E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
Assessment Program.
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Pesticide
Information
Profile
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Phosmet
Publication Date: 9/93
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TRADE OR OTHER NAMES
Trade names for products containing the compound include Appa,
Decemthion, Imidan, Kemolate, Fesdan, Prolate, PMC and Safidon. It is also
found in combination with other insecticides such as carbophenothion.
INTRODUCTION
Phosmet is a non-systemic, organophosphate insecticide used on both
plants and animals. Phosmet is mainly used on apple trees for control of
coddling moth, though it is used on a wide range of fruit crops, ornamentals
and vines for the control of aphids, suckers, mites and fruit flies. Phosmet
is used on approximately 1.1 million acres in the United States each year (5).
The compound is also an active ingredient in some dog collars (11). The pure,
off-white crystalline solid has an offensive odor.
Phosmet is a General Use Pesticide.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Phosmet is a moderately toxic compound by ingestion but requires the
signal word WARNING on the label because it is more highly toxic by other
routes of exposure. It has a moderately high toxicity through the skin and a
very high toxicity through inhalation.
Typical of other organophosphates, phosmet is an inhibitor of the enzyme
cholinesterase. Symptoms of acute phosmet poisoning include nausea, vomiting,
abdominal cramps and diarrhea. Acute exposure at high levels may result in
muscle spasms, loss of muscle coordination, mental confusion and
drowsiness. The insecticide may also adversely affect breathing and
salivation (12).
The oral LD50 of phosmet ranges from 113 to 369 mg/kg in rats of both
sexes and 23.1 to 50.1 mg/kg in mice. Signs of acute poisoning are rapid,
generally occurring within 30 minutes after exposure. The dermal LD50 for
phosmet in the rabbit ranges from 1,560 to 4,640 mg/kg. Inhalation
experiments showed that 50 to 800 ml/l resulted in behavior changes but no
mortality to rats (1). The compound appears to be more toxic to many domestic
animals such as cattle, sheep and goats than to rodents. The LD50 values for
these animals range from 25 to 50 mg/kg.
CHRONIC TOXICITY
Rats fed phosmet for sixteen weeks at moderate to very high doses (22.5
mg/kg to 300 mg/kg) suffered some mortality and exhibited a number of toxic
effects. Over a six month period, doses of phosmet of 1 mg/kg/day in the
diets of rats produced no observable chronic effects (NOEL). In another
study conducted over two years the NOEL was 2 mg/kg/day. These two studies
indicate that even small amounts of phosmet can cause chronic toxic effects
(8).
Dogs also had a 1 mg/kg/day NOEL in a two-year feeding study. In a 20-
week experiment, dogs exhibited changes in their blood enzyme activity
(cholinesterase) at doses at or above 3.7 mg/kg/day. Cattle also showed a
blood enzyme activity decrease when fed varying amounts of phosmet (1 to 2
mg/kg) for eight weeks (1).
No delayed neurotoxic effects were noted in chickens fed diets with
moderate levels of phosmet for six weeks (3).
Rabbits which had phosmet applied to their skin for five days a week for
three weeks suffered high mortality rates at doses of 300 to 600 mg/kg/day.
At 50 mg/kg/day there was significant brain enzyme (cholinesterase)
depression (1).
Estimates place field worker exposure to the pesticide at levels ranging
from 0.1 to 1.4 mg/kg/day one day following field application. The worst case
estimate of homeowner exposure was no greater than 0.005 mg/kg/day (11).
Despite its high toxicity, over an eight year reporting interval only sixteen
cases of phosmet poisoning were reported in California. One year during this
period (1986) approximately 240,000 pounds of phosmet were sold in the state
indicating the relative safety with which the product was handled (11).
The signs and symptoms of chronic toxicity are generally consistent with
those for the class of organophosphate insecticides.
Reproductive Effects
A three-generation study with rats indicated that there were no
reproductive effects when the animals were fed small amounts (2.0 mg/kg) of
the compound for the first generation and slightly higher amounts (4 mg/kg)
for the second and third generations (3). Female rabbits given phosmet both
dermally and orally for three weeks prior to mating and for 18 consecutive
days of gestation showed no effects on reproductive parameters. The doses
tested ranged from 10 to 60 mg/kg for both routes of exposure (1).
Teratogenic Effects
No birth defects were noted in studies with pregnant rabbits fed 10 to 60
mg/kg for three weeks during pregnancy or in monkeys given 8 to 12 mg/kg on
days 22 to 32 of gestation (3). Rats fed 10 to 30 mg/kg on days 6 through 15
of gestation suffered some maternal toxicity at the higher doses but no
abnormalities appeared in the pups. In another study however, single moderate
doses of 30 mg/kg administered to rats between day nine and thirteen of
gestation, produced an increase in brain damage (hydrocephaly) in 33 of
the 55 embryos examined. Embryo toxicity was dose-dependent (1). The
results of these studies, viewed together, are somewhat ambiguous and make
it difficult to draw firm conclusions about possible teratogenic effects in
humans.
Mutagenic Effects
The tests on the mutagenicity of phosmet have produced mixed results.
Several tests with bacteria did not cause any mutations though there was one
positive test with one strain of bacteria (S. typhimurium) (4). There have
been no tests conducted directly on animal or human cells (8). However,
among workers producing the compound Safidon, some changes in their
chromosomes were noted (12).
Carcinogenic Effects
A group of rats fed diets containing 1 to 20 mg/kg/day of phosmet for two
years showed no differences with respect to neoplasms when compared to the
controls. However, the study has been deemed inadequate because too few
rats were analyzed at the end of the test (1).
A two-year mouse study showed that phosmet is associated with a
significant increase in liver tumors in male mice. The dose in this test was
not noted in the report. In female mice, there was a positive dose-related
trend for liver tumors and carcinomas (4). Phosmet has a "tentative" category
C carcinogen rating (possible carcinogen). The EPA has requested that
additional testing be conducted.
Organ Toxicity
Observations of occupationally exposed workers indicate that the
compound may cause a reduction in enzyme activity (peripheral cholinesterase).
No other observable adverse effects were noted among the workers (1).
Phosmet is a mild irritant to the eyes, and only mildly irritating to the
skin (9).
Fate in Humans and Animals
Phosmet is rapidly absorbed, distributed, and eliminated in mammals.
Rats given single doses of 23 to 35 mg/kg phosmet excreted greater than three
quarters of the dose in urine, about fifteen percent in the feces. Less
than three percent was found in body tissues after two days (1). Other
figures show nearly eighty percent eliminated in the urine and twenty percent
eliminated in the feces after three days (4).
Phosmet applied to a steer's back was moderately absorbed and rapidly
broken down in the blood to phthalamic and phthalic acids (3). Rat studies
indicate that phosmet crosses the placenta (1). Phosmet also appeared in the
milk of goats fed a single dose of 70 mg/kg. The level in the milk after
eight hours was 0.38 mg/kg but after 24 hours and 48 hours none could be
detected. Cows fed silage with an average residue level of 19 mg/kg for
nearly two months showed no residues in the milk above the detection level of
0.01 mg/kg (2). Cattle fed dietary levels of 20 to 100 ppm showed no residues
in the tissues at levels higher than 0.005 ppm (3).
Metabolic breakdown is primarily by hydrolytic pathways and the breakdown
products are similar to those resulting from other organophosphate pesticides.
The major metabolite is phthalamic acid with phthalic acid produced in smaller
quantities (3).
ECOLOGICAL EFFECTS
The LD50 for phosmet in mallards is 1,830 mg/kg but is much more
toxic to red-winged blackbirds with an LD50 of 18 mg/kg. The LD50 in
ring-necked pheasants is from 237 mg/kg to greater than 250 mg/kg. The
variation among species is also evident in dietary LC50 values (for mallards,
greater than 5,000 ppm; for Japanese quail, 2,041 to 2,072 ppm; and for
northern bobwhite quail, 501 ppm (5). Phosmet can cause reproductive
difficulties in birds whose feed contains phosmet residues (4).
Phosmet also ranges from highly to very highly toxic to fish, depending on the species. The 96-hour LC50 for phosmet is 56 ug/l for rainbow trout, 9,000 ug/l for fathead minnows, and 70 ug/l for bluegill. Bluegill are sensitive to temperature increases in relation to phosmet exposure. The toxicity of the compound increases nine-fold from 10 degrees C to 25 degrees C. Trout are more sensitive to the compound at 5 degrees C than at 10 degrees C (6).
The insecticide is highly toxic to aquatic invertebrates and crustaceans.
LC50 values in these species range from 2.0 to 6.0 ug/l (8).
Phosmet has a bioconcentration factor of 6 to 37 in fish, indicating that
there is little likelihood that the compound accumulates significantly in
aquatic organisms.
Phosmet is very toxic to honeybees.
ENVIRONMENTAL FATE
Phosmet is rapidly broken down in soil to non-toxic products (5, 9). In
sandy loam and loamy soil, half of the initial amount of the compound is
broken down in 3 to 19 days. The compound persists longer in dry soil than in
moist soil. Degradation is by hydrolysis (the chemical action of water) and
microbial action (5). Breakdown is also faster under basic conditions. There
is little leaching or runoff associated with the compound, even after repeated
applications, partly because it is only slightly soluble in water (3).
In water, phosmet is rapidly broken down by the chemical action of the
water (hydrolysis) and by sunlight (photolysis). The half-life of the
compound varies with the acidity of the water. Under moderately acidic
conditions (pH 5) half of the compound degrades within nine days. In a
neutral solution (pH 7) the half-life is 18 hours. Under alkaline conditions
(pH 9) the half-life is as short as 16 hours.
Plants break down phosmet quickly, primarily through the action of air
(oxidation) and water (hydrolysis). On apricots and nectarines treated at an
unknown rates, there were residues of less than 5 mg/kg seven days after
treatment and less than 1 mg/kg 21 days after treatment (1). Maize used for
silage showed a rapid decline in residues before being made into silage, but
the half-life of the silage residue was about 92 days (2). Washing and
blanching of fruits and vegetables can reduce residue levels by 50 to 80
percent and thus reduce the potential human exposure to the pesticide (3).
PHYSICAL PROPERTIES AND GUIDELINES
Exposure Guidelines:
| NOEL: | 2 mg/kg/day (rats) |
| LEL: | 20 mg/kg/day (rats) |
| RfD: | 0.02 mg/kg/day |
| ADI: | 0.02 mg/kg/day |
Physical Properties:
| CAS #: | 732-11-6 |
| Solubility in water: | 20 mg/l |
| Solubility in solvents: | acetone 65g/100g; kerosene 0.5g/100 g; xylene 25g/100g; methanol 5g/100g. |
| Melting point: | 72.5 degrees C |
| Vapor pressure: | 4.9 x 10 to the minus 7 power mmHg |
BASIC MANUFACTURER
Zeneca Ag Products
Wilmington, DE 19897
Telephone: 800-759-4500
Review by Basic Manufacturer
Comments solicited: April, 1993
Comments received:
REFERENCES
Food and Agriculture Organization of the United Nations. 1978.
Pesticide Residues in Food - 1978. FAO Plant Production and Protection
Paper, 15 sup.
Food and Agriculture Organization of the United Nations. 1986.
Pesticide Residues in Food - 1986. FAO Plant Production and Protection
Paper 77.
Food and Drug Administration. 1986. The FDA Surveillance Index.
Bureau of Foods, Department of Commerce, National Technical Information
Service, Springfield, VA.
U.S. Environmental Protection Agency. 1983-85. Chemical Information
Fact Sheet. Office of Pesticides and Toxic Substances, Office of
Pesticide Programs (TS-766C).
Smith, G.J. 1993. Pesticide Use and Toxicology in Relation to
Wildlife: Organophosphorus and Carbamate Compounds, United States
Department of the Interior, Fish and Wildlife Service. C.K. Smolley, Boca
Raton, FL.
Johnson, W.W. and M.T. Finley. 1980. Handbook of Acute Toxicity of
Chemicals to Fish and Aquatic Invertebrates. U.S. Department of the
Interior, Fish and Wildlife Service, Resource Publication 137.
Maddy, K. T., S. Edmiston, C. Kahn, T Jackson and L. Rivera. A Study
of the Decay of Phosmet (Imidan) on the Foliage of Peach Trees in
Stanislaus County, California June-July 1977. California Department of
Food and Agriculture. Division of Pest Management, Environmental
Protection and Worker Safety. Worker Health and Safety Branch.
Walker, M.M. and L.H. Keith. 1991. EPA's Pesticide Fact Sheet
Database. Lewis Publishers. Chelsea, MI.
The Agrochemical Handbook. 1991. The Royal Society of Chemistry.
Cambridge, England.
The Farm Chemicals Handbook. 1992. Meister Publishing. Willoughby,
OH.
Blewett, C.T. and R.I. Krieger. 1988. Estimation of Exposure of
Persons in California to Pesticide Products That Contain Phosmet and
Estimation of Effectiveness of Exposure Reduction Measures. California
Department of Food and Agriculture. Division of Pest Management,
Environmental Protection and Worker Safety. Worker Health and Safety
Branch.
Toxnet. 1993. Hazardous Substance Data Base. Phosmet.
Disclaimer: Please read
the pesticide label prior to use. The information contained at this web
site is not a substitute for a pesticide label. Trade names used herein
are for convenience only; no endorsement of products is intended, nor is
criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
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