E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Publication Date: 9/93
TRADE OR OTHER NAMES
Commercial names for the product include Thiodan, Endocide, Beosit,
Cyclodan, Malix, Thimul and Thifor.
Endosulfan is a chlorinated hydrocarbon insecticide of the
cyclodiene subgroup which acts as a contact poison in a wide variety of
insects and mites. It can also be used as a wood preservative. It is
used primarily on food crops like tea, fruits, vegetables and on grains.
The commercial product is made up of a mixture of two separate
parts (isomers): the alpha and beta configurations. Endosulfan will be
considered as a single (homogenous) product unless otherwise stated in
Endosulfan is a highly toxic substance and carries the signal word
DANGER on the label. Toxicity is partly dependent on the manner with
which the pesticide is administered (7). Undiluted endosulfan is slowly
and incompletely absorbed into the body whereas absorption is more rapid
in the presence of alcohols, oils and emulsifiers.
Stimulation of the Central Nervous System is the major
characteristic of endosulfan poisoning (9). Symptoms of acute exposure
are indistinguishable from symptoms from other cyclodienes (10). They
include incoordination, even a loss of the ability to stand. Other
signs of poisoning include gagging, vomiting, diarrhea, agitation,
convulsions and loss of consciousness. Blindness has been documented
for cows which grazed in a field sprayed with the compound. The animals
completely recovered after a month following the exposure (10). In an
accidental exposure, sheep and pigs grazing on a sprayed field suffered
a lack of muscle coordination and blindness.
The oral LD50 in rats ranges from 18 - 220 mg/kg. Some other oral
LD50 values are: mice 7.36 mg/kg, hamsters 118 mg/kg, cats 2 mg/kg, and
dogs 76.7 mg/kg. The dermal LD50 for rats is 74 mg/kg while for rabbits
figures from 200 to 359 mg/kg are recorded. As noted before, the
solvents and emulsifiers used to dissolve endosulfan influence its
toxicity. Rats have an inhalation LC50 of 8.0 mg/m3 for four hours.
Dogs are less tolerant than rats to this compound and rats are nearly
twice as susceptible to endosulfan when they have been deprived of
Several chronic effects have been noted for animals exposed to
endosulfan. The pesticide is most likely to affect kidneys, liver,
blood chemistry and the parathyroid gland (9).
Rats fed low doses of endosulfan (2.5 mg/kg/day) for three
generations showed no ill effects. The same dose in dogs, however,
produced vomiting, tremors, and convulsions. These are the symptoms of
acute endosulfan poisoning. Higher doses of endosulfan (5.0 mg/kg/day)
caused death in rat dams, increased resorption and caused skeletal
deformities in the rat fetuses (10). Female mice fed the compound for
78 weeks (0.1mg/kg/day) had damage to their reproductive organs.
When moderate to high levels of endosulfan (5 or 10 mg/kg/day) were
given orally to female rats on days 6 to 14 of pregnancy, no soft tissue
defects were found in their offspring. Some delayed bone formation
occurred, however. It is possible that chronic exposure to endosulfan
may result in reproductive and/or developmental difficulties in humans.
There is no direct evidence of this in humans though.
Endosulfan is mutagenic to bacterial cells and to yeast cells. The
metabolites of endosulfan have also shown the ability to cause cellular
changes (10). This compound has also caused mutagenic effects in two
different mammalian species. It is possible that it would induce these
changes in humans.
In a National Cancer Institute study done with both mice and rats,
the males of both groups experienced such a high mortality rate that no
conclusions could be drawn (1). However, the females of both species
failed to develop any carcinogenic conditions 78 weeks after being fed
diets containing up to 445 ppm (about 23 mg/kg). There are no reports
of cancer in humans exposed to endosulfan. The EPA has placed
endosulfan in the "not classifiable" category due to the lack of data on
Fate in Humans and Animals
Endosulfan is rapidly degraded and eliminated in mammals with very
little absorption in the gastrointestinal tract. Cattle fed 0.15 mg/kg
for 60 days had no residues in the fat. The metabolite, endosulfan
sulfate, seems to show similar acute toxicity to the parent compound.
The beta isomer is cleared from blood plasma more quickly than the alpha
isomer (3). Most of the endosulfan seems to leave the body within a few
days to a few weeks.
Mice fed endosulfan had both isomers plus two breakdown products in
the feces. There were only traces of oxidized endosulfan in the kidney
Birds in general are fairly sensitive to endosulfan poisoning.
The oral LD50 is 33 mg/kg for young ducks (205-243 mg/kg for mature
mallards). The oral LC50 is 805 mg/kg for bobwhite quail and 1,275 mg/kg
for ring-necked pheasants. Male mallards from three to four-months-old
exhibited wings crossed high over their back, tremors, falling, and
other symptoms as soon as ten minutes after an acute, oral dose. The
symptoms persisted for up to a month in a few animals (3).
Several fish species are quite susceptible to endosulfan. The 96-
hour LC50 is 1.2 ppb for bluegill and 1.4 ppb for rainbow trout. In an
accidental fish kill, the initial water level was 30.9 ppb which
dropped to 0.01 - 6.5 ppb in four days. Endosulfan is also quite toxic
to birds and to shellfish.
It is moderately toxic to bees and is relatively non-toxic to
beneficial insects such as parasitic wasps, lady bird beetles and some
Endosulfan does not easily dissolve in water. It does stick to soil
particles readily. Transport of this pesticide is most likely occur if
endosulfan is attached to soil particles in surface runoff. Large
amounts of endosulfan can be found in surface water near areas of
application (9). It has also been found in surface water throughout the
country at very low concentrations and has been detected in the air at
minute levels. It is has been found, but not quantified, in well water
in California (11). It is not expected to pose a threat to groundwater.
In raw river water at room temperature and exposed to light, both
isomers disappeared in four weeks. A breakdown product first appeared
within the first week. The breakdown in water is faster (five weeks)
under neutral conditions than at more acidic conditions (five months).
Under strongly alkaline conditions the half-life of the compound is one
The two isomers have different degradation times in soil. The
half-life for the alpha isomer is 35 days and 150 days for the beta
isomer under neutral conditions. These two isomers will persist longer
under more acidic conditions. The compound is broken down in soil by
fungi and by bacteria (2).
The breakdown product, endosulfan sulfate, has been observed in
several field studies involving plants. The sulfate is more persistent
than the parent compound, accounting for 90% of the residue in 11 weeks.
Sulfate formation increases as temperatures increase (2). However,
sunlight may play a role in the reaction, perhaps in starting the
process. On most fruits and vegetables, 50% of the parent residue is
lost within three to seven days.
Endosulfan and endosulfan residues have been found in numerous food
products at very low concentrations. They have been detected in
vegetables (0.0005 - 0.013 ppm), in tobacco, in various seafoods (0.2
ppt - 1.7 ppb), and in milk.
|NOEL (rat): ||0.15 mg/kg/day
|TLV-TWA: ||0.1 mg/m3
|TLV STEL: ||0.3 mg/m3
|ADI: ||0.006 mg/kg/day (ppm) (WHO)
|RfD: ||0.00005 mg/kg/day (EPA); 0.0015 mg/kg/day (OPP)
|LEL: ||0.75 mg/kg/day (rat)
|CAS #: ||115-29-7
|Chemical name: ||6,7,8,10,10-hexachloro-1,5,51,6,9,9a-hexahydro-6,9-methano-2,4,3-benzadioxathiepin 3-oxide
|Chemical class/use: ||chlorinated hydrocarbon insecticide
|Solubility in water: ||alpha isomer: 0.32 mg/l; beta isomer: 0.33 mg/l
|Solubility in other solvents: ||toluene 20 g/100 g; hexane 2.4 g/100 g;
|Melting Point: ||alpha isomer: 109.2 degrees C; beta isomer: 213.3 degrees C; technical material 70-100 degrees C.
|Vapor Pressure: ||1.7 x 10 to the minus 7 power mm Hg
Agricultural Chemicals Group
2000 Market Street
Philadelphia, PA 19103
Review by Basic Manufacturer:
Comments solicited: October, 1992
National Cancer Institute (1978). Bioassay of Endosulfan for
Possible Carcinogenicity, U. S. Department of Health, Education and
Welfare, Public Health Service, National Institutes of Health, Technical
Report Series No. 62.
National Research Council Canada (1975). Endosulfan: Its Effects
on Environmental Quality. Subcommittee on Pesticides and Related
Compounds, NRC Associate Committee on Scientific Criteria for Environ
Quality, Report No. 11, Ottawa, Canada.
National Library of Medicine (1987). Hazardous Substances
Databank. TOX-NET, Medlars Management Section, Bethesda, MD.
Chemical Information Systems, Inc. (1988). Oil and Hazardous
Materials/Technical Assistance Data System, Baltimore, MD.
Food and Agriculture Organization of the United Nations
Pesticide Residues in Food - 1982. FAO Plant Production and Protection
National Institute for Occupational Safety and Health (1985-86)
Registry of Toxic Effects of Chemical Substances, U. S. Department of
Health and Human Services, Centers for Disease Control.
Maier - Bode, H. (1968). Properties, Effect, Residues, and
Analytics of the Insecticide Endosulfan, Residue Reviews 22:10-44.
Farm Chemicals Handbook. (1992). Meister Publishing Company.
US Department of Health and Human Services. 1990. Toxicological
Profile for Endosulfan. Draft. Public Health Service, Agency for Toxic
Substances and Disease Registry.
Smith, Andrew G. (1991). Chlorinated Hydrocarbon Insecticides.
in Handbook of Pesticide Toxicology, Volume 3, Classes of Pesticides.
Wayland J. Hayes Jr. and Edward R. Laws, Jr. editors. Academic Press,
Howard, Philip H. 1991. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals. Volume III, Pesticides. Lewis
Publishers, Chelsea, MI.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
Questions regarding the development of this web site should be directed to the
For more information relative to pesticides and their use in New York State, please contact the PMEP staff at:
5123 Comstock Hall
Ithaca, NY 14853-0901
This site is supported, in part, by funding from the