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
by the USDA/Extension Service/National Agricultural Pesticide Impact
Assessment Program.
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Pesticide
Information
Profile
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Triallate
Publication Date: 9/93
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TRADE OR OTHER NAMES
Some trade names include Avadex BW, CP 23426, Diptal, Far-Go, Buckle,
TDTC Technical and Carbamothoic acid.
REGULATORY STATUS
Formulations of triallate must bear the signal word "Caution" (11).
INTRODUCTION
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.
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
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).
CHRONIC TOXICITY
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).
ECOLOGICAL EFFECTS
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).
ENVIRONMENTAL FATE
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).
PHYSICAL PROPERTIES AND GUIDELINES
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) |
BASIC MANUFACTURER
Monsanto Agricultural Company
800 N. Lindbergh Blvd.
St. Louis, MO, 63167
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received: December, 1992
REFERENCES
Berg, G. L. (ed.). 1984 Farm chemicals handbook. Willoughby, OH:
Meister Publishing Company.
Cornell University. 1987. 1988 New York State pesticide
recommendations. Forty-ninth annual pest control conference. Nov. 9, 10, 11.
Ithaca, NY.
Hartley, D. and H. Kidd (eds.). 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
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.
National Institute for Occupational Safety and Health (NIOSH). 1981-
1986. Registry of toxic effects of chemical substances (RTECS). Cincinnati,
OH: NIOSH.
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. 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.
_____. 1984 (December). Users manual for the pesticide root zone
model (PRZM). Release 1. Athens, GA: Environmental Research Laboratory.
_____. 1980 (Nov.). Triallate decision document. Office of
Pesticides and Toxic Substances. Washington, DC: U.S. Government Printing
Office.
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.). 1991. Farm Chemicals Handbook '91. Meister
Publishing Company, Willoughby, OH.
Monsanto Company. 1989 (Sept.). Material Safety Data for Triallate
Technical. Monsanto Co., St. Louis, MO.
Weed Science Society of America. 1989. Herbicide Handbook, 6th
Edition. WSSA, Herbicide Handbook Committee, Champaign, IL.
Bruce Hammond, Manager of Toxicology, Monsanto Agricultural Company.
Letter of 23 December, 1991.
Monsanto Company. 1989 (May). Toxicology Information Summary for
Triallate. Monsanto Co., St. Louis, MO.
Occupational Health Services, Inc. 1991 (21 Feb.). MSDS for
Triallate. OHS Inc., Secaucus, NJ.
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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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