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Biomonitoring Summary


CAS No. 60-51-5


CAS No. 1113-02-6
Also a Metabolite of Dimethoate

General Information

Dimethoate is a systemic and contact organophosphorus insecticide registered for use in the U.S. in 1962 and used on several field grown agricultural crops (e.g., leaf greens, citrus, and melons), tree crops, and ornamentals. Residential and non-agricultural uses were cancelled in 2000. Use on alfalfa, wheat, cotton, and corn crops accounts for more than 60% of the total dimethoate use in the U.S. (U.S. EPA, 2006). Dimethoate is nonvolatile, water soluble, and not mobile in soil, where it degrades with a half-life of approximately 2-4 days, based on soil conditions.

In plants and in the environment, omethoate occurs as a break down product within a few days after dimethoate application. Similar to dimethoate, omethoate is broken down in the environment within two weeks. Omethoate appears to be responsible for dimethoate toxicity in insects and mammals (IPCS, 1989). Omethoate is a toxic organophosphate insecticide. Although never registered for use in the U.S., omethoate has been registered in other countries. Neither dimethoate nor omethoate bioaccumulate, but both are highly toxic to honey bees, birds, and freshwater invertebrates (U.S. EPA, 2006).

Dimethoate is absorbed from the gastrointestinal tract, the lungs, and through the skin. General population exposure to dimethoate or omethoate can occur by eating foods treated with dimethoate or by drinking water. Estimated intakes of dimethoate and omethoate from these sources have not exceeded the U.S. EPA levels of concern (U.S. EPA, 2006). The FDA has detected both insecticides in food samples tested as part of the Total Diet Study that monitors U.S. foods (FDA, 2006). Estimated average daily intakes have been below acceptable limits (Gunderson, 1995). Among professional pesticide applicators and formulators, dimethoate exposure can occur by skin contact or from inhaling aerosols or dust. Workers in treated fields can have exposure to dimethoate, omethoate, or both by skin contact.

Human health effects from dimethoate or omethoate at low environmental doses or at biomonitored levels from low environmental exposures are unknown. High doses of dimethoate, omethoate, and other organophosphate pesticides inhibit acetylcholinesterase enzymes in the nervous system, resulting in excess acetylcholine at nerve terminals. Acute cholinergic symptoms include nausea, vomiting, weakness, paralysis, and seizures. Dimethoate has moderate acute toxicity in mammals (e.g., the LD50 in mice and rats is 150 and 400 mg/kg bodyweight, respectively) (IPCS, 1989). Omethoate is about 10 times more toxic and a more potent cholinesterase inhibitor than dimethoate (FAO/WHO, 1997; Hassan et al, 1969).

In insects, dimethoate metabolizes to omethoate, but mammals appear to have lower levels of the enzyme responsible for this metabolic conversion. In animal studies, dimethoate was rapidly absorbed after oral dosing and more slowly after skin application (Sanderson and Edson, 1964). Dimethoate is widely distributed to body tissues and metabolized in the liver to omethoate (most likely via the cytochrome P450 enzyme system), which is then rapidly broken down to several methylated dialkyl phosphate metabolites that are eliminated in urine within 1-2 days (IPCS, 1989; Menzer and Best, 1968). Serial urine measurements of dimethoate in an adult who mistakenly ingested a large amount of the insecticide revealed an elimination half-life of 23.8 hours and first-order kinetics (Huffman and Papendorf, 2006). In another case, an adult ingested food containing 17 ppm dimethoate (dose approximately 0/1 mg/kg) and provided serial urine specimens. Over the next 50 hours, 97-99% of the ingested dimethoate was recovered as urinary dialkyl phosphate metabolites and <1% as dimethoate (Krieger and Thonginthusak, 1993).

In animal studies, inhibition of erythrocyte but not plasma cholinesterase appeared to be the most sensitive indicator of dimethoate exposure and toxicity (Sanderson and Edson, 1964; IPCS, 1989). In short-term feeding studies, laboratory animals showed reduced cholinesterase activity in red blood cells, plasma, and the brain despite a lack of clinical signs of toxicity (IPCS, 2003).

Carcinogenicity studies in animals have been inconsistent, with tumors of spleen, skin, and lymph systems in male but not female rats, and lung tumors and lymphoma in male mice and liver tumors in female mice. Dimethoate is considered mutagenic, but it is not a teratogen. Reproductive toxicity was seen at doses that also caused overt maternal toxicity (IPCS, 2003; U.S. EPA, 1995). The U.S. EPA classified dimethoate as a possible human carcinogen (U.S. EPA, 1995). The National Toxicology Program (NTP) and International Agency for Research on Cancer (IARC) have not evaluated dimethoate or omethoate with regard to human carcinogenicity. Additional information about external exposures (i.e., environmental levels) and health effects is available from the U.S. EPA at:

Biomonitoring Information

Urine levels of dimethoate and omethoate reflect recent exposure. These insecticides generally were not detectable in urine specimens collected from subsamples of NHANES 2003-2004 and 2005-2006 participants (CDC, 2013). In urine specimens from 499 largely Hispanic pregnant women and children living in the California agricultural area of the Salinas Valley, the geometric mean urine dimethoate concentration was 0.25 µg/L (detection frequency, 0.6%) and omethoate concentration was 1.28 µg/L (detection frequency, 0.6%) (Montesano et al., 2007). In workers who formulate and package dimethoate, dialkyl phosphate metabolite concentrations in urine correlated with hand dimethoate contamination and were highest among workers who formulated or bottled liquid insecticide (Aprea et al., 1998).

Finding measurable amounts of dimethoate or omethoate in the urine does not imply that the levels of dimethoate or omethoate cause an adverse health effect. Biomonitoring studies on levels of dimethoate and omethoate provide physicians and public health officials with reference values so they can determine if people have been exposed to higher levels of these insecticides than the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.


Aprea C, Sciarra G, Sartorell P, Mancini R, di Luca V. Environmental and biological monitoring of exposure to mancozeb, ethylenethiourea, and dimethoate during industrial formulation. J Toxico Environ Health Part A 1998;53:263-81.

Centers for Disease Control and Prevention (CDC). Fourth National Report on Human Exposure to Environmental Chemicals. Updated Tables. March 2013. [online] Available at URL: 4/20/13

Food and Agriculture Organization/World Health Organization (FAO/WHO). 4.10 Dimethoate, omethoate, and formothion (T**). In: Pesticide Residues in Food-1996. Report of the Joint Meeting of the FAO Panel of Experts on Pesticide Residues in Food and the Environment and the WHO Core Assessment Group. FAO Plant Production and Protection Paper, 140, 1997. Rome, 1997. 4/4/13

Food and Drug Administration (FDA). US Food and Drug Administration-Total Diet Study Market Baskets 1991-3 through 2003-2004. Revision 3, 1991-2003, December 2006. Available at: 4/20/13

Gunderson EL. FDA Total Diet Study, July 1986-April 1991, dietary intakes of pesticides, selected elements, and other chemicals. JAOAC Int. 1995;78(6):1353-63.

Hassan A, Zayed SMAD, Bahig MRE. Metabolism of organophosphorus insecticides—XI. metabolic fate of dimethoate in the rat. Biochem Pharmacol 1969;18(10):1419-38.

Huffmann U, Papendorf T. Organophosphate poisonings with parathion and dimethoate. Intensive Care Med 2006;32:464-8.

International Programme on Chemical Safety (IPCS). Environmental Health Criteria 90. Dimethoate [online]. 1989. Available at URL: 4/20/13

International Programme on Chemical Safety (IPCS). Pesticide residues in food-2003-Joint FAO/WHO Meeting on Pesticide Residues. Dimethoate (addendum). 2003. Available at: 4/20/13

Krieger RI, Thonginthusak T. Metabolism and excretion of dimethoate following ingestion of overtolerance peas and a bolus dose. Food Chem Toxicol. 1993;31(3):177-82.

Montesano MA, Olsson AO, Kuklenyik P, Needham LL, Bradman A, Barr DB. Method for determination of acephate, methamidophos, omethoate, dimethoate, ethylenethiourea and propylenethiourea in human urine using high-performance liquid chromatography-atmospheric pressure chemical ionization tandem mass spectrometry. J Expo Sci Environ Epidemiol 2007;17:321-30.

Menzer RE, Best NH. Effect of phenobarbital on the toxicity of several organophosphorus insecticides. Toxicol Appl Pharmacol 1968;13:37-42.

Sanderson DM, Edson EF. Toxicological properties of the organophosphorus insecticide dimethoate. Br J Ind Med 1964;21:52-64.

U.S. Environmental Protection Agency (U.S. EPA). Interim reregistration eligibility decision for dimethoate. Case No. 0088. June 12, 2006. Available at URL: 4/20/13

U.S. Environmental Protection Agency (U.S. EPA). Dimethoate; pesticide tolerance. Proposed rule. In: Federal Register volume 60, Number 128, July 5, 1995. Pages 34945-7.

Available at: 4/20/13 The U.S. Government's Official Web PortalDepartment of Health and Human Services
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