several decades on, the Bhopal disaster has been all but forgotten by most of the world. This assignment was completed for a Public health topic on environmental health
All Time Service Available Call Girls Marine Drive 📳 9820252231 For 18+ VIP C...
Lingering health impacts decades after the Bhopal disaster
1. 1. Scenario
Bhopal is a industrial city of approximately 1.6 million people situated in central Indian in the
state of Madhya Pradesh (Figure 1). Residents in the city and nearby tend to be of low socio-
economic status. Two large man-made lakes are situated in Bhopal, collectively known as the
Bhoi Wetland. Their combined catchment is approximately 370km2, and the upper lake
(which has the largest catchment) feeds into the Kolans River.1
Figure 1: Location of Madhya Pradesh2 Figure 2: residential settlements next to UCIL factory3
The city is situated on the sandstone Malwa Plateau4 which contains an aquifer that provides
drinking, cleaning and agricultural water for surrounding lands. Surrounding lands are hilly.
Madhya Pradesh is renowned for its forests – about one third of the state is forested, although
deforestation is progressing rapidly.5 Bhopal hinterlands are largely used for agriculture.
In 1969, US owned Union Carbide (now owned by Dow Chemicals) established a factory on
the north west edge of the city, on the banks of the larger upper lake. ‘Squatter settlements’ of
workers in very substandard housing grew around the plant6 (Figure 2), housing up to 10,000
people within 1km radius of the factory.7 Union Carbide chose the site because of its
effective railway system and cheap local labour. The factory was licensed to produce
phosgene, mono-methyl amine, methyl isocyanate, and carbaryl.8
Early in the morning of 3 December 1984 water entered storage tank 610 of the Bhopal union
Carbide Factory, producing 40 empirical tons of methyl isocyanate (MIC) gas, causing the
1
www.answers.com/tpic/bhopal?method=5 Accessed 4 February 2006
2
ibid
3
Agarwal R. Nair A. Wankhade K. Surviving Bhopal 2002: Toxic present – toxic future. A report on
the human and environmental chemical contamination around the Bhopal disaster site. Srishti. Fact
finding Mission on Bhopal. www.bhopal.net/oldsite/documentlibrary/survivingbhopal2002.doc
accessed 7 February 2006
4
www.worldrom.com/pages/cg_bhopal/fastfacts/bhopal_fastfacts.phtml Accessed 4 February 2006
5
“Madhya Pradesh” encyclopedia Britannica Online. www.britannica.com/eb/article?tocId=46063
accessed 4 February 2006
6
Weir D. The Bhopal Syndrome: Pesticides, environment and health. Sierra Club Books, San
Francisco. 1987. P36
7
Muller R. A significant toxic Event: The Union Carbide Pesticide Plant Disaster in Bhopal, India,
1984. www.tropmed.org/rreh/vol1_10.htm accessed 7 February 2006
8
Boybeyi Z, Raman S. Zanetti P. Numerical investigation of Possible Role of Local Meteorology in
Bhopal Gas Accident. Atmospheric Environment. Vol 29. No 4. Pp479-496. UK
1
2. temperature and pressure within the tank to rise and releasing a plume of gas through a safety
pressure valve. (Other gases may also have been involved.) Of the ~1 million 1984 Bhopal
residents, between 8,000 and 20,000 people are thought to have died in the disaster with
possibly a further 250,000 being exposed9 (estimates vary widely, up to 40,000 dead and
400,000 injured10 indicating a fair degree of confusion at the time). Bhopal residents also have
higher than normal rates of miscarriage and cancer, and children born to the victims who
survived have congenital deformities such as stunted growth and small heads.11 The gas also
affected plants and animals in the same area, both wild and agricultural12, entered the lakes
and permeated the porous sandstone under the city, entering the aquifer. No data was
collected on the Kolans River.
Following the disaster the factory was closed and the site remains untouched. Chemicals
remained stockpiled at the site. The site is not secured – animals graze and children play on
the site. Concerns about past and current soil and water contamination remain. Evaporation
ponds used for toxic waste disposal were covered in plastic and buried under soil. This cover
has been breached in at least one place.13 Run-off from the site reached the underground
aquifer (and may have while the site was operational) which supplies water for the city and
hinterlands.14
This Health Assessment will look at the acute and chronic effects in the population, as well as
the remaining hazards through inter-generational transfer and toxins remaining in the soil and
the uncleaned site, water supplies and foodstuffs such as animals and plants.
The Bhopal disaster has been an emotive issue on an international scale, and is used by green
groups as a symbol of the 'evils' of globalisation and the chemical industry generally. A large
number of highly emotive articles, documents and websites have been dedicated to this cause.
Where possible these sources have not been used, nor those of Union Carbide, as the claims
they contain are difficult to verify. Sources with a known bias are noted as such.
9
Cullinan P. Acquilla S. Ramana Dhara V. Respiratory morbidity 10 years after the Union Carbide gas
leak at Bhopal: a cross sectional survey. BMJ 1997;314:338
10
TED Case Studies: Bhopal disaster. www.american.edu/TED/bhopal.htm Accessed 4 February 2006
11
Harari F. Time Capsule 03/12/1984 Gas Leak Kills Thousands in Bhopal Tragedy. The Weekend
Australian Magazine 3-4 December 2005 p10.
12
Agarwal R. Nair A. Wankhade K. Surviving Bhopal 2002: Toxic present – toxic future. A report on
the human and environmental chemical contamination around the Bhopal disaster site. Srishti. Fact
finding Mission on Bhopal. www.bhopal.net/oldsite/documentlibrary/survivingbhopal2002.doc
accessed 7 February 2006
13
Stringer R. Johnston P. Technical guidelines for cleanup at the Union Carbide India Ltd (UCIL) site
in Bhopal, Madya Pradesh, India. Oct 2002. Greenpeace Research Laboratories, University of Exeter,
UK.
14
Acharya VN, Naik SR, Potnis AV, Bhalerao RA. Sequential study of thiocyanate levels in Bhopal
water following methyl isocyanate gas leakage. Journal of Post-Graduate Medicine. 1986. Vol 32.
Issue 4, p192-194.
2
3. 2. Hazard identification
“The process of determining whether an agent can cause an adverse health condition.”15
Pesticides are biologically active compounds, designed to kill plants, insects, fungi or
animals.16
Approximately 40 empirical tons of methyl isocyanate (MIC), an ingredient in the
manufacture of carbaryl and aldicarb pesticides (sold as Sevin and Temik brands),17 18 was
released from a storage tank pressure release valve approximately 33m above the ground.
Due to prevailing north to north to northwesterly light winds and a temperature inversion over
the city, the gas was taken from the release valve to the residential areas of the city.
MIC is an extremely toxic chemical. It is lighter than water but twice as heavy as air, and
hence once released into the atmosphere it tends to settle close to the ground. MIC has a very
high vapor pressure and may be the most toxic of all isocyanates due to its ability to affect
many systems. Table 1 contains an excerpt of the Cheminfo data on MIC (some of this
information may not have been available in 1984).
CHEMINFO record No. 164
Chemical family Isocyanic acid ester
Molecular Formula C2-H3-N-O
Structural Formula CH3-N=CO
Appearance and odour Colourless liquid with sharp unpleasant pungent odour,
lachrymator (vapour irritates eyes and causes tears)
Odour threshold 2.1 ppm. Three out of 7 people could still smell MIC at 5 ppm
Emergency overview ….EXTREMELY FLAMMABLE LIQUID AND VAOUR.
Vapour is heavier than air and may spread long distances.
Distant ignition and flashback is possible. Can decompose at high
temperatures forming toxic gases such as nitrogen oxides and
hydrogen cyanide. Closed containers may develop pressure and
rupture on prolonged exposure to heat. Reacts violently with
water…VERY TOXIC. May be fatal if inhaled or swallowed.
Vapour is extremely irritating to eyes and respiratory tract.
Causes lung injury – effects may be delayed. CORROSIVE to
eyes and skin. Can cause blindness and permanent scarring.
SKIN SENSITIZER. May cause allergic skin reaction.
MUTAGEN – may cause genetic damage, based on animal
information.
Carcinogenicity No human information is available on the carcinogenicity of
MIC. One animal study provides limited evidence of
carcinogenicity after a very brief exposure…... The International
Agency for Research on Cancer (IARC) has not evaluated the
carcinogenicity of this chemical.
Table 1: Excerpt of Cheminfo Data on Methyl isocyanate19
15
National Short Cause in Environmental Health Case Study 2005 documents
16
Cox C. From Factories and Tank Cars to You: Hazards of Manufacturing and transporting pesticides.
Journal of Pesticide Reform. Summer 1993 Vol 13 No2. P6.
17
TED Case Studies: Bhopal disaster. www.american.edu/TED/bhopal.htm Accessed 4 February 2006
18
Cox C. Aldicarb. Journal of pesticide reform. Summer 199. Vol 12, No 2.
19
CCOHS Cheminfo database. Methyl isocyanate.
3
4. Many other toxic compounds, identified and otherwise, are also present on the factory site
and in the local environment. These include, but are not limited to: ingredients used to
manufacture MIC, metabolites and breakdown products of MIC, and other chemicals
manufactured in the factory.
Chemical stockpiles at the site include: Aldicarb (Temik), BHC,20 an organochloride pesticide
which includes chlorobenzene. DDT isomers have been isolated on the site and nearby,
although the factory did not use or produce DDT.21 Heavy metals including mercury have
been detected.22 The solar evaporation ponds contain high levels of organochlorine.23
MIC can be converted into methylamine (methyl carbylamine isocyanatomethane) by cellular
enzymes in the human body, or by bacterial enzymes in water or in soil. This breakdown
product can yield cyanide.24 Studies have shown that the presence of bacteria in soil can
accelerate the breakdown of MIC.
MIC can be broken down by pyrolysis and interaction with water. MIC is more toxic than its
breakdown products.25 MIC is not biopersistent in the environment, although some of its
breakdown products including thiocyanate, can persist in water.26 Studies comparing Bhopal
water to Bombay water over before and after the leak show that the MIC had reached the
lakes and the aquifer providing water to the population of Bhopal and surrounding districts
(Bombay water showed no changes over this period). By August 1985, thiocyanate levels in
Bhopal water had returned to normal. 27 (Bhopal plaintiffs claim studies have shown other
chemicals remain present in the water supply.28) The half-life of MIC in soil is between 2.7
and 6.9 days (longer times recorded in river soils), degradation accomplished by microbial
and abiotic processes.29
As the Bhopal leak was the largest known human exposure, much of the data comes from
studies of this site. Other relevant studies include:
♦ Studies on a MIC leak at Union Carbide's aldicarb and carbaryl plant in West Virginia
(1985)30 with the same root causes as the Bhopal leak, resulting in 135 people being
hospitalised.
♦ metam sodium spill in the Sacramento River (1991)31 a derailed freight train which spilled
metam sodium in the Sacramento River. (Metam Sodium turns into methol isocyanate in
the presence of water.) The chemical affected local residents, fish, ducks, otters, insects
and ‘all living things’ for some months. Residents experienced an abnormally high rate
of miscarriage which may have been linked to the spill.32
20
ibid
21
ibid
22
ibid
23
ibid
24
Acharya VN, Naik SR, Potnis AV, Bhalerao RA. Sequential study of thiocyanate levels in Bhopal
water following methyl isocyanate gas leakage. Journal of Post-Graduate Medicine. 1986. Vol 32.
Issue 4, p192-194.
25
Varma DR. Guest I. The Bhopal Accident and methyl isocyanate toxicity. Journal of Toxicol environ
health. 1993 Dec; (40):513-29
26
ibid
27
ibid
28
Greenpeace. (1999) The Bhopal Legacy. Quoted on www.bhopal.net/oldsite/poisonpapers.html
29
Taylor GE. Schaller KB. Geddes JD. Gustin MS. Lorson GB. Miller GC. Microbial Ecology,
Toxicology and Chemical Fate of Methyl Isocyanate in Riparian Soils from the Upper Sacramento
river. Environmental Toxicology and Chemistry. Vol 15. Issue 10. Pp1694-1701
30
ibid
31
ibid
32
California Department of Health Services. Environmental Epidemiology and Toxicology Program.
Questions and Answers related to the Cantara loop spill: Metam sodium and MITC in the environment.
April 1992
4
5. ♦ spill of 50 gallons of MIC at FMC Corporation facility in Middlepost, New York (1984)33
caused permanent lung damage and asthma in children in a school nearby
♦ An invitro model has shown that MIC is cytogenic, causing sister chromatid exchange.
These findings were supported by an epidemiological study of exposed persons in
Bhopal.34
♦ Cheminfo data cites two laboratory studies of human subjects exposed to MIC vapour35
animal studies demonstrated high oral toxicity
MIC can cross cell membranes and hence penetrate the body’s defences, accessing organs
throughout the body. (MIC can also cross into breast milk.) It is linked to a number of
systemic effects, and it is believed its mechanism may be through the formation of a
reversible conjugate with glutathione. Aldicarb and sevin act through disrupting the normal
communication between nerve cells.36
MIC is converted into methylamine (methyl carbylamine isocyanatomethane) by cellular
enzymes in the human body or bacterial enzymes in soil and water.37
Reported adverse outcomes from MIC include:
• Death • Eye problems
• Respiratory problems • Miscarriage
• Nervous system problems • Congenital defects
• Gastrointestinal symptoms (abdominal • Neuromuscular abnormalities
pain, anorexia and diarrhoea) • Immuno-suppressant effects
• Non-specific airways irritation • Haematological effects
• Reproductive effects • Gene mutation38 39
Physical effects were stronger in the very young and very old, the infirm and smokers.
Early radiological investigations of Bhopal victims showed lung oedema and over-inflation,
enlarged heart, pleural scars and consolidation. Later investigations showed interstitial
deposits40 (these were also discovered in the autopsies of newborns). Cheminfo data states
that 49% of pregnant Bhopal leak victims did not give birth to live babies, a 3-4 fold increase
of fetal loss.41
High levels of psychological distress have been identified in survivors who may have seen
large numbers of their family and neighbours dying and dead.42 (Of the children identified as
having been psychologically affected, some were reported to have been thought dead and
placed in morgues only to wake and find themselves surrounded by dead bodies.)43
33
Journal of Pesticide Reform 9(1):2-5
34
Goswami HK. Cytogenic effects of methyl isocyanate exposure in Bhopal. Human genetics.
September 1986. Vol 74, No1. p81-84.
35
ibid
36
ibid
37
ibid
38
ibid
39
Goswami HK. Cytogenic effects of methyl isocyanate exposure in Bhopal. Human genetics. Vol 74
No1. Sept 1986. Pp81-84
40
Kamat SR, Patel MH, Pradhan PV, Taskar SP, Vaidya PR. Kolhatkar VP. Gopalani JP. Chandarana
JP. Dalal N. Naik M. Sequential respiratory, psychological and immunological studies with relation to
methyl isocyanate exposure over two years with model development. Environ Health Perspectives.
1992 Jul;97:241-53
41
ibid
42
ibid
5
6. 3. Dose response relationship
“The relationship between the dose (amount and/or duration) of an agent and the risk and
severity of an adverse health effect.”44
Cheminfo data cites studies exposing human subjects to varying concentrations of MIC
vapour. At 2ppm, irritation to nose and throat occurred, at 4ppm irritation was stronger and at
21ppm exposure was unbearable.45 Given the toxicity of this chemical such studies are
unlikely to be repeated in human subjects. The threshold for MIC toxicity in humans is 0.02
ppm of air.46 47
A definite dose response relationship is evidenced by studies of Bhopal victims. Those
closest to the factory leak had a much higher death rate.
A study of effects 105 days after the leak compared symptoms in two groups of children, one
group resided 1/2km to 2 km from the factory, and a second group who resided 8-10 kms
away from the factory. (It should be noted that due to the low socio-economic status in the
area, over 91% of those affected remained in the area and hence were easily tracked for these
sorts of studies. This also meant their exposure to the contaminated site continued.) A table
of the results is below:
Symptom / test result Group 1 Group 2
Respiratory abnormalities (rhonchi, rales, wheezing) 48.1% nil
Respiratory obstructive disability 28 8
Abnormal radiological findings 66.1% 8.1%
Conjunctivitis 79.8% nil
Vision abnormality 10.3% nil
Table 2: Dose response: level of symptoms to MIC in children
It should be noted that the children living closer to the factory may have been exposed to a
number of other pollutants prior to the MIC leak and hence general worsening of health
related to proximity to the factory may not be directly linked to the leak, but may still be
attributable to the Union Carbide Factory.
Another study looking at the damage to eyes noted a dose response relationship associated
with the distance from the factory and death rate in the community as a proxy for
concentration of exposure.48 (Meteorological modelling and comparison of vegetation
scorching supports distance from the factory as a proxy a measure of concentration gradient –
see notes above.) Highest death rate was in JP Nagyar colony, directly south of the factory.
(Figure 2)
4. Exposure assessment
43
Irani SF. Mahashur AA. A survey of Bhopal children affected by methyl isocyanate gas. Journal of
postgraduate medicine. 1986. Vol 32. Issue 4. P195-98
44
ibid
45
ibid
46
Acharya VN. Potnis AV. Bhopal gas tragedy; Medical Hazards. Science today, May 1985 pp22-23
47
Determination of Noncancer Chronic Reference Exposure Levels batch 2B December 2001. Chronic
Toxicity Summary Methyl Isocyanate. CAS Registry Number: 624-83-9
48
Andersson N. Muir MK, Mehra V, Salmon AG. Exposure and response to methyl isocyanate: results
of a community based survey in Bhopal. British Journal or Indian Medicine. 1988 Jul;45(7):469-75
6
7. “The process of measuring of estimating the intensity, frequency and duration of exposure to
a hazardous agent.”49
Exposure routes are multiple. Initially exposure was through the respiratory tract and eyes.
More long term, exposure is through the GI tract from ingestion of contaminated food and
water. Specific mention of milk from cows being grazed on the old factory site. As MIC is
able to cross membrane barriers, these exposure routes potentially open up all organ systems
to adverse effects, particularly as MIC is cytogenic. (A 2002 study found mercury and
organochlorides in breast milk of Bhopal women.50)
However, exposure assessment is somewhat confounded by a number of factors. A number
of contaminants remain on site so it would be difficult to link an illness specifically to the
MIC leak exposure. Some symptoms do not become apparent until a long time, sometimes
decades, after exposure. Many of the studies on pesticide exposure relate to small numbers of
workers and hence results are not statistically viable. Often exposures are to multiple
chemicals which makes it difficult to compare statistics. (Several relevant studies are listed
above)
Union Carbide is not the only chemical factory in Bhopal and other industries may also have
contaminated the local environmental and the aquifer. A number of those most affected were
workers at the plant and their families (who lived nearby) who may have been exposed at
work previously. Industrial Indian cities like Bhopal often have heavy air pollution. The local
population is of low socio-economic status and are probably exposed to a number of the risk
factors associated with this.
Smokers and those with existing ill health were particularly affected. Activities being
undertaken at the time also affected exposure – those doing physical activity outside in the
morning would have had a high dose than those remaining indoors (although it should be
noted that these houses were not by any means hermetically sealed). Some people would be
particularly susceptible to the exposure.
Length and intensity of exposure for individuals is difficult to estimate due to the number of
local climactic factors affecting the dispersion and distribution of the gas plume. The leak
itself lasted from 0030 hours to approximately 0200 – 90 minutes, however the gas remained
in the area for many hours afterwards. A nocturnal inversion was present on the night of the
gas leak. It’s position 250m above the ground meant that the warmer gas escaping from the
33m high vent remained trapped below the inversion as it cooled in the night air.51 While the
relative weight of the compound meant it could be expected to settle rapidly as it cooled, this
appears not to have been the case. Winds were calm and initially northwesterly and the
northerly, directing the plume over the populated areas of Bhopal rather than the agricultural
hinterlands.
Other local environmental factors also played a part in determining where the strongest doses
were experienced. Heat rising from parts of the city caused localised weak low pressure cells
which sucked the gas in but funneled it upwards. In some areas these temperature differences
also “sucked” clean air off the cooler lakes, dispersing the gas. (The average temperature in
the agricultural lands was about 16C, but in the town it rose to 22C.52) The area is also quite
hilly, creating funnels directing air flow. However, the urban areas are quite ‘rough’ for the
wind to flow over and hence the air slows over the city. A complex model factoring in all of
49
ibid
50
ibid
Murthy ASV. Varghese S. Nocturnal Temperature Inversions under calm clear conditions:
51
An analytical study. Council of Scientific and industrial research, New Delhi.
52
ibid
7
8. these factors demonstrates the gas plume moving slowly south east from the factory with little
mixing and the concentration mainly at the emission height of 33m, until it reaches the
turbulence over the warmer city. Between 210 to 270 minutes after the release the gas is
mixed with other air, cooler and descending on the city, still moving downwind.53 The change
from northwesterly to northerly win direction had the effect of narrowing the gas plume but
increasing the concentration54, meaning fewer people experienced the plume but those who
did received a more toxic dose.
Local reports are varied as to the length of exposure: one area was reportedly ‘clear’ by 0530,
while JP Nagyar colony next to the factory was still observably in the gas cloud five hours
after the release concluded (0700). 55 It is important to note that these were by observation of
the gas cloud – lower (but still toxic) concentrations may have remained in the area although
not visible and not causing the acute symptoms.
Overall, using the model mentioned above, vegetation scorching and pattern of deaths as
indicators, a small area to the southeast of the factory received the most concentrated gas
plumes, with the exposure generally lessening in concentration albeit unevenly, as the plume
travelled further from the initial site and was generally dispersed. Death rates coincided with
other indicators, and these areas also experienced the highest rate and most serious adverse
effects. JP Nagyar had the highest death rate.
While MIC is not biopersistent in the body or in the environment, it does remain for up to 9
days in soil and over 3 months in water (discussed previously). The ongoing contamination
source could be replenishing the exposure of soils, water (particularly in the lakes and
aquifers) and locals.
5. Risk Characterisation
“The process of predicting the incidence of a health effects resulting from exposure to a
hazardous agent by combining the dose response relationship with the exposure
assessment”56.
As noted above the particular local climactic conditions have made accurate characterisation
of exposure difficult due to the number of variable factors and the large number of people
involved. Estimates vary between 200,000 and 400,000 people affected by the initial gas
plume. Considering the ongoing environmental exposure through contaminated water in the
aquifer, contaminated milk from cattle grazing on the factory site, and contaminated local
agriculture products, the potential exposure numbers expand to the entire area. Bhopal does
not seem to have an agricultural export industry, so presumably most if not all agriculture
products are consumed locally. Any ongoing contamination, particularly the milk from cattle
grazing on the factory site that are subject to ‘fresh’ contamination, will also affect any new
residents who consume this product. The city of Bhopal is now approximately 1.6 million.
No data is available on the agricultural hinterland population, who would also draw upon the
contaminated aquifer.
Intergenerational effects such as congenital defects and miscarriages / stillbirths also increase
the number of people affected. There is no data on whether a third generation would also be
affected by the exposure but with a genetic-based defect this is entirely probable, providing
53
ibid
54
ibid
55
ibid
56
ibid
8
9. the defects do not affect fertility (studies on the congenital effects seem to focus on small
heads not on infertility other than the high miscarriage rate).
Some victims might experience only low-level effects, but considering the low threshold for
MIC, it is likely that all who are exposed would have some effects. Sensitive individuals
would experience stronger reactions, as would smokers, the unwell (particularly those with
respiratory conditions), the very young especially those exposed dring the first trimester of
pregnancy57 and the elderly.
Survivors would also have additional susceptibility to further toxic assaults and infections.
6. Risk Management
6.1 Costs
Although Union Carbide’s safety standards at the Bhopal factory were substandard even by
American international standards, the Indian government, on behalf of the victims, reached a
settlement of $470million USD – depending on estimates this is as little as $1000 per person.
This settlement was intended to cover compensation, but with no ongoing funding, it I now
having to cover the ongoing health costs for the victims, and the cleanup of the site58. In
addition, there is the cost to the agricultural land, products and industry, the loss of jobs to
locals, DALYs (including the costs of supporting victims unable to work). Some, but not all
of the money was distributed to victims. Greenpeace cites a US legislation, Superfund, which
places the responsibility for cleanup with the polluter, and has some limited ‘extraterritorial
provisions’, dependent on agreement between the US government and the government of the
affected country.59
6.2 Minimising Ongoing Risk
While the main incident of exposure occurred 22 years ago, there is evidence of ongoing risk
and exposure, which can only be addressed by a full-scale clean-up of the site and affected
areas. Even if it were possible to relocate a city of over a million people, the low socio-
economics of the affected populace means they are unlikely to be able to relocate and re-
establish easily without significant funding.
Greenpeace Research Laboratories have written a document detailing specifications for
cleanup for the Bhopal site60. (While Greenpeace cannot be considered to be a disinterested
party, their specifications do draw on previously published standards and studies.)
Their conclusions are that an effective cleanup would include:
• Closed loop technologies that do not produce further emissions
• Inventory, analysis and quantification of stockpiles to determine actual content, using
accredited laboratories
• Appropriate UN standards for containment, packaging, removal and transport of toxic
chemical stockpiles
• Chemicals which cannot be destroyed such as heavy metals and metallic compounds
should be stabilised and placed in monitored above-ground storage
• Recognition that a large number of toxic chemicals are on site and a number of potential
toxic combinations could be created through any mixture or cleaning process.
57
ibid
58
ibid
59
ibid
60
ibid
9
10. • Close ongoing evaluation of effectiveness and any potential for hazard production
• Remaining buildings will need to be deconstructed. Materials which can be demonstrated
to be free from contamination may be disposed of as normal. Contaminated materials
will need to be removed and treated or disposed of according to appropriate standards
• Workers in the clean-up will need to be appropriately protected. In addition to the
chemicals, there may be asbestos on site, and physical danger from the deteriorating
structures.
• Sludge from drains around the site will need to be dug out, analysed for toxins and dealt
with appropriately
• Sludge from storage tanks will need to be analysed and dealt with appropriately
• Contaminated soils, particularly the lime pit and solar evaporation ponds which were used
for waste disposal, and any other landfill waste disposal are present on sit, as well as
generally across the factory site. Soils will need to be systematically sampled and
analysed using a grid pattern, toxins identified including quantity, concentration and
depth, analysis should include metals such as mercury and should be broad spectrum,
seeking to identify unknown compounds, not just the chemicals known to have been
present on the site. The presence of DDT, a chemical not manufactured onsite indicates
the importance of this. Contaminated soils should be removed then remaining soils
retested.
• Ground water also needs to be decontaminated. Samples from wells and boreholes within
2km of the site should be tested. Where tests are positive in wells and bores near the
perimeter of this zone, the testing zone should be extended until no contamination is
detectable. Analyses should include heavy metals, solvents, organics and any other toxins
present. Water should be pumped from the contaminated wells and treated by a method
appropriate to the contaminant, without causing any further contamination (such as
evaporation of solvents which would cause further air pollution). Once cleaned, the water
could be used to recharge the aquifer.61
This clean-up would be a major undertaking, involving many tonnes of soil, chemicals and
thousands of litres of water. This will be costly and a long term undertaking, and provision
will need to be made for the local community to overcome the inconvenience – clean grazing
land for the cattle, an alternative playground for the children, alternative water sources while
wells are decontaminated. Cooperation of the local community is necessary on a number of
levels including use of the alternative resources, and the identification of bores and wells,
which may not be regulated.
At all stages the appropriate international standards should be identified and applied.
7. Uncertainties
There are a number of areas of uncertainty regarding this exposure. Primarily, identification
of the major contaminant does not allow for the large number of identified and potentially
unidentified contaminants. No history on pre-existing contamination is available. Actual
numbers of people exposed vary considerably and the level of exposure for each individual is
established by deduced averages for geographical area.
Most of the knowledge about MIC toxicity in humans comes from this exposure, so long term
effects, and ongoing intergenerational effects are not yet available. No knowledge is
available on interactions between the many toxicants in the Bhopal district.
Little is available about the toxic effects from ingestion of contaminated agriculture products
or the intergenerational effects on livestock.
61
ibid
10
11. The Bhopal population had a number of pre-existing risk factors including low socio-
economic status, poor housing quality and air pollution. They may also have had dietary and
lifestyle risk factors such as smoking. There is little general commentary on the pre-existing
health of the population or access to health services prior to the disaster. There is little
comparative epidemiological data on rates of various diseases, congenital malformations etc
prior to the exposure.
Finally, much of what has been written about Bhopal has come from Union Carbide, anti-
chemical industry campaigners, lobby groups on behalf of the victims of Bhopal and other
interested parties. Objective data, particularly for an event that occurred 22 years ago, can be
difficult to identify.
8. Communication
Affected persons must be informed and involved in the planning of any clean-up and
relocation involved. Significant disillusionment has already occurred with the population
over the compensation funding which has been held back for cleanup costs.
Significant distrust and fear as been engendered in a population that is largely dependant on
local industry as their employers.
The population would need to be made aware of what health effects can or cannot be linked to
the gas plume and toxins from the factory. They would need to be made aware of what they
can do to minimise their exposure and the harmful effects any damage may already have
caused, ie: don’t graze cattle on the factory site, keep children away from the factory site,
don’t drink from affected wells until they have been cleared (which would required the
provision of a viable local alternative source) and try to quit smoking.
The population would need to be made aware of what is being done to clean up the area.
They would need provision of health facilities adequate for their increasing needs and with
the appropriate equipment to run the screening tests and treatment required, either free or at a
fee that this low socio-economic population can afford and is willing to prioritise.
11
12. 9. References
Acharya VN, Naik SR, Potnis AV, Bhalerao RA. Sequential study of thiocyanate levels in
Bhopal water following methyl isocyanate gas leakage. Journal of Post-Graduate Medicine.
1986. Vol 32. Issue 4, p192-194.
Acharya VN. Potnis AV. Bhopal gas tragedy; Medical Hazards. Science today, May 1985
pp22-23
Agarwal R. Nair A. Wankhade K. Surviving Bhopal 2002: Toxic present – toxic future. A
report on the human and environmental chemical contamination around the Bhopal disaster
site. Srishti. Fact finding Mission on Bhopal.
www.bhopal.net/oldsite/documentlibrary/survivingbhopal2002.doc accessed 7 February 2006
Andersson N. Muir MK, Mehra V, Salmon AG. Exposure and response to methyl isocyanate:
results of a community based survey in Bhopal. British Journal or Indian Medicine. 1988
Jul;45(7):469-75
Boybeyi Z, Raman S. Zanetti P. Numerical investigation of Possible Role of Local
Meteorology in Bhopal Gas Accident. Atmospheric Environment. Vol 29. No 4. Pp479-496.
UK
California Department of Health Services. Environmental Epidemiology and Toxicology
Program. Questions and Answers related to the Cantara loop spill: Metam sodium and MITC
in the environment. April 1992
CCOHS Cheminfo database. Methyl isocyanate.
Cox C. Aldicarb. Journal of pesticide reform. Summer 199. Vol 12, No 2.
Cox C. From Factories and Tank Cars to You: Hazards of Manufacturing and transporting
pesticides. Journal of Pesticide Reform. Summer 1993 Vol 13 No2. P6.
Cullinan P. Acquilla S. Ramana Dhara V. Respiratory morbidity 10 years after the Union
Carbide gas leak at Bhopal: a cross sectional survey. BMJ 1997;314:338
Determination of Noncancer Chronic Reference Exposure Levels batch 2B December 2001.
Chronic Toxicity Summary Methyl Isocyanate. CAS Registry Number: 624-83-9
Goswami HK. Cytogenic effects of methyl isocyanate exposure in Bhopal. Human genetics.
September 1986. Vol 74, No1. p81-84.
Greenpeace. (1999) The Bhopal Legacy. Quoted on
www.bhopal.net/oldsite/poisonpapers.html
Harari F. Time Capsule 03/12/1984 Gas Leak Kills Thousands in Bhopal Tragedy. The
Weekend Australian Magazine 3-4 December 2005 p10.
Irani SF. Mahashur AA. A survey of Bhopal children affected by methyl isocyanate gas.
Journal of postgraduate medicine. 1986. Vol 32. Issue 4. P195-98
Journal of Pesticide Reform 9(1):2-5
12
13. Kamat SR, Patel MH, Pradhan PV, Taskar SP, Vaidya PR. Kolhatkar VP. Gopalani JP.
Chandarana JP. Dalal N. Naik M. Sequential respiratory, psychological and immunological
studies with relation to methyl isocyanate exposure over two years with model development.
Environ Health Perspectives. 1992 Jul;97:241-53
Madhya Pradesh. Encyclopedia Britannica Online. www.britannica.com/eb/article?
tocId=46063 accessed 4 February 2006
Muller R. A significant toxic Event: The Union Carbide Pesticide Plant Disaster in Bhopal,
India, 1984. www.tropmed.org/rreh/vol1_10.htm accessed 7 February 2006
Murthy ASV. Varghese S. Nocturnal Temperature Inversions under calm clear conditions: An
analytical study. Council of Scientific and industrial research, New Delhi.
National Short Cause in Environmental Health Case Study 2005 documents
Stringer R. Johnston P. Technical guidelines for cleanup at the Union Carbide India Ltd
(UCIL) site in Bhopal, Madya Pradesh, India. Oct 2002. Greenpeace Research Laboratories,
University of Exeter, UK.
Taylor GE. Schaller KB. Geddes JD. Gustin MS. Lorson GB. Miller GC. Microbial Ecology,
Toxicology and Chemical Fate of Methyl Isocyanate in Riparian Soils from the Upper
Sacramento river. Environmental Toxicology and Chemistry. Vol 15. Issue 10. Pp1694-1701
TED Case Studies: Bhopal disaster. www.american.edu/TED/bhopal.htm Accessed 4
February 2006
Varma DR. Guest I. The Bhopal Accident and methyl isocyanate toxicity. Journal of Toxicol
environ health. 1993 Dec; (40):513-29
Weir D. The Bhopal Syndrome: Pesticides, environment and health. Sierra Club Books, San
Francisco. 1987. P36
www.answers.com/tpic/bhopal?method=5 Accessed 4 February 2006
www.worldrom.com/pages/cg_bhopal/fastfacts/bhopal_fastfacts.phtml Accessed 4 February
2006
13