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
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).
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.
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.
Disulfoton has also been shown to be mutagenic in studies on
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.
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
PHYSICAL PROPERTIES AND GUIDELINES
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-
|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 |
|Drinking Water Equivalent Level: 0.0014 mg/L (10)
|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)
P.O. Box 4913
Kansas City, MO 64120
Review by Basic Manufacturer:
Comments solicited: November, 1992
American Conference of Governmental Industrial Hygienists (ACGIH).
1984-5. Disulfoton. Threshhold Limit Values for Chemical Substances in
the Work Environment. Cincinnati, OH.
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.
Di-syston insecticide. Technical information. Kansas City, Mo:
Chemagro Agricultural Division, Mobay Chemical Corp. January 1976.
U.S. Environmental Protection Agency. Office of Pesticide
Programs. Chemical fact sheet for disulfoton. No. 43. 12/31/84.
Goesslin, R.E.; Smith, R.P.; Hodge, H.C.; Braddock, J.E. 1984.
Clinical Toxicology of Commercial Products. 5th ed. Williams &
Matsumura, F. 1975. Toxicology of Insecticides. p. 224. Plenum
Miller, D.M., ed. 1985 Crop Protection Chemicals Reference. New
York: Chemical and Pharmaceutical Publishing Corp.
National Library of Medicine. Hazaradous Substances Databank.
Disulfoton. March, 1922.
Occupational Health Services Inc. Material Safety Data Sheet for
U.S. Environmental Protection Agency. Office of Drinking Water.
"Disulfoton Health Advisory." Draft Report. August 1987.
Vettorazzi, G. Disulfoton. 1979. International Regulatory Aspects
for Pesticide Chemicals. Vol 1. CRC Press.
Wagner, S.L. 1983. Clinical Toxicology of Agricultural
Chemicals. p. 227. Noyes Data Corp.
Windholz, M. et al., eds. 1983. The Merck Index, 10th Ed., p.
492. Merck & Co.
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.
U.S. Environmental Protection Agency. 1989. Office of Water.
Health Advisory Summaries.
Howard, Philip H. (1991). Handbook of Environmental Fate and
Exposure Data for Organic Chemicals. Volume III. Pesticides. Lewis
Publishers, Inc. Chelsea, MI.
Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet
Database. Lewis Publishers, Inc. Chelsea, MI.