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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 Avadex BW, CP 23426, Diptal, Far-Go, Buckle, TDTC Technical and Carbamothoic acid.


Formulations of triallate must bear the signal word "Caution" (11).


Triallate belongs to the thiocarbamate chemical class. It is a preemergence selective herbicide used to control grass weeds in field and pulse crops (11). It is used selectively to control wild oats, black grass, and annual meadow grass in barley, wheat, peas, lentils, rye, maize, beets, brassicas, carrots and onions (1, 3, 13). Depending on the crop that is treated, the herbicide is incorporated in the soil before or after planting (13). Triallate is available as emulsifiable concentrates and as granular formulations.



Technical triallate is slightly toxic by ingestion to humans. It is practically nontoxic via dermal exposure or inhalation (11, 14). In rats fed triallate at doses of 50 to 2,000 mg/kg, abnormal behavior was observed at doses of 100 mg/kg and above. No changes in nerve tissue occurred. At doses of 600 mg/kg and above, death and reduced body weight occurred (15). Sheep may be poisoned by 300 mg/kg of triallate, with symptoms of depression, lack of appetite, mouth watering, weakness, and convulsions (6). Inhalation exposure to large amounts of thiocarbamates may cause itching, scratchy throat, sneezing and coughing (13). Triallate is moderately irritating to the skin and is a mild eye irritant (14). Tests on guinea pigs indicate that technical triallate does not cause allergic skin reactions (15).

Although triallate is a carbamate, it does not inhibit cholinesterase activity. No symptoms occurred and cholinesterase activity was not affected in rats fed a single dose of 1,500 and 3,000 mg/kg (14, 16). (For more information on cholinesterase, please refer to the Toxicology Information Brief on Cholinesterase-Inhibition).

The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for technical triallate in rats is 800 to 2,165 mg/kg, and for mice is 930 mg/kg (3, 5, 11, 16). The oral LD50 for emulsifiable concentrate formulations is 2,700 mg/kg, and for granular formulations is greater than 12,000 mg/kg (13). The dermal LD50 for technical triallate in rabbits is 8,200 mg/kg, and for rats is 3500 mg/kg. The inhalation LClo for cats is 400 mg/m3/4 hours.(16).


Prolonged or repeated exposure to triallate may cause symptoms similar to those caused by acute exposure.

Technical triallate fed to rats, hamsters and dogs for 30 to 90 days caused abnormal behavior, reduction of body weight and food consumption, changes in blood composition, effects on the gastrointestinal tract, sex organs, liver, thymus, spleen and kidneys, and some deaths.

Oral doses of 2,000 ppm triallate to hamsters for 22 months resulted in decreased body weight gain, changes in blood chemistry, slight anemia, increased liver weights, and decreased spleen weights. The NOEL in this study was 300 ppm. Mice fed 60 and 250 ppm triallate for two years exhibited increased liver and heart weights, changes in the liver and spleen, and mineralization of the brain and cornea. The NOEL was 20 ppm. No adverse effects were observed in dogs fed 1.5, 5 and 15 mg/kg/day of triallate for two years (14, 15).

At high dose levels in subchronic exposure studies, neurological effects have been observed in rats. Rat deaths at these high levels were probably due to a variety of systemic effects such as liver and stomach pathological changes, and loss of food consumption and body weight. Neurological effects were not observed in rats at doses of 50 mg/kg or below (14).

Reproductive Effects

Reduced body and pup weights, reduced pregnancy rate and length, reduced pup survival and effects on other reproductive parameters occurred when rats were fed 600 ppm triallate during mating, pregnancy and nursing for two successive generations. The reproductive NOEL for this study was set at 150 ppm (14, 15).

Teratogenic Effects

No birth defects were observed in the offspring of rabbits given doses of 0, 5, 15, and 45 mg/kg/day on days 6 through 28 of pregnancy. No birth defects were observed in the offspring of rats given doses of 0, 10, 30, 90 mg/kg on days 6 through 20 of pregnancy. In both of these studies, the highest dose administered caused poisoning symptoms in both the mothers and their offspring (15).

Mutagenic Effects

No genetic changes occurred in tests using live animals (fruit flies, hamsters, and mice). In tests using bacterial and animal cell cultures, both positive and negative results have been reported (14, 15).

Carcinogenic Effects

Tests suggest that carcinogenicity to the general public and/or applicators is unlikely at usual exposure rates (9). When fed dietary doses of 20, 60 and 250 ppm technical triallate over a long time, the incidence of liver tumors increased in a strain of mice normally prone to spontaneous production of liver tumors. Several other long term feeding studies involving test animals showed no incidence of tumors (14). Triallate did not produce tumors in rats fed up to 250 ppm for two years (15). No tumors appeared when hamsters were fed dietary doses of 50, 300 or 2,000 ppm triallate for 22 months (14).

Organ Toxicity

Changes in the cellular processes of the brain, liver and spleen were observed in pigs given triallate (6).

Fate in Humans and Animals

In general, thiocarbamates, the chemical class in which triallate is included, are rapidly absorbed into the bloodstream from the gastrointestinal tract, readily broken down into polar metabolites and then excreted by treated animals. It is rarely possible to detect thiocarbamates in the blood (4).

A single oral dose of 500 mg/kg of triallate was rapidly absorbed from the gastrointestinal tract of rabbits. It was then found to be present in all organs tested within 15 to 20 minutes after dosing. The largest amount of the herbicide accumulated in the liver, lungs, kidneys, and spleen. All traces were gone by the seventh day. Triallate was reported to be completely eliminated from the body of rabbits within 7 to 10 days (6). The meat of sheep poisoned by 300 mg/kg of triallate had detectable traces 84 days later in cold storage. No traces of the herbicide were detected in the eggs, meat, or internal organs of hens fed 1/240 of a LD50 dose (6, 15).


Effects on Birds

Triallate is slightly toxic to relatively non-toxic to birds. The acute oral LD50 for triallate in bobwhite quail is 2,251 mg/kg. The eight-day dietary LD50 is greater than 5,000 ppm in both mallards and bobwhite quail (13, 15).

Effects on Aquatic Organisms

Triallate is highly toxic to fish and other aquatic organisms. 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 96-hour LD50 for technical triallate in bluegill is 1.3 mg/l, and 1.2 mg/l in rainbow trout. The 48-hour LD50 for Dapnia magna, a small freshwater crustacean, is 0.43 mg/l (11). The 96-hour LC50 for algae is 0.12 mg/l (15).

When technical triallate concentrations were measured in bluegill sunfish over a 7-week period, it was determined that marked bioaccumulation occurred. However, after a two week depuration period, triallate was rapidly and nearly completely eliminated by the fish (15).

Effects on Other Animals (Nontarget species)

Triallate is non-toxic to bees (3).


Breakdown of Chemical in Soil and Groundwater

Triallate adsorbs well to loam and clay soils (Koc = 2,400 g/ml) and is not readily dissolved in water (4 ug/ml). This information indicates that triallate is not likely to move through the soil, even though it has a lengthy soil half-life (82 days) (12, 13). However, if there is significant moisture and/or low levels of organic matter in the soil, triallate may become desorbed, from soil particles. Leaching and groundwater contamination is possible in such situations. EPA suggests that triallate does not pose a threat to the environment due to leaching because it is generally used where the water table is relatively low. In areas of heavy rainfall, or where the water table is near the surface, triallate could enter the groundwater (9).

Triallate is reported to be degraded in soil primarily by soil microbes (13). Plants also degrade triallate, lessening its potential to accumulate in the soil (9). If applied to the soil surface at high temperatures, without incorporation into the soil, triallate can be lost to the atmosphere through volatilization. Its volatility increases with soil water content. Triallate must be incorporated into the soil after application to prevent its loss from soil at high temperatures (6, 9, 13). Photodecomposition, or breakdown in the presence of ultraviolet light of the sun, is considered an insignificant method of degradation for triallate (6). Triallate can persist into the next growing season, especially in colder climates in which it is less likely to be broken down (9).

Breakdown of Chemical in Vegetation

Studies indicate that triallate also does not bioaccumulate in plants. Triallate is absorbed and metabolized by plants (13).


Triallate is an amber oily liquid which is nonflammable and noncorrosive under dry conditions (3, 13). It is indefinitely stable, and insensitive to heat and light (13). Triallate is hydrolyzed by strong acids and alkalis (3). It is usually compatible with sprayable fluid fertilizers, but a preliminary test is recommended (3, 13).

There are no unusual fire or explosion hazards associated with triallate. Hazardous thermal decomposition products include hydrogen chloride, carbonyl sulfide and carbonyl chloride, and oxides of nitrogen and sulfur (12, 16).

Triallate is highly resistant to decomposition by UV irradiation. It is insensitive to light or heat (13).

Applicators who work with emulsifiable concentrate formulations are subject to somewhat higher levels of exposure than those who work with granular formulations (9). Rubber gloves and safety goggles should be worn when handling triallate (13).

Occupational Exposure Limits:

No occupational exposure limits have been established for triallate by OSHA, ACGIH, or NIOSH (16).

Physical Properties:

CAS #: 2303-17-5
Specific gravity: 1.273 at 25/15.6 degrees C (16)
H20 solubility: 4 mg/l at 20-25 degrees C; 4 ppm at 25 degrees C (9, 13, 14)
Solubility in other solvents: At 25 degrees C, it is soluble in acetone, ether, ethyl alcohol, heptane, benzene, ethyl acetate, and most organic solvents (13, 16).
Melting point: 29 - 30 degrees C (86 degrees F) (13)
Boiling point: 117 degrees C at 0.3 mm Hg; 1.36 degrees C at 1 mm Hg (13); 298 degrees F at 2 mm Hg (14); 329 degrees F (165 degrees C) at 6.0 mm Hg (16).
Decomposition temperature: 200 degrees C (16)
Flashpoint: 113 degrees F (11), greater than 300 degrees F (12)
Vapor pressure: 1.1 x 10-4 mm Hg at 25 degrees C (13)
Koc: 2220 (7)
Chemical Class/Use: (Mono)thiocarbamate herbicide
Degradation rate
constant in soil
root zone (days-1):
.0231-.0713 (8)


Monsanto Agricultural Company
800 N. Lindbergh Blvd.
St. Louis, MO, 63167

Review by Basic Manufacturer:

Comments solicited: October, 1992
Comments received: December, 1992


  1. Berg, G. L. (ed.). 1984 Farm chemicals handbook. Willoughby, OH: Meister Publishing Company.
  2. Cornell University. 1987. 1988 New York State pesticide recommendations. Forty-ninth annual pest control conference. Nov. 9, 10, 11. Ithaca, NY.
  3. Hartley, D. and H. Kidd (eds.). 1983. The agrochemicals handbook. Nottingham, England: Royal Society of Chemistry.
  4. 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.
  5. National Institute for Occupational Safety and Health (NIOSH). 1981- 1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati, OH: NIOSH.
  6. 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.
  7. U.S. Environmental Protection Agency. 1986 (Jan.). Estimating pesticide sorption coefficients for soils and sediments. Richard E. Green and Samuel W. Karickhoff. Environmental Research Laboratory. Office of Research and Development. Athens, GA.
  8. _____. 1984 (December). Users manual for the pesticide root zone model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
  9. _____. 1980 (Nov.). Triallate decision document. Office of Pesticides and Toxic Substances. Washington, DC: U.S. Government Printing Office.
  10. Hayes, W.J. and E.R. Laws (eds.). 1990. Handbook of Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., NY.
  11. Meister, R.T. (ed.). 1991. Farm Chemicals Handbook '91. Meister Publishing Company, Willoughby, OH.
  12. Monsanto Company. 1989 (Sept.). Material Safety Data for Triallate Technical. Monsanto Co., St. Louis, MO.
  13. Weed Science Society of America. 1989. Herbicide Handbook, 6th Edition. WSSA, Herbicide Handbook Committee, Champaign, IL.
  14. Bruce Hammond, Manager of Toxicology, Monsanto Agricultural Company. Letter of 23 December, 1991.
  15. Monsanto Company. 1989 (May). Toxicology Information Summary for Triallate. Monsanto Co., St. Louis, MO.
  16. Occupational Health Services, Inc. 1991 (21 Feb.). MSDS for Triallate. OHS Inc., Secaucus, NJ.