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Trichlorfon

Publication Date: 9/93

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).

ADI: 0.01 mg/kg (15)

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

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  5. Hayes, W. J. 1982. Pesticide studies in man. Baltimore, MD: Williams and Wilkins.
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  7. 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.
  8. Melnikov, N. N. 1971. Chemistry of pesticides. NY: Springer- Verlag, Inc.
  9. 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.
  10. 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.
  11. National Institute for Occupational Safety and Health (NIOSH). 1981- 1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati, OH: NIOSH.
  12. 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.
  13. Sax, N. I. 1975. Dangerous properties of industrial materials. Fourth Edition. NY: VanNostrand Reinhold Co.
  14. Thomson, W. T. 1986. Insecticides, acaricides and avicides. Agricultural Chemicals, Book I. Fresno, CA: Thomson Publications.
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  16. U. S. Environmental Protection Agency. 1985 (Oct. 31). EPA Chemical Profile: Trichlorophon.
  17. _____. 1984. (June 30). Chemical fact sheet for trichlorfon. Washington, DC.
  18. _____. 1984. (June 30). Guidance for registration of pesticide products containing trichlorfon as the active ingredient (057901). Washington, DC.
  19. _____. 1984. (Dec.). User's manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  20. _____. 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.
  21. Windholz, M. (ed.). 1983. The Merck Index. Tenth edition. Rahway, NJ: Merck and Company.
  22. Worthing, C. R. (ed.) 1983. The pesticide manual: A world compendium. Croydon, England: The British Crop Protection Council.
  23. Hayes, W.J. and E.R. Laws (eds.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  24. Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92. Meister Publishing Company, Willoughby, OH.
  25. 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.
  26. Occupational Health Services, Inc. 1991 (Nov. 18). MSDS for Trichlorfon. OHS Inc., Secaucus, NJ.
  27. Cheminova Agro A/S. 1991 (June 11). Material Safety Data Sheet : Dimethoate. Cheminova, Lemvig, Denmark.
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