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    and the World Health Organization

    World Health Orgnization
    Geneva, 1984

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    1.1. Summary
         1.1.1. Properties and analytical methods
         1.1.2. Uses and sources of exposure
         1.1.3. Environmental concentrations and exposures
         1.1.4. Kinetics and metabolism
         l.l.5  Studies on experimental animals
         1.1.6. Effects in man
    1.2. Recommendations


    2.1. Identity
    2.2. Physical and chemical properties
    2.3. Analytical methods


    3.1. Production and uses
    3.2. Transport and distribution
         3.2.1. Air
         3.2.2. Water
         3.2.3. Soil
         3.2.4. Abiotic degradation


    4.1. General population exposure
    4.2. Occupational exposure
    4.3. Wildlife


    5.1. Animal studies
    5.2. Human studies


    6.1. Single exposures
    6.2. Short-term exposures
         6.2.1. Dermal toxicity
    6.3. Long-term exposures and carcinogenicity studies
    6.4. Reproduction and teratology studies
    6.5. Mutagenicity
    6.6. Behavioral studies
    6.7. Neurotoxicity
    6.8. Other studies


    7.1. Poisoning incidents in the general population
    7.2. Occupational exposure
    7.3. Treatment of poisoning in man


    8.1. Aquatic organisms
    8.2. Terrestrial organisms
    8.3. Microorganisms
    8.4. Bioaccumulation and biomagnification
    8.5. Population and community effects
    8.6. Effects on the abiotic environment
    8.7. Appraisal



    10.1. Chlordecone toxicity
    10.2. Exposure to chlordecone
    10.3. Effects on the environment
    10.4. Conclusions




Dr Z. Adamis, National Institute of Occupational Health, 
   Budapest, Hungary

Dr D.A. Akintonwa, Department of Biochemistry, Faculty of 
   Medicine, University of Calabar, Calabar, Nigeriaa

Dr R. Goulding, Chairman of the Scientific Sub-committee, UK
   Pesticides Safety Precautions Scheme, Ministry of
   Agriculture, Fisheries & Food, London, England  (Chairman)

Dr S.K. Kashyap, National Institute of Occupational Health
   (Indian Council of Medical Research), Meghaninager,
   Ahmedabad, India

Dr D.C. Villeneuve, Environmental Contaminants Section,
   Environmental Health Centre, Tunney's Pasture, Ottawa,
   Ontario, Canada  (Rapporteur)

Dr D. Wassermann, Department of Occupational Health, The
   Hebrew University, Haddassah Medical School, Jerusalem,
   Israel  (Vice-Chairman)

 Representatives of Other Organizations

Dr C.J. Calo, European Chemical Industry Ecology and
   Toxicology Centre (ECETOC), Brussels, Belgium

Mrs M.Th. van der Venne, Commission of the European 
   Communities, Health and Safety Directorate, Luxembourg

Dr D.M. Whitacre, International Group of National Associations
   of Agrochemical Manufacturers (GIFAP), Brussels, Belgium


Dr M. Gilbert, International Register for Potentially Toxic
   Chemicals, United Nations Environment Programme, Geneva,

Mrs B. Goelzer, Division of Noncommunicable Diseases, Office
   of Occupational Health, World Health Organization, Geneva,

Dr Y. Hasegawa, Division of Environmental Health,
   Environmental Hazards and Food Protection, World Health
   Organization, Geneva, Switzerland

a   Unable to attend.

 Secretariat (contd.)

Dr K.W. Jager, Division of Environmental Health, International
   Programme on Chemical Safety, World Health Organization,
   Geneva, Switzerland  (Secretary)

Mr B. Labarthe, International Register for Potentially Toxic
   Chemicals, United Nations Environment Programme, Geneva,

Dr I.M. Lindquist, International Labour Organisation, Geneva,

Dr M. Vandekar, Division of Vector Biology and Control,
   Pesticides Development and Safe Use Unit, World Health
   Organization, Geneva, Switzerland

Mr J.D. Wilbourn, Unit of Carcinogen Identification and
   Evaluation, International Agency for Research on Cancer,
   Lyons, France


    While every effort has been made to present information in 
the criteria documents as accurately as possible without unduly 
delaying their publication, mistakes might have occurred and are 
likely to occur in the future.  In the interest of all users of 
the environmental health criteria documents, readers are kindly 
requested to communicate any errors found to the Manager of the 
International Programme on Chemical Safety, World Health 
Organization, Geneva, Switzerland, in order that they may be 
included in corrigenda, which will appear in subsequent volumes. 

    In addition, experts in any particular field dealt with in 
the criteria documents are kindly requested to make available to 
the WHO Secretariat any important published information that may 
have inadvertently been omitted and which may change the 
evaluation of health risks from exposure to the environmental 
agent under examination, so that the information may be 
considered in the event of updating and re-evaluation of the 
conclusions contained in the criteria documents. 

                        *     *     *

    A detailed data profile and a legal file can be obtained from 
the International Register of Potentially Toxic Chemicals, Palais 
des Nations, 1211 Geneva 10, Switzerland (Telephone no. 988400 - 


    Following the recommendations of the United Nations 
Conference on the Human Environment held in Stockholm in 1972, 
and in response to a number of World Health Assembly Resolutions 
(WHA23.60, WHA24.47, WHA25.58, WHA26.68), and the recommendation 
of the Governing Council of the United Nations Environment 
Programme, (UNEP/GC/10, 3 July 1973), a programme on the 
integrated assessment of the health effects of environmental 
pollution was initiated in 1973.  The programme, known as the WHO 
Environmental Health Criteria Programme, has been implemented 
with the support of the Environment Fund of the United Nations 
Environment Programme.  In 1980, the Environmental Health 
Criteria Programme was incorporated into the International 
Programme on Chemical Safety (IPCS).  The result of the 
Environmental Health Criteria Programme is a series of criteria 

    A WHO Task Group on Environmental Health Criteria for 
Organochlorine Pesticides other than DDT met in Geneva from 28 
November to 2 December, 1983.  Dr K.W. Jager opened the meeting 
on behalf of the Director-General.  The Task Group reviewed and 
revised the draft criteria document and made an evaluation of the 
health risks of exposure to chlordecone. 

    This document is a combination of drafts prepared by Dr D.C. 
Villeneuve of Canada and Dr S. Dobson of the United Kingdom. 

    The efforts of all who helped in the preparation and 
finalization of the document are gratefully acknowledged. 

                            * * *

    Partial financial support for the publication of this 
criteria document was kindly provided by the United States 
Department of Health and Human Services, through a contract from 
the National Institute of Environmental Health Sciences, Research 
Triangle Park, North Carolina, USA - a WHO Collaborating Centre 
for Environmental Health Effects. 


1.1.  Summary

1.1.1.  Properties and analytical methods

    Chlordecone (Kepone) is a tan- to white-coloured solid.

    Gas chromatography with electron capture detection is the 
method most widely used for the determination of chlordecone. 

1.1.2.  Uses and sources of exposure

    Chlordecone was used as an insecticide and as a base material 
in the manufacture of the insecticide kelevan.  Its production in 
the USA was discontinued in 1976; information about its production
elsewhere is lacking. 

    Exposure of the general population through its normal use can 
be regarded as minimal and is mainly related to residues in food.  
Poisoning amongst workers and severe contamination of the 
surrounding area and rivers have occurred where manufacture and 
formulation were carried out in a careless and unhygienic manner.  
The exposure of people living near these plants must have been 

    Small children may be exposed through playing with insect 
traps containing chlordecone. 

1.1.3.  Environmental concentrations and exposures

    Chlordecone presents a major hazard for aquatic ecosystems 
because of its stability and persistence in sediments, its 
bioaccumulation in food chains, and its acute and chronic 
toxicity.  Low concentrations cause reductions in both algal 
growth and invertebrate populations, thereby affecting productivity 
at other trophic levels.  The few data available on terrestrial 
ecosystems indicate low acute toxicity but some long-term effects 
on vertebrate reproduction. 

1.1.4.  Kinetics and metabolism

    Chlordecone is readily absorbed following ingestion by 
animals and human beings.  It is also absorbed following 
inhalation and dermal exposure.  It is widely distributed in the 
body; accumulation occurs mainly in the liver.  The half-life in 
the body is of the order of several months and excretion is slow, 
mainly via the faeces. 

1.1.5.  Studies on experimental animals

    Chlordecone is moderately toxic with single exposures. Acute 
toxic symptoms in all species tested included severe tremors.  It 
can cause skin irritation.  In long-term studies, lower doses 
caused tremors and other neurological symptoms, liver hypertrophy 

with induction of mixed function oxidases, hepatobiliary 
dysfunction, and centrilobular hepatocellular necrosis. 

    Chlordecone interferes with reproduction, and it is fetotoxic 
in experimental animals. 

    It is not generally active in short-term tests for genetic 
activity.  Chlordecone is carcinogenic in both sexes of mice and 
rats producing hepatocellular carcinomas. 

1.1.6.  Effects in man

    No accidental poisonings have been reported.

    A large number of cases of occupational poisoning were 
reported in a manufacturing plant where work-hygiene and safety 
precautions were insufficient.  Neurological symptoms, especially 
nervousness and tremors, together with oligospermia and joint 
pains were reported. 

1.2.  Recommendations

1.  Careful surveillance should be maintained over the future 
    production of chlordecone and the nature and extent of its 

2.  The levels in the environment should continue to be 

3.  It is desirable that a long-term follow-up study should be 
    conducted on workers whose health has been affected by 


2.1.  Identity


Molecular formula:          C10Cl10O

CAS chemical name:          1,1a,3,3a,4,5,5,5a,5b,6-decachloro-

Synonyms:                   decachloro-pentacyclo[5,2,1,02,6,03,
                            9,O5,8]decan-4-one, dec-

Trade names:                GC 1189, Kepone, Merex

CAS registry number:        143-50-0

Relative molecular mass:    490.6

2.2.  Physical and Chemical Properties

    Chlordecone is a tan- to white-coloured solid that sublimes 
with some decomposition at 350 C (IARC, 1979).  Its vapour 
pressure is less than 3 x 10-7 at 25 C. 

    In the anhydrous form, chlordecone is soluble in organic 
solvents such as benzene and hexane.  The hydrated compound is 
less soluble in apolar solvents.  Oxygenated solvents such as 
alcohols and ketones are recommended for the hydrated form 
(Blanke et al., 1977).  Chlordecone is also soluble in light 
petroleum and may be recrystallized from 85 - 90% aqueous ethanol 
(Information Canada, 1973).  It is readily soluble in acetone 
(IARC, 1979). 

    Early reports did not include any evidence of chlordecone 
degradation in the natural environment (Dawson, 1978; Geer, 
1978), but, in a more recent study, microbial action has been 

shown to transform chlordecone into monohydro and possibly 
dihydro-chlordecone (Orndorff & Colwell, 1980a). 

    Technical grade chlordecone contains from 88.6% to 99.4% 
chlordecone (Blanke et al., 1977), 3.5 - 6.0% water (Dawson, 1978) 
and 0.1% hexachlorocyclopentadiene.  It has been formulated as a 
wettable powder (50% chlordecone), emulsifiable concentrates, 
granules, and dust (Information Canada, 1973). 

2.3.  Analytical Methods

    Various methods for the determination of chlordecone are 
summarized in Table 1. 

Table 1.  Methods for the determination of chlordecone
Sample type      Sampling method,                Analytical          Limit of   Reference
or medium        extraction/clean-up             method              detection
general                                          gas chromato-       0.005-     Moseman et al.     
                                                 graphy electron     0.01 g    (1978)
                                                 capture detection

formulations,    extract (acetone),              infrared (IR)       -          Allied Chemicals
concentrations,  decant, evaporate               (c = o band)                   Corporation (1966)
wettable powders to dryness, dissolve
                 (decane), boil, cool

technical grade  extract (acetone-decane),       infrared (IR)       -          Allied Chemicals
                 heat to remove                  (c = o band)                   Corporation (1966)
                 acetone, boil, cool

air              trap on filter and back up      gas chromato-       0.1 g/m3  NIOSH (1977)
                 up impinger containing          graphy electron
                 sodium hydroxide solution,      capture detection
                 extract filter (benzene-        (GC/ECD)
                 methanol), acidify extract
                 (benzene), bulk extracts  

  apples         extract (benzene), decant,      gas chromato-       80 g/kg   Brewerton & Slade
                 filter                          graphy electron                (1964)
                                                 capture detection

  potatoes       extract (methylene chloride),   thin-layer          200 g/kg  Proszynska (1977)
                 column chromatography (CC)      chromatography
                                                 (TLC) (revelation:
                                                 silver nitrate/
                                                 gas chromato-
                                                 graphy electron
                                                 capture detection

Table 1.  (contd.)
Sample type      Sampling method,                Analytical          Limit of   Reference
or medium        extraction/clean-up             method              detection    
  bananas        extract (isopropanol-benzene),  gas chromato-       3 g/kg    Allied Chemicals
                 evaporate to dryness, dissolve  graphy (GC)/                   Corporation (1963)
                 (hexane), liquid/liquid         micro coulo-
                 partition, extract (benzene)    metric detection

water            add XAD-2 resin to water,       gas chromato-       0.015      Harris et al. (1980)
                 extract (toluene ethyl          graphy electron     g/kg        
                 acetate), column                capture detection                
                 chromatography (CC)             (GC/ECD)                         
soil and         extract (50% methanol           gas chromato-       10-20      Blanke et al. (1977);
sediment         in benzene), column             graphy electron     g/kg      Moseman et al. (1977);
                 chromatography (CC)             capture detection              Saleh & Lee (1978);
                                                 (GC/ECD)                       Orndorff & Colwell
biological       extract (toluene in             gas chromato-       10 g/kg   Mady et al. (1979)
tissues          ethyl acetate), column          graphy electron                  
                 chromatography (CC)             capture detection                


3.1.  Production and Uses

    The synthesis of chlordecone was first reported in 1952 by 
Gilbert & Giolito (1952).  Commercial production in the USA 
started in 1966 (IARC, 1979). 

    Chlordecone is manufactured by the condensation of 2 
molecules of hexachlorocylopentadiene in the presence of sulfur 
trioxide, followed by hydrolysis to the ketone.  It is also 
produced during the synthesis of mirex and is a contaminant of 
technical grade mirex.  From the 1950s until 1975, some 1 600 000 
kg of chlordecone were produced in the USA, of which between 90% 
(Sterrett & Boss, 1977) and 99.2% (US EPA, 1976b) was exported to 
Africa, Europe, and Latin America.  The bulk of the remainder,  
12 000 - 70 000 kg (US EPA, 1976b) was used in ant and cockroach 
traps in the USA or, after 1978, stored until it could be 
disposed of safely.  It has been reported that most of the 
chlordecone exported was used in the manufacture of kelevan 
(Cannon et al., 1978). 

    Chlordecone has been used extensively in the tropics for the 
control of banana root borer (Anonymous, 1978a; Langford, 1978).  
It is regarded as an effective insecticide against leaf-cutting 
insects, but less effective against sucking insects (Information 
Canada, 1973).  It can be used as a fly larvicide, as a fungicide 
against apple scab and powdery mildew (Information Canada, 1973), 
and to control the Colorado potato beetle (Motl, 1977), rust mite 
on non-bearing citrus, and potato and tobacco wireworm on gladioli
and other plants (Suta, 1978). 

    Life Science Products in Hopewell, Virginia, produced up to 
2700 kg of chlordecone a day between April, 1974 and June, 1975, 
when the plant was closed (Lewis & Lee, 1976).  Chlordecone 
production was discontinued in the USA in 1976.  However, a year 
later it was reported that a French company was considering the 
establishment of production facilities in France (Anonymous, 
1978b), but no further information on this proposal is available. 

3.2.  Transport and Distribution

3.2.1.  Air

    Laboratory and field observations indicate that chlordecone 
does not volatilize to any significant extent (Dawson, 1978).  
However, in the past, the release of copious quantities of 
chlordecone dust from production facilities has represented a 
major source of environmental and human contamination.  It has 
been suggested that chlordecone emissions from the Hopewell plant 
"were of a fine particle size having a long residence time in the 
atmosphere" (Lewis & Lee, 1976). 

3.2.2.  Water

    The solubility of chlordecone in water is low (1 - 2 mg/litre) 
and, as in the case of mirex, contamination is more likely to be 
associated with the particulate matter in the water than with the 
water itself (Orndorff & Colwell, 1980b).  With the exception of 
contamination in the James River system, very little information 
is available on chlordecone residues in water.  Sampling after 
the closure of the Life Science Plant revealed chlordecone levels 
of 1 -4 g/litre in Bailey Creek, 0.1 g/litre in the Appomattox 
River, and 0.3 g/litre in the James River and at the mouth of 
Bailey Creek (Smith, 1976).a  Chlordecone was not detected (limit 
of determination 0.01 mg/kg) in samples taken from the James River
several months after the plant was shut down (Huggett et al., 
1977).  However, it was detected periodically in the water table
of Hopewell at levels as high as 3.4 g/litre but typically 0.1
g/litre (Dawson, 1978) and was also detected in the New York 
water supply of the Great Lakes Basin by Suta (1978). 

    Residues as high as 0.21 g chlordecone/litre have been
reported in runoff from a banana plantation in Guadeloupe
(Snegaroff, 1977).

3.2.3.  Soil

    Chlordecone has a high affinity for soils and sediments such 
that, at equilibrium in the environment, residue levels in 
particulate matter will be 104 - 105 times that in any surrounding
water (Dawson, 1978).  Consequently, sediments act as sink for
chlordecone-contaminated water and soils provide a sink for most
atmospheric contamination.  Again, most of the residue data result
from work in and around Hopewell and the James River system.
Sediment levels were as high as 10 mg/kg in Bailey Bay, and it has
been estimated that as much as 47 000 kg of chlordecone lie on the
bottom of the James River (Chigges, unpublished data, 1977). 

    Soil residue levels in Hopewell ranged from as high as 10 000 
to 20 000 mg/kg near the plant to 2 - 6 mg/kg at a distance of 1 
km (US EPA, 1976a) and it was estimated (Anonymous, 1978) that 
1000 kg of chlordecone lay within a 1 km radius of the plant.  
Most of the soils tested in Hopewell contained detectable levels 
of chlordecone with concentrations generally decreasing with 
increasing distance from the plant (Dawson, 1978).  Chlordecone 
residues may be expected in sediments of waterways in the vicinity
of other production-formulation facilities, but no data are
available on this. 

a   Smith, W.C. (1976)   Kepone discharges from Allied Chemical
     Corporation, Hopewell, Virginia, Denver, Colorado, US EPA,
    National Field Center (Internal EPA Memorandum).

    The US EPA (Anonymous, 1978a) estimated that a field that had 
been treated with chlordecone (4.2 kg active ingredient/ha) should
have a residue level of 100 mg/kg in the top 3 cm of soil, after
application.  Reports of actual determinations in soil are scarce,
but the United Fruit Company (Anonymous, 1978a) described a 
residue level of 15 - 25 mg/kg, 6 months after an application of 
6.73 kg active ingredient/ha.  Snegaroff (1977) reported soil 
residue levels of 9.5 mg/kg and a level of 0.135 mg/kg in 
sediments in streams neighbouring on a banana plantation in 

3.2.4.  Abiotic degradation

    Chlordecone is an extremely stable compound and, as mentioned 
in section 2, it is not expected to be degraded in the environment
to any significant extent.  However, there have been reports of
trace amounts of monohydro chlordecone being found (Carver et al.,
1978, Orndorff & Colwell, 1980b), but the mechanism of its 
formation is not clear.  Solar irradiation of chlordecone in the
presence of ethylenediamine will result in 78% degradation after
10 days, but no study of the degradation products or their 
toxicity has been undertaken (Dawson, 1978). 


4.1.  General Population Exposure

    Precise information on general population exposure to 
chlordecone is not available.  However, a summary of the daily 
exposure from several sources in different regions in the USA has 
been compiled (Suta, 1978). 

    (a)  Air

    Airborne chlordecone has been known to spread 60 miles from a 
point source (Feldmann, 1976), and the potential exists for 
further dispersion of fine particles (Lewis & Lee, 1976). 

    (b)  Water

    At present, exposure via drinking-water does not present a 
health hazard with the possible exception of that in the Hopewell 
area.  Values quoted for the lower James River ranged from 0.1 to 
10 g/litre (Suta, 1978). 

    (c)  Food

    The USA action levels for chlordecone residues in foods are 
0.3 mg/kg for shellfish, 0.3 mg/kg for finfish, 0.4 mg/kg for 
crabs, and 0.01 mg/kg for banana peels (Suta, 1978).  While the 
majority of shellfish taken from the polluted James river in 1976 
contained less than the 0.3 mg/kg action level of chlordecone, 
oyster and clam samples in certain areas contained 0.21 - 0.81 
mg/kg, crab samples contained 0.45 - 3.44 mg/kg, and finfish 
samples 0.02 - 14.4 mg/kg.  These data prompted a fishing ban on 
the James River (Shanholtz, 1976). 

    In 1978, samples of spot, flounder, mullet, trout, and croakers
from the James River contained chlordecone but in concentrations
below the 0.3 mg/kg action level (Suta, 1978).  In bluefish, one
sample was above 0.1 mg/kg (0.2 mg/kg) (US FDA, 1977).  The shell-
fish sampled in the same area contained chlordecone, but at levels
that could not be reliably determined (Reuber, 1977).  All crabs 
in the area contained chlordecone, but all levels were below the 
action level. 

    In 1976, samples from the polluted Chesapeake Bay contained 
levels of 0.037 mg/kg for 75 finfish samples and 0.61 mg/kg for 
11 crab samples, and levels in 3 samples of oysters and one 
sample of clams were non-detectable (US EPA, 1979). 

    Residues in Atlantic coast bluefish (66 samples) ranged from 
0.01 to 0.06 mg/kg, with the higher concentrations found off the 
Virginia coast (Peeler, 1976).  South Atlantic coastal fish were 
relatively free of chlordecone as only 1 out of 132 samples 
contained detectable levels (Reuber, 1977). 

    Residues of chlordecone in edible plants have only been 
reported in New Zealand (Brewerton & Slade, 1964).  No data are 
available in the literature for chlordecone residue levels in 
bananas (Suta, 1978). 

    Chlordecone has been found in 9 out of 298 samples of human 
milk, but the detection limit was relatively high (1 g/kg) 
(Suta, 1978).  Samples were taken in the southern USA, and 
chlordecone residues were only found in areas that had received 
bait treatment for fire ants. 

    (d)  Exposure in infants

    Two major sources of chlordecone exposure for infants are 
insect traps and human milk.  The USDA (1977)a has reported that 
of 56 cases of non-occupational exposure to chlordecone, 52 were 
children under the age of 5, and all but 9 of these had come into 
contact with insect traps.  This is understandable as children of 
this age group are fairly inquisitive and their activity areas 
are likely to overlap target areas for ant and cockroach traps.  
The same study also cited exposure of 2 adults and 2 persons of 
unspecified age. 

    To date, chlordecone contamination of human milk has only 
been reported in 9 samples (Suta, 1978) in the southeastern USA.  
However, relatively few samples have been tested for chlordecone. 

    (e)  Miscellaneous

    Since tobacco plants were treated with chlordecone, this may 
have also represented an exposure route, but again no residue 
data are available. 

4.2.  Occupational Exposure

    Chlordecone received its notoriety when severe and wide-
spread industrial poisoning was discovered at the Life Science 
Plant (LSP) in Hopewell in 1975.  From March 1974 to June 1975, 
the LSP recorded output of chlordecone was 769 390 kg (Dawson, 
1978).  The total production was certainly above this figure, but 
massive amounts of chlordecone found their way into the soil, 
water, and air surrounding the plant.  The workers in the plant 
and the families in the area were exposed to extremely high 
concentrations of chlordecone dust.  High volume air samplers 
(Pate & Tabor, 1962), 200 m from the plant, recorded chlordecone 
levels as high as 54.8 mg/m3, which constituted 50% of the total 
particulate load.  Lower concentrations of chlordecone were 
detected in the air 25 km away from the plant.  Concentrations of 
a   Comments of the Secretary of Agriculture in response to 
    the Notice of Intent to cancel pesticide products
    containing chlordecone, trade name "Kepone". Washington DC
    vs. USDA, January 11, 1977.

chlordecone dust within the plant were not monitored, but levels 
reaching 11.8 mg/litre were found in blood samples of workers 
from the LSP (Heath, 1978).  Illness was found in 76 of the 133 
current and former workers of the plant examined.  Families of 
the LSP workers were also examined, as well as Allied Chemical 
Corporation people working in the area of the plant, workers from 
the sewage treatment plant that received chlordecone sludge, and 
residents of Hopewell.  It was found that the blood levels of 
workers who were ill, averaged 2.53 mg/litre, whereas the average 
level in workers not reporting ill was 0.60 mg/litre (Heath, 

4.3.  Wildlife

    Residue levels for phytoplankton in the James River were 
found to average 1.3 mg/kg (Huggett et al., 1977). 

    Chlordecone residues were also found in several species of 
birds that inhabit the southeastern USA coast, such as the blue 
heron, mallard duck, coot, black duck, wood duck, herring gull, 
Canada goose, hooded mersanger, and the bald eagle (Dawson, 
1978).  Residue levels were as high as 13.23 mg/kg (Dawson, 
1978), but typically between 0.02 and 2 mg/kg.  Eggs from the 
bald eagles and the osprey in Virginia were also examined and 
were found to contain residue levels ranging from 0.14 to 0.19 
mg/kg, and 0.06 to 1.5 mg/kg, respectively (Dawson, 1978). 

    Studies on marsh plants in the James River Basin indicated 
that there was no translocation of chlordecone from root to 
aerial plant tissue (Lunz, 1978). 


    Only limited information is available on the absorption, 
distribution, metabolism, and excretion of chlordecone in human 
beings and animals.  These aspects of the chemical are therefore 
discussed together, rather than in separate sections. 

5.1.  Animal Studies

    The results of earlier studies by Huber (1965) indicated that,
after dietary exposure, chlordecone was accumulated mainly in the
liver of mice.  The brain, fat, and kidneys also contained some
residues.  Chlordecone was well absorbed and distributed through-
out the body of rats after oral administration.  Following a 
single oral dose at 40 mg/kg body weight, the highest concentrations
were found in the adrenal glands and liver, followed by the fat 
and lung (Egle et al., 1978).  The compound had a long biological
half-life and disappeared more slowly from the liver that from
other tissues.  Excretion occurred mainly in the faeces, a total
of 66% of the dose being removed in the faeces and 2% in the urine
urine in the 84 days following administration.  Faecal excretion
of chlordecone in rats was increased by the adminstration of an
ionic exchange resin, cholestyramine (Boylan et al., 1977).
Excretion of chlordecone by the gastrointestinal tract, in addition
to the biliary route, occurs in rats as well as human beings
(Boylan et al., 1979).  A small amount of chlordecone alcohol was
found in rat faeces suggesting that chlordecone under went
reductive biotransformation in the rat (Blanke et al., 1978). 

5.2.  Human Studies

    A number of studies were conducted to investigate the 
kinetics of chlordecone in workers who were exposed to this 
chemical.  Chlordecone was present in high concentrations in the 
liver (mean and range) (75.9 mg/kg; 13.3 - 173 mg/kg), whole 
blood (5.8 mg/litre, 0.6 - 32 mg/litre), and subcutaneous fat 
(21.5 mg/kg, 2.2 - 62 mg/kg) of 32 male workers (Cohn et al., 
1976).  Adir et al. (1978) reported that, in occupationally-
exposed workers, serum chlordecone concentrations ranged from 120 
to 2109 g/litre.  Six to 7 months later, the concentration 
dropped to 37 - 486 g/litre. The half-life was estimated to be 
63 - 148 days.  Chlordecone was eliminated, primarily in the 
faeces, at a mean daily rate of 0.075% of the estimated total 
store in the body (Cohn et al., 1976).  Cholestyramine was found 
to increase the faecal excretion of chlordecone by a factor of 6 
- 7, presumably by interfering with reabsorption from the 
intestine.  Chlordecone underwent extensive biliary excretion and 
enterohepatic circulation.  Elimination by the gastrointestinal 
tract also played an important role (Boylan et al., 1979).  
Chlordecone alcohol was identified in human faeces (Blanke et 
al., 1978). 


6.1.  Single Exposures

    Toxicity data resulting from single exposures to chlordecone 
in several animal species are summarized in Table 2.  Toxic 
symptoms included severe tremors in all species tested.  These 
tremors usually reached a maximum within 2 - 3 days, then 
gradually subsided.  Tremors were exacerbated by excitement. 

    In dermal studies on rats and rabbits, no skin irritation was 
observed when chlordecone was administered in oil, but in aqueous 
solution it produced marked irritation, oedema, and scab formation 
(Epstein, 1978). 

6.2.  Short-Term Exposures

    The effects of chlordecone following short-term exposures are 
summarized in Table 3.  In general, they include nervous symptoms,
liver hypertrophy, induction of mixed-function oxidases (EC, 
and structural and ultrastructural changes in the liver, thyroid, 
adrenals, and testes.  Death sometimes followed. 

6.2.1.  Dermal toxicity

    A study has been reported (Epstein, 1978) in which 
chlordecone concentrations equivalent to 5 and 10 mg/kg body 
weight were tested on groups of 6 male albino rats for 3 weeks, 
totalling 15 applications; the animals were killed 2 weeks after 
termination of exposure.  Two out of 6 animals in the low-dose 
group and 1 out of 6 in the high-dose group showed testicular 
atrophy.  Otherwise, there were no consistent or significant 
pathological changes. 

6.3.  Long-Term Exposures and Carcinogenicity Studies

    The long-term and carcinogenic effects of chlordecone are 
summarized in Table 4.  Effects in these studies were similar to 
those reported following short-term exposures.  The data indicate 
that chlordecone is carcinogenic in mice and rats.  These studies 
were reviewed by IARC (1979) and it was concluded that chlordecone 
produced hepatocellular carcinomas in both sexes of mice and rats. 

Table 2.  Acute toxicity of chlordecone
Species  Sex    Route of           LD50 (mg/kg     Reference
                administration     body weight)
dog      M & F  oral               250             Larson et al. (1979b)

rabbit   ?      oral               65              NIOSH (1978)

chicken  ?      oral               480             NIOSH (1978)

rat      ?      oral               95              NIOSH (1978)

rabbit   ?      dermal             345             NIOSH (1978)

rat      M      oral (oil)         132             Larson et al. (1979b)

rat      F      oral (oil)         126             Larson et al. (1979b)

rat      M      oral (aqueous)     96              Epstein (1978)

rabbit   M      oral (oil)         71              Larson et al. (1979b)

rabbit   M      oral (aqueous)     65              Epstein (1978)

rabbit   M      dermal (oil)       410             Epstein (1978)

rabbit   M      dermal (aqueous)   435             Epstein (1978)

pig      M      oral (approx.)     250             Epstein (1978)

rat      M      oral (aqueous)     9.6a            Epstein (1978)

rat      M      oral (peanut oil)  125             Gaines (1969)

rat      F      oral (peanut oil)  125             Gaines (1969)

rat      M      dermal (xylene)    2000            Gaines (1969)

rat      F      dermal (xylene)    2000            Gaines (1969)
a  These animals were dosed for 20 consecutive days excluding Sundays.

Table 3.  Summary of short-term studies with chlordecone
Species  Sex     Duration        Doses used      Effects                          Reference          
mouse    M       14 days         1, 10, or       induction of hepatic mixed-      Fabacher & Hodgson 
                                 50 mg/kg diet   function oxidases                (1976)             
                                                 at 2 highest levels                                 
rat      M       8 days          200 mg/kg       ultrastructural changes in       Baggett et al.     
                                 diet            the liver and adrenal            (1977, 1980)       
                                                 medulla, decreased adrenal                          
                                                 catecholamines, and                                 
                                                 increased P-450 values                              
rat      F       15 days         50, 100, or     decreased body weight gain       Mehendale et al.   
                                 150 mg/kg diet  and induction of mixed-          (1978)             
                                                 function oxidases at all                            
                                                 3 levels of treatment                               
rat      M       15 days         10, 50, or      decreased biliary excretion      Mehendale et al.   
                                 150 mg/kg diet  at 10 mg/kg and higher;          (1978)             
                                                 body weight gain affected                           
                                                 at 50 mg/kg and higher;                             
                                                 liver enlargement at                                
                                                 all 3 levels of treatment                           
rat      M & F   3 months        25 mg/kg diet   tremors after 4 weeks; liver     Cannon & Kimbrough 
                 followed by                     hypertrophy; liver and adrenals  (1979)             
                 "clean" diets                   both showed histological                              
                 for 4.5 months                  changes; after recovery                         
                                                 period, liver still showed                          
                                                 histological abnormalities                          
rat              14 days         1 mg/kg diet    induction of hepatic mixed-      Baker et al.       
                                                 function oxidases                (1972)             

Table 4.  Summary of long-term and carcinogenicity studies with chlordecone
Species   Duration         Doses used   Effects                                            Reference
rat       2 years          5, 10, 25,   all rats on 2 highest doses died during first      Larson et al.        
                           50, or 80    6 months; depressed growth occurred at 10 mg/kg    (1979b)
                           mg/kg diet   and higher; liver hypertrophy occurred at levels
                                        of 10 mg/kg and higher; histopathological find-
                                        ings in liver, kidneys, and testes at 25 mg/kg;
                                        haematological changes at 25 mg/kg

dog       127 weeks        1, 5, or 25  weight gain reduced at 25 mg/kg; no treatment-     Larson et al.        
                           mg/kg diet   related histological abnormalities observed        (1979b)

mouse     90 weeks         20-40 mg/kg  survival reduced at high dose level in males;      Anonymous       
                           diet         hepatocellular carcinomas induced in both males    (1976)
                                        and females

rat       up to 24 months  1-80 mg/kg   hepatocellular carcinomas observed in some         Larson et al.        
                           diet         intermediate dose groups, but not all              (1979b)

mouse     12 months        0-100 mg/kg  tremors observed after 4 weeks in all mice         Huber (1965)
                           diet         fed 30 or more mg/kg; deaths observed
                                        at 2 highest doses; liver enlargement
                                        observed at 40 mg/kg and higher; micro-
                                        scopic and electron microscopic changes
                                        observed in dose-dependent manner

rat       exposure for 80  8-26 mg/kg   increased incidence of hepatocellular carcinomas   Anonymous       
          weeks followed   diet         observed in high-dose females                      (1976)
          by 16 weeks of

rat       up to 2 years    1 mg/kg      increased incidence of malignant tumours in        Reuber (1978,      
                           diet         male and female rats                               1979)

6.4.  Reproduction and Teratology Studies

    The reproductive performance of mice fed 0, 10, 30, or 37.5 
mg chlordecone/kg diet was impaired in terms of offspring and 
litter size (Huber, 1965).  No litters were produced by females 
fed 40 mg/kg, but litter production did resume within 7 weeks 
following withdrawal of the chlordecone, although litters were 
still smaller than those of untreated controls.  Histological 
examination of the testes showed they were normal, but corpora 
lutea were virtually absent from the ovaries.  The authors 
concluded that reproductive failure was largely due to an effect 
in females characterized by prolonged FSH and estrogen 
stimulation, inducing constant estrus, large follicles and 
absence of corpora lutea but with levels of LH subminimal for 

    In a study reported by Good et al. (1965), male and female 
mice fed chlordecone in the diet at levels ranging from 10 to 375 
mg/kg for 1 month, were randomly paired with animals at the same 
feeding level and then maintained on the same diet for 4 months.  
The results indicated that chlordecone caused a dose-dependent 
effect on reproduction, even at 10 mg/kg. 

    Similar effects on reproduction were noted by Hammond et al. 
(1978) in rats fed 30 mg/kg; the estrogenic properties of this 
chemical were also noted (Couch et al., 1977; Bulger et al., 
1979; Hammond et al., 1979).  In female rats fed 25 mg 
chlordecone/kg diet for 3 months, followed by a control diet for 
4.5 months, reproduction was completely inhibited during the 
treatment period.  Two months after exposure was discontinued, 
reproduction was only partially restored (Cannon & Kimbrough, 
1979).  Chlordecone has also been shown to interfere with egg 
production in both quails (McFarland & Lacy, 1969) and hens 
(Naber & Ware, 1965). 

    Chlordecone was administered by gastric intubation in doses 
of 2, 6, and 10 mg/kg body weight per day to rats and 2, 4, 8, 
and 12 mg/kg body weight per day to mice on days 7 - 16 of 
gestation (Chernoff & Rogers, 1976).  In rats, the highest dose 
caused 19% maternal mortality and fetuses exhibited reduced 
weight, reduced degree of ossification, oedema, undescended 
testes, enlarged renal pelvis, and enlarged cerebral ventricles.  
Lower dose levels induced reductions in fetal weight and degree 
of ossification.  Male rats born to treated dams did not show any 
reproductive impairment.  In the mouse, fetotoxicity was observed 
only at the highest dose level and consisted of increased fetal 
mortality and clubfoot. 

    In a study by Rosenstein et al. (1977), rats were 
administered chlordecone by gavage from day 2 of gestation at 
levels of 1, 2, or 4 mg/kg body weight per day.  At parturition, 
all control pups and those from mothers receiving 1 mg/kg body 
weight were normal.  Two-thirds of the females receiving 2 mg/kg 
and all females receiving 4 mg/kg aborted or had still births. 

    Chlordecone was administered to female rats at concentrations 
of 2.5 mg/kg body weight per day and to mice at 6.0 - 24 mg/kg 
body weight per day on days 7 - 16 of gestation and also 
postpartum (Chernoff et al., 1979a).  Although there were toxic 
manifestations in the mother (death) and fetuses (litter 
mortality, decreased litter weight), ophthalmological studies did 
not reveal cataracts or outlined lenses. 

6.5.  Mutagenicity

    Chlordecone was found to be negative at dose levels of 3.6 or 
11.4 mg/kg body weight per day for 5 days in a dominant lethal 
study on rats (Simon et al., 1978).  Chlordane gave negative 
results when tested for enhancement of unscheduled DNA synthesis 
in primary cultures of adult rat hepatocytes (Williams, 1980; 
Prohst et al., 1981) and was not mutagenic in  Salmonella 
 typhimurium(Prohst et al., 1981). 

6.6.  Behavioural Studies

    In studies on rats administered 40 - 80 mg chlordecone/kg 
diet, behavioural changes including hyperactivity, decreased 
ambulation in an open field, and delayed emergence from the home 
cage were seen at both dose levels within one week (Reiter et 
al., 1977; Reiter & Kidd, 1978; Tilson et al., 1979).  Chlordecone
was given intragastrically, 5 - 6 days per week, at dosages of 1, 
5, and 10 mg/kg body weight for 4 - 76 days to male and female 
Zivic-Miller rats.  A dose of 1 mg/kg body weight disrupted the 
multiple-fixed-ratio test and the fixed-interval test after 3 
injections and a dose of 5 mg/kg decreased the spaced-responding 
test after 9 - 10 injections.  Gradual recovery occurred after 
discontinuation of treatment (Dietz & McMillan, 1978). 

6.7.  Neurotoxicity

    Chickens (Naber & Ware, 1965), quail (McFarland & Lacy, 
1969), fish (Couch et al., 1977), hamsters (Martinez et al., 
1976), mice (End et al., 1979), rats (Epstein, 1978), and man 
(Martinez et al., 1978) have all displayed neurotoxic symptoms on 
exposure to chlordecone.  Biochemically, chlordecone has been 
shown to inhibit Mg-ATPases in fish brain (IARC, 1979) and rat 
liver (Desaiah et al., 1977) and also to cause disruption of rat 
brain synaptosomal membranes (End et al., 1979). 

6.8.  Other Studies

    Chlordecone has been shown to inhibit several enzymes  (in 
 vitro) including maleate dehydrogenase (Anderson et al., 1977), 
lactate dehydrogenase (EC (Anderson & Noble, 1977; 
Anderson et al., 1978), and succinic acid dehydrogenase (Kawatski 
& Hecker, 1979). 

    Chlordecone has been demonstrated to enhance the hepatotoxic 
effects of both chloroform and carbon tetrachloride (Cianflone et 
al., 1980), but had no similar effect on the response of the rat 
liver to polyhalogenated biphenyls (Chu et al., 1980).  It was 
able to increase the detoxification of lindane in weanling rats 
(Chadwick et al., 1979).  Pretreatment of rats with low non-toxic 
levels of dietary chlordecone (10 mg/kg, 15 days) potentiated the 
hepatotoxicity (Curtis et al., 1979) and lethality of carbon 
tetrachloride (Klingensmith & Mehendale, 1982a) about 70-fold in 
male rats and 25-fold in female rats (Agarwal & Mehendale, 
1982a).  Comparative doses of other inducers of microsomal 
enzymes such as mirex, photomirex, and phenobarbital did not 
potentiate carbon tetrachloride toxicity to such an extent 
(Curtis & Mehendale, 1980; Klingensmith & Mehendale, 1982b). 
Hepatobiliary dysfunction, elevation of hepatic enzymes in serum, 
and centrilobular hepatocellular necrosis were the characteristic 
features for the rat.  The hepatotoxicity and lethality of 
bromotrichloromethane were also potentiated about 5-fold by 
chlordecone (Agarwal & Mehendale, 1982b). 

    Like mirex, chlordecone has been shown to modify 
hepatobiliary function (Mehendale, 1979), possibly due to 
interference with energy production and utilization. 

    In an inhalation study reported in a review (Epstein, 1978), 
male rats were exposed to test and control dusts for 2 h per day 
for 10 days and killed 2 weeks later.  Air flow was maintained at 
10 - 12 litre/min, and the effective chlordecone concentrations 
were 3.7 and 15.4 g/litre.  The reviewer concluded, contrary to 
the authors of the actual study, that chlordecone at both dose 
levels induced toxic effects, including hepatomegaly and 
histopathological changes in the liver and lungs. 


7.1.  Poisoning Incidents in the General Population

    No information is available concerning such incidents.

7.2.  Occupational Exposure

    Life Sciences Products Co. (LSPC) was formed in November 1973 
and went out of production in July 1975.  In a study carried out 
by the Center for Disease Control (Cannon et al., 1978), 133 
employees, including 33 currently employed, were interviewed, 
examined, had blood samples taken, and completed a standard 
questionnaire.  Of the 133 examined, 76 (57%) had developed 
clinical illness described as nervousness, tremor, weight loss, 
opsoclonus, pleuritic and joint pain, and oligospermia.  Illness 
rates were higher for production workers than non-production 
workers, and the mean blood-chlordecone level for workers with 
illness was 2.53 mg/litre compared with a level of 0.60 mg/litre 
in workers without disease.  Laboratory findings from the above 
study showed an increase in serum alkaline phosphatase (EC activity in several patients (Taylor et al., 1978) and 
morphological changes in peripheral nervous tissue (Martinez et 
al., 1978). 

7.3.  Treatment of Poisoning in Man

    The treatment is symptomatic.

    Administration of cholestyramine will increase the excretion 
of chlordecone, and so reduce the body burden of the chemical 
(Cohn et al., 1976, 1978; Anonymous, 1977). 


8.1.  Aquatic Organisms

    The results of studies on the toxicity of chlordecone for a 
variety of algae are given in Table 5. 

    Acute and short-term toxicity values for invertebrate species 
are also tabulated (Table 6).  A more comprehensive table listing 
different conditions and exposure times is available on request 
from the IRPTC, Geneva.  A life cycle study is available for 
mysid shrimps,  Mysidopsis bahia (Nimmo et al., 1977).  This test 
was long enough to cover the production of several broods.  The 
average number of young produced by each female was reduced from 
the control level of 15.3 to 8.9 on exposure to 0.39 g 
chlordecone/litre.  Juveniles produced grew more slowly than 
controls.  Young females exposed to as little as 0.072 g 
chlordecone/litre for 14 days were shorter than controls.  The 
authors pointed out that reproductive success was related to body 
size, the number of eggs produced being greater in bigger 
females.  In a life cycle study of a copepod,  Eurytemora affinis,  
a dominant zooplankter, the intrinsic rate of natural increase 
was reduced by all concentrations of chlordecone greater than 
5 g/litre (Allan & Daniels, 1982).  This was due to a combination 
of a reduced rate of survival, delayed onset of reproduction, and 
reduced fecundity. 

    The toxicity of chlordecone for fish varies with species 
(Table 6).  Juvenile fish are generally less susceptible to 
chlordecone than adults.  Symptoms of chlordecone poisoning 
(Hansen et al., 1976) progressed from scoliosis (darkening of the 
posterior third of the body) through haemorrhaging near the brain 
and anterior point of darkening, oedema, fin rot, incoordinated 
swimming, and cessation of feeding.  Symptoms increased in 
severity before death, which occurred between 5 and 8 days after 
initial exposure.  Juveniles showed reduced growth at 0.08 g 
chlordecone/litre with some showing scoliosis during a 36-day 
test.  Embryo survival was reduced when adults were exposed to 
chlordecone.  When adults were exposed to 1.9 g/litre, their 
embryos developed abnormally or died, even when incubated in 
chlordecone-free water.  Fry from embryos exposed to 6.6 or 33 g 
chlordecone/litre were visibly affected within 24 h of hatching.  
Symptoms of poisoning in fry less than 1 week old included 
diminished activity, loss of equilibrium, cessation of feeding, 
and emaciation.  Fry more than 1 week old had symptoms identical 
to those in adult fish, except for haemorrhaging and oedema.  
Sixty percent of juvenile fish that had survived 36 days' 
exposure to 0.08 g chlordecone/ litre had scoliosis and 
blackened tails.  In clean water, symptoms persisted for more 
than ten days (Hansen et al., 1976). 

Table 5.  Toxicity of chlordecone for algae
Alga          Flow/  Temp    Salinity  End point    Parameter   Concentration  Reference
              stat   (C)    o/oo                               (g/litre)
 Chlorococcum  stat   200.5  30        growth       7-day EC50  0.35           Walsh et al. (1977)
 sp.                                   retardation

 Dunaliella    stat   200.5  30        growth       7-day EC50  0.58           Walsh et al. (1977)
  tertiolecta                           retardation

 Nitzschia     stat   200.5  30        growth       7-day EC50  0.60           Walsh et al. (1977)
 sp.                                   retardation

 Thalassiosira stat   200.5  30        growth       7-day EC50  0.60           Walsh et al. (1977)
  pseudonana                            retardation

Table 6.  Toxicity of chlordecone for aquatic organisms
Organism       Flow/  Temp   Salinity   End point     Parameter    Concen-      Reference                  
               stat   (C)   o/oo                                  tration                               
grass shrimp   flow                                   96-h LC50    121          Schimmel & Wilson (1977)   
 (Palaemonetes  flow   25-28  10-20                    19-day LC50  1.4          Nimmo et al. (1977)      
blue crab      flow                                   96-h LC50    >210         Schimmel & Wilson (1977)   
 (Callinectes   flow                                   48-h LC50    1000a        Butler (1963)              
easter oyster  flow   14                inhibition    96-h EC50    57a          Butler (1963)              
 (Crassostrea                            shell depos-                                                     
  virginica)                             ition                                                            
American eel   flow   19     flesh                    96-h LC50    35           Roberts & Bendl (1982)     
 stage VIA                                                                                               
sheepshead     flow                                   96-h LC50    69.5         Schimmel & Wilson (1977)   
spot           flow                                   96-h LC50    6.6          Schimmel & Wilson (1977)   
bluegill       flow   19-21                           96-h LC50    50           Roberts & Bendl (1982)     
 sunfish, juv                                                                                            
channel        flow   20-23                           96-h LC50    514          Roberts & Bendl (1982)     
 catfish, juv                                                                                            
a  Nominal concentration, not measured.
    Estimation of the long-term effects of chlordecone on 
juvenile fish, from the results of acute tests can result in 
severe underestimation.  When juvenile spot were fed sublethal 
doses of chlordecone (0.3 and 0.7 mg/kg diet per day) for 56 
days, they developed bone damage including fracturing and 
thickening of vertebrae (Stehlik & Merriner, 1983). 

    Desaiah & Koch (1975) conducted  in vitro studies on brain 
ATPase activity in channel catfish  (Ictalurus punctatus) and 
demonstrated a significant inhibition of oligomysin-sensitive 
(mitochondrial) Mg2+, oligomysin-insensitive Mg2+ and NA+-K+
ATPases with increasing concentrations of chlordecone. Inhibition 
was 25.7% and 36.7% at chlordecone concentrations of 1.25 and 2.5 
M, respectively.  The authors noted that the resulting reduction 
in energy supply could have physiological consequences.  
Winkelhake et al. (1983) showed the inducement of an acute phase 
(C-reactive) protein in the serum of rainbow trout after 
administration of chlordecone at 5 mg/kg.  The formation of these 
proteins is the initial reaction to bacteria or response to 
foreign proteins. 

8.2.  Terrestrial Organisms

    (a)  Plants

    Little work on the effects of chlordecone on plants has been 
reported.  In one experiment, chlordecone increased both the 
quality and quantity of the cotton yield (Gawaad et al., 1976).  
Residues in seeds were always, 1 mg/kg, despite different 
application rates. 

    (b)  Insects

    In a study on bees, Atkins & Anderson (1962) reported an LT50 
value for a 200 mg dose of chlordecone of 68 h.  They tested 
chlordecone in 1961 on bee colonies that had shown a progressive 
resistance to DDT over a 5-year period.  They obtained an LT50
value of 45 h for chlordecone, in 1952, when tested on a 
different strain of DDT-susceptible bees.  The authors implied 
that DDT resistance carries over to other organochlorine 
insecticides; but though lower susceptibility to chlordecone was 
shown by DDT-resistant bees, the results do not directly 
demonstrate this.  The results of later studies by Atkins et al. 
(1973) suggest that chlordecone would have to be used at 5 times 
the recommended application rate to kill 50% of bee populations.  
At the recommended usage rate of 2.25 kg/ha, chlordecone was not 
harmful to 3 out of 4 predatory insect species and arthropods, 
monitored in an apple orchard. 

    There is no information on the effects of chlordecone on 
amphibians or reptiles. 

    (c)  Birds

    Chlordecone was shown not to be very toxic when fed to either 
young or adult birds (Table 7).  Species tested were not very 
representative.  Birds fed lethal doses of the insecticide 
developed characteristic whole-body tremor, prior to death 
(DeWitt et al., 1962; Naber & Ware, 1965; McFarland & Lacy, 
1969).  Japanese quail injected daily with 0.5 mg chlordecone/
bird showed liver damage (damage to hepatic parenchymal cells, 
including disruption of mitochondria, with cellular debris in the 
bile and bile ducts), with increased numbers of phagocytic Kupffer 
cells lining the liver sinusoids (US EPA, 1979). 

    Sublethal effects of chlordecone on birds are pronounced 
despite the compound's low acute toxicity.  A sublethal dose of 
200 mg chlordecone/kg diet administered to Japanese quail caused 
structural changes in the liver, adrenals, and gonads (Eroschenko 
& Wilson, 1975).  Many sublethal effects of the compound are 
attributable to its estrogenic effects.  Dosing with chlordecone 
caused oviduct maturation in sexually immature females held on 
non-stimulatory daylengths, but mature females were not affected 
(Eroschenko & Wilson, 1975).  Ovaries from chlordecone-treated 
females contained more primary oocytes and smaller follicles than 
those from controls.  A central effect on follicle-stimulating 
hormone production was postulated by McFarland & Lacy (1969), but 
direct hormone measurement does not seem to have been carried 
out.  Estrogen-like stimulation of secondary sexual characteristics
caused male pheasants to develop female plumage at dietary doses of 
50, 100, and 150 mg chlordecone/kg (DeWitt et al., 1962).  Males 
also showed malformed sperm and reduced reproductive success.  
Eroschenko & Wilson (1975) reported effects on the testicles in 
both immature and adult quail; seminiferous tubules were distended 
with watery fluid that caused a significant weight increase in the 
testes, germinal epithelium and spermatozoa were reduced, and 
abundant intraluminal cellular debris was common. 

    Both egg laying and chick survival were reduced in domestic 
hens fed 75 or 150 mg chlordecone/kg diet for 12 weeks.  Only 56% 
of chicks hatched from hens treated with 75 mg/kg survived for 20 
days, no chicks or hens treated with 100 mg/kg survived.  Residues 
were still detectable in eggs laid 3 weeks after treatment ceased 
(Naber & Ware, 1965).  Eggshell deposition was affected by 
chlordecone.  A peculiarly thick spongy layer developed leading to 
blockage of shell pores and suffocation of the embryo (Erben, 
1972).  Changes in shell structure occurred in Japanese quail fed 
225 mg chlordecone/kg diet (US EPA, 1979). 

    There is no information on the toxicity of chlordecone for
non-laboratory mammals.

Table 7.  Toxicity of chlordecone for birds
Species               Age     Route   Parameter   Concentration   Reference
mallard duck          young   diet    LC50        400             Dewitt et al. (1962)

bobwhite quail        young   diet    LC50        600             Dewitt et al. (1962)

bobwhite quail        adult   diet    LC50        530             Dewitt et al. (1962)

ringnecked pheasant   young   diet    LC50        600             Dewitt et al. (1962)

ringnecked pheasant   adult   diet    LC50        115             Dewitt et al. (1962)
8.3.  Microorganisms

    Effects of chlordecone on soil microorganisms were investigated 
by Gawaad et al. (1972a).  Application of chlordecone to 3 soil 
types in the Nile Delta altered fungal, actinomycete, and other 
bacterial populations for as long as 45 days, compared with 
controls (Gawaad et al., 1972a).  Unfortunately, chlordecone was 
applied at a very high rate (22.0 kg/ha) and therefore the results 
are difficult to interpret in terms of likely effects on crops.  
The magnitude and duration of effects on populations differed with 
soil type, but the general pattern was a fall in numbers in the 
first week followed by an increase in the second week with numbers 
eventually returning to normal levels.  In a second experiment in 
which effects on nitrogen transformation in treated soils were 
studied, chlordecone was shown to affect fungi and bacteria 
responsible for ammonification, and  Nitrobacter, which is 
responsible for changing nitrite to nitrate, but not  Nitrosomonas, 
which is responsible for changing ammonia to nitrite (Gawaad et 
al., 1972b). 

    Similar effects on microbial populations were found by Meyers 
et al. (1982), when chlordecone at 0.5 mg/litre was applied to 
static carbon metabolism microcosms; no significant total 
treatment variation was seen in either bacterial or fungal 
populations after 10 days incubation.  Similar results were 
obtained in response to continuous application of chlordecone.  
Chlordecone is probably highly toxic for sludge microorganisms, 
since massive amounts of beneficial bacteria in a sludge digester 
were killed after chlordecone wastes were discharged into the 
sewage system (Bray, 1975).  Portier & Meyers (1982) stated that 
microcosms (simulated aquatic microenvironmental systems) were 
"sensitive" to chlordecone "under a variety of regimes".  Among 
response criteria used were microbial diversity, enzymatic 
activity, ATP, and material turnover. 

    The toxicity of chlordecone for mixed populations of 
microorganisms was determined by standard plate assays on Zobell 
marine medium containing 0.02, 0.2, or 2 mg chlordecone/litre 
(Mahaffey et al., 1982).  All these concentrations of chlordecone 

reduced the number of colony-forming aerobes but did not affect 
anaerobes.  Gram-positive organisms were more sensitive to 
chlordecone than gram-negative organisms.  Oxygen uptake by gram-
negative isolates was reduced by 25 - 100% by chlordecone at 20 
mg/litre.  A significant reduction in the specific activities of 
NADH oxidase and succinooxidase by the addition of chlordecone at 
0.49 mg/litre indicated that chlordecone can inhibit electron 

8.4.  Bioaccumulation and Biomagnification

    Data on the bioconcentration of chlordecone are given in Table 
8.  It should be noted that none of the exposures were representative 
of realistic environmental levels.  Bioaccumulation in detritus, 
such as decomposing  Spartina cyanosuroide, was demonstrated by 
Odum & Drifmeyer (1978).  As detritus is a major energy source in 
aquatic environments, this could represent an important entrance 
for chlordecone into aquatic food webs.  Both aquatic invertebrates 
and fish bioaccumulate chlordecone to very high levels.  Depuration 
is slow in fish, thus residues tend to be high.  Levels of chlordecone 
accumulated in edible fillets were almost the same as the whole 
body concentrations in sheepshead minnows and spot; therefore one 
of the largest residue reserves in contaminated fish is in the 
edible portion (Bahner et al., 1977). 

    Residues were higher in female sheepshead minnows than in males 
(Bahner et al., 1977), and residues in juveniles tended to increase 
with increasing concentrations of chlordecone in the water (Hansen 
et al., 1976).  When chlordecone was fed to juvenile spot for 28 
days, the body burden of chlordecone increased additively and 
equilibrium was not attained (Stehlik & Merriner, 1983).  Chlordecone 
accumulation in an estuarine food chain (composed of green algae, 
oysters, mysids, grass shrimps, sheepshead minnows, and spot) 
occurred at concentrations as low as 0.023 g/litre (Bahner et al., 
1977).  All species had equilibrated tissue concentrations of 
chlordecone 8 - 17 days after the beginning of the exposure.  
Clearance of chlordecone from oysters was rapid; levels were non-
detectable, 7 - 20 days after exposure ceased.  Clearance was slow 
in shrimp and fish, with tissue levels of chlordecone decreasing by 
30 - 50% in 24 - 28 days.  When oysters were fed chlordecone-
contaminated algae, the maximum overall accumulation and transfer 
of chlordecone (or "food-chain potential") from water to algae and 
then to oysters was 2.1 (Bahner et al., 1977).  However, the 
transfer potential (transfer from one trophic level to the next) 
from algae to oysters was only 0.007; therefore, transfer of 
chlordecone from algae to oyster and retention in oyster were 
inefficient.  When spot were fed mysids that had eaten chlordecone-
contaminated brine shrimp, the food-chain potential from water to 
brine shrimp to mysids and finally to fish ranged from 3.9 to 10.5.  
The transfer potential from shrimp to mysids was 0.53 and from 
mysids to spot, 0.85.  This indicated that much of the chlordecone 
was being transferred through the trophic levels. 

    No data are available on the bioconcentration of chlordecone 
by terrestrial organisms. 

Table 8.  Bioaccumulation of chlordecone
Organism            Temp   Salinity Flow/   Bioconc.   Exposure      Time        Reference                        
                    (C)   o/oo     stat    factor     concentration                                              
                                            (BCF)      (g/litre)                                                 
algae,              19.5-  30       stat    230-800    100           24 h        Walsh et al. (1977)              
unicellular         20.5                                                                                          
oyster                                      9354       0.03          19 d        Bahner et al. (1977)             
 (Crassostrea                                9278       0.39          21 day                                       
grass shrimp                                698        12-121        96 h        Schimmel & Wilson                
 (Palaemonetes                              (425-933)                            (1977)                           
 pugio)                                      5127       0.023         28 day      Bahner et al. (1977)             
                                            11425      0.4           28 day      Bahner et al. (1977)             
spot                                        3217       0.029         30 day      Bahner et al. (1977)             
spot                                        1120       1.5           96 h        Bahner et al. (1977)             
fathead minnow                      flow    16600      0.004         56 day      Huckins et al. (1982)            
sheepshead minnow,  28-32  11-31    flow    1800       0.041         life        Goodman et al. (1982)            
juv 21-day                                                           cycle test                            
sheepshead minnow,  28-32  11-31    flow    2400       0.041         life        Goodman et al. (1982)            
juv 42-day                                                           cycle test                            

Table 8.  (contd.)
Organism            Temp   Salinity Flow/   Bioconc.   Exposure      Time        Reference                        
                    (C)   o/oo     stat    factor     concentration                                              
                                            (BCF)      (g/litre)                                                 
sheepshead minnow   28-32  11-31    flow    3900       0.041         life        Goodman et al. (1982)            
adult male                                                           cycle test                                   
sheepshead minnow   28-32  11-31    flow    3700       0.041         life        Goodman et al. (1982)            
adult female                                                         cycle test                                   
sheepshead minnow,  28-32  11-31    flow    2900       0.041         life        Goodman et al. (1982)            
embryos                                                              cycle test                                   
sheepshead minnow,  28-32  11-31    flow    2400       0.041         life        Goodman et al. (1982)            
juvenile progeny                                                     cycle test                                   
8.5.  Population and Community Effects

    Chlordecone is strongly adsorbed on sediment.  Effects on 
aquatic organisms are therefore partly from material in the water 
and partly from material obtained from sediment.  D'Asaro & Wilkes 
(1982) examined the effects of sediments, previously exposed to 
chlordecone at a known concentration, and of James River sediments 
contaminated with chlordecone, on an estuarine community established 
in aquaria supplied with non-filtered sea water.  Mysid shrimps 
showed a dose-related mortality rate, when exposed to sediments 
previously equilibrated at 0.1, 1.0, or 10 g chlordecone/litre.  
Mysids were not affected by James River sediment.  Oysters showed 
dose-dependent reduced shell growth, when exposed to chlordecone-
equilibrated sediments, and also responded adversely to river 
sediment.  Lugworms  Arenicola cristata disappeared from aquaria 
after 28 days of treatment with sediment exposed to 10 g 
chlordecone/litre, though numbers were not affected by lower doses.  
Both lugworms and oysters concentrated chlordecone from the 

8.6.  Effects on the Abiotic Environment

    No data are available on the effects of chlordecone on the 
abiotic environment. 

8.7.  Appraisal

    As actual levels of chlordecone in natural waters are extremely 
low, because most of the chlordecone is transferred rapidly to 
sediments, bioconcentration and toxicity test levels are often 
unrealistically high.  However, bearing in mind the potential for 
bioaccumulation, data suggest that chlordecone is both acutely and 
chronically toxic for aquatic organisms.  A major omission in the 
aquatic toxicity data is the toxicity of chlordecone for detritus 
feeders that will be exposed to significant concentrations in 
contaminated sediments.  Exposure of the lowest level of the 
aquatic food chain to concentrations of chlordecone above a 
threshold of 0.35 - 1 mg/litre will cause disturbance or destruction, 
sufficient to affect productivity at other levels of the food chain.  
Few data are available on the sublethal effects of chlordecone on 
aquatic organisms.  In fish, such effects include:  retardation of 
growth, which will ultimately affect fecundity, scoliosis, inhibition 
of ATPase; and stimulation of some immune response.  Juvenile fish 
appear to be less sensitive to chlordecone than adults. 

    Chlordecone appears to have little effect on soil 
microorganisms at concentrations that would result from 
agricultural use.  However, discharges directly into sewage 
systems are highly toxic for sludge microbes.  Agricultural 
application rates cause little acute toxicity to non-target 
invertebrates or birds, but chlordecone at higher dosages can 
have pronounced effects on many reproductive variables in birds.  
No data are available on effects on amphibia, reptiles, or non-
laboratory mammals. 


    IARC (1979) evaluated the carcinogenic hazard resulting from 
exposure to chlordecone and concluded that "there is sufficient 
evidence for its carcinogenicity in rats and mice.  In the absence 
of adequate data in humans, it is reasonable for practical  
purposes to regard chlordecone as if it presented a carcinogenic 
risk to humans". 

    No acceptable daily intake (ADI) for chlordecone has been 
proposed by FAO/WHO. 

    In recent years, official registrations for a number of uses 
of chlordecone have been withdrawn in certain countries for 
various reasons (IRPTC, 1983). 

    Regulatory standards established by national bodies in 12 
different countries (Argentina, Brazil, Czechoslovakia, the 
Federal Republic of Germany, India, Japan, Kenya, Mexico, Sweden, 
the United Kingdom, the USA, and the USSR) and the EEC can be 
found in the International Register of Potentially Toxic 
Chemicals Legal File (IRPTC, 1983). 


10.1.  Chlordecone Toxicity

    Chlordecone is moderately toxic in acute studies on rats, 
i.e. the oral LD50 values range from 95 to 132 mg/kg body weight.  
It can enter the body via ingestion, inhalation, and via the 
skin.  It is not metabolized to any significant extent.  It 
bioaccumulates mainly in the liver, and it is excreted very 
slowly via the faeces. 

    Toxic effects include neurological symptoms, especially 
tremors, liver hypertrophy with enzyme induction, centrilobular 
hepatocellular necrosis, and hepatobiliary dysfunction.  It can 
impair reproduction (mouse, 10 mg/kg diet or 0.5 mg/kg body 
weight per day) and is fetotoxic (rat, 2 mg/kg body weight per 

    Chlordecone was not generally active in short-term tests for 
genetic activity.  There is sufficient evidence of its 
carcinogenicity for mice and rats. 

    Careless occupational handling in a manufacturing plant 
caused a series of poisonings with neurological symptoms, 
especially nervousness and tremors, oligospermia, and joint 

10.2.  Exposure to Chlordecone

    Exposure of the general population through the normal use of 
chlordecone can be regarded as minimal and is mainly related to 
residues in food. 

    Small children may be exposed when playing with insect traps. 

10.3.  Effects on the Environment

    The environmental hazard posed by chlordecone is associated 
with its stability and persistence in sediments, which provide a 
long-term source of contamination, in conjunction with its massive 
bioaccumulation in aquatic food chains.  One of the largest 
reserves of chlordecone in food is in the edible portion of 
contaminated fish.  Although chlordecone has a low solubility in 
water, between 0.35 and 1 mg/litre is sufficient to reduce algal 
growth, thereby affecting productivity at other trophic levels.  
Chlordecone is acutely and chronically toxic for aquatic 
invertebrates and causes loss of equilibrium, reduction in 
reproductive success, and decreased shell growth at sublethal 
concentrations.  Reduction in mysid populations due to low-level 
chlordecone contamination has important consequences for fish 
productivity.  Symptoms of exposure range from diminished activity 
and emaciation to abnormal development and death. 

    The few data available indicate that chlordecone is not 
acutely toxic for terrestrial invertebrates.  Subacute doses of 
chlordecone induce significant toxic effects in birds including 
tremors, liver damage, and reproductive failure. 

    Excretion of chlordecone is extremely slow.

10.4.  Conclusions

1.  Serious illness has been suffered by workers occupationally 
    over-exposed to chlordecone.

2.  Based on the findings in mice and rats, this chemical should 
    be considered, for practical purposes, as being potentially 
    carcinogenic for human beings. 

3.  For the above reason, reservations must remain about the 
    occurrence of residues of chlordecone in food. 

4.  Adverse effects on the organisms studied, as well as 
    persistence, suggest that chlordecone presents a long-term 
    hazard for the environment. 

5.  Taking into account these considerations, it is felt that the 
    use of this chemical should be discouraged, except where there 
    is no adequate alternative. 


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KLINGENSMITH, J.S. & MEHENDALE, H.M.  (1982b)  Potentiation of
CCl4 lethality by chlordecone.  Toxicol. Lett.,  11: 149-154.

LANGFORD, H.D.  (1978)  Kepone, mirex pesticide residues
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BORZELLECA, J.F.  (1979b)  Acute, subchronic, and chronic
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LEWIS, R.G. & LEE, R.E.  (1976)  Air pollution from
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MADY, N., SMITH, D., SMITH, J., & WEZWICK, C.  (1979)
Analysis of Kepone in biological samples.  NBS (US) Spec.
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S.A.  (1976)  Kepone poisoning ultrastructure of nerves and
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ISAACS, E.  (1978)  Chlordecone intoxication in man: II.
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McFARLAND, L.Z. & LACY, P.B.  (1969)  Physiologic and
endocrinologic effects of the insecticide Kepone in the
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MEHENDALE, H.M.  (1979)  Modification of hepatobiliary
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Effect of pre-exposure to Kepone on hepatic mixed-function
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MEYERS, S.P., GAMBRELL, & DAY,  (1982)   Determination of
 environmental impact of several substitute chemicals in
 agricultural affected wetlands,  Washington DC, US
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(1977)  Electron capture gas chromatographic determination of
Kepone residues in environmental samples.  Arch. environ.
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MOSEMAN, R.F., WARD, M.K., CRIST, H.L., & ZEHR, R.D.  (1978)
A micro derivatization technique for the confirmation of trace
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MOTL, M.L.  (1977)  EPA develops process to destroy Kepone.
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ODUM, W.E. & DRIFMEYER, J.E.  (1978)  Sorption of pollutants
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REITER, L. & KIDD, K.  (1978)  The behavioral effects of
subacute exposure to Kepone or mirex on the weanling rat.
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L.E., Jr  (1977)  Comparative behavioural toxicology of mirex
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REUBER, M.D.  (1977)  Kepone carcinogenicity affirmed by
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REUBER, M.D.  (1978)  Carcinogenicity of Kepone.  J. Toxicol.
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REUBER, M.D.  (1979)  The carcinogenicity of Kepone.  J.
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ROBERTS, M.H., Jr & BENDL., R.E.  (1982)  Acute toxicity of
Kepone to selected freshwater fish.  Estuaries,  5: 158-164.

Neurotoxicity of Kepone in perinatal rats following  in utero
exposure.  Toxicol. appl. Pharmacol.,  41: 142-143 (Abstract 28).

SALEH, F.Y. & LEE, G.F.  (1978)  Analytical methodology for
Kepone in water and sediment.  Environ. Sci. Technol.,  12:

SALEH, F.Y., LEE, G.F., & BUTLER, J.S.  (1978)  Kepone and
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SCHIMMEL, S.C. & WILSON, A.J. Jr  (1977)  Acute toxicity of
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SHANHOLTZ, M.I.  (1976)   Emergency rule, Virginia State Board
 of Health. Prohibiting the taking of crabs from the James
 River and its tributaries and the taking of fish for human
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(1978)  Failure of Kepone and hexachlorobenzene to induce
dominant lethal mutations in the rat.  Toxicol. appl.
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SNEGAROFF, J.  (1977)  Organochlorine insecticidal residues in
the soil and rivers of banana-growing region of Guadeloupe.
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STEHLIK, L.L. & MERRINER, J.V.  (1983)  Effects of accumulated
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STERRETT, F.S. & BOSS, C.A.  (1977)  Careless Kepone.
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SUTA, B.E.  (1978)   Human population exposures to mirex and
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(1978)  Chlordecone intoxication in man. I. Clinical
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TILSON, H.A., BYRD, M., & RILEY, M.  (1979)  Neurobehavioral
effects of exposing rats to Kepone via the diet.  Environ.
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US EPA  (1976a)   Preliminary report on Kepone levels found in
 environmental samples from the Hopewell, Virginia area,
Research Triangle Park, North Carolina, US Environmental
Protection Agency, Health Effects Research Laboratory.

US EPA  (1976b)   Review of the Chesapeake Bay Program. Seminar
 on kepone held at Virginia Institute of Marine Sciences, 12-13
 October, 1976,  Research Triangle Park, North Carolina, US
Environmental Protection Agency.

US EPA  (1979)   Reviews of the environmental effects of
 pollutants. 1. Mirex and Kepone,  Washington DC, US
Environmental Protection Agency (EPA Report No.
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US FDA  (1977)   Compliance program evaluation-FY77 Kepone and
 mirex contamination,  Washington DC, US Department of Health,
Education and Welfare.

WALSH, G.E., AINSWORTH, K., & WILSON, A.J., Jr  (1977)
Toxicity and uptake of Kepone in marine unicellular algae.
 Chesapeake Sci.,  18: 222-223.

WILLIAMS, G.M.  (1980)  Classification of genotoxic and
epigenetic hepatocarcinogens using liver culture assays.  Ann.
 N.Y. Acad. Sci.,  349: 273-282.

Induction in rainbow trout of an acute phase (C-reactive)
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    See Also:
       Toxicological Abbreviations
       Chlordecone (HSG 41, 1990)
       Chlordecone (ICSC)
       Chlordecone (IARC Summary & Evaluation, Volume 20, 1979)