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Methoprene Introduction Methoprene,
an insect growth regulator, is being applied to many home and community
pest control problems as a general use, slow-acting insecticide. This
chemical can be used to control a number of pests, including fleas (PrecorTM),
mosquitoes (AltosidTM), pharaoh ants, leaf miners and hoppers, and cucmber
beetles. It is also used as an insect control in food production and
agriculture (U.S. EPA 1991). EPA estimated in 1982 that 57% of use at that
time was as an additive to cattle feed and mineral supplements to control
horn flies. Mode
of Action
This
chemical is an analog to a unique insect-growth regulating hormone, which
does not ressemble any known mammalian hormones. Use requires careful
attention to timing and patience. Applied at very low rates, while insect
populations are still in the egg or larval stage of their life cycle,
methoprene prevents development to the adult reproductive stages so that
insects die in arrested immaturity. Methoprene is not toxic when applied
to adult stages of the target insect. Because the chemical interferes with
the insect’s normal life cycle and is not directly toxic to the pest, it
is considered to be a biochemical pesticide (EXTOXNET 2001).
Toxicity
According
to information contained in a 1982 EPA Registration Standard, methoprene
is of extremely low acute toxicity to mammals (LD50 equals 36,500 mg/kg).
It is not a skin or eye irritant, although it is slightly toxic via dermal
absorbtion. For this effect, methoprene is a toxicity category III with
the signal word CAUTION required on the label (U.S. EPA 1991). No
adverse effects have been reported in animal bio-assays for long-term
health effects and short-term tests for mutagenicity were all negative.
EPA reviewers found that animals rapidly metabolize and excrete the
material, the major non-water soluble metabolite in animal assays being
cholesterol.
Ecological
Effects
Methoprene
may have severe developmental effects on frogs. It was found to be a
possible cause of a sharp rise in the incidence of frog deformities
throughout North America. A 1997 study linked pesticides to frog
deformities when they found a higher number of hindlimb frog deformities
occurring in agricultural areas (Oulette 1997). It
is believed that a breakdown product of methoprene mimics retinoic acid,
an important chemical to the development of fish and frog embryos.
Laboratory tests involving raised levels of retinoic acid have resulted in
a majority of the limb deformities found in the North American frogs (Conlan
1996). Methoprene
also has a moderate toxicity towards both warm and cold water, freshwater
fish, although exposure of these organisms is limited due to
methoprene’s rapid degradation in unshaded water. It is highly acutely
toxic to estuarine and marine invertebrates, which play an important role
in the delicate estuarine ecosystem.
The LC50 (concentration needed to kill half of the test
population) for fresh water shrimp is greater than 0.1 ppb (parts per
billion) and the LC50 for the estuarine mud crabs is greater
than .0001 ppb. Meanwhile, the level of methoprene released into an
environment from a general application is expected to be around 10 ppb (EXTOXNET
2001). Environmental
Fate
Studies
reviewed by EPA indicate that if protected from light, methoprene is quite
stable in water within the pH range 5-9, not degrading after 30 days in
the dark. The BioIntegral Research Center of Berkeley, CA reports that
methoprene used inside homes is active for at least 6 months against
developing fleas. When exposed to light, however, methoprene degrades
within 7 days to more than 50 products, not all of which have been
identified. The
chemical’s soil half-life is between 10-14 days in four soils tested,
where it is microbially degraded to carbon dioxide and soil-bound
products. Although
the mode of action and low persistence of methoprene imply that resistance
problems should be slow to develop, resistance to insect growth hormones
has been induced experimentally and therefore might be possible in the
field. Data
Gaps
A
Reregistration Eligibility Document has been created for methoprene and
most products were accepted for reregistration for use in the United
States. However, the U.S. EPA is still requiring an estuarine invertebrate
life cycle study in order to determine adverse effects of methoprene on
those species from long term exposures to briquette formulations of the
pesticide (EXTOXNET 2001). References Brown,
T.M. et al. 1974. “Experimental induction of resistance to a juvenile
hormone mimic.” Journal of Economic Entomology 67(6):799-801. Coats,
J.R. 1982. “Insecticide Mode of Action.” Academic Press, New York, NY. Conlan,
Michael. 1996 “Clue Found in Deformed Frog Mystery.” Environment
Canada. <http://www.on.ec.gc.ca/herptox/methoprene.html>.
Enviro
Control, Inc. 1981. “Methoprene. Task 2: Topical Discussions.”
Submitted to U.S. EPA. Washington D.C. Extension
Toxicology Network (EXTOXNET) Pesticide Information Profile. 2001. “Methoprene.”
<http://pmep.cce.cornell.edu/profiles/extoxnet/haloxyfop-methylparathion/methoprene-ext.html>. Oulette,
M. et al. 1997. “Hindlimb deformities (ectromelia, ectodactyly) in free
living anurans from agricultural habitats.” Journal of Wildlife
Diseases 33(1):95-104. Thomson,
W.T. 1984. “Agricultural Chemicals: Insecticides.” Thomson
Publications. Fresno CA. U.S.
EPA. 1991. “Reregistration Eligibility Document: methoprene.” Office
of Pesticide Programs, Washington D.C. <http://www.epa.gov/oppsrrd1/REDs/index_h2z.html#M>. U.S.
EPA. 1982. “Methoprene: Pesticide Registration Standard.” Office of
Pesticide Programs. Washington D.C. U.S. EPA. 1981. “Report on methoprene.” Ecological Effects Branch. Office of Pesticides Programs. Washington D.C.
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