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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.


Publication Date: 9/93


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.


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.



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.


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).


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.


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).


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


Zeneca Ag Products
Wilmington, DE 19897
Telephone: 800-759-4500

Review by Basic Manufacturer

Comments solicited: April, 1993
Comments received:


  1. Food and Agriculture Organization of the United Nations. 1978. Pesticide Residues in Food - 1978. FAO Plant Production and Protection Paper, 15 sup.
  2. Food and Agriculture Organization of the United Nations. 1986. Pesticide Residues in Food - 1986. FAO Plant Production and Protection Paper 77.
  3. Food and Drug Administration. 1986. The FDA Surveillance Index. Bureau of Foods, Department of Commerce, National Technical Information Service, Springfield, VA.
  4. U.S. Environmental Protection Agency. 1983-85. Chemical Information Fact Sheet. Office of Pesticides and Toxic Substances, Office of Pesticide Programs (TS-766C).
  5. 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.
  6. 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.
  7. 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.
  8. Walker, M.M. and L.H. Keith. 1991. EPA's Pesticide Fact Sheet Database. Lewis Publishers. Chelsea, MI.
  9. The Agrochemical Handbook. 1991. The Royal Society of Chemistry. Cambridge, England.
  10. The Farm Chemicals Handbook. 1992. Meister Publishing. Willoughby, OH.
  11. 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.
  12. Toxnet. 1993. Hazardous Substance Data Base. Phosmet.