Biomonitoring Summary

Acephate

CAS No. 30560-19-1

General Information

Acephate is a contact and systemic organophosphate insecticide registered in the U.S. in 1973 and used to control insects on field (e.g., tobacco) and food crops (e.g., beans, lettuce, bell peppers), on ornamental plants, sods and turf, in food handling establishments, residential and commercial buildings. Acephate is nonvolatile, very water soluble, has low binding to soils, and has a moderate potential for runoff into surface waters. In the environment, acephate breaks down within a few days to degradation products including methamidophos, a more toxic organophosphate insecticide. A similar conversion occurs in insects, so that acephate toxicity to insects results largely from its conversion to methamidophos. Acephate does not bioaccumulate but is acutely toxic to honey bees in the immediate post-application period (U.S. EPA, 2006).

General population exposure to acephate may occur from consuming foods that have been treated with acephate and by direct contact with treated surfaces. Estimated dietary and water intakes have not exceeded recommended limits (Gunderson, 1995), but potential exposures from residential use have posed concern, so residential indoor and lawn registrations have been discontinued (U.S.EPA, 2006). Applicators and formulators may be exposed through dermal and inhalational (e.g., dust or aerosol) routes.

Human health effects from acephate at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses, acephate 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. Acephate has moderate acute toxicity in mammals. In insects, acephate is converted to methamidophos, but in mammals, this conversion appears to be limited to about 1-2%, regardless of the acephate dose (Chang et al, 2009; Mahajna et al., 1997). Acephate is quickly absorbed from the gastrointestinal tract, lungs, and through the skin, widely distributed to body tissues, and rapidly eliminated in the urine over 12-24 hours (IPCS, 2002). Human studies demonstrated a plasma acephate half-life of 3-7 hours (IPCS, 2002). Acephate produced altered sperm motility and counts in male mice, but reproductive toxicity was only seen in pregnant mice at doses that produced maternal toxicity (Farag et al., 2000a, 2000b). Acephate has not consistently been shown to be teratogenic, mutagenic or genotoxic (Carver et al., 1985; IPCS, 2002). Evidence of carcinogenicity is limited to liver tumors that occurred in rats fed high doses of acephate over several months, and U.S. EPA considers acephate to be a possible human carcinogen (U.S.EPA, 2012). NTP and IARC have not made determinations regarding human carcinogenicity. Additional information about pesticides is available from U.S. EPA at: https://www.epa.gov/pesticides/.

Biomonitoring Information

Urinary levels of acephate reflect recent exposure. Urinary levels of acephate 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., acephate was measured above the detection limit of 0.8 µg/L in 6.4% of samples (Olsson et al., 2003). Geometric mean urine acephate was 1.43 µg/L (detection frequency 3.1%) 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). Urinary acephate was undetectable (detection limit 0.8 µg/L) in 59 samples obtained from 18 horticultural greenhouse workers and collected during and after a work shift (Bouchard et al., 2006). Four workers who formulated acephate and could have multiple exposure routes (e.g., ingestion, inhalation, and dermal) provided spot urine samples during and after work shifts. Urinary acephate concentrations ranged from 0.044-10 mg/L; at the end of work shift, medians were 0.4-1.1 mg/L (Maroni et al., 1990). These concentrations were up to ten thousand times greater than the acephate limits of detection (0.1 and 0.25 µg/L) reported in CDC's National Biomonitoring Program (CDC, 2013).

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

References

Bouchard M, Carrier G, Brunet RC, Dumas P, Noisel N. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Ann Occup Hyg 2006;50(5):505-15.

Carver JH, Bootman J, Cimino MC, Esber HJ, Kirby P, Kirkhart B, et al. Genotoxic potential of acephate technical: in vitro and in vivo effects. Toxicology1985;35(2):125-42.

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

Chang AS, Montesano MA, Barr DB, Thomas J, Geller RJ. Urinary elimination kinetics of acephate and its metabolite, methamidophos, in urine after acute ingestion. J Med Toxicol 2009;5(2):68-72.

Farag AT, Eweidah MH, El-Okazy AM. Reproductive toxicity of acephate in male mice. Repro Toxicol 2000a;14:457-62.

Farag AT, Eweidah MH, Tayel SM, El-Sebac AH. Developmental toxicity of acephate by gavage in mice. Repro Toxicol 2000b;14:241-5.

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.

International Programme on Chemical Safety (IPCS). Pesticide residues in food-2002-Joint FAO/WHO Meeting on Pesticide Residues. Acephate. Available at URL: http://www.inchem.org/documents/jmpr/jmpmono/2002pr02.htm. 4/4/13

Maroni M, Catenacci G, Galli D, Cavallo D, Ravazzani G. Biological monitoring of human exposure to acephate. Arch Environ Contam Toxicol 1990;19(5):782-8.

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.

Olsson AO, Nguyen JV, Sadowski MA, Barr DB. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Anal Bioanal Chem 2003;376(6):808-15.

U.S. Environmental Protection Agency (U.S. EPA). Acephate (CASRN 30560-19-1) Integrated Risk Information System (IRIS). Updated August 9, 2012. Available at URL: https://www.epa.gov/iris/subst/0354.htm. 4/4/13

U.S. Environmental Protection Agency (U.S. EPA). Reregistration eligibility decision (IRED). July 2006. Available at URL: https://www.epa.gov/oppsrrd1/reregistration/acephate/. 4/4/13