This report contains the collective views of an international group of
    experts and does not necessarily represent the decisions or the stated
    policy of the United Nations Environment Programme, the International
    Labour Organisation, or the World Health Organization.

    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    Draft prepared by Professor D. Beritc-Stahuljak and Professor
    F. Valic (University of Azgreb, Croatia) using texts made
    available by Dr R. Millischer (ATOCHEM, Paris, France), 
    Dr. S. Magda (Kali-Chemie, Hanover, Germany), Mr D.J. Tinston
    (ICI Central Toxicology Laboratory, United Kingdom), Dr. H.J.
    Trochimowicz (E.I. Du Pont de Nemours, Newark, Delaware, USA)
    and Dr G.M. Rusch (Engineered Materials Sector, Allied-Signal Inc.,
    Morristown, New Jersey, USA).

    World Health Orgnization
    Geneva, 1984

         The International Programme on Chemical Safety (IPCS) is a
    joint venture of the United Nations Environment Programme, the
    International Labour Organisation, and the World Health
    Organization. The main objective of the IPCS is to carry out and
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    toxicology. Other activities carried out by the IPCS include the
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    1.1. Identity, analytical methods, and sources of exposure
         1.1.2. Environmental concentrations and exposures
         1.1.3. Kinetics and metabolism
         1.1.4. Studies on experimental animals
         1.1.5. Effects on man
         1.1.6. Effects on the environment
    1.2. Recommendations


    2.1. Identity
    2.2. Properties and analytical methods
         2.2.1. Physical and chemical properties
         2.2.2. Analytical methods


    3.1. Uses
    3.2. Transport and distribution
    3.3. Levels of exposure


    4.1. Animal studies
    4.2. Human studies


    5.1. Short-term exposures
         5.1.1. Single exposure
         5.1.2. Repeated exposure
    5.2. Long-term exposures
    5.3. Reproduction studies
    5.4. Mutagenicity
    5.5. Teratogenicity
    5.6. Carcinogenicity
    5.7. Factors influencing toxicity


    6.1. Poisoning incidents
    6.2. Occupational exposure
    6.3. Treatment of poisoning


    7.1. Toxicity for aquatic organisms
    7.2. Toxicity for terrestrial organisms
         7.2.1. Plants
         7.2.2. Honey bees
         7.2.3. Birds
    7.3. Toxicity for microorganisms
    7.4. Bioaccumulation



    9.1. Evaluation of health risks for man
    9.2. Evaluation of overall environmental effects
    9.3. Conclusions




Dr E. Astolfi, Faculty of Medicine of Buenos Aires, Buenos
   Aires, Argentina

Dr I. Desi, Department of Environmental Hygienic Toxicology,
   National Institute of Hygiene, Budapest, Hungary

Dr R. Drew, Department of Clinical Pharmacology, Flinders
   University of South Australia, Bedford Park, South

Dr S.K. Kashyap, National Institute of Occupational Health,
   Ahmedabad, India

Dr A.N. Mohammed, University of Calabar, Calabar, Nigeria

Dr O.E. Paynter, Office of Pesticide Programs, US
   Environmental Protection Agency, Washington DC, USA

Dr W.O. Phoon, Department of Social Medicine and Public
   Health, Faculty of Medicine, University of Singapore,
   Outram Hill, Singapore  (Chairman)

Dr D. Wassermann, Department of Occupational Health, The
   Hebrew University, Hadassah Medical School, Jerusalem,

 Representatives of Other Organizations

Dr H. Kaufmann, International Group of National Associations
   of Agrochemical Manufacturers (GIFAP)

Dr V.E.F. Solman, International Union for Conservation of
   Nature and Natural Resources (IUCN), Ottawa, Ontario,


Dr S. Dobson, Institute of Terrestrial Ecology, Monks Wood
   Experimental Station, Abbots Ripton, Huntingdon, United
   Kingdom  (Temporary Adviser)

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

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

 Secretariat (contd.)

Dr D.C. Villeneuve, Health Protection Branch, Department of
   National Health and Welfare, Tunney's Pasture, Ottawa,
   Ontario, Canada (Temporary Adviser)  (Rapporteur)

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 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 (Endosulfan, Quintozene, 
Tecnazene, Tetradifon) was held at the Health Protection Branch, 
Department of National Health and Welfare Ottawa from 28 May - 1 
June, 1984.  The meeting was opened by Dr E. Somers, Director- 
General, Environmental Health Directorate, and Dr K.W. Jager 
welcomed the participants on behalf of the three co-sponsoring 
organizations of the IPCS (UNEP/ILO/WHO).  The Task Group reviewed 
and revised the draft criteria document and made an evaluation of 
the health risks of exposure to endosulfan. 

    The drafts of this document were 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. 



1.1.1.  Identity, analytical methods, and sources of exposure

    Technical endosulfan (6,7,8,9,10, 10-hexachloro-1,5,5a,6,9,9a, 
hexahydro 6,9-methano-2,4,3-benzodioxathiepin, 3-oxide) is a brown 
crystalline substance consisting of alpha- and beta-isomers in the 
ratio of approximately 70:30.  It is used in a formulated form as a 
broad-spectrum contact and stomach insecticide mainly in agriculture 
and, in some countries, in public health. 

    The method of choice for its determination is gas chromatography 
combined with electron capture detection.  In considering residue 
levels, the sum of the alpha- and beta-isomers plus the endosulfan 
sulfate metabolite, which is similar in toxicity to the parent 
compound, have to be considered. 

    The main source of exposure of the general population is food, 
but residues have generally been found to be well below the FAO/WHO 
maximum residue limits.  Because of its use in tobacco farming, 
smoking may be an additional source of endosulfan exposure. 

1.1.2.  Environmental concentrations and exposures

    Both endosulfan isomers are fairly resistant to photo-
degradation, but the metabolites endosulfan sulfate and endosulfan 
diol are susceptible to photolysis.  Its half-life in water is 
estimated to be 4 days, but anaerobic conditions and/or a low pH 
will lengthen the half-life.  In water, it is mainly degraded to 
endosulfan diol.  Fish are extremely sensitive to endosulfan and 
fish kills have been reported as a result of the discharge of 
endosulfan into rivers.  Agricultural run-off has not caused such a 

    In soil, the alpha-isomer disappears more rapidly than the beta-
isomer.  Endosulfan sulfate is the major degradation product in 
soil.  These compounds are not prone to leaching. 

    Biodegradation in soil and water is dependent on climatic 
conditions and on the type of microorganisms present. 

1.1.3.  Kinetics and metabolism

    Endosulfan can be absorbed following ingestion, inhalation, and 
skin contact.  Following oral or parenteral dosing, it is rapidly 
excreted via faeces and urine.  Following acute over-exposure, high 
endosulfan concentrations can temporarily be found in the liver; 
the concentration in plasma decreases rapidly.  The major 
metabolities are endosulfan sulfate and endosulfan diol. 

1.1.4.  Studies on experimental animals

    Endosulfan is moderately to highly toxic according to the scale 
of Hodge & Sterner (1956).  The oral LD50 in the rat ranges from 18 
to 355 mg/kg body weight.  WHO (1984) classified endosulfan in 
Class II: technical products moderately hazardous.  One of its 
metabolites, endosulfan sulfate, has the same order of toxicity as 

    Signs of acute intoxication include neurological manifestations, 
such as hyperactivity, muscular twitching, and convulsions, some- 
times followed by death. 

    In rats, induction of hepatic mixed-function oxidases was 
observed after administration of endosulfan for 7 days at 2.5 mg/kg 
body weight per day.  At higher doses (100 mg/kg in the diet for 
104 weeks), testicular atrophy and renal tubular damage with 
interstitial nephritis were observed.  The long-term, no-observed-
adverse-effect level in rats was 30 mg/kg of diet (1.5 mg/kg body 
weight) and 0.75 mg/kg body weight in dogs.  Protein-deficient rats 
are more sensitive to acute toxic effects of endosulfan. 

    Adequate data were not available on effects on reproduction, or 
teratogenic or embryotoxic effects.  Negative or conflicting 
results were obtained in short-term tests for genetic activity.  
Carcinogenicity studies on mice and rats were difficult to evaluate 
because of inadequate reporting or early death in males; however, 
there was no indication of carcinogenic activity in females. 

1.1.5.  Effects on man

    Several cases of accidental and suicidal poisoning have been 
reported.  In fatal cases, death occurred within a few hours of 
ingestion.  Signs of poisoning included vomiting, restlessness, 
irritability, convulsions, pulmonary oedema, and cyanosis.  EEG 
changes have been reported in occupationally overexposed persons.  
Cases of poisoning in production workers have been reported, but 
occurred only when safe handling procedures were neglected. 

1.1.6.  Effects on the environment

    Endosulfan is not readily bioaccumulated and it is not 
persistent in biological tissues.  It is hazardous as an acute 
poison for some aquatic species, particularly fish, even at 
application rates recommended for wetland areas.  It is moderately 
toxic for honey bees.  It is moderately to highly toxic for birds 
in a laboratory setting, but no poisonings have been reported under 
field conditions. 

1.2.  Recommendations

    1.  Precautions should be taken to avoid contamination 
        of surface and drinking-water supplies during
        spraying.  Where necessary, residue levels of 
        endosulfan in drinking-water should be reduced by 
        proper water treatment.

    2.  In countries where endosulfan is used for tsetse
        fly control, exposed populations should be monitored
        for potential adverse health effects.

    3.  Research is required to determine whether biological 
        monitoring can be used as an early warning of 
        endosulfan exposure.

    4.  Further research is required to investigate possible
        reproductive, teratological, and embryotoxic effects.

    5.  An adequate carcinogenicity study should be
        carried out.


2.1.  Identity

Chemical Structure

Molecular formula:            C9H6Cl6O3S

CAS chemical name:            6,7,8,9,10,10-hexachloro-1,5,5a,6,9,9a

Common trade names:           Benzoepin, Beosit, Chlorthiepin,
                              Cyclodan, FMC 5462, Insectophene,
                              Kop-thiodan, HOE 2671, Malix,
                              NCI-C00566, NIA 5462, Thifor,
                              Thimul, Thiodan, Thiofor, Thiomul,
                              Thionex, Thiosulfan, Tionel, Tiovel.
                              Formulations under other trade names
                              may also exist.

CAS registry number:          115-29-7

Relative molecular mass:      406.9

    Endosulfan was developed and introduced in the mid 1950s 
(Maier-Bode, 1968).  Technical endosulfan is obtained through the 
Diels-Alder addition of hexachlorocylopentadiene and cis-butene-
1,4-diol, followed by reaction of the addition-product with thionyl 
chloride (Canada, National Research Council, 1975).  Technical 
endosulfan consists of a mixture of alpha- and beta-isomers in the 
approximate ratio of 70:30. 

2.2.  Properties and Analytical Methods

2.2.1.  Physical and chemical properties

    Technical endosulfan is usually sold in the form of brown 
crystalline flakes with a terpene odour (Maier-Bode, 1968).  It has 
a melting point of 79 - 100C (Canada, National Research Council, 
1975) and a vapour pressure of 1 x 10-5 mm Hg at 25C.  Its 
solubility in water is low:  60 - 150 g/litre (Canada, National 
Research Council, 1975), and increases with decreasing pH 
(Shuttleworth, 1971).  Solubility in other solvents varies from 5 - 
65% (Maier-Bode, 1968; Canada, National Research Council, 1975). 

    Endosulfan is available as a wettable powder, granules, 
emulsifiable concentrates, dusts, and as ultra-low-volume (ULV) 

2.2.2.  Analytical methods

    Methods for the clean-up and determination of endolsulfan have 
been summarized by Maier-Bode (1968), Canada, National Research 
Council (1975), and Goebel et al., (1982), but the sensitivities 
and recoveries for the various methods are not always given.  
Although colorimetric techniques, thin-layer chromatography, and 
bio-assays have been used for the determination of endosulfan, the 
most recent method involves a combination of gas chromatography 
with electron capture detection (GC-EC). 

    The sensitivity of assays in water ranged from 0.01 - 2.0 
g/litre with recoveries generally greater than 90% (Wegman & 
Greve, 1978; 1980;  Frank et al., 1979a).  In soil and sediment, 
assays were not as sensitive, ranging from 0.001 to 0.1 mg/kg with 
recoveries between 80 - 110% but usually less than 90% (Miles & 
Harris, 1973; Frank et al., 1976; Carey et al., 1979).  Biological 
samples such as animal and plant tissues, milk, etc., normally 
require more extensive clean-up procedures (i.e., column methods).  
Sensitivities from 0.2 to 10 g/kg were usual with most recoveries 
greater than 90% (Cheng & Braun, 1977; Chopra & Mahfouz, 1977; 
Frank et al., 1979a; Zanini et al., 1980).  Samples with a high 
sugar content gave erroneous results, but methods have been 
developed to overcome the problem (Shuttleworth, 1971).  Clean-up 
methods employing high-pressure liquid chromatography (HPLC) have 
been used, which reduce the time involved in the preparation of 
such samples (Demeter & Heyndrickx, 1979). 

    It should be noted that detection limits for the alpha- and 
beta-isomers of endosulfan usually differ, the alpha-isomer being 
easiest to detect (Goebel et al., 1982).  At low concentrations, 
the identification of endosulfan residues can be hampered by a 
variety of other pesticides or plant components.  Endosulfan 
residues in environmental samples can only be considered to be 
valid if alpha- and beta-together with endosulfan sulphate are 
found simultaneously.  Validation can be achieved by methods 
summarized by Goebel et al. (1982). 


3.1.  Uses

    Endosulfan is a contact and stomach poison that has been used 
to control insects such as the Colorado potato beetle, flea beetle, 
cabbageworm, peach tree borer, and tarnished plant bug, as well as 
several species of aphid and leafhopper (Canada, National Research 
Council, 1975).  It is used in countries throughout the world to 
control pests on fruit, vegetables, tea, and on non-food crops such 
as tobacco and cotton (FAO/WHO, 1968).  Depending on the type of 
crop and the area in which it is grown, application rates usually 
range between 0.45 kg ai and 1.4 kg/ha, but both smaller and larger 
doses have occasionally been used.  Minimum time intervals between 
the last application and harvesting are prescribed in most 
countries and vary between 0 and 42 days, depending on the crop, 
type of formulation used, the mode of application, tolerances, and 
agronomic needs (Hoechst, 1977). 

    In addition to its agricultural use, and its use in the control 
of the tsetse fly, endosulfan is used as a wood preservative and 
for the control of home garden pests (Canada, National Research 
Council, 1975).  A list of uses together with respective quantities 
used in some countries appear in Table 1. 

    Figures for world production are not available but, after DDT 
was banned, the use of endosulfan in Canada increased quite rapidly 
until the mid 1970s (Canada, National Research Council, 1975).  At 
present, world production might be in the order of 10 000 tonnes 
per year. 

    An estimated several tens of thousands of drums containing 
chemical waste including endosulfan, which have been found in and 
along the North Sea, are a potential source of pollution (Greve, 

3.2.  Transport and Distribution


    Endosulfan is most frequently applied using air-blast equipment 
or boom sprayers with a resulting potential for local drift and air 
pollution.  Keil et al. (1972) included 4-metre guard rows between 
treated and control plots.  The day after treatment, endosulfan 
levels of 0.091 - 0.529 mg/kg were found in the control plots, 
indicating a considerable drift of the insecticide between the 
plots.  Eighteen days after treatment, an endosulfan level of 0.037 
mg/kg was still detectable in the control plots.  Endosulfan was 
also found in the water and sediments of streams adjacent to 
sprayed crops (Canada, National Research Council, 1975). 

Table 1.  Usage data for endosulfan from selected countriesa
Area      Quantity      Year     Uses
Colombia  21 834 kg     1982     agricultural insecticide recommended
          15 918 kg     1981     in the growth of cotton, rice, corn,
          16 868 kg     1980     cabbage, sorghum

Malaysia                         insecticide

Sweden    2000 kg       1981     horticultural use against insects
                                 and mites

Tanzania  2130 tonne    1980-83  applied to various crops to control
                                 chewing, mining, and sucking pests

Thailand  63 420 kg     1982     insecticide
          114 800 kg    1981
          99 550 kg     1980
          27 587 kg     1979
          24 519 kg     1978
          18 482 kg     1977
          1540 kg       1976

United    27.58 tonne   1975-79  insecticide and acaricide
Kingdom   per year

USA       511-704 tonne 1980     insecticide on various crops;
          454 tonne     1971     insecticide on potatoes, tobacco,
                                 and fruits
a  From: IRPTC, personal communication, 1984.

    Residues of alpha- and beta-endosulfan have been detected in 
ambient air samples in the USA (Alabama, Arkansa, Illinois, Kansas, 
Kentucky, Louisiana, Maine, Montana, New Mexico, North Carolina, 
Ohio, Oklahoma, Oregon, Pennsylvania, South Dakota, Tennessee), 
though not frequently (Kutz et al., 1976).  Between 1970 and 1972, 
alpha-endosulfan was found in 2.11% of samples tested in the USA at 
a mean concentration of 111.9 ng/m3 and a maximum of 2256 ng/m3.  
During the same period, beta-endosulfan was present in 0.32% of the 
samples at a mean of 22.0 ng/m3 and a maximum concentration of 54.5 
ng/m3.  This information suggests that the alpha-isomer is more 
persistent in air.  Both alpha- and beta-endosulfan have been 
detected at levels up to 12 ng/litre in precipitation in the Great 
Lakes area of Canada and the USA (Strachan et al., 1980). 


    Endosulfan contamination does not appear to be widespread in 
the aquatic environment but has been found in agricultural run-off 
and rivers in industrialized areas where it is manufactured or 
formulated.  Estimates for the aquatic half-life of both isomers of 
endosulfan range from 4 days in river water subjected to municipal 
and industrial runoff (Eichelberger & Lichtenberg, 1971) to 7 days

(Greve, 1971a) in normal water (pH 7, with normal oxygen 
saturation).  However, the half-life was profoundly affected by pH 
and oxygen content; a drop in either of these two parameters 
inhibited endosulfan degradation.  Under anaerobic conditions at pH 
7, the half-life increased to approximately 5 weeks, and at pH 5.5, 
the half-life was nearly 5 months (Greve, 1971a).  More than 80% of 
the endosulfan present can be removed from water by filtration and 
almost all by treatment with activated charcoal (Greve, 1971a). 

    Studies of endosulfan in agricultural run-off, in the USA, 
indicate that, if rain follows within 4 days of application (0.35 
kg/ha), residues can average 16 g/litre run-off (Epstein & Grant, 

    A widespread fish kill was observed in 1969, when an estimated 
quantity of 30 kg of endosulfan was discharged into the section of 
the Rhine river that runs through the Federal Republic of Germany 
(Sievers et al., 1972).  Annual monitoring of endosulfan (drinking 
water, ground water, rain water, surface water) since 1969 in the 
Netherlands has revealed that maximum levels have dropped 
approximately 3 orders of magnitude, with maximum concentrations in 
1977 of 0.03 g/litre (Wegman & Greve, 1980). 

    Endosulfan was found only once in rivers draining orchard areas 
in Ontario, during 2-week sampling periods in 1973 at levels 
ranging from 0.47 to 0.083 g/litre (Frank, unpublished data, 
1973).  Studies on water samples from Lake Erie, Ontario, and the 
St. Lawrence River showed that approximately 15% of the samples 
contained endosulfan at levels ranging from 0.005 to 0.060 g/litre 
(Natural Research council, 1975).  In recent work in Western 
Canada, endosulfan was found (0.011 g/litre) in one out of 1400 
surface water samples, indicating that water contamination by this 
insecticide was not widespread (Gummer, 1980). 

    No alpha- or beta-endosulfan or endosulfan sulfate residues 
were detected (method sensitivity, 10 g/litre) in well waters 
located near treated fields in Wisconsin and Florida, USA, 282 and 
100 days, respectively, after the last endosulfan application.  The 
treated fields in Wisconsin received seven foliar applications of 
endosulfan at 0.56 kg/ha (2 in 1966 and 5 in 1969), while the 
fields in Florida were treated with 10 - 16 foliar applications of 
endosulfan at 1.12 kg/ha over a 5-year period (Niagara Chemical 
Division, 1971). 


    Early work by Byers et al. (1965) indicated that the alpha-
isomer dissipated more rapidly in the soil than the beta-isomer.  
The authors suggested that the latter was more strongly adsorbed on 
soil than the former.  The results of field studies have since 
confirmed that the alpha-isomer has a shorter half-life (60 days) 
than the beta-isomer (900 days) (Steward & Cairns, 1974). 

    It was also suggested that endosulfan sulfate (the major
degradation product in soil) accumulated at a rate comparable
to the rate of loss of alpha- and beta-endosulfan.  Endosulfan
sulfate tended to be more stable than either of the 2
endosulfan isomers, but none of the 3 compounds was prone to
leaching in soil (Stewart & Cairns, 1974).

    The degradation of endosulfan, which was substantially reduced 
when the compound was incorporated into soil, halted during winter 
months (Niagara Chemical Division, 1966, Stewart & Cairns, 1974).  
A survey of agricultural soils in North America showed that 
endosulfan residue levels were typically below 1 mg/kg, with a few 
exceptions (4.78 mg/kg, 4.93 mg/kg) (Frank et al., 1976; Harris et 
al., 1977).  A study from Italy revealed endosulfan soil residues 
ranging from 0.23 to 3.88 mg/kg (Sanna et al., 1979).  Endosulfan 
has been detected in the sediments of drainage ditches (Miles & 
Harris, 1971; Niagara Chemical Division, 1971), rivers (Miles, 
1976), and lakes (Canada, National Research Council, 1975). 
Concentrations ranged from trace amounts to 0.64 mg/kg dry weight 
(Miles et al., 1971). 

    Degradation of endosulfan appears to be different in sediments 
and in soil.  Martens (1977) studied soil samples under a variety 
of conditions, including flooding, and demonstrated that the 
percentage of endosulfan diol was increased in the flooded soil 
samples and that a lower percentage of the sulfate was observed.  
Carbon dioxide production was measured in all samples and was 
highest under aerobic condition (Martens, 1977). 

    Abiotic degradation and bioaccummulation

    Both alpha- and beta-endosulfan are fairly resistant to 
photodegradation (Schumacher et al., 1971; Schuphan et al., 1972), 
but the 2 dominant break-down products, endosulfan sulfate and 
endosulfan diol, are susceptible to photolysis (Fig. 1) (Schuphan 
et al., 1972).  Technical endosulfan is sensitive to moisture, 
acids, and alkali and will undergo slow hydrolyses producing sulfur 
dioxide (S02) and endosulfan alcohol via the intermediate 
endosulfan sulfate (FAO/WHO, 1968; Martens, 1977). 

    In soil and on plant surfaces, endosulfan sulfate is the 
primary degradation product of endosulfan (Cassil & Drummond, 1965; 
Martens, 1977) with lesser amounts of endosulfan diol and 
endosulfan lactone being produced.  Although sunlight may be 
involved in the initiation of sulfate production, Archer et al. 
(1972) felt that thermolysis was the principle formation mechanism. 

    In aquatic environments (water and sediment), endosulfan diol 
was present together with smaller amounts of the sulfate and other 
compounds (Eichelberger & Lichtenberg, 1971; Martens, 1977). 

    Martens (1972) demonstrated the production of endosulfan and 
endosulfan diol by fungi, but the role that these and other 
microorganisms play in environmental degradation is not clear. 


    As a result of the higher solubility in water of endosulfan 
compared with most other organochlorine pesticides, it does not 
have the affinity for lipids that most related compounds have.  
Consequently, biomagnification and accumulation of endosulfan in 
food chains is less likely to occur.  The typical response for most 
organisms exposed to endosulfan at below lethal levels, is to 
accumulate the compound up to a plateau, but clear the residues 
fairly rapidly once the source of contamination is removed.  The 
higher the exposure level, the longer it takes to reach a plateau 
and the higher the plateau is.  This response was demonstrated in 
mussels (Roberts, 1972), fish (Schoettger & Bier, 1970; Oeser & 
Knauf, 1973), and algae (Oeser & Knauf, 1973).  An estimate of the 
half-life of endosulfan in fish was 3 days (Oeser & Knauf, 1973).  
Similar results have been found in mammals; summaries of data have 
been made by Maier-Bode (1968), Goebel et al. (1982), and US EPA 
(1982).  Endosulfan sulfate was generally the only compound 
detected in tissues of animals exposed to endosulfan.  In cattle 
(FAO/WHO, 1967), the concentration factors were small (0.5 in milk, 
0.05 in muscle tissue, and 0.15 in fat), and residues cleared quite 
rapidly when endosulfan was removed from the diet.  Other diet 
studies have produced similar results in sheep (Maier-Bode, 1968) 
and dogs (FMC Corp., unpublished data, 1963).  No reports of 
endosulfan residues in human adipose tissue or breast milk were 

    In plants sprayed with endosulfan, initial residues on fruits 
and vegetables can vary from about 1 to 100 mg/kg; after 1 week, 
residues generally decrease to 20% or less of the initial amount 
(Canada, National Research Council, 1975). 

3.3.  Levels of Exposure


    Human exposure during endosulfan spraying for tsetse fly 
control using a helicopter in the Ivory Coast was assessed by means 
of exposure pads worn over or under light overalls (Copplestone et 
al., 1979).  Three male volunteers were positioned within a village 
and three more in the area deliberately being sprayed.  The men 
walked in the area during spraying and for 1 h afterwards.  The 
application rate of the compound is not stated.  Five cm square 
sections of 7 pads, 6 worn over and 1 worn under clothing, were 
analysed from each volunteer and the total exposure to endosulfan 
calculated assuming that all endosulfan measured on the pads was 
absorbed into the body, irrespective of clothing.  An addition of 
10% was made to the calculation as an estimate of respiratory 
absorption.  Calculated values were compared with the dermal LD50 
for rat of 74 mg/kg body weight.  The men outside the village 
received 0.27% and those in the village 0.007% of the rat LD50.  
The exposure calculated was an overestimate as it assumed that 
clothing offered no protection.  The authors showed that the cotton 
overalls reduced the dose of endosulfan by the pads by a factor of 
at least 20. 

    Endosulfan has been shown to be released from a wood 
preservative into a room atmosphere over a 1-year period of 
observation (Zimmerli et al., 1979). 

    It is well-known that the respiratory route is a potential 
route of exposure to endosulfan (Oudbier et al., 1974; Wolfe, 
1976), and a TLV has been established at 0.1 mg/m3 (ACGIH, 1982). 


    In the USA, endosulfan has been reported to be present in the 
market basket survey since 1967.  Between the 1967 and the 1974-75 
studies, the level of contamination decreased, but the proportion 
of food samples containing endosulfan increased.  Endosulfan 
(alpha-, beta-isomer and the sulfate derivative) was present in 3 
out of 360 food samples in the 1967-68 survey, at a concentration 
range of 0.008 - 0.134 mg/kg and was found in 1 sample of each of 3 
food groups:  garden fruits, leafy vegetables, and oils and fats 
(Corneliussen, 1969).  The 1968-69 survey revealed that endosulfan 
was present in 16 out of 360 food samples with a range from 0.01 to 
0.042 mg/kg.  It was present in 7 out of 20 food samples, but only 
in 2 food groups, leafy vegetables and garden fruits (Johnson & 
Manske, 1977).  Similar results for the above food groups were 
found in Canada (Canada, National Research Council, 1975). 

    Endosulfan sulfate was also present in cow's milk from tobacco 
farming areas at levels of up to 0.010 mg/litre (Frank et al., 
1970, 1979).  Beck et al. (1966) reported that endosulfan could not 
be detected in the milk of cows that had been fed forage containing 
endosulfan at 0.41, 0.70, or 2.35 mg/kg for 21 days. 

    No endosulfan residues have been reported in market basket 
surveys from other countries and there are no reports of the daily 
human intake of endosulfan exceeding the FAO/WHO temporary ADI of 
0.008 mg/kg body weight (FAO/WHO, 1982). 

    In general, endosulfan residues in food are well below the 
tolerance levels established for various food types by the FAO/WHO 
(1975a) (Table 2).  These residue tolerances refer to the total 
residue of alpha- and beta-endosulfan and endosulfan sulfate. 

Table 2.  Endosulfan tolerances in fooda
Food                           FAO/WHO toleranceb                 
Tea (dry, manufactured)        30 mg/kg                           
Fruits and vegetables          2 mg/kg                            
(other than exceptions noted)                                        
Carrots, potatoes, sweet       0.2 mg/kg                          
potatoes, bulb onions                                                
Cottonseed                     1.0 mg/kg                          
Cottonseed oil (crude)         0.4 mg/kg                          
Rice (in husk)                 0.1 mg/kg                          
Milk and milk products         0.5 mg/kg                          
(fat basis)                                                          
Fat and meat                   0.2 mg/kg                          
a  From:  FAO/WHO (1975a).
b  Calculated as the total of alpha- and beta-endosulphan plus 
   endosulfan sulfate.

    High endosulfan residues have been found in tobacco leaves in 
both Canada and the USA.  Pyrolysis studies on tobacco indicate 
that the alpha- and beta-isomers, the sulfate derivative, and a 
variety of other products are present in contaminated tobacco smoke 
(Chopra et al., 1978).  Levels as high as 30.9 and 20 g/m3 were 
detected in Canada and the USA, respectively (Dorough, 1973; Cheng 
& Braun, 1977).  Residues seem to consist primarily of endosulfan 
sulfate followed by the beta-isomer, then the alpha-isomer (Cheng 
& Braun, 1977). 

    Relative importance of different sources

    With good agricultural practice, endosulfan residues in food 
should not be significant.  Its use in tobacco farming has been 
discouraged (Cheng & Braun, 1977) but, if not regulated, could 
provide a significant route of exposure.  As a rule, endosulfan 
concentrations in air and water are very low and localized, and 
accordingly of no significance as far as risk for general 
population is concerned. 

    No reports of endosulfan in breast milk have appeared in the 
literature.  However, since endosulfan is used as a wood 
preservative and garden pesticide in some countries, direct 
exposure of infants and children remains a possibility. 

    Occupational exposure

    Only 2 reports on occupational exposure were found; both 
involved workers who filled sacks with endosulfan powder.  A total 
of 11 people were poisoned, all of whom experienced difficulties in 
concentration, vertigo, followed by epileptiform convulsions or 
stupor (FAO/WHO, 1975b).  No further information on workers exposed 
during the production or spraying of endosulfan was available. 


4.1.  Animal Studies

    Five days after a single oral administration (by gavage) of 
14C-labelled alpha-endosulfan in corn oil at 2 mg/kg body weight to 
female albino rats, totals of 75% and 13% of the dose were 
eliminated in the faeces and urine, respectively.  With the same 
dose of 14C-labelled beta-endosulfan, and under the same 
conditions, the values were 68% and 18.5%, respectively.  When 
radio-labelled endosulfan was fed to rats at 5 mg/kg diet for 14 
days, 56% was eliminated in the faeces and 8% in the urine.  
Maximum residues of endosulfan, which occurred in the kidney and 
liver, were 3 and 1 mg/kg, respectively.  Metabolism studies using 
alpha- and beta-endosulfan did not reveal any appreciable 
differences in the fate of the 2 isomers in the rat (Dorough et 
al., 1978).  Endosulfan was metabolized in rats to endosulfan diol, 
endosulfan hydroxyethers, endosulfan lactone, endosulfan sulfate, 
and some unidentified polar metabolites (Dorough et al., 1978).  
Similar metabolites of endosulfan were identified in mice (Deema et 
al., 1966; Schuphan et al., 1968). 

    Sheep given daily doses of endosulfan at 15 mg/kg body weight 
for 28 days, eliminated 20% of the dose in the faeces as the 
unchanged compound; only a small amount of endosulfan diol was 
detected in the urine.  Endosulfan sulfate (0.1 mg/kg) was found in 
perirenal and mesenteric adipose tissues (Gorbach, 1965). 

    In rabbits, after a single intravenous (iv) injection of 
endosulfan at 2.0 mg/kg, the concentration in plasma declined 
rapidly.  Thirty-seven percent of the dose was excreted in the 
urine as alpha-endosulfan and 11% as beta-isomer in the first 5 
days (Gupta & Ehrnebo, 1979). 

    The distribution pattern of endosulfan in the plasma and brain 
was studied when rats were administered daily doses of 5 or 10 
mg/kg body weight in peanut oil by gavage (approximately 1/20 and 
1/10 LD50) (2 alpha-:1 beta-isomer ratio) for 15 days (Gupta, 
1978).  On day 16, the rats that were dosed with 5 mg/kg had the 
following concentrations of the alpha-isomer in the brain: 
cerebrum, 3.76 mg/kg, cerebellum, 2.04 mg/kg; remaining parts of 
the brain, 2.66 mg/kg.  The concentrations of the beta-isomer were 
0.06 mg/kg in the cerebrum and 0.02 mg/kg in the cerebellum; no 
beta-isomer was detected in the other parts of the brain (Gupta, 
1978).  When the rats were fed the higher dose level the same 
pattern of isomers and metobolite was found, the only difference 
being that the concentrations were higher than in rats receiving 
the lower dose.  Distribution of endosulfan was also investigated 
in the cat brain.  Following a single iv administration of 3 mg/kg 
body weight, groups of animals were sacrificed at selected time 
intervals and analysed for endosulfan content.  The cerebrum had 
the highest concentration followed by the spinal cord, cerebellum, 
and the brain stem (Khanna et al., 1979). 

4.2.  Human Studies

    Some human data were obtained following the analysis of a case 
of suicide in which an unknown amount of endosulfan was ingested 
(Demeter et al., 1977) in combination with alcohol.  The individual 
died within 6 h after ingestion of the chemical.  The tissue 
distribution of endosulfan is given in Table 3.  It could not be 
concluded that death was due solely to the effects of endosulfan. 

Table 3.  Tissue distribution of endosulfan
Tissue            alpha-endosulfan  beta-endosulfan               
                  (mg/kg)           (mg/kg)                       
Liver             12.4              5.2                           
Kidney            2.48              1.8                           
Blood             0.06              0.015                         
Urine             1.78              0.87                          
Stomach content   2610              1900                          
Small intestinal  190               99                            


    The toxicity and the residue data on endosulfan have been 
reviewed by the Joint Meeting on Pesticide Residues (JMPR) in 1965, 
1967, 1968, 1971, 1974, and 1982 (FAO/WHO, 1965, 1968, 1969, 1972, 
1975a, 1983).  For their conclusion, refer to section 8.  We refer 
to these reports, which contain more detailed information on the 
toxicity studies and residue data than the present report.  
Moreover, several unpublished studies have been evaluated and 
reported there. 

5.1.  Short-Term Exposures

5.1.1.  Single exposure

    The LD50 of endosulfan varied widely depending on the route
of administration, species, vehicle, and sex of the animal.  The 
available acute toxicity data are summarized in Table 4.  The 
clinical signs of toxicity include hyperactivity, tremors, and 
convulsions, followed by death (Boyd, 1972; Gosselin et al., 1976; 
Gupta, 1976). 

    Limited short-term studies on the dog showed that as little as 
30 mg/kg body weight could be fatal (Canada, National Research 
Council, 1975), and 2.5 mg/kg body weight per day for 3 days 
induced toxic symptoms (FAO/WHO, 1968).  The 2 stereoisomers have 
comparable LD50 values for the rat (Lindquest & Dahm, 1957). 

    Male rats given a single oral dose of endosulfan at 40 mg/kg 
body weight displayed acute neurotoxic manifestations and showed a 
significant increase in blood glucose, blood ascorbic acid, and 
blood and brain glutathione (Garg et al., 1980).  There have been 
no published data on skin irritation or sensitization. 

5.1.2.  Repeated exposures

    Endosulfan sulfate was fed to rats in the diet for 3 months at 
levels as high as 500 mg/kg (Canada, National Research Council, 
1975); no effects were detected other than increased liver or 
kidney weight. 

    The same compound was administered to dogs for 3 months at 
levels ranging from 0.75 to 2.5 mg/kg body weight per day.  The 
lowest dose did not have any effect, but the highest dose was not 
tolerated and the 1.5 mg/kg dose induced occasional signs of 
toxicity.  It was concluded that endosulfan sulfate appeared to 
have the same order of toxicity as endosulfan (Canada, National 
Research Council, 1975). 

Table 4.  Acute toxicity of endosulfan in different animal species
Species  Sex  Route       Vehicle      LD50      Reference
Rat      NS   oral        olive oil    64        Truhaut et al.

Rat      NS   oral        95% alcohol  40 - 50   FAO/WHO (1968)

Rat      M    oral        peanut oil   43        Gaines (1969)

Rat      M    oral        cottonseed   121       Boyd (1972d)

Rat      F    oral        peanut oil   18        Gaines (1969)

Rat      NS   oral        NS           355       Boyd & Dobos

Rat      NS   ip          95% alcohol  8         FAO/WHO (1965)

Rat      N    dermal      xylene       130       Gaines (1969)

Rat      F    dermal      xylene       74        Gaines (1969)

Rat      NS   dermal      cottonseed   681       Gupta & Gupta
                          oil                    (1979)

Rat      NS   inhalation  NS           350       Gupta & Gupta
                                       (mg/m3)a  (1979)

Mouse    F    ip          95% alcohol  7.5       Gupta (1976)

Mouse    F    ip          alcohol &    13.5      Gupta (1976)
                          peanut oil

Mouse    M    ip          95% alcohol  6.9       Gupta (1976)

Mouse    M    ip          alcohol &    12.6      Gupta (1976)
                          peanut oil

Rabbit   NS   dermal      cottonseed   147       Gupta & Gupta
                          oil                    (1979)

Rabbit   NS   percutan-   cottonseed   360       Gupta & Gupta
              aneous      oil                    (1979)

Rabbit   NS   dermal      oil solvent  359       Martin (1968)

Table 4.  (contd.)
Species  Sex  Route       Vehicle      LD50      Reference
Rabbit   NS   dermal      chloroform   187       Gupta &
                                                 Chandra (1975)

Guinea-  NS   dermal      cottonseed   1000      Gupta & Gupta
pig                       oil                    (1979)

Hamster  NS   oral        olive oil    118       Truhaut et
                                                 al. (1974)
a  Value represents the LC50 in mg/m3 for a 4-h exposure period.
NS = Not stated.
 M = Male.
 F = Female.

    When rats were treated with daily oral doses of endosulfan at 
1.6 - 3.2 mg/kg body weight, for 12 weeks, no effects were observed 
on growth-rate (FAO/WHO, 1967).  Administration of dietary levels 
of endosulfan ranging from 2 to 200 mg/kg to male rats for 2 weeks, 
resulted in changes in mixed-function oxidase activity (Den 
Tonkelaar et al., 1974).  Endosulfan at the highest level (200 
mg/kg, approximately 10 mg/kg body weight per day) was found to 
induce mixed-function oxidases activity (aniline hydroxylase and 
aminopyrine demethylase). 

    Endosulfan was administered to female rats at daily oral doses 
of 1.0, 2.5, or 5.0 mg/kg body weight for 7 or 15 days (Gupta & 
Gupta, 1977).  No changes were observed in body, ovary, or adrenal 
weights.  Liver weight increased and pentobarbital sleeping time 
decreased at the 2 highest dose levels and both time intervals.  
The results of subsequent studies (Agarwal et al., 1978) showed 
that the 2 highest levels resulted in induction of aminopyrine 
demethylase and aniline hydroxylase activities as well as a dose-
related increase in amino-transferase activity and spontaneous 
lipid peroxidation. 

    Male rats were dosed by oral intubation with endosulfan at 
levels of 5 or 10 mg/kg body weight per day for 15 days (Gupta, 
1978).  A reduction in body weight gain was observed at the higher 
dose, and 3 out of 12 animals died during testing. 

    In a separate study (Garg et al., 1980), male rats were dosed 
orally with endosulfan at 0.625, 5.0, or 20 mg/kg body weight, 6 
days per week, for 7 weeks.  Animals receiving the highest dose 
showed a slight increase in blood glucose and a decrease in plasma 
calcium levels. 

    Endosulfan was administered orally to 4 dogs for 3 days at 2.5 
mg/kg body weight (FAO/WHO, 1967).  Vomiting was observed in one 
dog and vomiting, tremors, convulsions, rapid respiration, and 
mydriasis in the 3 remaining animals.  Three other groups of dogs, 
2 males and 2 females per group, were administered endosulfan 
orally at levels of 0.075, 0.25, or 0.75 mg/kg body weight for 6 
days a week over a 1-year period (FAO/WHO, 1968).  No signs of 
toxicity were observed.  At autopsy, gross and microscopic 
examination of the tissues did not reveal any differences between 
treated and control animals. 

    When endosulfan was administered to cats (Misra et al., 1980) 
at levels of 2, 3, or 4 mg/kg body weight, muscular twitching 
was observed in all treatment groups, followed by convulsions.  At 
the 2 higher dose levels, there was a marked rise in blood glucose 
levels after 15 and 30 min with a gradual fall up to 4 h.  
Adrenalectomy prevented this rise.  Cats were fasted for 1 - 2 h 
before this study and were then injected with a single intravenous 
dose of endosulfan (2, 3, or 4 mg/kg) through a cannula inserted 
into the femoral vein.  Blood was drawn from the femoral vein after 
0, 15, and 30 min, and 1, 2, and 4 h. 

    Endosulfan is able to inhibit sodium-, potassium-, and 
magnesium-dependent ATPase enzymes in rainbow trout brain (Davis & 
Wedemeyer, 1971). 

5.2.  Long-Term Exposures

    Groups of 25 male and 25 female rats received technical grade 
endosulfan at 10, 30, and 100 mg/kg diet for 104 weeks (FAO/WHO, 
1968).  Survival of the female rats in the 10 and 30 mg/kg groups 
was lower than that in the female control group, during the second 
year of exposure.  In the 100 mg/kg female group, survival was 
significantly lower after 26 weeks and abnormalities were observed 
in weight gain and haematological parameters.  At autopsy, the 
relative weight of the testes in the 10 mg/kg male group was 
significantly lower than in the control group.  Significant 
histopathological findings were apparent only in the 100 mg/kg male 
group.  In these animals, the kidneys were enlarged and there were 
signs of renal tubular damage with interstitial nephritis.  
Hydropic changes were seen in liver cells.  The tumor incidence in 
all test groups was within the range of the control group. 

    In a study reported by the Commission of European Communities 
(CEC, 1981), male and female dogs were dosed with endosulfan (by 
capsule), 6 days a week for 10 months.  The dose levels ranged from 
0.075 to 0.75 mg/kg body weight.  No gross or microscopic evidence 
of toxicity was noted. 

    The Joint Meeting on Pesticide Residues (JMPR) reviewed the 
toxicity data on endosulfan in its 1982 meeting (FAO/WHO, 1983) and 
concluded that the following levels did not cause any toxicological 

    rat:    30 mg/kg diet, equivalent to 1.5 mg/kg body weight;

    dog:    0.75 mg/kg body weight per day (administered by

5.3.  Reproduction Studies

    Adequate data are not available.

5.4.  Mutagenicity

    Endosulfan was not mutagenic in  E. coli or  S. typhimurium
(Fahrig, 1974; Moriya et al., 1982).  It did not induce mitotic 
conversion in  Saccharomyces cerevisae (Fahrig, 1974).  However, in 
one study, technical grade endosulfan was reported to induce reverse 
mutations, cross overs, and mitotic gene conversions in  Saccharomyces 
 cerevisiae (Yadav et al., 1982).

    Endosulfan did not induce chromosomal abberations in bone 
marrow cells or spermatogonia of male rats treated with 5 daily 
oral doses of 11 - 55 mg/kg body weight (Dikshith & Datta, 1978). 

    An increased number of micronuclei induced in the bone marrow 
erythrocytes of mice treated with endosulfan in the drinking-water 
(43.3 mg/litre) for 2 consecutive days was not statistically 
significant (Usha Rani et al., 1980).  Negative results were 
observed in a dominant lethal test in mice (Canada, National 
Research Council, 1975). 

5.5.  Teratogenicity

    Adequate data are not available.

5.6.  Carcinogenicity

    The carcinogenicity of technical grade endosulfan was tested 
using Osborne-Mendel rats and B6C3F1 mice (NCI Tech. Series, 1978).  
The time-weighted average high and low endosulfan concentrations in 
the diet for male rats were 952 and 408 mg/kg; for female rats 445 
and 223 mg/kg; for male mice 6.9 and 3.5 mg/kg; and for female mice 
3.9 and 2.0 mg/kg.  Testing of high-dose male rats was terminated 
during week 82 and low dose male rats during week 74. 

    Female rats were administered endosulfan for 78 weeks followed 
by a 33-week observation period.  Mice were administered the 
chemical for 78 weeks and observed for an additional 14 weeks.  A 
high early mortality rate in male rats and mice precluded any 
conclusions concerning carcinogenicity.  Under the conditions of 
the assay, it was concluded that endosulfan was not carcinogenic 
for female Osborne-Mendel rats or female B6C3F1 mice. 

    In a large scale screening study, 2 strains of male and female 
hybrid mice [(C57BL/6 x C3H/Anf)F1] and [(C57BL/6 x AKR)F1] were 
given 2.15 or 3.0 mg/kg body weight endosulfan by oral intubution 
on days 7 - 28 of age followed by the feeding of diets containing 
concentrations of 3 or 6 mg/kg diet for 78 weeks (Innes et al., 
1969).  Although no conclusion could be drawn about its 
carcinogenic potential, endosulfan was reported as being one of the 
compounds requiring further study. 

5.7.  Factors Influencing Toxicity

    Rats subjected to protein-deficient diets were more susceptible 
to the acute toxic effects of endosulfan (Boyd, 1972).  The LD50 
for rats on normal lab chow was reported to be 121 mg/kg body 
weight, compared with 5 mg/kg for rats on a protein-deficient diet. 


6.1.  Poisoning Incidents

    A report from Bulgaria described the circumstances, clinical 
symptoms, and morphological changes in 5 cases associated with 
endosulfan poisoning (Terziev et al., 1974).  These cases comprised 
2 suicides and 3 accidental poisonings.  Death generally followed a 
few hours after ingestion.  The clinical symptoms included 
vomiting, agitation, convulsions, cyanosis, dyspnoea, foaming at 
the mouth, and noisy breathing. 

    Another report lists the findings on 2 cases (apparently 
suicides) of men who died after ingesting endosulfan (Demeter & 
Heyndrickx, 1978).  Again, death was noted to occur within a few 
hours of ingestion, and significant post-mortem findings included 
congested and oedematous lungs and cyanosis.  Tissue analysis for 
residues indicated the possible synergistic effect of endosulfan 
and alcohol in one patient (Demeter et al., 1977) and endosulfan, 
alcohol, and dimethoate, an organophosphorous insecticide, in the 

6.2.  Occupational Exposure

    Three cases of poisoning in workers employed in a chemical 
factory have been reported (Israeli et al., 1969; Tiberin et al., 
1970).  Poisoning occurred when the men filled bags with 
insecticide without wearing protective clothing and masks.  
Symptoms developed after 3 weeks, 1 month, and 18 months, 
respectively, following daily exposure, and consisted of headaches, 
restlessness, irritability, vertigo, stupor, disorientation, and 
epileptiform convulsive seizures. 

    Electroencephalogram changes were noted.  Endosulfan has been 
shown to persist on the hands of pest control operators for up to 
31 days after exposure.  No clinical symptoms were observed (Kazen 
et al., 1974). 

6.3.  Treatment of Poisoning

    In case of overexposure, medical advice should be sought 

    If the pesticide has been ingested, gastric lavage should be 
performed with 2 - 4 litres of tap water followed by saline 
purgatives (30 g sodium sulfate in 250 ml of water).  Barbiturates 
or diazepam should be given intraveneously in sufficient dosage to 
control restlessness or convulsions.  Mechanical respiratory 
assistance with oxygen may be required.  Calcium gluconate (10% in 
10 ml) should be injected 4-hourly.  Contraindications are oily 
purgatives, epinephrine, and other adrenergic drugs and central 
stimulants of all types (FAO/WHO, 1975b). 


7.1.  Toxicity for Aquatic Organisms

    The most representative studies on the toxicity of endosulfan 
for aquatic organisms are summarized in Table 5.  A more 
comprehensive table, listing different conditions and exposure 
times, is available on request from IRPTC, Geneva, Switzerland. 

    Ramachandran et al. (1981) looked at the effects of a low 
concentration of endosulfan (50 g/litre) on photosynthesis and 
respiration in some common seaweeds.  The red alga  Gracilaria 
 verrucosa showed the highest tolerance to endosulfan.  Photo-
synthesis was 96.2% of control levels and respiration was 
stimulated to 112.32%.  The 3 other algal species  Gratiloupia, 
 Enteromorpha intestinalis, and  Cheatomorpha linum showed photo-
synthetic rates of 80.4, 83.6, and 84.6% of control levels and 
respiration rate of 107.38, 86.97, and 93.6%, respectively.  The 
respiration to photosynthesis ratio was lower than control levels 
for all 4 species. 

    The toxic effects of endosulfan, determined for 1 freshwater 
and 2 seawater species of crustacea, are summarized in Table 5.  
McLeese & Metcalfe (1980) studied the effects of including sediment 
in test vessels.  For the shrimp  Crangon, 96-h LC50 values for 
endosulfan increased from 0.2 g/litre to 6.9 g/litre with the 
inclusion of sediment.  The mortality rate estimate of Butler 
(1963) for the brown shrimp included animals immobilized by the 
material and showing no clear signs of life.  Twenty-four- and 48-h 
LC50 values for the freshwater scud  Gammarus lacustris were 9.2 
and 6.4 g/litre, respectively (Sanders, 1969). 

    McLeese et al. (1982) tested the toxicity of endosulfan for the 
ragworm  Nereis virens with and without sediment in the test 
vessels.  The LC50 for endosulfan in 288-h tests were 100 g/litre 
with sea water and 340 g/kg with sediment.  Symptoms of stress in 
the worms included eversion of the proboscis, lost equilibrium, and 
immobilization.  Stressed worms in sediment tests emerged from the 
sediment and subsequently did not burrow, even after the sediment 
was changed. 

Table 5.  Toxicity of endosulfan for aquatic organisms
Organism          Size/  Grade Temp  pH   Stat/ Sal    Effect    Parameter    Conc.       Reference
                  age          (C)       flow  (0/00)                        (g/litre)
eastern oyster                 28               22     decrease  96-h EC50    65          Butler (1963)
 (Crassostrea                                           in shell
 virginical)                                            growth

polychaete worm   adult        9-10       stat         death     12-day LC50  100         McLeese et al.
 (Nereis nereis)                                                                           (1982)

                  adult        9-10       stat         death     12-day LC50  340a        McLeese et al.

Cladoceran                     10    7.4        45b    death     96-h LC50    52.9        Schoettger 
 (Daphnia magna)                                 38c                                       (1970)

shrimp            adult        20         stat         death     96-h LC50    0.2         McLeese & 
                                                                                          Metcalfe (1980)

 (Crangon          adult        10         stat         death     96-h LC50    6.9a        McLeese & 
 septemspinosa)                                                                            Metcalfe (1980)

blue crab         juv.         30         stat         death or  24-h EC50    55          Butler (1963)
 (Callinectes                                           loss of   48-h EC50    35          Butler (1963)
 sapidus)                                               equilib-

freshwater mite   adult  tech  25-   7.8- stat         immobil-  48-h EC50    2.8         Nair (1981)
 (Hydrachna                     31    8                 isation

stonefly          nymph        15.5  7.1  stat         death     96-h LC50    2.3         Sanders & Cope
 (Pteronarcys                                                                              (1968)

rainbow trout     1.3g   tech                          death     96-h LC50    1.4         Johnson & 
 (Salmo gairdneri)        96%                                                              Finley (1980)

fathead minnow    0.7g   tech                          death     96-h/LC50    1.5         Johnson & 
                         96%                                                              Finley (1980)

Table 5.  (contd.)
Organism          Size/  Grade Temp  pH   Stat/ Sal    Effect    Parameter    Conc.       Reference
                  age          (C)       flow  (0/00)                        (g/litre)
channel catfish   1.7g   tech                          death     96-h LC50    1.5         Johnson & 
 (Ictalurus               96%                                                              Finley (1980)

catfish           6-10g  35%   18.2  6.9- stat         death     96-h LC50    0.67        Verma et al. 
 (Mystusvittatus)  80-    EC          7.4                                                  (1980)

                  6-10g  35%   18.2  6.9- stat         death     96-h LC0     0.06        Verma et al. 
                  80-    EC          7.4                                                  (1980)

                  6-10g  35%   18.2  6.9- stat         death     96-h LC50    3.50        Verma et al. 
                  80-    EC          7.4                                                  (1980)
                  100mm              8.4  flow  152b   death     96-h LC50    2.2         Rao & Murty 
                                                330c                                      (1982)

catfish                              8.4  flow  152b   death     96-h LC50    1.1         Rao & Murty 
 (Heteropneustes                                 330c                                      (1982)
                  41.8  35%         7.8  stat  120c   death     96-h/LC50    14.7        Singh & Narain
                  4.7g                                                                    (1982)
                  197   EC

                  11.3  35%         7.8  stat  120c   death     96-h/LC50    7.3         Singh & Narain
                  1.6g                                                                    (1982)
                  102   EC

catfish                              8.4  flow  152b   death     96-h LC50    1.9         Rao & Murty (1982)
 (Mystuscavasius)                                330c

catfish           40-55g 35%   18.2  6.9- stat         death     96-h LC50    22          Verma et al. 
 (Ophiocephalus    90-    EC          7.4                                                  (1981)
 punctatus)        100mm
a  Sediment present in test vessel.
b  Hardness mg CO3/litre.
c  Alkalinity mg HCO3-/litre.
    Nair (1981) tested endosulfan toxicity with a range of 
concentrations from 2.6 and 2.9 g/litre on the freshwater mite 
 Hydrachna trilobata viets and reported a 48-h LC50 value of 
2.8 g/litre.  The small difference between the no-effect and 
lethal dosages of endosulfan is typical for many different aquatic 
organisms.  A 96-h LC50 of 1890 g/litre was reported by Holcombe 
et al. (1983) for adult freshwater snails  Aplexa hypnorum.  Roberts 
(1972) reported that endosulfan at a concentration of 1000 g/litre 
delayed the onset of spawning and prolonged the spawning period for 
the common mussel  Mytilus edulis.  At a lower dose of 100 g/litre, 
a slight reduction in the length of the spawning period was 
considered by the author to reflect the experimental tank 
conditions rather than the endosulfan treatment. 

    Endosulfan has a high acute toxicity for fish.  There have been 
studies on many species of teleosts with 96-h LC50 values ranging 
from 0.67 g/litre to 4.8 g/litre.  Where commercial preparations 
of endosulfan have been used, it is not always clear how the dose 
is presented.  Where LC50 values exceed 4.8, it seems clear that 
the values given are for a preparation that usually contains only 
35% endosulfan. 

    Singh & Narain (1982) looked at variations in LC50 values
in 96-h tests on the catfish  Heteropneustes fossilis in
relation to season, and size and weight of the fish.  Tolerances of 
the fish to the Thiodan preparation (35% endosulfan) showed a 
significant seasonal variation.  Fish were more tolerant to 
endosulfan during the colder months of the year.  The toxicity of 
endosulfan was directly proportional to the length and weight of 
fish; LC50 values increased from 5 to 4.7 g/litre with an increase 
in fish weight from 4.8 to 41.8 g and an increase in length from 
6.2 to 19.7 cm.  The relative toxicity of technical endosulfan, 
endosulfan isomers, and formulations, was investigated in the 
freshwater fish  Labeo rohita by Rao et al. (1980), and in  Channa 
 punctata, a catfish, by Devi et al. (1981).  In  Labeo rohita, 
endosulfan-A was 3.33 times and endosulfan-B 0.16 times more toxic 
than technical endosulfan; the alpha-isomer was 30 times and the 
beta-isomer 0.7 times more toxic than technical material in  Channa 
 punctata.  Rao & Murty (1982) demonstrated in 3 species of catfish 
that the relative toxicity between species could not be determined 
using LC50 values alone.  The slopes of endosulfan toxicity curves 
were different for different species.  The same authors (Rao & 
Murty, 1980), reported that endosulfan metabolites were eliminated 
mainly with faeces and urine, the principal sites of detoxification 
of endosulfan being the liver and kidney.  Using the freshwater 
catfish  Saccobranchus fossilis, Verma et al. (1982a) calculated the 
safe levels of 2 preparations of endosulfan to be 0.14 g/litre 
(Thiotox) and 0.23 g/litre (Thiodan).  Verma et al. (1980) looked 
for synergism and antagonism between endosulfan, dichlorvos and 
carbofuran on the test fish  Mystus vittatus and  Ophiocephalus 
 punctatus, but did not find any evidence of either. 

    Histopathological, biochemical, and physiological changes in 
fish after exposure to endosulfan have been reported in a large 
number of studies.  Gopal et al. (1981a) measured blood glucose 
levels in catfish during 96-h of exposure to endosulfan at 10 
g/litre.  A marked rise, at 4 h, of 66.4% over control levels 
increased to a peak of 101.6% at 48 h compared with control levels 
and then declined to match control levels at 72 h.  At the end of 
the study, after 95 h, the glucose level was not significantly 
different from controls.  Singh & Srivastava (1981) exposed Indian 
catfish to a high sublethal concentration of endosulfan of 1.5 
g/litre (representing 75% of the 96-h LC50 for the species).  The 
average mortality rate for all fish groups was 5% over the 96-h 
experimental period.  Muscle glycogen was depressed for most of the 
experimental period.  Liver glycogen was the least affected of all 
the variables measured.  Blood glucose was significantly elevated 
at 3, 6, 48, and 96 h of exposure, but not at 12 h.  Blood pyruvate 
was elevated at 6 and 48 h only, whereas blood lactate was 
significantly elevated for the first 6 h of exposure and 
significantly depressed for the remainder of the observation 
period.  Endosulfan was shown by Sastry & Siddiqui (1982) to reduce 
intestinal uptake of glucose by the fish  Channa punctatus at doses 
of 1 mg/litre and above.  Using endosulfan concentrations of 
between 0.17 and 2.3 g/litre on 3 species of Indian catfish, Verma 
et al. (1983) found elevation of blood glucose ranging from 67.31% 
to 98.36%.  The concentrations of endosulfan used represent 25% of 
the 96-h LC50 for each species.  Murty & Devi (1982) demonstrated 
that changes in tissue protein, glycogen, and lipid levels in the 
fish  Channa punctatus were greater with exposure to the alpha- than 
to the beta-isomer of endosulfan. 

    A clear dose-related reduction in both oxygen consumption and 
total nitrogen excretion was shown by Rao et al. (1981) in the fish 
 Macrognathus aculeatum with endosulfan concentrations ranging from 
1 to 15 g/litre.  Verma et al. measured the activity of 3 
phosphatases in the liver, brain, and gills of  Saccobranchus 
 fossilis after 30 days exposure to endosulfan at concentrations 
from 0.63 g/litre.  The depression in the activity of these 
enzymes was increased by the addition of ascorbic acid to the food 
of the fish.  Dalela et al. (1979) reported that acute (5 h of 
exposure) and short-term exposure (up to 32 days) of the fish 
 Channa gachua to endosulfan at respectively 11.76 and 3.5 g/litre 
produced histological changes in the gills.  On acute exposure to 
11.76 g/litre, there was separation of the respiratory gill 
epithelium from the basement membrane, pronounced hyperaemia, 
necrosis, fusion of adjacent gill lamellae, erosion at the distal 
end of gill filaments, and loss of cell membrane.  With exposure to 
a sub-lethal dose of 3.5 g endosulfan/litre, damage to the gill 
was not as severe after 8 days, but was found to be progressively 
more pronounced with increasing exposure time. 

    A detailed field study was conducted in relation to tsetse fly 
control operations in the Okavango delta region of Botswana.  Fox & 
Matthiessen (1982) reported that in laboratory studies, 24-h LC50 
values for Okavango fish ranged from 1.2 to 7.4 g/litre, depending 
on species.  Field concentrations of endosulfan after spraying at 
9.5 g/ha ranged between 0.2 and 4.2 g/litre.  The authors 

determined pre-spraying population densities and, thereby, the 
apparent mortality rate in a variety of fish species after 
spraying.  Estimated mortality rates ranged from 0.2 to 4.3% for 
individual species with an overall estimate of 0.9%.  Matthiessen & 
Roberts (1982) reported pathological changes in the liver and brain 
of fish exposed to endosulfan spray, and Matthiessen (1981) 
reported a significant elevation in blood cell counts during 

7.2.  Toxicity for Terrestrial Organisms

    The toxicity of endosulfan for terrestrial organisms is 
summarized in Table 6. 

7.2.1.  Plants

    Some phytotoxic effects of endosulfan have been reported. 
Gentile et al. (1978) reported that 24% endosulfan reduced the 
germination of cucumber pollen to 54.6% of control levels at a 
concentration of 1000 mg ai/litre, half the recommended 
concentration for field use.  At the same concentration, 
pollentube length was only 8.1% of controls.  Morey & Singh (1980) 
examined the effects of endosulfan on several species of  Cucurbitae  
and found that it was phytotoxic to all but one species and 
moderately phytotoxic to the latter.  Concentrations ranged from 
0.035 to 0.14%.  Phytotoxicity was estimated by necrotic spots on 
leaves.  Agarwal & Beg (1982a) studied the effects of endosulfan on 
the germination and seedling growth of  Cicer arietinum.  They found 
reduced viability and delayed germination with endosulfan 
treatment.  Inhibition, at lower concentrations of 0.01, 0.1, and 1 
mg/litre in an agar bed used as the germination medium, was 
reversed as germination progressed, whereas at 10 mg/litre 
inhibition persisted.  Endosulfan affected all major stages of 
germination and seedling growth.  The results of a simple  in vitro 
experiment suggested that endosulfan changed the permeability of 
root membranes.  Gupta & Gupta (1977) examined 4 concentrations of 
endosulfan between 0.35 g/kg and 3 g/kg for effects on Green Gram, 
 Vigna radiata.  Toxic effects were dose-dependent.  At 0.35 g/kg 
and 0.7 g/kg, no adverse effects were observed in any of the 
parameters studied, but, at higher concentrations of 1.5 g/kg and 3 
g/kg, symptoms of toxicity were visible.  These included coiling of 
the radical, inhibition of root growth, stunting of shoots, and 
burning of the tips and margins of leaves.  Plants were dwarfed and 
chlorotic, having damaged pollen grains and low productivity. 
Agarwal & Beg (1982b) reported that exposure of germinating  Cicer 
 arietinum seeds to endosulfan resulted in a fall in the pectin, 
hemicellulose, and cellulose contents of cell walls at all stages 
of germination compared with untreated controls.  It must be stated 
that these were very isolated phytotoxic effects.  In normal usage, 
endosulfan has not been shown to be significantly toxic to plants. 

Table 6.  Toxicity of endosulfan for terrestrial organisms
Organism            Size/       Grade       Temp  Route    Parameter      Concentration   Reference
                    age                     (C)                          (mg/kg)a
braconoid parasite  adult       technical   24    contact  24-h LC50      494 mg/litre    Hagley et al.
 (Apanteles ornigis)                                                                       (1981)

ladybird beetle     adult       technical         contact  72-h LC83      200 mg/litre    Makar & Jadhav

 (Menochilus         1-day-old   technical         contact  72-h LC78      200 mg/litre    Makar & Jadhav
 sexmaculatus)       larva                                                                 (1981)
                    3rd instar

honey bee, worker               95%               contact  LD50           7.1 g/bee       Stevenson et 
 (Apis mellifera)                                  oral     LD50           6.9 g/bee       al. (1978)

mallard             36 h        96%               oral     acute LD50     27.8            Hudson et al.
( Anas                                                                     (22.8-33.8)     (1972)
                    7 day       96%               oral     acute LD50     6.47            Hudson et al.
                                                                          (5.19-9.05)     (1972)
                    30 day      96%               oral     acute LD50     7.89            Hudson et al.
                                                                          (5.77-10.8)     (1972)
                    3-4 month   96%               oral     acute LD50     33 (23.8-45.8)  Tucker & 
                                                                                          Crabtree (1970)
                    6 month     96%               oral     acute LD50     34.4            Hudson et al.
                    16 day      96%               diet     5-day LC50     1053            Hill et al. 
                                                                          (781-1540)      (1975)
                    young       35%b              diet     < 10-day LC50  1000            DeWitt et al.
                    adult       35%b              diet     < 10-day LC50  > 5000          DeWitt et al.
                    adult       35%b              diet     < 100-day LC50 1000            DeWitt et al.

Table 6.  (contd.)
Organism            Size/       Grade       Temp  Route    Parameter      Concentration   Reference
                    age                     (C)                          (mg/kg)a
ringnecked pheasant 10 day      96%               diet     5-day LC50     1275            Hill et al. 
 (Phasianus                                                                (1098-1482)     (1975)
 colchicus)          young       35%b              diet     < 10-day LC50  500             DeWitt et al.
                    young       35%b              diet     < 100-day LC50 > 300          DeWitt et al.
                    adult       35%b              diet     < 100-day LC50 1000           DeWitt et al.

Japanese quail      14-day      96%               diet     5-day LC50     1250            Hill et al. 
 (Coturnix coturnix                                                                        (1975)

bobwhite quail      9-day       96%               diet     5-day LC50      805 (690-939)  Hill et al. 
 (Colinus                                                                                  (1975)
 virginianus)        young       35%b              diet     < 10-day LC50   300            DeWitt et al.
                    young       35%b              diet     < 100-day LC50  100            DeWitt et al.
                    adult       35%b              diet     < 100-day LC50  > 250          DeWitt et al.

cowbird                         35%b              diet     10-day LC50     1000           DeWitt et al.
a  Concentrations are mg/kg body weight for oral dosing and mg/kg diet for dietary dosing.
b  Preparation used is "thiodan", which is a 35% formulation of endosulfan.

7.2.2.  Honey bees

    Endosulfan is considered of moderate or low toxicity for honey 
bees.  Stevenson et al. (1978) reported a contact LD50 of 7.1 g/bee 
and an oral LD50 of 6.9 g/bee for endosulfan.  Endosulfan has never 
been implicated in episodes of poisoning of bees investigated in 
Great Britain (Stevenson et al., 1978). 

7.2.3.  Birds

    The toxicity of endosulfan for birds is summarized in Table 6.  
Hudson et al. (1972) examined the effects of age of mallard ducks 
on their sensitivity to endosulfan.  The acute oral LD50s for ducks 
at 36 h, 7 days, 30 days, and 6 months of age were 27.8, 6.47, 
7.89, and 34.4 mg/kg body weight, respectively. 

    Field studies on birds in the Okavango delta of Botswana 
related to endosulfan sprays for tsetse fly control failed to show 
any change in bird numbers or species diversity (Douthwaite, 1980).  
Douthwaite (1982) looked specifically at kingfishers that fed on 
fish killed or incapacitated by the spray.  The feeding rates of 
kingfishers were greatly increased by the availability of 
debilitated fish, but these rates fell when spraying ended.  The 
kingfisher population in the study area survived and numbers at a 
communal roost were steady. 

7.3.  Toxicity for Microorganisms

    Endosulfan is toxic for a wide variety of microorganisms. 
Srivastava & Misra (1981) found a dose-related increase in oxygen 
consumption by the yeast  Rhodotorula gracilis at concentrations of 
endosulfan between 10 and 200 mg/litre medium.  Further increases 
in dose up to 400 mg/litre did not show any increased effects.  
The authors suggested that endosulfan affects membrane components.  
Butler (1963) reported that endosulfan (thiodan) at a concentration 
of 1 mg/litre, decreased productivity in a natural phytoplankton 
community by 86.6% during a 4-h exposure.  The bacterial 
insecticide,  Bacillus thuringiensis, was reported by Kahlon et al. 
(1981) to show reduced viable count and spore count on incubation 
with solutions of endosulfan at 0.5 or 1 g/litre.  Endosulfan was 
the most effective inhibitor of sporulation of the 3 insecticides 
tested.  Tarar & Salpekar (1980) reported that endosulfan was the 
most toxic of 6 organochlorines for soil algae.  Of algal species 
present in the soil (18 species present in the control soil), 17 
were eliminated by endosulfan concentrations of 2 g/kg.  Only 1 
species survived endosulfan at 4 and 6 g/kg.  This species, 
 Chlorococcum humicolo, was unaffected by any of the organochlorines 
with which the soil was treated.  El Beit et al. (1981) examined 
the microbial metabolism of pesticides and effects of the 
pesticides on the growth of bacterial and actinomycete colonies.  
Endosulfan either as the alpha- or beta-isomer applied at 4000 
mg/litre prevented the growth of any bacterial or actinomycete 
colonies from any soil type tested.  Alpha-endosulfan seemed to be 
broken down by both bacteria and fungi whereas the beta-isomer was 
degraded more by bacteria than by fungi.  Results suggest that 

while both isomers can be degraded by microbial organisms, the 
degradation materials released counteract the growth of the 

7.4.  Bioaccumulation

    In aquatic ecosystems, endosulfan residues tend to reach a 
plateau level in tissues.  Schoettger (1970) exposed western white 
suckers to water containing 14C-labelled endosulfan at 29 g/litre 
for 12 h.  In the tissues concentrating the most endosulfan, a 
plateau level of the compound was reached within 12 h.  A plateau 
was maintained over a prolonged period in studies on goldfish 
exposed to endosulfan solutions at 7 g/litre.  Residue levels in 
muscle were 2.54 mg/kg after 5 days and 1.09 mg/kg after 20 days 
(Schoettger, 1970).  Accumulation appeared to be transitory, 
because endosulfan disappeared rapidly in mussels (Roberts, 1972) 
and goldfish after the source was removed (Schoettger, 1970).  
Oeser & Knauf (1973) calculated the half-life for the elimination 
of endosulfan from goldfish to be 2 - 3 days.  This followed a 5-
day exposure to 1 g of the pesticide/litre, during which time 
residues reached a mean level of 0.35 mg/kg.  Little accumulation 
of endosulfan seems to have been reported in the field.  The mean 
residue level in fish living in endosulfan-contaminated natural 
surface water was 0.4 mg/kg (Gorbach & Knauf, 1971). 

    Roberts (1972) reported concentration factors of 17, 11, and 
8.1 after exposing mussels to 0.1, 0.5, and 1.0 mg endosulfan/litre, 
respectively, for 112 days.  Although the mussels assimilated more 
pesticide at higher dose levels, the greatest concentration factors 
were achieved with the lowest dose of 0.1 mg/litre, a maximum BCF 
of 22.5 being reached after 70 days.  Roberts (1972) found that the 
major storage site for endosulfan in scallops was the digestive 
gland.  He suggested this would also be the case for mussels and 
other bivalves. 

    In a study by Ernst (1977) on the uptake and elimination of 
endosulfan, a somewhat higher BCF value of 600 was measured in 
mussels, with an initial concentration of endosulfan in the water 
of 2.05 g/litre.  The concentration factor is based on a steady 
state concentration of 0.14 g endosulfan/litre water.  If the BCF 
is calculated on the initial concentration, a BCF of 41, a more 
typical value for aquatic organisms, is obtained.  Bioaccumulation 
data are summarized in Table 7. 

Table 7.  Bioaccumulation of endosulfan
Organism             Grade   Temp  Organ   Exposure   Concen-  Dose    References
                             (C)          time       tration  (g/
                                                      factor   litre)              
green alga                         WBc     initial    2500             Oeser et al. 
 (Chlorella sp.)                            BCF                         (1971)
mussel                             WB      112 day    17       100     Roberts (1972)
 (Mytilus edulis)                   WB      112 day    11       500     Roberts (1972)
                                   WB      112 day    8.1      1000    Roberts (1972)
                     alpha-        WB                 600a     0.14a   Ernst (1977)
                     isomer                           (41)b    (2.05)b 
goldfish                           liver   11-20 day  781      7       Schoettger (1970)
 (Carassius auratus)                muscle  5-20 day   314      7       Schoettger (1970)
western white                19    muscle  12 h       65       20      Schoettger (1970)
sucker                       19    muscle  9 h        55       20      Schoettger (1970)
 (Catostomus                  19    liver   12 h       550      20      Schoettger (1970)
 commersoni)                  19    liver   9 h        695      20      Schoettger (1970)
a  Higher BCF based on steady state concentration of endosulfan.
b  Values in () based on original concentration of endosulfan (static test).
c  WB = whole body.

    Koeman et al. (1974) measured residues in animal species in    
Java, following BIMAS programmes for the control of paddy-stem     
borer that had continued over several years.  No residues were     
found (detection limit 0.03 mg/kg); animals used included fish,    
molluscs, crabs, and shrimps.  Matthiessen et al. (1982) studied   
the accumulation of endosulfan in fish and their predators         
following aerial spraying to control the tsetse fly in Botswana.   
Residue levels in fish predators, birds, and crocodiles, were      
similar to those in their prey.  Risk to predators was consequently 
deemed to be low.  Although endosulfan residues in insects were not 
measured, low residues in insectivorous birds suggested rapid      
degradation and little accumulation.  According to Matthiessen et 
al. (1982), lean fish have a lower survival rate than fat ones at 
subacute concentrations of endosulfan in the water. 

    There do not seem to be any accumulation data available for 
wild mammals. 


    The Joint Meeting on Pesticide Residues (JMPR) have reviewed 
residues and toxicity data on endosulfan on several occasions in 
the past:  1965, 1967, 1968, 1971, 1974, and 1982 (FAO/WHO, 1965, 
1968, 1969, 1972, 1975a, 1983). 

    In 1982, the estimate of a temporary acceptable daily intake 
for man was made at 0 - 0.008 mg/kg body weight (total of alpha- 
and beta-endosulfan and endosulfan sulfate).  This was based on 
no-observed-adverse-effect levels of: 

    rat:    30 mg/kg diet, equivalent to 1.5 mg/kg body weight;

    dog:    0.75 mg/kg body weight per day (administered by

    The FAO/WHO (1975b) in its series of "Data sheets on chemical 
pesticides" issued one on Endosulfan.  Based on a brief review of 
use, exposure, and toxicity, practical advice is given on 
labelling, safe-handling, transport, storage, disposal, 
decontamination, selection, training, and medical supervision of 
workers, and first aid and medical treatment. 

    WHO (1984), classified endosulfan in the list of technical 
products being moderately hazardous. 

    Regulatory standards established by national bodies in 12 
different countries (Argentina, Brazil, Czechoslovakia, 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 IRPTC (International Register of Potentially Toxic Chemicals) 
Legal file (IRPTC, 1983). 


9.1.  Evaluation of Health Risks for Man

    Endosulfan toxicity

    Endosulfan is moderately to highly toxic according to the scale 
of Hodge & Sterner (1956).  The oral LD50 in the rat ranges from 18 
- 355 mg/kg body weight, depending on such parameters as sex, 
strain, and vehicle used. 

    WHO (1984) classified endosulfan in the category of technical 
products that are moderately hazardous. 

    Endosulfan can be absorbed following ingestion, inhalation, and 
skin contact.  It is readily metabolized and excreted and does not 
accumulate in the body. 

    On acute intoxication, neurological manifestations may occur, 
such as irritability, restlessness, muscular twitchings, and  
convulsions.  Lung oedema and cyanosis may precede death. 

    Endosulfan was negative or produced conflicting results in 
short-term tests for genetic activity.  It showed no carcinogenic 
activity in mice or rats but studies were limited by inadequate 
reporting or survival. 

    Several cases of suicidal and occupational poisoning have been 
reported, the latter resulting, in most cases, from neglect of 
safety precautions. 

    Exposure to endosulfan

    Food is the main source of exposure of the general population 
to endosulfan.  Endosulfan residues in food (the sum of its alpha- 
and beta-isomers and endosulfan sulfate) have been found to be 
generally well below FAO/WHO maximum residue limits. 

    In occupationally-exposed persons, both skin contact and 
inhalation can be important routes of absorption when adequate 
safety precautions are not taken. 

    Hazard assessment

    The main hazard associated with endosulfan is acute 
intoxication through overexposure.  Such situations may be due to 
intentional or accidental overexposure or to gross negligence in 
occupational situations. 

    In all other exposure situations, especially as far as the 
general population is concerned, the toxicity profile and the 
present exposure pattern do not indicate any appreciable hazard. 

9.2.  Evaluation of Overall Environmental Effects

    Degradation of endosulfan in soil and water by photolysis, 
chemical reactions, and biotransformation is governed by a wide 
range of climatic factors and the type of microorganisms present. 

    Endosulfan does not appear to be a problem with regard to 
persistence.  It is not readily bioaccumulated.  In aquatic 
organisms, loss soon balances uptake and a fairly low plateau level 
of residues is achieved. 

    Endosulfan is hazardous in acute overexposure for some aquatic 
species, especially fish.  There has been large-scale field 
experience with endosulfan without any long-term adverse effects on 
the environment. 

    Careful application to avoid overexposure of non-target 
organisms does not eliminate kills in local fish populations when 
endosulfan is applied to wetland areas at recommended rates.  
Because there is little or no biomagnification, endosulfan, when 
applied at recommended rates, is not hazardous to terrestial 
animals.  Toxicity for bees is low to moderate. 

    The reported toxicity of endosulfan for microorganisms in the 
laboratory is low; it is unlikely to have an appreciable effect in 
the field. 

9.3.  Conclusions

    1.  The general population does not appear to be at risk
        from endosulfan residues in food.  Exposure of the
        general population via air and drinking-water is
        generally low.

    2.  Occupational exposure has resulted in some incidents
        of poisoning.  These appear however, only to have
        occurred when adequate safety precautions were not

    3.  In terms of the general environment, endosulfan is
        highly toxic for some aquatic species, particularly 
        fish.  Endosulfan is moderately toxic for honey bees.

    4.  Endosulfan does not accumulate in food chains and is
        excreted from the body rapidly.


ACGIH  (1982)   TLV's (R) threshold limit values for chemical
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American Conference of Governmental Industrial Hygienists,
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AGARWAL, S. & BEG, M.U.  (1982a)  Biochemical changes in  Cicer
 arietinum seedling on exposure to endosulfan.  Indian J.
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AGARWAL, S. & BEG, M.U.  (1982b)  Effect of endosulfan on
endogenous IAA, cell wall polysaccharide peroxidase activity
and its isoenzymatic pattern in germinating  Cicer arietinum
seeds.  Indian J. exp. Biol., 20: 319-323.

AGARWAL, D.K., SETH, P.K., & GUPTA, P.K.  (1978)  Effect of
endosulfan on drug metabolizing enzymes and lipid peroxidation
in rat.  J. environ. Sci. Health, Part C, Environ. Health Sci.,
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    See Also:
       Toxicological Abbreviations
       Endosulfan (HSG 17, 1988)
       Endosulfan (PDS)
       Endosulfan (PIM 576)
       Endosulfan (FAO Meeting Report PL/1965/10/1)
       Endosulfan (FAO/PL:1967/M/11/1)
       Endosulfan (FAO/PL:1968/M/9/1)
       Endosulfan (WHO Pesticide Residues Series 1)
       Endosulfan (WHO Pesticide Residues Series 4)
       Endosulfan (WHO Pesticide Residues Series 5)
       Endosulfan (Pesticide residues in food: 1982 evaluations)
       Endosulfan (Pesticide residues in food: 1989 evaluations Part II Toxicology)
       Endosulfan (JMPR Evaluations 1998 Part II Toxicological)