanies wouldbe done for free. It is an
interesting prqj oct.
David Lean
NSERCIndistriai Chair mEcotoxicology
Department of Biolow
University of Ottawa
P.O. Box'150 Station A
Ottawa KI N6N5
CANADA
e-mai 1: dean@sd ence.iidhrwa. ca
2 of?
6/28/01 2:07 PN
Letter to expeir
Dear Dr. T^an -
I got yoir name from Susannah Scott.
I have a question that I hojje will be simple for you to answer.
In one case, I am helping a lawyer in a tropical country represent a
community living next to a field containing thousands of abandoned.
broken and leaking mercury thermometers. The company responsible for
the mess says 'hot to worry"because the rate of mercury methylation is
"nil "in water (compared to the rate in soil) and that the rate of
mctlrslationis much dower in the relatively colckr temperatires that
jrevail in groundwater (comparedto the tem|X3ratires of soil or surface
water).
What is void uncferstandng of how the rate of mercury methyl atation is
affected by water satur ation or temperature?
Is it really true that the rate of merciny methylation is insignificant
in surface water and'or
colder temperatures that prevail in groundwater?
RESPONSE OF EXPERT
I am pleased to see that tfere are people who do kind of work that you
ar e doing It is valuable. A situation like this must be corrected I
also got void- phone message and ifyou need more informal! on call me on
Mondi)7 afternoon (my time).
A few years ago T would have been sympathetic to the argument that
elemental merctuy (Ilgo) cannot form methyl mercury. I then would have
followed the conventional wisdom and said that it is the sulfate
reduditg bacteria that methylate mercury7 and that they7 only7 use oxi died
mercury (HgH) as a substrate. Since then we have learned that Hgo does
get oxi d zed both photocheni cally and by bacteri a. We have al so 1 earned
that McBgmay be foniicd without nriaolial activity'. We are dill
looking at the cheni cal mechanism involved but it is certain that MeHg
can be formedin natui e under certain contitions (as in soil
groundwater) without tfe necessity for microbial activity.
finally, a very’ little mercury goes a very’ 1 ong way. A gram of mercury
is a million micrograms (ug). Title human consumption guideline is 05 ug
mercury7 per gr am wet weight of food so in one fish fillet (200^ you
will take up 100 ug of mercury.
There is a big problem of methyl mercury formation in tlie Arctic (wher e
we are now doing some work) and the temper ature is near za o all year
round The col d temperature may result in slow production but al so slow
cfegr adation so accumiiiatioii may even be ingiiei.
In water logged soils, oxygen levels usually d op. This is exactly the
right condtions tor MeHg formation.
Merctuy metlylatioii does indeed occur in both surface waters and
groundwater. The form of mercury7 that is methyl atedis not well known
and under soiw condtions elemental mercury7 can remain uncharged for
6/26/01 9:54 AM
upnal exp to Hg
Subject: Fw: Occupnal exp to Hg
Date: Thu, 21 Jun 2001 22:23:30 +0530
From: ’’Thelma & Ravi Narayan” <tnarayan@vsnl.com>
To: <sochara@vsnl.com>
------- Original Message ---From: <nity68@vsnl.com>
To: <navrozmo@vsnl.net>; <eco.matser@ams.greenpeace.org >;
<r.1.stringer@exeter.ac.uk>; <p.johnston@exeter.ac.uk>
Cc: <tnarayan@vsnl.com>
Sent: Saturday, June 16, 2001 6:32 AM
Subject: Occupnal exp to Hg
> hello all:
> Below is some more information on mercury methylation and occupational
exposure, will share the dossier under preparation^as soon as it arrives
next week from the USA.
> ciao, nity
>
Dear Mohan and Nity >
> What follows are some quick replies to your queries. I will give you a
> more FORMAL memorandum next week. The argument that mercury methylation
> does not occur in water and/or the temperatures prevailing Kodaikanal is
> incredulous. Mercury methylation is primarily a biological process and
> occurs primarily in water. While it is true that the rate of
> methylation is faster in warmer water (because of increased biological
> activity), you would need to chill water to near 0 C to slow methylation
> to an insignificant rate. I suppose that even COLDER water in
> Kodaikanal (in a tropical region) is still quite warm.
>
> Mark
>
* * *
> *
>
> 1. SCIENTIFIC STUDIES ABOUT OCCUPATIONAL EXPOSURE TO MERCURY AND HEALTH
> EFFECTS.
>
> There are two good recent ones showing kidney disease and neurological
> deficits.
>
> Neurotoxicology 2000 Aug;21(4):459-74
>
> Related Articles, Books, LinkOut
>
> Residual neurologic deficits 30 years after
> occupational exposure to elemental mercury.
>
> Letz R, Gerr F, Cragle D, Green RC, Watkins Jf
> Fidler AT.
>
> Department of Behavioral Science and Health
> Education, Rollins School of Public Health, Emory University, Atlanta,
> GA 30322, USA. rletzQsph.emory.edu
>
> A battery of tests of peripheral and central
> nervous system function was administered to 205 former workers of a
> large heavy industrial plant, 104 of whom were
> previously exposed to inorganic mercury. The
> mean age of these examined was 71 years. Exposed subjects had
> participated in a urine-mercury exposure monitoring
> program during the time of operation of a
> process that required the use of mercury and its subsequent clean-up.
> Mercury exposure had been high (mean peak urine
> mercury concentration was >600 microg/1) and
FT dA cn
1 of 4
6/26/01 10:15 AN
Fw: Occupnal exp to Hg
> had ended JO years or more prior to the investigation. Peripheral nerve
> function outcomes that were statistically
> significantly associated with cumulative
> mercury exposure after controlling for covariates included
> classification as having peripheral neuropathy, peroneal motor nerve
> conduction velocity, ulnar motor nerve
> conduction velocity, and peroneal motor nerve F-wave latency.
> Quantitative assessment of resting tremor was nearly
> significantly associated with cumulative
> mercury exposure (p=Q.O7). Among tests of central nervous system
> function, results of the Handeye Coordination test were
> significantly associated with cumulative
> mercury exposure after controlling for covariates. Cumulative mercury
> exposure was not observed to be associated with a
> quantitative measure of dementia or with a
> number of cognitive neurobehavioral test outcomes. The statistically
> significant associations with mercury exposure were
> observed in spite of greater mortality among
> the exposed group than the unexposed group. These results suggest that
> substantial occupational mercury exposure can
> have long-term adverse effects on the
> peripheral nervous system detectable decades after cessation of
> exposure. Such long-term adverse effects were not observed for a
> measure of dementia or other measures of
> cognitive function.
>
> PMID: 11022856 [PubMed - indexed for MEDLINE]
>
> Neurotoxicology 2000 Aug;21(4):459-74
>
> Related Articles, Books, LinkOut
>
>
> Residual neurologic deficits 30 years after
> occupational exposure to elemental mercury.
>
> Letz R, Gerr F, Cragle D, Green RC, Watkins J,
> Fidler AT.
>
> Department of Behavioral Science and Health
> Education, Rollins School of Public Health, Emory University, Atlanta,
> GA 30322, USA. rletz@sph.emory.edu
>
> A battery of tests of peripheral and central
> nervous system function was administered to 205 former workers of a
> large heavy industrial plant, 104 of whom were
> previously exposed to inorganic mercury. The
> mean age of those examined was 71 years. Exposed subjects had
> participated in a urine-mercury exposure monitoring
> program during the time of operation of a
> process that required the use of mercury and its subsequent clean-up.
> Mercury exposure had been high (mean peak urine
> mercury concentration was >600 microg/1) and
> had ended 30 years or more prior to the investigation. Peripheral nerve
> function outcomes that were statistically
> significantly associated with cumulative
> mercury exposure after controlling for covariates included
> classification as having peripheral neuropathy, peroneal motor nerve
> conduction velocity, ulnar motor nerve
> conduction velocity, and peroneal motor nerve F-wave latency.
> Quantitative "assessment of resting tremor was nearly
> significantly associated with cumulative
> mercury exposure (p=0.07). Among, tests of central nervous system
> function, results of the Handeye Coordination test were
> significantly associated with cumulative
> mercury exposure after controlling for covariates. Cumulative mercury
> exposure was not observed to be associated with a
> quantitative measure of dementia or with a
f4
6/26/01 10:15/
Fw: Occupnal exp to Hg
> number of cognitive neurobehavioral test outcomes. The statistically
> significant associations with mercury exposure were
> observed in spite of greater mortality among
> the exposed group than the unexposed group. These results suggest that
> substantial occupational mercury exposure can
> have long-term adverse effects on the
> peripheral nervous system detectable decades after cessation of
> exposure. Such long-term adverse effects were not observed for a
> measure of dementia or other measures of
> cognitive function.
>
> PMID: 11022856 [PubMed - indexed for MEDLINE]
>
> 2. MERCURY LEVELS IN URINE: ACCORDING TO THE LITERATURE AT HAND, MERCURY
> LEVELS ABOVE 20 MICROGRAMS/LITRE OF URINE IS CONSIDERED UNACCEPTABLE.
> ARE THERE DOCUMENTED EFFECTS ABOVE THESE LEVELS? WHAT ARE THEY?
>
> Will answer later (next week)
>
> 3. FATE OF INORGANIC MERCURY IN ENVIRONMENT: UNILEVER ARGUES THAT
> INORGANIC MERCURY DOES NOT CONVERT READILY TO METHYL MERCURY IN THE
> ENVIRONMENT IN KODAIKANAL AND SURROUNDINGS. THEIR ARGUMENT IS THAT IN
> THE PRESENCE OF WATER AND COLD TEMPERATURES, METHYLATION IS RETARDED, IF
> NOT, NIL. CAN YOU PLEASE FORWARD ME STUDIES THAT DEAL WITH THESE
> ASPECTS?
>
>
> See some info on factors affecting methylation
>
> by C.
> Mark Smith
> Massachusettes
> Department of Environmental Protection (MA DEP)
> Office of
> Research and Standards
> E-mail:
> C.Mark.Smith@state.ma.us
> In water andv..sediments the amount
> of methylation is affected by:
> l.the amount of dissolved oxygen present;
> 2.the amount of sulfur present;
> 3.the pH of the water or sediment; and,
> 4.the presence of particles of clay or organic material.
>
> Where the amount of oxygen is limited, as in deeper layers of the
> surface water or sediments, more methyl mercury is formed. The presence
> of sulfur may be important because it is thought that
> sulfate-dependent bacteria are involved in the methylation process.
> Low pH is associated with an increase in methylation. (This means that
> methylation may occur more readily in water affected by acid
> rain.) If clay particles are present in the water, the mercury may
> attach to the particles, and may not be as available for methylation.
>
> Methyl mercury may also be formed in soil. As in lakes, rivers, or
> sediments, the oxygen and sulfur levels and the pH may affect the amount
> of methylation that occurs. Methyl mercury formed in the
> soil may be transported to surface water as runoff and ultimately
> enter lakes, ponds or the ocean.
>
> The concentrations of different forms of mercury found in soil,
> water, or air, or in living things, is the result of the amount of
> releases, how they have been transported, and how the mercury is
> transformed. Figure 2-2 displays the overall process of cycling of
> mercury through the environment.
>
>
>
> http://response.restoration.noaa.gov/cpr/sediment/mercury.html
6/26/01 10:17 AM
3 of 4
Fw: Occupnal exp to Hg
>
> Mercury in Aquatic Habitats . . .
>
> Methylation is influenced by environmental variables that affect both
> the availability of mercuric ions for methylation and the growth of the
> methylating microbial populations. Methylation
> rates are higher under anoxic conditions, in freshwater compared
> to saltwater, and in low pH environments. The presence of organic matter
> can stimulate growth of microbial populations
> (and reduce oxygen levels) f thereby enhancing the formation of
> methylmercury. Sulfide can bind mercury and limit methylation.
> Methylmercury production can vary due to seasonal changes
> in nutrients, oxygen, temperature, and hydrodynamics. In most
> studies, methylation increased during the summer months when biological
> productivity was high, and decreased during the
> winter months.
>
>
tof4
6/26/01 10:17/
I
I
MERCURY {Hq) FACTSHEET
Mercury is probably best known as the silver liquid in thermometers. However, it has
over 3000 industrial uses. Mercury and its compounds are widely distributed in the
environment as a result of both natural and man-made activities. The utility, and the
toxicity, of mercury have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous.
HISTORY & OCCURRENCE
Mercury occurs naturally in the environment as mercuric sulfide, also known as
Cinnabar. It is also present in some fossil fuels. Cinnabar has been refined for its
mercury content since the 15th or 16th century B.C.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and
cannot be broken down into less hazardous compounds.
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room
temperature, ease of vaporizing and freezing, and electrical conductivity make mercury
an important industrial metal In 1973, U.S. consumption of mercury was 1900 metric
tons. Primary among its over 3000 industrial uses are battery manufacturing and
chiorine-alka-i production. Paints and industrial instruments have also been among the
major uses. Until paint manufacturers agreed to eliminate the use of mercury in interior
paints, 480,000 pounds of mercury in paints and coatings were produced each year.
Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems (i.s. when it comes into contact with micro organisms in soil
or water).
STATUS OF CONTA^ATION
Not only are these methylated mercury compounds toxic, but highly bioaccumulative as
well. Mercury biomagnifies upto 100,000 times in predatory fish. The consumption of
such fish led to the poisoning of Japanese fisherman and their families in Minamata.
Japan, in the 1950s as a result of consumption of methyl mercury contaminated fish.
The magnification of ieveis of mercury as it rises in the aquatic food chain results in
relatively high level's of mercury in fish consumed by humans. The US Food and Drug
Administration (news - web sites) (FDA) recommends that pregnant women and those
who may become pregnant avoid eating shark, swordfish, king mackerel, and tile fish
known to contain elevated levels of methylmercury, an organic form of mercury that can
accumulate in the food chain.
ECOS, an association of state and territorial environmental commissioners from the
United States, is expected to adopt the resolution during its annual meeting currently
underway in Tampa Bay, Fla. In terms of national vision, the ECOS resolution calls on
the White House and Congress "to articulate a goal of virtual elimination of mercury'
discharge into the environment at the national and international levels."
<http://www.eenews.net>
To date, more than 40 US states and the Food and Drug Administration
have adopted at least 2,073 public health advisories warning about
mercury contamination. In addition, several states and large municipalities
- mostly located in the Northeast - are cracking own on the amount of
mercury in the environment by outlawing mercury thermometers, which,
some say, could render drinking water supplies unusable if even one
thermometer contaminates a source.
In addition to the early workers in the cinnabar mines, modern workers in industries
using mercury are at risk from overexposure. The Occupational Safety and Health
Administration (OSHA) has been reviewing the current occupational exposure standard
of 0.1 mg/m3 (milligrams per cubic meter of air) to determine if they should reduce the 8
hour acceptable exposure limit to 0.05 mg/m3. Although no regulatory limit exists for
airborne exposure to mercury outside of an occupational setting, the ERA suggests that
0.3 ug/m3 (micro-grams per cubic meter of air) of mercury is a no-effect level (or
reference dose = Rfd) for chronic inhalation exposure.
EXPOSURE SCENARIOS
Humans come in contact with mercury through environmental, occupational or
accidental exposure scenarios. An estimated 80% of utilized mercury is eventually
released back into the environment. Because it is easily vaporized, air around chlorine
alkali plants, smelters, municipal incinerators, sewage treatment plants and even
contaminated soils may contain increased levels of mercury. A primary route of
exposure is through transport into surface waters, where mercury becomes biomagnified
in fish tissues.
Workplace exposure to mercury occurs through inhalation of contaminated air, direct
skin contact with liquid mercury, or oral exposure through contaminated hands, food,
etc.
HEALTH EFFECTS AND TOXICITY
Exposure to mercury can occur through inhalation, ingestion or dermal absorption, the
amount of mercury absorbed by the body -and thus the degree of toxicity - is dependent
upon the chemical form of mercury. For instance, ingested elemental mercury is only
0.01% absorbed, but methyl mercury is nearly 100% absorbed from the gastrointestinal
tract. The biological half-life of mercury is 60 days. Thus, even though exposure is
reduced, the body burden will remain for at least a few months.
Elemental mercury is most hazardous when inhaled. Only about 25% of an inhaled dose
is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the
total dose). Derma! contact with liquid mercury can significantly increase biological
levels. The primary focus of this article is elemental mercury, since that is the form of
exposure to health care workers involved with mercury-containing instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury
may cause acute or chronic health effects. Acute exposure (i.e., short term, high dose)
is not as common today due to greater precautions and decreased handling. However,
severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5
hours may cause headaches, salivation, metallic taste in the mouth, chills, cough, fever,
tremors, abdominal cramps, diarrhea, nausea, vomiting, tightness in the chest, difficulty
breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a number of
hours.
Chronic effects include central nervous system effects, kidney damage and birth
defects. Genetic damage is also suspected. Nervous system effects. These are the
most critical effects of chronic mercury exposure from adult exposure as they are
consistent and pronounced, some elemental mercury is dissolved in the blood and may
be transported across the blood/brain barrier, oxidized and retained in brain tissue.
Elimination from the brain is slow, resulting in nerve tissue accumulation. Symptoms of
chronic mercury exposure on the nervous system include: Increased excitability, mental
instability, tendency to weep, fine tremors of the hands and feet, and personality
changes. The term "Mad as a Hatter" came from these symptoms which were a result of
mercury exposure in workers manufacturing felt hats using a mercury-containing
process.
Kidney effects: Kidney damage includes increased protein in the urine and may result
in kidney failure at high dose exposure.
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild
exposure include delayed developmental milestones, altered muscle tone and tendon
reflexes, and depressed intelligence.
Mercury exposure in children can cause a severe form of poisoning termed acrodynia.
Acrodynia is evidenced by pain in the extremities, pinkness and peeling of the hands,
feet and nose, irritability, sweating, rapid heartbeat and loss of mobility.
For more information:
www.ban.org
www.noharm.org
www.greenpeaceindia.org
£ AT.
MERCURY (Hg)- a profile
Mercury is probably best known as the silver liquid in thermometers. However, it has
over 3000 industrial uses. Mercury and its compounds are widely distributed in the
environment as a result of both natural and man-made activities. The utility, and the
toxicity, of mercury have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous.
HISTORY & OCCURRENCE
Mercury occurs naturally in the environment as mercuric suifide, also known as
cinnabar. It is also present in some fossil fuels. Cinnabar has been refined for its
mercury content since the 15th or 16th century B.C.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and
cannot be broken down into less hazardous compounds.
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room
temperature, ease of vaporizing and freezing, and electrical conductivity make mercury
an important industrial metal. In 1973, U.S. consumption of mercury was 1900 metric
tons. Primary among its over 3000 industrial uses are battery manufacturing and
chlorine-alkali production. Paints and industrial instruments have also been among the
major uses. Until paint manufacturers agreed to eliminate the use of mercury in interior
paints, 480,000 pounds of mercury in paints and coatings were produced each year.
Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems (i.e. when it comes into contact with micro organisms in soil
or water).
STATUS OF CONTAMINATION
Not only are these methylated mercury compounds toxic, but highly bioaccumulative as
well. Mercury biomagnifies upto 100,000 times in predatory fish. The consumption of
such fish led to the poisoning of Japanese fisherman and their families in Minamata,
Japan, in the 1950s as a result of consumption of methyl mercury contaminated fish.
The magnification of levels of mercury as it rises in the aquatic food chain results in
relatively high levels of mercury in fish consumed by humans. The US Food and Drug
Administration (news - web sites) (FDA) recommends that pregnant women and those
who may become pregnant avoid eating shark, swordfish, king mackerel, and tile fish
known to contain elevated levels of methylmercury, an organic form of mercury that can
accumulate in the food chain.
*
«
.X
ECOS, an association of state and temtonaj en^
meeting curr tly
United States, is expected to ^opt^
vjsi0n9 the ECOS resolution calls on
underway in Tampa Bay, Fla^
rticu|ate a goal of virtual elimination of mercury
a, .eve. ■
<http7/www .eenews.net>
have adopted at least 2 0731 p
gnd large municipalities
X^ay" coUld"r=endrin«rng water supples unusabte /even one|
thermometer contaminatesajource.-----—----------------------- —-
—
ln addition to the early workers in the
using mercury are at risk from o^r®xPos '
ent occupational exposure standard
Administration (OSHA) has bee"/e^X 9f air) to determine if they should reduce the 8
of 0.1 mg/m3 (milligrams per cubic meter of air) Although no regulatory limit exists for
XSoXX™ /onto inhalation exposure.
exposure scenarios
Humans come in contact »lh
WA 0^7X0°//“^*
accidental exposure scenarios^ An esbmat d 80 /
air arOund chlonnereleased back into the environment. Because
treatment plants and even
alkali plants, smelters, municipal 'ncm^tor
A p
rout of
™X"h SspXo surface waters, where mercuw becomes hiomagnthed
in fish tissues.
HEALTH EFFECTS AND TOXICITY
Exposure to mercury
0CC“\“X¥'Xthus B^d^’e^XSSSlir^te’rtependenl
FAM1I HILLS eOMSElSVALIOll CCUTieiL (PHCC)
PAMBAR SHOLA: A BIODIVERSITY TREASURE TROVE UNDER THREAT
"Pambar Shola, c. 2000m, Kodaikanal, perched on the edge of the precipe with the Falls cascading
down for several hundred metres. This extremely biodiverse Shola, now shrunk to less than 3 kms in
circumference, is witnessing the last-ditch battle for survival by a number of plant species, the last
sentinels of a bygone age. The past has been glorious; several plant species were described as new to
science from here. But the development activities of recent decades have depleted its species richness;
a few are already extinct; at least four are now known from a single clump each for the entire Palai
hills. Pambar Shola is truly a living fossil, a relic among relics.
In 1997, Ponds India Ltd set up a mercury thermometer factory on the ridge of Pambar shola slope by
securing special exemption from the Tamilnadu Government on grounds that the factory is non
polluting. Over the years, the slopes leading into Pambar shola’s core have been used by the factory
management as a dumping ground for all kinds of wastes, including broken mercury-containing
thermometers and other potentially mercury-contaminated wastes. The slopes where the wastes are
dumped are part of the Pambar shola watershed, draining water through the Pambar River which
eventually ends up in the plains leading up to the temple city of Madurai through a network of canals.
Contiguous to the Pambar Shola is a remarkable slope of Strobi/anthes kunthiana, the folklore plant
endemic to the South Indian bills, known for the gregarious flowering regularly at intervals of 12 years.
The slope is probably the best preserved one for then plant for the entire Palm* hills. The secluded
location of these two localities saved them to some extent till now, but for the future, instant in site (on
S'te) conservation is imperative. Proposals and representations have been a plenty, and all hope is not
yet lost. The urgent task is to lock the stables before at least the last horses have escaped"
COver of the Handb00k of the Anglade Institute of Natural History, Shembaganur by
K.M. Matthew, 20.12.94.)
' 1
Another significant finding was that endemic species often occur together, for which we have used the
thA
PAMBAR SHOLA AND ENVIRONS - RED DATA LIST
!.
~
2.
3. Piectrantnus bourneae- a succulent herb endemic to from Pambar shola.
4.
Tnchoglottis tenera - an epiphytic orchid. Pambar Shola is its major habitat.
5. Phyllanthus chandrabosei- a shrub endemic to Pambar Shola
6. Hupzeria sp. - a fern of a kind endemic to Pambar Shola
7. Sdaginella sp. b - a delicate creeping fern endemic to Pambar Shola
8. Psydrax ficiformis -- a tree, until recently thought extinct
9.
Ut/eria salicifolia - endemic to Palni hills
10. Elaeocarpus munroni-- found only in one other known location in the Palni hills
11. Elaeocarpus blascoi - a tree believed extinct until this year
12.
crinita - tree fern, believed extinct in India (Botanical Survey of India)
13. Aeschynanthus perrottetn - known only from one other shola in the Palni hills
14.
. SP' " 3 nGW SpeCies for the Pa,ni hi,ls nrst collected in April 2000
15.
~
tree be,ieved extinct (Botanical
°f Ma). TWO trees found in Pambar
16. Ceropegia thwaitesii - vine, vulnerable, endemic to Pambar shola
17.
’ herb' P055^'7 extinct' ori9inal|y found in Pambar ^ola grasslands
18.
acum anamallayannum - gentian, only one other known location in Palni hills 9
Paln^ r±±L3
°f NatUral hiStOrY in Kodaika™1' contact:
raim Hills Conservation Council
Endhavin, Lower Shola Road, Kodaikanal 624101
Tel: +91 4542 40157
Email: kannan@vsnl.com
Condon WC9°nSerVatiOn
°f SOU,I, India" P'a"tS '' K M
Biodiversity and
I
!■
total dose). Dermal contact with liguid mercury can significantly increase biological
levels. The primary focus of this article is elemental mercury, since that is the form of
exposure to health care workers involved with mercury-containing instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury
may cause acute or chronic health effects. Acute exposure (i.e., short term, high dose) is
not as common today due to greater precautions and decreased handling. However,
severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5
hours may cause headaches, salivation, metallic taste in the mouth, chills, cough, fever,
tremors, abdominal cramps, diarrhea, nausea, vomiting, tightness in the chest, difficulty
breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a number of
hours.
Chronic effects include central nervous system effects, kidney damage and birth defects
Genetic damage is also suspected. Nervous system effects. These are the most critica^
effects of chronic mercury exposure from adult exposure as they are consistent and
pronounced, some elemental mercury is dissolved in the blood a-d may be transpo. ied
across the blood/brain barrier, oxidized and retained in brain tissue. Elimination from the
brain is slow, resulting in nerve tissue accumulation. Symptoms of chronic mercury
exposure on the nervous system include: Increased excitability, mental instab]l'ty'
tendency to weep, fine tremors of the hands and feet, and personality changes. The
term "Mad as a Hatter" came from these symptoms which were a result of mercury
exposure in workers manufacturing felt hats using a mercury-containing process.
Kidney effects: Kidney damage includes increased protein in the urine and may result
in kidney failure at high dose exposure.
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild
exposure include delayed developmental milestones, altered muscle tone and tendon
reflexes, and depressed intelligence.
feet and nose, irritability, sweating, rapid heartbeat and loss of mobility.
For more information:
www.ban.org
www.noharm.org
www.greenpeaceindia.org
I ——
Page 1 of 2
fcJnilever - Policy and Strategy
o
Unilever
policy and strategy
ENVIRONMENT
policy and strategy
news and events
profiles
our performance report
SITE MAP
UNDERSTANDING OUR IMPACT
MEETING OUR RESPONSIBILITIES
We have an environmental policy that applies
to all Unilever companies world-wide.
Linked to our broader business strategy is our
environmental strategy. This outlines our future direction
and is designed to ensure that we are closely connected
with the needs and demands of consumers who, research
shows, expect us to care for the environmental impact of
products on their behalf.
TAKING ACTION
USEFUL INFORMATION
CONTACT US
The environment strategy has three key elements:
1.
Continue to improve the environmental performance
of our manufacturing operations and extend the use
of eco-efficiency measures along the supply chain
where we have influence and where we can get
major environmental improvements.
2.
Pursue the integration of environmental
sustainability into key business activities by ensurinc
that environmental factors are accounted for in
product design. We call this eco-innovation.
3.
Meet goals set for our three sustainability initiatives
which support long-term accessibility of fish,
agriculture and water.
Our Policy Statement:
Unilever is committed to meeting the needs of customers
and consumers in an environmentally sound and
sustainable manner, through continuous improvements in
environmental performance in all our activities.
Accordingly, Unilever's aims are to:
. ensure the safety of its products and operations for
the environment
. exercise the same concern for the environment
wherever we operate
. develop innovative products and processes'which
reduce levels of environmental impact and develop
methods of packaging which combine effective
protection and presentation with the conservation of
raw materials and convenient, environmentally
appropriate disposal
. reduce waste, conserve energy and explore
opportunities for re-use and recycling
To achieve these aims, we will:
. Assess the environmental impacts of all its business
activities from research, through manufacture,
distribution, use and disposal
http://www. unilever.com/en/en_ps.html
23/2/01
1
Page 2 of 2
Unilever - Policy and Strategy
• Apply more stringent criteria than those required by
law when we believe this to be appropriate
• Use standards of environmental impact assessment
which are robust, scientifically sound and generally
acceptable within the present state of knowledge, at
the same time attempting to develop superior
methods and to improve on current practice
.
Develop and apply systems of environmental
management, as part of day-to-day operational
practice and on-going management reporting and
control procedures
.
Encourage our suppliers to develop environmentally
superior processes and ingredients and co-operate
with other members of the supply chain to improve
overall environmental performance
. Work with industry bodies, government agencies,
business partners and other concerned
organisations, to promote environmental care,
increase knowledge and disseminate
. best practice
.
Remain alert and responsive to developing issues,
knowledge and public concerns
Unilever will communicate actively in order to:
. Provide whatever information and advice is
necessary on the safe use and disposal of our
products
.
Ensure that employees are aware of the company’s
environmental policy and motivated to apply it; are
aware of their own responsibilities and given the
support and training necessary to fulfill them
.
Publish relevant and meaningful information on
environmental performance and progressively
introduce a more comprehensive reporting system.
Unilever hom
http://www.unilcver.com/en/en_ps.hlml
23/2/01
MERCURY: A FACT SHEET FOR
HEALTH PROFESSIONALS
Mercury is probably best know as the silver liquid m thermometers. However, it has over 3000 industrial uses.
Mercury and its compounds are widely distributed in the environment as a result of both natural and man-made
activities. The utility, and the toxicity, of mercury have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous. The purpose of this document is to provide health
professionals with updated information on mercury and guidance on preventing toxic exposures in health care
workers and their clients.
HISTORY & REGULATIONS
Mercury occurs naturally in the environment as mercuric sulfide, also known as cinnabar. It is also present in some
fossil fuels. Cinnabar has been refined for its mercury content since the 15th or 16th century B.C. Its health hazards
have been known at least since the roman conquest of Spain. Due to the toxicity of mercury in cinnabar, criminals
sentenced to work in quicksilver mines by the Romans had a life expectancy of only 3 years.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and cannot be broken down into
less hazardous compounds. Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems. Not only are these methylated mercury compounds toxic, but highly bioaccumulative
as well. The increase in mercury as it rises in the aquatic food chain results in relatively high levels of mercury in
fish consumed by humans. Widespread poisoning of Japanese fisherman and their families occurred in Minamata,
Japan in the 1950's as a result of consumption of methyl mercury contaminated fish. Today, we continue to be
exposed to mercury in our diets, primarily from fish and shellfish. As a result, the U.S. Food and Drug
Administration (FDA) has an action level for mercury of 1 part per million (ppm) in fish and the Michigan
Department of Public Health issues fish consumption advisories to anglers when mercury levels exceed 0.5 ppm in
fish tissue.
Widespread industrial production of mercury, along with lack of careful handling and disposal practices, has
contributed to environmental contamination. The U.S. Environmental Protection Agency (EPA) has made efforts to
regulate the continued release of mercury into the environment. EPA regulates industrial discharges to air and water,
as well as regulating some aspects of mercury waste disposal. In 1976, EPA banned most pesticide uses of mercury with the exceptions of fungicidal uses in paints and outdoor fabrics, and for control of Dutch Elm disease. In 1990,
mercury use as a fungicide in interior latex paint was halted by the EPA. This action stemmed from requests by
Michigan officials after a child was poisoned from over formulated mercury-containing paint used in his home.
More recently, the use of mercury compounds in exterior latex paint has also been halted.
In addition to the early workers in the cinnabar mines, modem workers in industries using mercury are at risk from
overexposure. The Occupational Safety and Health Administration (OSHA) has been reviewing the current
occupational exposure standard of 0.1 mg/m3 (milligrams per cubic meter of air) to determine if they should reduce
the 8 hour acceptable exposure limit to 0.05 mg/m3. Although flo regulatory limit exists for airborne exposure to
mercury outside of an occupational setting, the EPA suggests that 0.3 ug/m3 (micro-grams per cubic meter of air) of
mercury is a no-effect level (or reference dose = Rfd) for chronic inhalation exposure.
................ .... .................. .... ................................................. ..... ••••.........................................................
...........
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room temperature, ease of vaporizing
and freezing, and electrical conductivity make mercury an important industrial metal. In 1973, U.S. consumption of
mercury was 1900 metric tons. Primary among its over 3000 industrial uses are battery manufacturing and chlorine
alkali production. Paints and industrial instruments have also been among the major uses. Until paint manufacturers
agreed to eliminate the use of mercury in interior paints, 480,000 pounds of mercury in paints and coatings were
produced each year. Table 1 provides a list of mercury uses.
EXPOSURE SCENARIOS
Humans come in contact with mercury through environmental, occupational or accidental exposure scenarios. An
estimated 80% of utilized mercury is eventually released back into the environment. Because it is easily vaporized,
air around chlorine-alkali plants, smelters, municipal incinerators, sewage treatment plants and even contaminated
soils may contain increased levels of mercury. A primary route of exposure is through transport into surface waters,
where mercury becomes biomagnified in fish tissues.
Workplace exposure to mercury occurs through inhalation of contaminated air, direct skin contact with liquid
mercury, or oral exposure through contaminated hands, food, etc. A recent edition of the television show 60 Minutes
highlighted concerns about mercury exposure in patients receiving silver dental fillings with mercury-containing
amalgam. Insufficient scientific evidence exists at this time to either support or refute the claims that dental fillings
may result in harmful exposure to mercury.
Accidents have resulted in several cases of mercury poisoning in Michigan in the past two years. Four members of a
Lincoln Park family were killed after one member attempted to refine dental amalgam in his home while attempting
to recover silver. High levels of mercury were found throughout the house, including wrapped food inside the
freezer. The entire house had to be demolished and disposed of in a hazardous waste landfill.
A number of children have developed mercury poisoning after playing with small vials of mercury which they found
at home or school. These children were hospitalized when symptoms became so severe that they could not longer
walk. One contamination incident involved closing a school for weeks and entailed environmental investigation of
residences, cars, school buses and day care centers.
METABOLISM & TOXICITY
Exposure to mercury can occur through inhalation, ingestion or dermal absorption, the amount of mercury absorbed
by the body -and thus the degree of toxicity - is dependent upon the chemical form of mercury For instance
ingested elemental mercury is only 0.01% absorbed, but methyl mercury is nearly 100% absorbed from the ’
gastromtestmal tract. The biological half-life of mercury is 60 days. Thus, even though exposure is reduced, the
byrden^n remam for at Ieast a few months. Elemental mercury is most hazardous when inhaled. Only about
/o of an inhaled dose is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the total
ose). Dermal contact with liquid mercury can significantly increase biological levels. The primary focus of this
article is elemental mercury, since that is the form of exposure to health care workers involved with mercurycontainmg instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury may cause acute or chronic
health effects. Acute exposure (i.e., short term, high dose) is not as common today due to greater precautions and
decreased handling. However, severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5 hours may cause headaches
1
"J?3 lC St.r^ th,e T0Uth’ Chllls’ C0U8h’ fever’ tremors> abdominal cramps, diarrhea, nausea, vomiting
number ofhours^’ d'ffiCU ty breath,n& fatigue, or lung irritation. Symptoms may be delayed in onset for a
Chrome effects include central nervous system effects, kidney damage and birth defects. Genetic damage is also
oilbp vvlvCl.
™n^7Stiem f'CCtS' TheS^ are the ?10St CriticaI effects of chronic mercury exP°sure from adult exposure as they
are consistent and pronounced, some elemental mercury is dissolved in the blood and may be transported across the
blood/brain bamer, oxidized and retained in brain tissue. Elimination from the brain is slow, resulting in nerve tissue
htstabihv ZrfeT0™ ° Cnr°n'C merCU7- eXP°SUre °n the nerVOUS system include Increased excitability, mental
^ability, tendency to weep, fine tremors of the hands and feet, and personality changes. The term "Mad as a
X a mZX°m t- SymPt°mS WhiCh
3 reSUlt °f merCUry exP°sure in workers manufacturing felt hats
using a mercury-containing process.
&
e^oXf^ Kidney dama8e 'nC1UdeS inCreaSed PrOte'n the Urine and may result in kidney failure at high dose
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild exposure include delayed
developmental milestones, altered muscle tone and tendon reflexes, and depressed intelligence
V
Mercury exposure in children can cause a severe form of poisoning termed acrodynia Acrodynia is evidenced bv
C of mobSy6"1’1168’ P"11”685 and P6611"8 °fhandS’
and n°Se’ irritabili‘y, sweating, rapid heartbeat and
... .
PRECAUTIONS FOR HEALTH CARE WORKERS
Substitutes for mercury-containing medical devices should be used whenever possible e g thermometers and
sShoufdT™"^616^ Whei? TCUly deV'CeS mUSt be USed’ speciaI Precaut‘ons should be taken These devices
should never be used on a cloth surface, such as upholstered chair or in a room with a carpeted floor If a snill
occurred in such an area, the upholstery or carpeting would need to be discarded as it could not be effectively
-
SPILL RESPONSE
If a spill occurs, evacuate the immediate area and ventilate as well as possible. An environmental consultant will
need to be contacted for clean-up and disposal. DO NOT attempt to clean-up a mercury spill using rags or an
ordinary vacuum. This will only serve to disperse the mercury and encourage volatilization. For further assistance,
contact your local health department and/or the Michigan Department of Public Health, Division of Health Risk
Assessment. For assistance with a large spill, call the Fire Department for assistance. For assistance with clean-up,
you may look in your local phone book for environmental consultants. Table 2 contains a list of consultants known
to respond to mercury spills.
DISPOSAL
The best method of mercury disposal is reclamation. Attached is a list of agencies in Michigan that will take used
mercury. Button batteries can be recycled at many jewelry stores and other retail outlets that sell batteries. Larger
quantities of mercury will need to be disposed of by a licensed hazardous waste hauler. Contact the Michigan
Department of Natural Resources, Waste Management Division for assistance with mercury disposal.
Back to the Ingham County Pamphlet List Page
Back to the AWARE Home Page
A#
TOXICITY SUMMARY FOR
METHYL MERCURY
February, 1992
Prepared by:
Robert A. Young, Ph.D., D.A.B T.
Chemical Hazard Evaluation and Communication Group
Biomedical and Environmental Information Analysis Section
Health and Safety Research Division
Oak Ridge National Laboratory
Oak Ridge, Tennessee
t
.■
v
i
Prepared for:
OAK RIDGE RESERVATION ENVIRONMENTAL
RESTORATION PROGRAM
i
* Managed by Martin-Marietta Energy' Systems, Inc. for the U.S. Department of Energy under Contract
No. DE-AC05-84OR21400
This page intentionally left blank
EXECUTIVE SUMMARY
Methyl mercury is formed by biotic and abiotic methylation of mercury (McComish and Ong. 1985).
Methyl mercury has been used as a fungicide, disinfectant, and in industrial processes (Singer and Nowak.
1980; Berlin et al.. 1983).
e oc 7 -
Methyl mercury is highly toxic and is readily absorbed by the body following ingestion or inhalation
(Abcrg et al.. 1969; Meittenen. 1973; Berlin et al., 1983). Methyl mercury may be metabolized to inorganic
mercury by the liver and kidneys, with further transformation occurring to form the divalent cation (ATSDR,
1989). Methyl mercury is excreted as inorganic mercury, primarily in the feces (Norseth and Clarkson. 1971).
(
The target organ for methyl mercury toxicity is the central nervous system (CNS), especially the brain,
and may occur at doses as low as 3 ig/kg in humans (WHO, 1976). Methyl mercury is neurotoxic to several
species of experimental animal and to humans. The LD5o values for various rodent species range horn 21 to
57.6 mg/kg (RTECS, 1986). Manifestation of toxic effects (neurobehavioral alterations and degenerative
changes in the central and peripheral nervous system) is probably a function of accumulation of critical levels
of mercury (Goyer, 1991). Histopathologic correlates have been identified in the brains of humans and animals
prenatally exposed to methyl mercury (Choi et al., 1987; Hughes and Annua, 1976).
Exposure to methyl mercury in the diet (fish and contaminated grain) has caused epidemic poisonings
in Iraq and Japan, characterized by severe developmental effects (impaired motor and cognitive functions) in
infants of exposed mothers (Baku ct al.. 1973; Amin-Zaki et al., 1974; WHO, 1976). The primary target organ
for oral exposure to methyl mercury is the brain; the effects on this organ accounting for the developmental
toxicity of the chemical (Magos, 1980; Goyer, 1991). Data on the effects of inhalation exposure to methyl
mercury are lacking for both humans and animals.
A reference dose (RfD) of 3E-04 mg/kg/day has been calculated by the U.S. EPA and is based on the
intake that would be required to produce a blood mercury level of 200 ig/mL, which is a level associated with
minimal health effects in humans (U.S. EPA^ 1991; U.S. EPA, 1990). In deriving the RfD, an uncertainty
factor of 10 was applied for extrapolation from a LOAEL to NOAEL. Confidence in the RfD is medium.
An inhalation reference concentiation (RfC) for methyl mercury' is not available.
No data were available for assessing the carcinogenic potential of methyl mercury.
1
*
1. INTRODUCTION
Mercury may undergo biotic and abiotic methylation to form methyl mercury (McComish and Ong.
1988). Commercially produceu iiicuiyi mercury (CAS No. 2269-92-6) has been used as a fungicide, seed
disinfectant, alkylating agent in organic synthesis of odier organometallic compounds, and as a preservative in
paints (Singerand Nowak, 1980; Berlin, 1983).
2. METABOLISM AND DISPOSITION
2.1.
ABSORPTION
Data are available showing that methyl mercury is readily absorbed from the gastrointestinal tract of
humans and animals. Based on retention and excretion data from humans, Aberg et al. (1969) reported that
95% of a single oral dose of methylmercuric nitrate was absorbed. Efficient absorption of methyl mercury was
also demonstrated in another study using human volunteers receiving an oral dose of protein-bound methyl
mercury (Miettinen, 1973). Up to 80% of volatile methyl mercury compounds such as methyl mercury
chloride vapor may be absorbed upon inhalation (Berlin, 1983). Dermal absorption of methyl mercury is
known to occur in both humans and animals but quantitative data are lacking.
2.2.
DISTRIBUTION
Methyl mercury is transported in red blood cells with a small fraction being bound to plasma proteins
(Beilin, 1983). The compound readily penetrates membranes resulting in widespread distribution in the body;
however, higher concentrations (up to 10% of total dose) accumulate in the central nervous system (CNS). In
theCNS, methyl mercury remainsm the organic form but in other tissues is converted and stored as inorganic
mercury with the highest concentrations generally occurring in the liver and kidney. Methyl mercury readily
traverses the placenta and results in higher levels of the compound in fetal relative toinatemal-blood (ATSDR,
1989). Incorporation of methyl mercury in hair during hair formation in die follicle results in concentrations
dial are up to 250 times greater than that in other tissues. A report by Dutczak et al. (1991) provided data from
guinea pigs, hamsters and a macaque monkey indicating extensive absorption of methyl mercury by the gall
bladder and subsequent biliary-hepatic cycling of the compound, which may contribute to the long biologic
half-life of methyl mercury.
2.3.
J
METABOLISM
Methyl mercury may be metabolized to inorganic mercuiy by the liver and kidneys, with the inorganic
form then entering an oxidation-reduction cycle in the red blood cells, lungs, and liver resulting in formation of
the divalent cation (Hg ) (ATSDR, 1989). Methyl mercury remaining in the gastrointestinal tract is converted
to inorganic mercury by the intestinal flora (Nakamura et al., 1977; Rowland et al., 1980). Available data
suggest that metabolism of methyl mercury is similar in animals and humans (ATSDR. 1989).
2.4.
EXCRETION
I
1
2
Methyl mercury is excreted primarily in the feces as inorganic mercury- (Norseth and Clarkson. 1971).
ITiiS is the result ol biliary excretion of the compound and subsequent conversion to he inorganic form bv
intestmal flora. Some of the methyl mercury excreted in the bile may also be reabsorbed thereby creating
enterohepahc circulation of the organic fonn. Less than 1% of the body burden of methyl mercury is excreted
daily resulting m a biological halt-life ot approximately Todays (Berlin. 1983). Over a 4-dav period, a human
volunteer excreted only about 6% of the ingested dose of radiolabeled, protein-bound methyl mercury the
biological half-hfe ultnnately being 76 days (Miettinen, 1973). Methyl mercury- is also secreted in breast milk
with concentrations being about 5% of that in the blood. Removal of inorganic mercury via exhalation saliva,
and sweat results from die metabolism of the organic form (ATSDR, 1989).
3. NONCARCINOG ENIC HEALTH EFFECTS
3.1. ORAL EXPOSURES
3.1.1.
Acute Toxicity
<
3.1.1.1. Human
z—7— —ngfrn .
ese blood concentrations correspond to bod}- burdens of 30 to 50 me He/70 ke and are
equivalent to daily intakes of3 to 7 ig/kg. It is important to note that the onset of methyl mwcuiy poisoning
may be delayed for weeks or even months depending on the total body accumulation of the compound.
3.1.1.2. Animal
Oral LD5o values of 29.9 mg/kg, 57.6 mg/kg, and 21 mg/kg have been reported for rats, mice, and
guinea pigs, respectivelyflRTECS, 1986). Acute toxic effects including neurological effects (behavioral
alteration^ brain cell death) have been reported for animals orally exposed to various methyl mercury
compounds, including methylmercunc chloride, methylmercuric hydroxide, methvlmercuric acetate and
methyhnercunc dicyandiamide (ATSDR, 1989).
3.1.2.
Subchronic Toxicity
3.1.2.1. Human
Depending on the exposure and subsequent accumulation of methyl mercury in the bods , toxic effects
may appear within weeks or months (Clarkson, 1989). As noted by Berlin (1983). seventy of exposure will
determine the onset of toxic effects, and that toxicity may occur following less than chronic exposure (see
Section 3. .3.1.). The signs and symptoms include sensory disturbances, constricted visuaHield. deafness, and
motor aberrations. Primary targets for methyl meicuiy damage uTadult humans are the cerebellumTcalcarine
nssure, and the precentral gyrus of the brain.
3
3.1.2.2. Animal
Subchronic exposure of cats to methyl mercury at doses of 0.01 mg/kg/day for 11 months, or 0.45
mg/kg/day for 83 days caused behavioral and pathological changes in nervous tissue (U.S. EP A. 1985).
Similar effects were also reported for rats given methyl mercury dicyandiamide at 1 mg/kg/day for 8 weeks
(Magos et al., 1972). An impairment of spatial vision at high and low luminescence was observed in newborn
cynomolgus monkeys fed methyl mercury at 0.05 mg/kg/day for 3-4 years. Evans et al. (1977) reported
reduced visual sensitivity, restricted visual field, intention tremors, somasethic impairment, and incoordination
in monkeys receiving 100 day-exposure to methyl mercury doses that produced steady-state blood mercun
levels of 100-400 ig/dL.
Wakita (1987) reported an increase in systolic blood pressure in rats receiving methylmercuric chloride
by gavage at 0.4 mg Hg/kg/day for 3-4 weeks. The effect persisted for at least 9 months.
Gavage administration of methylmercuric chloride at a dose of 1 mg/kg (0.8 mg Hg/kg) to rats for up to 11
weeks resulted in neuronal degeneration of the cerebellum and dorsal route ganglia, and clinical signs of
neurotoxicity (Chang and Hartmann, 1972). Hind leg weakness and degenerative changes in the corpus
striatum, cerebral cortex, thalamus, and hypothalamus were seen in mice receiving methyl mercury by gavage
at doses of 1.0 or 4.0 mg/kg/day (0.8 or 3.2 mg Hg/kg/day) for 60 days (Berthoud et al.. 1976).
3.1.3.
Chronic Toxicity
3.13.1. Humans
The chronic toxicity of methyl mercury is best exemplified by the epidemic poisonings in Iraq, and
Minamata and Niigata, Japan. In Iraq, over 6000 individuals were hospitalized and 459 individuals died as a
result of consuming bread prepared with flour made from wheat and barley treated with a methylmercurial
fungicide (Bakir et al., 1973). Methyl mercury concentration in the wheat flour ranged from 4.8-14.6 ig/g
(mean=9.1 ig/g). The clinical symptoms included paresthesia, visual disorders, dysarthria, and deafness. The
most severe cases resulted in coma and death due to CNS failure. Based on data obtained during this incident,
a dose-response relationship between blood mercury levels (<10 ig/dL to 500 ig'dL), and frequency and
severity of symptoms showed that mild symptoms occurred at the lower blood mercuiy levels and that deaths
occurred at levels >300ig/dL.
In Minamata and Niigata, Japan, methyl mercury poisoning resulted from the ingestion of fish that had
accumulated methyl mercury and other mercury compounds that were released from industrial sources into
surface waters (WHO, 1976).
3.1.3.2. Animals
Charbonneau et al. (1976) fed methyl mercury to cats for 2 years and found that doses as low as 0.046
mg Hg/kg/day impaired reflexes and diminished sensitivity to pain. At higher doses, these effects became
progressively more severe to the point of convulsions. Histopathological correlates included degenerative
changes in the dorsal root ganglia, and sensory nerve pathways.
Incoordination and weakness was observed in three of 16 kittens ted tuna containing methyl mercury
(dose equivalent to 0.015 mg Hg/kg/day) for 11 months (Chang et al.. 1974). However, degenerative changes
4
■
in the cerebellum and cerebral cortex were found in most of the treated kittens.
Mice given methyl mercury (0.8 mg Hg/kg/day) in the drinking water for 110 days followed by 8-16
mg Hg/kg/day for 14 months exhibited unspecified neurotoxic effects (Ganser and Kirschner. 1985). Rice and
Gilbert (1982) reported impaired spatial vision for monkeys given methyl mercury at a dose of 0.05 mg/kg/day
(0.04 mg Hg/kg/day) from birth until 3-4 years of age.
3.1.4.
Developmental and Reproductive Toxicity
3.I.4.I. Human
Relative to the effects on the adult brain, the effects of methyl mercury on the developing brain in
uiero are more diffuse and may involve derangement of cortical cells layers and ectopic neurons.
Depolymerization of microtubular structures by methyl mercury may be a possible mechanism for these
prenatal effects (Clarkson, 1989).
Although no evidence of teratogenicity was observed. Amin-Zaki et al. (1974) found other severe
dgvelopmgnial. effects (impaired motor and mental function, hearing loss and blindness) in infants of mothers
exposed to methyl mercury via contaminated gram during the Iraqi epidemic. The most severely affected
infants had mercury blood levels ranging from 319 to 422 ig Hg/dL. It is also important to note that a 45%
mortahty rate was reported for pregnant women with signs of mercury poisoning versus a 7% mortality rate for
the general population.
Harada (1978) reported that at about 6 months of age 13 of the 220 infants prenatally exposed to
methyl mercury during the Minamata Bay incident showed signs of mercury poisoning characterized by
mstability of the neck, convulsions, and severe neurological and mental impainnent.
Choi et al. (1978) reported abnormal cytoarchitecture of the brain in infants prenatally exposed to
methyl mercury. No other significant anatomical defects have been reported.
3.1.4.2. Animal
<
A 100% incidence of neonatal deaths and failure of dams to defiver was reported for rats receiving
dietary methylmercuric chloride equivalent to 5 mg Hg/kg/day (Kliera and Tabacova, 1973). The investigators
reported no maternal toxicity.
Ultrastructuial changes in die nervous system of mice exposed in uiero to methylmercuric hydroxide
(up to 10 mg Hg/Tg/day) were reported by Hughes and Annau (1976). A dose of 3 mg Hg/kg/day produced
significant behavioral changes in the mice. Ultrastructural changes in the nervous system have also been
reported for rats prenatally exposed to methylmercuric chloride (4 mg Hg/kg/day) (Chang et al.. 1977).
Exposure of rats to methyl mercury in die drinking water (0.25-0.50 mg Hg/kg/day) from one month
prior to mating to the end of gestation resulted m ultrastructural changes the livers of the fetuses (Fowler and
Woods, 1977).
In their study using monkeys exposed from birth to 3 or 4 years of age (Section 3.1.3.1.). Rice and
I
5
Gilbert (1982) noted that the young, developing monkeys were especially vulnerable to the toxic effects of
methyl mercury on visual function as demonstrated by the low dose at which these effects occurred.
Pregnant monkeys (Macaco Jascicularis) given methyl mercury in apple juice (50 or 90 ig methyl
mercury/kg/day resulted in blood mercury' levels of L0±0.13 ppm or 2.0±0.33 ppm, respectively) exhibited a
decrease in pregnancy rate and increased abortion rate for mercurv blood levels above I ppm (Mottet et al
1985).
3.1.5.
Reference Dose
3.1.5.1. Subchronic
ORAL RfDs:
UNCERTAINTY FACTOR: 10
3E-4 mg/kg/day (U.S. ERA, 1991)
NOAEL:
LOAEL:
None
200 ng mercury/mL of blood equivalent to 0.003 mg/kg/day
3.1.5.2. Chronic
ORAL RfDc:
UNCERTAINTY FACTOR: 10
MODIFYING FACTOR:
1
NOAEL:
LOAEL:
3E-4 mg/kg/day (U.S. EPA, 1990; U.S. EPA, 1991)
None
200 ng mercury/mL of blood equivalent to 0.003 mg/kg/day
CONFIDENCE:
Study:
Data base:
Rff):
VERIFICATION DATE:
Medium
Medium
Medium
12/02/85, revised 12/01/88
PRINCIPAL STUDY:
Clarkson et al., 1976; Nordberg and Strangert, 1976;
WHO, 1976.
COMMENTS: Hie RfD is based on the fact that the earliest effects of mercury poisoning in humans
(both pre- and postnatal exposures) have been shown to occur when blood concentrations are between 200
and 500 ng Hg/mL. A blood concentration of 200 ng Hg/mL corresponds to a body burden of 30 mg
Hg/70 kg, which is equivalent to an intake of 3 ig Hg/kg/day. (WHO, 1976).
3.2.
INHALATION EXPOSURES
3.2.1.
Acute Toxicity'
3.2.1.1. Human
6
any r<
......
3.2.1.2. Animal
N„ d» co a.—
3.2.2.
Subchronic Toxicity
3.2.3.
Chronic Toxicity
““ ■“* "f
^.2.3.1. Human
No d» are av.i.M. re^ X^—iy —
-j in humans. As
the body burden of
3.2.3.2. Animal
No data ar e avarlatio ^d,n81.0 oinon.e inhaMon roxicity of mchyl mccoy in
I
3.2.4.
Developmental and Reproductive Toxicity
3.2.4.I. Human
No doo. „
devebpmonul and ^roduodve .oxicry of mChyl
»
humans following inhalation exposure.
*
3.2.4.2. Animal
No data are available regarding the developmental and reproductive toxicity of methyl mercury in
animals following inhalation exposure.
3.2.5.
Reference Concentration
3.2.5.I. Subchronic
Not calculated.
7
3.2.S.2. Chronic
Not calculated.
3.3. OTHER ROUTES OF EXPOSURE
3.3.1.
Acute Toxicity
Information on the acute toxicity of methyl mercury by other routes m humans or animals was not
available.
3.3.2.
Subchronic Toxicity
Information on the subchronic toxicity of methyl mercury by other routes in humans or animals was
not available.
Z
3.3.3.
Chronic Toxicity
Postnatal mercury poisoning may occur via exposure to methyl mercury in breast milk.
3.3.4.
Developmental Toxicity
No information regarding the developmental toxicity of methyl mercury by other routes in humans or
animals was available.
3.4. TARGET ORGANS/CR1T1CAL EFFECTS
3.4.1. Oral Exposures
3.4.1.1. Primary Targets)
1. CNS: Hie primary target for methyl meicury toxicity is the brain. Data indicate that the fetal brain
is more sensitive than that of the adult (Magos, 1980). Methyl mei:rcury-induced developmental toxicity also
involves the central nervous system.
3.4.1.2. Other Targets)
No information was available indicating additional target organs for methyl mercury.
3.4.2. Inhalation Exposures
Inhalation exposure to methyl mercury has not been shown to be a significant route of e.xposuie.
However, due to the rapid absorption of methyl mercury by biological systems and its affinity for the CNS, it
may be assumed that the critical organ (CNS) would be the same as for oral exposure.
8
4
4. CARCINOGENICITY
4.1. Oral Exposures
4.1.1. Human
Information on the carcinogenicity of methyl mercury in humans is not available.
4.1.2. Animal
Mitsiunon «.,<«.)
"ZX1
but not female mice fed methyl mercury chloride (15 ppm) for 5. weeks.
available regarding the carcinogenicity of methyl mercury.
'
4.2. Inhalation Exposure
tar„n„.»n o .he
of methyl
«■ >— and amm* following «*««"
exposure is not available.
4.3. Other Routes of Exposure
Information on the carcinogenicity of methyl mercury in humans and animals is not available.
4.4. Weight-of-Evidence
The potential carcinogenicity of methyl mercury has not been evaluated by the U.S. EP A and.
therefore, does not receive a weight-of-evidence classification.
4.5. Carcinogenicity Slope Factor
i
Not calculated.
I
5. REFERENCES
tain-Zaki. L„ S. Eltasaani, MA Majeed, T.W. Cto U.
G“””d- 1974-
utenne methyl mercury poisoning. Ped.atncs 54:587-595. (cited in USAF. 1990)
ATSDR (Agency for Toxic Substances and Disease Registiy). 1989. Toxicological Profile for Mercury.
ATSDR/U.S. Public Health Service. Dec., 1989. pp. 169.
Baku; F. S.F. Kamluji, L. Amin-Zaki, et al. 1973. Methylmercury poisoning in Iraq. Science 181:2.’0-241.
Berlin I. 1983. Organic compounds of mercuiy. In: Encyclopedia of OccupationalI Health and Safety. 3rd.
Ed., ed. L. Panneggiani, International Labour Organization. Geneva, Switzerland, pp. 036-1.^ .
9
t
Berthoud, H R, R.H. Garman and B. Weiss. 1976. Food intake, body wegit, and brain histopathology in
mice following chronic methylmercuiy treatment. Toxicol. Appl. Pharmacol. 36:19-e0
Chang, L. and H.A. Hartmann. 1972. Cltrastructural studies of the nervous system after mercury intoxication.
Acta Neuropathol (Berl) 20:122-138.
Chang. L.W.. S. Yamaguchi and J.A.W. Dudley. 1974. Neurological changes> in.cats following long-term diet
ofmercuiy contaminated tuna. Acta Neuropathol. (Berl) 27:171-176 (cited in ATSDR. 1989).
Chang, L.W.. K.R. Reuhl and G.W. Lee. 1977. Degenerative changes in the developing nervous system as a
result of in utero exposure to methyhnercury. Environ. Res. 14:414-425.
Charbonneau, S.M., I. Munro and E. Nera.
Toxicology7 5:337-340.
1976. Chronic toxicity of methylmercuiy' in the adult cat.
Choi, CM, L.W. Lapham, L. Amin-Zake, et al. 1978. Abnormal neuronal migration, deranged cerebral
cortical organization and diffuse white matter astrocytosis of human fetal brain: a major effect ot
methylmercury poisoning in utero. J. Neuropathol. Exp. Neurol. 37:719-732 (cited in ATSDR, 1989).
Clarkson, T.W. 1989. Mercury. J. Am. Coll. Toxicol. 8:1291-1295.
Clarkson, T.W., L. Amin-Zaki and S.K. Al-Tiknti. 1976. An outbreak of methylmercury poisoning due to
consumption of contaminated grain. Fed. Proc. 35.2j95-2399.
Dutczak. W„ T.W. Clarkson and N. Ballatori. 1991. Biliary-hepatic recycling of a xenobiotic: gallbladder
absorption of methyl mercury. Amer. J. Physiol. 260:G873-G880.
Evans, H.L., R. Garman and B. Weiss. 1977. Methylmercury: Exposure duration and regional distribution as
determinants of neurotoxicity in nonhuman primates. Toxicol. Appl. Pharmacol. 4115-33.
Fowler, B. and J.S. Woods. 1977. The transplacental toxicity of methylmercury to fetal rat liver mitochondria
Lab. Invest. 36:122-130 (cited in ATSDR. 1989).
Ganser, A.L. and D.A. Kirschner. 1985. The interaction of mercurials with myelin: Comparison of m vitro
and in vivo effects. Neurotoxicology 6:63-78 (cited in ATSDR, 1989).
Goyer. R. 1991. Toxic effects of metals. In: Amdur, M.O., J.D. Doull and C D. Klassen. Eds. Casarett and
Doull's Toxicology. 4th ed. Pergamon Press, New York, pp.623-680.
Harada M. 1978. Congenital Minamata disease: Intrauterine methylmercury poisoning. Teratology 18:285-
288.
Hughes J.A. and Z. Annau. 1976. Postnatal behavioral effects m mice after prenatal exposure to
methyhnercury Pharmacol. Biochem. Behav. 4:385-391. (cited in ATSDR, 1989).
9
10
4
Khera, K..S. and S.A. Tabacova. 1973. Effects of methyl mercuric chloride on the progeny of mice and rats
treated before or during gestation. Food Cosmet. Toxicol. 11:245-254. (cited in ATSDR. 1989).
Magos, L. 1980. Factors affecting the neurotoxicity of mercury and mercurials. In: Manzo, L., N. Lery, Y.
Lacasse and L. Roche. Eds. Advances in Neurotoxicology. Pergamon Press, New York. pp. 17-25.
Magos, L. and W.H. Butler. 1972. Cumulative effects of methyl mercury dicyandiamide given orally to rats.
Ed. Cosmet. Toxicol. 10:513-517. (cited in USAF, 1990)
McComish, M.F. and J.H. Ong. 1988. Trace metals. In: Bodek. I. et al. Eds. Environmental Inorganic
Chemistry. Propcities, Processes, and Estimation Methods. Pergamon Press, New York. pp. 7.10-1 - 7.10-17.
Mitsumori, K., K. Maita, T. Saito, S. Tsuda and Y. Shikasu. 1981. Carcinogenicity of methylmercury chloride
in ICR mice: Preliminary note on renal carcinogens. Cancer Lett. 12:305-310.
Mottet N.K., C.-M. Shaw and T.M. Bubacher. 1985. Health risks from increases in methylmercury exposure.
Environ. Health Perspect. 63:133-140.
Nakamura, L, K. Hosokawa, H. Tamara, et al. 1977. Reduced mercury excretion with feces in gennffee mice
after oral administration of methylmercury chloride. Bull. Environ. Contain. Toxicol. 17:5 (cited in ATSDR,
1989)
Nordberg, G.F. and P. Strangert. 1976. Estimations of a dose-response curve for long-term exposure to
methylmercuric compounds in human beings taking into account variability of critical organ concentration and
biolgoical half-time: A preliminary communication. In: G.F. Norberg, ed. Effects and Dose-Response
Relationships of Toxic Metals. Elsevier, Amsterdam. Pp. 273-282.
Norseth, T. and T.W. Clarkson. 1971. Intestinal transport of 2O3Hg-labeled methylmercuiy chloride; role of
biotransfoimation in rats. Arch. Environ. Health. 22:258. (cited in ATSDR, 1989)
Rice, D.C. and S.G. Gilbert. 1982. Early chronic low-level methylmercuiy poisoning in monkeys impairs
spatial vision. Science 216:759-761. (cited in ATSDR, 1989).
Rowland, I., M. Davies and J. Evans. 1980. Tissue content of mercury in rats given methylmercury chloride
orally: influence of intestinal flora. Arch. Environ. Health 35: 155 (cited in ATSDR. 1989)
RTECS (Registry of Toxic Effcts of Chemical Substances). 1985-1986. U.S. Dept, of Health and Human
Services, Washington, D.C.
Singer, W. and M. Nowak. 1980. Mercury compounds. In: Grayson, M. ed., Kirk-Othmer Encyclopedia of
Chemical Technology, 3rd. Ed, Vol. 15, John Wiley and Sons, New York, pp. 143-171.
USAF (United States Air Force). 1990. The Installation Restoration Program Toxicology' Guide. Harry G.
Armstrong Aerospace Medical Research Laboratory, Wright-Patterson AFB, OH. pp.73-1 - 73-84.
U.S. EPA. 1985. Drinking Water Criteria Document for Mercury7. Prepared by Environmental Criteria and
11
1
Assessment Office, Cincinnati, OH. Prepared for the Office of Drinking Water. Washington, D.C. (cited in
USAF, 1990)
U.S. EPA. 1990. Integrated Risk Infonnation System (IRIS). Health Risk Assessment for Methyl Mercury.
On-line (Verification date 12/01/88) Office of Health and Environmental Assessment, Environmental Criteria
and Assessment Office, Cincinnati, OH.
U.S. EPA. 1991. Health Effects Assessment Summary Table. Fourth Quarter, 1990. Prepared by the Office of
Health and Environmental Assessment. Environmental Criteria and Assessment Office, Cincinnati, OH for the
Office of Emergency and Remedial Response, Washington, D.C. NTIS PB90-921104.
WHO (World Health Organization). 1976. Environmental health criteria for mercury. In: Environmental
Health Criteria 1. Mercuiy. World Health Organization, Geneva, Switzerland.
.'X
12
•C"
. /
. L
JData and trends on MERCURY
Professor Dr. Gerrit H. Vonkeman, Utrecht University and Institute for European
Environmental Policy
Mercury presence, mining and prices
Introduction
Like cadmium, mercury is a rare element of the lib group of the periodic system.
However, being a noble metal, it appears (or is easily transformed) in metallic form and
has been known since ancient times. Having a melting point of 38,87 °C, the silvery
liquid metal has always roused much imagination, the more so because it has a very high
density of 13,6 and is an extremely good 'solvent* for gold and silver, via the
formation of amalgams. Although it is rare, it is found in many areas, including the
United States and Mexico, Southern Europe (Spain, Italy, the Balkan) and several states
of the former Soviet Union and Central Asia. Unsurprisingly, the natural mercury content
in soil and water is relatively high in these areas. .
The most important ore for production is cinnabar (HgS). Important deposits are found in
mountain areas of late formation and in volcanic areas, particularly in the belt from
Spain into the Himalayas and the one around the pacific basin. Five areas within these
belts have for a long time dominated the mercury production, viz. Almaden in Spain,
Monte Amiata in Italy, Idria in Slovenia, California in the United States and
Huancavelica in Peru.
Mercury is a *volatile' element; not only literally: its boiling point being as low as
356,9 °C, but also in a metaphorical sense. The latter is caused by the feet that Hg is
very easily 'methylated' in nature, thus forming an organic compound that enters living
organisms easily. As a consequence, Hg is usually present as an impurity in the fossil
fuels: coal, oil, and natural gas as well. In addition, it can appear in metal ores as a
trace element, as is often the case in lead, copper, zinc and gold ores. Natural
emissions from (erosion of) minerals, volcanic eruptions and forest fires, in later
times supplemented by anthropogenic releases, have caused a presence of on average 0,08
ppm (parts per million) of Hg everywhere on earth.
Mercury mining is a relatively simple process, because HgS easily decomposes when heated
in air. This roasting' results in sulphur dioxide (SO2) and mercury vapour. The latter
can be condensed and further purified by distillation. Given its high density, the Hg is
sold in cast iron ‘flasks' of about 2,5 liters, having a mercury content of some 34 5
kgUses of mercury and mercury compounds
Throughout the history, mercury uses have changed considerably. In the 16th century the
potential of Hg to recover silver and gold via the patio amalgamation process was widely
recognised and the demand for Hg began to increase rapidly. Large amounts were
transported from Spain to Latin America, whereby the ships carried silver and gold on
their way back. Its role in silver and gold production has remained the dominant
application until the 20th century, with an all times production peak in the second half
of the 19th century. By that time, silver amalgam also began to find an important
application m dentistry, as an easily applicable tooth filling material with a lon<’
lifetime.
As of the sixteenth century, also applications in physics began to be developed. The
liquid metal was applied in thermometers, manometers and barometers and other devices
Many new applications were added in tlie nineteenth century, as a consequence of the
• 10
rapid develop-ment of chemistr}' and electricity. Both inorganic and organic compounds
were used as dyes and later organic explosives and pesticides were developed as well. In
addition, Hg served as a catalyst in some important chemical production processes
Also mercury metal found many new applications in electrical devices and
electrochemistry. It became a much-used component of switches (eg. in thermostats),
lighting devices (e.g. fluorescent tubes) and electrolysis cells, the latter
particularly for the production of chlorine and caustic soda from rock salt brine After
the Second World War, the preparation of lithium for the hydrogen bomb and the use in
batteries were added to this list and the defence industry became an important consumer.
Finally, we mention the use of mercury metal in the extraction of gold from shallow
sediments (in addition to large-scale mining). During the many 'gold rushes', the
prospectors 'wash' the sediments with mercury, whereby the gold enters into the meremy
as gold amalgam. This amalgam is then heated in very primitive devices, whereby most of
the mercury disappears into the environment.
All mentioned applications have been developed in spite of the high toxicity of mercury
and its compounds, as has been the case with many other toxic substances and products.
It took until the 1960ies, when a mercury-based catastrophe had occurred in the Japanese
Bay of Minamata, before the toxicity of mercury got world wide attention. Since then,
mercury (and its compounds) have been designated as a 'sunset metal' by the Organisation
for Economic Co-operation and Development (OECD) and put as a 'black listed substance'
in several international legislative texts. As a consequence, many of the aforementioned
applications have been considerably reduced or even abandoned. Evidently, this resulted
in a drastic change of the mercury production scene, the more so where mercury recovery
developed rapidly into an important source.
World production, resources and reserve bases
Unsurprisingly, world production has followed the sketched developments and fluctuated
considerably overtime. The top production in the United States has already been as
early as 1877. This production amounted to 2.700 mt (metric tonnes), In 1965 (here were
still 130 mines active in the US, however producing only 675 mt. As of 1991 all US
mercury mines have been abandoned and only some indirect production is left, mainly from
gold mining.
For Europe a similar scene can be sketched and only one producing mine has sun ived
the Almaden mine in Spain, with an annual capacity of some 3.500 mt but a production of
1.500.mt or less.
Table 1 gives an overview of the world production in the 1990ics; in Table 2 the world
mercury reserves have been presented.
Country
1993 1994 1995 1996 1997 1998
Algeria
459 414 292 368 370 300
China
520 470 780 510 500
Finland
98
Kyrgyzstan
1000 379 380 584 61 1
Mexico
12
12 15
15
Morocco
0
0
0
0
0
83 90
88
90
15
Russia
60
50 50
50
50
Slovakia
50
50 50
20
20
600
0
Slovenia
6
5
5
5
Spain
64 393 1497 862 1000 1000
Tajikistan
80
55 50
45
40
Ukraine
50
50 40
30
25
Other
countries
700
United
States
400 400 400 400 400 400
Total
2793 2362 3649 2977 3126 3000
Table 1 World primary and secondary mercury production in metric tonnes
Country
Reserves Reserve
base
United
States
7.000
Algeria
2.000 3.000
Italy
- 69.000
Kyrgyzstan
7.500 13.000
Spain
76.000 90.000
Other
38.000 61.000
countries
World
total
123.500 243.000
Table 2 Word mercury reserves and reserve base, in metric tonnes
The total world mercury resources are estimated at nearly 600.000 mt, principally in
Kyrgyzstan, Russia, Slovenia, Spain and Ukraine. Given the present annual production of
3000 mt, an increasing secondary and production and a declining demand, a future
shortage of Hg is thus unlikely.
Mercury prices
As could have been expected, the mentioned developments have also influenced mercury
prices, as is shown in Figure 1. In this figure, we have opted to express the prices in
1992 US $, to better highlight die price fluctuations. Expressed in current US S. the
1965 peak corresponds with 555 US $ and die 1968 one with some 510 US $. In all other
years, current prices remained below 500 US $.
Please note that the first year is 1959 and the last 1998.
Figure 1 Annual Average US Mercury prices in 1992 US $ per flask
*
The present level is in the order of 150 US $ per tlask, or about 4.350 US $ per metric
’ tonne. This implies that the total world mining production of 3000 mt annually amounts
to only slightly over 10 million US S in value or, in other words, that mercury mining
contributes virtually nothing to the-gross domestic products of the producing countries
Evidently, this does not imply that mercury products or applications may not play a
crucial role in productions with a high contribution to GDI’.
Having the data at hand now, we also wish to note that the annual Hg production from
mining has a volume of only 220 m3 and would fit in a cube with ribs of only 6 metres
This means on the one hand that storage of even the entire Hg production o( this centuiy
would be feasible, and, on the other, that it will be extremely difficult to recover the
mercury once it has been dispersed in the environment.
Mercury world production
Introduction
In section 1.2 we have already presented the annual world production from direct and
indirect mining, that is in the order of 3.000 mt annually. However, there is also a
secondary production from recovered Hg and Hg products that is rapidly growing in
importance, because of the world wide efforts to prevent Hg from entering the
environment. It is difficult to produce reliable figures for the entire world, but,
whereas the aim of this study is the provision of sufficient data for policy
development, this is no problem, as long as trends and orders of magnitude can be gi\ en.
The latter can best be derived form the developments in the United States.
Secondary production in the United States
Year
1993 1994 1995 1996 1997 1998
Production in mt 350 466 534 446 389 400
Table 3 Secondary production of Hg by the US industry in mt
As Table 3 indicates, the US secondary production alone amounts already to 13% of the
world primary production. About 70% of this is accounted for by the chloralkali industry
(that reuses most of the reclaimed Hg itself) and another 25% came from discarded
instruments and switches. Laboratory' wastes, fluorescent lamps and dental amalgam made
up for the remaining less than 5%. Except for the chloralkali industry', the problem is
that each individual waste item usually contains only a minute amount of Hg. The
collection, transport and recovery costs are therefore high, as compared with the value
of the recycled product, and recycling will only develop if supported by legal or
financial incentives.
The situation in Europe
Exports to: Year
1990 1991 1992 1993 1994 1995
Netherlands tonnes
297 296 125 14 7
161
1231 773 621 21 28
476
kEUROs
kEURO/tonne 4.1 2.6 5.0 1.5 4.0 3.0
Europe
tonnes
kEUROs
402 379 223 69 39
286
1678 1166 1005 196 147 926
kEURO/tonne 4.2 3 1 4.5 2 8 3.8 3.2
tonnes
1
10
0
0
0
7
kEUROs
5
43
0
0
1
29
Africa
4.1
kEURO/tonne 5.0 4.3
tonnes
0
28
12
0
0
14
kEUROs
0
57
10
0
0
45
USA
Meso
tonnes
America
kEUROs
3.2
2.0 0.8
kEURO/tonne -
23
14
14 17
22
64
103 63
5
19
42 64
kEURO/tonne 7.4 2.7 2.9 3.0 3.8 3.8
Amazonia
tonnes
kEUROs
82
42 30 24
73
31
15
85
213 147 98
96
kEURO/tonne 5.5 3.1 2.9 3.5 3.3 3.5
Southern
tonnes
5
Cone
kEUROs
42
42
0
1
109 17
kEURO/tonne 8.4 2.6 South Asia tonnes
kEUROs
20 77
0
2
12 8
12.0-
14
7.0
13 478 25 43
98 240 30
1400 69 150
kEURO/tonne 4.9 3.1 2.3 2.9 2.8 3.5
East Asia tonnes
kEUROs
19
154 552 564 1687 559
100 476 1462 1505 1245 1800
kEURO/tonne 5.3 3.1 2.6 2.7 0.7 3.2
Total
tonnes
kEUROs
476 744 895 1168 1798 940
2108 2250 2801 33021632 3068
kEURO/tonne 4.4 3.0 3.1 2.8 0.9 3.3
Table 4 Total Spanish metallic mercury exports as reported to Eurostat
The only Hg mine in the European Union, owned by MAYAS A, is situated in Almaden, Spain,
with a production capacity of 3.500 mt and an actual annual production of about 1000 mt
per year. Table 4 gives the exports of metallic mercury from Spain; in addition some 150
mt of mercuric oxide (most commonly used for batteries) is sold each year. Table 6
presents the relative importance of these activities for the company.
Year
1994
1995
MAYASA
Within
For Within
For
sales of:
Spain export Spain export
♦
Mercury
533
2 504
1 100 3 519
Mercury
products
30
584
11
Total
income*
27 391
524
3 088 36 249 4 044
The 'Totals' row includes all the company's sources of income - much the largest being
contract works for various public bodies.
Table 6 Share of mercury based activities in MAYASA income, in thousands of EUROs
World stocks and strategic stockpiles of mercury
It is an impossible task to obtain reliable data under this heading. Stocks may be
maintained by mining companies, trading companies and users for varying reasons and
under varying conditions. The Spanish mine keepts stock of 3-4 months production,
motivated by the remark that this contributed to their reputation as a reliable supplier
that could also meet unexpected demands. This provides an indication that this is not
common practice and that the total world stocks at the mines will probablv be less than
some 750 mt
Given the decline in both demand and price, the risks and costs of maintaining a stock
are high and it is unlikely that substantial stocks are present at commercial trading
and manufacturing companies. It would therefore surprise us if their total stocks would
match the ones at the mines.
Another, and even more difficult case is presented by governments and the defence
industry. Some years ago, it became apparent that some governments had built up
considerable stocks, notably for the production of lithium for hydrogen bombs. The US
has been selling some 1.735 tonnes from surplus stocks between 1979 and 1994. Followinn.
nuclear disarmament agreements, 5.200 additional tonnes became available, but have been
withheld because of the possible environmental consequences of putting almost twice the
annual world production additionally on the market. Taking into consideration that it is
uidcnown how much mercury has been retained for military purpose and that, moreover, the
US federal government holds a stock of 5000 mt for other purposes in addition, we may
conclude that the total US government stockpile probably amounts to well over 10 000
tonnes. Whereas it is also known that much of the Russian Hg sales in the mid-1990ies
originated from government stocks, and it is likely that other (potential) nuclear
powers have followed similar strategies, the least we can conclude is that government
stockpiles may amount to over five years of annual world production and then outweigh bv
tar the stocks at producing, trading and industrial companies.
Consumption and trade
The annual primary world demand for mercury is uncertain but below 5.000 tonnes, or 360
m3. The value of the total world Hg market was estimated at $75 million in 1982. but
just one-third of this, $25 million, ten years later in 1992. It is difficult to net a
detailed picture ofglobal mercury flows. By far the largest consumers arc die
industrialised countnes of the OECD family, but an 'eastward' shift is observed.
Global mercury consumption
2000
In previous years
Tout accumulation (excl. Chlorine plant 2100
inventories)
Environmental burden ofHg on the EU 12
754
Domestic burden
Emissions .mported from third countries
31
Emissions exported to third countries
27
Total accumulation in the EU 12 environment 758
Table 9 Annual flows of mercury through the EU 12 economy and env.ronment m i 989
eCoLly.i^relse the stock
It should be noted that, with a
14.000 mt tf the tnventory of the mercury cefls of
the EU chloralkali industry is included.
The following nsded.K. uTtfeU0jncompleie (for
“SSWSSSSXSnX „ iuen -«-■ «»" ™
The EU12 in 1995
Imported tonnes Exported tonnes
ofHg
''fu’
from: ofHg to:
EU12
EU12
745
745
Other 513 Other 87
Europe,
Europe,
CIS
CIS
N.
47
America
N.
22
America
Africa 42
Africa
26
0
South
Asia
132
South
Asia
East Asia 0
East Asia 815
Amazonia 0
Amazonia 40
Total
1347
Total
1919
Table 10 EU imports and exports of mercury in 1995
Typical uses of mercury
Refernng to Table 8, we will now pay more attention to each of the mentioned uses.
Wiring, switches and measuring devices
In this area, a considerable replacement by electronic solutions and a rcducUon of the
mere uy content has taken place in mercury sensitive countries, some of which have
banned these uses almost completely. We note here that, although Hg is the only metal
element that is liquid at room temperature, some alloys have the same propertv L- u
commercially available gallium-indium-tin alloy called Galinstan has a melting point 19
ai^l H b®1.in|g P01”1 ofover 1-300 °C) and is claimed to be non-toxic and recyclable.
Although it lacks the high density necessary for barometers et cetera, it can be a good
replacement in (fever) thermometers (if electronic devices are not an option),
speedometers, thermostats and other tilt switches, liquid mirrors, ct cetera.
Whereas all mercury containing devices will be discarded at some moment, a good
collection system is anyhow of great importance here.
Lighting
Whereas fluorescent bulbs have an important role to play in energy conservation and no
alternative for the use ofHg is available as yet, it would be unwise to ban this
application. In the past, the amount of Hg per device has already been reduced and
rther reduction, c.q. replacement, should be encouraged via research. It is likewise
important that the discarded lamps are collected. In spite of their low Hg content
Denta?usenUmber S°
‘hat “ SUmS UP ‘O 3 considcrable amo,'nt 1 'll P<=r year.
Although in Denmark and Sweden composite fillings and titanium and gold inlays have
Urgely replaced silver amalgam as filling material, and the discussion about the danger
ofHg in fillings and then release of Hg into the body continues many dentists cl .i.n
that composite fillings are inadequate for molars of adolescents and that inlays are too
expensive.
°fmo/H8 US6d 10 dentiStry endS *n the fillin8'Firet of al1'''is important
that the other lO/o is recovered. The remaining 90% ultimately ends up in the
Xn“ % reStnC,'°n Ofamal8am fi,linSS t0 adult molars only would reduce the
Other (small) uses; Batteries
larsest use of Hg in the us in 1989’and the second
«m V
’
Char'gCd POS't,0n Wlth paints'(See hereafter). It was used both
as the key component in mercury battenes and as an additive in other types Mercun.batteries have vntually disappeared from OECD countries and alkaline battenes have
become mercury
Outs.de OECD, the situation is less reassuring
Other (small) uses; Paints
and fimgictde m latex pamts. Whereas the first appheatton directiy polluted the
aquatm environment and the second could threaten human health £ a consequence of the
Other (small) uses; Chemicals
“=’,s
Table*7 presents an overall view of world mercury consumption in 1993. Given the tact
’ that CIS has no significant chloralkali production based on mercury cells, its figure is
remarkably high.
World Mercury Consumption
(tonnes, 1993)
1379
CIS
USA
558
Europe
448
Iran
414
China
345
India
.345
Other
345
Total
3834
Sources: Lawrence, B.,
"Mercury",
E&Mj, March 1994;
US Geological Survey
Table 7 World mercury consumption in 1993
Mercury consumption in the United States
In the United States, the use of mercury has dropped by 80% from a peak thirty years
ago. The remaining U.S. use during 1997 is presented in Table 8.
Application
Tonnes % %
1997 1997 1993
chlorine production
160
46 33
wiring and switches
57
17
15
measuring devices
24
7
12
lighting (fluorescent
bulbs)
29
8
7
12c
6
(many) other smaller
uses
36
10
Total
100 100
dentistry
40
346
27
Table 8 US mercury uses in 1997
Mercury flows in the European Union
Because comprehensive updated mercury flows are not available for the EU as a whole, we
have compiled a flow data sheet based upon our work for DG XI in 1991 (sec I able 9).
’ These data apply only to 1989, and only to the EU12 (less the former Eastern Germany).
They were the most complete data compiled at that time. Even today, they mav be taken to
approximate EU15 flows, given the quantities and trends shown in recent, aggregated data
for the present EU.
Imports extra EU 12 and primary production Tonnes
Imported waste and used products containing
Hg
- for reprocessing
- for disposal
0
40
Imported products
125
Primary (mined) Hg
967
Secondary Hg
361
Imported refined Hg
803
Imported ores, fuels, et cetera
172
Reprocessed for domestic use
0
‘ • Total mercury flow
2468
EU 12 economy
Consumer products
650
Industry/commercial products
Other uses
250
200
EU 12 reprocessing
0
EU 12 exports
Primary Hg
1000
Reprocessed Hg
Hg products
0
408
Exported Hg waste
206
Total EU 12 mercury exports
1614
Accumulation of Hg in the EU 12 economy
In 1989
100
should not disappear completely out if sight.
Other (small) uses; Gold mining
Apart from application in some industrial gold mining and production operations, mercury
is widely used by individual gold seekers to 'wash' the gold from sandy river sediments
and collect it as amalgam. The amalgam is subsequently heated to recover the gold,
whereby most of the mercury is lost into the environment. This practice is known to
cause considerable damage in the Amazon area of Brazil, but similar use has also been
reported in Kampuchea, Vietnam, Colombia, Ecuador, Peru, Panama, Papua New Guinea and
(perhaps) Ghana and Zimbabwe. Greenpeace estimated total world wide mcrcurv use for gold
mining as 400-500 tonnes in 1993-4. Some industry observers consider this estimate loo
high, and suggest that 1996 use may be 350-450 tonnes At some point all of this enters
the environment, after first having caused considerable damage to human health. Even if
this application does not consume the greatest slice of world mercury consumption, it
certainly merits the greatest attention due to the devastating environmental and health
effects.
Chlorine production
The production of chlorine and caustic soda (NaOH) from brine is one of the largest bulk
chemical processes in the world, with a capacity of well over ten million tonnes of each
product In feet it is rather peculiar that one often speaks of chlorine production,
because in many years the market demand for NaOH rather then C12 determines production.
Three electrolytic processes are applied in industry, based on the mercury, diaphragm
and membrane cell, respectively. Each process has its advantages and disadvantages in
chemical, economic and technological terms. After 1970, environmental considerations
dominantly entered the scene and no new Hg cells have been installed in the US since
then, contrary to Europe. Whereas the diaphragm cell is 'technologically mature'
improvements are unlikely, and, moreover, most diaphragms contain asbestos, US EP A
states: 'The modern membrane process has been improved over the past decade to become
more efficient than either the diaphragm or mercury cell and produces a higher qualitv
product than either cell'.
Region
Capacity Share share
world Hg
capacity cells
%
%
North America
14686
29,7
12,5
South America
1787
3,6
23,7
(1.000
tonnes)
European
Union
rest West
Europe
East Europe
21
10359
0,6
281
62,4
33,8
1791
3,6
66,9
former USSR
3676
7,4
6,4
Middle East
1294
2,6
21,3
Africa
584
1,2
38,5
Indian
2135 4,3 42,9
Subcontinent
Northeast
11794 23,9 0,4
Asia
Southeast
1050 2,1
19,8
II
Asia
Total World
49437
100
23,5
Table 11 Chloralkali production capacity; situation by world rcj’ioii m I'.'97.
In Table 11, the high percentage of the total production capacity of the European Union
that is covered by mercury cells is particularly striking: almost three times the world
average and five times that of North America (the NAFTA countries). The comparison with
the former USSR is even worse, not to speak of Northeast Asia (China, Japan and Korea),
that produces practically mercury free.
Of the world regions, only the East European countries (many of them accession
countries) have a worse record. The accession of the Central European candidate
countries would increase the EU production capacity by some 16%, based for 64.80-<> on 11g
techholdgy, the latter percentage being slightly above EU average.
Comparing Table 7 with Table 11, one must ask oneself what will be the use of the
mercury in cases where countries without Hg based chlorine production buy substantial
amounts of it This question is particularly relevant for CIS and China. The latter has
been £ large buyer in spite of its Hg based chlorine production capacity of only 50
tonnes out of 5186 total. But the question is relevant for other countries as well.
Mercury flows through the environment
Introduction
In this section, we will tre^f three types of Hg flows and try to quantify their
relative importance, 'fhe fitst are the natural flows. In addition, we will distinguish
two types of anthropogenic flows, in spite of the fact that their borderline is not
always easy to trace. The first group comprises inadvertent flows, caused by Hg that is
present as an impurity or contaminant in ores, substances or products. The other flow is
linked with the use of Hg in the economy.
Natural flows of mercury
As stated earlier, natural emissions of Hg may originate inter alia from volcanic
eruptions, natural degassing, vapourisation and erosion. It is estimated that these
processes emit some 1.000 mt annually into the United States and 5.000 mt world wide In
comparison with these figures, the amount of mercury that is annually trapped in
sedimentation and other processes is very small. Confronting this figure with an annua;
primary production of maximum 5.000 mt, that will only be partly emitted into the
environment, may give the impression that anthropogenic flows will be of less
importance. However, one must be aware that the deposition of Hg by natural emissions
will occur for more than 90% in the oceans and uninhabited areas of the world, whereas
most of the anthropogenic emissions will end in populated areas. Moreover, if mercury
immissions cause problems, the only thing we can do is to reduce the anthropogenic pan.
Mercury flows from impurities and contaminants
Fossil fuel combustion
Coal, oil and natural gas all contain varying amounts of Hg. For the US, an average
concentration ofHg of 0.21 ppm has been determined for 1990, 1’hus the 81 2 mfcoal n■.!
by the US in 1990 will have emitted some 130 mt of Hg. assuming 25% was irappc.l bv
emission control.
For oil, almost all the Hg it contains will be emitted during combustion. Typically,
crude oil contains 3,5 ppm, distillate oil 0,40 ppm and residual oil 0,06 ppm. For the
US, the oil that has been combusted during 1990 will thus have contributed some 1 0 m: • f
Hg in emissions.
Data on the role of natural gas are more difficult to obtain In the Netherlands, where
the gas has a rather high Hg content, about 8 tonnes arc captured annually and 6 of them
reprocessed.
I ,ime and cement manufacture
The Hg content of limestone is in the range of 0,02 to 2,3 ppm. US EPA has determined an
overall p.miccinn factor nfO 0R7 u nf Mo n#*r metric, tonne (if produced cement ;md
calculated an emission of 6 mt of Hg for the total US cement production of 1990. We do
not. have similar data for lime production
Municipal solid waste incineration
Althoueh municipal solid waste and refuse will deftnitelv cnntnin roninone.nis from .the
second anthropogenic category, we will briefly discuss this source of emissions here.
Evidentlv. the Hu content of refuse depends strongly on the wealth of the uomdaiion
that produced the waste and the state of advancement of the mercury and the waste policy
in place. The latter also includes the tvne of incinerator and its emission controls
For the US, it has been estimated that 97 mt of Hg was emitted in 1989 and 57 mt in
1990. the reduction being laruelv the result of the restriction of Hu batteries.
Also municipal sewage treatment plants collect Hg in their sludge; in the US the average
concentration in 1990 was 5 c/mt. The sludge was either burnt in incinerators that
emitted on average 0,018 g/mt if equipped with venturi control and 1,6 g/mt without this
equipment, contributing some 1.6 mt Hu out of 1.5 million tonnes of sludge, or
landfilled. An estimated 1 mt of Hg was placed in landfills via sludge.
In addition. 58.7 mt Hg was emitted to the atmosphere in the US in 1990 bv medical waste
incineration.
Mercury flows from economic uses of He
Mining and primary production of mercury mines
Evidently, the losses durine minine and production vary from site to site, whereas they
depend inter alia on the type of mine (closed or open pit), the characteristics of the
ores, and the quality and technology of the roasting and purification process. Until the
beginning of the 20th century, up to 40% of the Hg was lost in the condenser. This
amount was reduced to some 5% around 1930 and to less than I % in the last operating mine
in the US, at its closure in 1990.
Secondary production from other ores
As stated earlier, most non-ferrous ores contain trace amounts of Hg. Some of it is lost
during the mining and concentration process, but most of the Hg remains in the
concentrate. Potentially, the roasting process is therefore the most likely source of Hg
emission into the environment. Whether this happens and to what extent depends to a high
degree on the quality and technology of the roasting process and its emission controls.
It is therefore impossible to arrive at general estimates that make any sense.
Apart from being a source of Hg emission, some mines and ore refineries also produce
mercury as a by-product. Data on sources and quantities were already presented
Mercury recoveiy
Although it does not influence the total amount of mercury on earth, the recover/ and
recycling industry can play an important role in keeping the Hg in the economy and thus
reducing its emission. The size and state of development of this sector differs
considerably from country to country.
'Chemical time bombs'
Several years ago, William Stigliani from the International Institute for Advanced
Systems Analysis (DASA) introduced this suggestive name for the total quantity of any
persistent substance that had been produced in the past, and therefore must still 'be
around somewhere'. We have not borrowed his indication to suggest that mankind is in
imminent danger from its past Hg production, but rather to distinguish this kind of
stock from the stocks we addressed in section 3. However, one cannot deny that vast
amounts of mercury have been produced in the past. For die US alone, an estimated input
of over 100.000 mt has been calculated for the. period between 1900 and 1990 We also
know that US domestic production peaked in 1877, at 2.700 mt and had reached a, from
then on more or less stable, level of 1.000 mt annual production by 1900. Whereas US
mercury production began in 1850, it is not unreasonable to assume that the total Hg
I
input into the US may not have been far below 200.()()() mt
For the EU, the figures will be less dramatic, give die absence of the gold rushes that
absorbed most of the mercury input in the 19th century in the US. For the 20th centurv.
however, the similarity between the US and Europe will be much greater.
Chlorine and caustic soda production
The production in mercury cells results in losses to all three environment compartments.
Most of it is lost in wastewater, from which it can be partly reclaimed by retorting. (IS
EPA estimates that the total mercury losses in Hg cell chlorine production in the t IS i.
0,75 kg Hg per 100 tonnes of produced chlorine, or 7,5 g/mt. Foi the EU this would
amount to 67.500 kg annually.
The EPA Toxic Release Inventory (TRI) gives for 1990 a total Hg loss to the US
environment by chlorine and caustic soda production of 69.512 kg, for 21 of the then
active 23 plants. Assuming the same conditions, this would indicate a much higher
emission in the EU, viz. in the order of 240.000 kg or 240 mt per year.
Electrical and other uses
For most uses, we have already given the relevant data earlier. In spite of attempts to
abandon or reduce many of these uses, discarded products will continue to contribute to
the flow of mercury into the environment. E.g., US EPA estimates that broken fever
thermometers alone contribute some 15 mt of Hg annually to this flow.
ANNEX Chlorine production and chlorine based industry
As announced, we begin this annex with Table 12, that sheds more light on on the 1997
situation in the EU.
Country Hg Diaphragm Membraneother other Total% 11g
cell
Hg Hg
free
Austria
113
Belgium
508
Finland
40
France
718
Germany
2079
Greece
35
113 100
0
60
530
578
Portugal
70
Spain
Sweden
Total EU
20 162851,2
260 50 110 394953,9
5
5 0
165 175
Netherlands 205
UK
10040,0
245 115
1450
50 82768,2
35 100
Ireland
Italy
205 64
130
91882,0
300
63532,3
12
8285,4
652
42 20
71494,1
185
100
28564,9
735
190
83 25 35 106871,2
1035962,4
Hi
Table 12 Chloralkali production capacity in the EU in 199/
For East Europe details are given in Table 13
Country Hg
cell
Diaphragm Membraneother other Total% I Ig
Hg Hg
free
Albania
10
Bulgaria
10 100
105
105 0
Czech Republic +
Slovakia 141
Former
121
Yugoslavia
Hungary .155
88 50
27968,5
12
13391,0
155 100
Poland
230
232
Romania
217
45
46249.8
110 275
East Europe
647 76
179166,9
Table 13 Chloralkali production capacity in Eastern Europe in 1997
Chlorine is a bulk chemical with many applications. According to the EU chlorine
industry, total EU chlor-alkali production value in 1996 was over 3 billion Euro.
Chlor-alkali production is important for over 50% of the EU chemical industry and
chlorine based products contributed some 20 billion Euro in export earnings in 1996. In
spite of these impressive economic data and their major contribution to employment, both
the chlorine production and the chlorine-based chemical industry have come under severe
pressure based on environmental concerns.
Evidently both industries are inter linked and often combined into one chemical complex,
thus avoiding the risks of bulk chlorine transports. Elsewhere, we have described the
structure of the chlorine based industry, their most important end products and their
applications and the main chlorine streams through it. Here we iust present a Table for
the EU in 1995.
End Use
Chlorine
kt per %
annum
Polymers, mainly PVC
3271
36
Organic chemistry, dyestuffs,
pesticides, medical, ct cetera
1777
19
Inorganic chemistry, e.g. titanium 1345
dioxide
15
Intermediates for non-chlorinated 2171
polymers, PU, PC, epoxies
24
,
Elemental chlorine
258
3
Table 14 End uses of chlorine in the EU in 1995
Many applications and products have been banned or substantially reduced in the past ten
years, such as chlorine bleaching in the paper pulp industry, pesticides, organochlorine
solvents, PCBs and PCTs, CFCs and diffuse applications of PVC. Important environmental
NGOs such as Greenpeace have been campaigning for a 'chlorine free chemistry' since more
than a decade, initially on environmental grounds. Later, sustainable development
considerations have added new arguments to their position.
The least one can say, given this situation, is that the future of these industries
merits a serious scientific and political debate, followed by a long term, global
policy.
We could e.g. well imagine that, in a situation 10 or 20 years from now, the global
chlorine demand will not be higher than at present, in spite of the population increase
and the development of nonwestem countries. Moreover, a substantially increased
recovery and recycling of chlorine containing products could have further lowered the
demand for primary chlorine . Such a situation, combined with the expectable desire of
non-westem countries to have their own chlorine production and chlorine-based chemical
industry and the probability that, by then, they can use solar energy' as a cheap and
CO2-ffee energy source, could have very serious consequences for the chlorine producing
industry within the EU.
Presently, the European chlorine producing industry is strongly opposed to the OSPAR.COM
decision to phase out mercury cells by 2010 at the latest. Among its most important
economic arguments are that replacement by other (probably membrane) cell types would
result in a considerable capital destruction and a large investment demand that would
■ leave little room for investments in other promising areas. We return to its
environmental arguments later.
With regard to the capital destruction, it is evident that functioning equipment that
could be applied for another one or two decades would have to be dismantled On the
other hand, and apart from the fact that most of the installations were built at a
moment that Japan, the US, Canada and others already abstained from their use for
environmental reasons, the installations have all been depreciated several years ago. It
is also questionable whether they will be competitive on the world market, the more so
where their chlorine prices exceed already US and Middle East prices by almost 100 USS
per Electrochemical Unit.
Regarding the investment costs in new cells, one could question their necessity.
Investment in non-chlorine areas might be much more beneficial to the EU economy and
environment of the future.
Regarding the environmental side of the medal, the chlorine producing industry
highlights that the present and future mercury emissions from their cells are already so
low that the cost per kg of mercury that will be withheld by closing the cells is
extravagant and the effect insignificant. In addition, they stress that at least 1 1.800
tonnes of mercury will become available from the cell content alone. Although one can
question some parts of their calculations and, moreover, we cannot reconcile them with
our own and the fact that the EU chlorine industry buys some 60 tonnes of mercury per
year for replenishment, we leave this issue for the time being. Anyhow, the concern for
the stock in the cells is totally justified.
Theoretical background for framing future policies and legislation
Introduction
Before we enter into details, we wish to make a number of introductory remarks to
It,
position this text and explain and motivate our approach.
First and foremost, this text is intended to trigger and focus discussion. I lowevcr, this
rlrtac
mo-in
«♦ ic tirr,f+*»n <n o
tiroir
/7
f\ttr rr\ nc i zjr>r-i ti-x-i e .>o.l
suggestions are based on environmental concerns, in the conviction that the economic
actors are best placed to present their side of the coin and will be given ample
opportunity to do so.
In fact, environmental concerns is not the right expression: it should rather be slated
as "sustainable development" concerns.
The governments of the world have embraced the concept of sustainable development as the
base for policy making in any area and the European Union even adopted it as its central
goal in the Amsterdam Treaty. Sustainable development is a complicated concept that
cannot easily be defined in one short sentence. But, as we have explained elsewhere , it
is by no means vague.
In its report to the UN General Assembly , the World Commission on Environment and
Development (WCED) wrote:
Sustainable development is development that meets the needs of the present without
compromis-ing the ability of future generations to meet their own needs.
It contains within it two concepts:
the concept of'needs', in particular the essential needs of the world's poor, to
which overriding priority should be given; and
the idea of limitations imposed by the state of technology and social organi-sation on
the environment's ability to meet present and future needs.
The Commission also describes sustainable development as an ongoing process:
In essence, sustainable development is a process of change in which the ex-ploitation of
resources, the direction of investments, the orientation of techno-logical develop-ment
and institutional change are all in harmony and enhance both current and future
potential to meet human needs and aspirations .
Having discussed the report (and several other UN policy documents, such as the
voluminous Agenda 21 ) at the United Nations Conference on Environment and Development
(UNCED) in Rio de Janeiro, mid 1992, the representatives of the member states
governments concluded in Principle 25 of their Rio Declaration :
Environment, development and peace are inter-dependent and indivisible.
In our view, that is supported by other Principles from the Declaration, these
quotations imply that a reduction of the total global pressure on the environment and
its resources and a simultaneous reduction of the gap in wealth and quality of life
between the rich and the poor parts of the world are not only the central aims of
sustainable development, but a prerequisite for peace and societal stability as well.
Thus, sustain-able development becomes an expression of both intra- and
inter-generational solidanty. Keeping in mind that the environment and development
problems have been caused by the state of technology and social organi-sation, solutions
have to be found in these two areas, and predominantly in fundamental changes in the
latter. If we wish that future generations live in a world characterised by a higher
degree of equity, but also by a lower total pressure on the global environment and its
resources than at present, then a substantial reduction of the claims of the rich,
industrialised countries of the West, combined with a redistribution in the direction of
the poor countries, seems inevitable, the more so where the population in the latter is
bound to increase considerably . These changes in social organisation will particularly
have to focus on our economic system, perhaps even by imposing 'limits to competition'
and/or 'growth'.
Evidently, it is far beyond the scope of this text to enter into this economic part of
the debate. But, on the other hand, the commitment of the EU to move 'Towards
sustainable Development' and the scope of the present project will oblige us to consider
future strategies and policies in the heavy metals area within a global context and
against the background of the quoted principles of sustainable development
1-^ •
/■
Sustainable deveiopment ts a long-t«™ p^
Should not shy away front a tune h°nzon of« yean or
short- and medtum-term pohc.es coulrln< ™
not realistic that any EU pol.cy could dnast «dly
e
<l)
J does not nlean lllal,he
. ,s
By dc(,nlt,o„.
, ,avlng lbe
Whereas some of them are ess^tia'extent. In parallel their mining,
solar energy, will demand large amounts of solar cells
metals.
In spite of the mentioned problems and
heat y metals polic^Metals are
ssssaghsxsssr'
„„»»«»„
sssK. "X
„
.... “
BsatsfflS - “” n””“
. ©ssssgSs
possible means. The eventual impact on price o i
on the ability of the population to purchase a good
uave access io a service, is an
hvuacocs
decision to regulate or ban a certam
ofuse and promot.on of
sass?=”
should accompany such decision.
Another uoo.lJetahoo h based on the
” red““"" ■*”
i;,Xbfeon"h^'Xo'‘l a*
....... -
■ f<
I')
So, ideally and without considering economic and other consequences, mining and primary
production should be reduced as much as possible.
The awareness that a large stock of heavy metals has accumulated alicadv m the economic
compartment gives rise to two other considerations. The first is that a substantial
reduction in the use of heavy metals, in com-bi-nation with a massive recycling eflbtt.
might result in a tangible heavy metal stock that is too large for the needs of the
remaining applications, even if primary production by mining would be abandoned. In that
case, the option of complete recycling should be reconsidered and recovery, followed by
partial recycling and partial (safe) storage might be a better one. The second
consideration is that anyhow the existence of the accumulated stocks should be taken
into account when future policy options are considered. Even the most drastic,
’’far-reaching” option: discontinue mining and ban all applications, is no solution if it
is not combined with measures that address the existing, accumulated stock. In other
words, any policy option should include provisions for the management of this stock.
Obviously, if the mining and heavy metal input is continued sustainable management of
the existing stocks becomes even more urgent.
Before we enter into separate sections, wherein we develop in more detail what the
presented background philosophy might entail for each of the studied metals, we wish to
add a few more general considerations of different nature.
As stated, we will not focus in detail on economic restructuring, although we consider
it inevitable. But we should keep in mind that the poorer part of the world is entitled
to a similar level of development as the industrialised. Thus, if we wish that they do
not additionally contribute to heavy metal problems, the industrialised world has the
obligation to enable them to follow alternative developments.
In our view, any primary production of bulk material (e.g. above 100.000 tonnes per
year) is inherently unsustain-able, because of its high (fossil) energy demand and other
environmental consequences. In case the primary process is electrolysis, which tends to
be particularly energy intensive, the energy should at least be based on solar energy,
which means that the production should predominantly take place in areas receiving high
solar radiation mostly in developing countries. Another un-sus-tain-able element of
present primary bulk production is the fact that both the ores and the energy carriers
are transported over long distances. As a rule, the heavy metal production should take
place at or in the vicinity of the mine. This would have the additional advantage that
added value is often generated within developing countries, and that at least some of
the process waste could be return safely to the mine.
Finally, we wish to highlight again that an important part of our approach is based on
validation of agreed, general principles of international policy. With regard to ’our'
heavy metals, OECD has played an important role in providing a forum for presentation of
(frequently controversial) views and in reaching agreements in a number of cases. Wc
therefore end this introduction with the following quote from the OECD Risk Reduction
Monograph No. 4 , that holds for mercury and might be amended accordingly for other
heavy metals:
Mercury is a toxic substance having no known function in human biochemistry or
physiology. It is desirable on health grounds that human exposure to mercury' be kept as
low as practicable. Where contamination by mercury exists or is likely to arise, action
to reduce man-made contributions progressively should be taken as and when appropriate,
taking account not only of the desirability of improving safety margins, but also of
industrial economic viability, technical adequacy, and the availability of less
hazardous substances.
[Image]
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ZkT.II
Human exposure to mercury: a critical assessment of the evidence of adverse
health effects. Ratcliffe HE. Swanson GM. Fischer LJ. Journal of
Toxicology & Environmental Health. 49(3):221-70, 1996
Environmental health. Maeda K. Nitta H. Journal of Epidemiology.
6(Suppl):S121-4,1996
Minamata disease redress settled [news]. Ross C. Lancet. 346(89918992): 1695-6,1995 Dec 23-30.
Expansion of methyhnercury poisoning outside of Minamata: an
epidemiological study on chronic methyhnercury poisoning outside of
Environmental Research. 70(l):47-50,1995 Jul.
Neurologic features of chronic Minamata disease (organic mercury poisoning)
certified at autopsy. Uchino M. Okajima T. Eto K. Internal Medicine.
34(8):744-7, 1995 Aug.
Neurologic features of chronic minamata disease (organic mercury poisoning)
and incidence of complications with aging. Uchino M. Journal of
Environmental Science & Health - Part B: Pesticides, Food
Japan pledges new aid to Minamata victims [news]. Swinbanks D. Nature.
375(6534):711, 1995 Jun 29.
Minamata disease: methylmercury poisoning in Japan caused by
environmental pollution. Harada M. Critical Reviews in Toxicology.
25(l):l-24, 1995.
Concentration of mercury in hair of diseased people in Japan. Nakagawa R.
Chemosphere. 30(1): 135-40, 1995 Jan.
Atmospheric pollution due to mobile sources and effects on human health in
Japan. Kagawa J. Environmental Health Perspectives. 102 Suppl 4:93-9,
1994 Oct.
MR imaging of minamata disease: qualitative and quantitative analysis.
Korogi Y. Takahashi M. Sumi M. Hirai T. Okuda T. Shinzato J. Radiation
Medicine. 12(5):249-53, 1994 Sep-Oct.
Molecular analysis of mercury-resistant Bacillus isolates from sediment of
Minamata Bay, Japan. Nakamura K. Silver S. Applied & Environmental
Microbiology. 60(12):4596-9, 1994 Dec.
MR findings in seven patients with organic mercury poisoning (Minamata
disease). Korogi Y. Takahashi M. Shinzato J. Okajima T. Ajnr: American
Journal of Neuroradiology. 15(8): 1575-8, 1994 Sep.
Methylmercury induces apoptosis of rat cerebellar neurons in primary culture.
Kunimoto M. Biochemical & Biophysical Research Communications.
204(l):310-7,1994
e
[Health conditions among fishermen living in the Minamata disease prevalent
area]. Sugisawa A. Nippon Koshu Eisei Zasshi - Japanese Journal of
Public Health.
Profile of subjective complaints and activities of daily living among current
patients with Minamata disease after 3 decades. Kinjo Y. Environmental
Research. 63(2):241-51,1993 Nov.
The epidemiology of disasters and adverse reproductive outcomes: lessons
learned. Cordero JF. Environmental Health Perspectives. 101 Suppl 21316, 1993 Jul.
Environmental release of chemicals and reproductive ecology. Bajaj JS. Misra
A. Rajalakshmi M. Madan R. Environmental Health Perspectives. 101
Suppl 2:125-30, 1993 Jul.
Effects of methylmercury on the brain of infant rats reared artificially. Naruse
I. Arakawa H. Fukui Y. Tokushima Journal of Experimental Medicine
40(l-2):69-74, 1993 Jun.
Epidemiological and clinical features of Minamata disease. Igata A.
Environmental Research. 63(1): 157-69, 1993 Oct.
[Influence of age and sex on threshold dose of mercury in Minamata disease
as determined by hair mercury concentration]. Kinjo Y. Kato Nippon
Koshu Eisei Zasshi - Japanese Journal of Public Health.
Common factors contributing to intractable pain and medical problems with
insufficient drug uptake in areas to be treated, and their Acupuncture &
Electro-Therapeutics Research. 17(2): 107-48, 1992.
A fetal type of Minamata disease. An autopsy case report with special
reference to the nervous system. Eto K. Oyanagi S. Itai Y. Molecular &
Chemical Neuropathology. 16(1-2): 171-86, 1992 Feb-Apr.
An epidemiological study with risk analysis of liver diseases in the general
population living in a methyl mercury polluted area. Journal of
Epidemiology & Community Health. 46(3):237-40, 1992 Jun.
Truncal hypesthesia in patients with Minamata disease. Yoshida Y.
Kamitsuchibashi H. Hamada R. Kuwano Y. Mishima I. Igata A. Internal
Medicine. 31(2):204-7,1992 Feb.
The discovery of the causal agent of Minamata disease. Tsuchiya K.
American Journal of Industrial Medicine. 21 (2):275-80, 1992.
[A study of victims of methylmercury poisoning outbreaks by age and sex in
Minamata, Niigata and Iraqi outbreaks]. Kinjo Y. Nakano A. Nippon
Koshu Eisei Zasshi - Japanese Journal of Public Health.
Minamata disease: a story of mercury’s malevolence. Powell PP. Southern
Medical Journal. 84(11): 1352-8,1991 Nov.
Present mercury levels in red blood cells of nearby inhabitants about 30 years
after the outbreak of Minamata disease. Sakamoto M. Nakano
Ecotoxicology & Environmental Safety. 22(1 ):58-66, 1991 Aug.
The neurotoxicology and pathology of organomercury, organolead, and
organotin. Chang LW. Journal of Toxicological Sciences. 15 Suppl 4:12551, 1990 Dec.
M,"3™xxifteX™eofof
” 307'
AddiTJ? ?3y’ Japan' Tamura K c'lmercuiy‘P°,lufed sediment of
kvei seslva®
lienee & Medicine.
isease. Mizukoshi K.
- J3ta S. Saitoh H.
v<>'S"...
ProfeSX^^K B“"e<,n&
•«;=s=sss=:.
WO. Baxter DW. Barrows HS^o^n " northw«t Quebec Spitze
iTm 'zxs„
a
“’?“«<> sc.
==i=aE’5a=S“
[Diagnostic problems in chronic Minamata disease (organic mercury
pmsonmgj-with specml reference to the neurological features and Rinsho
Smnkeigaku - Clinical Neurology. 27(2):204-10,1987 Feb
Methylmercury exposure and mortality in southern Japan: a close look at
causes of death. Tamashiro H. Arakaki M. Futatsuka M. Lee ES. Journal
of Epidemiology & Community Health. 40(2):181-5,1986 Jun
Characteristics of Hg-resistant bacteria isolated from Minamata Bay sediment.
Nakamura K. Fujisaki T. Tamashiro H. Environmental Research.
40(l):58-67, 1986 Jun.
[Computed tomography in chronic Minamata disease (organic mercury
poisoning)—with special reference to comparison between the computed
Rinsho Shinkeigaku - Clinical Neurology. 25(10): 1204-9,1985 Oct
Mortality and survival for Minamata disease. Tamashiro H. Arakaki M. Akagi
198R°ht
Internat'Onal Journal of Epidemiology.
Cutaneous and auditory Junction in rats following methyl mercury poisoning.
Wu MF. Ison JR. Wecker JR. Lapham LW. Toxicology & Applied
Pharmacology. 79(3):377-88, 1985 Jul.
Effect of organic mercury on the ele
1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
file:///C|/Lever docs/Survey health guidelines.
ATJ 7-
1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
2. SUPPLEMENTARY INFORMATION ON INORGANIC MERCURY
3, REFERENCED DOCUMENTS
4, FURTHER READING
1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY *
BASELINE HEALTH SURVEILLANCE AT TIME OF EMPLOYMENT IN AN
INORGANIC MERCURY PROCESS
1.Collection of Demographic Data
• Name and unique company identification number.
• Date of birth.
• Sex.
• Address.
• Date of starting company service
• Descriptive job title. To include the Australian Bureau of Statistics’ Australian Standard
Classification of Occupations (ASCO)- and Australian Standard Industrial
Classification (ASIC)-.
• Places of previous employment.
Z.Occupational History
• Past work history, including previous exposure to inorganic mercury.
• Potential current exposure.
• Whether suitable personal protective equipment is used for that specific mercury
process.
3.Medical History
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GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
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• Presence of symptoms.
• Smoking history.
4.Physical Examination
With emphasis on neurological, gastrointestinal and renal systemsand skin.
S.lnvestigation
Spot creatinine corrected urine for inorganic mercury to be conducted. Where there is 50 pg
inorganic mercury or more per gram creatinine, a repeat spot creatinine corrected urine for
inorganic mercury should be performed at the same time of the day.
6.Health Advice
The appointed medical practitioner should inform the employee of the potential health effects
associated with exposure to inorganic mercury.
DURING EXPOSURE TO AN INORGANIC MERCURY PROCESS
7.Personal Protective Equipment
The availability, type, fit, maintenance and frequency of use of personal protective equipment
should be monitored regularly.
S.Urinary Inorganic Mercury
Baseline pev?!
Spot creatinine corrected urine for inorganic mercury to be conducted every 90 days. Where
there is 50 pg inorganic mercury or more per gram of creatinine, a repeat spot creatinine
corrected urihe for inorganic mercury should be performed at the same time of the day.
Action Level
On confirmation of a level of 50 jig inorganic mercury or more per gram of creatinine, a
medical examination with emphasis on the neurological, gastrointestinal, renal and
dermatological systems should be performed.
The employer should informed when abnormal findings are detected so that control
measures can be checked The employee should be informed of the results of the health
surveillance.
Removal
Removal from mercury work should be considered if clinical signs of mercury poisoning are
present or if the level of inorganic mercury in urine is greater than 100 pg per gram of
creatinine.
The person should be investigated every 30 days until the level falls below 50 pg inorganic
mercury per gram of creatinine on two successive occasions. The test may be performed more
frequently in individual circumstances.
6
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1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
file:///C|/Lcver docs/Survey health guidelines.!-
The 90 day protocol may then be resumed.
Return to Work
The person must be medically fit to return to mercury work.
AT TERMINATION OF EMPLOYMENT IN AN INORGANIC MERCURY PROCESS
9.Data that should be Collected:
• Date of termination.
• Reason for termination:
o ill-health (if'yes', give details).
o other reasons, and
o date and cause of death if in service.
lO.Final Physical Examination
A physical examination to determine persons with neurological or renal dysfunction due to
mercury.
2. SUPPLEMENTARY INFORMATION ON INORGANIC MERCURY
WORK ACTIVITIES THAT MAY REPRESENT A HIGH RISK EXPOSURE
Mercury exists m three forms: liquid and vapour states (Hg°) and inorganic mercury salts
Examples ot work activities involving inorganic mercury and its compounds which require
special attention when assessing exposure include:
manufacture of amalgams, for example, tin amalgam, amalgam of gold, copper and zinc
used in dentistry for filling teeth, amalgamated zinc used in electric batteries and
sodium amalgam used in the laboratory in conjunction with water as a reducing agent;
• dental work involving mercury;
manufacture of pigments and antifouling paints (mercuric oxide) and vermilion
(mercuric sulphide) in the paint and colour industry;
• extraction of gold and silver from roasted pyrites (mercuric sulphate);
• extraction of gold from tailings;
• laboratory work with mercury in closed or confined spaces; and
• the use of mercury-containing fungicides.
»f6
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1. guidelines for health surveillance for inorganic mercury
file.7//C|/Lever docs/Survey health guidelines!
may occur in the atov^prwessef
t0
exPosures, including mercury spills that
mercijryL health effects following exposure to inorganic
Route of Entry into the Body
Ino.gan.e meren^s absorpt.on and pote^ t0X]CIty
„„ . s
““ '",eS,'nal lract <less
than I pi
alveolar membranes into the bloodstream Percntan™
nt.ntn.at. „ mercu,
^ercury vaP°ur ls absorbed across
ingestion. rmuS«X“4ioi^no2icamel,,,le “’T'1®1 (<1° Per “"•) rollowing
nterenno sa.ts are more s„lub7ea„d
Acute Effects
gastromtestinaTsystem by SgS
merCUry Vap°ur’ and the
Stomatitis, colitis, nephrotic syndrome^nd sahv^ d
'C taSte in the mouthcorrosive bronchitis and inteJitiai^pnuemoXX" uXT
C0~ati<™ -use
central nervous system produces tremor and increased exchabl^1117 VaP°Ur
the
kidney are affected by ingestion of mercuiy salts
h gaStro,ntest,naI tract and later the
Chronic Effects
mercurial ^mpounl^
mer-W or the dust of inorganic
chronic diarrhoea. The characteristic features are stomaS
7 headach-> tiredness and
disturbances. Effects on the mouth may va^fZT
’ T™13’'tremors and Psychotic
26/05/01 1.21 PM
1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
r
file:///C|/Lever docs/Survey health guidelines, htr
surveillance and should be read in conjunction with the Introduction to the Guidelines for
Health Surveillance [NOHSC:7039(1995)J.
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1. GUIDELINES FOR HEALTH SURVEILLANCE FOR INORGANIC MERCURY
♦4
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Kidney dysfunction sometimes develops, especially in workers exposed to elemental mercury.
Its development is not clearly linked with the intensity of exposure. After inorganic salts are
ingested, a large amount of mercury may accumulate in the kidneys, producing a generalised
increase in the permeability of the tubular epithelium.
The soluble inorganic mercury salts, for example, mercuric chloride, will devitalise tissue by
denaturation and precipitation of the proteins present. Phenyl mercury acetate has a strong
corrosive action and will cause local blistering of the skin. Mercury fulminate is particularly
prone to cause a vesicular dermatitis, especially affecting the fingers, and irritation of the eyes
and eyelids. Workers exposed to mercury vapour may be found to have a discolouration of the
lens of the eye, which is indicative of mercury exposure rather than of intoxication.
3. REFERENCED DOCUMENTS
1.
2. Australian Bureau of Statistics, Australian Standard Classification of Occupations:
ASCO Coding System, Australian Bureau of Statistics,Canberra, 1993.
3.
4. Australian Bureau of Statistics, Australian Standard Industrial Classification,
Australian Bureau of Statistics, Canberra, 1985.
4. FURTHER READING
Agency for Toxic Substances and Disease Registry, Case Studies in Environmental Medicine
17: Mercury Toxicity, Agency for Toxic Substances and Disease Registry, United States
Department of Health and Human Services, Public Health Service, Atlanta, 1992.
Alessio L, Crippa M and Lucchini R, 'Inorganic Mercury', CEC Criteria Documentfor
Occupational Exposure Limit Values, Roi R and Scibbioni E (eds), European Chemicals
Bureau, Joint Research Centre, Ispra, 1994.
National Health and Medical Research Council, Inorganic Mercury, Occupational Health Guide NH15, National Health and Medical Research Council, Canberra, 1982.
International Programme on Chemical Safety, Environmental Health Criteria 1: Mercury,
International Programme on Chemical Safety, World Health Organization, Geneva, 1976.
Health and Safety Executive (United Kingdom), Mercury: Medical Surveillance, Guidance
Note MS 12, Health and Safety Executive, London, 1979.
International Agency for Research on Cancer, IARC Monographs on the Evaluation of the
Carcinogenic Risk of Chemicals to Humans, vol 58: Beryllium, Cadmium, Mercury and
Exposures in the Glass Manufacturing Industry, International Agency for Research on Cancer,
Lyon, 1993.
Lauwerys RR and Hoet P, Industrial Chemical Exposure Guidelines for Biological
Monitoring, 2nd Ed, Lewis Publishers, Boca Raton, 1993.
* These guidelines set out in a practical manner the minimum requirements for health
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'
312
VctyukUI
THE ANCIENT METALS
THE DISEASES OF OCCUP/mIONS
i
3X3
The Felt-hat Industry
In the felt-hat industry the occurrence of mercurialism has been notori
ous for centuries. Among hatters and hatters’ furriers the onset of poison
ing has usually been slow and the symptoms mild. In this industry the
mi
. T'
1
■
■
Fig. 103.—Workmen dipping Felt Hats in an Acid Solution of Mercuric Nitrate
(The Occupational Diseases, W. Gilman Thompson, D. Appleton & Co., New York, 1^14)
Fig. 102.---- ]Hatters’-furriers’ Workshop. The Bench is provided with Ex
haust Ventilation operating through Hoods
danger arises from the presence in the air of the workshops of fine fur
which has been treated with mercuric nitrate in the process of felting (fig,
102) The fine hairs which form the fur of rabbits, hares, muskrats and
beavers are smooth, resilient and straight. Treatment with some chemical
substance which makes them limp, twisted and rough greatly aids the felting
process, and many substances have been shown to produce such an effect.
Among them is an acid solution of mercuric nitrate, which is used in the
preparation of hatters’ fur in some countries (fig. 103).
Hazards of the Hatters’-furriers’Workshops
Neal and his colleagues (1941) examined 544 hatters employed in five
representative felt-hat factories in the United States of America. He
showed that 59 of these workers had signs of chronic mercurialism. Four
of the 21 men engaged in mixing and blowing, 8 of the 34 coners, 6 of the
29 hardeners, and 33 of the 179 starters, wetters-down, and sizers were so
diagnosed. Mixers and blowers were exposed to 5 milligrams of mercury
per 10 cubic metres of air, hardeners to 27 milligrams, and starters,
wetters-down and sizers to 2-1 milligrams. In any range of exposure above
100 micrograms of mercury per cubic metre of air the incidence of mer
curialism increases with increasing duration of employment. No cases were
found among hatters exposed to less than 100 micrograms per cubic metre
of air as measured by the Nordlander instrument.
Chronic Mercury Poisoning
Saliyation and tenderness of the gums and mouth are usually early
symptoms. The gums are swollen and bleed readily, but it is not easy to
distinguish an early mercurial gingivitis from the pyorrhoea of a neglected
mouth. Rarely a mercurial line is seen on the gums. It usually resembles the
blue line due to absorptipivofjead, but sometimes is dark brown. In a few
cases mercury causes dermatitis when it is constantly in contact with the skin,
as in men who fill the standard 76-lb. iron flasks and spill mercury on their
hands and feet. It is a papular erythema with slight hyperkeratosis which
affects the dorsum of the hand and foot and spreads to some
extent up the leg. With change of work the prognosis is always good.
The symptoms of mercury poisoning arising in industry are as a rule
slower in onset and more insidious in character than those which result
from the continued internal administration of mercury. In chronic cases,
as, for example, in mercury miners and thermometer makers, two charac
teristic sets of symptoms which are but rarely seen in medical cases occur,
namely tremor and erethism.
—>
GJ
Ii
THE ANCIENT METALS
3H
The Hatters’ Shakes
The most characteristic symptom, though it is seldom the first to appear
is mercurial tremor (fig. 104). It is neither so fine nor so regular as that of
hyperthyroidism. It may be interrupted every few minutes by coarse jerky
movements. It usually begins in the fingers, but the eyelids, lips and tongue
FiC. 104.—Tremor in a Mercury Miner of Idria, Yugoslavia
(By courtesy of Dr. Ivan Hribernik)
are affected early. It may become less severe when familiar tasks are performed. As it progresses it passes to the arms and then to the legs so that
it
it becomes
becomes very
very difficult
difficult for
for a man to walk about the workshop, and often
he has to be guided to his bench. At this stage the condition is so obvious
that it is known to the layman as the hatters shakes, and in the United
States of America as the Danbury shakes. The tremor often passes away 1
the patient gives up his work before it has reached a serious stage. AlcojioJism greatly favours its development and it is claimed that no total abstainer
'Tasever suffered from tremor in severe form (Hamilton, 1925).
Mercurial Erethism
The syniptoms known as erethism have been rare since silver took the
place of mercury in mirror making. The man affected is easily upset and
embarrassed, loses all joy of life and lives in constant fear of being dis
missed from his job. Sometimes he is quarrelsome and neglects his work
and his family. He has a sense of timidity and may lose self-control before
strangers. Thus if a visitor stops to watch such a man in the factory he
‘ will sometimes throw down his tools in anger and turn on the intruder,
saying that he cannot work if watched. Occasionally a man is obliged to
give up work because he can no longer take orders without losing his tem
per, or if he is a foreman because he has no patience with the men under
him. Drowsiness by day, depression, loss of memory and insomnia may
occur, but hallucinations, delusions and mania are now rare. That this has
not always been the case may be judged from the expression as mad as a
hatter.
3i5
THE DISEASES OF OCCUPATIONS
Mercurialentis
In
In 1943
1943 Atkinson
Atkinson added
added a new physical sign to the picture of chronic
L.
___
--omercurial poisoning. This
T.— was mercurialentis, detected by examination
with the slit-lamp microscope. His patient had inhaled mercury vapour for
•
rT
” change; in the lens
less than five years while making thermometers.
The
consists of a discoloration of the anterior capsule showing as ar reflex vary___brown. The change; is bilateral
ing in intensity from light brown to coffee
b------y fine-—
punctate
opacities in
and symmetrical, and is usualilly
J accompanied
4
_— ---------each lens, especially in the anterior cortex. Visual acuity is unaffected by
the changes. The discoloration of the lens capsule appears a long time
before the onset of general signs of mercury poisoning and is therefore of
value in the early detection of exposure to atmospheric mercury (Hunter
and Lister, 1953). Mercurialentis has been described by Locket and
Nazroo (1952) in twelve out of fifty-one men exposed to mercury vapour
and dust in repairing direct-current electric meters. It has also been seen
as the earliest sign of absorption of mercury in hatters’ furriers (Rosen, 1950).
Policemen poisoned from Fingerprint Photography
In photographing fingerprints at the site of housebreaking and other
crimes, a light-coloured powder is applied to a dark background. We have
seen (p. 266) how lead poisoning arose in Denmark in 1937 from the use of
white lead for this purpose. But the powder most commonly used is
mercury-with-chalk or grey powder (hydrargyrum cum creta, B.P.) pre
pared in the usual way by triturating one part by weight of metallic mer
cury with two parts of chalk in a mortar. The powder is dry and finely
divided. It is applied liberally with a well-loaded, flat squirrel-hair or
camel-hair brush and the excess is brushed or blown off. The brush itself
is often cleaned by rubbing against a convenient door-post, and powder
rises in a cloud. The Lancashire Constabulary sets particular value in
such techniques, and in 1949 Agate and Buckell found that of thirty-two
men engaged regularly on such work, four exhibited tremor and erethism
and three tremor alone. Exposures in excess of 250 hours per year were
considered to constitute a definite risk. Urinary mercury estimations were
of no assistance in diagnosing individual cases or estimating exposures, but
the average excretion of the group was abnormally high.
Subacute Mercury Poisoning
Subacute poisoning occurs, for example, in the men who clean the
flues of the recovery plant. At the Idria mines this is done once a year; it
takes three weeks and no man works more than one day
"''1
1953). As the workmen scrape the soot from ledges, wal
cury globules are visible everywhere in the soot. They v
because the flues are 100 per cent saturated with mercu
centration of 14 milligrams per cubic metre of air
they are protected in this way they develop a tyj
j
1 in: iJirm.iDiAo ur
which there is accentuation of the gastro-intestinal symptoms. Salivation
is uncommon, but sore gums occur. In addif
to the gingivitis,
the pharynx may be mildly inflamed and shallow uicers may occur on
the buccal mucosa and palate. Vomiting and mild diarrhcea with
perhaps four stools a day may be seen.
Excretion of Mercury
In their investigation of poisoning in men repairing direct-current
meters, Bidstrup and others (1951) estimated the urinary excretion of
mercury in twenty-four hours in
126 cases. To lessen the risk of
contamination from clothing and
atmosphere the men were asked to
collect the specimen away from
the workshop, preferably at week
ends. Of the twenty-seven who
showed clinical evidence of chronic
mercury poisoning, twenty-one
excreted more than 300 micro
grams of mercury in twenty-four
hours. On the other hand, sixteen
of 101 men with no clinical
evidence of poisoning excreted
more than 300 micrograms of mer
cury in twenty-four hours. When
the results of urine examinations
were known in these cases, six of
the men were recalled for further
clinical examination. No symptoms
or signs of poisoning were de
tected at the second interview, nor
was any past history of mercury
Fig. 105.—Respirator for Protection poisoning elicited. They therefore
against Mercury Vapour. The Can suggested that a high urinary ex
ister contains Iodized Carbon. Two
Exhaling Valves seen on the Face cretion of mercury is of diagnostic
piece are designed to reduce the significance only when symptoms
Breathing Resistance as much as and signs of poisoning can be
possible
demonstrated. The urinary ex
(Photo by Gerasimov, A. Photographic Labora
tory, School of Public Health, Zagreb, from I 'ouk,
cretion of more than 300 micro
V’. B., Topclnik, Z., ami Pugas, M., Brit. J.
Industr. Med., 1953, 10, 69)
grams of mercury in twenty-four
hours is likely to be accompanied
by clinical manifestations of chronic mercury poisoning. In a group of
men who had no contact with mercury in their work Buckell and others
(1946) found that the urinary excretion of mercury in twenty-four hours
was not more than 100 micrograms in any case.
J
THE ANCIENT METALS
31?
Renal Lesions
purring in Mercury Poisoning
The kidney is the organ in which the highest concentrations of mercury
are localized following absorption. Although albuminuria among workers
exposed to mercury has been reported on many occasions, and despite
the role of the kidney in the storage and elimination of mercury, there has
been some uncertainty in the past as to whether renal damage occurs as a
manifestation of mercury poisoning of occupational origin. A number of
reports are available now which indicate that the nephrotic syndrome
develops in certain persons exposed to mercury. The same is true of some
cases of chronic nephritis. On the evidence provided by these cases there
can be no doubt that occupational exposure to mercury can cause renal
damage. The nephrotic syndrome accompanied by an abnormally high
output of mercury in the urine is the usual manifestation, and recovery
follows removal from contact in most cases. It is of interest that in most
of the cases reported other symptoms and signs of mercury poisoning
have been absent. The condition of the patient is not necessarily related
to the duration of exposure.
Distribution of Mercury in Rat Tissue
Rothstein and Hayes (i960) studied the metabolism of mercury in the
rat using intravenous and intramuscular injections of mercuric nitrate in
which the isotope 203Hg was present. They demonstrated that the liver
acts as a reservoir for mercury for a few days after intravenous injection,
but that after about two weeks 85 per cent or more of a given dose is found
in the kidney and 66 per cent is subsequently excreted in the urine. In
animals given labelled mercuric nitrate by intramuscular injection, the
site of the injection acts as a reservoir from which clearance to the kidneys
occurs in about two weeks. The mercury accumulates in the collecting
tubules, the distal parts of the proximal convoluted tubules, and the wide
parts of Henle’s loops, but not in the glomeruli (Bergstrand and others,
1958).
Nephrosis in Workers making Chlorine from Brine
Benning (1958) refers to two cases of kidney disease among women
using a tamping compound containing 22 per cent mercury amalgamated
with copper in the manufacture of carbon brushes for generators. Friberg
and others (1953) review the relevant literature and refer to two cases
of nephrosis reported by Riva (1945) in men exposed for five months and
three years respectively in an ammunition factory, and to eight cases of
nephrosis reported by Lederberger (1949). Friberg and his colleagues
describe two cases of nephrotic syndrome in men employed for
than
one year in the production of chlorine by an electrochemical pr
this process, chlorine is formed from brine by electrolysis using
contained in a rubber-lined trough as the cathode and anodes o
which are horizontal plates suspended from the cell cover f
graphite stubs which protrude through the cover. The elec<
3I8
1 111; AM 1E2\ 1 MEIAL^
the diseases of occupations
319
nection to the mercury is by means of iron struct,
shaped like mush
rooms set in the rubber lining of the trough. Chlorine is discharged at the
anode and an amalgam of sodium and mercury forms at the cathode. 1 he
cells are sloped to allow the mercury amalgam to flow continuously to a
decomposer where it reacts with water to form caustic soda and hydrogen,
and the mercury is freed and recirculated. Hazards to operators exist
during maintenance procedures on the cell and from spills and leakage
at the pump end. Air analyses in the factory in which the two men who
developed nephrosis worked revealed mercury concentrations of 0-02-0-45
mg. Hg/m3. Before clinical evidence of renal involvement was apparent
the excretion of mercury in the urine on two occasions was in one case,
0-90 and o-68 mg/1. and in the other o-6o and 0-16 mg/1. Significantly large
amounts of mercury continued to be excreted in the urine for at least two
months after removal from exposure. Fatigue, irritability and oedema of
the face and ankles, and the presence of protein and hyaline casts in the
urine were the significant features of the illness. Both men recovered
completely several months after removal from exposure to mercury.
mercury. Neither ' these had had proteinuria before working with mer
cury. One of then, .ntinued to pass protein in the urine in small amounts
for three months after removal from contact with mercury, and the other
for an indefinite time. In the latter case the electrophoretic pattern of the
protein was different during and after exposure. The protein attributed
to the effect of mercury on the kidney was separable on electrophoretic
analysis into five components, the first three of which corresponded to
albumen, a2-globulin, and ^-globulin, but the remaining two, present only
in small amounts, were not identified. The results of analysis by ultra
centrifuging and amino-acid identification led the authors to conclude
that the proteins which appeared in the urine were serum proteins which
had been eliminated by the kidney by an undetermined mechanism.
Since the proteinuria ceased in two cases after removal from the mercury
hazard, it is assumed that the renal damage in these cases was reversible.
In the case in which the proteinuria persisted, the diagnosis of chronic
and supported by the results of biochemical investinephritis was made
1
gations; it was not possible to decide whether the chronic nephritis was
the result, of the preceding exposure to mercury.
Nephrosis in other Workers handling Mercury
Kazantzis and others (1962) report on four men with albuminuria who
had worked with mercury and its compounds in two different factories.
In one, men were exposed to metallic mercury, oxides of mercury, mer
curous and mercuric chloride, and phenyl mercury acetate, and in the
other to mercuric oxide; three of the four men developed symptoms and
signs characteristic of the nephrotic syndrome and all recovered com
pletely on removal from exposure to mercury and its compounds. Chmca
recovery coincided with disappearance of mercury from the urine, and
there was no evidence that the nephrotic syndrome in these cases was due
to any of the commonly-recognized underlying causes of this condition.
Estimation of the excretion of mercury in the urine revealed that all four
men were excreting more than 1000 /xg./l. at the onset of their illness, but a
survey made in the factories concerned demonstrated that a number of
men who had no symptoms nor signs of mercury poisoning were excreting
equally large, or larger, amounts of mercury in the urine. Kazantzis and
his colleagues suggest, therefore, that the occurrence of the nephrotic
syndrome in persons exposed to mercury results from an idiosyncrasy.
Friberg and his colleagues (1953) were unable to demonstrate hyper
sensitivity to mercury by means of skin tests, and conclude that the exact
mechanism for the origin of the kidney injury is not known. Although
complete recovery from the nephrotic syndrome following exposure to
mercury is the usual outcome, death attributed to damage to the kidney
caused by mercury has been reported (Lcdcrberger, 1949)-
Safe Substitutes for Mercury
The work of chemists leading
up to the discovery of safe sub
stitutes for mercury dates back
more than a hundred years. Mer
cury poisoning was common in
the mirror-making industry until
silvering was introduced. In 1835,
working on the oxidation of
alcohols, Justus von Liebig isolated
acetaldehyde (fig. 106). Seeking a
test for aldehydes he observed that
a test tube becomes coated with
silver if an ammoniacal solution of
silver nitrate is warmed with an
aldehyde. The mirror so formed
provided a more perfect reflecting
surface than one made with tin
amalgam, and mercury poisoning
Fig. 106.—Justus von Liebig,
disappeared in the trade. Similarly,
1803-73
powders containing mercury or its
compounds used for the identification of fingerprints must also disappear.
Salts of calcium, bismuth., barium, zinc or titanium should be used
instead (Agate and Buckell, 1949).
Electrophoretic Pattern of the Urinary Protein
By electrophoresis and ultra-centrifuging Smith and Wells (i960)
investigated protein in the urine of two of three men exposed to metallic
Invention of Electroplating
The introduction into commerce of electrolytic gold plati
also led to a great reduction of mercury poisoning because <
&
cAro jkbXxVK
6 Oak |) <h k
1^9. 2
14-c^aTr
■-1^
A
»
Mercury: chronic poisoning
x Periodic medical examinations should be made at
< intervals depending on the extent of the risk and should
\be aimed at the early detection of excessive exposure to
mercury and picking up early signs of mercury poisoning.
Xyialyses of urine mercury should be carried out regularly
and attention paid not only to individual levels but also
to \the trend in the distribution amongst groups of
workers subject to the same type of exposure.
Ara personal level a concentration of 50 pg/l urine has
been proposed as a maximum allowable concentration.
Certain authors have also recommended the analysis
of blood mercury, which should not exceed a concentra
tion of 3\0 pg/100 ml.
A careful check should be made for the first signs of
neurological and renal involvement. Various clinical or
laboratory Methods have been proposed for detecting
slight tremok An attempt should be made to detect
behavioural changes. Various authors have proposed the
regular use of a\battery of psychomotor tests. Proteinuria
analyses are alsq recommended.
I!
II
intensity as a function of the patient's mental and cultural
level.
The course of intoxication may vary considerably from
case to case. If exposure is terminated immediately upon
the appearance of the first symptoms, recovery occurshowever, if exposure is not terminated and the intoxica
tion becomes firmly established, no more than an
alleviation of symptoms can be expected in the majority
of cases.
The severe chronic form of mercury poisoning
encountered in places like Almaden up until the early
20th century and which presented spectacular renal,
digestive, mental and nervous disorders and terminated
in cachexia, was eliminated by means of preventive
measures. However, a chronic, "intermittent” poisoning
in which periods of active intoxication are interspersed
between periods of latent intoxication can still be
detected among mercury miners. In the latent periods,
symptoms remit to such a degree that they are visible
only on close search; only the vegetative manifestations
persist in the form of profuse sweating, dermographia
Treatment
and, to some extent, emotional instability. This form does
In cases of acuta poisoning symptomatic treatment
not. in itself, affect life expectancy but may aggravate or
should be supplemented by administration of BAL (2.3favour the appearance of mortal diseases.
dimercaptopropanof) intramuscularly.
Certain authorities described a condition of "microThere are no specific antidotes for chronic poisoning,
mercurialism
characterised by functional neurosis
which reinforces the importance of early detection of
(frequent hysteria, neurasthenia, and mixed forms),
incipient lesions since, depending on the severity of the
cardiovascular lability and secretory neurosis of the
clinical signs, it is possible that recovery may not be
stomach.
complete following terrr\ination of exposure. Various
Digestive system. Gingivitis is the most common
treatments have been proposed to stimulate mercury
gastrointestinal disorder, encountered in mercury pois
excretion, sweating sessions, administration of chelat
oning. It is favoured by poor oral hygiene and is
ing agents. Some of these hbve been used in man (BAL
accompanied by an unpleasant, metallic or bitter taste in
CaNa2EDTA. penicillamine,\J-acetyl-D-penicillamine)
the
mouth.
with varying results. Experimental studies suggest that
Ulceromembranous stomatitis is much less common
other chelating agents might be more effective (sodium
and is normally found in persons already suffering from
2,3-dimercaptopropane-1 -sulpnonate, dimercaptosuc
gingivitis who have accidentally inhaled mercury
cinic acid).
\
vapours. This stomatitis commences with the subjective
LAUWERYS. R.
symptoms of gingivitis with increased salivation (mer
curial ptyalism) and coating of the tongue. Eating and
drinking produce a burning sensation and discomfort in
Mercury. Environmental health criteria 1 kGeneva, World Health
the mouth, the gums become increasingly inflamed and
Organisation. 1976). 131 p. Ulus. 356 tef
swollen,
ulcers appear and there is spontaneous
Early detection of health impairment in occupational exposure
bleeding. In acute cases, there is high fever, inflamma
to health hazards. Report of a WHO meeting (Geneva. World
tion of the submaxillary ganglions and extremely fetid
Health Organisation, 1979).
\
"Individual mercury exposure of chloralkalXworkers and its
breath. Alveolodental periostitis has also been observed.
There may<be
bluish
on the
dge of the
relation to blood and urinary mercury levelsV. Lindstedt. G.;
-----a....
m m.. line twu
, tooth
Wl eUIC
i me in nartim
ilar’,ir> the vicinity of :„x
__ LTTi :— — —
•
Gottberg. I.; Holmgren. B.; Jonsson. T.\ Karlsson. G. ^ums^jn
infected~areas
this
... particuladn
<n me viuimiy ui iineuieu
areas; tnis
Scandinavian Journal of Work. Environment and Health ''line is. 1however, -----'
’
never encountered in persons without
(Helsinki), Mar. 1979. 5/1 (59-69). Ulus. 17 rdf.
teeth- Sj^-gre.Y-^unctifgmiDjgmenla.tion of the oral
CIS 79-791 "Evaluation of workers exposed t\ elemental
mucosae-the vestibular side of the gums (usually those
mercury using quantitative tests of tremor and neiAomuscular of the lower jaw), the palate, and even the inside of the
functions”. Langolf. G. D.; Chaffin. D. B.; Henderson. R.
cheeks-has also been observed.
Whittle. H. P. American Industrial Hygiene Association
Recurrent gingivitis affects the supporting tissues of
Journal (Akron). Dec. 1978. 39/12 (976-984). IlluX 14 ref.
the teeth, and in many cases the teeth have to be
extracted or merely fall out.
Non-specific pharyngitis is relatively common. A rarer
manifestation is that of Kussmaul's pharyngitis which
presents as a bright-red coloration of the pharynx, tonsils
and soft palate with fine arborisation.
Mercury: chronic poisoning
Other gastrointestinal disorders encountered in mer
cury poisoning include gastritis and gastroduodenitis.
In chronic mercury poisoning, digestive and nervous
symptoms predominate and. although the former are of
Kidney. Only in the case of poisoning by soluble mercury
earlier onset, the latter are more obvious; other signifi*j_
compounds does nephrosis occur in acute poisoning
2va.u
aUtbut
lter?s® ssymptoms
ymPtoms may
wui '^u irmieiise
may be
De present.
present. The
I he Wlth the chronic, intermittent form there are no more
duration of the- period
than a few- isolated cases of slight albuminuria mostly
i- —
" — of
** ■ mercury
■ ■ ■ vi
■ jr absorption
wwi
v* I I preceding
|^l
Illy
the appearance of clinical symptoms depends on the transitory in nature and with neither oedema nor other
level of absorption and individual factors. The main early,
changes.
Dremonitnn/
i___Kt in
.
..
premonitory Qinnc
signs innhirloinclude: clinkt
sHght Hi'/innt;.
drgestive disorders'
Nervous system. Nervous system involvement may occur
particular, anorexia; intermittent tremor, sometimes in
with or without gastrointestinal symptoms and may
specific muscle groups; and neurotic disorders varying in
evolve in line with two main clinical pictures:
1334
mm
'
1
m
i
r
(
I
Mercury : chronic poisoning
3l
n
n
n
V
3
</I
i
□
i
3
J
5
i
5
r
(a) fine-intention tremor reminiscent of that encoun
tered in persons suffering from multiple sclerosis,
and
(b) parkinsonism with tremor at rest and reduced motor
function.
Usually one of these two conditions is dominant in the
over-all clinical picture which may be further com
plicated by morbid irritability and pronounced mental
hyperactivity (mercurial erethism)./
Mercurial parkinsonism presents a picture of amimia,
unsteady and staggering gait, absence of balance
recovery reflexes and hypotonia; vegetative symptoms
are slight with mask-like facies, sialorrhea, etc. However,
parkinsonism is usually encountered in milder forms, in
pa rt i c u I a r a s micro-parkinsonism.
The most frequently encountered symptoms resemble
those presented by persons with multiple sclerosis,
except that there is no nystagmus and the two conditions
have a different serology and different clinical courses.
The most striking feature is tremor which is usually a late
symptom but may develop prior to stomatitis (figure 1).
When tolerated intoxication is on the point of
decompensation, the tremor is circumstantial and an
expression of mercurial erethism, appearing only in
predisposing situations, e.g. when the patient is tired,
i cold, hungry (hypoglycaemia), or emotionally aroused
(anger, embarrassment, etc.). The attack is usually of
short duration.
The tremor varies a good deal, and is by no means easy
to describe. There is a subtle trembling of the fingers, like
that observed in hyperthyroidism; more obvious trem
bling, at rest, reminiscent of parkinsonism; and major
oscillations, in intentional movements made by the
patient in an effort to get about, similar to those observed
in persons stricken with multiple sclerosis. I n fact, variety
in form and intensity is a characteristic feature of mercury
tremor.
Tremor usually disappears during sleep, although
sudden generalised cramps or contractions may occur;
however, it always igpreasRS under emotional stress and
this is such a characteristic feature that it provides firm
grounds for a diagnosis of mercury poisoning. Tremor is
particularly pronounced in situations where the patient
feels embarrassed or ashamed; often he will have to eat
in solitude since otherwise he would be incapable of
raising food to his lips.
Tremor usually begins with a subtle trembling of the
fingers. It then becomes more obvious, invading the
hand, the forearm, and so on, eventually reaching the
lower limbs and indeed the facial muscles, tongue and
larynx. In some cases, it begins with the eyelids, the area
round the mouth, and the tongue and, in rare cases, it
starts in the feet (in very slight cases, mercury poisoning
may be diagnosed by observation of the feet). The
patient does not himself perceive the tremor, but when it
reaches the knee he begins to feel unsafe. Tremor in the
limbs does not increase when the patient shuts his eyes
but it does increase when movement stops. •
In its most acute form, the tremor may invade all the
voluntary musclesand be continuous. Cases still occur in
which the patient has to be strapped down to prevent
him falling out of bed; such cases also present massive,
choreiform movements sufficient to wake the patient
from his sleep.
The patient often has difficulty in opening his hand
after he has been grasping an object firmly; this
phenomenon differs from myotonia in that it does not
regress after repeated contractions. One patient was
observed to take over 4 s to release his hand from a
handshake and eventually had to pull with the arm to
achieve the desired result.
Figure 1.
Mercurial tremor. The patient's attempt to sign his
name.
The patient tends to utter his words in staccato?
fashion, so that his sentences are difficult to'follow
(psellismus mercurialis); when a spasm ceases, the
words come out too fast. In cases more reminiscent of
parkinsonism, speech is slow and monotonous and the
voice may be low or completely absent; spasmodic
utterence is, however, more common.
K,
A highly characteristic symptom is a desire forslefiU. 4^
and the patient often sleeps for long periods although'
lightly and is frequently disturbed by cramps and spasms.
However, insomnia may occur in some cases.
It is widely agreed that loss of memory is an early and
dementia a terminal symptom. Descriptions have been
given of vegetative disturbances ("mercurial vegetative
syndrome") due to basically sympathicotonic or parasympathicotonic imbalance. Dermographia and pro
fuse sweating (for no obvious reason) are frequently
encountered.
Eyes. In chronic mercury poisoning, the eyes may show
the picture of "mercurialentis" characterised by a light
grey to dark, reddish-grey discoloration of the anterior
capsule of the crystalline lens due to the deposition of
finely divided particles of mercury. MercurialentisTian be
detected by examination with a slit-lamp microscope
and is bilateral and symmetrical; it usually appears some
considerable time before the onset of general signs of
mercury poisoning.
Blood. It is widely accepted that chronic intoxication is
accompanied by mild anaemia sometimes preceded by
polycythaemia resulting from bone_n]aiiQyy.jrritation.
Lymphocytosis and eosinophilia have also been
observed.
[Studies on the effects of mercury exposure on
enzyme production have shown increased lysosomal
enzymes in the plasma.]
PERALES Y HERRERO. N.
CIS 76-1048 "Effects of exposure to mercury in caustic soda
plants in Maharashtra". Singh. H ; Gupta. V. P. Indian Journal
of Industrial Medicine (Calcutta). Apr. 1975. 21 /2 (49-64).
10 ref.
CIS 78-484 "Occupational health problems of women working
in the mercury production industry" (Voprosy gigieny truda
enScin pri proizvodstve rtuti). GonSaruk. G. A. Gigiena truda
iprofessional'nyezabolevanija (Moscow). May 1977. 5 (1720). 4 ref. (In Russian)
CIS 77-460 "Patterns of some lysosomal enzymes in the plasma
and of proteins in urine of workers exposed to inorganic
mercury". Fo£. V.: Caimi, L; Amante, L; Antonini, C.:
Gattinoni. A.; Tettamanti, G.; Lombardo. A.: Giuliani. A.
International Archives of Occupational and Environmental
Health-Internationales Archiv fur Arbeits- und Umweltmedizin (West Berlin), 3 June 1976, 37/2 (115-124). Ulus
22 ref.
1335
Mercury, organic compounds of
Mercury, organic compounds of
Organic compounds of mercury may be considered as
the organic compounds in which the mercury is
chemically linked directly to a carbon atom. Carbon
mercury bonds have a wide range of stabilities; in
general, the carbon-to-mercury bond in aliphatic com
pounds is more stable than that in aromatic compounds.
According to one reliable estimate, more than
400 phenyl mercurials and at least that number of alkyl
mercury compounds have been synthesised. In addition
to these two large groups, mercury derivations have been
obtained from a wide range of organic compounds. The
three most important in common usage are the alkyls, the
aromatic hydrocarbons or aryls and the ^Ikoxyalkyls.
Uses. All the important uses of the organic mercury
compounds depend on the biological activity of these
substances. In medical practice organic mercury com
pounds are used as antiseptics, germicides, diuretics and
contraceptives. In the field of pesticides they serve as
algicides, fungicides, herbicides, slimacides and as
preservatives in paints, waxes and pastes; they are used
for mildew suppression, in antifouling paints, in latex
paints and in the fungus-proofing of fabrics, paper, cork,
rubber and wood for use in humid climates. In the
chemical industry they act as catalysts in a number of
reactions and the mercury alkyls are used as alkylating
agents in organic syntheses.
Aryl mercury compounds
Examples of aryl mercury compounds are phenylmer
curic acetate (PMA), nitrate, oleate, propionate and
benzoate. Most available information is about PMA.
Phenylmercuric acetate (C6H5HgC2H302)
ACETOXYPHENYLMERCURY. PMA
m.w.
336.8
m.p.
149’C
slightly soluble in water; soluble in ethanol, benzene and
acetone
small prismatic crystals.
Metabolism
Absorption. Absorption on occupational exposure may
occur through inhalation of aerosols containing PMA, by
the skin on skin contamination or by ingestion. The
solubility of the mercurial and the particle size of the
aerosols are determining factors for the extent of
absorption. PMA is more efficiently absorbed by
ingestion than inorganic mercuric salt.
Transport, distribution and excretion. Phenylmercury is
transported mainly in blood and distributed in the blood
cells (90%), accumulates in the liver and is there
decomposed into inorganic mercury. Some phenylmer
cury is excreted in the bile. The main portion absorbed in
the body is distributed in the tissues as inorganic mercury
and accumulated in the kidney. On chronic exposure,
mercury distribution and excretion follow the pattern
seen on exposure to inorganic mercury.
HAZARDS
Occupational exposure to phenylmercury compounds
occurs in the manufacture and handling of products
treated with fungicides containing phenylmercury com
pounds. Acute inhalation of large amounts may cause
lun§ damage. Exposure of the skin to a concentrated
solution of phenylmercury compounds may cause
chemical burns with blistering. Sensitisation to phenyl
mercury compounds may occur. Ingestion of large
amounts of phenylmercury may cause renal and liver
damage. Chronic poisoning gives rise to renal damage
1336
due to accumulation of inorganic mercury in the renal
tubules.
Available clinical data do not permit extensive
conclusions about dose-response relationships. They
suggest, however, that phenylmercury compounds are
less toxic than inorganic mercury compounds or long
term exposure.
Alkyl mercury compounds
From a practical point of view, the short-chained alkyl
mercury compounds, like methylmercury and ethylmer
cury compounds, are the most important. These
compounds have been extensively used in seed treat
ment.
Methylmercuric chloride (CH3HgCI)
m.w.
241
sp.gr.
4.06
m.p.
170 ’C
white crystals with a characteristic odour.
Ethylmercuric chloride (C2H5HgCI)
ETHYLMERCURY CHLORIDE; CHLOROETHYLMERCURY
m.w.
265.1
m.p.
192.5 °C
white leaflets, slightly soluble in ether.
Metabolism
Most available data about metabolism of short-chained
alkyl compounds are for methylmercury. Data pertaining
to ethylmercury confirm the close similarity between
methyl- and ethylmercury.
Absorption. Volatile methylmercury compounds, like
methylmercury chloride, are absorbed to about 80%
upon inhalation of vapour. More than 95% of shortchained alkyl mercury compounds is absorbed by
ingestion, although the absorption of methylmercury
compounds by the skin can be efficient, depending on
their solubility and concentration and the condition of
the skin.
Transport, distribution and excretion. Methylmercury is
transported in the red blood cells (> 95%). and a small
fraction is bound to plasma proteins. The distribution to
the different tissues of the body is rather slow and it takes
about four days before equilibrium is obtained. Methyl
mercury is concentrated in the central nervous system
and especially in grey matter. The highest concentration
is found in the occipital cortex and the cerebellum. About
10% of the body burden of mercury is found in the brain.
In pregnant women methylmercury is transferred in the
placenta to the fetus and especially accumulated in the
fetal brain.
Methylmercury is biotransformed to inorganic mer
cury as some inorganic mercury is accumulated in
kidneys and liver. This biotransformation probably
occurs in the liver. The excretion of methylmercury is
slow-1 % of the body burden is excreted daily, resulting
in a biological half-time of 70 days. In a small fraction of
the population, the half-time may be considerably
longer. Methylmercury is excreted in the bile. A large part
is reabsorbed in the intestines, causing an enterohepatic
recirculation.
Some mercury in the bile is in inorganic form.
Methylmercury can also be decomposed by the micro
organisms in the gut. As inorganic mercury is absorbed
only to about 5% this factor facilitates the elimination of
mercury. In lactating women methylmercury is excreted
with the breast milk at a concentration of about 5% of the
blood concentration, between 20 and 60% of mercury in
the breast milk is methylmercury, depending on the
blood concentration of methylmercury. Methylmercury
is also included in the hair at the formation of the hair
250 times
hair is about
concentration
icentration.
inhalation ot
nc mercury
—r
'mercury
of exchange
liBBSilia
BsSgBigSS
of alky'
St ^cumulation o' 0^Xgenin the senson< cortex,
protecbve equrpmen^a
compou^ s ou^
^gggsfeaasi
noisoning is the
symptoms may P
'
examination... . mercury compounds
.
,actation
BsssWasa sisssgss^
cury poisoning
between
sensitive^ Dartlydueto
sOiSsfSWi®
f
inhibition of the
.
to the r
a ■« • a*-*
LJ I .
^essssBi
brain.
WKoxvalKY. mercurv ^pounds
-t common al
^^.RSXin
gSSs--sSotheirhaz3,do"
ha,r \haTheChair concentration should t of biological
As mercury^analyse
d
= is
-=ta^cal sklll
j by an
^nt,ins^Leen
,rcurY acetate (CH30CH2CHaHg00CCH=)
ness.
Methoxyethylmei
of. mercury P^^compoS
crystals, soluble in water.
jpgCStlOO
cOmPound^eabsorbednVgan.c Sabs^bS'Se-cW
„„
rnore e{bcier^7 Jcretion patterns
distribution and ®^®nic mP^'s
follow those ofHno ga^
t .t__ ^Amtirmi Im111
.. .
-.sS££s sBsSSSsgSE
HS^-SsgSSs
gg^ssssrtfw •-
extem'unchanged alkoxyalkyl
man is unknown.
. ,i..^Athof.OnC“’’i'ov
The
I
5
What are the main health hazards associated with breathing in Mercury?
Harmful effects due to short-term exposure to elemental mercury are rarely seen any more because of
strict controls used in workplaces where mercury exposure might occur. Historically, short-term
exposure to high concentrations of mercury vapour caused harmful effects on the nervous, digestive
and respiratory systems, and the kidneys. In most cases, exposure occurred when mercury was
heated.
Initial exposure to high concentrations of mercury vapour produces symptoms similar to ’’metal fume
fever" including fatigue, fever, and chills. Respiratory system effects include cough, shortness of
breath, tightness and burning pains in the chest and inflammation of the lungs. Occupational exposure
to 1 to 44 mg/m3 of mercury vapour for 4 to 8 hours caused chest pain, cough, coughing up blood,
impaired lung function and inflammation of the lungs. In some cases, a potentially life-threatening
accumulation of fluid in the lungs (pulmonary edema) has occurred. Exposure to high, but unspecified,
concentrations of mercury vapour has caused death due to respiratory failure. All of the reported
deaths resulted from inhaling mercury vapours formed upon heating mercury.
Several case reports have described harmful nervous system effects following inhalation of high
concentrations of mercury vapour. The most prominent symptoms include tremors (initially affecting
the hands and sometimes spreading to other parts of the body), emotional instability (including
irritability, excessive shyness, a loss of confidence and nervousness), sleeplessness, memory loss,
muscle weakness, headaches, slow reflexes and a loss of feeling or numbness.
A classic sign of exposure to high concentrations of mercury is inflammation of inside of the mouth
(stomatitis), sometimes with a metallic taste, excessive salivation and difficulty swallowing. Other
digestive system effects include abdominal pains, nausea, vomiting and diarrhea.
Kidney injury is common following exposure to high concentrations of mercury. Reported effects range
from increased protein in the urine to kidney failure. Exposure to high concentrations of mercury has
I
l
r
V
I
s'
also caused increased blood pressure and heart rate.
toptop
What happens when Mercury comes into contact with my skin?
Elemental mercury is not known to directly irritate the skin. However, an allergic skin reaction may
develop following contact with mercury. For further information, refer to "What are the long term
health effects of exposure to Mercury?” below. Elemental mercury liquid and vapour can be absorbed
through the skin and may contribute to the overall absorption and toxicity.
I
J
toptop
Can Mercury hurt my eyes?
There is very little relevant information about the effects of getting liquid mercury in the eyes. It is
probably not a direct eye irritant. In one case, droplets of mercury accumulated under the surface of
the cornea in an person forcefully sprayed with mercury liquid. After two days, the cornea cleared and
vision was normal. High concentrations of mercury vapour can cause redness, burninq and
inflammation of the eyes.
*
What happens if Mercury is accidentally swallowed (enters the digestive system)?
Elemental mercury is poorly absorbed from the gastrointestinal tract and is more toxic following
inhalation. In one report, ingestion of 204 gm did not cause harmful effects. In a second report
ingestion of 220 ml (approximately 3.0 kg) caused immediate effects such as tremor, irritability
forgetfulness and fatigue. It is uncertain whether liver effects observed several months later were
related to the mercury exposure. Ingestion is not a typical route of occupational exposure. Although
airborne droplets of elemental mercury are actually more likely
likely to
to enter
enter the
the gastrointestinal
gastrointestinal system
system
@
rather than the lungs, resulting in lower absorption.
are the long term health effects of exposure to Mercury?
toptop
i
1
i
J
II
/
absorption through the skin are expected to be similar to those reported for long-term inhalation
exposure.
Mercury levels in urine are often used as a general indicator of how much exposure to mercury has
occurred. As a result, urine mercury levels rather than airborne levels are provided in some of the
reports which compare mercury exposures to specific health effects. Urine mercury levels are reported
in micrograms/gram of creatinine (a component of the urine). The relationship between airborne
mercury levels and urine mercury levels is complicated and depends on many factors, including other
sources of mercury exposure and between individual differences. Several studies indicate that an
airborne exposure of 0.025 mg/m3 mercury compares to approximately 37 micrograms of
mercury/gram of creatinine in the urine. Urine mercury levels in adults without occupational exposure
are typically less than 3 micrograms/gram of creatinine. Sources of non-occupational exposure to
inorganic mercury include new dental fillings.
In this review, urinary mercury levels below 35 micrograms/gram of creatinine are considered to
reflect relatively low mercury exposure; 35 to 50 micrograms/gram of creatinine reflects moderate
exposure; 50 to 100 micrograms/gram of creatinine reflects moderately high exposure and above 100
micrograms/gram of creatinine reflects high exposure.
EFFECTS ON THE NERVOUS SYSTEM: Effects on muscle coordination, mood, behaviour, memory,
feeling and nerve conduction have been reported following long-term occupational exposure to
mercury. These effects are often observed in employees with moderately high or high exposure to
mercury. At lower exposures, the results are inconclusive with no effects being reported in some
studies and mild effects reported in other studies. Although improvement has been observed upon
removal of the person from the source of exposure, it is possible that some of the changes may be
irreversible. The nervous system effects of mercury toxicity are sometimes referred to as "Mad
Hatter's Disease" since mercurous nitrate was used in making felt hats.
A classic sign of mercuryToxicity is a fine tremor, usually of the fingers, hands or arms and
occasionally the eyelids, lips, tongue, and whole body. Many occupational studies indicate that tremors
become more pronounced with longer exposures to mercury. Tremors are thought to be a sensitive
indicator for long-term low-level exposure to mercury vapour. One report described tremors in
employees with average exposures as low as 0.026 mg/m3 for an average of 15 years.
Behaviour and personality changes such as irritability, excitation and shyness, psychotic reactions
such as delirium and hallucinations, loss of appetite, tiredness, sleeplessness, short-term memory loss
and impaired nerve conduction have also been reported following long-term exposure. In one study,
subtle behaviourial effects were detected in dentists with moderate mercury exposure.
Damage to the nerves of the arms and legs (polyneuropathy) has been reported in employees with
high exposures. Reduced sensation and strength in the arms and legs, muscle cramps and decreased
nerve conduction have been observed. Employees with episodes of very high exposure appear to be
more at risk of developing these effects. Studies of employees in a chlor-alkali plant showed mild
polyneuropathy in employees exposed to high levels of mercury. Signs included abnormalities in nerve
conduction tests with reduced sensation and increased tremor of the arm.
EFFECTS ON THE KIDNEY: Many occupational studies indicate that moderate to high exposure to
mercury can cause harmful effects on the kidneys. When urine mercury levels are low to moderate,
the results are inconclusive with no effects being reported in some studies and mild effects reported in
others.
Early indicators of kidney injury include increased levels of protein in the urine (proteinuria) and
increased levels of certain enzymes in the blood and urine. Proteinuria is commonly observed in
studies reporting kidney effects. Less often, changes to the structure of the kidneys have been shown.
An increase in deaths from kidney disease in people occupationally exposed to mercury was not
observed in one study.
SKIN SENSITIZATION: Allergic skin sensitization has been reported in people with occupational
exposure to mercury liquid or vapour. Once a person is sensitized to a chemical, contact with even a
small amount causes outbreaks of dermatitis with symptoms such as skin redness, itching, rash and
swelling. This can spread from the hands or arms to other parts of the body. Occupational skin
sensitization to mercury has been observed in people exposed to mercury in dental amalgams, tattoos
or breakage of medical instruments. Positive patch tests were obtained in a dentist, five doctors, a
nurse’s aid, a mercury recycling employee and a pipeline repairman who had developed of red, dry,
itchy skin (contact dermatitis) following occupational exposure. Previous history of allergies was not
discussed for any of these cases. Skin sensitization to mercury has also been reported in the general
public.
EFFECTS ON THE DIGESTIVE SYSTEM: Limited information suggests that long-term exposure to
mercury vapour can cause inflammation and ulceration of the inside of the mouth, sore gums,
drooling, diarrhea and other effects on the digestive system. No exposure information is reported, but
presumably the concentrations were high.
EFFECTS ON THE HEART: Mercury may affect the heart producing increased blood pressure and/or
heart rate. Two studies of employees with long-term exposure to low levels of mercury showed no
effects on blood pressure or heart rhythm, as measured by electrocardiogram (ECG). A few other
studies have shown effects on the heart including increased blood pressure and heart rate and
abnormal ECG results. More deaths due to cardiovascular problems were observed in employees
exposed to mercury in the chlor-alkali industry. These studies are limited by factors such as exposure
to other potentially harmful chemicals at the same time and weak exposure information.
EFFECTS ON THE IMMUNE AND ENDOCRINE SYSTEMS: In most studies, effects on the immune and
endocrine systems were not observed in employees exposed to mercury. However, altered immune
response has been suggested in a few studies.
EFFECTS ON THE RESPIRATORY SYSTEM: Very little information is available regarding effects on the
respiratory system from long-term exposure. Two studies reported persistent cough in employees
exposed to mercury vapour for several weeks. Another study reported no respiratory symptoms, X-ray
abnormalities or impaired pulmonary function in employees exposed to mercury vapour levels up to
0.27 mg/m3 for more than 6 years.
EFFECTS ON THE EYE: Long-term occupational exposure to mercury has caused a grayish-brown or
yellow discoloration in the eyes of some people. This haze is not thought to affect vision. A gray band
through the cornea (band keratopathy) has also been reported in a few people. In one study, poor
a
colour vision was observed in 33 employees with moderately high to high urine mercury levels.
toptop
<
Will Mercury cause cancer?
The International Agency for Research on Cancer (IARC) has determined that there is inadequate
evidence in humans and animals for the carcinogenicity of mercury and mercury compounds. The
overall IARC evaluation for metallic mercury and inorganic mercury compounds is that they are not
classifiable as to their carcinogenicity to humans (Group 3).
In most studies, increased cancer rates were not observed in people with occupational exposure. Brain
tumours were increased in dentists and dental nurses exposed to metallic mercury, but this outcome
was not observed in other similar populations. In another study, prostate and lung cancers were
associated with exposure to metallic mercury. Other studies could not be interpreted because of study
desicjn limitations such as multiple chemical exposures.
-in
toptop
Will Mercury cause any problems with my reproductive system?
Although it is not possible to draw firm conclusions based on the limited human information available,
exposure to mercury may reduce fertility in females. Effects on male fertility have generally not been
observed. There is no relevant animal information available.
In one study, fertility was decreased in female dental assistants who prepared 30 or more dental
fillings per week and had poor work hygiene practices. There was also some evidence of decreased
fertility in a group of employees exposed to mercury at a lamp factory. Both of these studies had
design limitations. Complications during pregnancy and delivery and increased menstrual disorders
have also been seen in some studies. However, all of the studies had design limitations including
inadequate exposure assessment, inadequate controls and incomplete reporting of the data.
Effects on fertility were not seen in three studies of men occupationally exposed to mercury. One
study showed that the wives of men occupationally exposed to moderately high concentrations of
mercury had more miscarriages, but another study did not show this effect. Two studies showed no
harmful effects on pregnancy when the father was exposed to mercury.
toptop
Will Mercury cause effects on the fetus/unborn baby?
While it is not possible to draw firm conclusions based on the limited human information available,
exposure to mercury has generally not caused harmful effects in the unborn child or more
miscarriages. Two animal studies do indicate that mercury exposure during pregnancy can cause
subtle behavioral changes in offspring, in the absence of harmful effects in the mothers. Several
human population studies have investigated pregnancy outcome in women routinely exposed to low
levels of mercury in the workplace. Two large studies of dental assistants and dentists did not report
an increase in birth defects. Two smaller studies, both with study design limitations, reported birth
defects (such as spina bifida and dislocation of the hip). One incompletely reported study suggested
decreased birth weights.
A small number of case reports have not described harmful effects on the unborn child following brief
exposure of the mother to high levels of mercury during pregnancy. Another case report describes a
normal pregnancy outcome in a woman occupationally exposed to low levels of mercury vapour
throughout pregnancy. No conclusions can be drawn from one other case report where the infant was
also deprived of oxygen during delivery.
Most human population studies have not shown more miscarriages in women occupationally exposed
!wj
to mercury. A few studies with significant design limitations have shown more miscarriages.
toptop
Will Mercury act in a synergistic manner with other materials (will its effects be
more than the sum of the effects from the exposure to each chemical alone)?
In one animal study, the offspring of pregnant rats exposed to both methylmercury and elemental
mercury had more pronounced behaviourial effects than rats exposed to elemental mercury alone.
Similar effects were not observed in the offspring of rats exposed to methylmercury alone. No
conclusions can be drawn from one study which indicated that the mutagenic effects of elemental
mercury are enhanced by smoking. This study was incompletely reported.
Exposure to other metals at the same time, the use of penicillin-type antibiotics, and ingestion of
ethanol in alcoholic beverages can the influence excretion of elemental mercury.
toptop
Is there potential for Mercury to build-up or accumulate in my body?
Elemental mercury is a heavy liquid. The vapour evaporates from the liquid and evaporation occurs
more rapidly when the liquid is heated. The vapour is well absorbed following inhalation. It
accumulates in the kidney and the brain. Elemental mercury is excreted from the body slowly. It has
an elimination half-life of 40-60 days. Most elemental mercury is excreted in exhaled air, and small
amounts in the feces and urine. Very small amounts can be eliminated in sweat, saliva and milk.
Following ingestion, elemental mercury is poorly absorbed and most of it is excreted in the feces.
Elemental mercury liquid and vapour can be absorbed through the skin in small amounts. Elemental
mercury is transferred to the developing child in a pregnant women.
[ 100c Lu tp-rew
MERCURY: A FACT SHEET FOR
HEALTH PROFESSIONALS
Mercury is probably best know as the silver liquid in thermometers. However, it has over 3000 industrial uses.
Mercury and its compounds are widely distributed in the environment as a result of both natural and man-made
activities. The utility, and the toxicity, of mercury’ have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous. The purpose of this document is to provide health
professionals with updated information on mercury and guidance on preventing toxic exposures in health care
workers and their clients.
HISTORY & REGULATIONS
Mercury occurs naturally in the environment as mercuric sulfide, also known as cinnabar. It is also present in some
fossil fuels. Cinnabar has been refined for its mercury content since the 15th or 16th century B.C. Its health hazards
have been known at least since the roman conquest of Spain. Due to the toxicity of mercury in cinnabar, criminals
sentenced to work in quicksilver mines by the Romans had a life expectancy of only 3 years.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and cannot be broken down into
less hazardous compounds. Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems. Not only are these methylated mercury compounds toxic, but highly bioaccumulative
as well. The increase in mercury as it rises in the aquatic food chain results in relatively high levels of mercury in
fish consumed by humans. Widespread poisoning of Japanese fisherman and their families occurred in Minamata,
Japan in the 1950's as a result of consumption of methyl mercury contaminated fish. Today, we continue to be
exposed to mercury in our diets, primarily from fish and shellfish. As a result, the U.S. Food and Drug
Administration (FDA) has an action level for mercury of 1 part per million (ppm) in fish and the Michigan
Department of Public Health issues fish consumption advisories to anglers when mercury levels exceed 0.5 ppm in
fish tissue.
Widespread industrial production of mercury, along with lack of careful handling and disposal practices, has
contributed to environmental contamination. The U.S. Environmental Protection Agency (EPA) has made efforts to
regulate the continued release of mercury into the environment. EPA regulates industrial discharges to air and water,
as well as regulating some aspects of mercury waste disposal. In 1976, EPA banned most pesticide uses of mercury with the exceptions of fungicidal uses in paints and outdoor fabrics, and for control of Dutch Elm disease. In 1990,
mercury use as a fungicide in interior latex paint was halted by the EPA. This action stemmed from requests by
Michigan officials after a child was poisoned from over formulated mercury-containing paint used in his home
More recently, the use of mercury compounds in exterior latex paint has also been halted.
In addition to the early workers in the cinnabar mines, modern workers in industries using mercury are at risk from
overexposure. The Occupational Safety and Health Administration (OSHA) has been reviewing the current
occupational exposure standard of 0.1 mg/m3 (milligrams per cubic meter of air) to determine if they should reduce
the 8 hour acceptable exposure limit to 0.05 mg m3. Although no regulatory limit exists for airborne exposure to
mercury outside of an occupational setting, the EPA suggests that 0.3 ug/m3 (micro-grams per cubic meter of air) of
mercury is a no-effect level (or reference dose = Rfd) for chronic inhalation exposure.
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room temperature, ease of vaporizing
and freezing, and electrical conductivity make mercury an important industrial metal. In 1973, U.S. consumption of
mercury was 1900 metric tons. Primary among its over 3000 industrial uses are battery manufacturing and chlorine
alkali production. Paints and industrial instruments have also been among the major uses. Until paint manufacturers
agreed to eliminate the use of mercury in interior paints. 480,000 pounds of mercury in paints and coatings were
produced each year. Table 1 provides a list of mercury uses
EXPOSURE SCENARIOS
Humans come in contact with mercury through environmental, occupational or accidental exposure scenarios An
estimated 80% of utilized mercury is eventually released back into the environment. Because it is easily vaporized,
air around chlorine-alkali plants, smelters, municipal incinerators, sewage treatment plants and even contaminated
soils may contain increased levels of mercury. A primary route of exposure is through transport into surface waters,
where mercury becomes biomagnified in fish tissues.
Workplace exposure to mercury occurs through inhalation of contaminated air, direct skin contact with liquid
mercury, or oral exposure through contaminated hands, food, etc. A recent edition of the television show 60 Minutes
highlighted concerns about mercury exposure in patients receiving silver dental fillings with mercury-containing
amalgam. Insufficient scientific evidence exists at this time to either support or refute the claims that dental fillings
may result in harmful exposure to mercury.
Accidents have resulted in several cases of mercury poisoning in Michigan in the past two years. Four members of a
Lincoln Park family were killed after one member attempted to refine dental amalgam in his home while attempting
to recover silver. High levels of mercury w'ere found throughout the house, including wrapped food inside the
freezer. The entire house had to be demolished and disposed of in a hazardous waste landfill.
A number of children have developed mercury poisoning after playing with small vials of mercury which they found
at home or school. These children were hospitalized when symptoms became so severe that they could not longer
walk. One contamination incident involved closing a school for weeks and entailed environmental investigation of
residences, cars, school buses and day care centers.
METABOLISM & TOXICITY
<
Exposure to mercury can occur through inhalation, ingestion or dermal absorption, the amount of mercury absorbed
by the body -and thus the degree of toxicity - is dependent upon the chemical form of mercury. For instance,
ingested elemental mercury is only 0.01% absorbed, but methyl mercury is nearly 100% absorbed from the
gastrointestinal tract. The biological half-life of mercury is 60 days. Thus, even though exposure is reduced, the
body burden will remain for at least a few months. Elemental mercury is most hazardous when inhaled. Only about
25% of an inhaled dose is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the total
dose). Dermal contact with liquid mercury can significantly increase biological levels. The primary focus of this
article is elemental mercury, since that is the form of exposure to health care workers involved with mercurycontaining instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury may cause acute or chronic
health effects. Acute exposure (i.e., short term, high dose) is not as common today due to greater precautions and
decreased handling. However, severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5 hours may cause headaches,
salivation, metallic taste in the mouth, chills, cough, fever, tremors, abdominal cramps, diarrhea, nausea, vomiting,
tightness in the chest, difficulty breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a
number of hours.
Chronic effects include central nervous system effects, kidney damage and birth defects. Genetic damage is also
suspected.
Nervous system effects. These are the most critical effects of chronic mercury exposure from adult exposure as they
are consistent and pronounced, some elemental mercury is dissolved in the blood and may be transported across the
blood/brain barrier, oxidized and retained in brain tissue. Elimination from the brain is slow; resulting in nerve tissue
accumulation. Symptoms of chronic mercury exposure on the nervous system include: Increased excitability, mental
instability, tendency to weep, fine tremors of the hands and feet, and personality changes. The term "Mad as a
Hatter" came from these symptoms which were a result of mercury exposure in workers manufacturing felt hats
using a mercury-containing process.
Kidney effects: Kidney damage includes increased protein in the urine and may result in kidney failure at high dose
exposure.
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild exposure include delayed
developmental milestones, altered muscle tone and tendon reflexes, and depressed intelligence.
Mercury exposure in children can cause a severe form of poisoning termed acrodynia. Acrodynia is evidenced by
pain in the extremities, pinkness and peeling of the hands, feet and nose, irritability, sweating, rapid heartbeat and
loss of mobility.
PRECAUTIONS FOR HEALTH CARE WORKERS
Substitutes for mercury-containing medical devices should be used whenever possible, e g therroometers and
sphygmomanometers. When mercury devices must be used, special precautions should be taken. These devices
should never be used on a cloth surface, such as upholstered chair or in a room with a carpeted floor If a spill
occurred in such an area, the upholstery or carpeting would need to be discarded as it could not be effectively
decontaminated. Children should never be left unattended near these devices. If mercury thermometers are used, a
mercury spill kit should be kept readily accessible. The kit should contain a sulfur powder to suppress volatilization
and a collection device.
1
SPILL RESPONSE
If a spill occurs, evacuate the immediate area and ventilate as well as possible. An environmental consultant will
need to be contacted for clean-up and disposal. DO NOT attempt to clean-up a mercury spill using rags or an
ordinary vacuum. This will only serve to disperse the mercury and encourage volatilization. For further assistance,
contact your local health department and/or the Michigan Department of Public Health, Division of Health Risk
Assessment. For assistance with a large spill, call the Fire Department for assistance. For assistance with clean-up,
you may look in your local phone book for environmental consultants. Table 2 contains a list of consultants known
to respond to mercury spills.
DISPOSAL
The best method of mercury disposal is reclamation. Attached is a list of agencies in Michigan that will take used
mercury. Button batteries can be recycled at many jewelry stores and other retail outlets that sell batteries. Larger
quantities of mercury will need to be disposed of by a licensed hazardous waste hauler. Contact the Michigan
Department of Natural Resources, Waste Management Division for assistance with mercury disposal.
Back to the Ingham County Pamphlet List Page
Back to the AWARE Home Page
«•
Monitoring Mercury Exposure
Mercury can be monitored in the body two ways, biologically and medically. Monitoring mercury is necessary if
someone is exposed mercury, or think they might be exposed. Everyday objects such as lights and thermostats in the
home and in appliances are of no danger to humans unless they are broken and the mercury is released.
What is Biological Monitoring?
Biological monitoring is the measurement of chemical agents in the blood, urine, or other body tissue of exposed
individuals to determine how much of the chemical has been absorbed into the body. It serves as a back-up to
environmental exposure measurements, since air measurements cannot take into consideration skin exposure or the
effectiveness of protective equipment and work practices. Biological monitoring measures the amount of an agent
actually present in the body and is usually a better estimate of risk for adverse health effects than air monitoring.
There is no ideal biological monitor for evaluating the risks of mercury intoxication from metallic (mercury zero) or
inorganic mercury. Mercury can be measured in both blood and urine. Individual levels may vary greatly from day
to day and even within a given day. While proper interpretation of the results can be difficult, the measurements can
nevertheless provide information on potential overexposure. Measurements should be taken regularly (several times
a year) for chronically exposed workers. Individual results and also group results should be evaluated. To effectively
interpret the results, baseline levels need to be established before exposure begins for comparison purposes.
Mercury in the Urine
Measurement of mercury in urine is the recommended biological monitor for cases of metallic and inorganic
mercury exposure. Organic mercury is not passed out of the body in urine so it cannot be measured this way. Ideally,
the collection should be over 24 hours, but this is seldom feasible. Spot urine samples may also be taken, but they
must always be collected at the same time of day near the end of the work week after several months of steady
exposure. Overnight samples may also be collected. This collection extends from the time the employee goes to bed
through the first urination of the morning.
Samples must be collected in containers provided by the laboratory, since a preservative must be added. A minimum
of 25 milliliters of urine must be collected. Great care must be taken to prevent contamination of the sample
containers or the urine itself with mercury from the skin or workplace air.
When the results are interpreted, the urine values should be corrected for grams of creatinine in the sample, and
should be expressed as ug Hg/gram creatinine. In persons not occupationally exposed to mercury, urine levies rarely
exceed 5 ug Hg /g creatinine.
While many laboratories indicate that only levels above 150 ug/L should be considered toxic, there is strong
evidence that early signs of mercury intoxication can be seen in workers excreting more than 50 ug Hg/L of urine
(standardized for a urinary creatinine of 1 gram/L). This value of 50 ug/g creatinine is proposed by many experts as
’
Avnnciirft tn mercurv vapor. In 1980 this view was endorsed by a World
a biological thresnoid ilnlh vdiuu ivi CilxOH/V w--r
Health Organization study group.
Mercury in the Blood
in the Wood reflects exposure to organic mercury (including methylmercury) as well
Occurs
Samples *,uM .toys he — •>
»< “■>
“d <>' 1'“
”“k
”'hS °f
n
steady exposure. The blood should be collected in mercury-free heparinized tubes after careful skin cleansing.
In unexposed individuals, the amount of mercury in blood is usually less than 2 ug/100 mL. According to some
experts, an average airborne concentration of 50 ug/cubic meter corresponds to a mercury concentration in blood of
about 3-3.5 mg/lOOmL. Early effects of mercury toxicity have been found when the blood concentration exceeds 3
ug/100 mL. Levels above 2.8 ug/DL are required to be reported to the Health Department. Any worker exceeding
this level should be placed in a non-exposed job until dietary and workplace exposures have been evaluated and
blood levels have returned to baseline.
Medical Monitoring
Medical monitoring is the long-term periodic evaluation of exposed workers to insure that they are not experiencing
any adverse effects of potentially hazardous workplace exposures. Medical monitoring serves as a backup for a
program of routine air and biological monitoring, which are the primary means for insuring that exposure levels are
below those associated with adverse health effects. A medical monitoring program should be designed to detect
adverse effects of exposure early on, when they are still reversible, so that exposures can be controlled and serious
permanent effects can be prevented.
An initial medical examination should be performed on all employees exposed to potentially hazardous levels of
mercury. The purpose of this examination is to provide a baseline for future health monitoring.
The examination should include a complete medical history and symptom questionnaire, with attention given to the:
• nervous system (target organ for chronic exposure)
• kidneys (target organ for acute and chronic exposure)
• oral cavity (target organ for chronic exposure)
• lungs (target organ for acute exposure)
• eyes (affected by chronic exposure)
• skin (mercury is a known skin sensitizer)
Signs and symptoms of the earliest signs of mercury intoxication should be checked for; these include personality
changes, weight loss, irritability, fatigue, nervousness, loss of memory, indecision, and intellectual deterioration.
Complaints of tremors and loss of coordination should also be sought. Physical examination should focus on the
target organs described above. A baseline handwriting sample should be obtained. Laboratory evaluation should
include at minimum a complete urinalysis.
This examination should be repeated annually. Results should be compared with the baseline examination, looking
for changes suggestive of mercury toxicity. Handwriting samples should be compared to the baseline sample for
evidence of tremor. If symptoms suggestive of mercury intoxication are occurring, interim evaluations should be
conducted.
expose. htmTo Exposure to Mercury
© Copyright
rI
■ THE STATES
Ws2X.
in Kodaikanal
r
-
a wltalionol company in Kodaikanal is accused of being less ikon
: '“sposiigailtregtothe^nvironmenfof the region.
a
i-w
K
MS
NITYANAND JAYARAM
T^HE mist clears as a Breeze wafts in
X
che densely forested valley in the
east. The smell of eucalyptus and pine
hangs fresh in the air. This is Kodaikanal,
the popular tourist destination in South
nd'a known for its beautiful lakes, rich
forests and perennially cool weather.
Uniformed workers, wearing funny
■ndustnal hats and the logo HLLembroidered on their shirts, mil! around near a
gate, drinking hot tea, smoking beedis
chatting. It is rca timeat Hindustan Lever
imiteds (HLL) mercury thermometer
f
y. Heyond the gate and inside the
racuvfy, everything looks clean and orderIt fr ? i' aH,iS nOt Weli here- Residents of
■ Kodaikanal, and environmental pressure
■ groups including the Palni Hills
I
^onservatton Council (PHCC) and !
I
Greenpeace have accused HLL of dump
ing toxic waste in Kodaikanal.
.Raja Mohan, a. naturalist and an
aettvist ° rhe PHCC, leads you to the
area behind the factory, over a fence and
up a steep climb. “This is where the facW has dumped stuff," says Mohan,
P n ing to a patch of vegetation on the
the richest of terrestrial biodiversity The shola forest
ts In the Palni Hills
posttones. Virtually every shola drains region are
among
the richest of
into a perennial scream or river.
terrestrial biodiversity depositories.
The dump is spread out. A barrel lies
on its side with its contents - of broken
thermometers, some containing mercury can of waste dumping.”
Barely } km away, ar .Munjikal. a
- spilled on the forest floor. Plastic hor
c
ensely
populated part of the town, a scrap
des labelled Mercury. Poison" litter rhe
nearby area. A closer inspection reveals yard owner complains that he is stuck with
nearly 1 5 tonnes of mercury-laden broken
that the
bottles
tents
of refine
J and their erstwhile con thermometers that he was sold as broken
tents or renned mercury were supplied by glass scran bv HH
Lsix months ago. "I’m ;i
went to pick up scrap
t
factory, and they said I would eet
cleqrprl r ”
‘ «
- nave
the Other cmn /-.n
eared it, says Mohan. “Thev are obvi- f other scrap only if I took the broken
thermometers, sayS Piraviyam. "Nobody
ouslytrymg co hide what evidence they told
^'i me it was illegal or rhar
'
23s
-O‘
oiopcs.
the p^f^^all of the factory,
out in a
green hues. Sholas
) are unique to
la and are among
'
waste in the hill resort.
FRONTLINE, MARCH 30, 2001
47
4.
1-
I
I
UtE
pMCv
I
I
I
!
once a day. In another section, where they
heat thermometers in an oven, workers
were exposed to gusts of mercury' vapour
every time the oven door was opened.”
On its website, Unilever, the com
mercially thriving Anglo-Dutch multina
tional yvhich holds 51 per cent stake in
the equally thriving HLL, states that
Unilever s aims are to “exercise the same
concern for the environment yvherever we
operate.” At Kodaikanal itself. HLL has
extensively sponsored road-signs that
exhort people to “Keep Kodai Clean.”
I
company began production of
1 thermometers at Kodaikanal in 1983,
after a second-hand mercury- thermometer
plant owned by Cheseborough Por 'nc.
in Watenown, New York, closeu ,wn
Activists at a scrapyard where glass scrap was stated to contain
and was relocated in India under the own
mercury.
ership of Ponds India Ltd. In 1997. Ponds
dangerous substance. Last year my boys
more concerned than anvbody else about India merged with HLL, the Unilever sub
collected about half-a-litre of mercury' but
our emp.cvees and the environment,” he sidiary. The factory' enjoys a variety- ofgov
1 don’t knoyv what happened to it.” The said in cctennai. There is no hazardous
ernment benefits as a 100 per cent
broken thermometers now lie in
waste the: has gone outside the factory.” export-oriented unit (EOU).
Piraviyam s cluttered shop in open and
An ofr.c'-L response from the HLL to a
HLL imports the required glass and
torn sacks, exposed to the elements - and
questior.r_iire that this writer sent the mercury- (short of five tonnes a year), the
a stone s throw away from two schools.
compar stated that it had sold only the latter primarily from the U.S., and
Mercury- in the presence of soil or
glass waste from the non-mercury area,
water gets converted into compounds which is completely free rrom any mer exports all of its thermometers to the U.S.
.
-According to a spokesman of HLL'sthcrsuch as methyl mercury'. This poisonous
cury at al" (HLL stated in a press
|
release mometer division, the thermometers then
substance is bioaccumulative as it moves
on Marcc. 8 that pending a comprehen find their way into markets in the U.K.,
up the food chain, and biomagnifies by si
sive auo:: and review of the operation of Canada, Australia, Germany and Spain.
some 100,000 times in fish. In a well- the
’ facto- . the company had decided to
“ The entire operation reeks of envi
known case, the consumption of mer
suspend mermometer production there.) ronmental double-standards. All that talk
cury-bearing fish led to the poisoning of
■, some local res.dents and ex- .. ..........
Uu.l,,.1avJIlglcarn[al
esSOnrrom
industry'having
learnt a lesson
from
a number ofjapanese fishermen and their workers^;.-chatHLL sc aimsinth.smat- about
Bhopal is nonsense,” says R. Kannan, a
families in Minamata, Japan, in the t
a™*" diSPla’'S .PHCC i1™™- “No lessons have been
1950s.
The
Food
and
L.„
Drugb two buexet ofbroken thermometers pur
Administration (FDA) of the United chased rrom the scrapyard. Some of them learnt, either by the oig companies •“ ^y
5
States has advised pregnant women and have mercury in the bulbs. Others bear our regulatory' authorities.” In the 1.
women of childbearing age to avoid eat the brane names of companies in the years, the PHCC has sought, yvith signif
ing predatory fish such as shark, syvord- U.S., the L.K. and Germany that have icant success, to arrest the degradation of
precious natural heritage sites in
fish king mackerel and tile fish, which sourced thermometers
sourced thermometers
from
the Kodaikanal through encroachment and
could carry high levels of methyl mercury. T
J
JI
__
;
..........
Kodaikane. plant. “The brand names are
the b°ann^aoCfh I’ T J0 Pe0P,e,UI;der P™t«i "JSer the mercury is ruled m deforestation.
• mercury' is filled in
While the nearly 15 tonnes of mer
the banner of a broad coalmon including the stem.- says S. Sagavaraj. who left the
cury-contaminated
waste continues to
on7ind-8r°UPS’ CtTmer Or?anisa- ^Ploy ofthe company after his health
pose the threat of toxic exposure to the
tions, mdigenous people s groups, envi- suffered a setback in 1995
ronmentalists and former workers of the
As in the case of some other former community, agencies involved in safe
guarding public health and environment
yJTrhX'mfaChOd’frCaChtd thc Scrapi' WOrkeii dle Plant’
feels rh-«
ard. They marched from the scrapyard his ailments have somedrin? to do with restrict themselves to generalities and
to the factory holding placards that read what he terms the casual manner in which seem unaware of the evidence mounting
Mino ?°”e
Bhopals
No
more mercury is handled in the factory. “I saw against mercury in countries ofthe North.
“Mercury is a low-level hazardous
1J ■ and demandmg a public mercury daily on the floor and I saw peounder Indian law. If mercury is
apology from the factory management.j
A P1J^dling it intentionally or c :..b chemicalcause
coming going to cause aa ror
lot or
ofnarm,
harm, then
then we
yve need
need
team of ex-workers assisted L,
by into contact with it accidentally, he said, to look at various forms of reflation. If
Greenpeace cordoned off the scrapyard.
d.
Mahendra Babu, another ex-worker it
it is
established that
that aa plant
nUri.™,
is established
is causing mer
A spokesman ror HLL, hoyvever,
who is attempting to bring the affected cury pollution, the plant can be shut
denies the charges levelled with regard to
workers together, says: “\Vnen I worked
the Kodaikanal unit’s operation. “We’re there, the}- used to suck up the mercury down,” says Dr. Indrani Chandrarunning a very’ safe operation, and yve are from the hoor i suck up the mercury sekhran, Assistant Director, Ministry of
using a vacuum cleaner Environment and Forests. ■
•4S
FRONTLINE, MARCH 30, 2001
1
Or
MERCURY: A FACT SHEET FOR
HEALTH PROFESSIONALS
Mercury is probably best know as the silver liquid in thermometers. However, it has over 3000 industrial uses.
Mercury and its compounds are widely distributed in the environment as a result of both natural and man-made
activities. The utility, and the toxicity, of mercury have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous. The purpose of this document is to provide health
professionals with updated information on mercury and guidance on preventing toxic exposures in health care
workers and their clients.
HISTORY & REGULATIONS
Mercury occurs naturally in the environment as mercuric sulfide, also known as cinnabar. It is also present in some
fossil fuels. Cinnabar has been refined for its mercury content since the 15th or 16th century B.C. Its health hazards
have been known at least since the roman conquest of Spain. Due to the toxicity of mercury in cinnabar, criminals
sentenced to work in quicksilver mines by the Romans had a life expectancy of only 3 years.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and cannot be broken down into
less hazardous compounds. Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems. Not only are these methylated mercury compounds toxic, but highly bioaccumulative
as well. The increase in mercury as it rises in the aquatic food chain results in relatively high levels of mercury in
fish consumed by humans. Widespread poisoning of Japanese fisherman and their families occurred in Minamata,
Japan in the 1950's as a result of consumption of methyl mercury contaminated fish. Today, we continue to be
exposed to mercury in our diets, primarily from fish and shellfish. As a result, the U.S. Food and Drug
Administration (FDA) has an action level for mercury of 1 part per million (ppm) in fish and the Michigan
Department of Public Health issues fish consumption advisories to anglers when mercury levels exceed 0.5 ppm in
fish tissue.
Widespread industrial production of mercury, along with lack of careful handling and disposal practices, has
contributed to environmental contamination. The U.S. Environmental Protection Agency (EPA) has made efforts to
regulate the continued release of mercury into the environment. EPA regulates industrial discharges to air and water,
as well as regulating some aspects of mercury waste disposal. In 1976, EPA banned most pesticide uses of mercury with the exceptions of fungicidal uses in paints and outdoor fabrics, and for control of Dutch Elm disease. In 1990,
mercury use as a fungicide in interior latex paint was halted by the EPA. This action stemmed from requests by
Michigan officials after a child was poisoned from over formulated mercury-containing paint used in his home.
More recently, the use of mercury compounds in exterior latex paint has also been halted.
In addition to the early workers in the cinnabar mines, modern workers in industries using mercury are at risk from
overexposure. The Occupational Safety and Health Administration (OSHA) has been reviewing the current
occupational exposure standard of^JjngZmT (milligrams per cubic meter of air) to determine if they should reduce
the 8 hour acceptable exposure limit to 0.05 mg/m3. Although no regulatory limit exists for airborne exposure to
mercury outside of an occupational setting, the EPA suggests that 0.3 ug/m3 (micro-grams per cubic meter of air) of
mercury is a no-effect level (or reference dose = Rfd) for chronic inhalation exposure.
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room temperature, ease of vaporizing
and freezing, and electrical conductivity make mercury an important industrial metal. In 1973, U.S. consumption of
mercury was 1900 metric tons. Primary among its over 3000 industrial uses are battery manufacturing and chlorine
alkali production. Paints and industrial instruments have also been among the major uses. Until paint manufacturers
agreed to eliminate the use of mercury in interior paints, 480,000 pounds of mercury in paints and coatings were
produced each year. Table 1 provides a list of mercury uses.
EXPOSURE SCENARIOS
Humans come in contact with mercury through environmental, occupational or accidental exposure scenarios. An
estimated 80% of utilized mercury is eventually released back into the environment. Because it is easily vaporized,
air around chlorine-alkali plants, smelters, municipal incinerators, sewage treatment plants and even contaminated
)>
soils may contain increased levels of mercury. A primary route of exposure is through transport into surface waters,
where mercury becomes biomagnified in fish tissues.
Workplace exposure to mercury occurs through inhalation of contaminated air, direct skin contact with liquid
mercury, or oral exposure through contaminated hands, food, etc. A recent edition of the television show 60 Minutes
highlighted concerns about mercury exposure in patients receiving silver dental fillings with mercury-containing
amalgam. Insufficient scientific evidence exists at this time to either support or refute the claims that dental fillings
may result in harmful exposure to mercury.
Accidents have resulted in several cases of mercury poisoning in Michigan in the past two years. Four members of a
Lincoln Park family were killed after one member attempted to refine dental amalgam in his home while attempting
to recover silver. High levels of mercury were found throughout the house, including wrapped food inside the
freezer. The entire house had to be demolished and disposed of in a hazardous waste landfill.
A number of children have developed mercury poisoning after playing with small vials of mercury which they found
at home or school. These children were hospitalized when symptoms became so severe that they could not longer
walk. One contamination incident involved closing a school for weeks and entailed environmental investigation of
residences, cars, school buses and day care centers.
METABOLISM & TOXICITY
Exposure to mercury can occur through inhalation, ingestion or dermal absorption, the amount of mercury absorbed
by the body -and thus the degree of toxicity - is dependent upon the chemical form of mercury. For instance,
ingested elemental mercury_is only 0.01% absorbed, but methyl mercury is nearly 100% absorbed from the
gastrointestinal tract. The biological half-life of mercury is 60 days. Thus, even though exposure is reduced, the
body burden will remain for at least a few months. Elemental mercury is most hazardous whenjnhaled. Only about
25% of an inhaled dose is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the total
dose). Dermal contact with liquid mercury can significantly increase biological levels. The primary focus of this
article is elemental mercury, since that is the form of exposure to health care workers involved with mercurycontaining instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury may cause acute or chronic
health effects.jAcute exposure ^i.e., short term, high dose) is not as common today due to greater precautions and
decreased handling. However, severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5 hours may cause headaches,
salivation, metallic taste in the mouth, chills, cough, fever, tremors, abdominal cramps, diarrhea, nausea, vomiting,
tightness in the chest, difficulty breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a
number of hours.
Chronic effects include central nervous system effects, kidney damage and birth defects. Genetic damage is also
suspected.
Nervous system effects. These are the most critical effects of chronic mercury exposure from adult exposure as they
are consistent and pronounced, some elemental mercury is dissolved in the blood and may be transported across the
blood/brain barrier, oxidized and retained in brain tissue. Elimination from the brain is slow, resulting in nerve tissue
accumulation. Symptoms of chronic mercury exposure on the nervous system include: Increased excitability, mental
instability, tendency to weep, fine tremors of the hands and feet, and personality changes. The term "Mad as a
Hatter" came from these symptoms which were a result of mercury exposure in workers manufacturing felt hats
using a mercury-containing process.
Kidney effects: Kidney damage includes increased protein in the urine and may result in kidney failure at high dose
exposure.
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild exposure include delayed
developmental milestones, altered muscle tone and tendon reflexes, and depressed intelligence.
Mercury exposure in children can cause a severe form of poisoning termed acrodynia. Acrodynia is evidenced by
pain in the extremities, pinkness and peeling of the hands, feet and nose, irritability, sweating, rapid heartbeat and
loss of mobility.
PRECAUTIONS FOR HEALTH CARE WORKERS
Substitutes for mercury-containing medical devices should be used whenever possible, e.g. thermometers and
sphygmomanometers. When mercury devices must be used, special precautions should be taken. These devices
should never be used on a cloth surface, such as upholstered chair or in a room with a caipeted floor. If a spill
occurred in such an area, the upholstery or carpeting would need to be discarded as it could not be effectively
decontaminated. Children should never be left unattended near these devices. If mercury thermometers are used, a
mercury spill kit should be kept readily accessible. The kit should contain a sulfur powder to suppress volatilization
and a collection device.
SPILL RESPONSE
If a spill occurs, evacuate the immediate area and ventilate as well as possible. An environmental consultant will
need to be contacted for clean-up and disposal. DO NOT attempt to clean-up a mercury spill using rags or an
ordinary vacuum. This will only serve to disperse the mercury and encourage volatilization. For further assistance,
contact your local health department and/or the Michigan Department of Public Health, Division of Health Risk
Assessment. For assistance with a large spill, call the Fire Department for assistance. For assistance with clean-up,
you may look in your local phone book for environmental consultants. Table 2 contains a list of consultants known
to respond to mercury spills.
DISPOSAL
The best method of mercury disposal is reclamation. Attached is a list of agencies in Michigan that will take used
mercury. Button batteries can be recycled at many jewelry stores and other retail outlets that sell batteries. Larger
quantities of mercury will need to be disposed of by a licensed hazardous waste hauler. Contact the Michigan
Department of Natural Resources, Waste Management Division for assistance with mercury disposal.
Back to the Ingham County Pamphlet List Page
Back to the AWARE Home Page
Qr ^5-.
SUMMARY REPORT
n
Environmental Site Assessment and
Preliminary Risk Assessment for
Mercury
Kodaikanal Thermometer Factory,
Tamil Nadu
Preparedfor
Hindustan Lever Limited (HLL)
Hindustan Lever Ltd
Haji Bunder, Sewni
Mumbai
24 May 2001
<-
49032-002-353\REr;
.R001 ESA.DOC
*3•
Contents
1
j
1
Introduction
1-1
2
History
2-1
2.1
2.2
2.3
2.4
2-1
2-2
3
Process of Manufacture
Scrap Hand:
and Disposal
Kodaikanal (. site Scrapyard
Medical Surveillance
Mercury in the En\
2-3
2-4
;nent
3-1
Description
Intematior0’ C :deline^
3-1
Regulatory Considerations
4-1
4.1
4.2
4.3
4.4
4.5
Air Pollution Control
Water Pollution Control
Hazardous Subs’.:
Hazardous Waste Management
Air Quality
4-1
4-1
4-2
4-3
4-3
5
Site Description------------------------
5-1
6
Scope of work
6-1
7
Assessment of Analytical Results
7-1
7.1
7.2
7.3
7.4
7-1
7-1
7-2
7-2
3.1
3.2
4
General
Mercury Distribution Offsite
Mercury Distribution On Site
Methyl Mercury Results
8
Mercury Balance
9
Health Csues
9.1
9.2
10
3-1
8-1
9-1
Potential Exposure Pathways - Human Health
Potential Exposure Pathways - Environment
9-1
9-2
Conclusions and Recommendations -----------
10-1
10.1 Conclusions
10.2 Recommendations
10.2.1
Priority Actions
10.2.2
Clean L’p Criteria
10-1
10-1
10-1
10-2
C.'SHASM’S BACKUPS\510 ■ PAUL WHINCUP>=;?51 ES~
SUMMARY REPORT - 24-05-01 DOC'24-MAY-01
i
vj
List of Tables, Figures, PJates & Appendices
■j
1
Tables
1
Summary: Samples Tested for Mercury
2
Total Mercury Levels in Soil/Sediment/Lichen - March/April 2001
7-3
3
Total Mercury Levels in Water - March/April 2001
7-5
4
Methyl Mercury Levels in Soil/Sediment/Lichen Samples
7-6
5
Details of Areas Requiring Remediation
Figures
1
Site Location Map
2
Rainfall Recorded at Kodaikanal Weather Station
n
Wind Directions and Speed Recorded at Kodaikanal Weather Station
4
Topography Map
5
Site Layout and Sample Location Plan
6
Offsite Sample Locations
Plates
1
Kodaikanal Scrapyard. 3 and 4 Glass Scrap
7
Kodaikanal Scrapyard. View from Above
3
Soil Erosion, Hotspot A
4
Stream Draining Across Site
5
Grassed Area on site
6
Hotspot B
7
Offsite Discharge to Pambar Shola
8
Site Perspective
9
Precipice below Levange Path from East
10
Precipice below Levange Path from West
11
Tamil Nadu Plains below Pambar Shola
12
Kodai Lake from Carlton Hotel
C:\SHARM-S BACKUPSolO-PAUL WHINCUF\=001 ESA - SUMMARY REPOP T - 24-05 01 DOC24..MAY-01
ii
6-1
7-6
r ■
J
Introduction
SECTION t
n
URS Dames & Moore has been commissioned by Hindustan Lever Limited (HLL) to conduct an
environmental site assessment and preliminary risk assessment for mercury at its wholly owned
thermometer manufacturing facility located at Kodaikanal in Tamil Nadu State. This follows publicity by
Greenpeace and the Palini Hills Conservation Council after their discovery of glass scrap illegally
disposed from the manufacturing facility to a scrapyard in Kodaikanal townsite.
The site location plan is shown on Figure 1. •
)
C:\SHARM S BACKUPSXSIO - PAUL WHWCUPWOOi eSA - SUMMARY REPORT - JA-OS OI ^GZA-MAV-OI
;. .fevv..
- ----------------------------------------------
TTD<
1-1
' '
-
’
■
’
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SECTION 2
History
The Kodaikana! thermometer factory of former Ponds (India) Limited, commenced its manufacturing
operations in early 1984 using equipment relocated from a thermometer factory at Watertown, USA
belonging to Chesebrough Ponds. Kodaikanal was chosen as the most suitable location in South India
because of similar cool climatic conditions to those at Watertown. This was beneficial in terms of
occupational health and safety, and the manufacturing processes.
The factory came under •’ ' ownership of Hindustan Lever Limited (HLL) in 1998 consequent to the
merger with Ponds Indi.
aited. It manufactures thermometers mainly for export to Europe, USA,
South America, Australia and in recent years a small proportion within India under permission from the
Ministry of Commerce.
Thermometers in the factory are manufactured from imported glass and imported mercury. The mercury
used in thermometers is triple distilled (99.999%) and its importation requires clearances from the
Ministries of Commerce and Finance of the Government of India. Entry of glass or mercury on to site
and dispatch off site of finished products and wastes are carried out under certification by the customs
official posted at the Factory and recorded in the Annual Bond Account.
)
!
The factory operates under valid Consents for Discharge of Sewage and Trade Effluents granted by the
>. Tamil Nadu Foliation Control Board (TNPCB). In addition, the factory has authorisation from the
I TNPCB for collection/storage of hazardous wastes under Rule 3(c) and 5(5) of The Collection/Storage of
i Hazardous Waste (Management and Handling) Rules 1989 enacted under the Environmental Protection
/ Act 1986. This licence is for sludge derived from treatment of industrial effluent containing heavy metals
and was renewed in April 2000 with a validity of two years.
2.1
Process of Manufacture
The factory is divided into two main areas:
€'•
Non Mercury Area; and
Mercury Area.
Non Mercury Area
This is where glass-forming operations arc carried out before mercury is filled into fnermometers. This
area covers departments 1 and 2. Various processes that are carried out in this area are:
Stem cutting; Bulb cutting; End opening; End cutting; and Bulb forming.
Mercury Area
This is where all operations from mercury fill through to final thermometer manufar.uring operations are
carried out and covers departments 3 and 4. Various processes that are carried cut r this area are:
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History
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The Mercury and Non Mercury areas arc physically separated by partitions and walls.
2.2
Scrap Handling and Disposal
Glass scrap from the Non Mercury area departments 1 and 2 is bagged and has cither been disposed or is
held in the Custom Bonded Storage area on site. Another 45 tonnes was also buried m four shallow pits
on site. Tliis scrap is mercury free.
The glass scrap from the Mercury area departments 3 and 4 contains residual mercury and until 1990 was
stored as such. Residual mercury in this non-treated scrap approaches 6% by weight.
In 1990 recovery was commenced using a crusher and twin recovery ovens, which operated until 1998.
)
Approximately 60 tonnes of 3 and 4 glass have been processed, however this operation was not
considered particularly efficient as the grinder was unable to crush the glass to the desired level. Residual
mercury in this treated scrap is approximately 1%.
At the end of 1998, a new crusher and vacuum activated mercury recovery' plant were commissioned and
has been in operation since that tunc. This new plant is able to piocess and recover mercury from 200 kg
per day of glass on a round the clock basis. An order has been placed for three additional units to
augment the capacity for mercury' recovery from the accumulated backlog of o and 4 glass scrap.
Residual mercury' in this scrap is approximately 0.15%.
Sale of glass scrap commenced in 1992. A total of 98.3 tonnes was soid during this p^riou <u>d v^mp-rised
both 1 and 2 glass scrap and mercury-recovered 3 and 4 glass scrap. An sales up to October 1994
made to MLC Industries, a lamp/lamp casing manufacturer in Mysore^These sales were discontinued
when lead glass was replaced with soda lime glass. Thereafter, besides sales of 1 and 2 glass scrap, 11.5
tonnes of mercury-recovcrcd 3 and 4 glass scrap was sold to a dealer in Coimbatore in September 1998.
Of this quantity, approximately 8.0 tonnes was sold to Philips India Limited and 3.5 tonnes w€sold to
glass marble manufacturers. Of the 3.5 tonnes, about 1.3 tonnes (mc’uding mud) was traced by HLL in
Bangalore and retrieved in March 2001.
A further quantity of 19.42 tonnes of 1 and 2 glass scrap was sold to a glass recycler in Coimbatore
between June 1997 to June 1999 for manufacture of glass marbles. This manufacturer has confirmed that
all the material has been consumed except for 30 kg wliich has beer, retrieved by HLL. Anothei 6 tOu^vS
of 1 and 2 glass scrap has been retraced to a glass marble manufacturer xvho has consumed the total
quantity of the materials. Eighteen tonnes of 1 and 2 glass scrap w ere sold to a scrap dealer in Chennai
in December 1995 of which approximately' one tonne has beer, retrieved, the remainder has been
consumed in glass marble manufacture.
The last sale in November 1999 of 5.3 tonnes was made to a scrap dealer in Kodaikanal (which is die
material referred to by Greenpeace) and is lynng in the dealer’s yard in Kodaikanal.
History
U
SECTION 2
n
2.3
Koclaikanal Offsite Scrapyard
Approximately 5.3 tonnes of glass cullets, as 3 and 4 glass scrap, are stored in a scrapyard in Kodaikanal
Tins was sold to the scrapyard in November 1999 and is currently located in two small stockpiles
amongst other scrap waste. The glass scrap was treated for mercury recovery before disposal from the
factory and contains between 0.15% and 1.0% metallic mercury. On this basis the material contains
slightly more than b0 mg/kg of mercury and is classified as a Hazardous Waste.
The scrapyard is located within the residential/commercial area of Kodaikanal. where granite bedrock is
exposed and soil cover is no more than 0.2 to 0.3 m. There is surface runoff from the site durin- rainv '
periods whtch discharges across the adjacent road and then downhill across other roads which are located
at progressively lower elevations. It is considered essential that the glass scrap be removed from the
scrapyard before the onset of the monsoon season.
A preliminary protocol for recovery, transport and on-site storage of the Hass scrap was prepared hv URS
Dames & Moore, and submitted to the Tamil Nadu Pollution Control Board (T.XPC B) on 18 March 2001.
Comments made by Navroz Mody of the Tamilnadu Alliance Against Mercurx were returned on ' May
2001. These comments have been reviewed by URS Dames & Moore and its expert subconsultant Dr Van
Teunenbroek of TNO in the Netherlands. Together a revised protocol has been agreed and resubmitted to
TNPCB for approval. The protocols are in line with internationally accepted Guidelines for Chemical
Hazards of the U.S. Department of Health and Human Services. National Institute for Occupational
Safety and Health ( NIOSH) as published on their website htip://w ww.cdc.gov/niosh/npg/nengapdx.html.
It should be recognised that retrieval, drumming, transport and storage of the waste will occupy an
elapsed lime of no more than two days and will involve no more than 20y 200 Ittre drums of waste glass
and soil. The potential exposure of workers and nearby residents to mercury vapour and dust during the
operation is therefore limited. The proposed protocol involves the hallowing step.-:
I.
Cordon off access to the scrapyard immediately prior to commencement of operations and secure
the area with police.
!!.
Use a fine spray of water on the stockpiles, a'-oiding any surface runoff. : minimise dust
generation.
iii.
Erect tarpaulin/HDPE partition above man height anmnd the pen meter of that part of the
scrapyaid, which is to be disturbed to further minimise am dust emission; ofr ite.
iv.
Commence monitoring of mercury concentrations in air using a Jerome 431 -X Mercury Vapour
Analyzer accurate to 0.003 mg/m3 fef the NIOSH time weighted a > erage Ur mercurv vapour is
0.05 mg/ mg/m3).
Commence clearing and drumming of waste and soil with vmrker equit: .d
ith Personal
Protective Equipment (PPE) as recommended by MOSH i.e. rubber boo: . hand glme>. full
body overalls, eye and hair protection and respirator- dust rask<
c smarm s backupsvsio ■ paul whincupbxj esa - summa= < repop r - 24-0'..<-
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History
SECT2ON 2
I
vi.
The glass waste and soil, excavated down to bedrock, will be placed in open-top 2OO.litre steel
drums and sealed with steel lids.
vii.
The sealed drums will be manually loaded onto truck using ramps.
viii.
The truck will be lined with HDPE sheeting to contain any potential spills during loading and
transport, and secured with tarpaulin cover.
ix.
The truck will be driven to the HLL factory site under police escort.
x.
On arrival at the factory the drums will be unloaded, weighed, labeled and transferred to a secure
storeroom.
xi.
The PPE and implements used during the operation will be decontaminated by washing in the
factory and the water discharged to the factory effluent treatment plant.
xii.
Any springs or seeps of water down slope of the scrapyard should be identified before start of
operations and samples collected for mercury analysis. If concentrations exceed 0.0003 mg/1 an
alternative water supply will be provided by HLL until such time as mercury levels decline to the
above criterion.
2.4
Medical Surveillance
The work place atmosphere in the mercury area is monitored using a gold film mercury vapour analyser
with a self-calibrating facility. The intention is for the mercury' in the atmosphere to be controlled to 0.05
mg/m3 of air by adopting the following measures:
•
Exhaust fans fitted along the length of the Mercury Area in the factory to turnover the air every 45
minutes;
•
1 .^vision of vacuum cleaners in the factory to collect broken thermometers when breakage occurs;
and
•
Scrubbing and washing of the factory floor once a day with water tb remove traces of mercury. This
water is treated in the effluent treatment plant (ETP) and reused for floor washing.
Operators in the Mercury area are provided with safety masks to filter out mercury vapours. This is
backed by an emergency procedure when the mercury vapour exceeds 0.05 mg/m3 which includes
opening all windows and cleaning the entire floor with water after which the water is brushed into the
ETP.
Records of mercury vapour levels have been maintained for the period 1983 to 2000. The records for
1994 to 1999 have not been sighted and are currently being traced. During this time there have been
instances of readings exceeding the maximum level mainly during the month of May 2000 in the mercury
distillation and crusher areas. The maximum spot reading of mercury in air, from the records available,
has been 0.480 mg/m3.
______
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History
1
The medical surveillance comprises an annual medical checkup of all employees and monthly monitoring
of mercury in urine. The annual medical check up consists of physical examinations with special attention
to mouth, gums, skin, teeth, hair and neurological symptoms such as tremors or unsteady gait. The
medical tests comprise blood tests (haemoglobin estimation, total white blood cell counts, differential
white blood cell counts) and routine urine examinations for albumen, red blood cells, casts, crystals and
sugar). Records of these examinations for 130 employees are available from 1988. The medical records
of 30 employees who left the company others, whose services of were terminated in the recent past are
available and are within normal limits.
The monthly urine examinations of all employees are done for mercury and compared to the maximum
regulated level of 100 micrograms of mercury per litre of urine. Employees whose mercury levels
exceeded this level were re-deployed from the mercury area. In all such cases mercury levels of the re
deployed staff reduced to acceptable limits in the subsequent readings. The monthly urine monitoring
was commenced in 1986 and the records since 1988 are available.
Results of the most recent urine examinations conducted io the year 2000 indicate that the mercury
concentrations in the urine of all employees, ex-employees and scrap dealers are well below the WHO
recommended acceptable upper limit of 100 micrograms per litre. Of the 255 included in the survey. 3%
of those surveyed had between 40 and 60 micrograms of mercury per litre of urine, another 3% between
30 and 40 micrograms per litre and the remaining 94% had mercury levels of less than 30 micrograms per
litre of urine.
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Mercury in the Environment
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3.1
SECTION 3
Description
The most significant anthropogenic activities giving rise to mercury (Hg) discharge to land, water and air
are:
Mining and smelting of copper and zinc ores;
. ?•
Burning of fossil fuels, mainly coal;
Industrial production processes, in particular the mercury cell chlor-alkali process for production of
chlorine and caustic soda;
Consumption related discharges, including waste incineration; and
•
Use of agricultural fertilisers, fungicides and seed disinfectants.
All chemical compounds of Hg are toxic to humans although Hg° may have to be oxidised to ionic forms
to show toxic effects. Organomercurials, in particular methyl mercury appears to show strong teratogenic
effects, and carcinogenic and mutagenic activity have also been implied.
Occupational Health and Safety Guidelines applicable to mercury in the workplace arc therefore very
strict. The most applicable guidelines arc those published by the US Department of Health and Human
Services, National Institute for Occupational Safety and Health (NIOSH). The Kodaikanal Thermometer
Factory closely follows the NIOSH guidelines for mercury vapour which include a maximum time
weighted average mercury concentration of 0.05 mg/n? in air and regular monitoring of mercury levels in
urine of all employees.
Handling, storage and transport of glass scrap with residual mercury is also planned to be undertaken
under NIOSH guidelines.
3.2
International Guidelines
There exist a number of international guidelines for total inorganic (metallic') mercury and methyl
mercury in soil that are relevant to the assessment of potential exposure via incidental contact with soil.
Examples are listed below:
CASHARM'S BACKUPS\510 - PAUL WHINCUPRC01 ESA - SUMMARY REPORT • 24-05-01.DOC'2*-JW’-AY-01
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SECTION 3
Mercury in the Environment
Mercury Concentration (nig/kg)
USEPA Region 9
Total Hg
Canadian
Australian
Dutch
Intervention
Methyl Hg
Value
Residential
23
6.1
Commercial
Industrial
15
6.6
10
24
610
88
75
50
The Dutch do not provide a value for industrial land use. the value provided is for both the protection of human
health and terrestrial ecosystems. A risk assessment study recommended when values are in excess of 10 mg/kg.
Note:
It should be noted that the above guidelines provide a basis for identifying conditions that may warrant
further assessment, they do not signify conditions that would represent an unacceptable risk. They have
been developed at a generic level to be over protective. SUe specific risk assessments normally result in
relaxation of these values.
Based on URS Dames & Moore’s current understanding of the site conditions, the above guidelines form
an appropriate basis for the assessment of risks to human health for both on site workers and the
surrounding population.
A
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SECTION 4
Regulatory Considerations
o
1
The following environmental legislation sets out policies and regulations to control environmental
pollution in India:
The Air (Prevention and Control of Pollution) Act, 1981 and subsidiary Rules;
The Water (Prevention and Control of Pollution) Act, 1974 and subsidiary' Rules;
The Water (Prevention and Control of Pollution) Cess Act, 1977 and subsidiary Rules; and
The Environment (Protection) Act, 1986 and subsidiary Rules.
Under the Environment (Protection) Act, all industries requiring a consent under Section 25 of the Water
(Prevention and Control of Pollution) Act or under Section 21 of the Air (Prevention and Control of
Pollution) Act or both, or requiring authorisation under the Hazardous Wastes (Management and
Handling) Rules, 1989, are required to submit an environmental statement for the financial year ending 31
March in Form V to the State Pollution Control Board on or before 30 September every year.
4.1
Air Pollution Control
Air emissions are controlled by The Air (Prevention and Control of Pollution) Act, 1981. The State
Pollution Control Boards (formed under Section 3 of The Water Act) are responsible for laying down, in
consultation with the Centra] Board, standards for emissions of air pollutants from industries and any
other source. The Environment (Protection) Rules 1986 provide the national standards for emissions and
discharges of environmental pollutants from various sources. Since the States have not laid down more
stringent standards, the national standards as prescribed in Schedule I of the Rules are applicable.
Prior to its amendment in 1987, The Air Act was enforced through mild court-administered penalties on
violators. The 1987 Amendment strengthened enforcement and introduced stiffer penalties. Now. Boards
maY d^e down a defaulting industrial plant or may stop its supply of electricity or water. The Boards
may al.-Jo apply in court to restrain emissions that exceed prescribed standards. The Act was extended to
include noise as an air pollutant.
The Environment (Protection) Rules of 1986. with amendments up to April 1999. specify the standards of
emission and or discharge of environmental pollutants from 80 industries, operations or processes. No
standard has been established for mercury.
4.2
Water Pollution Control
The Indian legal system provides four mjjor sources of law for addressing water pollution problems:
•
Administrative permit system under the Water (Prevention and Control of Pollution » Act. 1974 and
subsequent Rules of 1975 and amendments in 1978
•
Provisions under the Environment (Protection) Act and Rules of 1986 relating to water quality
standards------ .
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Regulatory CGnsicfferations
SECTION 4
Public nuisance actions
Common riparian law.
The Water Act empowers the State Pollution Control Boards to:
Establish and enforce effluent standards for factories discharging pollutants
?
"
Control sewage and industrial effluent by approving, rejecting or conditioning applications for
permission to discharge
Minimise water pollution by advising on appropriate sites for new industry
Prescribe standards for the discharge of effluent or quality of receiving waters
Monitor compliance with permitted effluent discharge standards.
Prior to its amendment in 1988, enforcement under the Water Act was achieved through criminal
prosecutions initiated by boards, and through applications to magistrates for injunctions to restrain
polluters. The 1988 Amendment strengthened the Act’s implementation provisions. Now, the Board may
close a defaulting industrial plant or withdraw its supply of power or water by administrative order,
penalties are more stringent, and a citizens’ suit provision bolsters enforcement machinery.
Effluent standards have been stipulated under the Water (Prevention and Control of Pollution) Act of
1974. The standards for discharge of mercury are as follows:
Inland surface water—O.Olppm
Public sewers—O.Olppm
•
Marine coastal areas--0.CJ ppm.
The Water Prevention and Control of Pollution Cess Act of 1977 was passed to help meet the expenses of
the Central and State Water Boards. The Act creates economic incentives for^pollution control and
requires local authorities and certain designated industries to pay cess (tax) for water consumption. These
revenues are used to implement the Water Act.
4.3
Hazardous Substances
The Manufacture, Storage & Import of Hazardous Chemical Rules, 1989, apply to industries that use or
store specified hazardous chemicals. These Rules pertain to directives and procedures for:
Storage of hazardous chemicals;
Inventory of hazardous chemicals;
•
Identification of major hazards posed;
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Regulatory Considerations
SECTION 4
1I
Preparation of on-site emergency plans;
Workers’ operational safety; and
Disclosure of product safety information in material data sheets.
Amendments passed in 1987 to the 1948 Factories Act introduced special provisions on hazardous
industrial activities. The 1987 Amendment, among other things, empowers states to appoint site appraisal
committees to advise on the initial location of factories using hazardous processes. The Act also requires
the occupier of a factory to maintain workers' medical records and employ operations and maintenance
personnel who are experienced in handling hazardous substances. A Schedule to the Act prescribes
permissible limits of exposure to toxic substances and requires the creation of safety committees to
consist of workers and managers who are required to review a factory’s safety measures periodically.
A review of the list of specified chemicals indicates that mercury, in the forms of alkyl mercury, mercury
fulminate, and methyl mercury, are listed under these Rules.
4.4
Hazardous Waste Management
The first comprehensive rules to deal with hazardous wastes were issued in 1989 under the framework of
The Environment (Protection) Act of 1986. These rules. The Hazardous Waste (Management and
Handling) Rules apply to designated categories of waste generated in quantities exceeding specified
limits, and provide for their proper handling, storage and disposal with the requirement for a permit.
Waste Category No. 4 under the rules is mercury bearing waste. Any operation that generates more than
a total of 5 kilograms per year (calculated as pure metal) must ensure proper collection, reception,
treatment, storage, and disposal of this waste. Rule 3i(b) refers Schedule 2 of the Hazardous Waste Rules
and was updated on 6 January 2000. Class A. and specifically Class A6. mercury and mercury
compounds, is nominated as Hazardous Waste if the con^ntration exceeds 50 mg/kg.
/
4.5
Air Quality .
The Indian Occupational Health and Safety Regulations for air quality in the Workplace specifies a
maximum time weighted average of 0.05 mg/m3 of Hg. There are no regulations or guidelines for
mercury in air emissions or ambient air.
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SECTION 5
Site Description
"7
The HLL factory site is located at an elevation of approximately 2.180 m. The site is irregular in shape
and occupies an area of approximately 87,250 square meters. The southern boundary of the site slopes
steeply into a protected nature sanctuary of the Tamil Nadu government, the Pambar Shola Forest.
Meteorological recrds are available for the six year period 1995 to 2000 and have been used to construct a
monthly average rainfall chart (Figure 2) and wind rose (Figure 3). The dominant wind directions are
northeast/northnortheast, northwest/northnorthwest and southeast, consistent with the monsoons.
Mercury vapour in air will therefore disperse predominantly to the northwest/northnorthwest, northeast/
northnortheast and to the southeast.
The access road to the site, St. Mary’s Road, forms the drainage divide between the factory site and the
Pambar River subcatchment to the south and Kodai Lake to the north. Drainage across the site is
primarily via a small stream which originates at the northeastern comer of the site and flows in a
southwest direction prior to discharging to the precipitous slopes which fall 1,300 m from the southern
boundary to the Pambar River. This river is for the most part inaccessible until the Kumbakarrai Falls
located about 7 km to the southeast. There is a second smaller drainage traversing the western part of the
site and other seepage areas. The topography of the site and its sunoundings are provided on Figure 4.
The general land use to the north and east is largely low density private residential properties along St
Mary’s Road. A few squatter cottages and St Mary’s Church are located to the west. A large television
broadcast antenna tower is located about 200 meters to the east of the site. The nearest surface water body
to the site is the Pambar River (approximately 0.5 km to the south), which flows in a southwest direction to
the Kumbakarrai Falls, thence draining eastward across the Tamil Nadu Plain.
The whole site is underlain by shallow Archaean bedrock, mainly granite gneiss and charnockite, which is
impermeable apart from limited fracture porosity related to vertical and subhorizontal joints and
exfoliation joints in the uppermost weathering profile down to 5 or 6 m depth. Two shallow wells on site
are blasted into the rock, but have limited supplies which decline markedly, in the summer season. There
is also a spring in the central/Iower part of the site adjacent to the stream, fmd this again becomes dry
during summer. The soil profile is very thin, and comprise a few centimetres of predominantly sandy
material in the upper part of the site grading down into densely vegetated peaty soils in the south.
Maximum thickness of soil intersected across the site is 1.5 m. A narrow access path, the Levange Path,
is in the Forest Reserve immediately to the south of the site boundary and can be traversed on foot with
the approval and presence of the Forestry Department in Kodaikanal. This path lies immediately above
the precipitous slopes and is primarily on bedrock with only a thin veneer of soil. There is no easy access
to the slopes below the Levange Path. The stream discharging from the site forms a waterfall which has.
over time eroded a small shallow basin in the rock along the Levange Path. This shallow pool contains at
most approximately 25 to 50 kg of sediment washed down from the factory site. This is termed location
DFE and both sediment and water samples have been collected for analysis. There is also some offsite
seepage of water and sediment from the soil/rock contact and possibly exfoliation joints which has been
sampled at location DFNE.
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SECTION 6
work
As part of the environmental investigations and the risk assessment for mercury, URS Dames cE Moore
has cairied out a review oi meteorology, topography, drainage, soils, geology and hydrogeology to assess
sources and pathways for release of mercury onsite and offsite. The main sources arc the Mercury area
departments 3 and 4, the distillation plant, the crushing plant, the industrial ETP and the onsite storage
areas for glass scrap. These have been examined to evaluate potential sources of mercury release.
This has been followed by a comprehensive sampling programme whereby in excess of 150 samples have
been collected for total mercury analysis. This sampling programme is dynamic in that additional
samples arc collected for analysis as results progressively come to hand. Selected samples have also been
tested (or are currently being tested) for methyl mercury. The sampling locations are shown on Figures 5
and 6. Particular emphasis has been placed on following internationally accepted QA/QC protocols for
collection and analysis of samples; eg., chain of custody and preservation procedures, duplicate samples
and blanks, and storage times. The break down of the samples for which results have been received is as
follows; with additional samples of soil, sediment, water and lichen also submitted for analysis but not yet
available for review.
Table 1
Summary: Samples Tested for Mercury
Total Onsite
Total Offsite
Soil
66
13
Sediment
8
7
Water
5
6
Lichen
0
2
Analytical testing of the soil/sedimcnt/lichen samples for total mercury has been primarily conducted at
the MGT Environmental Laboratories in Melbourne, Australia.
Testing for methyl mercury is highly specialised and for this study has been conducted at the
Commonw'ealth Scientific and Industrial Research Organisation (CSIRO) laboratory in Sydney, Australia
with additional lichen samples submitted to the TNO Laboratory in Holland for total mercury and methyl
mercury analysis.
Air quality monitoring data plus medical records (mercury levels in urine and blood) for on site workers
have also been examined by HRS Dames & Moore.
The Hindustan Lever Research Centre (HLRC) Laboratory in Mun.bai has a quick turnaround which is
important in a study of this nature and at total mercury concentrations of 10 mg/kg and above has been
found to show' good correlation with the MGT results. The HLRC total mercury analyses have therefore
been very useful in delineating “hotspots” with higher mercury concentrations.
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SECTION
Assessment of Analytical Results
i
7.1
General
i
Results of (he analytical testing for total mercury arc provided in Table 2. Results of the water samples
arc presented in Table 3 and methyl mercury results arc presented in Table 4.
i
7.2
i
Mercury Distribution Offsite
The distribution of mercury analyses received to date follows a pattern which is in accordance with the
identified sources and pathways. There arc slightly elevatcdsconcentrations of mercury, up to 2.5 mg/kg,
over the whole site and offsite to the immediate north and south. Offsite concentrations in lichen arc
higher, up to 4.8 mg/kg immediately north of the site. These arc attributable to dispersion of metallic
mercury vapour by air from the mercury production, distillation and crushing areas. Conservative
calculation of air discharges indicate a maximum total discharge to atmosphere over the 18 years of plant
operation of approximately 70 kg of mercury.1 Based on contouring of low level mercury concentrations
some 10 kg of this mercury has transferred offsite in air and deposited in the uppermost soil profile to 0.1
m depth, and on lichen and other organic matter, to the north (6 kg) and south (4 kg) of the site. All on
site sample locations, those on the private properties located on St. Marys Road to the immediate north of
the site and the sample locations along the Levangc Path arc shown on Figure 5. All the offsite sampling
locations on Upper and Lower Shola Roads and Lake Road (to the immediate south of the Kodai Lake)
arc shown on Figure 6. The sediment sample and the water sample from the Kumbakarrai Falls were
collected from the access point marked on Figure 4.
Mercury levels ol the surface soils along the Levangc Path immediately south of the boundary fence were
measured to be between 0.7 and 6 mg/kg. The slightly elevated readings (6 mg/kg) at KP2 and DFNE arc
related to sediment discharge from the west stream and groundwater seepage. The sediments in the small
depression on Levangc Path receiving waler from the main stream from the site had total mercury
concentrations ranging between 26 and 110 mg/kg (at locations LP5 and DFE). These elevated values arc
within the top 10 to 20 cm ol the profile. Mercury levels in the soils/sediments along Upper Shoala and
Lower Shoala Roads located about 400m to 500 m north of the site were found to be less than 0.1 mg/kg.
Soil samples collected from the southern periphery of the Kodai Lake, 800 m to the northeast also
contained mercury levels of less than 0.1 mg/kg. The water sample from the lake contained less thair*$
0.0003 mg/L mercury. Water and sediment samples were also collected and tested from the Kumbakarai
Falls understood to be the closest location to the site accessible to humans. /This water sample contained
less than 0.0003 mg/L of mercury and the sediment sample contained less than 0.1 mg/kg of total
mercury.
J
(
C
Maximum Hg concentration in air 0.05 mg/nr. Air space of mercury area 15,145 m3. ban operation 16 hours per
day, 310 days per year for 18 years. Air turnover every 45 minutes. Total discharge 70 kg.
C.ASHARM’S BACKUPS510 ■ PAUL WHINCUPWOOI ESA - SUMMARY REPORT - 24-05-01 CXXA24-MAY-01
7-1
J
t i?
/ Assessment of Ar=a»y
7.3
E'CGSOncS
SECTION 7
Mercurv Distribution On Site
Four ‘hotspots’ with metallic mercury concentrations in soil in excess of 50 mg/kg have been located
within the site. These arc illustrated on Figure 5.
/
I
Hotspot A (Area A) is adjacent to the mercury distillation unit and industrial ETP immediately south of
the Mercury area in the factory’. The maximum mercury' concentration recorded in this hotspot is 3
mg/kg (location CT 1) at a depth of 10 cm, reducing to 47 mg/kg at a depth of 80 cm and 14 mg/kg on
bedrock at 1.30 m.
Hotspot B (Area B) is at the old bakery where 3 and 4 glass scrap was stored and also where some
glass/stccl mercury containers were discarded. Maximum mercury' concentration recorded here is 62
mg/kg (location P2) to a depth estimated to be about 40 cm.
Hotspot C (Area C) is located southeast of Area B. Subsequent to the initial sampling at locations FiN4
and FN5, 48 additional locations have been sampled and tested. 'Hie average concentration oi lota!
mercury of these 51 samples is zS.O mg’kg. Additional sampling is m progress.
•lotspot D (Area D) relates to elevated mercury in sediment along the stream below the diSiuiation room
and as far as tlic Levange Path.. The maximum concentration of mercury’ in the sediment on site is 270
/
mg/kg (at location DD).
Details of these impacted areas arc provided in Table 5.
Additionally an estimated SOJcg of mercury at low levels of concentration is distributed across the She
with the primary source considered to be from air discharged from the mercury working areas.
7.4
Methyl Mercury Resuits
The available methyl mercury results are provided in Tabic
The samples being tested lor mctly I
mercury include those with higher than axerage total mercury concentrations for on site samples ns well
as on site locations such as those from the banks of Kodai Lake, the sediments at tlic main stream
discharge on to the Lcvangc Path, the sediments of Kumbakarrai Falls and lichen samples from the
Charlcmont Property. Additional on-sitb lichen samples and soil, sediment, water and lichen from the
area between the Levange Path and the Kumbakarai Falls have recently been collected.
All methyl mercury analyses indicate concentrations so low that they do not constitute cither a health or
ecological risk.
-:1 US' t
■-'V,?
SECTION 7
c Assessment of Analytical Results
Table 2
Total Mercury Lewis in SoibScdiment/Lichen - March/April 2001
Sample Location
Type of
Sample Depth
Hg in mg/kg,
Hg in mg/kg,
Sample
(cm)
(HLRC)
(MGT)
BE-05_____________________
Soil
BE-1______________________
Soil
5
10
59
0.51
BE-2______________________
Soil
BE-3______________________
Soil
BGE-05___________________
Soil
5
22
BGW-05___________________
Soil
5
2.5
BN-1______________________
Soil
10
33.3
35
BN-1-40___________________
Soil
40
8.4
6.7
BS-1______________________
Soil
10
BS-2______________________
Soil
10
BS-3___________________ .
Soil
10
BS-4______________________
Soil
10
2.7
BS-5______________________
Soil
10
0.99
10
X
10
0.13
2.0
0.26
0.14
0.1
9.9
6.2
BW-05____________________
Soil
5
9.4
CC-1 (Carlton Compound)
Soil
10
1.1
CD-05_____________________
Soil
5
14
CD-50_____________________
Soil
50
71
CM-05 (Charlemont Property)
Soil
10
2.2
CM-1 (Charlemont Property)
Soil
10
1.3
CM-2 (Charlemont Property)
Soil
10
0.70
CML (Charlemont Property)
Lichen
From tree trunk
4.5
CML-2 (Charlemont Property)
Lichen
From tree trunk
CTJ___________________ _
Soil
10
CJ-MJ0
Soil
130
_____
CT-1-80___________________
DD
DD-40____________________
4.8
108.0
330
14
Soil
80
5,9
47
Sediment
Surface
73.0
270
4^_
9.1
25
Soil
DFE-05 (Levange Path)
Sediment
Surface
DFE-1 (Main Stream Outfall)
Sediment
Surface
DFNE-05 (Levange Path)
Sediment
Surface
DP-05____________________
__Soil__
p
DP-1-10___________________
Soil
10
18.8
36
DP-1-40___________________
Soil___
40
31.0
155
DP-2___ _________________
Soil
10
5.3
DP-3 __________
__Soil__
JO
DP-4______________
Soil___
JO
DP-4-50
Soil
50_
DPS______________________
Soil
10
DP-50_____________________
Soil
50
DP6
Soil
10
85
26.0
110
6
40
5.9
—
3.2
5J?
40
20
20
CASHARifS BACKUPS\510 - PAUL WHWCUPVUWI ESA - SUMMARY REPORT - 24-05-01.00CV4-MAY-01
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__ _ ___ J.
______ __ • ■
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? 'L
SECTION 7
Assessment of Analytical Results
-o
Table 2 (cont’d)
Total Mercury Levels in Soil/Sediment/Lichcn - March/Apri! 2001
Sample Location
FC-1____________
FC-2____________
FC-3___________
FC-4_______ ___ _
FC-5____________
FN-1____________
FN-2____________
FN-3____________
_FN-4____________
FN-4-80__________
FN-5____________
HL-1____________
HL-1-80__________
LK1 (Kodai Lake Bank)
LK2 (Kodai Lake Bank)
LK3 (Kodai Lake Bank)
LP-2 (Levange Path)
LP-3 (Levange Path)
LP-4 (Levange Path)
LP-5 (Levange Path)
LP-6 (Levange Path)
LP-7 (Levange Path)
Type of
Sample Depth
Hg in mg/kg,
Hg in mg/kg,
Sample
(cm)
(HLRC)
(MGT)
Soil
10
1.7
Soil
10
1.3
Soil
10
Soil
10
8.9
16
Soil
10
3.2
Soil
' 10
2.5
Soil
10
JL9_
Soil
10
Soil
10
Soil
80
Soil
10
0.75
62.8
60
171.6
8.3
240
W_
Soil
10
Soil
80
2.9
Soil
10
<0.1
Soil
10
<0.1
Soil
10
<0.1
Soil
10
6.0
Soil
10
2.4
7.3
Soil
10
Sediment
Surface
Soil
10
1.1
Soil
10
0.63
20
1.4
12.6
55
MD-05_______________
Soil
5
MD-50_______________
Soil
10
11
NS-05__________ __
Soil
5
4.5
PI-05________
Soil
P1S-10___________
P1S-40___________
P2-05______ .
_
P2S-10___________
P2S-40___________
P3-05
________
P3S-10___________
P3S-30__________
P4-05
Soil
Soil
5
10
40
5
10
40
10
10
30
5
10
Soil
80
P4S
Soil
10
20
1.9
0.59
62
4.1
5.3
25
4.7
5.7
9.4
20
5.0
31
P4SE_________________
Soil_____ j
10
PPE-05
Soil
5
P4E-10_______
P4E-80
___
T
Soil
Soil
Soil
Soil
Soil
Soil
Soil
Soil
17.1
11.9
22.9
d
6.2
—r
10
4.6
C:\SHARM S BACKUPS^ 10 - PAUL WHINCUP^OOI ESA - SUMMARY REPORT - 24-05-01.DOC\24-MAY-01
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7-4
URS
SECTION 7
Assessment of Analytical Results
Table 2 (cont’d)
Total Mercury LevtSs in ^>OH/Sediment/Lichen — March/Apri! 2091
r
Sample Location
PPS___________________
PPS-1_________________ _
■
Type of
Sample
Sample Depth
(cm)
Soil
10
32
Soil
10
6.7
Hg in mg/kg,
(HLRC)
Hg in mg/kg,
(MGT)
PPS-2__________________
Soil
10
PPS-3
Soil
PPW-05________________
Soil
10
5
SR (Kumbakarai Falls)
Sediment
Surface
<0.1
SS-05__________________
_ Soil
\ 10
6.6
SS-1____________________
Soil
10
3.5
SS-2____________________
Soil
10
2.6
5
31
0.35
t
I
3.0
13
TB-05___________________
Soil
TBD____________________
Sediment
Surface
US-1 (Upper Shola Road)
Sediment
Surface
US-2 (Upper Shola Road)
Sediment
Surface
<0.1
US-3 (Upper Shola Road)
Sediment
Surface
<0.1
US4 (Upper Shola Road)
Soil
10
<0.1
USS (Upper Shola Road)
Soil
10
<0.1
USS (Upper Shola Road)
Soil
10
VE-1
Soil
10
41.9
110
<0.1
1
<0.1
1.1
Note: All sample locations are from within the HLL site unless otherwise noted in parenthesis.
Table 3
Total Mercury Levels in Water - March/ApriI 2001
Sample Location
Hg (mg/L)
BRW
0.085
DFE (Main Stream Outfall)
<0.0003
<0.0003
<0.0003
<00003
_
_
___
ES
<0.0003
LKW (Kodai Lake)
^2
<0.0003 __
0.31
<0.0003
<0.0003
<0.0003
~
<0.0003
<0.0003
.
<0.0003
DFE-W1 (Main Stream Outfall)
DFNE (Levange Path)
______
DW-1 (Main Stream Outfall)
MDRW_____
MSYW (Scrap Yard)
PM (Pambar River)
SRW (Kumbakarrai Falls)
SW__
SY (Kodaikanal Scrap Yard)
USW (Upper Shola Road)
WS
j________
~
<0.0003
NQtg?: All sample locations are from within the HLL site unless otherwise noted in parenthesis.
Samples BRW and MDRW were slightly silty.
CASHARM’S BACKUPS510 - PAUL WHINCUFAR001 ESA - SUMMARY REPORT • 24-05-01 00024-MAY^J
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a
, Assessment of Analytical Results
Tabic 4
Methyl Mercury Levels in Soil/Scdinicnt/Lichen Samples
I
: Sample Location
Sample Depth (cm)
CM-05 (Chariemont Property)
5
0 0011
!
Lichen from tree trunk
0.0019
4.5
CML-2 (Chariemont Property)
Lichen from tree trunk
CT1_______________________
10
130
80
0.0019
0.0029
0.0001
<0.0001
0.0026
0.126
4.8
330
14
47
240
85
CT1-80
DFE-05 (Levange Path)
Surface Sediments
5~
DFE1(Levange path)
Surface Sediments
0.060
110
5
0.0008
6
DP____________________
DFNE-05 (Levange Path)
DP1-10
10
0.0002
36
DP1-40
40
<0.00005
155
0.0094
40
DPS
T
I
10
FN4
T
10
!
FN5
10
I
LK1 (Kodai Lake)
LK3 (Kodai LakeJ
10
_______ 10________
LP5
Surface Sediments
--7
0.0026
240
0.0008
<0J
<0.1
55
0.0014
20
50
0.0005
11
SRA (Kumbakarrai falls)
Surface Sediments
0.0001
<0.1
TBD
Surface Sediments
0.003
110
i
Tabic 5
Details of Areas Requiring Remediation
Location
Approx.
Average
Volume
Approx.
Average
Approx.
Area
Depth
(m'J)
Weight
Concen
Weight of
(-2)
(cm)
tration
mercury
(mg/kg)
(hg)
1200
500
600
1200
45
55
Area B
2400
400
950
1900
27
50
Area C
1600
400
640
1280
28
Area D
160
300
rn
100
45
2240
4480
TOTALS
I
(tonnes)
Area A
I
I
60
0.0002
MD-50
-
r\r\ a r\
0.0062
MD-05
■ iiii
2.2
CML (Charlemont Property)
CT1-130
: >\
Total Hg
Methyl Mercury
(mg/kg)
____ ;
5
146
SECTJON 8
A mercury balance has been prepared in order to estimate tlic total unacountcd losses of mercury' over the
18 years life of the operation. These unaccounted losses comprise dispersion of airborne mercury' to soil
and lichen, both onsite and offsite, mercury' retained in sludge from the industrial effluent treatment plant,
mercury- in soil and sediment hotspots derived from accidental spillages, and mercury in suspended
sediment discharging offsite southwards to Pambar Shola.
Tlic elements of tlic mcrcuiy' balance arc:
MI:
Mercury imported to site in containers from the USA and Spain, d'lie customs
bond register records a total of 125,676 kg and the supplier has a tolerance of
+/- 0.0625%.
TE:
Mercury exported from site in thermometers. Tlic weight of mcrcuiy in each
thermometer is dependent on type of thermometer and grading. I ILL has made
an exhaustive review and collation of the recorded numbers and types of
thermometers dispatched from site. The total number of thermometers is
165,078,561 and average mercury content ranges between 0.66819 gm and
0.66666 gm per thermometer, a range of +/- 0.0012%.
GSS and GSO:
Tills represents glass scrap stored onsite (GSS) and glass scrap disposed olisite
(GSO). Tills has been calculated from tabulated records of unrccovcred 3 and 4 I
glass (6% residual mercury), 3 and 4 partially recovered (1% mercury), and 3 and'
4 enhanced recovery' (0.15% mcrcuiy). Tlic figures have been further supported"
by sampling each batch of unrccovercd glass scrap in GSS and measuring
mercury- recovery'. The accuracy of tlic GSS figure is assumed to be T/- 3% (any
larger percentage could result in a potential net gain in the mercurv balance.
which is clearly not die ease). GSO is assumed accurate to +/- 5%.
ST and WIP:
Mercury' in stock (S f) correct to +/- 0.0625% and work in progress (WIP) correct
to 0.0012%.
1
Ihcrefor? the mean figures, in kg of mercury, arc as follows:
MI
TE
125,676
110,178
GSS
+
9,741
GSO
+
284
ST
4-
2,983
WIP
+
1,931
AU
Unaccounted losses, AU, therefore total 559 kg.
Statistical analysis using two standard deviations gives a range of probability for AU of between 43 kg(
minimum and 1,075 kg maximum.
• L
0
Mercury Balance
SECTION 8
I he unaccounted losses can also be c,xprcsscd as the following equation;
AU
I1
J
1
A + SS + ETP + PS
where;
A
airborne emission of mercury vapour, estimated to be 70 kg.
SS
mercury contained in soil and sediment, namely hotspots A, B, C, and D (150 kg)
plus widespread low level dispersion (90 kg, of which 70 kg is derived from A).
Total SS unrelated to air dispersion is therefore 170 kg.
ETP
mercury in stored sludge from the industrial ETP, estimated to be 20 kg.
PS
discharge offsite to the south to the Pamber Shola.
PS
AU
A
SS
ETP
559
70
170
20
and
j
1
4
1'
i
Therefore estimated offsite discharge to the Pambar Shola is approximately 300 kg.^I
This figure is considered to be of the correct order of magnitude based on the grassed nature of the site,
limited evidence of soil erosion and comparison to the current level of mercury recognised onsite
(i.e. 260 kg).
C:\SHARM S BACKUPS'510 - PAUL WHINCUP\RW1 ESA - SUMMARY REPORT - 24-05-01 DOC^-MAY-01
8-2
SECTION 9
Health issues
9.1
Potential Exposure Pathways - Human Health
Human exposure to mercury in the environment external to the mercury working areas in the factory may
occur via the following mechanisms or pathways:
Incidental ingestion of soil through hand to mouth contact;
o
Inhalation of dusts;
Inhalation of vapours;
Ingestion of water; and
Consumption of food grown in contaminated soil, or exposed to mercury vapours, or fish from
methyl mercury contaminated waterbodies.
In relation to the site, the following issues arc relevant to the assessment of exposure pathways.
1 he area, including the site, is heavily vegetated and therefore there exists limited opportunity for the
generation of dust through wind erosion.
e
The prime source of mercury vapours is via emissions from the factory extractor fans. When in
operation, the site workers would represent the population most at risk from inhalation of vapours
due to their proximity to the source. 1 he mercury intake of workers has been assessed through a
medical monitoring program.
o
The potential for exposure to mercury via food consumption is likely to be low for the following
reasons:
air dispersion from the site is limited due to the location of the extractor fan outlets (ground
level) and the occurrence ol dense vegetation including moderately sized trees;
the surrounding area is not used extensively for food production or fisheries; and
metallic mercury, as opposed to methyl mercury, does not bioaccumulate.
•
As surface water run off occurs predominantly to the south of the site into the forest, there is limited
potential for ingestion of surface water that may be affected by mercury attached to suspended
sediment.
On the basis of the above, there arc no pathways for human exposure to mercury which are of concern
and this is applicable to both on site workers and the off site population.
Consideration of potential exposure to mercury vapours for site workers remains an occupational health
safety issue relevant to the management of the site.
'J.\SHARM S BACKUPS\510 - PAUL WHINCURR001 ESA - SUMMARY REPORT - 24-V5-01 OOC\2A-MAY-O1
9-1
URS
SECTION 9
Health Issues
9.2
Potential Exposure Pathways - Environment
The available data confirm that elevated concentrations of total mercury relative to expected background
concentrations in soil arc present within the site boundaries. Slightly elevated mercury concentrations
also extend a short distance to the north and south of the site. The available data suggest a background
concentration of less than 0.1 mg/kg of total mercury. Whilst there are offsite concentrations greater than
the background, the values are generally low and only marginally above apparent background. I he
mechanisms by which mercury may have migrated beyond the site boundaries are:
Via sediment in surface water run off principally to the South of the site; and
Via dispersion in air from (he factory extractor fans.
The prime form of mercury released to air from the factory extractor fans was elemental mercury vapour.
Mercury vapour may be absorbed by vegetation or disperse into the atmosphere. Given the low water
solubility of elemental mercury, there exists limited potential for deposition in rainfall. The apparently
elevated concentrations of mercury in the lichen samples near to the site reflect absorption of mercury
vapour from the air.
The prime direction for surface water run off is to the south into the Painbar Shola. This area is
precipitous and heavily forested and not frequented by humans until a substantial distance downstream.
The mercury balance which has been derived in order to assess the amount of mercury discharged to (he
Pambar Shola indicates a total of 300 kg, equivalent to about 17 kg/year over the IS years of factory
operation.
Additional soil, sediment, water and lichen samples have been collected below the Levange Path and
from the Pambar River upstream of Kumbakarrai Falls. It is considered extremely unlikely, pending
receipt of these analyses that the flora and fauna of the Pambar Shola and Pambar River arc at risk from
the calculated mercury discharges.
Kodai Lake is on a separate drainage catchment to the Factory and receives only infinitesimal mercury
input from sediment on the northern margin of St Mary's Road. AU soil, sediment and water samples al
the Lake return total mercury concentrations below detection level.
C VSHARM'S BACKUPS\510 - PAUL WHINCUPWOO! ESA - SUMMARY REPORT - 24-05-01.DOC2«-MAY-G1
9-2
Conclusions and Recommendations
10.1
SECTION 1O
Conclusions
Mercury impacted soil has been identified on the Kodaikanal site. The total estimated volume of
impacted soil requiring remediation is 2,240 m3 equivalent to 4,480 tonnes of soil containing
approximately 150 kg of mercury. An estimated 80 kg of mercury has also been deposited across the site
to shallow depth, primarily from airborne mercury. There has also been offsite transfer of mercury in air
to the north and south, totalling approximately 10 kg and by runoff to the south via the stream which
traverses the site, crosses the Levange Path and falls 1,300 m down to the Pambar River. Based on
mercury balance calculations and site disposition ic limited evidence of soil erosion on site, the maximum
discharge to the Pambar River catchment may be of the order of 300 kg of mercury over a period of
18 years.
The available soil and water data suggests that risk to human health is negligible. The available data and
the mechanisms by which mercury is believed to have migrated beyond (he site, also suggest a low
potential for adverse effects on the environment.
10.2
Recommendations
10.2.1 Priority Actions
The highest priority is to recover the 3 and 4 glass scrap from the dealer’s scrapyard in Kodaikanal. This
is an cxcicisc that will only occupy two days or so, and should be undertaken as soon as approval is uiven
by the FNPCB. Any delays could result in offsite discharge of mercury to adjacent residential areas
during periods of high rainfall. Appropriate occupational health and safety protocols have been detailed.
The second priority action is to prevent discharge of sediment south from the site before the advent of the
southwest monsoon. I his can be accomplished by installing silt traps and sediment settling ponds along
the stream (Area D) which receives stormwater runoff from the three hotspots (Areas A to C) identified
on site. A preliminary engineering design has been prepared maximising the use of existing facilities, and
also requires the approval of the TNPCB.
Following the installation of silt traps, soil should be excavated from the hotspots (Areas A, B, C and D in
Figure 3) and temporarily stored on site in steel drums. Manual excavation is recommended in order to
minimise the volume of soil to be excavated and suitable protocols will be developed to ensure full
protection of workers. Mercury levels in urine and blood will be tested before and after excavation is
completed, PRE will be nominated and monitoring of mercury vapour levels will be undertaken
throughout the duration of the works.
In the longer term the soil, together with stored ETP sludge and treated 3 and 4 glass scrap should be
liansfcncd to an approved landfill site. Although an approved landfill site docs apparently exist in Tamil
Nadu it is recommended that 11LL either purchase or use an existing FILL industrial site in the lowlands
and obtain approval from the TNPCB v ia the environmental impact process for construction of such a
C:\SHARM S BACKUPS\510 - PAUL WHINCUPVIOOI ESA - SUMMARY REPORT - 24-05 01.DOC\24-MAY 01
10-1
11
Conclusions and Recommendations
SECTION 1O
landlill. Allowing lor over excavation and some bulking, the area required for landfill is provisionally
estimated to be 40 m by 40 m by 3 m deep allowing for 1.5m of clean soil cover.
[
10.2.2 Clean Up Criteria
Risk Based Corrective Action (RBCA) is a USEPA accepted system lor determining appropriate clean
up levels in soil based on assessment ol sources, pathways, receptors and evaluation of health and
ecological risk. 1 he I icr 1 RBCA uses Risk Based Screening Levels (RBSLs) derived from published
F
data. Should observed values be elevated above Tier 1, then further analysis can be undertaken using
exposure data, human body weight, published loxicologicabdata etc to derive site specific Tier 2 and Tier
3 clean-up criteria. Clean-up criteria are progressively relaxed from Tier 1 through to Tier 3.
I he Dutch Intervention value ol 10 mg/kg is based on multi-functional use of land over a shallow
F
diinking waler aquifer and is therefore very conservative for most sites. It is accepted that if the
Intervention Value is exceeded a risk assessment should be undertaken to calculate a site specific value,
and at (he Kodaikanal Site this would be signiIicanlly higher than 10 nm/kc.
r
i
I lowever. because of the publicity surrounding (his site it is highlx recommended by I RS Dames .V
Mooie that risk assessment should not be undertaken on this occasion. Rather it is proposed that the
consei vative Dutch Intervention Value ol 10 mg/kg total mercury should be used
criteria tor the Kodaikanal site, on (he basis of future residential use.
PAUL WHINCUP
Senior Vice President, Asia
UPS Dames & Moore
25 May 2001
C:\SHAnwS DACKUPS\510 • PAUL kVHINCUPVIO01 I SA • SUMMAHY nCPCR T - 24.0',-Gl DOCK'S MAY-f.-
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KODAIKANAL town
x *■
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Health Efferfs
All forms of mercury are poisonous. However, organic mercury, such as methylmercury, is a
particular concern because organic mercury accumulates in the tissues of living creatures
including people. Any form of mercury can be converted to methylmercury by microbes in water
ano soil.
PM
nave been mistakenly diagnosed as having symptoms of alcohol intoxication or diabetes.
Exposure
Major pathways of mercury exposure are as follows:
Ingestion: eating foods that are contaminated with mercury. Fish are a great concern
because mercury bioaccumulates: airborne mercury that falls on the surface of lakes and
rivers and settles in sediments is accumulated by the tiny organisms in the water and
sediments. Fish eat these organisms, accumulating higher concentration in the flesh. In this
way, the mercury concentration in the flesh of predatory fish reaches levels 10,000 to
100,000 times that in the water. The wildlife—bears, eagles, panthers, etc.-and people who
eat the fish accumulate even higher levels of mercury in their flesh. Native peoples who
hunt wildlife and eat fish accumulate mercury levels that are higher yet.
Inhalation: through the respiratory system, breathing latex paint and airborne emissions.
Absorption: through the skin, coming in direct contact through air pollutants and
precipitation containing mercury.
Prenatal and postnatal exposure: before birth, mercury passes from the mother to the
developing fetus; after birth, mercury passes from the mother to the nursing infant in the
breast milk.
«
In exposed populations, such as Native peoples and others living subsistence lifestyles, developing
f“tuses and nursing infants are potentially most exposed to mercury.
Mercury in deep sediments in rivers and lakes remains relatively isolated until disturbed by
removal of vegetation or by the development of reservoirs or dredging of river bottoms. With
these activities, large amounts of methylmercury can be dispersed into the surrounding water to
be ingested by microbes and fish and, ultimately, people.
When anv form of mercnrv is burned, the metal vanorizes and is released as a <>as. Gaseous
7/06/01 6:13 PM
6“
4 - Mercury Poisoning of Native Pcoplcs</1icad>
. 5-0
file.///C|/Leverdocs/Hgdocs/mercindians.htm
MERCURY POISONING OF NATIVE AMERICANS
Environmental Network have
healthy environment.
Native Environmental Justice
T reCeived
less ^•ronn.en.al
‘
and parishes have. It wasn't untildecent years thaat NSSf,StanACe"than StatCS’CitieS’t0Wns’counties’
Mercury
Mercury is a neural element that doesn't break down in the environment Pur,, mon
mercury can
found in small quantities in some ore deposits. Mercury most commnnlvnrr
combination with other elements, such as oxygen, sulfer, and chlorine, as so-called inorganic*1^ 'H
mercury. However, mercury also occurs in combination with carbon-based substances for
cxumple, as methylmercury, an "organic" form of mercury.
’
The amount of mercury that occurs naturally in any one place is usually very small. However,
increased. More than half pf pH airborne mercury now comes from human activities.
I
Some common consumer products in which mercury can be found are thermostats, heater
laW teSs’ourcerefCent
f!3™’
and fun8icides-In household wastes, the single
la
4 source of mercury is battenes-rechargeables, lead-acid, alkaline, mercuric-oxide button
cellar com shaped, and nickel cadmium rechargeable batteries and battery packs such as NiCd
Of the 341 tons of mercury emitted annually into the air in the U.S. because of human activities
most common from four sources:
activities,
• Coal-fired power plants, 117 tons
Medical waste incinerators, 64.7 tons
• Municipal waste incinerators, 63.5 tons
• Oil-fired industrial boilers, 22.5 tons
7/06/01 6:08 PM
- Mercury Poisoning of Native Peoples</head>
file :///C (/Lever docs/H gdocs/mcrcindians htm
mercury and mercury bound to airborne particles are transported by air currents until they are
removed by rain, snow, or fog or absorbed by vegetation. Weather conditions, including
prevailing winds, are a major factor in determining where airborne mercury is eventually
deposited. Although local sources-such as power plants and incinerators-are important, sources
up to 1,560 miles away or farther can account for mercury deposition from rain and snow.
Many Native communities are being affected, especially communities relying on fishing and
hunting as a large portion of their lifestyle. A pregnant woman with mercury in her system can
pass it through the placenta to accumulate in the brain of the fetus, as well as through breast
feeding. Infants and children are also at a great risk.
In Northern Quebec two-thirds of the Cree Indian community of Chisasibi learned that they have
been poisoned by mercury contamination of the fish that are a mainstay of their diet. Some of the
elders developed numbness of limbs, loss of peripheral vision, shaking, and neurological damage.
They were downstream of the first phase of the La Grande hydroelectric complex. Hydro-Quebec
diverter three rivers into the La Grande River in the largest water diversion of volume on Earth.
Incineration facilities that burn hazardous waste, municipal waste, and medical waste in
communities where people of color, including Native Americans, live pose a serious threat to the
development of future generations. Incinerators are the largest source of mercury in Florida.
Studies show a dramatic rise in mercury found in water, alligators, fish, and panthers, thus
affecting the traditional Seminole communities.
Burning is not the answer: When an incinerator burns tons of wastes per year, an undetermined
ount of some of the most toxic chemicals known to science is released into our environement.
Incinerator regulations are based on ’’acceptable” rates of death and disease, allowing a
predetermined number of people to be harmed. According to regulations, which are based on the
approach of risk assessment, it is acceptable to kill as many as one in 1,000,000, one in
100,000—even one in 10,000—of the people exposed. In other words, a certain number of people
are expendable.
Groups most likely to be exposed to high levels of mercury are Native Americans who have
land-based cultures that subsist on fish and foods from the natural food chain. A 1990 Wisconsin
study of mercury concentration in blood taken from Anishinabe Ojibwa shows a direct
relationship between blood levels of mercury and the number of walleye eaten. Mercury
contamination is affecting many Native American populations. In most cases, Native American
communities do not know whether these mercury issues are affecting their communities or what
their options are.
All life is sacred. Much of the Native American lifestyle is connected to hunting, fishing, and
westing and is part of the continuing Circle of Life.
The Indigenous Environmental Newtwork is an alliance of grassroots Indigenous Peoples whose mission is to protect the
sacredness of Mother Earth from contamination and exploitation by strenghtening, maintaining and respecting the traditional
teachings and the natural laws.
GreenpeaceThere are a few simple truths that we still believe in:
Every species has the right to clean air, clean water, clean soil, and an unthreatened existence.
For over twenty years, whenever any of these environmental rights has been violated, we have called attention to this
injustice by speaking out and, when necessary, by using nonviolent direct action and dramatic images bearing witness for the
Earth.
4
7/06/01 6:13 PM
Beefing
MERCURY (Hg) - a profile
Mercury is probably best known as the silver liquid in thermometers. However, it has
over 3000 industrial uses. Mercury and its compounds are widely distributed in the
environment as a result of both natural and man-made activities. The utility, and the
toxicity, of mercury have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous.
HISTORY & OCCURRENCE
Mercury occurs naturally in the environment as mercuric sulfide, also known as
cinnabar. It is also present in some fossil fuels. Cinnabar has been refined for its
mercury content since the 15th or 16th century B.C.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and
cannot be broken down into less hazardous compounds.
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room
temperature, ease of vaporizing and freezing, and electrical conductivity make mercury
an important industrial metal. In 1973, U.S. consumption of mercury was 1900 metric
tons. Primary among its over 3000 industrial uses are battery manufacturing and
chlorine-alkali production. Paints and industrial instruments have also been among the
major uses. Until paint manufacturers agreed to eliminate the use of mercury in interior
paints, 480,000 pounds of mercury in paints and coatings were produced each year.
Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems (i.e. when it comes into contact with micro organisms in soil
or water).
STATUS OF CONTAMINATION
Not only are these methylated mercury compounds toxic, but highly bioaccumulative as
well. Mercury biomagnifies upto 100,000 times in predatory fish. The consumption of
such fish led to the poisoning of Japanese fisherman and their families in Minamata,
Japan, in the 1950s as a result of consumption of methyl mercury contaminated fish.
The magnification of levels of mercury as it rises in the aquatic food chain results in
relatively high levels of mercury in fish consumed by humans. The US Food and Drug
Administration (news - web sites) (FDA) recommends that pregnant women and those
who may become pregnant avoid eating shark, swordfish, king mackerel, and tile fish
known to contain elevated levels of methylmercury, an organic form of mercury that can
accumulate in the food chain.
ECOS, an association of state and territorial environmental commissioners frcm the
United States, is expected to adopt the resolution during its annual meeting currently
underway in Tampa Bay, Fla. In terms of national vision, the ECOS resolution calls on
the White House and Congress "to articulate a goal of virtual elimination of mercury
discharge into the environment at the national and international levels."
<http://www.eenews.net>
To date, more than 40 US states and the Food and Drug Administration
have adopted at least 2,073 public health advisories warning about
mercury contamination. In addition, several states and large municipalities
- mostly located in the Northeast - are cracking own on the amount of
mercury in the environment by outlawing mercury thermometers, which,
some say, could render drinking water supplies unusable if even one
thermometer contaminates a source.
In addition to the early workers in the cinnabar mines, modern workers in industries
using mercury are at risk from overexposure. The Occupational Safety and Health
Administration (OSHA) has been reviewing the current occupational exposure standard
of 0.1 mg/m3 (milligrams per cubic meter of air) to determine if they should reduce the 8
hour acceptable exposure limit to 0.05 mg/rn3. Although no regulatory limit exists for
airborne exposure to mercury outside of an occupational setting, the EPA suggests that
0.3 ug/m3 (micro-grams per cubic meter of air) of mercury is a no-effect level (or
reference dose - Rfd) for chronic inhalation exposure.
EXPOSURE SCENARIOS
Hurnans come in contact with mercury through environmental, occupational or
accidental exposure scenarios. An estimated 80% of utilized mercury is eventually
released back into the environment. Because it is easily vaporized, air around chlorine
alkali plants, smelters, municipal incinerators, sewage treatment plants and even
contaminated soils may contain increased levels of mercury. A primary route of
exposure is through transport into surface waters, where mercury becomes biomagnified
in fish tissues.
Workplace exposure to mercury occurs through inhalation of contaminated air, direct
skin contact with liquid mercury, or oral exposure through contaminated hands, food, etc.
HEALTH EFFECTS AND TOXICITY
Exposure to mercury can occur through inhalation, ingestion or dermal absorption, the
amount of mercury absorbed by the body -and thus the degree of toxicity - is dependent
upon the chemical form of mercury. For instance, ingested elemental mercury is only
0.01% absorbed, but methyl mercury is nearly 100% absorbed from the gastrointestinal
tract. The biological half-life of mercury' is 60 days. Thus, even though exposure is
reduced, the body burden will remain for at least a few months.
Elemental mercury is most hazardous when inhaled. Only about 25% of an inhaled dose
is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the
total dose). Dermal contact with liquid mercury can significantly increase biological
levels. The primary focus of this article is elemental mercury, since that is the form of
exposure to health care workers involved with mercury-containing instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury
may cause acute or chronic health effects. Acute exposure (i.e., short term, high dose) is
not as common today due to greater precautions and decreased handling. However,
severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5
hours may cause headaches, salivation, metallic taste in the mouth, chills, cough, fever,
tremors, abdominal cramps, diarrhea, nausea, vomiting, tightness in the chest, difficulty
breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a number of
hours.
Chronic effects include central nervous system effects, kidney damage and birth defects.
Genetic damage is also suspected. Nervous system effects. These are the most critical
effects of chronic mercury exposure from adult exposure as they are consistent and
pronounced, some elemental mercury is dissolved in the blood and may be transported
across the blood/brain barrier, oxidized and retained in brain tissue. Elimination from the
brain is slow, resulting in nerve tissue accumulation. Symptoms of chronic mercury
exposure on the nervous system include: Increased excitability, mental instability,
tendency to weep, fine tremors of the hands and feet, and personality changes. The
term "Mad as a Hatter" came from these symptoms which were a result of mercury
exposure in workers manufacturing felt hats using a mercury-containing process.
Kidney effects: Kidney damage includes increased protein in the urine and may result
in kidney failure at high dose exposure.
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild
exposure include delayed developmental milestones, altered muscle tone and tendon
reflexes, and depressed intelligence.
Mercury exposure in children can cause a severe form of poisoning termed acrodynia.
Acrodynia is evidenced by pain in the extremities, pinkness and peeling of the hands,
feet and nose, irritability, sweating, rapid heartbeat and loss of mobility.
For more information:
www.ban.org
www.noharm.org
www.qreenpeaceindia.org
pami HiisLs
eomteiL (pmco
PAMBAR SHOLA: A BIODIVERSITY TREASURE TROVE UNDER THREAT
"Pambar Shola, c. 2000m, Kodaikanal, perched on the edge of the precipe with the Falls cascading
down for several hundred metres. This extremely biodiverse Shola, now shrunk to less than 3 kms in
circumference, is witnessing the last-ditch battle for survival by a number of plant species, the last
sentinels of a bygone age. The past has been glorious; several plant species were described as new to
science from here. But the development activities of recent decades have depleted its species richness;
a few are already extinct; at least four are now known from a single clump each for the entire Palai
hills. Pambar Shola is truly a living fossil, a relic among relics.
In 1997, Ponds India Ltd set up a mercur/ thermometer factory on the ridge of Pambar shola slope by
securing special exemption from the Tamilnadu Government on grounds that the factory is non
polluting. Over the years, the slopes leading into Pambar shola's core have been used by the factory
management as a dumping ground for ali kinds of wastes, including broken mercury-containing
thermometers and other potentially mercury'-contaminated wastes. The slopes where the wastes are
dumped are part of the Pambar shola watershed, draining water through the Pambar River which
eventually ends up in the plains leading up to the temple city of Madurai through a network of canals.
Contiguous to the Pambar Shola is a remarkable slope of Strobi/anthes kunthiana, the folklore plant
endemic to the South Indian bills, known for the gregarious flowering regularly at intervals of 12 years.
The slope is probably the best preserved one for then plant for the entire Palni hills. The secluded
location of these two localities saved them to some extent till now, but for the future, instant in site (on
site) conservation is imperative. Proposals and representations have been a plenty, and all hope is not
yet lost. The urgent task is to lock the stables before at least the last horses have escaped".
(From the inside cover of the Handbook of the Anglade Institute of Natural History', Shembaganur, by
K.M. Matthew, 20.12.94.)
"Another significant finding was that endemic species often occur together, for which we have used the
term "enedemic poskeets". The most prominent of these, Pambar Shola ca. 1900 m, with an
accumulation of the highly vulnerable Sonerifa pufneyensis, Hcya wighli ssp. Pulneyensis, Ptectranthus
boumeae, Trichog/otb's tenera and PhyHanthus chandrabosei, along with Huperzia sp. Virtually from a
single population with ArtocarpusbirsutuswightiiQn a slope opposite."1
PAMgARSHOLA AND ENVIRONS - RED DATA .LIST
1. Sonerilapulneyensis- a delicate succulent herb endemic from Pambar Shola in all of the Palni Hills
2. Hoya wigfitiissp. pulneyensis - a succulent vine with waxy flowers endemic to Pambar Shola.
3.
Plcctranthus bourneae — a succulent herb endemic to from Pambar shola.
4.
Trichoglottis tenera - an epiphytic orchid. Pambar Shola is its major habitat.
5.
Phyllanthus chandiabosei- a shrub endemic to Pambar Shola
6. Hupzeria sp. - a fern of a kind endemic to Pambar Shola
7. Selaginella sp. b - a delicate creeping fern endemic to Pambar Shok:
8.
Psydrax ficiformis - - a tree, until recently thought extinct
9.
Ut/eria salicifolia - endemic to Palni hills
10. Elaeocarpus munroni- found only in one other known location in the Palm hills
11. Elaeocarpus blascoi - a tree believed extinct until this year
12. Cyathea crinita - tree fern, believed extinct in India (Botanical Survey of India)
13. Aeschynanthus perrottetii - known only from one other shola in the Palni hills
14. Eulophia sp. - a new species for the Pain: hills first collected in April 2000
15. Actinodaphne bourneae - Laurel tree believed extinct (Botanical Smvey of India). Two trees found in Pambar
Shola
16. Ceropegia thwaitesii - vine, vulnerable, endemic to Pambar shola
17. Pimpenella pulneyensis - herb, possibly extinct, originally found in Pambar shola grasslands
13. Exacum anamallayannum - gentian, only one other known location in Pah!! hills
For more information about the status of Natural history in Kodaikanal, contact:
Palni Hills Conservation Council
Endhavin, Lower Shola Road, Kodaikanal 624101
Tel: 4-91 4542 40157
Email: kajnan@vsnl.com
1 Report on the "Conservation Status of South Indian Plants," K.M Matthew, Biodiversity and
Conservation 1999.
Unilever - Policy and Strategy
Unilever
ENVIRONMENT
policy and strategy
news and events
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UNDERSTANDING OUR IMPACT
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Page 1 of2
policy and strategy
We have an environmental policy that applies
to all Unilever companies world-wide.
Linked to our broader business strategy is our
environmental strategy. This outlines our future direction
and is designed to ensure that we are closely connected
with the needs and demands of consumers who, research
shows, expect us to care for the environmental impact of
products on their behalf.
The environment strategy has three key elements:
CONTACT US
1.
Continue to improve the environmental performance
of our manufacturing operations and extend the use
of eco-efficiency measures along the supply chain
where we have influence and where we can get
major environmental improvements.
2.
Pursue the integration of environmental
sustainability into key business activities by ensuring
that environmental factors are accounted for in
product design. We call this eco-innovation.
3.
Meet goals set for our three sustainability initiatives
which support long-term accessibility of fish,
agriculture and water.
Our Policy Statement:
Unilever is committed to meeting the needs of customers
and consumers in an environmentally sound and
sustainable manner, through continuous improvements in
environmental performance in all our activities.
Accordingly, Unilever's aims are to
•
ensure the safety of its products and operations for
the environment
.
exercise the same concern for the environment
wherever we operate
.
develop innovative products and processes which
reduce levels of environmental impact and develop
methods of packaging which combine effective
protection and presentation with the conservation of
raw materials and convenient, environmentally
appropriate disposal
-
reduce waste, conserve energy and explore
opportunities for re -use and recycling
To achieve these aims, we will:
.
http://www.unilcvcr.com/en/en_ps.htinl
Assess the environmental impacts of all its business
activities from research, through manufacture,
distribution, use and disposal
23/2/01
Unilever - Policy and Strategy
Page 2 of 2
. Apply more stringent criteria than those required by
law when we believe this to be appropriate
. Use standards of environmental impact assessment
which are robust, scientifically sound and generally
acceptable within the present state of knowledge, at
the same time attempting to develop superior
methods and to improve on current practice
. Develop and apply systems of environmental
management, as part of day-to-day operational
practice and on-going management reporting and
control procedures
. Encourage our suppliers to develop environmentally
superior processes and ingredients and co-operate
with other members of the supply chain to improve
overall environmental performance
. Work with industry bodies, government agencies,
business partners and other concerned
organisations, to promote environmental care,
increase knowledge and disseminate
• best practice
. Remain alert and responsive to developing issues,
knowledge and public concerns
Unilever will communicate actively in order to:
. Provide whatever information and advice is
necessary on the safe use and disposal of our
products
. Ensure that employees are aware of the company's
environmental policy and motivated to apply it; are
aware of their own responsibilities and given the
support and training necessary to fulfill them
. Publish relevant and meaningful information on
environmental performance and progressively
introduce a more comprehensive reporting system.
Unilever hom
http://www.nn ilcver.com/cn/en_ps.htnil
23/2/01
MERCURY (Hg) ■ FACTSHEET
Mercury is probably best known as the silver liquid in thermometers. However, it has
over 3000 industrial uses. Mercury and its compounds are widely distributed in the
environment as a result of both natural and man-made activities. The utility, and the
toxicity, of mercury have been known for centuries. New evidence demonstrates that
even low levels of mercury exposure may be hazardous.
HISTORY & OCCURRENCE
Mercury occurs naturally in the environment as mercuric sulfide, also known as
cinnabar. It is also present in some fossil fuels. Cinnabar has been refined for its
mercury content since the 15th or 16th century B.C.
Mercury is present in numerous chemical forms. Elemental mercury itself is toxic and
cannot be broken down into less hazardous compounds.
USES
Desirable properties such as the ability to alloy with most metals, liquidity at room
temperature, ease of vaporizing and freezing, and electrical conductivity make mercury
an important industrial metal. In 1973, U.S. consumption of mercury was 1900 metric
tons. Primary among its over 3000 industrial uses are battery manufacturing and
chlorine-alkali production. Paints and industrial instruments have also been among the
major uses. Until paint manufacturers agreed to eliminate the use of mercury in interior
paints, 480,000 pounds of mercury in paints and coatings were produced each year.
Elemental or inorganic forms can be transformed into organic (especially methylated)
forms by biological systems (i.e. when it comes into contact with micro organisms in soil
or water).
STATUS OF CONTAMINATION
Not only are these methylated mercury compounds toxic, but highly bioaccumulative as
well. Mercury biomagnifies upto 100,000 times in predatory fish. The consumption of
such fish led to the poisoning of Japanese fisherman and their families in Minamata,
Japan, in the 1950s as a result of consumption of methyl mercury contaminated fish.
The magnification of levels of mercury as it rises in the aquatic food chain results in
relatively high levels of mercury in fish consumed by humans. The US Food and Drug
Administration (news - web sites) (FDA) recommends that pregnant women and those
who may become pregnant avoid eating shark, swordfish, king mackerel, and tile fish
known to contain elevated levels of methylmercury, an organic form of mercury that can
accumulate in the food chain.
ECOS, an association of state and territorial environmental commissioners from the
United States, is expected to adopt the resolution during its annual meeting currently
underway in Tampa Bay, Fla. In terms of national vision, the ECOS resolution calls on
the White House and Congress "to articulate a goal of virtual elimination of mercury
discharge into the environment at the national and international levels."
< http://www.eenews.net>
To date, more than 40 US states and the Food and Drug Administration
have adopted at least 2,073 public health advisories warning about
mercury contamination. In addition, several states and large municipalities mostly located in the Northeast - are cracking own on the amount of
mercury in the environment by outlawing mercury thermometers, which,
some say, could render drinking water supplies unusable if even one
thermometer contaminates a source.
In addition to the early workers in the cinnabar mines, modern workers in industries
using mercury are at risk from overexposure. The Occupational Safety and Health
Administration (OSHA) has been reviewing the current occupational exposure standard
of 0.1 mg/m3 (milligrams per cubic meter of air) to determine if they should reduce the 8
hour acceptable exposure limit to 0.05 mg/m3. Although no regulatory limit exists for
airborne exposure to mercury outside of an occupational setting, the ERA suggests that
0.3 ug/m3 (micro-grams per cubic meter of air) of mercury is a no-effect level (or
reference dose = Rfd) for chronic inhalation exposure.
EXPOSURE SCENARIOS
Humans come in contact with mercury through environmental, occupational or
accidental exposure scenarios. An estimated 80% of utilized mercury is eventually
released back into the environment. Because it is easily vaporized, air around chlorine
alkali plants, smelters, municipal incinerators, sewage treatment plants and even
contaminated soils may contain increased levels of mercury. A primary route of
exposure is through transport into surface waters, where mercury becomes
biomagnified in fish tissues.
Workplace exposure to mercury occurs through inhalation of contaminated air, direct
skin contact with liquid mercury, or oral exposure through contaminated hands, food,
etc.
HEALTH EFFECTS AND TOXICITY
Exposure to mercury can occur through inhalation, ingestion or dermal absorption, the
amount of mercury absorbed by the body -and thus the degree of toxicity - is dependent
upon the chemical form of mercury. For instance, ingested elemental mercury is only
0.01% absorbed, but methyl mercury is nearly 100% absorbed from the gastrointestinal
tract. The biological half-life of mercury is 60 days. Thus, even though exposure is
reduced, the body burden will remain for at least a few months.
Elemental mercury is most hazardous when inhaled. Only about 25% of an inhaled dose
is exhaled. Skin absorption of mercury vapor occurs, but at low levels (ex. 2.2% of the
total dose). Dermal contact with liquid mercury can significantly increase biological
levels. The primary focus of this article is elemental mercury, since that is the form of
exposure to health care workers involved with mercury-containing instrument accidents.
In the human body, mercury accumulates in the liver, kidney, brain, and blood. Mercury
may cause acute or chronic health effects. Acute exposure (i.e., short term, high dose)
is not as common today due to greater precautions and decreased handling. However,
severe acute effects may include severe gastrointestinal damage, cardiovascular
collapse, or kidney failure, all of which could be fatal. Inhalation of 1-3 mg/m3 for 2-5
hours may cause headaches, salivation, metallic taste in the mouth, chills, cough, fever,
tremors, abdominal cramps, diarrhea, nausea, vomiting, tightness in the chest, difficulty
breathing, fatigue, or lung irritation. Symptoms may be delayed in onset for a number of
hours.
Chronic effects include central nervous system effects, kidney damage and birth
defects. Genetic damage is also suspected. Nervous system effects. These are the
most critical effects of chronic mercury exposure from adult exposure as they are
consistent and pronounced, some elemental mercury is dissolved in the blood and may
be transported across the blood/brain barrier, oxidized and retained in brain tissue.
Elimination from the brain is slow, resulting in nerve tissue accumulation. Symptoms of
chronic mercury exposure on the nervous system include: Increased excitability, mental
instability, tendency to weep, fine tremors of the hands and feet, and personality
changes. The term "Mad as a Hatter" came from these symptoms which were a result of
mercury exposure in workers manufacturing felt hats using a mercury-containing
process.
Kidney effects: Kidney damage includes increased protein in the urine and may result
in kidney failure at high dose exposure.
Birth defects: Neurologic damage from methyl mercury. The manifestations of mild
exposure include delayed developmental milestones, altered muscle tone and tendon
reflexes, and depressed intelligence.
Mercury exposure in children can cause a severe form of poisoning termed acrodynia.
Acrodynia is evidenced by pain in the extremities, pinkness and peeling of the hands,
feet and nose, irritability, sweating, rapid heartbeat and loss of mobility.
For more information:
www.ban.org
www.noharm.org
www.greenpeaceindia.org
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