|Jmol-3D images||Image 1|
|Molar mass||215.68 g mol−1|
|Melting point||175 °C (347 °F; 448 K)|
|Boiling point||200 °C (392 °F; 473 K)|
|Solubility in water||7 mg/100 mL|
|Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)|
Atrazine is a herbicide of the triazine class. Atrazine is used to prevent pre and post-emergence broadleaf weeds in crops such as maize (corn) and sugarcane and on turf, such as golf courses and residential lawns.
As of 2001, Atrazine was the most commonly detected pesticide contaminating drinking water in the United States.:42 Studies suggest it is an endocrine disruptor, an agent that may alter the natural hormonal system in animals. In 2006 the U.S. Environmental Protection Agency (EPA) stated that "the risks associated with the pesticide residues pose a reasonable certainty of no harm", and in 2007 the EPA said that atrazine does not adversely affect amphibian sexual development and that no additional testing was warranted. The EPA opened a new review in 2009 that concluded that "the agency’s scientific bases for its regulation of atrazine are robust and ensure prevention of exposure levels that could lead to reproductive effects in humans."
Atrazine is a pesticide/herbicide that is used to stop pre and post-emergence broadleaf and grassy weeds in crops such as sorghum, maize, sugarcane, lupins, pine and eucalypt plantations, and triazine tolerant (TT) canola.
In the United States as of 2014, atrazine was the second most widely used herbicide after glyphosate, with 76 million pounds of it applied each year. Atrazine continues to be one of the most widely used herbicides in Australian agriculture. Its use is banned in the European Union.
Its effect on yields has been estimated from 6% to 1%, with 3–4% being the conclusion of one economics review. In another study looking at combined data from 236 university corn field trials from 1986–2005, atrazine treatments showed an average of 5.7 bushels more per acre than alternative herbicide treatments.
Chemistry and biochemistry
Atrazine is prepared from cyanuric chloride, which is treated sequentially with ethylamine and isopropyl amine. Like other triazine herbicides, atrazine functions by binding to the plastoquinone-binding protein in photosystem II, which animals lack. Plant death results from starvation and oxidative damage caused by breakdown in the electron transport process. Oxidative damage is accelerated at high light intensity.
Atrazine remains in soil for a matter of months and can migrate from soil to groundwater; once in groundwater, it degrades slowly. It has been detected in groundwater at high levels in some regions of the U.S. where it is used on some crops and turf. The US Environmental Protection Agency expresses concern regarding contamination of surface waters (lakes, rivers, and streams).
- Hydrolysis of the C-Cl bond, followed by the ethyl and isopropyl groups, catalyzed by the hydrolase enzymes called AtzA, AtzB, and AtzC. The end product of this process is cyanuric acid, itself unstable with respect to ammonia and carbon dioxide. The best characterized organisms that use this pathway are of Pseudomonas sp. strain ADP.
- Dealkylation of the amino groups to give 2-chloro-4-hydroxy-6-amino-1,3,5-triazine, the degradation of which is unknown. This path also occurs in Pseudomonas species as well as a number of bacteria.
Rates of biodegradation are affected by atrazine's low solubility, thus surfactants may increase the degradation rate. Though the two alkyl moieties readily support growth of certain microorganisms, the atrazine ring is a poor energy source due to the oxidized state of ring carbon. In fact, the most common pathway for atrazine degradation involves the intermediate, cyanuric acid, in which carbon is fully oxidized, thus the ring is primarily a nitrogen source for aerobic microorganisms. Atrazine may be catabolized as a carbon and nitrogen source in reducing environments, and some aerobic atrazine degraders have been shown to use the compound for growth under anoxia in the presence of nitrate as an electron acceptor, a process referred to as a denitrification. When atrazine is used as a nitrogen source for bacterial growth, degradation may be regulated by the presence of alternative sources of nitrogen. In pure cultures of atrazine-degrading bacteria, as well as active soil communitites, atrazine ring nitrogen, but not carbon are assimilated into microbial biomass. Low concentrations of glucose can decrease the bioavailability, whereas higher concentrations promote the catabolism of atrazine.
The genes for enzymes AtzA-C have been found to be highly conserved in atrazine-degrading organisms worldwide. In Pseudomonas sp. ADP, the Atz genes are located noncontiguously on a plasmid with the genes for mercury catabolism. AtzA-C genes have also been found in a Gram-positive bacterium, but are chromosomally located. The insertion elements flanking each gene suggest that they are involved in the assembly of this specialized catabolic pathway. Two options exist for degradation of atrazine using microbes, bioaugmentation or biostimulation. Recent research suggests that microbial adaptation to atrazine has occurred in some fields where the herbicide is used repetitively, resulting in a decrease in herbicidal effectiveness. Like the herbicides trifluralin and alachlor, atrazine is susceptible to rapid transformation in the presence of reduced iron-bearing soil clays, such as ferruginous smectites. In natural environments, some iron-bearing minerals are reduced by specific bacteria in the absence of oxygen, thus the abiotic transformation of herbicides by reduced minerals is viewed as "microbially induced".
Health and environmental effects
According to Extension Toxicology Network in the U.S., "The oral median Lethal Dose or LD50 for atrazine is 3090 mg/kg in rats, 1750 mg/kg in mice, 750 mg/kg in rabbits, and 1000 mg/kg in hamsters. The dermal LD50 in rabbits is 7500 mg/kg and greater than 3000 mg/kg in rats. The 1-hour inhalation LC50 is greater than 0.7 mg/L in rats. The 4-hour inhalation LC50 is 5.2 mg/L in rats." The maximum contaminant level is 0.003 mg/L and the reference dose is 0.035 mg/kg/day.
Atrazine contamination of surface water (lakes, rivers, and streams) is a concern to the U.S. Environmental Protection Agency (EPA). As of 2001, Atrazine was the most commonly detected pesticide contaminating drinking water in the United States and the EPA has stated that "Drinking water from a contaminated groundwater or surface water source can be a significant medium of exposure for children.":2
In animals, including humans, the endocrine system is the primary target of atrazine. The U.S. EPA says that "studies thus far suggest that atrazine is an endocrine disruptor". According to a US EPA chemical summary, implications of possible endocrine disruption for children’s health are related to effects during pregnancy and during sexual development, though few studies are available. Increased risks for preterm delivery and intrauterine growth retardation have been associated with atrazine exposure. Atrazine exposure has been shown to result in delays or changes in pubertal development in experimental animal studies.
In August 2009, the risks of atrazine were discussed in a page 1 article in the New York Times as a potential cause of birth defects, low birth weights and menstrual problems when consumed at concentrations below federal standards. A Natural Resources Defense Council's Report on Atrazine suggested that the EPA is ignoring atrazine contamination in surface and drinking water in the central United States.
Research results from the U.S. National Cancer Institute's Agricultural Health Study published in 2011 concluded that "there was no consistent evidence of an association between atrazine use and any cancer site." The study tracked 57,310 licensed pesticide applicators over 13 years. EPA also determined in 2000 "that atrazine is not likely to cause cancer in humans."
A 2012 epidemiological study showed that women who lived in counties in Texas with the highest levels of atrazine being used on agricultural crops were 80 times more likely to give birth to infants with choanal atresia or stenosis compared to women who lived in the counties with the lowest levels. 
In 2006 the U.S. Environmental Protection Agency (EPA) stated that "the risks associated with the pesticide residues pose a reasonable certainty of no harm", and in 2007 the EPA said that atrazine does not adversely affect amphibian sexual development and that no additional testing was warranted. The EPA opened a new review in 2009 that concluded that "the agency’s scientific bases for its regulation of atrazine are robust and ensure prevention of exposure levels that could lead to reproductive effects in humans."
Effect on amphibians
Atrazine is a suspected teratogen, causing demasculinization in male northern leopard frogs even at low concentrations, and an estrogen disruptor. A 2002 study by Tyrone Hayes, of the University of California, Berkeley, found that exposure to atrazine caused male tadpoles to turn into hermaphrodites – frogs with both male and female sexual characteristics. But a 2005 study, requested by the EPA and funded by Syngenta, one of the companies that produce atrazine, was unable to reproduce these results. Hayes noted that all of the studies that failed to conclude that atrazine caused hermaphroditism were plagued by poor experimental controls and were funded by Syngenta suggesting conflict of interest.
The U.S. Environmental Protection Agency (EPA) and its independent Scientific Advisory Panel (SAP) examined all available studies on this topic and concluded that "atrazine does not adversely affect amphibian gonadal development based on a review of laboratory and field studies." The EPA and its SAP made recommendations concerning proper study design needed for further investigation into this issue. As required by the EPA, Syngenta conducted two experiments under Good Laboratory Practices (GLP) and inspection by the EPA and German regulatory authorities. The paper concluded "These studies demonstrate that long-term exposure of larval X. laevis to atrazine at concentrations ranging from 0.01 to 100 microg/l does not affect growth, larval development, or sexual differentiation." A report written in Environmental Science and Technology (May 15, 2008) cites the independent work of researchers in Japan, who were unable to replicate Hayes' work. "The scientists found no hermaphrodite frogs; no increase in aromatase as measured by aromatase mRNA induction; and no increase in vitellogenin, another marker of feminization."
A study published in 2007 examined the relative importance of environmentally relevant concentrations of atrazine on trematode cercariae versus tadpole defense against infection. The principal ﬁnding of the present study was that susceptibility of wood frog tadpoles to infection by E. trivolvis is increased only when hosts are exposed to an atrazine concentration of 30 ng/L and not to 3 ng/L.
A 2008 study reported that tadpoles developed deformed hearts and impaired kidneys and digestive systems when exposed to atrazine in their early stages of life. Tissue malformation may have been induced by ectopic programmed cell death, although a mechanism was not identified.
In 2010, the Australian Pesticides and Veterinary Medicines Authority (APVMA), found the chemical safe to use:
The conclusion of the APVMA at that time, based on advice from DEWHA, was that atrazine is unlikely to have an adverse impact on frogs at existing levels of exposure. This advice was consistent with findings by the US EPA in 2007 (see below) that atrazine does not adversely affect amphibian gonadal development.
Furthermore, the APVMA responded to Hayes' 2010 published paper, by stating that his findings "do not provide sufficient evidence to justify a reconsideration of current regulations which are based on a very extensive dataset."
Effects on fish and insects
A 2010 study conducted by scientists from the U.S. Geological Survey observed substantial adverse reproductive effects on fish from atrazine exposure at a threshold concentration of 0.5 μg/L, which is below the threshold levels previously defined for fish toxicity and within the surface water concentrations found in agricultural areas; the authors concluded: "The effects on egg production and spawning in fathead minnow suggest the reproductive risks of atrazine exposure to feral fish populations in high use, agricultural areas may be under estimated by current evaluations."
A recent study demonstrated that exposure of beetles to environmentally relevant doses of Atrazine during development as larvae confounded the sexual selection process so that females selected less fit mates, and speculated that it may have played a role in the declines in the federally endangered American Burying Beetle.
Class action lawsuit
In 2012 Syngenta corporation, manufacturer of atrazine, was the defendant in a class action lawsuit concerning the levels of atrazine in human water supplies. Syngenta agreed to pay $105 million to reimburse more than a thousand water systems for "the cost of filtering atrazine from drinking water", although the company denied all wrongdoing. 
Personal attacks on scientists
In 2014, New Yorker writer Rachel Aviv reported that Syngenta might have been orchestrating an attack on the "scientific credibility" of not just Tyrone Hayes, the lead critic of atrazine use, but other scientists as well whose studies have shown atrazine to have negative effects on the environment and/or human and animal health.
Paul Winchester, a professor of pediatrics at the Indiana University School of Medicine, wrote a paper that was published in Acta Paediatrica reviewing national records for thirty million births, found that children conceived between April and July, when the concentration of atrazine, mixed with other pesticides, in water is highest, were more likely to have genital birth defects. Professor Winchester subsequently received a subpoena requesting that he turn over to Syngenta every e-mail he had written about atrazine in the past decade.
Deborah Cory-Slechta, a professor at the University of Rochester Medical Center, and a former member of the EPA’s science advisory board, said that she, too, had felt that Syngenta was trying to "undermine" her work, after she published a study showing that the herbicide paraquat may contribute to diseases of the nervous system. "The folks from Syngenta used to follow me to my talks and tell me I wasn’t using ‘human-relevant doses'," Cory-Slechta said. "They would go up to my students and try to intimidate them. There was this sustained campaign to make it look like my science wasn’t legitimate.”
In one of the e-mails obtained by class-action suit plaintiffs, the company’s communications consultants had written in 2005 that they "wanted to obtain Hayes’s calendar of speaking engagements," so that Syngenta could “start reaching out to the potential audiences with the Error vs. Truth Sheet,” which would provide “irrefutable evidence of his polluted messages.” Syngenta subsequently stated that many of the documents unsealed in the lawsuits refer to "ideas that were never implemented."
In response to the allegations, Ann Bryan, Syngenta's senior manager for external communications, stated to the New Yorker writer that "atrazine does not and, in fact, cannot cause adverse health effects at any level that people would ever be exposed to in the real-world environment." She added she was "troubled by a suggestion that Syngenta have ever tried to discredit anyone. The company's focus has always been on communicating the science and setting the record straight.”
- Pesticides in the United States – Atrazine
- Endocrine disruptor
- Pesticide Properties Database record for Atrazine
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- Pesticide Information Profile: Atrazine, Extension Toxicology Network (Cooperative Extension Offices of Cornell University, Oregon State University, the University of Idaho, and the University of California at Davis and the Institute for Environmental Toxicology, Michigan State University), June 1996.
- USGS Pesticide Use Maps
- "How the EPA is Ignoring Atrazine Contamination in Surface and Drinking Water in the Central United States". Natural Resources Defense Council (The New York Times). August 2009.
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- Study: Exposure to herbicide may increase risk of rare disorder
- Jennifer Lee (2003-06-19). "Popular Pesticide Faulted for Frogs' Sexual Abnormalities". The New York Times.
- Tyrone Hayes, Kelly Haston, Mable Tsui, Anhthu Hoang, Cathryn Haeffele, and Aaron Vonk (2003). "Atrazine-Induced Hermaphroditism at 0.1 ppb in American Leopard Frogs" (Free full text). Environmental Health Perspectives 111 (4): 568. doi:10.1289/ehp.5932. PMC 1241446.
- Mizota, K.; Ueda, H. (2006). "Endocrine Disrupting Chemical Atrazine Causes Degranulation through Gq/11 Protein-Coupled Neurosteroid Receptor in Mast Cells". Toxicological Sciences 90 (2): 362–8. doi:10.1093/toxsci/kfj087. PMID 16381660.
- Briggs, Helen. (April 15, 2002), Pesticide 'causes frogs to change sex'. BBC News. Retrieved on 2007-10-16.
- Jooste et al.; Du Preez, LH; Carr, JA; Giesy, JP; Gross, TS; Kendall, RJ; Smith, EE; Van Der Kraak, GL; Solomon, KR (2005). "Gonadal Development of Larval Male Xenopus laevis Exposed to Atrazine in Outdoor Microcosms". Environ. Sci. Technol. 39 (14): 5255–5261. doi:10.1021/es048134q. PMID 16082954.
- Hayes, TB (2004). "There Is No Denying This: Defusing the Confusion about Atrazine". BioScience 54 (112): 1138–1149. doi:10.1641/0006-3568(2004)054[1138:TINDTD]2.0.CO;2. ISSN 0006-3568.
- Kloas, W; Lutz, I; Springer, T; Krueger, H; Wolf, J; Holden, L; Hosmer, A (2009). "Does atrazine influence larval development and sexual differentiation in Xenopus laevis?". Toxicological sciences : an official journal of the Society of Toxicology 107 (2): 376–84. doi:10.1093/toxsci/kfn232. PMC 2639758. PMID 19008211.
- Renner, Rebecca (May 2008). "Atrazine Effects in Xenopus Aren't Reproducible (Perspective)". Environmental Science & Technology 42 (10): 3491–3493. doi:10.1021/es087113j.
- Koprivnikar, Janet; Forbes, Mark R.; Baker, Robert L. (2007). "Contaminant Effects on Host–Parasite Interactions: Atrazine, Frogs, and Trematodes". Environmental Toxicology and Chemistry 26 (10): 2166–70. doi:10.1897/07-220.1. PMID 17867892.
- Lenkowski JR et al. Perturbation of Organogenesis by the Herbicide Atrazine in the Amphibian Xenopus laevis Environ Health Perspect. Feb 2008; 116(2): 223–230. PMID 18288322
- "Pesticide atrazine can turn male frogs into females" (Press release). University of California. Retrieved March 5, 2010.
- 'Chemicals in the News: Atrazine', Australian Pesticides and Veterinary Medicines Authority, June 30, 2010
- Hayes, TB; Khoury, V; Narayan, A; Nazir, M; Park, A; Brown, T; Adame, L; Chan, E et al. (2010). "Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis)". Proceedings of the National Academy of Sciences of the United States of America 107 (10): 4612–7. Bibcode:2010PNAS..107.4612H. doi:10.1073/pnas.0909519107. PMC 2842049. PMID 20194757.
- McCallum, Malcolm L.; Matlock, Makensey; Treas, Justin; Safi, Barroq; Sanson, Wendy; McCallum, Jamie L. (2013). "Endocrine disruption of sexual selection by an estrogenic herbicide in the mealworm beetle (Tenebrio molitor)". Ecotoxicology 22 (10): 1461–1466. doi:10.1007/s10646-013-1132-3. PMID 24085605.
- City of Greenville v. Syngenta Crop Protection, Inc., and Syngenta AG Case No. 3:10-cv-00188-JPG-PMF, accessed August 23, 2013
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- Winchester, Paul. "Agrichemicals in surface water and birth defects in the United States", Acta Paediatrica, Volume 98, #4, pp. 664–669, April 2009
- atrazine.com – Syngenta's page about atrazine
- Atrazinelovers: an anti-atrazine website – maintained by Tyrone Hayes
- Atrazine - CDC - NIOSH Pocket Guide to Chemical Hazards
- Pesticide Properties Database record for Atrazine