PMEP Home Page --> Pesticide Active Ingredient Information --> EXTOXNET: The Extension Toxicology Network --> 2,4-D to Captan --> Atrazine

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.


Publication Date: 9/93


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" (25).


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 ab-sorbed 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 mg/kg.

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).

Reproductive Effects

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).

Teratogenic Effects

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).

Mutagenic Effects

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).

Carcinogenic Effects

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).

Organ Toxicity

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, 29).

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 (Agro-Ecosystems 7(3):225238.1981).

Breakdown of the Chemical in Water

Atrazine is not very water soluble. Chemical hydrolysis, followed by bio-degradation, 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 (28).

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 grapes) (7).


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)

Physical Properties

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:
SolventT (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


Agricultural Division
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, Champaign, IL.
  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. Croydon, England.
  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: Merck.
  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. 1989.
  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).