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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


Some trade names include AC 8911, Agromet, Geomet, Granutox, Phorate 10G, Rampart, Thimenox, Thimet, Vegfru Foratox, Timet and Vegfru.


Phorate, an organophosphorus compound, is an insecticide and acaricide that controls pests by systemic, contact, and fumigant action. It is used against sucking and chewing insects, leafhoppers, leafminers, mites, some nematodes and rootworms. Phorate is used in pine forests and on root and field crops, including corn, cotton, coffee, some ornamental and herbaceous plants and bulbs.

Phorate is a Restricted Use Pesticide (RUP) and is among the most poisonous chemicals commonly used for pest control. Restricted Use Pesticides may be purchased and used only by certified applicators.



Phorate is extremely toxic, and phorate products are labeled with a DANGER signal word. Symptoms of acute oral exposure may include blurred vision, headache, inability to concentrate, fatigue, nausea, diarrhea, irregular heart and respiration rates, tremors, excessive sweating, confusion and convulsions. Death can occur at high doses due to respiratory arrest or lung constriction. Phorate causes toxicity by inhibiting cholinesterase, an enzyme necessary for normal functioning of the nervous system. This enzyme is found at the ends of individual nerve fibers and plays an important role in nerve transmission. Symptoms resulting from phorate inhalation or skin contact may occur from a few minutes up to 12 hours after exposure. Skin absorption is greater at higher temperatures and increases if the skin is irritated or broken. Toxicity appears to vary with age, with the young being more susceptible (4). Several poisoning cases involved workers from 16-18 years old, wearing inadequate protection while applying phorate to crops, or working around machines used to apply phorate.

The oral LD50 for rats is 1.0 mg/kg (5, 6). The oral LD50 for mice ranges from 3.5 to 6.59 mg/kg (6, 9). Guinea pigs have an oral LD50 of 20 mg/kg. (5). The dermal LD50 for rats is 5.7 mg/kg, while rabbits have a dermal LD50 of 5.2 mg/kg (9). Guinea pigs have a dermal LD50 of 20-30 mg/kg during a 24-hour exposure (9). During a one-hour exposure, rats had an inhalation LC50 of 11 mg/m3 (6).


Repeated exposures to small quantities - by inhalation, ingestion, or dermal routes - can result in cholinesterase inhibition for as long as three months. Workers habitually exposed to organophosphates have shown slow thinking, memory defects, irritability, delayed reaction time, and anxiety (6). A survey of workers exposed to phorate revealed toxic effects in 60% of the males tested (after a two week exposure). Symptoms included a lowering of the heart rate. Effects on cholinesterase in the blood of the workers was also noted in this study (5).

Reproductive Effects

Long-term studies of mice fed high doses of 98.7% pure phorate showed no effects on fertility, gestation, and viability (5, 9). This suggests that phorate is unlikely to cause reproductive effects in humans.

Teratogenic Effects

No birth defects were found in two studies on the rat (5, 10). This suggests that phorate does not cause birth defects. There was some maternal and embryo toxicity at relatively low doses (0.5 mg/kg) (14).

Mutagenic Effects

Available mutagenicity studies involving microbial and mammalian cells have shown no adverse effects on genes or chromosomes (5). Thus it appears that phorate does not cause mutations. Valid studies on the carcinogenicity of phorate are not available.

Carcinogenic Effects

Cancer studies have been conducted on rats and mice. These studies produced no evidence of carcinogenicity (14). A maximum tolerated dose was not achieved in the study on mice.

Organ Toxicity

Phorate, like the other organophosphates, interferes with the working of the nervous system by inhibiting a vital chemical, cholinesterase. In one study, dogs were fed moderate to high doses of phorate six days each week for 13-15 weeks. The dogs experienced lower cholinesterase activity, but did not show any tissue damage (9). Other studies indicate that direct eye exposure may cause blurring, tearing, and ocular pain (6).

Fate in Animals and Humans

The major breakdown products of phorate in mammals are more toxic and have greater anticholinesterase activity than phorate. Phorate's most toxic metabolite has an oral LD50 of 0.5 to 0.8 mg/kg (4).

Phorate is readily absorbed by the skin and the gastrointestinal tract. In rats, less than 40% of a high oral dose of phorate was excreted in six days. The liver, kidney, lung, brain, and glandular tissue held the remaining residues (11).


Phorate is very highly toxic to, and extremely fast-acting on bird species, freshwater fish, and aquatic invertebrates (14). Symptoms occurring in mallards at very low doses include tremors and wing beat convulsions. Fish species which have been studied include bluegill and rainbow trout (5).


In the environment, phorate is degraded by microorganisms and interaction with water. Phorate itself is not persistent in plants. However, phorate protects plants for a long time because its breakdown product persists in plants and soils. For example, a field study of corn treated with a 10% granular formulation at one pound a.i./acre showed that phorate residues were very low after 14 days. Its degradation products persisted for 28 days. After 83 days, no detectable phorate or breakdown product residues were detected in the kernels, cobs, or husks.

Soil treatments often leave more residues in plants than foliar treatments, because the compound persists in the soil and is readily taken up by plant roots.

Phorate binds to soil organic matter and clay particles and is almost immobile in soils. Thus, it does not leach easily and is mainly transported with runoff via sediment and water.

Phorate is moderately persistent in the soil. Its half-life under aerobic laboratory conditions is 82 days, while a field study noted a half- life of 7.5 days (12). It is least persistent in clay soil, while it is slowly released from peat/sand and sandy soils. Phorate almost completely disappears from sand/muck soils within one year. Phorate is unstable in water, especially under alkaline (basic) conditions. As it breaks down in water, non-toxic, water-soluble products are formed.

The half-life in acidic water solutions is between a few days and a few weeks, depending on temperature (9). The half-life in alkaline (basic) water is much shorter (2).

In storage, phorate and its metabolites are stable at room temperatures for at least two years (8). Significant amounts of phorate are lost due to evaporation especially right after being soil-applied, but the loss rapidly stabilizes.

Phorate and its soil metabolites are absorbed from the soil by plant roots and are translocated to above-ground portions of the plant.

Phorate has some potential, though minimal, to leach through the soil and contaminate ground water, particularly where soils are sandy and aquifers are shallow. Phorate is unlikely to leach in clay soils. One study of various soil types (watered every two days for a total of about 100 inches over 24 days) showed that more than 80% of the compound remained near the surface of silt loam and muck soils, while only 50% remained in sandy soil and 76% stayed near the surface of quartz sand (5). Thus, phorate has the potential to be carried in runoff and to contaminate surface water.


Phorate is a clear liquid with a skunk-like odor. It is a member of the organophosphate chemical family. This compound is a derivative of dithio- phosphoric acid. Its chemical name is o,o-diethyls[(ethylthio)methyl] phosphorodithioate. Its molecular weight is 260.39.

Exposure Guidelines:

NOEL: 0.66 ppm (rats); 0.01 mg/kg (dogs) (5)
ADI: 0.0001g/kg/day (5) in drinking water; 0.000 in crop residues (13)
TLV: air: 0.05 mg/m3 (skin)
TWA: 0.2 mg/m3 (skin) STEL (1)

Physical Properties:

CAS #: 298-02-2
Solubility in water: 50 ppm (considered to be of low solubility)
Solubility in solvents: miscible with xylene, carbon tetrachloride, dioxane, methyl cellosolve, dibutylphthalate vegetable oils, ethanol, ether, aliphatic hydrocarbons.
Melting point: -43.7 degrees C (4); <-15 degrees C (8)
Boiling point: 188 degrees C at 2 torr; (6) 118-120 degrees C at 0.8 torr (7)
Vapor pressure: .00084 torr at 20 degrees C; 0.01 torr at 40-42 degrees C (9)


American Cyanamid
One Cyanamid Plaza
Wayne, NJ 07470
Telephone: 201-831-2000

Review by Basic Manufacturer:

Comments solicited: November, 1992
Comments received: December, 1992


  1. American Conference of Governmental Industrial Hygienists 1984-85. Phorate. Threshold Limit Values for Chemical Substances in the Work Environment. Cincinnati, OH: ACGIH.
  2. Buchel, K.H., ed., and G. Holmwood, translator. 1983. Chemistry of Pesticides. John Wiley & Sons, Inc.
  3. Gosselin, R.E.; R.P. Smith, H.C. Hodge and J.E. Braddock. 1984. Clinical Toxicology of Commercial Products, 5th edition. Williams & Wilkins.
  4. Hayes, W.J. 1982. Pesticides Studied in Man. pp. 390-391. Williams & Wilkins.
  5. National Library of Medicine. Hazardous Substances Databank. Phorate. 1992
  6. Occupational Health Services, Inc. Material Safety Data Sheet on Phorate. 7 April 1987.
  7. Sax, N. 1984. Phorate. Dangerous Properties of Industrial Materials. 6th Edition. Van Nostrand Reinhold Co. p. 2208.
  8. Technical Information Sheet on Thimet. February 1987. Cyanamid Agricultural Division: Wayne, NJ.
  9. Toxicological Information. Cyanamid. Organophosphate Pesticides. Thimet. Cyanamid Agricultural Division: Wayne, NJ.
  10. U.S. Environmental Protection Agency. Office of Pesticide Programs. Pesticide Fact Sheet for Phorate. Fact Sheet No. 34.1. February 1985.
  11. Vettorazzi, G. 1979. Phorate. International Regulatory Aspects for Pesticide Chemicals. Vol 1. CRC Press.
  12. Wagner, S.L. 1983. Clinical Toxicology of Agricultural Chemicals. p. 239.
  13. Ware, G.W., ed. 1987. Reviews of Environmental Contamination and Toxicology. Vol. 98. Springer-Verlag.
  14. Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet Database. Lewis Publishers. Chelsea, MI.