| Atrazine | |
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1-Chloro-3-ethylamino-5-isopropylamino-2,4,6-triazine |
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Other names
Atrazine |
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| Identifiers | |
| CAS number | 1912-24-9 |
| PubChem | 2256 |
| ChemSpider | 2169 |
| UNII | QJA9M5H4IM |
| DrugBank | DB07392 |
| KEGG | C06551 |
| ChEBI | CHEBI:15930 |
| ChEMBL | CHEMBL15063 |
| Jmol-3D images | Image 1 |
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| Properties | |
| Molecular formula | C8H14ClN5 |
| Molar mass | 215.68 g mol−1 |
| Appearance | colorless solid |
| Density | 1.187 gcm−3 |
| Melting point |
175 °C, 448 K, 347 °F |
| Boiling point |
200 °C, 473 K, 392 °F |
| Solubility in water | 7 mg/100 mL |
| Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) | |
| Infobox references | |
Atrazine, 2-chloro-4-(ethylamino)-6-(isopropylamino)-s-triazine, an organic compound consisting of an s-triazine-ring is a widely used herbicide. Its use is controversial due to widespread contamination in drinking water and its associations with birth defects and menstrual problems when consumed by humans at concentrations below government standards.[1] Although it has been banned in the European Union,[2] it is still one of the most widely used herbicides in the world.
Contents |
Atrazine is used to stop pre- and post-emergence broadleaf and grassy weeds in major crops. The compound is both effective and inexpensive, and thus is well-suited to production systems with very narrow profit margins, as is often the case with maize. Atrazine is the most widely used herbicide in conservation tillage systems, which are designed to prevent soil erosion.
Its effect on yields has been estimated from 6% to 1%, with 3-4% being the conclusion of one review.[3] 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.[4]
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.[5]
Atrazine degrades in soil primarily by the action of microbes. The half-life of atrazine in soil ranges from 13 to 261 days.[6] Atrazine biodegradation can occur by two known pathways:
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,[9] 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.[10] Low concentrations of glucose can decrease the bioavailability, whereas higher concentrations promote the catabolism of atrazine.[11]
The genes for enzymes AtzA-C have been found to be highly conserved in atrazine-degrading organisms worldwide. The prevalence of these genes could be due to the mass transfer of AtzA-C on a global scale. In Pseudomonas sp. ADP, the Atz genes are located noncontiguously on a plasmid with the genes for mercury catabolism. This plasmid is conjugatable to Gram-negative bacteria in the laboratory and could lead to the worldwide distribution, in view of the extensive release of atrazine and mercury. AtzA-C genes have also been found in a Gram-positive bacterium, but are chromosomally located.[12] The insertion elements flanking each gene suggest that they are involved in the assembly of this specialized catabolic pathway.[8] Two options exist for degradation of atrazine using microbes, bioaugmentation or biostimulation.[8] 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.[13] 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".[14]
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." [15]
Atrazine was banned in the European Union (EU) in 2004 because of its persistent groundwater contamination.[3] In the United States, however, atrazine is one of the most widely used herbicides, with 76 million pounds of it applied each year, in spite of the restriction that used to be imposed.[17], [18] Its endocrine disruptor effects, possible carcinogenic effect, and epidemiological connection to low sperm levels in men has led several researchers to call for banning it in the US.[3]
In August 2009, Atrazine was prominently featured 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.[1] 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.[19] Findings from further studies released in early 2010 have tended to support the conclusion that even low doses can increase health risks, leading to calls for further testing and renewed EPA evaluation of atrazine's safety.[20]
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 pesticied applicators over 13 years. [21] EPA also determined in 2000 "that atrazine is not likely to cause cancer in humans."[22]
Atrazine is a suspected teratogen, causing demasculinization in male northern leopard frog even at low concentrations,[23][24] and an estrogen disruptor.[25] A 2010 study found that atrazine rendered 75 percent of male frogs sterile and turned one in 10 into females.[26] A 2002 study found that exposure to atrazine caused male tadpoles to turn into hermaphrodites - frogs with both male and female sexual characteristics.[27] But another study, requested by EPA and funded by Syngenta, was unable to reproduce these results.[28]
Tyrone Hayes, Department of Integrative Biology, University of California, notes that all of the studies that failed to conclude that atrazine caused hermaphroditism were plagued by poor experimental controls and were funded by Syngenta, one of the companies that produce the chemical.[29] The U.S. Environmental Protection Agency (EPA) and its independent Scientific Advisory Panel (SAP) examined all available studies on this topic — including Hayes' work — and concluded that there are "currently insufficient data" to determine if atrazine affects amphibian development. Hayes, formerly part of the SAP panel, resigned in 2000 to continue studies independently.[30] 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."[31] Another independent study in 2008 determined that "the failure of recent studies to find that atrazine feminizes X. laevis calls into question the herbicide's role in that decline." 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." [32]
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 [33]
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.[34]
In 2009, University of Tennessee Department of Plant Sciences researchers found the combination of the herbicides mesotrione and atrazine can make sweet corn more nutritious. They found the herbicides directly up-regulate the carotenoid biosynthetic pathway in corn kernels, which is associated with the nutritional quality of sweet corn. Enhanced accumulation of lutein and zeaxanthin is important because dietary carotenoids function in suppressing aging eye diseases such as macular degeneration, now affecting 1.75 million older Americans.[35]
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 effect amphibian gonadal development.[36]
Furthermore, the APVMA responded to Hayes' 2010 published paper, Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis), 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."[36]
A 2010 study conducted by the U.S. Geological Survey observed substantial adverse reproductive effects on fish from atrazine exposure at concentrations below the USEPA water-quality guideline.[37]
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