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| Name Of Product |
CAS NO. |
Specification |
MSDS |
| Methidathion |
950-37-8 |
95% TC, 400 g/l EC, 25% WP |
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Methidathion Basic information
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Methidathion Chemical Properties
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Methidathion Usage And Synthesis
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Description
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Methidation is used as an insecticide. Cross-sensitivity was described to dichlorvos.
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Chemical Properties
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Crystalline solid. Almost insoluble in water; soluble in common organic solvents.
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Chemical Properties
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Methidathion is a colorless crystalline pesticide at room temperature. It is sparingly soluble in water, but very soluble in octanol, ethanol, xylene, acetone, and cyclohexane. Methidathion is a non-systemic organophosphorous insecticide and acaricide with stomach and contact action. It is used to control a variety of insects and mites on crops and fruit plants. Methidathion is highly toxic to animals and humans. The US EPA grouped methidathion as a class I toxic substance and as an RUP.
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Chemical Properties
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Methidathion is a colorless crystalline solid.
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Uses
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Insecticide and acaricide.
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Uses
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Methidathion is an organophosphate insecticide and was examined for human health and toxicological concerns.
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Uses
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Insecticide, acaricide.
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Uses
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Methidathion is used to control a wide range of insects in many different crops.
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General Description
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Methidathion is a colourless crystalline pesticide at room temperature. It is sparingly soluble in water but very soluble in octanol, ethanol, xylene, acetone, and cyclohexane.
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Air & Water Reactions
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Stable in neutral or weak acid solution. Hydrolyzed by alkali. [EPA, 1998].
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Reactivity Profile
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Organophosphates, such as Methidathion, are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrides. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides.
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Hazard
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Toxic by ingestion, a cholinesterase inhibitor.
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Health Hazard
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Methidathion is poisonous to humans. Its toxic effects are by action on the nervous system. Human volunteers ingesting 0.11 mg/kg/day for 6 weeks had no clinical effects.
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Health Hazard
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Acute and prolonged exposures to methidathion cause poisoning in animals and humans. The symptoms include, but are not limited to, nausea, vomiting, cramps, diarrhea, salivation, headache, dizziness, muscle twitching, diffi culty breathing, blurred vision, and tightness in the chest, pulmonary edema, respiratory depression, and respiratory paralysis. Acute exposures to high concentrations of methidathion cause intense breathing problems, including paralysis of the respiratory muscles.
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Fire Hazard
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(Non-Specific -- Organophosphorus Pesticide, n.o.s.) Container may explode in heat of fire. Fire and runoff from fire control water may produce irritating or poisonous gases. Stable in neutral or weak acid solution. Hydrolyzed by alkali.
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Agricultural Uses
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Insecticide: A U.S. EPA restricted Use Pesticide (RUP). Not approved for use in EU countries . There are no residential uses for methidathion. Methidathion is a non-systemic organophosphate 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 nuts, artichokes, olives, cotton, fruits, vegetables, tobacco, alfalfa, and sunflowers, and also in greenhouses and on rose cultures. It is especially useful against scale insects.
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Contact allergens
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Methidation is an organophosphorus compound used as an insecticide. Cross-sensitivity was described to Dichlorvos.
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Safety Profile
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Poison by ingestion and skin contact. Moderately toxic by inhalation. Human mutation data reported. Human systemic effects: coma, lachrymation, miosis. A severe eye irritant. An insecticide. When heated to decomposition it emits very toxic fumes of NOx, POx, and SOx
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Carcinogenicity
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In a chronic toxicity/carcinogenicity study, rats were fed diets with 0, 4, 40, or 100 ppm methidathion (equivalent to 0, 0.16, 1.72, or 4.91 mg/kg/day (males) and 0, 0.22, 2.20, or 6.93 mg/kg/day (females)) for 2 years, and there was no evidence of carcinogenicity in either males or females . Body weight decreases occurred in both sexes at the highest dose throughout the study.
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Environmental Fate
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Photolytic. When methidathion in an aqueous buffer solution (25C and pH 7.0) was exposed to filtered UV light (l >290 nm) for 24 hours, 17% decomposed to 5-methoxy- 3H-1,3,4-thiadiazol-2-one. At 50C, 56% was degraded after 24 hours. Degradation occurred via hydrolysis of the thiol bond of the phosphorodithioic ester. Under acidic and alkaline conditions, hydrolytic cleavage occurred at the C-S and P-S bonds, respectively (Burkhard and Guth, 1979). Smith et al. (1978) demonstrated that methidathion degraded to methidathion oxon at a faster rate in six air-dried soils than in moist soils. Half-lives for methidathion in the air-dried soils ranged from 19 to 110 days. In addition, methidathion degraded faster in an air-dried soil exposed to ozone (half-lives 2.5 to 7.0 days).
Chemical/Physical. Emits toxic fumes of phosphorus, nitrogen and sulfur oxides when heated to decomposition (Sax and Lewis, 1987). Methidathion oxon was also found in fogwater collected near Parlier, CA (Glotfelty et al., 1990). It was suggested
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Metabolic pathway
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The main route of methidathion metabolism in animals and plants is via hydrolysis or oxidation (or hydrolysis of the oxon) to yield the 3- thiomethyl-5-methoxy-1,3,4-thiadiazoldee rivative. This may either lose methanethiol to yield the methoxy-1,3,4thiadiazolinone or be conjugated as the cysteine derivative via a route involving desmethylmethidathion (in plants). In plants and mammals an additional route involves the methylation of the thiomethyl methoxy-1,3,4-thiadiazolinone derivative by S-adenosylmethionine followed by oxidation to the corresponding sulfoxide and sulfone which are excreted in the urine in mammals. Another route of detoxification in insects, plants and mammals is via demethylation of the 5-methoxy group of the 1,3,4-thiadiazolinone ring to form a metabolite which may be conjugated in plants. As is common with many phosphorothioates, the active acetylcholinesterase inhibitor, methidaoxon, is usually detected in metabolism studies but at very low concentration due to its rapid rate of hydrolysis.
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Metabolism
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The principal degradation route is similar both in animals and plants, that is, cleavage of the P?S bond via oxidative desulfuration (activation) to the oxon followed by hydrolysis to O,O-dimethyl hydrogen phosphorothioate and the 3-thiomethyl-5-methoxythiadiazole derivative, which is further degraded or conjugated. Methidathion is rapidly degraded in soil; DT50 in soil is 3C18 d.
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Shipping
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Color codeBlue: Health Hazard/Poison: Store in a secure poison location. Prior to working with this chemical, personnel should be trained on its proper handling and storage. Store in tightly closed containers in a cool, wellventilated area
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Toxicity evaluation
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The acute oral LD50 for rats is 25C54 mg/kg. Inhalation LC50 (4 h) for rats is 3.6 mg/L air. NOEL (2 yr) for rats is 4 mg/kg diet (0.2 mg/kg/d). ADI is 1 g/kg b.w. Methidathion administered to animals is rapidly metabolized and excreted.
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Degradation
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Methidathion is rapidly hydrolysed in alkaline solution but it is relatively stable in neutral and slightly acidic media. The DT50 for hydrolysis at pH 13 (25 C) was 30 min (PM).
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Waste Disposal
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Treat with strong alkali, mix with soil and bury in the case of small quantities. For large quantities, use incineration with effluent gas scrubbing
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Precautions
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Occupational workers should be very careful during use and chemical management of methidathion. As this chemical substance is a highly toxic pesticide, it has been grouped by the US EPA as toxicity class I. The containers and labels of the products should bear the signal word DANGER. Methidathion is an RUP, except for use in nurseries, and on saffl ower and sunfl owers.
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Methidathion Preparation Products And Raw materials
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