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.
EXTOXNET primary files maintained and archived at Oregon State
TRADE OR OTHER NAMES
G-30027, Aatrex, Aktikon, Alazine, Atred, Atranex, Atrataf,
Atratol, Azinotox, Crisazina, Farmco Atrazine, Gesaprim, Giffex
4L, Malermais, Primatol, Simazat, Zeaphos (25).
Atrazine has been classified as a Restricted Use Pesticide
(RUP), due to its potential for groundwater contamination (32).
RUPs may be purchased and used only by certified applicators.
Products containing atra-zine must bear the signal word "Caution"
Atrazine is a selective triazine herbicide used to control
broadleaf and grassy weeds in corn, sorghum, sugarcane,
pineapple, Christmas trees and other crops, and in conifer
reforestation plantings. It is also used as a non-selective
herbicide on non-cropped industrial lands and on fallow lands.
It is available as dry flowable, flowable liquid, liquid, water
dispersible granular, and wettable powder formulations (25, 28).
Atrazine is slightly to moderately toxic to humans and other
animals. It can be absorbed into the bloodstream through oral,
dermal and inhalation exposure. Symptoms of poisoning include
abdominal pain, diarrhea and vomiting, eye irritation, irritation
of mucous membranes, and possible skin reactions (14). At very
high doses, rats showed excitation followed by depression, slowed
breathing, incoordination, muscle spasms, and hypothermia (24).
After consuming a large oral dose, rats exhibited muscular
weakness, hypoactivity, breathing difficulty, prostration,
convulsions and death (33).
Atrazine is a mild skin irritant. Rashes associated with
exposure have been reported. Moderate to severe eye irritation
can occur. Exposure to large concentrations of airborne
particles or droplets may cause irritation of the mucous
membranes (24, 30).
The amount of atrazine 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 atrazine in
rats is 672 to 3,000 mg/kg, in mice is 850 to 1,750 mg/kg, in
rabbits is 750 mg/kg, and in hamsters is 1,000 mg/kg. The dermal
LD50 in rabbits is 7,500 mg/kg, and in rats is greater than 3,000
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 one-hour inhalation LC50 in rats is greater than 700 mg/m3.
The 4-hour inhalation LC50 in rats is 5,200 mg/m3 (24, 25, 33,
NIOSH RTECS Online File # 85/8408).
Forty percent of rats receiving oral doses of 20 mg/kg/day
for 6 months died with signs of respiratory distress and
paralysis of the limbs. Morphological and biochemical changes in
the brain, heart, liver, lungs, kidney, ovaries and endocrine
organs were observed (30). Rats fed 5 or 25 mg/kg/day of
atrazine for 6 months exhibited growth retardation. Examination
of these rats revealed no lesions (24). In a 2-year study with
dogs fed 0, 0.75. 7.5 or 75 mg/kg/day, the NOAEL was 0.75 mg/kg.
At 7.5 mg/kg, decreased food intake and increased heart and liver
weights were observed. At 75 mg/kg, there were decreases in food
intake and body weight gain, increased adrenal weight, lowered
blood cell counts, and occasional tremors or stiffness in the
rear limbs (29).
The EPA has established a Lifetime Health Advisory level for
atrazine in drinking water of 3 micrograms per liter (ug/l).
Water containing atrazine at or below this level is acceptable
for drinking every day over the course of one's lifetime, and
does not pose any health risk. Long-term consumption of high
levels of atrazine has caused adverse health effects in animals,
including tremors, changes in organ weights and damage to the
liver and heart (29).
Subcutaneous injection of atrazine of near lethal doses of
800 mg/kg/day on days 3, 6 and 9 of gestation resulted in the
death and resorption of some or all the pups in each litter of
rats. Dosages as high as 200 mg/kg/day by this route did not
affect the number of pups per litter or their weight at weaning.
Dietary levels up to 1,000 ppm (about 50 mg/kg/day) caused no
adverse effects (24).
In mice, atrazine did not cause abnormalities in fetuses
whose dams were given doses of 46.4 mg/kg/day during days 6
through 14 of gestation (24).
The weight of evidence from more than 50 studies reported in
the literature indicates that atrazine is not mutagenic (24). In
tests with mice, atrazine induced dominant lethal mutations and
increased the frequency of chromatid breaks in bone marrow (29).
Atrazine did not cause tumors when mice were given oral
doses of 21.5 mg/kg/day from age 1 to 4 weeks followed by dietary
doses of 82 mg/kg for an additional 17 months. Mammary tumors
were observed in rats after lifetime administration of atrazine
(24). EPA has classified atrazine as a possible human carcinogen
because it has caused cancer in rats receiving high doses over
the course of their lifetimes (29).
Lethal doses in test animals have caused severe damage, in
the form of congestion and/or hemorrhaging, to the lungs,
kidneys, liver, spleen, brain and heart (29).
Fate in Humans and Animals
Ingested atrazine is readily absorbed into the body through
the gastrointestinal tract. When a single dose of 0.53 mg
atrazine was administered to rats by gavage, 20% of the dose was
excreted in the feces within 72 hours. The other 80% was
absorbed across the lining of the gastrointestinal tract into the
bloodstream. After 72 hours, 65% was eliminated in the urine and
15% was retained in body tissues, mainly in the liver, kidneys
and lungs (24).
Effects on Birds
Atrazine is only slightly toxic to birds. The LD50 in
mallard ducks is greater than 2,000 mg/kg. The NOELs for
bobwhite quail and ring-necked pheasants fed atrazine were both
greater than 5,000 ppm.
Effects on Aquatic Organisms
Atrazine is only slightly toxic to fish and other pond or
stream life. In whitefish, atrazine accumulates in the brain,
gall bladder, liver and gut (Arch. Hydrobiol. Suppl.
59(2-3):252-87. 1981). Fish may bioaccumulate atrazine to levels
of 11 times the concentration in surrounding water. This is a
low level of bioaccumulation. Atrazine is easily broken down.
Effects on Other Animals (Nontarget species)
Atrazine is not toxic to bees (25).
Breakdown of the Chemical in Soil and Groundwater
Atrazine is moderately to highly mobile in soils, especially
where soils have low clay or organic matter content. Because it
does not absorb strongly to soil particles (Koc = 100 g/ml) and
it has a lengthy soil half-life (60 to 100+ days), it is expected
to have a high potential for groundwater contamination, even
though it is only moderately soluble in water (33 ug/ml) (26,
Atrazine is not normally found below the first foot of soil,
even after years of continuous use.
Chemical hydrolysis, followed by degradation by soil
microorganisms probably account for most of the breakdown of
atrazine in soil. Hydrolysis is rapid in acidic or basic
environments, but is slower at neutral pHs. Addition of humic
material increased the rate of hydrolysis. Atrazine is also
subject to photo-decomposition and volatilization when high
temperatures and prolonged sunlight occur after precipitation,
but these effects are small under normal field conditions.
Atrazine can persist for longer than one year under conditions
which are not conducive to chemical or biological activity, such
as dry or cold climates (27, 28). Atrazine usually lasts about 4
months at the surface and 2 months at deeper sites
Breakdown of the Chemical in Water
Atrazine is not very water soluble. Chemical hydrolysis,
followed by biodegradation, may be the most important route of
disappearance from aquatic environments. Hydrolysis is rapid
under acidic or basic conditions, but is slower at neutral pHs.
Addition of humic material increased the rate of hydrolysis.
Atrazine is not expected to strongly adsorb to sediments.
Bioconcentration and volatilization of atrazine are not
environmentally important (27).
Trace amounts of atrazine have been found in drinking water
samples from Louisiana and Iowa and in groundwater samples from
Pennsylvania, Iowa, Nebraska, Wisconsin and Maryland (27, 29, NRC
Drinking Water and Health 1977). Atrazine has been detected in
each of 146 water samples collected at 8 locations from the
Mississippi, Ohio and Missouri Rivers and their tributaries. For
several weeks, 27% of these samples contained atrazine at
concentrations above the EPA's maximum concentration level (MCL)
for atrazine of 3 ppb. The MCL is the maximum permissible level
of a contaminant in water delivered to any user of a public water
system (30). A five year survey of drinking water wells
detected trace amounts of atrazine in an estimated 1.7% of
community water systems and 0.7% of rural domestic wells
nationwide. Levels detected in rural domestic wells sometimes
exceeded the MCL (31).
Breakdown of the Chemical in Vegetation
Atrazine is absorbed by plants mainly through the roots, but
also through the foliage. Once absorbed, atrazine is
translocated upward and accumulates in the growing tips and the
new leaves of the plant. In susceptible plant species, atrazine
inhibits photosynthesis. In tolerant plants, it is metabolized
Most crops can be planted one year after application of
atrazine. Atrazine blocks the plant's ability to carry on
photosynthesis (Hartley. Agrochem Hdbk 1983). Atrazine
increases the uptake of arsenic by treated plants (such as
PHYSICAL PROPERTIES AND GUIDELINES
Atrazine is a white, crystalline solid (25). It is stable
under normal temperatures and pressures, but may burn if exposed
to heat or flame. Excessive heating of atrazine may cause the
production of toxic and corrosive fumes of chlorides and of toxic
fumes of nitrogen. Atrazine is stable in neutral, slightly
acidic, or basic material, but it is hydrolyzed by alkali or
mineral acids at higher temperatures (24, 33).
Occupational Exposure Limits:
5 mg/m3 OSHA TWA
5 mg/m3 ACGIH TWA
5 mg/m3 NIOSH recommended TWA
2 mg/m3 DFG MAK TWA (total dust)
CAS #: 1912-24-9
Specific gravity: 1.187 g/cubic cm (7, 33)
H20 solubility: 33 ppm at 25 degrees C (25, 26). 0.007% at 25
degrees C (33)
Solubility in other solvents:
Solvent T (degrees C) Solubility
_______ _____________ ___________
Chloroform 25 52,000 ppm (22)
Diethyl ether 27 1.2% (2)
Dimethyl sulfoxide 27 18.3% (2)
Ether 25 12,000 ppm (22)
Ethyl acetate 27 2.8% (2)
Methanol 25 18,000 ppm (22)
N-pentane 27 360 ppm (2)
Melting point: 173-175 degrees C (25).
Vapor pressure: 3.0 x 10 to the minus 7th power mm Hg at 20
degrees C (2, 28). Atrazine is slightly volatile.
Koc: 100 g/ml (26): 0.6 on sandy loam; 1.8 on gravelly sand; 5.6
on silty clay; 7.9 on clay loam; 8.7 on sandy loam, 11.6 on silty
clay loam; and greater than 21 on peat (29)
Chemical Class/Use: triazine herbicide
PO Box 18300
Greensboro, NC 27419-8300
Review by Basic Manufacturer:
Comments solicited: January, 1992
Comments received: April, 1992
(1) Meister, R.T. (ed.) 1987. Farm Chemicals Handbook.
Willoughby, OH: Meister Publishing Co.
(2) WSSA Herbicide Handbook Committee. 1983. Herbicide
Handbook of the Weed Science Society of America. 5th Ed. WSSA,
(3) EPA-SAB-74-001 Herbicide Report Chemical Analysis,
Environmental Effects, Agriculture and Other Applied Uses.
Hazardous Materials Advisory Committee. EPA. May 1974.
(4) Tucker, Richard. 1970. Handbook of toxicity of pesticides
to wildlife. USDI Fish & Wildlife Service.
(5) Worthing, C.R. (ed.). 1987. The pesticide manual: A world
compendium. 8th Ed. The British Crop Protection Council.
(6) Hayes, Wayland, Jr. 1982. Pesticides studied in man.
Baltimore, MD: Williams & Wilkins.
(7) Kearney, P.C. & D.D. Kaufman (eds.). 1975. Herbicides:
chemistry, degradation, and mode of action. 2nd Ed. Vol. 1 & 2.
New York: M. Dekker.
(8) Hartley, D. and H. Kidd, (eds.) 1983. The agrochemicals
handbook. Nottingham, England: Royal Society of Chemistry.
(9) Crop Protection Chemicals Reference. 1986. 2nd Ed. New
York: Chemical and Pharmaceutical Pub. Corp.
(10) Shepard, T.H. 1973. Catalog of teratogenic agents.
Baltimore, MD: John Hopkins University Press.
(11) Schardein, James. 1985. Chemically induced birth defects.
New York: Marcel Dekker.
(12) U.S. Department of Health, Education and Welfare. 1976.
Suspected Carcinogens. A subfile of the registry of toxic
effects of chemical substances. Washington, DC: EPA.
(13) Department of Transportation. 1984. Emergency Response
Guidebook: Guidebook for hazardous materials incidents.
Washington, DC: U.S. DOT.
(14) Hallenbeck, W.H. & K.M. Cunningham-Burns. 1985.
Pesticides and human health. New York: Springer-Verlag.
(15) Lef'evre, M.J. 1980. First aid manual for chemical
accidents. New York: Van Nostrand Reinhold.
(16) TOXNET. 1985. National library of medicine's toxicology
data network. Hazardous Substances Databank. Public Health
Service. National Institute of Health. U.S. Department of
Health and Human Services. Bethesda, MD: NLM.
(17) Sax, N.I. 1975. Dangerous properties of industrial
materials. 4th Ed. New York: Van Nostrand Reinhold Co.
(18) Casarett, L.J. 1980. Casarett & Doull's Toxicology: the
basic science of poisons. 2nd Ed. New York: Macmillan.
(19) Gosselin, R.E. 1984. Clinical toxicology of commercial
products. 5th Ed. Baltimore, MD: Williams & Wilkins.
(20) National Fire Protection Association (NFPA). 1978. Fire
Protection Guide. Hazardous Materials.
(21) Morgan, D.P. 1982. Recognition and management of
pesticide poisonings. Iowa Pesticide Hazardous Assessment
Project. 1982. Iowa City, IA.
(22) Windholz, M. (ed.) 1976. The Merck Index: an
encyclopedia of chemicals and drugs. 9th Ed. Rahway, NJ:
(23) Sunshine, Irving. 1969. Handbook of analytical
toxicology. Cleveland, OH: Chemical Rubber Co.
(24) Hayes, W.J. and E.R. Laws (ed.). 1990. Handbook of
Pesticide Toxicology, Vol. 3, Classes of Pesticides. Academic
Press, Inc., New York.
(25) Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92.
Meister Publishing Company, Willoughby, Ohio.
(26) USDA SCS. 1990 (Nov). SCS/ARS/CES Pesticide Properties
Database: Version 2.0 (Summary). USDA - Soil Conservation
Service, Syracuse, NY.
(27) Howard, P.H. (ed.). 1989. Handbook of Environmental Fate
and Exposure Data for Organic Chemicals, Vol. III: Pesticides.
Lewis Publishers, Chelsea, Michigan.
(28) WSSA Herbicide Handbook Committee. Herbicide Handbook of
the Weed Science Society of America, 6th Ed. WSSA, Champaign, IL.
(29) US EPA. 1988 (August). Atrazine: Health Advisory. Office
of Drinking Water, US EPA, Washington, DC.
(30) USGS. 1991 (Nov. 20). Spring sampling finds herbicides
throughout Mississippi River and tributaries. U.S. Geologic
Survey, Dept. of the Interior, Reston, Virginia.
(31) US EPA. 1990 (Fall). National Pesticide Survey: Atrazine.
Office of Water and Office of Pesticides and Toxic Substances, US
EPA, Washington, DC.
(32) Food Chemical News, Inc. 1990 (Jan. 31). Atrazine use
restricted; other label changes imposed by EPA. Pesticide and
Toxic Chemical News. Washington, DC.
(33) OHS MSDS for Atrazine. 1991 (March 20).
This PIP is part of the EXTOXNET Pesticide Information
Notebook. For more information, contact the Pesticide Management
Education Program, Cornell University, 5123 Comstock Hall,
Ithaca, N.Y. 14853.
DISCLAIMER: The information in this profile does not in any way
replace or supersede the information on the pesticide product
label/ing or other regulatory requirements. Please refer to the
pesticide product label/ing.