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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 Assessment Program.


Publication Date: 9/93


Trade names include Bay S276, Disyston, Disystox, Dithiodemeton, Dithiosystox, Frumin AL, and Solvirex.


Disulfoton is a selective, systemic organophosphate insecticide and acaricide that is especially effective against sucking insects. It is used to control aphids, leafhoppers, thrips, beet flies, spider mites, and coffee leaf miners. Disulfoton products are used on cotton, tobacco, sugar beets, cole crops, corn, peanuts, wheat, ornamentals, cereal grains, and potatoes.

All products formulated at greater than 2% disulfoton are classified as Restricted Use Pesticides (RUP). This precaution is taken due to the high toxicity of disulfoton (4). Restricted Use Pesticides may be purchased and used only by certified applicators.



Disulfoton is very highly toxic to all mammals by all routes of exposure. It is labeled with a DANGER signal word. Whether absorbed through the skin, ingested, or inhaled, early symptoms in humans may include blurred vision, fatigue, headache, dizziness, sweating, tearing, and salivation. Symptoms occurring at high doses include defecation, urination, fluid accumulation in the lungs, convulsions, or coma. Death can occur if high enough doses lead to stoppage of respiratory muscles and/or constriction of the windpipes.

Ingestion of high doses can lead to rapid onset of effects on the stomach while symptoms resulting from skin exposure may be delayed for up to 12 hours. Complete recovery from acute poisoning takes at least one week, but complete restoration of the blood to normal enzyme (cholinestrase) levels may take up to three months (9).

The oral LD50 ranges from 6.2 to 12.5 mg/kg in male rats and from 1.9 to 2.5 mg/kg in female rats (12, 10). Weanling male rats have an oral LD50 of 5.4 mg/kg (10, 5). The dermal LD50 is 3.6 mg/kg for female rats and 15.9 mg/kg for male rats (4, 10). The inhalation LC50 for one hour is 180 ppb for male rats, and 90 ug/L for female rats (3).


Disulfoton is rapidly absorbed through the skin. This chemical inhibits cholinesterase, and, as a result, may affect the eyes, respiratory system, and central nervous system (9). Continual daily absorption may cause flu-like symptoms, loss of appetite, weakness, and uneasiness. While repeated exposure to disulfoton may inhibit the cholinesterase enzyme and thus interfere with the nervous system, 30-day human exposures have not resulted in significant enzyme inhibition (10). Workers chronically exposed to organo-phosphates, of which disulfoton is a member, have developed irritability, delayed reaction times, anxiety, slowness of thinking, and memory defects (9). Chronic exposure of workers may also lead to cataracts.

Rats have survived daily doses of 0.5 mg/kg/day for 90 days. Some studies have shown that rats can acquire a tolerance for the chemical, so they are able to adjust to the lower cholinesterase levels resulting from chronic lower level exposures (8).

Reproductive Effects

In a long-term reproduction study, 98.5% pure disulfoton was fed at doses ranging from 0.05 to 0.5 mg/kg/day to both male and female albino rats. At the high dose, the number of animals per litter was reduced by 21% in the first and third generations and a 10 to 25% lower pregnancy rate was noted. Some third-generation litters whose parents were exposed to this dose, developed fatty deposits and swelling in their livers. Exposed adults and litters had a 60% to 70% inhibition of red blood cell cholinesterase (10). This suggests that long-term exposures to high doses of disulfoton may cause reproductive effects in humans.

Teratogenic Effects

In one study, pregnant rats were given disulfoton (98.2% pure) at doses ranging from 0.1 to 1.0 mg/kg/day through a stomach tube during the sensitive period of gestation. Cholinesterase activity was decreased. In the fetuses, no developmental defects were seen except at high doses, where incomplete bone development was noted (4, 10). In another study, rabbits were given disulfoton (97.3% pure) during the sensitive period. At the higher doses (1.5 and 2.0 mg/kg/day), the mothers experienced tremors, incoordination, and death, while fetal growth was not affected (10). These studies indicate that disulfoton is very unlikely to cause birth defects in humans.

Mutagenic Effects

Disulfoton has also been shown to be mutagenic in studies on bacteria (10).

Carcinogenic Effects

Studies of rats and mice fed high doses for two years did not show significant tumor growth (4, 10). The EPA has determined that there is no evidence that disulfoton is carcinogenic.

Organ Toxicity

In a 2-year rat study, males fed disulfoton (95.5% pure) daily at levels below the LD50 had increased spleen, liver, kidney, and pituitary weights, while females with similar treatment had decreased weights in these organs. Also, at all dietary levels, male brains decreased in weight while female brain weights increased. At the highest doses, cholinesterase activity was inhibited in both sexes in the brain, plasma, and red blood cells (10).

In a 23-month mouse study, kidney weights increased in females fed daily high doses. At that level, cholinesterase activity was decreased in both sexes (10).

Fate in Humans and Animals

Disulfoton is rapidly absorbed by the gastrointestinal tract, metabolized, and excreted via urine. In one study, in which both male and female rats received single doses, females excreted the chemical at a slower rate than did the males. Males excreted 50% of the dose in the urine within four to six hours after dosing, while it took females 30 to 32 hours to excrete 50% through the urine. Within 10 days after dosing, both male and female rats lost, on average, 81.6% of the initial dose via the urine, 7.0% in the feces, and 9.2% in expired air (10).


Disulfoton-containing products are highly toxic to cold and warm fish, crab, shrimp, birds, and other wildlife (7, 8). The acute dietary LC50 for disulfoton in mallard ducks is 692 mg/kg, and 544 mg/kg in quail. The EPA has stated that use of disulfoton on certain crops may pose a risk to some aquatic and terrestrial endangered species (17).


When applied to the soil, disulfoton is actively taken up by plant roots and is translocated to all parts of the plant (14). Such systemic distribution is especially effective against sucking insects, while predators and pollinating insects are not destroyed. Control may persist for six to eight weeks (3, 4).

Disulfoton is strongly bound to soil. Some metabolites are more mobile than the parent disulfoton in sandy loam, clay loam, and silty clay loam soils. Mobility decreases as organic matter content of soil increases. In addition, these metabolites can persist longer than disulfoton. In a study on sandy loam soils, disulfoton had a half-life of one week, and 90% loss in five weeks. One metabolite had a half-life of 8 to 10 weeks, and another was fairly stable for 42 weeks (10). Higher temperatures and higher chemical concen-trations appear to decrease the rates of metabolism and degredation of disulfoton (2).

Like other organophosphorous insecticides, disulfoton will break down in water under alkaline conditions, and is most stable at normal surface water acidities. The degradation of the compound is temperature dependant (2). Humic (organic) substances found in the soil can make the pesticide sensitive to degredation by sunlight.

Disulfoton was not found in any of 835 groundwater samples taken at 764 sites (10) but was found but not quantified in groundwater in California (16).


Disulfoton, a member of the organophosphate chemical family, is a yellowish oil with a molecular weight of 274.38. At 25 degrees C, disulfoton is a pale yellow liquid. Thermal decomposition may release toxic oxides of phosphorus and toxic oxides of sulfur. Chemically, disulfoton is known as o,o-diethyl s-[2-(ethylthio)ethyl]phos-phoro- dithioate.

Exposure Guidelines:

NOEL: 0.75 mg/kg body weight/day (human) (11)
LOAEL: 0.04 mg/kg/day (10)
ADI: 0.0025 mg/kg/day (4)
TLV: 0.1 mg/m3 (skin, TWA); 0.3 mg/m3 (STEL) (1)
Drinking water
health advisory:
Drinking Water Equivalent Level: 0.0014 mg/L (10)

Physical Properties:

CAS #: 298-04-4
Solubility in water: 25 ppm at 23 degrees.
Solubility in solvents: soluble in most organic solvents and fatty oils.
Melting point: 25 degrees C
Boiling point: 62 degrees C at 0.01 torr (3); 132-135 degrees C at 1.5 torr.
Vapor pressure: 1.8 x 10 to the minus 4 power mm Hg at 20 degrees C (13)


Miles Inc.
P.O. Box 4913
Kansas City, MO 64120
Telephone: 816-242-2000

Review by Basic Manufacturer:

Comments solicited: November, 1992
Comments received:


  1. American Conference of Governmental Industrial Hygienists (ACGIH). 1984-5. Disulfoton. Threshhold Limit Values for Chemical Substances in the Work Environment. Cincinnati, OH.
  2. Clapp, D.W.; Naylor, D.V.; and Lewis, G.C. 1976. The Fate of Disulfoton in Portneuf Silt Loam Soil. J. Environ. Qual. 5:207-210.
  3. Di-syston insecticide. Technical information. Kansas City, Mo: Chemagro Agricultural Division, Mobay Chemical Corp. January 1976.
  4. U.S. Environmental Protection Agency. Office of Pesticide Programs. Chemical fact sheet for disulfoton. No. 43. 12/31/84.
  5. Goesslin, R.E.; Smith, R.P.; Hodge, H.C.; Braddock, J.E. 1984. Clinical Toxicology of Commercial Products. 5th ed. Williams & Wilkins.
  6. Matsumura, F. 1975. Toxicology of Insecticides. p. 224. Plenum Press.
  7. Miller, D.M., ed. 1985 Crop Protection Chemicals Reference. New York: Chemical and Pharmaceutical Publishing Corp.
  8. National Library of Medicine. Hazaradous Substances Databank. Disulfoton. March, 1922.
  9. Occupational Health Services Inc. Material Safety Data Sheet for Disulfoton. 4/13/87.
  10. U.S. Environmental Protection Agency. Office of Drinking Water. "Disulfoton Health Advisory." Draft Report. August 1987.
  11. Vettorazzi, G. Disulfoton. 1979. International Regulatory Aspects for Pesticide Chemicals. Vol 1. CRC Press.
  12. Wagner, S.L. 1983. Clinical Toxicology of Agricultural Chemicals. p. 227. Noyes Data Corp.
  13. Windholz, M. et al., eds. 1983. The Merck Index, 10th Ed., p. 492. Merck & Co.
  14. Spear, Robert. (1991). Recognized and Possible Exposure to Pesticides. in Handbook of Pesticide Toxicology: General Principles Volume 1. eds, Wayland J. Hayes, Jr. and Edward R. laws, Jr. Academic Press, Inc., NY.
  15. U.S. Environmental Protection Agency. 1989. Office of Water. Health Advisory Summaries.
  16. Howard, Philip H. (1991). Handbook of Environmental Fate and Exposure Data for Organic Chemicals. Volume III. Pesticides. Lewis Publishers, Inc. Chelsea, MI.
  17. Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet Database. Lewis Publishers, Inc. Chelsea, MI.