EXTOXNET PIP - METHIDATHION (original) (raw)

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The information in this profile may be out-of-date. It was last revised in 1996. EXTOXNET no longer updates this information, but it may be useful as a reference or resource.

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E X T O X N E T

Extension Toxicology Network

Pesticide Information Profiles

A Pesticide Information Project of Cooperative Extension Offices of Cornell University, Oregon State University, the University of Idaho, and the University of California at Davis and the Institute for Environmental Toxicology, Michigan State University. Major support and funding was provided by the USDA/Extension Service/National Agricultural Pesticide Impact Assessment Program.

EXTOXNET primary files maintained and archived at Oregon State University

Revised June 1996

Methidathion

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

RegulatoryStatus**:**Methidathion is an highly toxic compound in EPA toxicity class I. Labels for products containing it must bear the Signal Word DANGER. Methidathion is a Restricted Use Pesticide (RUP), except for use in nurseries, and on safflower and sunflowers.

Chemical Class:organophosphate

Introduction**:**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, and also in greenhouses and on rose cultures. It is especially useful against scale insects. It works by inhibiting certain enzyme actions in the target pests. It is available in emulsifiable concentrate, wettable powder, and ultra-low volume (ULV) liquid.

Formulation: It is available in emulsifiable concentrate, wettable powder, and ultra-low volume (ULV) liquid formulations.

Toxicological Effects:

• Acute toxicity: Methidathion is highly toxic via the oral route, with reported acute oral LD50 values of 25 to 54 mg/kg in the rat, and 18 to 25 mg/kg in the mouse [2,13]. Other reported oral LD50 values include 25 mg/kg in guinea pigs, 80 mg/kg in rabbits, and 200 mg/kg in dogs [2]. It is highly toxic via the dermal route as well, with reported dermal LD50 values of 85 to 94 mg/kg in the rat [2]. Methidathion is only a mild skin irritant and is nonirritating to the eyes (in rabbits). Via the inhalation route, it may be slightly toxic, with a reported 4-hour inhalation LC50 of 3.6 mg/L in rats [13]. Effects due to acute methidathion exposures are similar to those caused by other organophosphate pesticides, and may include nausea, vomiting, cramps, diarrhea, salivation, headache, dizziness, muscle twitching, difficulty breathing, blurred vision, and tightness in the chest [2]. High acute exposure may cause intense breathing problems, including paralysis of the respiratory muscles.
• Chronic toxicity: Beagle dogs fed small doses of the compound for 2 years experienced no compound related effects at or below the dose of 0.10 mg/kg/day [2,8]. At doses of 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) [2]. Rats also have a low tolerance for the compound. Compound related effects were first noted in the rats at doses of 2 mg/kg and above and included cholinesterase inhibition in the blood and brain and some nerve related effects. 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 [2,8,81]. 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 at doses of 0.11 mg/kg/day for 6 weeks had no noticeable clinical effects [8]. 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) [82].
• Reproductive effects: Moderate amounts of methidathion caused a number of adverse reproductive effects. When male and female rats were fed moderate amounts of methidathion over two successive litters, the parents experienced tremors, decreased food consumption and decreased ovary weights at 1.25 mg/kg/day [2,8]. The low dose of 0.25 mg/kg/day disrupted mating behavior and also affected nursing offspring. At 2.5 mg/kg/day (the highest dose tested), stillbirths and decreased pup survival were observed [2]. Reproductive effects in humans as a result of methidathion exposure are unlikely under normal circumstances.
• 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 [2]. The compound is unlikely to pose a developmental risk to humans.
• 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 [2]. These data indicate that methidathion is not mutagenic.
• Carcinogenic effects: Methidathion caused malignant and benign liver tumors (adenomas) in male mice fed 2.5 mg/kg/day for 2 years. Additional tumors (carcinomas) were found in the male mice fed 5 mg/kg/day over the same period. This higher feeding level also produced numerous other signs of toxicity [2,8]. Since these results apply to only one sex in one species, the carcinogenic potential of methidathion is unclear.
• Organ toxicity: Target organs in animal studies include the nervous system, liver, gall bladder, and ovaries.
• Fate in humans and animals: Methidathion is rapidly absorbed, broken down, and eliminated in animals [8]. Following absorption of the compound, the majority is lost as a breakdown product through the lungs [2,6]. Between 30 and 50% of the ingested amount is eliminated (as breakdown products) in urine [2,6]. Half of the initial amount of the compound is removed from mammals within 6 hours [2,6]. The breakdown products of the parent compound are not of toxicological concern [8]. Only very small amounts of various metabolic products of methidathion have been detected in milk from cows [6] and in chicken eggs [2].

Ecological Effects:

• Effects on birds: Methidathion is highly toxic to birds following acute exposure. The reported oral LD50 values for the compound are 23 mg/kg to 33 mg/kg in mallards, 8.41 mg/kg in Canadian geese, 33.2 mg/kg in the ring-necked pheasant, and 225 mg/kg in the chukar partridge [8,6].
• Effects on aquatic organisms: The compound is very highly acutely toxic to aquatic organisms (both vertebrate and invertebrate); the reported LC50 values of the compound are 10 to 14 ug/L in rainbow trout and 2 to 9 ug/L in bluegill sunfish [13,72]. 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 [13]. Studies with bluegill sunfish indicate that there is only a slight potential that the compound would accumulate in fish tissues [6]. Maximum levels of the residues of the pesticide after 1 month of exposure to very low concentrations in the water, 0.05 ug/L, were 1.0 ug/kg in the edible tissue, 3.9 ug/kg in nonedible tissue, and 2.4 ug/kg in whole fish. These concentrations indicate a low bioconcentration factor of 46 for whole fish. After 2 weeks in water without methidathion, the concentration in whole fish fell by nearly 80% [2].
• Effects on other organisms: Methidathion is slightly toxic to bees [13].

Environmental Fate:

• Breakdown in soil and groundwater: Methidathion is of low persistence in the soil environment; reported field half-lives are 5 to 23 days, with a representative value of about 7 days [19]. Breakdown of the compound in soil occurs through the action of soil microorganisms [83]. Under alkaline conditions, methidathion is rapidly degraded by chemical action [8]. Methidathion and its breakdown products are poorly bound by soils, and so may be mobile [19,81]. However, they have not been detected in any groundwater sources. This is probably due to the short half-life of the compound and its degradates.
• Breakdown in water: No data are currently available.
• Breakdown in vegetation: In plants, methidathion is rapidly metabolized [13]. Oranges sprayed with Supracide at a rate of nearly 2 pounds per acre had residues of the compound of about 0.1 ug/ml [81]. Within 2 days over 60% of the compound was removed from the outside of the fruit, and within 1 week, less than 1% of the compound remained [81].

Physical Properties:

• Appearance: Methidathion is a colorless crystalline compound at room temperature [13].
• Chemical Name: S-2,3-dihydro-5-methoxy-2-oxo-1,3,4-thiadiazol-3-ylmethyl O,O-dimethylphosphorodithioate [13]
• CAS Number: 950-37-8
• Molecular Weight: 302.33
• Water Solubility: 240 mg/L @ 20 C [13]
• Solubility in Other Solvents: v.s. in octanol, ethanol, xylene, acetone, and cyclohexane [13]
• Melting Point: 39.5 C [13]
• Vapor Pressure: 186 mPa @ 20 C [13]
• Partition Coefficient: 4.7243 [8]
• Adsorption Coefficient: 400 (estimated) [19]

Exposure Guidelines:

• ADI: 0.001 mg/kg/day [38]
• MCL: Not Available
• RfD: 0.001 mg/kg/day [53]
• PEL: Not Available
• HA: Not Available
• TLV: Not Available

Basic Manufacturer:

Ciba-Geigy Corporation
P.O. Box 18300
Greensboro, NC 27419-8300

• Phone: 800-334-9481
• Emergency: 800-888-8372

References:

References for the information in this PIP can be found in Reference List Number 5

DISCLAIMER: The information in this profile does not in any way replace or supersede the information on the pesticide product labeling or other regulatory requirements. Please refer to the pesticide product labeling.