E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
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University of California at Davis. Major support and funding was provided
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Pesticide
Information
Profile
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Phorate
Publication Date: 9/93
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TRADE OR OTHER NAMES
Some trade names include AC 8911, Agromet, Geomet, Granutox, Phorate 10G,
Rampart, Thimenox, Thimet, Vegfru Foratox, Timet and Vegfru.
INTRODUCTION
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.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
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).
CHRONIC TOXICITY
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).
ECOLOGICAL EFFECTS
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).
ENVIRONMENTAL FATE
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.
PHYSICAL PROPERTIES AND GUIDELINES
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) |
BASIC MANUFACTURER
American Cyanamid
One Cyanamid Plaza
Wayne, NJ 07470
Telephone: 201-831-2000
Review by Basic Manufacturer:
Comments solicited: November, 1992
Comments received: December, 1992
REFERENCES
American Conference of Governmental Industrial Hygienists 1984-85.
Phorate. Threshold Limit Values for Chemical Substances in the Work
Environment. Cincinnati, OH: ACGIH.
Buchel, K.H., ed., and G. Holmwood, translator. 1983. Chemistry of
Pesticides. John Wiley & Sons, Inc.
Gosselin, R.E.; R.P. Smith, H.C. Hodge and J.E. Braddock. 1984.
Clinical Toxicology of Commercial Products, 5th edition. Williams & Wilkins.
Hayes, W.J. 1982. Pesticides Studied in Man. pp. 390-391. Williams
& Wilkins.
National Library of Medicine. Hazardous Substances Databank.
Phorate. 1992
Occupational Health Services, Inc. Material Safety Data Sheet on
Phorate. 7 April 1987.
Sax, N. 1984. Phorate. Dangerous Properties of Industrial
Materials. 6th Edition. Van Nostrand Reinhold Co. p. 2208.
Technical Information Sheet on Thimet. February 1987. Cyanamid
Agricultural Division: Wayne, NJ.
Toxicological Information. Cyanamid. Organophosphate Pesticides.
Thimet. Cyanamid Agricultural Division: Wayne, NJ.
U.S. Environmental Protection Agency. Office of Pesticide Programs.
Pesticide Fact Sheet for Phorate. Fact Sheet No. 34.1. February 1985.
Vettorazzi, G. 1979. Phorate. International Regulatory Aspects for
Pesticide Chemicals. Vol 1. CRC Press.
Wagner, S.L. 1983. Clinical Toxicology of Agricultural Chemicals.
p. 239.
Ware, G.W., ed. 1987. Reviews of Environmental Contamination and
Toxicology. Vol. 98. Springer-Verlag.
Walker, M.M. and L.H. Keith. 1992. EPA's Pesticide Fact Sheet
Database. Lewis Publishers. Chelsea, MI.
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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