CAS No. 10265-92-6
Also a Metabolite of Acephate
Methamidophos is an organophosphate insecticide registered for use in the U.S. in 1972, and all uses were voluntarily cancelled in 2009 (U.S. EPA, 2009). It was used mainly on commercial crops of potatoes, cotton, and tomatoes, had limited use in commercial and public buildings, but it was not registered for any residential uses. Current sources of methamidophos include environmental degradation or metabolism of acephate. Methamidophos is water soluble and had a moderate potential for runoff into surface waters, but degrades within a few weeks. It may enter surface waters as a result of application or via degradation from acephate. Methamidophos does not bioaccumulate. It is acutely toxic to bees, birds, fish, and aquatic invertebrates (U.S. EPA, 2002).
General population exposure to methamidophos may occur through the diet. Estimated intakes from diet (Gunderson, 1995) and ground water sources have not exceeded recommended intake limits (U.S.EPA, 2002). Applicators, formulators, and workers who re-enter treated agricultural areas may have higher exposures, with the potential for absorption from ingestion, dermal and inhalational (as dust or aerosol) routes. Dermal absorption, approximately 5% of an applied dose, is substantially lower than gastrointestinal absorption. Methamidophos is quickly absorbed following ingestion or inhalation of dust or aerosols. It is widely distributed to body tissues, and in laboratory animals, it undergoes extensive metabolism involving deamination and demethylation, and the metabolites are eliminated in the urine. Approximately 50% of an administered dose of methamidophos was recovered in the urine within 1-3 days (IPCS, 2002).
Human health effects from methamidophos at low environmental doses or at biomonitored levels from low environmental exposures are unknown.At high doses, methamidophos and other organophosphate pesticides inhibit acetylcholinesterase enzymes in the nervous system, resulting in excess acetylcholine at nerve terminals and acute cholinergic symptoms including nausea, vomiting, weakness, paralysis, and seizures. Methamidophos has high acute toxicity in animals; for example, the rat LD50 is 13-23 mg/kg body weight. Methamidophos or associated impurities may have caused a delayed peripheral neuropathy reported in some human poisonings (Brown et al., 1989; Senanayake and Johnson, 1982; Senanayake and Karalliede, 1987). Inappropriate or misapplication of methamidophos has been responsible for food poisoning episodes (Goh et al., 1990; Wu et al., 2001). In animal studies, reproductive and developmental toxicity was observed at methamidophos doses that were maternally toxic, and methamidophos did not appear to be teratogenic, genotoxic, or carcinogenic (IPCS, 2002).The NTP, IARC and U.S. EPA do not have ratings regarding human carcinogenicity. Additional information about pesticides is available from U.S. EPA web site at:https://www.epa.gov/pesticides/external icon.
Urinary levels of methamidophos reflect recent exposure. Urinary levels of methamidophos were generally not detectable in the NHANES 2003-2004 and 2005-2006 subsamples (CDC, 2013). In urine samples from 140 adults and children in the U.S. and from 69 Italian adults, methamidophos was measured above a detection limit of 0.8 µg/L in 5.0% and a detection limit of 7 µg/L in 2.8% of samples, respectively (Olsson et al., 2003; Saieva et al., 2004). Geometric mean urine methamidophos was 1.97 µg/L (detection frequency, 1.3%) in a sample of 499 largely Hispanic pregnant women and children residing in the California agricultural area of the Salinas Valley (Montesano et al., 2007). Seven children living near potato fields sprayed with methamidophos provided urine samples on days before, during, and after spraying occurred. Urine analyzed for the methamidophos metabolite, O,S-methyl hydrogen phosphorothioate (O,S-DMPT), had median urinary O,S-DMPT concentrations of 61 µg/L on the day before, 170 µg/L on the day of, and 114 µg/L on the day after spraying (Weppner et al., 2006). High concentrations (up to 10 mg/L) of acephate but not methamidophos were detected in urine samples from four workers after acephate exposure (Maroni et al., 1990). In contrast, methamidophos was measured in urine from a child who ingested a toxic dose of acephate, and serial measurements ranged from 13,170 µg/L shortly after the ingestion to 190 µg/L two days later (Chang et al., 2009).
Finding measurable amounts of methamidophos in the urine does not imply that the levels of methamidophos cause an adverse health effect. Biomonitoring studies on levels of methamidophos provide physicians and public health officials with a reference values so that they can determine whether people have been exposed to higher levels of methamidophos than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.
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