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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 for products containing methidathion include Somonic, Somonil, Supracide, Suprathion and Ultracide. The compound may be found in formulations with many other pesticides.


Methidathion is a non-systemic organophosphorous insecticide and acaricide with stomach and contact action. The compound is used to control a variety of insects and mites in many crops such as fruits, vegetables, tobacco, alfalfa and sunflowers. It is also used in greenhouses and on rose cultures. It is especially useful against scale insects. It works by inhibiting certain enzyme actions in the target pests.



Methidathion is a highly toxic compound that carries the signal word DANGER on its label. The acute oral LD50 for the compound ranges from 25 mg/kg in the mouse to 225 mg/kg in the chukar partridge. The oral LD50 for the compound to rats is between 25 mg/kg and 54 mg/kg (1).

The compound is poisonous to humans, because of its capacity to interfere with enzymes related to breathing and other nervous system activities. Symptoms of acute methidathion poisoning may include nausea, vomiting, cramps, diarrhea, salivation, headache, dizziness, muscle twitching, difficulty breathing, blurred vision, and tightness in the chest (2). Acute exposure may cause intense breathing problems including paralysis of the respiratory muscles. The symptoms of acute methidathion poisoning are similar to acute exposure to parathion.

The compound is also very highly toxic through exposure on the skin. The dermal LD50 in rabbits is about 200 mg/kg. The dermal LD50 is much higher (less toxic) to rats (1,546 mg/kg) (2). Methidathion is also highly toxic through inhalation (3) (based on studies with a product containing 40 percent methidathion). The technical product, a solid, has not been evaluated for inhalation toxicity.

Methidathion is only a mild skin irritant and is non-irritating to the eyes (for rabbits).


Beagle dogs fed small doses of the compound for two years experienced no compound related effects at or below the dose of 0.10 mg/kg/day. At doses above this amount (0.4 mg/kg/day and above) the dogs experienced enzymatic changes, and liver alterations. Inhibition of red blood cell cholinesterase, an enzyme, was observed only at the highest dose tested (1.6 mg/ kg/day) (3).

Rats also have a low tolerance for the compound; the methidathion lifetime NOEL is 0.20 mg/kg/day. Compound related effects were first noted in the rats at doses of 2 mg/kg and above and included cholinesterase inhibition in the blood, brain and some nerve related effects (3). At the highest dose of 5 mg/kg, the rats ate more food but had less body weight gain. They also developed skin lesions and foam in their lungs.

Rhesus monkeys fed small amounts of the compound developed changes in blood cholinesterase activity at doses of 1 mg/kg/day and above. Humans ingesting very small amounts of the compound (0.11 mg/kg/day) for six weeks, had no noticeable clinical effects (2). A study of exposure levels of mixer/loaders of methidathion (Supracide applications) in California showed that the greatest exposure potential to the compound was through the skin (dermal). The workers' clothing contained the greatest concentrations of the compound. Total amounts of the compound inhaled were between 13 ug/l and 21 ug/l per day of application activity. No estimates for total exposure were given owing to the difficulty in determining the amount of the compound being absorbed into the body through the skin (4).

Reproductive Effects

Moderate to low amounts of methidathion caused a number of adverse reproduction related effects. Male and female rats were fed low to moderate amounts of methidathion over two successive litters. The parents experienced tremors and decreased food consumption at 1.25 mg/kg. The low dose of 0.25 mg/kg disrupted mating behavior and also affected nursing offspring. At the highest dose tested (2.5 mg/kg), stillbirths and decreased pup survival was observed (3).

Teratogenic Effects

Small to moderate amounts of methidathion administered to pregnant rats and rabbits produced no birth defects in the offspring. The pregnant females experienced several compound related effects, most of which were typical of cholinesterase inhibition (3). The compound is unlikely to pose a significant developmental risk to humans exposed to small amounts.

Mutagenic Effects

Methidathion did not induce any genetic changes in a number of tests for gene mutation, chromosomal aberrations and DNA damage. The various gene mutation studies were conducted on hamster bone marrow cells, in mammalian cells, and on several species of bacteria (3). There is no evidence that the compound poses a genetic threat to organisms.

Carcinogenic Effects

Methidathion caused malignant and benign liver tumors in male mice. The tumors (adenomas) appeared in the mice fed 2.5 mg/kg/day for two years. Additional signs of cancer (carcinomas) were found in the male mice fed higher doses of the compound (5 mg/kg/day) for two years. This higher feeding level also produced numerous other signs of toxicity (3).

The EPA has classified the compound as a possible human carcinogen. The committee stated that this one study constitutes only limited evidence of carcinogenicity because it induced common tumors in only one sex of one species and that the mutagenic tests were not supportive of a higher classification (3).

Organ Toxicity

In addition to the changes in relation to its carcinogenicity the compound can also affect liver weight, induce other liver changes, affect the gall bladder, and decrease ovary weights at moderate doses (3).

Fate in Animals and Humans

Methidathion is rapidly absorbed, broken down and eliminated in animals (2). The breakdown products of the parent compound are not of toxicological concern (3). Only very small amounts of various metabolic products of methidathion have been detected in milk from cows (8) and in chicken eggs (3).

Following exposure to the compound, the majority of it is lost as a breakdown product through the lungs as carbon dioxide indicating complete metabolism (3, 8). Between 30 and 50 percent of the ingested amount is eliminated (as breakdown products) in urine. Half of the initial amount of the compound is removed from mammals within six hours. The compound does not significantly accumulate in rat tissue.


Methidathion is highly toxic to birds following acute exposure. The LD50 for the compound ranges from 23 mg/kg to 33 mg/kg in mallards, 8.41 in Canadian geese, 33.2 mg/kg in the ring-necked pheasant and 225 mg/kg in the chukar partridge (3, 8). When the mallards were fed methidathion in their diets, the compound was moderately toxic.

The compound is highly acutely toxic to all aquatic organisms (vertebrates and invertebrates) and thus can pose substantial risk to these populations if the compound gets into surface water through actions like pesticide drift, in surface water run-off or by entry into the sewer system. Methidathion is potentially hazardous to freshwater and saltwater species because it is highly toxic to both. In addition, tests on lobsters indicated that the combination of methidathion and another organophosphate insecticide, phosphamidon, was more toxic than either compound separately or than would be expected if the toxicities were added together (2).

The LC50 of the compound is 0.01 mg/l (rainbow trout) and 0.002 mg/l (bluegill sunfish). Methidathion is highly toxic to honey bees and products containing the compound require cautionary labeling to that effect (2, 3).

Studies with bluegill sunfish indicate that there is only a slight potential that the compound would accumulate in the tissues of organisms (7). Maximum levels of the residues of the pesticide after one month of exposure to very low concentrations in the water (0.05 ug/l) were 1.0 ug/l in the edible tissue, 3.9 ug/l in non-edible tissue, and 2.4 ug/l in whole fish. These concentrations indicate a bioconcentration factor of 46 for whole fish. After two weeks in water without methidathion the concentration in whole fish fell by nearly eighty percent (3).


Methidathion degrades quickly in soil. Half of the initial amount of the compound is usually degraded within two to three weeks. The breakdown of the compound in soil occurs through the action of soil microorganisms (7). Under alkaline conditions, methidathion is rapidly degraded by chemical action. In field tests, the half-life of the compound ranges from one to four weeks. The elimination of the compound from the application site may occur through any of the breakdown avenues or may be lost by movement. Both the parent compound and its breakdown products are mobile in soil (3), however, they have not been detected in any groundwater sources.

Little or no information is available about the fate or residence time of methidathion in water. The compound is soluble in water.

In plants, methidathion is rapidly metabolized. Oranges sprayed with Supracide at a rate of nearly two pounds per acre had residues of the compound around 0.1 ug/cm3. Within two days over sixty percent of the compound was removed from the outside of the fruit. Within one week, less than one percent of the compound remained.

Exposure Guidelines:

NOEL (dog): 0.1 mg/kg/day (liver toxicity)
ADI: 0.0005 mg/kg (human)
RfD: 0.001 mg/kg/day

Physical Properties:

Common Name: methidathion
CAS #: 950-37-8
Chemical Name: O,O-dimethyl S-(2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadiazol-3-methyl) phosphorodithioate
Chemical class: organophosphate, thiadiazole
Chemical Use: insecticide and acaricide
Solubility in water: 240 mg/l at 20 degrees C
Solubility in solvent: 53 g/kg (octanol), 260 g/kg (ethanol), 600 g/kg (xylene), 690 g/kg (acetone), 850 g/kg (cyclohexane)
Melting Point: 39-40 degrees C
Vapor pressure: 186 mmPa at 20 degrees C


Ciba-Giegy Agricultural Division
P.O. Box 18300
Greensboro, NC 27419-8300
Telephone: 919-632-6000
Fax: 919-299-8318

Review by Basic Manufacturer:

Comments solicited: June, 1993
Comments received: June, 1993


  1. The Agrochemicals Handbook. 1991. The Royal Society of Chemistry. Cambridge, England.
  2. Integrated Risk Information System. 1993. Methidathion. National Library of Medicine, Medlars.
  3. Guidance for the Reregistration of Pesticide Products containing Methidathion as the Active Ingredient. 1988. Office of Pesticides and Toxic Substances. Environmental Protection Agency. Washington, DC. 870 pages.
  4. Maddy, K.T., Dennis Gibbons, D.M. Richmond and S.A. Fredrickson. 1983. Potential Exposure of Leader/Applicators to Methidathion (SUPRACIDE) During Applications to Citrus In Riverside County, California in 1982. California Department of Food and Agriculture, Division of Pest Management, Environmental Protection and Worker Safety, Worker Health and Safety Unit. Sacramento, CA.
  5. Gauthier, M.J., J.B. Berge, A. Cuany, V. Breittmayer and D. Fournier. 1988. Microbial Degradation of Methidathion in Natural Environments and Metabolism of this Pesticide by Bacillus coagulans. Pesticide Biochemistry and Physiology 31: 61-66.
  6. Maddy, K.T., K.C. Jacobs and C. Cooper. 1984. A Degradation Study of Dislodgeable Methidathion Residues on Orange Foliage in Fresno County. California Department of Food and Agriculture, Division of Pest Management, Environmental Protection and Worker Safety, Worker Health and Safety Unit. Sacramento, CA.
  7. Asztalos, I., B.J. Nemcsok, I. Benedeczky, R. Gabriel, A. Szabo and O.J. Refaie. 1990. The Effects of Pesticides on Some Biochemical Parameters of Carp (Cyprinus carpio L.)
  8. Smith, G.J. 1993. Toxicology and Pesticide Use in Relation to Wildlife: Organophosphorous and Carbamate Compounds. C.K. Smoley. Boca Raton, FL.
  9. Gallo, M.A. and N.J. Lawryk. 1991. Organic Phosphorous Pesticides. In Handbook of Pesticide Toxicology, Volume 2, Classes of Pesticides. Wayland J. Hayes and Edward R. Laws (eds.). Academic Press, NY.