The insecticide dimethoate, an organophosphate, was first introduced in 1962 for broad spectrum control of a wide range of insects including mites, flies, aphids, and plant hoppers. It inhibits AChE activity, resulting in nerve damage, which may lead to death. It is considered highly toxic to insects although dimethoate resistance has been observed. Dimethoate has both a low vapor pressure (0.247 mPa) and Henry's law constant (l.42x10(-6) Pa m3/mol), thus volatilization is not a major route of dissipation from either water or moist soils. Photolysis is considered a minor dissipation pathway. However, studies have shown that in the presence of a catalyst, the rate of photolysis does increase. The insecticide has high water solubility (39,800 mg/L) and under alkaline conditions, hydrolysis predominates representing a major degradation pathway. It has a low soil sorption capacity (Koc=20) which varies by soil type and organic matter content. Dimethoate is degraded by microbes under anaerobic conditions and bacterial species have been identified that are capable of using dimethoate as a carbon source. Although many intermediate by-products have been identified by abiotic and biotic processes, the major degradation product is omethoate. Dimethoate has been found to adversely impact many organisms. In plants, photosynthesis and growth are highly impacted, whereas birds exhibit inhibition in brain enzyme activity, thus sublethal effects are apparent. Furthermore, aquatic organisms are expected to be highly impacted via direct exposure, often displaying changes in swimming behavior. Toxicity results include inhibition in growth and more importantly, inhibition of acetylcholinesterase activity.
Keywords: Dimethoate; Fate; Insecticide; Organophosphate; Toxicity.