E X T O X N E T
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.
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Pesticide
Information
Profile
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Amitrole
Publication Date: 9/93
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TRADE OR OTHER NAMES
Amitrole is known as amino-triazole in Great Britain, France, New
Zealand and the former USSR. Trade names include Amerol, Amino
Triazole, Amitrol, Amizine, Amizol, Azolan, Azole, Cytrol, Diurol, and
Weedazol (24, 25, 28).
REGULATORY STATUS
Amitrole is a Restricted Use Pesticide (RUP). RUPs may be
purchased and used only by certified applicators. Products containing
amitrole must bear the signal word "Caution" (25).
INTRODUCTION
Amitrole is a nonselective systemic triazole herbicide. It is used
on non-cropland for control of annual grasses and perennial and annual
broadleaf weeds, for poison ivy control, and for control of aquatic
weeds in marshes and drainage ditches (25). All use of amitrole on food
crops was canceled by the EPA in 1971 because it has caused cancer in
experimental animals (31). It is available as soluble powders, soluble
concentrates, suspension concentrates, water dispersible granules,
liquid solutions, and wettable powders (25).
Amitrole was the chemical that gave rise to the Cranberry Crisis of
1959. This event involved the first enforcement of the Delaney Clause
which prohibits any amount of any cancer causing substance to be in or
on food. It also prompted growers to read and follow pesticide label
directions more carefully. At the time, amitrole was registered for
post harvest use on cranberries. This practice would leave no
detectable levels on berries harvested the following year. However,
misuse of this pesticide, either through over application the previous
season or through pre-harvest application, led to residues on portions
of the cranberry crops of 1957 and 1959. In 1959, just thirteen days
before Thanksgiving, Arthur Flemming, then Secretary of Health,
Education and Welfare, announced that the current crop of cranberries
was contaminated with amitrole, a cancer causing weed killer. The
actual levels detected on the berries were very low. 1587 metric tons
of cranberries were seized by the Food and Drug Administration and, just
three days before Thanksgiving, a plan was implemented to certify
sufficient cranberries to meet holiday demands (6, 24).
TOXICOLOGICAL EFFECTS
ACUTE TOXICITY
Amitrole is a compound of very low acute toxicity to humans and
other animals. Associated symptoms in humans include skin rash,
vomiting, diarrhea, and nose bleeds. Poisoning of several species by
amitrole is characterized by increased intestinal peristalsis (this may
lead to diarrhea), fluid in the lungs, and hemorrhages of various
organs. No toxic effects were observed in a woman who ingested 20
mg/kg. A single dose of 1,200 mg/kg reduced iodine uptake by the
thyroid in healthy persons (6, 24, 30).
Amitrole is a mild skin and eye irritant (24, 28, 30).
The amount of amitrole 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 and dermal LD50 for amitrole in
rats is greater than 5,000 mg/kg. Studies have reported oral LD50s as
high as 15,000 mg/kg in mice and 24,600 mg/kg in rats. In one study,
the largest doses tested, 4,080 mg/kg orally and 2,500 mg/kg dermally,
produced no toxic effects on rats. The dermal LD50 in rabbits is
greater than 200 mg/kg (24, 25, 28).
CHRONIC TOXICITY
Amitrole has not been shown to be hazardous to workers, even after
long term exposure (6). Amitrole has caused liver, thyroid and
pituitary tumors in laboratory animals. Long term exposure to amitrole
can cause reversible goiters (14, 30).
Reproductive Effects
In a 2-generation study in rats, the number of pups per litter and
their weight at weaning were reduced for dams fed 5 or 25 mg/kg.
Atrophy of the thymus and spleen also occurred at these high doses.
Within a week after weaning, most of these pups died of a condition
resembling runt disease. Similar effects have been observed in mice.
Dietary doses of 1.25 or 5 mg/kg/day had no significant effect on
reproduction (24).
Teratogenic Effects
Birth defects have occurred in the pups of pregnant rabbits, rats
and mice exposed to amitrole, but only at doses high enough to also
produce signs of toxicity in the mothers (31).
Mutagenic Effects
One laboratory assay has shown amitrole to be weak mutagen. All
other assays have shown no mutagenic effects by amitrole (24, 31).
Carcinogenic Effects
Amitrole has induced thyroid and liver tumors in rats and mice. It
has been classified as an human carcinogen by EPA because of the
probable evidence for cancer induction in experimental animals in the
absence of direct evidence for carcinogenic effects in humans (24,
29, 30, 31).
Organ Toxicity
Feeding of amitrole to rats at dietary levels of 3 or 6 kg/mg/day
for 2 weeks caused enlargement of the thyroid and reduced uptake of
radio iodine by the thyroid. A dietary level of 50 mg/kg/day produced
significant enlargement of the thyroid after three days of feeding.
Several studies have shown that amitrole inhibits the activity of
various liver enzymes. Atrophy of the thymus and spleen occurred in
pups of rat dams fed 5 or 25 mg/kg amitrol (24).
Fate in Humans and Animals
Amitrole is rapidly and completely absorbed into the body through
the gastrointestinal tract when eaten. No metabolites are found in
humans. Amitrole is excreted through the urine. The highest
concentrations in all tissues generally occurs within one hour after
exposure, and concentrations begin to decline after 2 to 6 hours (24).
When radio-labeled amitrole was administered to rats by stomach
tube, 70 to 95.5% of the radioactivity was excreted in the urine during
the first 24-hours. Radioactivity was detected in the rats' feces for 2
to 5 days after dosing. After six days, only 0.28 to 1.36% of the
total dose remained in the rats' bodies, mainly in the liver (24).
ECOLOGICAL EFFECTS
Effects on Birds
Amitrole has a very low acute toxicity to upland game birds (29).
The LD50 for amitrole in mallard ducks is 2,000 mg/kg (4).
Effects on Aquatic Organisms
Amitrole is slightly toxic to various species of freshwater fish
and freshwater invertebrates (29).
Effects on Other Animals (Nontarget species)
Amitrole inhibits the growth of bacteria (7). It is non-toxic to
bees (25).
ENVIRONMENTAL FATE
Breakdown of the Chemical in Soil and Groundwater
Because amitrole does not adsorb strongly to soil particles (Koc =
100 g/ml) and it is readily soluble in water, it has a moderate
potential for groundwater contamination. Its soil half-life is 14 days
(26). Microbial breakdown of amitrole takes 2-3 weeks in warm, moist
soil (28). Some chemical degradation may occur in soils. Loss of
amitrole from soils by volatilization or photodegradation is minor (27).
Amitrole residues were not detected in crops planted into soil 1 to 50
days after treatment with amitrole (29).
Breakdown of the Chemical in Water
In aquatic environments, amitrole is not expected to breakdown by
hydrolysis or photolysis, to volatilize, nor to bioaccumulate in aquatic
organisms. The biodegradation half-life for amitrole in water is about
40 days. Degradation of amitrole in open waters may occur through
oxidation by other chemicals. The main route of removal from waters may
be through adsorption to sediment particles (27). Amitrole may persist
in surface waters for longer than 200 days.
Breakdown of the Chemical in Vegetation
Amitrole is readily absorbed and rapidly translocated in the roots
and leaves of higher plants (29). Plants are able to metabolize
amitrole. This takes 1-4 weeks (7). Microbes break amitrole down to
carbon dioxide (16).
PHYSICAL PROPERTIES AND GUIDELINES
Amitrole is a white, odorless crystalline powder with a bitter
taste (24). Technical amitrole is an off-white powder (25). There is a
slight fire hazard when amitrole is exposed to heat or flame. It may
burn, but does not readily ignite (30).
Amitrole is mildly corrosive to iron, aluminum, copper and copper
alloys. It forms chelates with these metals (22). If strongly heated,
amitrole will emit very toxic fumes (16). The activity of amitrole is
increased by ammonium thiocyanate (6).
Occupational Exposure Limits:
0.2 mg/m3 OSHA TWA
0.2 mg/m3 ACGIH TWA
0.2 mg/m3 NIOSH Recommended TWA
0.2 mg/m3 DFG MAK TWA (total dust) (30)
Physical Properties:
| CAS #: | 61-82-5 |
| Chemical name: | 3-amino-1,2,4-triazole |
| Specific gravity: | 1.138 at 20 degrees C (28) |
| H20 solubility: | 280 gm/liter at 25 degrees C (24) |
| Solubility in other solvents: | Soluble in chloroform, ethanol and methanol. Slightly soluble in acetonitrile, ethyl acetate and methyl chloride. Insoluble in oils, kerosene, ether and acetone and nonpolar solvents (24, 25) |
| Melting point: | 157 - 159 degrees C (318 degrees F) (24) |
| Flashpoint: | aqueous and dry powder forms - nonflammable (2) |
| Vapor pressure: | negligible, 4.4 x 10 to the minus 7th power mm (26) |
| Koc: | 100 g/ml (26) |
| Chemical Class/Use: | triazole herbicide |
BASIC MANUFACTURER
Rhone Poulenc Ag Co.
PO Box 12014
2 T.W. Alexander Dr.
Research Triangle Park, NC 27709
Review by Basic Manufacturer:
Comments solicited: October, 1992
Comments received:
REFERENCES
Meister, R.T. (ed.) 1987. Farm Chemicals Handbook. Willoughby,
OH: Meister Publishing Co.
WSSA Herbicide Handbook Committee. 1983. Herbicide Handbook of
the Weed Science Society of America. 5th Ed. WSSA, Champaign, IL.
Hazardous Materials Advisory Committee. 1974. EPA-SAB-74-001
Herbicide Report Chemical Analysis, Environmental Effects, Agriculture
and Other Applied Uses. EPA: May.
Tucker, Richard. 1970. Handbook of toxicity of pesticides to
wildlife. USDI Fish & Wildlife Service.
Worthing, C.R. (ed.). 1987. The pesticide manual: A world
compendium. 8th Ed. The British Crop Protection Council. Croydon,
England.
Hayes, Wayland, Jr. 1982. Pesticides studied in man. Baltimore,
MD: Williams & Wilkins.
Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides:
chemistry, degradation, and mode of action. 2nd Ed. Vol. 1 & 2. New
York: M. Dekker.
Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals handbook.
Nottingham, England: Royal Society of Chemistry.
Crop Protection Chemicals Reference. 1986. 2nd Ed. New York:
Chemical and Pharmaceutical Pub. Corp.
Shepard, T.H. 1973. Catalog of teratogenic agents. Baltimore,
MD: John Hopkins University Press.
Schardein, James. 1985. Chemically induced birth defects. New
York: Marcel Dekker.
Suspected Carcinogens. A subfile of the registry of toxic effects
of chemical substances. US Dept. of Health, Education and Welfare.
1976.
Department of Transportation. 1984. Emergency Response
Guidebook: Guidebook for hazardous materials incidents. Washington,
DC: U.S. DOT.
Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985. Pesticides and
human health. New York: Springer-Verlag.
Lef'evre, M.J. 1980. First aid manual for chemical accidents.
New York: Van Nostrand Reinhold.
TOXNET. 1985. National library of medicine's toxicology data
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National Institute of Healtyh. U.S. Department of Health and Human
Services. Bethesda, MD: NLM.
Sax, N.I. 1975. Dangerous properties of industrial materials.
4th Ed. New York: Van Nostrand Reinhold Co.
Casarett, L.J. 1980. Casarett & Doull's Toxicology: the basic
science of poisons. 2nd Ed. New York: Macmillan.
Gosselin, R.E. 1984. Clinical toxicology of commercial products.
5th Ed. Baltimore, MD: Williams & Wilkins.
National Fire Protection Association (NFPA). Fire Protection
Guide. Hazardous Materials. 1978.
Morgan, D.P. 1982. Recognition and management of pesticide
poisonings. Iowa Pesticide Hazardous Assessment Project. 1982. Iowa
City, IA.
Windholz, M. (ed.) 1976. The Merck Index: an encyclopedia of
chemicals and drugs. 9th Ed. Rahway, NJ: Merck.
Sunshine, Irving. 1969. Handbook of analytical toxicology.
Cleveland, OH: Chemical Rubber Co.
Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of Pesticide
Toxicology, Vol. 3, Classes of Pesticides. Academic Press, Inc., New
York.
Meister, R. T. (ed.). 1992. Farm Chemicals Handbook '92.
Meister Publishing Company, Willoughby, Ohio.
USDA SCS. 1990 (Nov.). SCS/ARS/CES Pesticide Properties
Database: Version 2.0 (Summary). USDA - Soil Conservation Service,
Syracuse, NY.
Howard, P.H. (ed.). 1989. Handbook of Environmental Fate and
Exposure Data for Organic Chemicals, Vol. III: Pesticides. Lewis
Publishers, Chelsea, MI.
WSSA Herbicide Handbook Committee. 1989. Herbicide Handbook of
the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL.
US EPA. 1984 (March). Amitrole: Pesticide Registration Standard
and Guidance Document. Office of Pesticides and Toxic Substances, US
EPA, Washington, DC.
Occupational Health Services, Inc. 1991 (Sept. 16). MSDS for
Amitrole. OHS Inc., Secaucus, NJ.
U.S. Environmental Protection Agency. 1992 (Oct. 8). Amitrole;
Preliminary determination to terminate Special Review. Federal Register
57(196):46448-55.
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in nature and may no longer be applicable.
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