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Acephate This systemic,
broad-spectrum organophosphate insecticide, known by the trade-name
OrtheneTM, is produced by the Chevron Chemical Co. It is widely
used in agriculture, seed production, in greenhouses, on turf and on
commercially grown ornamentals, sometimes in combination with other
pesticides. EPA has not produced a Reregistration Eligibility Document for
acephate, but they required acephate product labels to contain the signal
work CAUTION because of its toxicity category III rating (EXTOXNET 2001).
They have also imposed an interim worker reentry period of 24 hours for
commercial use, and protective clothing requirements. Acute Toxicity Although acephate is only
moderately acutely toxic, with an oral rat LD50 (lethal dose needed to
kill 50% of the test population) of 500 to 1000 mg/kg, the state of
California reported 39 incidents of acephate poisoning between 1982 and
1986, most (25/39) involved applicators who were exposed to the
concentrated material. In common with other organophosphates, acephate
inhibits acetylcholine esterase (AchE), an essential nervous system
enzyme, causing characteristic symptoms such as headaches, fatigue,
stomach cramps, nausea, and in extreme cases, respiratory depression. Interestingly, technical
acephate is more acutely toxic than the purified form, because technical
acephate contains as much as 30% of a more toxic breakdown product,
methamidophos, another organophosphate pesticide known as MonitorTM.
Another impurity, methylthioacetate (MTA), can be found in small amounts
in acephate formulations, and further testing is being required to address
its significance. One acute dermal toxicity study in rabbits found that
MTA could cause blindness when applied at concentrations between 1500 and
3000 mg/kg. EPA published a
Registration Standard on acephate in September, 1987, which reviewed the
existing database and data gaps needing to be filled. According to the
Agency, acephate is quickly cleared, does not bioaccumulate, and is
excreted mostly as the unchanged compound, although a small amount of
methamidophos (also quickly excreted) is formed by intestinal microbes in
the rat. Chronic ToxicityChronic toxicity effects
were all related to AchE inhibition. A single, insensitive, neurotoxicity
test found no delayed neurotoxicity. Acephate has not been found to cause
birth defects in rats and rabbits. However, in a reproductive effects
test, a “non-observable-effects-level (NOEL)” was never established,
and low pregnancy rates, high loss of litters and decreased numbers of
live fetuses were observed in every treatment group, 50 ppm (parts per
million) and higher. EPA has classified
acephate as a Category C or possible human carcinogen. Oncogenicity test
results found an increased incidence of adrenal medullary tumors and
pituitary tumors in male rats when compared with experimental controls. In
female mice, an increased incidence of liver tumors and liver hyperplastic
nodules, thought to be precursors to tumors, was seen at the highest doses
tested. Acephate is mutagenic in shor-term assays, but not in tests
conducted in vivo, on live animals. Environmental Effects Although acephate
dissipates rapidly from aerobic soil with half-lives of three to six days,
it is, according to EPA,” mobile in most soils [therefore] the potential
for groundwater contamination exists …[however]…most of the applied
acephate and the breakdown product methamidophos degrade to immobile
compounds within 20 days…[and therefore]…the probability of
contamination is limited.” The USDA reviewed studies conducted by
Chevron in the early 1970’s and reported in a review, “OrtheneTM
has a longer half-life on foliar surfaces than in soil or water…in
studies using lettuce, broccoli and cotton leaves, only an average of 5%
of the applied OrtheneTM could be washed off leaves three,
seven and fourteen days after treatment at two lbs/acre.” Ecological Effects Acephate, and especially
methamidophos, are highly toxic to bees, and moderately toxic to birds.
EPA stated, “studies indicate that acephate treatments may result in
local population reductions in some avian species as well as a high
incidence of sublethal AchE inhibition…,” although EPA did not feel
that long-lasting harm to bird populations would occur. References: California Department of
Food and Agriculture. 1986. “Summary of toxicological data on acephate.”
Medical Toxicology Branch, Sacramento, CA. Extension Toxicology
Network. 2001. “Acephate.” Pesticide Information Profiles. Farm Chemicals Handbook.
1988. “Acephate.” Meister Publication. Willoughby, OH. Gosselin, R.E. et al.
1983. “Clinical Toxicology of Commercial Products. 5th
edition. Williams & Wilkins. Baltimore, MD. Thomson, W.T. 1983.
“Agricultural Chemicals: Book 1.” Thomson Publications. Fresno, CA. U.S. EPA. 1987.
“Guidance for the Reregistration of pesticide Products Containing
Acephate as the Active Ingredient.” Office of Pesticide Programs.
Washington, D.C. U.S. EPA. 1985.
“Toxicology One-Liner for Acephate (o,S-dimethyl acetyl-phosphoramidothioate.”
Office of Pesticide Programs. |
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BEYOND PESTICIDES |
