| Atrazine | |
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| IUPAC name | 1-chloro-3-ethylamino-5-isopropylamino-2,4,6-triazine |
| Other names | Atrazine See also synonyms |
| Identifiers | |
| CAS number | [1912-24-9] |
| SMILES |
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| Properties | |
| Molecular formula | C8H14ClN5 215.683477 g/mol |
| Appearance | colorless solid |
| Density | 1.187 g/cm³ |
| Melting point |
175 °C (448 K) |
| Boiling point |
200 °C (473 K) |
| Solubility in water | 0.007 g/100 mL (?°C) |
| Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) Infobox references |
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Atrazine, 2-chloro-4-(ethylamine)-6-(isopropylamine)-s-triazine, an organic compound consisting of an s-triazine-ring is a widely used herbicide. Its use is controversial due to its effects on nontarget species, such as on amphibians.[1] Like many commercial products, it is sold under numerous trade names. Although banned in the European Union, it is one of the most widely used herbicides in the U.S. with 77 million lb applied in 2003.
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Atrazine is used to stop pre- and post-emergence broadleaf and grassy weeds in major crops by binding to the plastoquinone-binding protein in photosystem II, inhibiting electron transport. Atrazine and its derivatives are also used in many industrial processes, including the production of some dyes and explosives.[citation needed] 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 an extensive review.[2]
The half-life of atrazine in soil is 13 to 261 days.[3] Atrazine biodegradation can occur by two known pathways:
1) Atrazine can be dechlorinated followed by removal the other ring substituents via amidohydrolases by the enzymes AtzA, AtzB, and AtzC. The end product is cyanuric acid. The best characterized organism that performs this pathway is Pseudomonas sp. strain ADP.
2) The other pathway involves dealkylation of the amino groups. Subsequent dechlorination yields cyanuric acid. The end result is 2-chloro-4-hydroxy-6-amino-1,3,5-triazine, which currently has no known path to further degradation. This path occurs in Pseudomonas species and a number of bacteria.[4][5]
Atrazine degrades in soil by the action microbes. Rates of biodegradation affected by atrazine's low solubility , thus surfactants increase the accelerate degradation. Atrazine itself is a poor energy source due to the highly oxidized carbons in the ring. It is catabolized as a carbon and nitrogen source in limiting environments. Inorganic nitrogen accelerates atrazine catabolism whereas organic nitrogen decreases it. Low concentrations of glucose can decrease the bioavailability, whereas higher concentrations promote the catabolism of atrazine.[6]
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 non-contiguously 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 of atrazine and mercury. AtzA-C have also been found in a Gram positive bacterium but are chromosomally located.[7] The insertion elements flanking each gene suggests that they are involved in the assembly of this specialized catabolic pathway.[5] Two options exist for degradation of atrazine using microbes: bioaugmentation or biostimulation.[5]
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It has been suggested that this article be split into articles entitled Atrazine controversy, accessible from a disambiguation page. (Discuss) |
Atrazine was banned in the European Union (EU) in 2004 because of its persistent groundwater contamination[2] In the United States, however, atrazine is one of the most widely used herbicides, with 76 million pounds of it applied each year.[9] It is probably the most commonly used herbicide in the world, and is used in about 80 countries worldwide.[10] Its endocrine 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.[2]
It is a teratogen, causing demasculinization in male frogs even at low concentrations,[11] and an estrogen disruptor.[12] Male frogs affected by atrazine could reach testosterone levels below females.[10]
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 is "currently insufficient data" to determine if atrazine affects amphibian development. Hayes, formerly part of the SAP panel, resigned in 2000 to continue studies independently.[13] Hayes 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, the company that produces the chemical.[14] In 2006 the U.S. EPA considered re-registration of Atrazine final when it issued a cumulative risk assessments on the triazine herbicides, and concluded that they posed "no harm that would result to the general U.S. population, infants, children or other...consumers."[15] A former scientist working for the Minnesota Pollution Control Agency believes he was fired for attempting to testify against atrazine.[16]
As reported in February 2008, young tadpoles undergoing organ morphogenesis were found to develop deformed hearts and impaired kidneys and digestive systems when exposed to atrazine. Tissue malformation may be induced by ectopic programmed cell death, althrough a mechanism was not identified.[17]
According to Extension Toxicology Network, "The oral 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." [18]