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: 5/94
TRADE OR OTHER NAMES
Agridip, Asunthol, Meldane, Muscatox, Umbethion, Co-Ral, Asuntol, Bay 21,
Baymix, Dilice, Resistox, Suntol, Negashunt.
The U.S. Environmental Protection Agency (EPA) classifies most
formulations of coumaphos as general use pesticides. Certain formulations
have been classified as Restricted Use Pesticides (RUP) because they pose a
hazard of acute poisoning from ingestion. These RUPs are 11.6% EC and 42%
flowable concentrate end-use products (20). RUPs may be purchased and used
only by certified applicators. Check with specific state regulations for
local restrictions which may apply.
Coumaphos is an insecticide used for control of a wide variety of
livestock insects, including cattle grubs, screw-worms, lice, scabies, flies,
and ticks. It is used against ectoparasites, which are insects that live on
the outside of host animals such as sheep, goats, horses, pigs, and poultry
(15). It is added to cattle and poultry feed to control the development of
fly larvae that breed in manure. It is also used as a dust, dip, or spray to
control mange, horn flies, and face flies of cattle (11). Coumaphos is
considered a selective insecticide because it kills specific insect species
while sparing other nontarget organisms.
Coumaphos is one of a class of pesticides referred to as
organophosphates. These chemicals act by interfering with the activity of
naturally-occurring enzymes called cholinesterases. Cholinesterases are
essential for the proper working of the nervous systems in the bodies of both
humans and insects. Please refer to the Toxicology Information Brief on
cholinesterase-inhibition for a more detailed discussion of this enzyme.
Coumaphos is highly toxic by inhalation and ingestion, and moderately
toxic by dermal absorption (19). As with all organophosphates, coumaphos is
readily absorbed through the skin. Skin which has come in contact with this
material should be washed immediately with soap and water and all contaminated
clothing should be removed. Skin and eye contact with this insecticide may
cause mild irritation, as well as cholinesterase-inhibition. Coumaphos does
not cause skin sensitization allergies (20). Toxic symptoms in humans are
largely caused by the inhibition of cholinesterase. Individuals with
respiratory ailments, impaired cholinesterase production, or with liver
malfunction may be at increased risk from exposure to coumaphos. High ambient
temperatures or exposure to UV light may increase the toxicity of coumaphos
(19). Signs of poisoning include diarrhea, drooling, difficulty in breathing,
leg and neck stiffness (3). Some of the symptoms of acute inhalation of
coumaphos begin immediately, or within four to 12 hours, of exposure. These
include headaches, dizziness and incoordination. Moderate poisoning is
characterized by muscle twitching and vomiting. Severe poisoning is indicated
by diarrhea, fever, toxic psychosis, fluid retention (edema) of the lungs, and
high blood pressure. Symptoms of sublethal poisoning may continue for 2 to 6
The organophosphate insecticides are cholinesterase inhibitors. They are
highly toxic by all routes of exposure. When inhaled, the first effects are
usually respiratory and may include bloody or runny nose, coughing, chest
discomfort, difficult or short breath, and wheezing due to constriction or
excess fluid in the bronchial tubes. Skin contact with organophosphates may
cause localized sweating and involuntary muscle contractions. Eye contact
will cause pain, bleeding, tears, pupil constriction, and blurred vision.
Following exposure by any route, other systemic effects may begin within a few
minutes or be delayed for up to 12 hours. These may include pallor, nausea,
vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred
vision, constriction or dilation of the eye pupils, tears, salivation,
sweating, and confusion. Severe poisoning will affect the central nervous
system, producing incoordination, slurred speech, loss of reflexes, weakness,
fatigue, involuntary muscle contractions, twitching, tremors of the tongue or
eyelids, and eventually paralysis of the body extremities and the respiratory
muscles. In severe cases there may also be involuntary defecation or
urination, psychosis, irregular heart beats, unconsciousness, convulsions and
coma. Death may be caused by respiratory failure or cardiac arrest (19).
Some organophosphates may cause delayed symptoms beginning 1 to 4 weeks
after an acute exposure which may or may not have produced immediate symptoms.
In such cases, numbness, tingling, weakness and cramping may appear in the
lower limbs and progress to incoordination and paralysis. Improvement may
occur over months or years, and in some cases residual impairment will remain
The amount of a chemical that is lethal to one-half (50%) of experimental
animals fed the material is referred to as its acute oral lethal dose fifty,
or LD50. The oral LD50 for coumaphos in rats is 13-41 mg/kg, 28 to 55 mg/kg
in mice, 58 mg/kg in guinea pigs, and 80 mg/kg in rabbits (8, 10, 2, 18, 19).
An oral dose of 8 mg/kg of the insecticide killed sheep. Other sheep survived
a 20 mg/kg dose, but were severely affected for several days (11). The dermal
LD50 in rats is 860 mg/kg, and 500 to 2400 mg/kg in rabbits (19, 20). The
eye, or ocular, LD50 in rabbits is 2.6 mg/kg (8).
The lethal concentration fifty, or LC50, is that concentration of a
chemical in air or water that kills half of the experimental animals exposed
to it for a set time period. The 1-hour inhalation LC50 for coumaphos in rats
is 341 mg/m3 for females and 1080 for males mg/m3 (20).
Repeated or prolonged exposure to organophosphates may result in the same
effects as acute exposure including the delayed symptoms. Other effects
reported in workers repeatedly exposed include impaired memory and
concentration, disorientation, severe depressions, irritability, confusion,
headache, speech difficulties, delayed reaction times, nightmares,
sleepwalking and drowsiness or insomnia. An influenza-like condition with
headache, nausea, weakness, loss of appetite, and malaise has also been
reported (8, 19).
Coumaphos has a residual period of two to three weeks on livestock.
During this time, traces of the chemical may still be active (4). No adverse
effects were seen in cattle that were sprayed weekly with a concentration of
200-400 parts per million (ppm) of coumaphos, or dipped over a two-year period
in a solution containing 200 ppm (11).
Rats tolerated a two-year diet with 5 mg/kg/day of coumaphos. Rats that
were given daily doses of 1.25 or 5 mg/kg in a two-year chronic feeding study
had shortened life spans by 10% and 25%, respectively. A dose-related
inhibition of cholinesterase was observed at 0.5 mg/kg or higher. In other
words, as the dosage of coumaphos increased, cholinesterase inhibition also
increased. No pathological changes were seen that could be attributed to
Once in the bloodstream, coumaphos may cross the placenta. Mice fed
coumaphos at a dietary level of 100 ppm exhibited a decrease in the number of
pregnancies, litter size, and surviving offspring. No reproductive effects
were observed in 3 generations of mice fed a dietary doses of 1.25 mg/kg/day
Based on studies with rats and rabbits, EPA has determined that coumaphos
is not teratogenic (20). When rats were given doses of 0, 1, 5 and 25 mg/kg
on days 6 through 15 of pregnancy, the mothers given 25 mg/kg exhibited
tremors, but no developmental effects occurred in offspring at any dose.
Similar results were observed when pregnant rabbits were given doses of up to
18 mg/kg on days 7 through 19 of pregnancy. The mothers exhibited signs of
cholinesterase inhibition at the highest dose tested (18 mg/kg), but no
evidence of developmental effects on the offspring were seen at any dose (21).
No increase in embryonic deaths or teratogenesis was observed in heifers given
dermal application of coumaphos at a rate of 14.2 grams (g) or 28.5 g/kg
during various stages of gestation (11).
Gene mutation and DNA damage studies performed on bacterial cultures
showed no evidence of mutagenicity (20, 21).
Coumaphos was not found to be cancer-causing, or carcinogenic, in tests
done on mice and rats. There was no increase in the number of tumors reported
in rats given doses of 1.25 or 5 mg/kg/day of coumaphos in a 2-year chronic
feeding study (13).
Coumaphos primarily affects the nervous system through cholinesterase
inhibition, by which there is a deactivation of cholinesterase, an enzyme
required for proper nerve functioning. No organ effects were seen in acute or
chronic studies of coumaphos. The toxic effects of coumaphos are limited to
those related to cholinesterase inhibition.
Fate in Humans and Animals
Following its oral administration to mammals, coumaphos was rapidly
broken down into nontoxic products which were eliminated in urine and feces
with no evidence of bioaccumulation (20). Seventy percent of an oral dose
given to rats was eliminated in 7 days. With dermal doses, 5% was eliminated.
Single oral doses produced no changes in metabolism and no evidence of
bioaccumulation in rats (21).
Significant amounts of organo-soluble substances were found in the livers
and kidneys of cattle that had coumaphos applied to the skin. Coumaphos was
also found in the milk of dermally treated cows (5).
Unchanged coumaphos and other breakdown products were found in the
excreta of hens that were dusted with the insecticide. Similar results and
substances were found after oral treatment of hens coumaphos (5).
Effects on Birds
Coumaphos is highly toxic to birds (20). The symptoms of acute toxicity
in mallards given dietary concentrations of 29.8 mg/kg include spraddle-legged
walking, wing twitching, wing drop, tearing of the eyes, and spread wings.
These symptoms persisted in some survivors for up to 13 days, accompanied by
weight loss. Death usually occurred between 2 and 12 hours after treatment.
(12). Severe acute toxicity, and eventual death, was caused in hens after
they were given daily oral doses of 10 mg for 1 to 8 days. Hens given single
oral doses of 50 mg/kg recovered from the initial effects of cholinesterase-
inhibition and developed signs of delayed nerve poisoning, or neurotoxicity
(11). The oral LD50 for coumaphos in wild birds is 3 mg/kg, 29.4 mg/kg in
mallard ducks, and 7.94 mg/kg in pheasants, and 14 mg/kg in chickens (7, 9,
20). When they were fed the insecticide at 100 mg/kg, chickens developed leg
Effects on Aquatic Organisms
Coumaphos is moderately toxic to fish and highly toxic to aquatic
invertebrates (20). The 96-hour LC50 for coumaphos (95-97% technical) in
channel catfish is 0.8 ppm at 18 degrees C, in largemouth bass is 1.1 ppm, and
in walleyes is 0.8 ppm (11). The 96-hour LC50 in rainbow trout is 5.9 ppm, in
bluegill sunfish is 5 ppm, and in freshwater invertebrates (amphipods) is 0.15
parts per billion (ppb) (20).
Effects on Other Animals (Nontarget Species)
Coumaphos poses a moderate hazard to honey bees and a slight hazard to
other beneficial insects (4).
Breakdown of Chemical in Soil and Groundwater
Coumaphos was relatively immobile in a sandy loam soil and is unlikely to
contaminate groundwater. However, because coumaphos use patterns create
potential concentrated or point sources of pollution at animal treatment
sites, EPA has called for additional data related to coumaphos's potential for
groundwater contamination (20).
A general characteristic of organo-phosphates such as coumaphos is that
they adsorb, or bind, fairly well to soil particles. Chemicals that have a
high tendency to bind to soil do not readily move (leach) with water
percolating through the soil (17).
Breakdown of Chemical in Water
Coumaphos is relatively resistant to breakdown in water (hydrolysis). It
is nearly insoluble in water, and is relatively stable over a wide pH range in
water (18, 23).
Breakdown of Chemical in Vegetation
No information was found on the breakdown of coumaphos in vegetation.
PHYSICAL PROPERTIES AND GUIDELINES
Technical coumaphos is a tan crystalline solid with a slight sulfur odor
(15, 5). Although it is stable in water, coumaphos hydrolyzes slowly in
alkaline conditions. Alkaline and strong oxidizing materials should be
avoided when using this material (11). It is also incompatible with
pyrethroids and piperonyl butoxide (4).
Coumaphos is stable under normal temperatures and pressures (19). It may
burn, but does not ignite readily. When heated to decomposition, coumaphos
emits very toxic fumes of sulfur oxides, phosphorous oxides, and chlorides
(15). These gases can pollute (14). Efforts should be made to keep containers
of this insecticide cool, as they may explode in the heat of fire (8). The
runoff from fire control water may give off poisonous gases or cause pollution
Depending on formulation and use rate, coumaphos should not be used to
treat lactating dairy cattle, or any cattle within three weeks of calving. It
should also not be used for treatment of any animals or poultry within two
weeks of shipping, vaccinations or other stressful situations (11).
Persons who work with organo-phosphate materials for long periods of time
should have frequent blood tests of their cholinesterase levels. If the
cholinesterase level falls below a critical point, no further exposure should
be allowed until it returns to normal (22).
Protective clothing must be worn when handling coumaphos. Before
removing gloves, wash them with soap and water. Always wash hands, face and
arms with soap and water before smoking, eating or drinking.
After work, remove all work clothes and shoes. Shower with soap and
water. Wear only clean clothes when leaving the job. Wash contaminated
clothing and equipment with soap and water after each use. Keep contaminated
work clothes separate from regular laundry.
No occupational exposure limits have been established for coumaphos by
OSHA, NIOSH or ACGIH (19).
|CAS #: ||56-72-4
|Specific gravity: ||1.474 (19); 30.06 lb/cu ft (21)
|H2O solubility: ||insoluble in water (5); 1.5 mg/liter at 20 degrees C (6)
|Solubility in other solvents: ||slightly soluble in acetone, chloroform, corn oil; soluble in organic solvents; slightly soluble in ethanol (5)
|Melting Point: ||90-92 degrees C (1)
|Boiling point: ||20 degrees C at 10 to the minus 7 mm Hg (20)
|pH: ||7.23 at 1 g/100 ml (20)
|Vapor pressure: ||1 x 10 to the minus 7 mm Hg at 20 degrees C (5)
|Partitioning model: ||PCMC1 (mole fraction) - 7.45 x 10 to the minus 8; PMCM2 (mg/l): 1.5; PCMC3 (mcm/l): 4 (16)
|Chemical Class/Use: ||Organophosphate insecticide
Anthelmintic for animal use (a remedy for the destruction or elimination of intestinal worms)
P.O. Box 390
Shawnee Mission, KS 66201-0390
Review by Basic Manufacturer
Comments solicited: November, 1992
Comments received: January, 1994
Berg, G. L., ed. 1986. Farm chemicals handbook. Willoughby, OH:
Meister Publishing Company.
Dreisbach, R. H. 1983. Handbook of poisoning: Prevention, diagnosis
and treatment. Eleventh edition. Los Altos, CA: Lange Medical Publications.
Gosselin, R. E., et al. 1976. Clinical toxicology of commercial
products. Fourth edition. Baltimore, MD: Williams and Wilkins.
Harding, W. C. 1979. Pesticide profiles. Part one: Insecticides and
miticides. Bulletin 267. Cooperative Extension Service. University of
MEDLARS II. 1983. National Library of Medicine. National interactive
retrieval service toxicology data bank file.
Melnikov, N. N. 1971. Chemistry of pesticides. NY: Springer-Verlag,
National Institute for Occupational Safety and Health (NIOSH). 1981-
1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati,
Occupational Health Services, Inc. 1986. Material safety data sheet.
Secaucus, NJ: OHS, Inc.
Pimentel, D. 1971 (June). Ecological effects of pesticides on
nontarget species. Executive Office of the President's Office of Science and
Technology. Washington, DC: U.S. Government Printing Office.
Sax, N.I. 1984. Dangerous properties of industrial materials. Sixth
edition. NY: VanNostrand Reinhold Co.
TOXNET. 1975-1986. National library of medicine's toxicology data
network. Hazardous Substances Data Bank (HSDB). Public Health Service.
National Institute of Health, U. S. Department of Health and Human Services.
Bethesda, MD: NLM.
Tucker, R. and D. G. Crabtree. 1970. Handbook of toxicity of
pesticides to wildlife. U. S. Department of Agriculture, Fish and Wildlife
Service. Bureau of Sport Fisheries and Wildlife. Washington, DC: U.S.
Government Printing Office.
U.S. Department of Health, Education and Welfare. 1979. Bioassay of
coumaphos for possible carcinogenicity. National Cancer Institute Technical
Report Series No. 96. NCI-CG-TR-96. Public Health Service. Bethesda, MD:
National Institutes of Health.
U. S. Department of Transportation. 1983. 1984 emergency response
guidebook. Guidebook for hazardous materials incidents. G-31. Washington,
U. S. Environmental Protection Agency. 1985 (Oct. 31). EPA chemical
profile: coumaphos. Washington, DC.
_____. 1984 (Dec.). User's manual for the pesticide root zone model
(PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
Witt, J. M., ed. 1985. Chemistry, biochemistry, and toxicology of
pesticides. Proceedings of Extension Service Short Course at Oregon State
University. Pest control education program. Eugene, OR.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Occupational Health Services, Inc. 1991 (Feb. 12). MSDS for Coumaphos.
OHS Inc., Secaucus, NJ.
US Environmental Protection Agency. 1989 (Sept. 27). Pesticide Fact
Sheet: Coumaphos (Fact Sheet Number 207). US EPA, Washington, DC.
_____. 1989 (Sept.). Registration Standard for Pesticide Products
Containing Coumaphos as the Active Ingredient. Office of Pesticide Programs,
US EPA, Washington, DC
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
Review by Miles, Inc. January 17, 1994.