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Methoprene Fact Sheet

Isopropyl (2E-4E)-11-methoxy-3,7,11-trimethyl-2,4
-dodecadienoate (56)


Methoprene is a slow-acting larvicide that is used in homes, communities, agriculture and food production. A “general-use” pesticide, it is used to control various types of fleas, mosquitoes, ants, flies, lice, moths, and beetles (EXTOXNET 2001). Brand names of pesticides containing methoprene include AltosidTM and PrecorTM.

How it works

Methoprene is effective because it interferes with regular insect life-cycles. Most insects pass through egg, larval, and pupal stages before becoming reproductively mature adults. By mimicking an insect growth regulating hormone, methoprene prevents pupae from developing into reproductively mature adults. Thus, applying methoprene at the right stage of insects’ life cycles causes them to die before they can reproduce. It has no significant effect on adult target insects. (EXTOXNET 2001)


Since methoprene does not resemble any mammalian growth hormone, its toxicity to humans has been of minimal concern. It is consequently classified as a “practically non-toxic compound in EPA toxicity class IV” – a low risk chemical compared to many other pesticides in common use (U.S. E.P.A. 1991). For adult rats, the LD50 (the amount of a chemical required to kill 50% of a test population) is 36 when 500 mg is administered per kilogram of body weight (EXTOXNET 2001). It is slightly toxic when absorbed through the skin, but does not irritate skin or eyes. Results from animal experiments suggest there is no risk of long term health problems for humans exposed to methoprene (NCAMP 2001).

Conversely, the potential effects of methoprene on amphibian populations are alarming. Frogs, toads, and salamanders, in particular, have displayed severe developmental effects in response to methoprene exposure. For example, agricultural methoprene use has been linked to a massive rise in the incidence of frog limb deformities across North America (Oulette 1997). Such malformations, including extra or missing limbs, are often caused by exposure to a family of chemical agents called retinoids (Conlan 1996). While methoprene does not contain any retinoids, one of its breakdown products (methoprene acid) imitates one by binding to and activating a retinoic acid cell receptor (La Clair et al. 1998). Given that the global frog population has plummeted by 40% since the 1950s, the ongoing large-scale application of methoprene to frog habitats, including standing water and riparian zones, cannot be ignored (Houlahan et al. 2000).

Methoprene is toxic to fish and marine and estuarine invertebrates. For example, the lethal concentration required to kill half of a fresh water shrimp population (LC50) is greater than 0.1 parts per million (ppm) and the LC50 for the estuarine mud crabs is greater than .0001 ppm (EXTOXNET 2001). While methoprene’s rapid degradation in unshaded water decreases its threat to freshwater fish, it is still considered to be moderately toxic to a range of fish species (NCAMP 2001).

Despite the fact that methoprene is considered to be of low toxicity to humans in general, it is important to note that comprehensive studies have not been done to determine the effects of long-term methoprene exposure on children. Such a knowledge gap is significant, considering that children are generally more susceptible to the health risks associated with pesticide use. Because they differ from adults in terms of size, weight, immunology, and behaviour, children must be considered separately when deciding whether methoprene is a safe general-use pesticide.


Given methoprene’s low level threat to humans, it may be tempting to support its widespread use. However, condoning pervasive methoprene use is short sighted and irresponsible, given its serious detrimental effects on amphibian and fish populations. Many of these species are already dying out, and applying a known toxic chemical to their habitats is unacceptable. More desirable alternatives must be adopted, such as Bti (Bacillus thuringiensis israelensis), a biological general-use pesticide that is nearly non-toxic to both humans and animals.

Works cited

Conlan, M. 1996. Clue Found in Deformed Frog Mystery.” Environment Canada.

Extension Technology Network (EXTOXNET) Pesticide Information Profile. 2001. “Methoprene.”

Houlahan, J.E., C. S. Findlay, B. R. Schmidt, A. H. Meyer, and S. L. Kuzmin. 2000. “Quantitive evidence for amphibian declines.” Nature 404: 752-755.

La Clair, J.J., Bantle, J.A. and Dumont, J. 1998. “Photoproducts and metabolites of a common insect growth regulator produce developmental deformities in Xenopus.” Environ. Sci. Technol. 32: 1453-1461.

National Colalition Agianst the Misuse of Pesticide (NCAMP). 2001. “Chemical WATCH Factsheet: Methoprene.”

Oulette, M. et al. 1997. “Hindlimb deformalities (ectromelia, ectodactyly) in free living anurans from agricultural habitats.” Journal of Wildlife Diseases 33(1): 95-104.

U.S. E.P.A. 1991. “Reregistration Eligibility Document: methoprene.” Office of Pesticide Programs. Washington, D.C.

Additional References

Coats, J.R. 1982. “Insecticide Mode of Action.” Academic Press, New York, NY.

Enviro Control, Inc. 1981. « Methoprene. Task 2 : Topical Discusssions/ » submitted to U.S. EPA. Washington D.C.
Extension Toxicology Network (EXTOXNET) Pesticide Information Profile. 2001. “Methoprene.”

Hayes, W. J. and E. R. Laws (ed.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.

Hudson, R. H., et al. 1984. Handbook of toxicity of pesticides to wildlife. Second edition. United States Department of the Interior. Fish and Wildlife Service. Resource Publication 153. Washington, DC.

Judy, D. and B. Howell. 1993. “Concentrations of methoprene found in freshwater microcosms treated with sustained release Altosid formulations.” Zoecon Study #1540. ABC Final Report #39541, MRID #42811202.

McEwen, F. L. and G. R. Stephenson. 1979. The use and significance of pesticides in the environment. NY: John Wiley and Sons, Inc.

Menzie, C. M. 1980. Metabolism of pesticides. Update III. U.S. Department of the Interior. Fish and Wildlife Service. Special Scientific Report. Wildlife No. 232. Washington, DC: U.S. Government Printing Office.

Mortimer, M. R. and H. F. Chapman. 1994. A comparison of the toxic effects of Altosid® Liquid Larvicide (S-methoprene) and Abate® (temephos) to some non-target aquatic crustacean species common in eastern Australia. Griffith University, Queensland, Australia.

National Pest Control Association, Inc. 1980 (Nov.). Technical release on new pesticide - Precor 5E. Vienna, VA.

Thompson, W.T. 1984. “Agricultural Chemicals: Insecticides.” Thomson Publications. Fresno CA.

Thomson, W. T. 1976. Insecticides, acaricides and ovicides. Agricultural Chemicals, Book I. Indianapolis, IN: Thomson Publications.

US Environmental Protection Agency. December, 1994. Pesticide rejection rate analysis -- ecological effects. Washington, DC. EPA Doc. 738- R-94-035.

World Health Organization. Methoprene.

Worthing, C. R., ed. 1983. The pesticide manual: A world compendium. Croydon, England: The British Crop Protection Council.


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