Toxicologic Information About Insecticides
Used for Eradicating Mosquitoes
(West Nile Virus Control)
April 2005
Resmethrin is a synthetic pyrethroid used for control of flying and crawling insects in homes, greenhouses, indoor landscapes, mushroom houses, industrial sites, and for mosquito control. It is also used for fabric protection, pet sprays and shampoos, and it is applied to horses or in horse stables (Exotoxnet 2003). Resmethrin is currently used for mosquito control by aerial application (WHO 1989).
Section 1. Environmental Factors
Pyrethroids are rapidly degraded in the environment through photolysis, hydrolysis, and biodegradation. Resmethrin is released to the environment as a result of its use as an insecticide. Resmethrin is one of the least persistent pyrethroids because it rapidly degrades when exposed to air or light. Resmethrin is rapidly photodegraded; in sunlight, aqueous solutions have a half-life of 47 minutes in pure water and 20 minutes in sea water. A range of photoproducts is formed from ester cleavage and oxidation reactions. Resmethrin is also very rapidly degraded in soil, with 2% of the applied parent compound remaining after 16 days. Rapid degradation also occurs on plants; after 5 days, no resmethrin is detected on plants (WHO 1989).
Direct releases to water are expected to be low for pyrethroids because these compounds are primarily applied aerially or from ground-based sprayers directly to crops and vegetation. Spray drift after application of these compounds, however, can contaminate nearby waters. Pyrethroids such as resmethrin, which often are used in mosquito control, are prohibited from being applied to open water or within 100 feet of lakes, rivers, and streams because of their high toxicity to fish (EPA 2000). In addition, resmethrin is highly toxic to bees.
Section 2. Potential for Exposure
Occupational exposure to resmethrin may occur through inhalation and dermal contact with this compound at workplaces where resmethrin is produced or used. Since resmethrin is a widely used insecticide that can be employed for the control of a variety of insects, mosquitoes and in pet sprays and shampoos, the general population may be exposed to resmethrin through use of insecticides containing this compound (HSDB 2003). The general population may also be exposed to resmethrin to a minor extent via dietary residues (WHO 1989).
Section 3. Health Effects/Toxicity
Almost all systemic effects resulting from exposures to pyrethroids are related to their action on the nervous system. Pyrethroids exert their profound effect by prolonging the open phase of the sodium channel gates when a nerve cell is excited. In rodents, effects such as tremors are induced if the open state is prolonged for brief periods; effects such as sinuous writhing (choreoathetosis) and salivation occur if the open state is prolonged for longer periods. Neurologic signs typically result from acute toxicity. Low-level chronic exposures to pyrethroids usually do not cause neurologic signs in mammals, largely because of rapid metabolism and elimination. Data from animal studies do not indicate that pyrethroids significantly affect end points other than the nervous system, although changes in liver weight and metabolism of chemicals sometimes have been used as an index of adverse effect levels for pyrethroids. A few recent animal studies indicate the potential for adverse neurodevelopmental, reproductive, and immunologic effects at exposure levels below those expected to result in overt signs of neurotoxicity. Data do not indicate that pyrethroids should be considered a carcinogenic concern to humans. No data in humans are available regarding the potential for pyrethroids to cross the placental barrier and enter a developing fetus. Limited data from animals indicate that transfer of pyrethroids across the placenta to the fetus may result in persistent effects on neurotransmitters later in life. Although pyrethroids have not been identified in human breast milk, very low levels of pyrethroids (<1% of an orally administered dose) are excreted into milk of lactating animals (ATSDR 2001).
Studies of laboratory animals exposed to resmethrin are summarized in Table 1, with no-observed adverse effect levels (NOAELs) and lowest-observed adverse effect levels (LOAELs) indicated.
The dermal LD50 for resmethrin is 2,500 mg/kg for rats, 2,500 mg/kg for rabbits, and >5,000 mg/kg for mice. Oral LD50 values for technical-grade resmethrin in rats range from 1,244 to >2,500 mg/kg. Its oral LD50 for mice range from 300 to 940 mg/kg. The 4-hour inhalation rat LC50 for resmethrin is >9,490 mg/m3; the inhalation LC50 for dogs is >420 mg/m3, and for rabbits, >12,000 mg/m3 (HSDB 2003). However, the toxicity is influenced by the isomeric properties of the compound. For example, the oral LD50 (rats) of 1R cis resmethrin is about 168 mg/kg, but the value for the 1R trans isomer is >8,000 mg/kg (Dorman and Beasley 1991). Resmethrin was found to be a slight dermal irritant in a 24-day dorsal/ventral rabbit ear test. However, it showed no compound-related lesions of the skin when applied twice a week for 3 weeks to the shaved skin of rabbits (WHO 1989).
In longer animal toxicity studies, resmethrin caused tremors, decreased body weights, and increased liver and kidney weights at levels ranging from 679 mg/kg/day to 5,000 mg/kg (Swentzel et al 1977; Miyamoto 1976). Skeletal development was delayed in rats at 80 mg/kg/day (Penwick Corp. 1979b), and a slight increase in pups cast dead and lower mean pup weight was seen at 25 mg/kg/day (Penwick Corp. 1979a). However, in another study, no teratogenicity was seen in rats at doses up to 1,500 mg/kg (Swentzel et al. 1977). In a 2-year rat study, minimal hypertrophy of hepatocytes and decreased spleen weights were seen at 39.5 mg/kg/day (Penwick Corp. 1980a). No oncogenicity was observed in rats and mice fed resmethrin. Resmethrin was not mutagenic to Salmonella typhimurium or Chinese hamster cells (WHO 1989).
In cows administered resmethrin orally, 43% of the administered dose was excreted in the urine as resmethrin metabolites (Ridlen et al. 1984). In rats administered resmethrin at 1 mg/kg, 53%–73% was excreted in the urine and feces in 6 days. When it was administered orally to rats at 500 mg/kg, it was absorbed rapidly from the gastrointestinal tract and was completely eliminated in the urine (36%) and feces (64%) in 3 weeks (HSDB 2003).
Table 1. Health Effect Levels of Resmethrin
in Humans and Laboratory Animals (PDF Version 64k)
Section 5. Standards and Guidelines for Protecting Human Health
Regulatory standards and guidance values are summarized in Table 2.
EPA has established an oral RfD for resmethrin of 0.03 mg/kg/day based on a three-generation reproduction rat study (Penwick Corp. 1980a), in which a LOAEL of 500 ppm (25 mg/kg/day) for increased pups cast dead and lower mean pup weight was identified. An uncertainty factor of 1,000 was used to account for interspecies and intraspecies differences and lack of an established NOAEL (IRIS 2003).
| Table 2. Regulatory Standards and Guidance Values for Resmethrin | ||
| Standard/Guidance | Value | Reference |
| Environmental Protection Agency Reference Dose (RfD) | 0.03 mg/kg/day | IRIS 2003 |
ATSDR. 2001. Toxicological profile for pyrethrins and pyrethroids [Draft], Atlanta: US Department of Health and Human Services, ATSDR.
Becci PJ, Knickerbocker M, Parent RA. 1979. Teratological evaluation of SBP-1382 in albino rabbits. Waverly, New York: Food and Drug Research Laboratories: 17 pp. Report No. 6288. Unpublished proprietary data supplied by Roussel Uclaf. (Cited in WHO 1989)
Coombs DW, Hardy CJ, Clark GC, et al. 1985. Resmethrin 90-day inhalation toxicity study in the rat. Huntingdon, UK: Huntingdon Research Centre, 80 pp. Report No. SBP 6/84997. Unpublished proprietary data supplied by Roussel Uclaf. (Cited in WHO 1989)
Cox GE, Knickerbocker M, Parent RA. 1979. Evaluation of dietary administration of SBP-1382 in CD-1 outbred albino mice over an 85-week period. Waverly, New York: Food and Drug Research Laboratories; Report No. 5270. Unpublished proprietary data supplied by Roussel Uclaf. (Cited in WHO 1989)
Dorman DC, Beasley VR. 1991. Neurotoxicology of pyrethrin and the pyrethroid insecticides. Vet Hum Toxicol 33:238– 43.
EPA. 2000. Synthetic pyrethroids for mosquito control. Washington, DC: US Environmental Protection Agency. 735-F- 00-004.
Extension Toxicology Network Extoxnet. (EXTOXNET). 2003. Pesticide information profile. Available at http://pmep.cce.cornell.edu/profile/extoxnet.
Gephart LA, Johnson WD, Becci PJ, Parent RA. 1980. 180-day subchronic oral dosing study with resmethrin in beagle dogs. Waverly, New York, Food and Drug Research Laboratories. Report No. 6289. Unpublished proprietary data supplied by Roussel Uclaf. (Cited in WHO 1989)
HSDB. 2003. Hazardous Substances Data Bank (HSDB), National Library of Medicine. National Toxicology Program. http://www.toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB Accessed January 30, 2003.
Integrated Risk Information System (IRIS). 2003. US Environmental Protection Agency. Resmethrin. Available at http://www.epa.gov/iris/subst/0343.htm.
Knickerbocker M, Becci PJ, Cox GE, Parent RA. 1980. A lifetime evaluation of the dietary administration of SBP-1382 to Wistar albino rats. Waverly, New York: Food and Drug Research Laboratories. Report No. 5271. Unpublished proprietary data supplied by Roussel Uclaf. (Cited in WHO 1989)
Machi RA, Kam C, Gallo MA, Stevens KR, Gagliardi JJ. 1979. Teratological evaluation of SBP-1382 technical in the albino rat. Florham Park, New Jersey: Booz, Allen & Hamilton Inc. Report No. 2054-066. Unpublished proprietary data supplied by Roussel Uclaf. (Cited in WHO 1989)
Miyamoto J. 1976. Degradation, metabolism and toxicity of synthetic pyrethroids. Environ Health Perspect 14:15–28. (Cited in WHO 1989)
Penwick Corporation. 1979a. MRID No. 00081276. Available from EPA. Write to FOI, EPA, Washington DC. 20460. (Cited in IRIS 2003)
Penwick Corporation. 1979b. EPA Accession No. 241765-66, 241768-70. Available from EPA. Write to FOI, EPA, Washington DC. 20460. (Cited in IRIS 2003)
Penwick Corporation. 1980a. EPA Accession No. 242782–242786. Available from EPA. Write to FOI, EPA, Washington DC. 20460. (Cited in IRIS 2003)
Penwick Corporation. 1980b. EPA Accession No. 244514. Available from EPA. Write to FOI, EPA, Washington DC. 20460. (Cited in IRIS 2003)
Ridlen RL, Christopher RJ, Ivie GW, et al. 1984. Distribution and metabolism of cis- and transresmethrin in lactating Jersey cows. J Agric Food Chem 32:1211–7.
Swentzel KL, Angerhofer RA, Haight EA. 1977. Toxicological evaluation of pyrethroid insecticide (5-benzyl-1,3-furyl) methyl-2,2-dimethyl-3-(2-methylpropenyl)cyclopropane-carboxylate (resmethrin). Aberdeen Proving Ground, Maryland: US Army Environmental Hygiene Agency. Report No. 51-0830-77. (Cited in WHO 1989)
WHO. 1989. Environmental health criteria 92: Resmethrins–Resmethrin, Bioresmethrin, Cisresmethrin. Geneva: World Health Organization.
« Permethrin |
Temephos »
Table of Contents
