Toxicological Profile for Atrazine

Chemical Formulation & Use Profile

Atrazine (6-chloro-N-ethyl-N’-isopropyl-1,3,5-triazine-2,4-diamine) is a triazine selective control herbicide, used as a pre- and post-emergent on broadleaf and grassy weeds in fruit and vegetable crops and in lumber reforestation plantings. It effectively prevents photosynthesis in plants, thereby stopping growth and eventually causing death. It is one of the two most widely used pesticides in the United States. Commercially, atrazine is available in liquid, granular and powder formulations. It is similar in structure and mode of action to other triazines such as hexazinone and simazine.

Human Health Risk Summary

Acute Effects: If ingested, atrazine is likely to cause abdominal pain, diarrhea and vomiting. If inhaled via airborne particulates, respiratory tract injury and increased risk of asthma may occur. Atrazine is also toxic through dermal absorption and may cause skin reactions, such as rashes and allergic eczema. , The EPA has identified congestion of the heart, lungs and kidneys; low blood pressure; muscle spasms; weight loss; and, damage to adrenal glands as acute exposure toxicity endpoints. Following acute, high oral dosing, test animals exhibited loss of muscle function, convulsions and behavioral disturbances.

Chronic Effects: Carcinogenicity: Animal studies have linked atrazine to mammary tumors, leukemia and lymphoma. , In farming community epidemiological studies, atrazine exposure has correlated with higher incidences of ovarian, breast, testicular, stomach, brain and non-Hodgkin’s lymphoma forms of cancer.
Reproductive & Developmental Toxicity: Both animal and human studies have indicated that atrazine is likely to be both a reproductive and developmental toxicant. Animal studies have shown that atrazine can cause premature birth; reduced birth weight; delayed bone development and sexual maturation; and growth retardation. Epidemiological studies in humans have shown that exposure to atrazine from drinking water contamination is associated with premature birth; low birth weight; physical birth defects; and reduced semen quality.
Organ Toxicity: Atrazine has been shown to cause liver, kidney and heart damage in animals, and is therefore likely to cause the same in humans.
Mutagenicity: Several animal studies have linked atrazine to genetic damage, including, chromosome breaks and rearrangement; and, disrupted DNA repair and synthesis.
Immunotoxicity: Several studies in both animals and humans have indicated a direct association between exposure to atrazine and adverse effects on the immune system, including suppression of antibodies and autoimmune reactions.

Ecological Hazard Summary

Environmental Fate: A major concern about atrazine is that it is highly persistent and mobile in soil environments, and extremely persistent in aquatic systems. Depending on soil conditions, atrazine can persist from several days to over a year. In water systems, it can persist for weeks to years depending on conditions such as temperature, pH, movement, etc. Atrazine does not bind to soil particles well, and is therefore likely to migrate into aquatic systems. Because of its widespread use, long persistence, and high mobility, atrazine is the most commonly detected pesticides in surface and ground water, and is often found in drinking water systems as well.
Risk to Non-Target Flora & Fauna: Atrazine can travel away from its use site via airborne dust particles, over-spray, and translocation by soil and/or water movement, and can consequently impact plants and animals in the natural environment. At very low concentrations atrazine can disrupt entire ecosystems by inhibiting photosynthesis and killing plants that offer protection and nutrients to animals. Aside from general ecosystem disturbance, atrazine can be toxic to most aquatic and amphibious animals. Because atrazine is a potent disruptor of hormones, exposure has shown to have reproductive and developmental toxicity to numerous animal species, including fish, frogs, salamanders, and alligators. Some of these toxicity endpoints include: reduced reproductive success, altered gender ratios, birth defects and behavioral disruptions.


Atrazine and its associated compounds are of particular concern to human health and the environment, due to: 1) evidence of carcinogenicity, reproductive/developmental effects, organ toxicity, immune system effects, and genotoxicity to humans; 2) likely adverse effects to non-target plants and animals, specifically reproductive and developmental toxicity to aquatic and amphibious species; and 3) the extensive contamination of surface, ground and drinking water systems.

Common Commercial Names

Aatrex, Purge II, Azinotox 500, Gesaprim, Alazine, Atred, Atranex, Atrataf


U.S. EPA. “Atrazine: HED’s revised preliminary human health risk assessment for the reregistration eligibility decision.” Washington, D.C. 2001.

Ibid, pg. 5.

Stevens, J.T. and Sumner, D.D. Herbicides. In Handbook of Pesticide Toxicology. Hayes, W.J., Jr. and Laws, E.R., Jr., Eds. Academic Press, New York, 1991.

Ellenhorn, M.J., S. Schonwald, G. Ordog, J. Wasserberger. Ellenhorn’s Medical Toxicology: Diagnosis and Treatment of Human Poisoning. 2nd ed. Baltimore, MD: Williams and Wilkins. 1997.

Ibid ref. #3.

Ibid ref. #4.

U.S. EPA. “Technical Fact Sheet on Atrazine”.

U.S. National Library of Medicine. Hazardous Substances Data Bank. Bethesda, MD, 1995.

Podda, M.V. et al. “Effect of atrazine administration on spontaneous and evoked cerebellar activity in the rat”. Pharmacological Research. 36(3):199-202. 1997.

OEHHA/CAEPA. “Public Health Goal for Atrazine in Drinking Water”. Feb. 1999.

Ueda, M. et al. “Possible enhancing effects of atrazine on growth of 7,12-dimethylbenz(a) anthracene-induced mammory tumors in ovariectomized Sprague-Dawley rats”. Cancer Science. 96(1):19-25. 2005.

Donna, A. et al. “Triazine Herbicide Exposure and Ovarian Epithelial Neoplasms”. Scandinavian Journal of Work and Environmental Health. 15:47-53. 1989.

Kettles, M.A. et al. “Triazine Herbicide Exposure and Breast Cancer Incidence: an ecological study of Kentucky counties”. Environmental Health Perspectives. 105: 1222-1227. 1997.

Mills, P.K. “Correlation Analysis of Pesticide use data and Cancer Incidence Rates in California Counties”. Archives of Environmental Health. 53:410-413. 1998.

Van Leeuwen, J.A. et al. “Associations Between Stomach Cancer Incidence and Drinking Water Contamination with Atrazine and Nitrate in Ontario (Canada) Agroecosystems.” International Journal of the Epidemiological Association. 28:836-840. 1999.

Weisenburger, D.D. “Environmental epidemiology of non-Hodgkin’s lymphoma in Eastern Nebraska.” American Journal of Industrial Medicine. 18:303-305. 1990.

Ibid ref. #10, pg. 11-12.

Ibid ref. #1, pg. 28-31.

Rayner, J.L., Enoch, R.R., and Fenton, S.E. “Adverse effects of prenatal exposure to atrazine during a critical period of mammary gland growth”. Toxicological Sciences. 87(1):255-66. 2005.

Savitz, D.A. et al. “Male pregnancy exposure and pregnancy outcome.” American Journal of Epidemiology. 146:1025-1036. 1997.

Munger, R. et al. “Birth defects and pesticide-contaminated water supplies in Iowa.” American Journal of Epidemiology. 136:959. 1992.

Swan, S.H. “Semen quality in fertile US men in relation to geographical area and pesticide exposure”. International Journal of Andrology. 29(1):62-8. 2006.

Munger, R. et al. “Intrauterine growth retardation in Iowa communities with herbicide-contaminated drinking water supplies.” Environmental Health Perspectives. 105:308-314. 1997.

ATSDR. “Toxicological Profile for Atrazine.” pg. 5. 2003.

Pino, A., Maura, A. and Grillo, P. “DNA damage in stomach, kidney, liver and lungs of rats treated with atrazine.” Mutational Research. 209:145-147. 1988.

Tennant, A.H., Peng, B., Kligerman, A.D. “Genotoxicity studies of three triazine herbicides: in vivo studies using the alkaline single cell gel (SCG) assay.” Mutational Research. 493:1-10. 2001.

Roloff, B.D., Belluck, D.A., Meisner, L.F. “Cytogenetic studies of herbicide interactions in vitro and in vivo using atrazine and linuron.” Archives of Environmental Contamination and Toxicology. 22:267-271. 1992.

Rowe, A.M. et al. “Immunomodulatory effects of maternal atrazine exposure on male Balb/c mice.” Toxicology and Applied Pharmacology. Jan. 2006.

Hurbankova, M. et al. “Some bronchoalveolar lavage and blood parameters in response to intratracheal instillation of atrazine in rats.” Biologia (Bratislava). 51(6):729-734. 1996.

National Toxicology Program. “NTP report on the immunotoxicity of atrazine in female B6C3F1 mice.” 1994.

Hooghe, R.J., et al. “Effects of selected herbicides on cytokine production in vitro.” Life Sciences. 66:2519-2525. 2000.

Filipov, N.M., et al. “Immunotoxic effects of short-term atrazine exposure in young male C57BL/6 mice.” Toxicological Sciences. Aug:86(2):324-32. Epub May 11, 2005.

Howard, P.H., (ed.). Handbook of Environmental Fate and Exposure Data for Organic Chemicals: Pesticides. Lewis Publishers, Boca Raton, FL. 1989.

U.S. EPA. “Reregistration Eligibility Chapter for Atrazine: Environmental Fate and Effects Chapter.” April, 2002.

Ibid ref. #1, pg. 82.

Ibid ref. #10, pg. 4-6.

Ibid ref. #34, pg. 80.

Kettle, W.D. et al. “Diet and reproductive success of bluegill recovered from experimental ponds treated with atrazine.” Bulletin of Environmental Contamination and Toxicology. 38:47-52. 1987.

Hayes, T., et al. “Atrazine-induced hermaphroditism at 0.1 ppb in American leopard frogs: laboratory and field evidence.” Environmental Health Perspectives. 111(4):568-75. 2003.

Crain, D.A. et al. “Alterations in steroidogenesis in alligators exposed naturally and experimentally to environmental contaminants.” Environmental Health Perspectives. 105:528-533. 1997.


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