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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Trichlorfon
Publication Date: 9/93
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TRADE OR OTHER NAMES
Trade names include Anthon, Bovinos, Briten, Chlorophos, Ciclosom, Dylox,
Dipterex, Ditrifon, Dylox, Dyrex, Equino-Aid, Foschlor, Leivasom, Neguvon,
Masoten, Trichlorophon, Trinex, Phoschlor, Proxol, Trichlorophene, Totalene,
Tugon and Vermicide Bayer 2349. The common name used in Great Britain is
trichlorphon, in Turkey is dipterex, and in the former USSR is chlorofos (24).
When this material is used as a drug, it is called metrifonate or metriphonate
(23).
REGULATORY STATUS
Trichlorfon is classified by the U.S. Environmental Protection Agency
(EPA) as a general use pesticide. Trichlorfon underwent pre-special review
based on its potential to cause tumors, genetic mutations, and reproductive
effects. It was, however, returned to the normal review process after a final
determination was made. A registration standard was issued in June, 1984. A
24-hour reentry interval was set for trichlorfon (18). Products containing
trichlorfon must bear the signal word "Warning" (24). Check with specific
state regulations for local restrictions which may apply.
INTRODUCTION
Trichlorfon is an organophosphate insecticide used to control
cockroaches, crickets, silverfish, bedbugs, fleas, cattle grubs, flies, ticks,
leafminers and leaf-hoppers (14). It is applied to vegetable, fruit and field
crops; livestock; ornamental and forestry plantings; in agricultural premises
and domestic settings; in greenhouses, and for control of parasites of fish in
designated aquatic environments (17). It is also used for treating domestic
animals for control of internal parasites (5, 23). Trichlorfon is available
in dust, emulsifiable concentrate, granular, fly bait, and soluble powder
formulations (24).
Trichlorfon is a selective insecticide, meaning that it kills selected
insects, but spares many or most other organisms. Trichlorfon is toxic to
target insects through direct applications and by ingestion. In other words,
it works both by contact and stomach poison action (17).
Trichlorfon is one of a family of insecticides referred to as
organophosphates. These chemicals act by interfering with an essential
nervous system enzyme, cholinesterase. Please refer to the Toxicology
Information Brief on cholinesterase-inhibition for a more detailed description
of this topic.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Trichlorfon is moderately toxic by ingestion or dermal absorption. As
with all organophosphates, trichlorfon is readily absorbed through the skin.
Skin which has come in contact with this material should be washed immediately
with soap and water and all contaminated clothing should be removed. Skin
sensitivity (allergies) can result from dermal exposure (16). Human exposure
to trichlorfon can be decreased with the use of approved respirators and other
protective clothing during handling, applying and reentry procedures (18).
Application by ground and aerial equipment increases the potential for
exposure to humans, livestock and wildlife, due to spray drift (17).
The organophosphate insecticides are cholinesterase inhibitors. They are
highly toxic by all routes of exposure. When inhaled, the first effects are
usually respiratory and may include bloody or runny nose, coughing, chest
discomfort, difficult or short breath, and wheezing due to constriction or
excess fluid in the bronchial tubes. Skin contact with organo-phosphates may
cause localized sweating and involuntary muscle contractions. Eye contact
will cause pain, bleeding, tears, pupil constriction, and blurred vision.
Following exposure by any route, other systemic effects may begin within a few
minutes or be delayed for up to 12 hours. These may include pallor, nausea,
vomiting, diarrhea, abdominal cramps, headache, dizziness, eye pain, blurred
vision, constriction or dilation of the eye pupils, tears, salivation,
sweating and confusion. Severe poisoning will affect the central nervous
system, producing incoordination, slurred speech, loss of reflexes, weakness,
fatigue, involuntary muscle contractions, twitching, tremors of the tongue or
eyelids, and eventually paralysis of the body extremities and the respiratory
muscles. In severe cases there may also be involuntary defecation or
urination, psychosis, irregular heart beats, unconsciousness, convulsions and
coma. Death may be caused by respiratory failure or cardiac arrest. Persons
with respiratory ailments, recent exposure to cholinesterase inhibitors,
impaired cholinesterase production, or with liver malfunction may be at
increased risk from exposure to trichlorfon. High environmental temperatures
or exposure of ethion to visible or UV light may enhance its toxicity (26).
Some organophosphates, including trichlorfon, may cause delayed symptoms
beginning 1 to 4 weeks after an acute exposure which may or may not have
produced immediate symptoms. In such cases, numbness, tingling, weakness and
cramping may appear in the lower limbs and progress to incoordination and
paralysis. Improvement may occur over months or years, but some residual
impairment will remain (26).
The amount of a chemical that is lethal to one-half (50%) of test animals
to which it is given is referred to as its lethal dose fifty, or LD50. The
oral LD50 for trichlorfon in rats is 150 to 649 mg/kg, 300 to 1370 mg/kg in
mice, 97 mg/kg in cats, 400 mg/kg in dogs, 420 mg/kg in guinea pigs, and 160
mg/kg in rabbits. The dermal LD50 in rats is 2,000 to 5,000 mg/kg, and 1,500
to greater than 2,100 mg/kg in rabbits (1, 11, 18, 23, 24).
The lethal concentration fifty, or LC50, is that concentration of a
chemical in air or water that kills half of the experimental animals exposed
to it for a set time period. The LC50 for trichlorfon in rats is 1300 mg/m3
(26).
CHRONIC TOXICITY
Repeated or prolonged exposure to organophosphates may result in the same
effects as acute exposure including the delayed symptoms. Other effects
reported in workers repeatedly exposed include impaired memory and
concentration, disorientation, severe depressions, irritability, confusion,
headache, speech difficulties, delayed reaction times, nightmares,
sleepwalking and drowsiness or insomnia. An influenza-like condition with
headache, nausea, weakness, loss of appetite, and malaise has also been
reported (26).
When 45 mg/kg/day was administered to dogs for three months, serum
cholinesterase was reduced to 60% of normal. A dietary level of about 10.5
mg/kg/day for twelve weeks produced a similar effect. During a 60-day testing
period with repeated doses of trichlorfon at 100 mg/kg/day, the cholinesterase
activity of rats was reduced to less than half of normal levels. Doses of 50
mg/kg/day reduced the activity to 50 to 75% of normal levels (5). Trichlorfon
produced no pathological changes in rats that were fed 500 mg/kg of the
insecticide for one year (7).
Reproductive Effects
Trichlorfon is suspected of having negative reproductive effects (3).
Fetal abnormalities were produced in rats, hamsters and mice, when doses
approaching the LD50 level were administered during pregnancy, or 'gestation'
(5). An increased number of embryonic deaths, a decreased number of live
fetuses and an increased number of fetal abnormalities was observed in rats
given a single oral dose of 80 mg/kg body weight, by stomach tube, on the 13th
day of pregnancy (15). During a 3-generation study of the effect of
trichlorfon on rat reproduction, a dietary level of 3,000 parts per million
(ppm), or about 150 mg/kg/day, resulted in a marked decrease in the rate of
pregnancy, and underdeveloped rat pups at birth, none of which survived to
weaning. A dietary dose of 50 mg/kg/day reduced the number of pups per
litter, as well as the weight of individual pups. A dietary level of 300 ppm
(about 15 mg/kg/day) had no detectable effect on reproduction (5). Once in
the bloodstream , trichlorfon may cross the placenta (26).
Teratogenic Effects
Since trichlorfon breaks down into a byproduct that is suspected of being
a teratogen, an agent that causes birth defects, the EPA has called for
additional data to assess the teratogenicity of this insecticide (17). A 50
mg/kg dose of trichlorfon was teratogenic in a litter of pigs (5). Dipterex
was teratogenic when given to pregnant rats through a stomach tube, at a dose
level of 480 mg/kg/day, on days 6 through 15 of pregnancy, but not when
administered only on days 8 or 10 of pregnancy. Teratogenic effects were also
seen in hamsters given 400 mg/kg/day on days 7 through 11 of pregnancy (15).
There was no evidence of teratogenesis in a 3-generation study with rats fed
dietary doses of as high as 150 mg/kg/day (23). It should be noted that these
doses are within the range of LD50's reported for rats (see Acute Toxicity).
Mutagenic Effects
In vitro studies indicate that trichlorfon, or its degradation products,
can be mutagenic in bacterial and mammalian cells (18). The insecticide
produced mutations in mice when it was given in the highest tolerable single
dose and in smaller, repeated doses (5). Additional data are needed by EPA on
the mutagenicity of trichlorfon, in order to complete the risk assessment for
this insecticide (17).
Carcinogenic Effects
Available data suggest that at high dietary levels (500 and 1,000 ppm),
trichlorfon contributes to the production of tumors (18). Carcinogenic
effects were seen in rats given oral doses of 186 mg/kg or intramuscular doses
of 183 mg/kg for six weeks (11). No evidence of carcinogenicity was found in
rats given the insecticide orally or intraperitoneally for 90 weeks (5).
Organ Toxicity
Trichlorfon primarily affects the nervous system through cholinesterase
inhibition, by which there is a deactivation of cholinesterase, an enzyme
required for proper nerve functioning.
Benign tumors called 'papillomas' developed in the lining of the forward
portion of the stomach when trichlorfon was administered to rats orally or
subcutaneously. Rats that survived for 6 months had varying degrees of liver
damage (5). Excessive accumulation of fluid, 'edema,' of the brain,
congestion of organs, breakdown of various parts of the liver, inflammation of
the lungs, and heart muscle changes were observed in rats given daily oral
doses of 300 mg/kg body weight technical trichlorfon for 5 days. 300 mg/kg
falls within the range of LD50's reported for trichlorfon in rats. Brain
disturbances and changes in the liver, kidneys, spleen, lungs and testicles
were seen in bulls that were given oral doses of 1, 2, or 5 mg/kg formulated
trichlorfon (chlorophos) daily, or 5 mg/kg in weekly intervals for 6 months
(15).
Fate in Humans and Animals
The absorption, distribution and excretion of trichlorfon is rapid.
About 70 to 80% of a dose administered orally to mice was excreted during the
first twelve hours following treatment (15). A breakdown product of
trichlorfon, dichlorvos (DDVP), was found in some body tissues of exposed
cows. Trichlorfon was found in cows' milk following "pour-on" applications of
the insecticide (5).
ECOLOGICAL EFFECTS
Effects on Birds
Trichlorfon is highly toxic to birds. The acute bird, or 'avian,' oral
toxicity is 40-47 mg/kg (17). Signs of intoxication in birds include
regurgitation, imbalance, trembling, slowness, lack of movement and wing-beat
convulsions. Signs of poisoning appeared as soon as 10 minutes after
exposure, and deaths usually occurred within 30 minutes to 3 hours of
treatment (6).
The LC50 for trichlorfon in bobwhites was 700 to 800 ppm. Its LC50 was
1,800 to 2,000 ppm in two-week-old coturnix that were fed treated feed for
five days, followed by untreated feed for three days. Seventy-seven percent
of exposed hen embryos were killed when 100 ppm of trichlorfon (in acetone)
was injected into their eggs (12). The oral LD50 for wild birds is 37 mg/kg
(11). The acute oral LD50 for trichlorfon in mallards is 36.8 mg/kg, 22.4
mg/kg in old bobwhite quail, 59.3 in California quail, 95.9 mg/kg in male
pheasant, and 23 mg/kg in rock doves (6).
Effects on Aquatic Organisms
Trichlorfon is highly toxic to both cold and warm water fish; its acute
toxicity to freshwater fish is between 1.67 and 180 ppm (17). The 24-hour LC50
for striped bass was 10.4 ppm. The 48-hour LC50 for rainbow trout was 3.2
ppm. The 96-hour LC50 for fathead minnow was 180.0 ppm (12). Studies did not
show a potential for trichlorfon to accumulate in nontarget fish (18).
Effects on Other Animals (Nontarget species)
Trichlorfon has moderate to high acute toxicity toward certain beneficial
or nontarget insects and aquatic invertebrates (7). This pesticide is toxic
to wildlife (18). Data indicate that trichlorfon has a low toxicity to bees;
it can be used around bees with minimum injury (17, 10).
ENVIRONMENTAL FATE
Most organophosphates tend to persist and bioconcentrate environmental
systems (28). Studies on the dissipation of trichlorfon in forest and aquatic
environments did not show a potential for the insecticide to persist in
leaves, leaf-litter, soil, water or sediment (18).
Breakdown of Chemical in Soil and Groundwater
Trichlorfon does not adsorb strongly to soil particles, is readily
soluble in water, and it is very mobile in soils of varying textures and
organic contents. It is therefore likely to contaminate groundwater (24).
Soil organic matter content does not appear to influence trichlorfon's
movement in soil (17).
Trichlorfon breaks down, or degrades, rapidly in aerobic soils, in which
it has half-lives between 1 and 27 days under nonsterile conditions.
Trichlorfon is stable with a half-life greater than 40 days in sterile soils.
A half-life of 27 days has been reported (25). It has been reported to
persist in soil for up to two weeks(15). The major breakdown product is
dichlorvos (DDVP). Trichlorfon should not be applied to lime-treated surfaces
(15).
Breakdown of Chemical in Water
Further studies on the behavior of trichlorfon in water are needed by the
EPA to complete the assessment of the environmental effects of this material
(17). State Fish and Game Agencies should be consulted before applying
trichlorfon products to public waters. It should not be applied to water or
wetlands that are not under forest canopy. Runoff and drift from treated
areas may be hazardous to aquatic organisms in neighboring areas (18).
Trichlorfon should not be discharged into lakes, streams, ponds or public
water without a permit. It degrades rapidly in alkaline pond water (pH 8.5).
Approximately 99% of applied trichlorfon was broken down within 2 hours. It
was stable in the same pond water kept under acidic (pH 5.0) conditions for 2
hours. The major breakdown product of trichlorfon in water is dichlorvos
(DDVP) (17). This insecticide persists at detectable levels for 526 days in
water at 20 degrees C (12).
Breakdown of Chemical in Vegetation
Further studies are needed regarding trichlorfon's behavior in vegetation
(17). The approximate residual period is 7 to 10 days on plants. Injury has
been reported on the foliage of apples, and on carnations and zinnias (4). A
manufacturer has cautioned against aerial spray drifts into sorghum. Care
must be taken when using this insecticide for seed soaks (7).
PHYSICAL PROPERTIES AND GUIDELINES
Trichlorfon is a pale clear, white or yellow crystalline solid with an
ethyl ether odor (1, 24, 26). The pure form is thought to be less toxic than
technical material (5). It is chemically related to dichlorvos (20, 23). It
is stable at normal temperatures and pressures, but is decomposed at higher
temperatures and at a pH of less than 5.5, forming dichlorvos (23).
Trichlorfon will also decompose in the presence of alkalis, and is
incompatible with strong oxidizing agents (26). It should be kept well packed
in a cool, dry place (16, 1). Heat may cause the decomposition of trichlorfon
and the release of dichlorvos, highly toxic fumes of hydrogen chloride and
phosphorous oxides. Containers may explode in the heat of a fire (13, 26).
This material may burn, but it does not readily ignite. As with other
organophosphate pesticides, it is advisable to stay upwind from trichlorfon
treatment areas. Keep this material out of low areas (16). Treated fields
should not be reentered for 24 hours, unless protective clothing is worn (18).
Persons who work with organophosphate materials for long periods of time
should have frequent blood tests of their cholinesterase levels. If the
cholinesterase level falls below a critical point, no further exposure should
be allowed until it returns to normal (27).
Protective clothing must be worn when handling trichlorfon. Before
removing gloves, wash them with soap and water. Always wash hands, face and
arms with soap and water before smoking, eating or drinking.
After work, remove all work clothes and shoes. Shower with soap and
water. Wear only clean clothes when leaving the job. Wash contaminated
clothing and equipment with soap and water after each use. Keep contaminated
work clothes separate from regular laundry.
Exposure Guidelines:
No occupational exposure limits have been established for trichlorfon by
OSHA, NIOSH or ACGIH (26). The maximum permissible concentration in air is
0.5 mg/m3 (8).
Physical Properties:
| CAS #: | 52-68-6 |
| Specific Gravity: | 1.73 at 20 degrees C (23) |
| H20 solubility: | 120,000 mg/l at 20-25 degrees C (19); readily soluble (24); 136 gm/l at 20 degrees C (1); 15.4 g/100 ml at 25 degrees (21) |
| Solubility in other solvents: | Soluble in alcohols, ketones, dichloromethane, 2-propanol, methylene chloride and toluene.
Slightly soluble in aromatic solvents.
Nearly insoluble in n-hexane (1, 17, 24). |
| Melting point: | 75 - 84 degrees C (24) |
| Boiling point: | 212 degrees F (100 degrees C) (26) |
| Vapor pressure: | 7.8 mm Hg at 20 degrees C (17) |
| PCMC1: | 8.40 x 10 to the minus 3 power mole fraction |
| PCMC2: | 120,000 mg/l |
| PCMC3: | 466,000 mcm/l (19) |
| Kow: | 4 (7) |
| Koc: | 2 g/ml (25) |
| Chemical Class/Use: | Organophosphate insecticide |
BASIC MANUFACTURER
Miles, Inc.
Crop Protection and Animal Health Div.
PO Box 4913
Kansas City MO 64120
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received:
REFERENCES
Berg, G. L. (ed.). 1986. Farm Chemicals Handbook. Meister
Publishing Co. Willoughby, Ohio.
Gosselin, R. E., et al. 1976. Clinical toxicology of commercial
products. Fifth edition. Baltimore, MD. Williams and Wilkins.
Hallenbeck, W. H. and K. M. Cunningham-Burns. 1985. Pesticides and
human health. NY: Springer-Verlag.
Harding, W. C. 1979. Pesticide profiles. Part one: Insecticides
and miticides. Bulletin 267. Cooperative Extension Service. University of
Maryland.
Hayes, W. J. 1982. Pesticide studies in man. Baltimore, MD:
Williams and Wilkins.
Hudson, R. H., et al. 1984. Handbook of toxicity of pesticides to
wildlife. Second edition. United States Department of the Interior. Fish and
Wildlife Service. Resource Publication 153. Washington, DC: U.S. Government
Printing Office.
Lambert, W. P. No date given. Dylox: A profile of its behavior in
the environment. Submitted by Roy F. Weston, Inc. West Chester, PA.
Submitted to the U.S. Department of Agriculture, Animal and Plant Inspection
Service.
Melnikov, N. N. 1971. Chemistry of pesticides. NY: Springer-
Verlag, Inc.
Morgan, D. P. 1982 (Jan.). Recognition and management of pesticide
poisonings. Third edition. U. S. Environmental Protection Agency.
Washington, DC: U. S. Government Printing Office.
Morse, R. A. 1987. Bee poisoning. In 1988 New York State pesticide
recommendations. Forty-ninth annual pest control conference. Nov. 9, 10, 11.
Cornell University. Ithaca, NY.
National Institute for Occupational Safety and Health (NIOSH). 1981-
1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati,
OH: NIOSH.
Pimentel, D. 1971 (June). Ecological effects of pesticides on
nontarget species. Executive Office of the President's Office of Science and
Technology. Washington, DC: U. S. Government Printing Office.
Sax, N. I. 1975. Dangerous properties of industrial materials.
Fourth Edition. NY: VanNostrand Reinhold Co.
Thomson, W. T. 1986. Insecticides, acaricides and avicides.
Agricultural Chemicals, Book I. Fresno, CA: Thomson Publications.
TOXNET. 1975-1986. National library of medicine's toxicology data
network. Hazardous Substances Data Bank (HSDB). Public Health Service.
National Institute of Health, U. S. Department of Health and Human Services.
Bethesda, MD: NLM.
U. S. Environmental Protection Agency. 1985 (Oct. 31). EPA Chemical
Profile: Trichlorophon.
_____. 1984. (June 30). Chemical fact sheet for trichlorfon.
Washington, DC.
_____. 1984. (June 30). Guidance for registration of pesticide
products containing trichlorfon as the active ingredient (057901).
Washington, DC.
_____. 1984. (Dec.). User's manual for the pesticide root zone
model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
_____. 1983. (June) 1983 status report on rebuttable presumption
against registration (RPAR) or special review process, registration standards
and the data call-in programs. Office of Pesticide Programs, Washington, DC.
Windholz, M. (ed.). 1983. The Merck Index. Tenth edition. Rahway,
NJ: Merck and Company.
Worthing, C. R. (ed.) 1983. The pesticide manual: A world
compendium. Croydon, England: The British Crop Protection Council.
Hayes, W.J. and E.R. Laws (eds.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister
Publishing Company, Willoughby, OH.
U. S. Department of Agriculture, Soil Conservation Service. 1990
(Nov.). SCS/ARS/CES Pesticide Properties Database: Version 2.0 (Summary).
USDA - Soil Conservation Service, Syracuse, NY.
Occupational Health Services, Inc. 1991 (Nov. 18). MSDS for
Trichlorfon. OHS Inc., Secaucus, NJ.
Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet :
Dimethoate. Cheminova, Lemvig, Denmark.
Witt, J. M. (ed.). 1985. Chemistry, biochemistry, and toxicology of
pesticides. Proceedings of an Extension Service Short Course at Oregon State
University. Pest control education program. Eugene, OR.
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site is not a substitute for a pesticide label. Trade names used herein
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criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
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