|Molar mass||215.68 g·mol−1|
|Melting point||175 °C (347 °F; 448 K)|
|Boiling point||200 °C (392 °F; 473 K) decomposes|
|7 mg/100 mL|
|Flash point||noncombustible |
|US health exposure limits (NIOSH):|
|TWA 5 mg/m3|
IDLH (Immediate danger)
Except where noted otherwise, data is 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 EPA said that atrazine does not adversely affect amphibian sexual development and that no additional testing was warranted. 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 an 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 was banned in the European Union in 2004, when the EU found that the data provided by the manufacturer was insufficient to show that groundwater and soil contamination would not exceed acceptable limits under the intended uses for atrazine.:4
Its effect on corn yields has been estimated from 8% 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. Effects on sorghum yields have been estimated to be as high as 20%, owing in part to the absence of alternative weed control products that can be used on sorghum.
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 (although in some soils can persist to at least 4 years) 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 more rapid biodegradation. 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 monitored by EPA and has consistently exceeded levels of concern in 2 Missouri watersheds and 1 in Nebraska. As of 2001, Atrazine was the most commonly detected pesticide in US drinking water.:2 Monitoring of atrazine levels in community water systems in 31 high use atrazine states found that atrazine levels exceeded levels of concern for infant exposure during at least one year between 1993-2001 in 34 of 3670 community water systems using surface water, and in none of 14,500 community water systems using groundwater. Surface water monitoring data from 20 high atrazine use watersheds found peak atrazine levels of up to 147 parts per billion, with daily averages in all cases below 10 parts per billion.
In 2006 EPA stated that "the risks associated with the pesticide residues pose a reasonable certainty of no harm", 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."
In 2007 the U.S. EPA said that "studies thus far suggest that atrazine is an endocrine disruptor". The implications for children’s health are related to effects during pregnancy and during sexual development, though few studies are available. In people, risks for preterm delivery and intrauterine growth retardation have been associated with exposure. Atrazine exposure has been shown to result in delays or changes in pubertal development in female rats; conflicting results have been observed in males. Male rats exposed via milk from orally exposed mothers exhibited higher levels of prostate inflammation as adults; immune effects have also been seen in male rats exposed in utero or while nursing.
A 2014 systematic review, funded by atrazine manufacturer Syngenta, assessed its relation to reproductive health problems. The authors concluded that the quality of most studies was poor and without good quality data the results were difficult to assess, though it was noted that no single category of negative pregnancy outcome was found consistently across studies. The authors concluded that a causal link between atrazine and adverse pregnancy outcomes was not warranted due to the poor quality of the data and the lack of robust findings across studies. Syngenta was not involved in the design, collection, management, analysis, or interpretation of the data and did not participation in the preparation of the manuscript.
A 2011 review of the mammalian reproductive toxicology of atrazine jointly conducted by the World Health Organization and the Food and Agriculture Organization of the United Nations concluded that atrazine is not teratogenic. Reproductive effects in rats and rabbits were only seen at doses that were toxic to the mother. Observed adverse effects in rats included fetal resorption in rates (at doses > 50 mg/kg per day), delays in sexual development in female rats (at doses >30 mg/kg per day), and decreased birth weight (at doses >3.6 mg/kg per day).
Research results from the U.S. National Cancer Institute's 2011 Agricultural Health Study 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."
Atrazine is a suspected teratogen, with some studies reporting 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 caused male tadpoles to turn into hermaphrodites – frogs with both male and female sexual characteristics. An EPA review of this study concluded that overcrowding, questionable sample handling techniques and the failure of the authors to disclose key details including sample sizes, dose-response effects and the variability of observed effects made it difficult to assess the study's credibility and ecological relevance. A 2005 Syngenta-funded study, requested by EPA and conducted under EPA guidance and inspection, was unable to reproduce these results.
According to Hayes, all of the studies that rejected the hermaphroditism hypothesis were plagued by poor experimental controls and were funded by Syngenta, suggesting conflict of interest. A recent EPA review article discussed the Hayes/Syngenta conflict to illustrate both financial and non-financial conflicts of interest. The authors concluded that "Statements by Hayes and Syngenta suggest that their scientific differences have developed a personal aspect that casts doubt on their scientific objectivity" and noted that "The inability of the scientific community to resolve this straightforward issue is an embarrassment." (
EPA's Scientific Advisory Panel (SAP) examined all relevant studies and concluded that "atrazine does not adversely affect amphibian gonadal development based on a review of laboratory and field studies." SAP made recommendations concerning proper study design for further investigation. As required by EPA, Syngenta conducted two experiments under Good Laboratory Practices (GLP) and inspection by 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 2008 report cited 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 2007 study examined the relative importance of environmentally relevant concentrations of atrazine on trematode cercariae versus tadpole defense against infection. Its principal ﬁnding was that susceptibility of wood frog tadpoles to infection by E. trivolvis is increased only when hosts were 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 chronically exposed to atrazine concentrations of 10,000 ppb 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), tentatively concluded that environmental atrazine were not affecting amphibian populations in Australia:
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."
Fish and insects
A 2004 study found no statistically significant reproductive effects in fathead minnow at atrazine levels up to 50 μg/L. The study examined endpoints including survival, egg production, number of spawns, eggs/spawn, relative gonad weight, and gonad histology, among others. Trends were observed in relative testis weight, testis maturity, and percentage embryo fertilization in atrazine-exposed fish, the but were not statistically significant. In contrast, in fish exposed to estradiol at 0.5 ug/mL as a positive control all endpoints were significantly different from atrazine-exposed fish and control fish. The authors concluded that atrazine does not have strong estrogenic effects in adult fathead minnows or cause overt reproductive toxicity at environmentally relevant concentrations
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 2014 study found similar results in Japanese medaka fish.
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 one thousand water systems for "the cost of filtering atrazine from drinking water". The company denied all wrongdoing. 
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