Atrazine

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Atrazine
Atrazine
Atrazine
Identifiers
CAS number1912-24-9 YesY
PubChem2256
ChemSpider2169 YesY
UNIIQJA9M5H4IM YesY
DrugBankDB07392
KEGGC06551 YesY
ChEBICHEBI:15930 YesY
ChEMBLCHEMBL15063 YesY
Jmol-3D imagesImage 1
Properties
Molecular formulaC8H14ClN5
Molar mass215.68 g mol−1
Appearancecolorless solid
Density1.187 gcm−3
Melting point175 °C; 347 °F; 448 K
Boiling point200 °C; 392 °F; 473 K
Solubility in water7 mg/100 mL
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
Infobox references
 
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Atrazine
Atrazine
Atrazine
Identifiers
CAS number1912-24-9 YesY
PubChem2256
ChemSpider2169 YesY
UNIIQJA9M5H4IM YesY
DrugBankDB07392
KEGGC06551 YesY
ChEBICHEBI:15930 YesY
ChEMBLCHEMBL15063 YesY
Jmol-3D imagesImage 1
Properties
Molecular formulaC8H14ClN5
Molar mass215.68 g mol−1
Appearancecolorless solid
Density1.187 gcm−3
Melting point175 °C; 347 °F; 448 K
Boiling point200 °C; 392 °F; 473 K
Solubility in water7 mg/100 mL
Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)
Infobox references

Atrazine is a herbicide of the triazine class. It is the most widely used herbicide in the United States[1] and one of the most widely used herbicides in Australian agriculture.[2] It was banned in the European Union in 2004.[3] 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.

Atrazine is the most commonly detected contaminant of drinking water in the United States. It is a potential endocrine disruptor, an agent that may alter the natural hormonal system in animals.[1][4] 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",[5] and in 2007 the EPA said that atrazine does not adversely affect amphibian sexual development and that no additional testing was warranted.[6] However, in 2009 the EPA began a new scientific evaluation of health effects on atrazine.[7] Numerous studies have stated that atrazine has substantial adverse reproductive effects even at levels said by the EPA to be safe.[8][9][4][10]

Uses[edit]

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.[2] 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 (corn). Although it is banned in the European Union,[3] Atrazine is one of the most widely used herbicides in the United States[1] and in Australian agriculture.[2]

Its effect on yields has been estimated from 6% to 1%, with 3–4% being the conclusion of one review.[11] 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.[12]

Chemistry and biochemistry[edit]

Atrazine was invented in 1958 in the Geigy laboratories as the second of a series of 1,3,5-triazines.[13]

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.[14]

Atrazine's effects in humans and animals primarily involve the endocrine system. Studies suggest that atrazine is an endocrine disruptor that can cause hormone imbalance.[1]

Biodegradation[edit]

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).[1]

Atrazine degrades in soil primarily by the action of microbes. The half-life of atrazine in soil ranges from 13 to 261 days.[15] Atrazine biodegradation can occur by two known pathways:

  1. 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.
  2. 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.[16][17]

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,[18] 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.[19] Low concentrations of glucose can decrease the bioavailability, whereas higher concentrations promote the catabolism of atrazine.[20]

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.[21] The insertion elements flanking each gene suggest that they are involved in the assembly of this specialized catabolic pathway.[17] Two options exist for degradation of atrazine using microbes, bioaugmentation or biostimulation.[17] 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.[22] 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".[23]

Health and environmental effects[edit]

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."[24]

Atrazine use in pounds per square mile by county. Atrazine is one of the most commonly used herbicides in the United States.[25]

Atrazine was banned in the European Union (EU) in 2004 because of its persistent groundwater contamination.[11] 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.[26][27] 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.[11]

Atrazine contamination of surface water (lakes, rivers, and streams) is a concern to the U.S. Environmental Protection Agency. It is the most commonly detected pesticide in U.S. surface waters and drinking water from a contaminated groundwater or surface water source can be a significant medium of exposure for children. 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.[1] Syngenta corporation, manufacturer of atrazine, was the defendant in a class action lawsuit concerning the adverse effects of atrazine in human water supplies. The suit was settled for 105 million dollars in May 2012.[28] A similar case involving six states is currently in federal court.[29][30]

In 2009, University of Tennessee Department of Plant Sciences researchers noted the combination of the herbicides mesotrione and atrazine can potentially make sweet corn more nutritious by increasing carotenoid levels, though in some cases atrazine decreased carotenoid levels. 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.[31]

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.[9] 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.[32]

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.[33] EPA also determined in 2000 "that atrazine is not likely to cause cancer in humans."[34]

One study suggests that chemicals that act as endocrine disrupters may put an unborn infant at risk. A 2012 epidemiological study looked at atrazine, a commonly used herbicide in the U.S., and found that women who lived in counties in Texas with the highest levels of this chemical being used to treat 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. [35]

Although the U.S. EPA states that thus far studies show atrazine to be an endocrine disruptor,[1] a 2013 op-ed written by Jon Entine in Forbes called it a novel theory, "widely circulated notion popular with the Environmental Working Group, Center for Food Safety, Natural Resources Defense Council and other anti-chemical activists".[36] According to Entine, the current scientific consensus is that atrazine is safe, restrictions too severe, and has prompted the WHO to significantly raise the allowable amount of atrazine in drinking water.[36]

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.[37]

Effect on amphibians[edit]

Atrazine is a suspected teratogen, causing demasculinization in male northern leopard frog even at low concentrations,[38][39] and an estrogen disruptor.[40] 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.[41] 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.[42] 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.[43]

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."[44] Hayes was formerly part of the SAP panel, but resigned in 2000 to continue studies independently.[45] 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."[46] 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."[47]

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.[48]

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.[49]

A 2010 Hayes study found that atrazine rendered 75 percent of male frogs sterile and turned one in 10 into females.[50]

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.[51]

Furthermore, the APVMA responded to Hayes' 2010 published paper,[52] 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."[51]

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.[8]

See also[edit]

References[edit]

  1. ^ a b c d e f g Atrazine: Chemical Summary. Toxicity and Exposure Assessment for Children’s Health (Report). U.S. Environmental Protection Agency. 4/24/2007. http://www.epa.gov/teach/chem_summ/Atrazine_summary.pdf.
  2. ^ a b c "Chemical Review: Atrazine". Australian Pesticides and Vetinary Medicines Authority. Retrieved 2014-02-05. 
  3. ^ a b "EDEXIM Chemical Information for Atrazine". Retrieved 2014-2-10. 
  4. ^ a b Hayes, Tyrone B.; Anderson, Lloyd L.; Beasley, Val R.; de Solla, Shane R.; Iguchi, Taisen; et al. (2011). "Demasculinization and feminization of male gonads by atrazine: Consistent effects across vertebrate classes". The Journal of Steroid Biochemistry and Molecular Biology 127 (1-2): 64–73. doi:10.1016/j.jsbmb.2011.03.015. 
  5. ^ Triazine Cumulative Risk Assessment and Atrazine, Simazine, and Propazine Decisions, June 22, 2006, EPA.
  6. ^ Atrazine Updates, April 2010, EPA.
  7. ^ EPA Begins New Scientific Evaluation of Atrazine, October 7, 2009, EPA.
  8. ^ a b Commonly Used Atrazine Herbicide Adversely Affects Fish Reproduction, ScienceDaily (May 20, 2010)
  9. ^ a b Duhigg, Charles (August 22, 2009). "Debating How Much Weed Killer Is Safe in Your Water Glass". The New York Times. Retrieved 2009-09-10. 
  10. ^ Rachel Aviv: The Scientist Who Took on a Leading Herbicide Manufacturer : The New Yorker
  11. ^ a b c Ackerman, Frank (2007). "The economics of atrazine". International Journal of Occupational and Environmental Health 13 (4): 437–445. PMID 18085057. 
  12. ^ Fawcett, Richard S. (2008) Twenty Years of University Corn Yield Data: With and Without Atrazine. North Central Weed Science Society.
  13. ^ Wolfgang Krämer (2007). Modern Crop Protection Compounds, Volume 1. Wiley-VCH. ISBN 9783527314966. 
  14. ^ Appleby, Arnold P.; Müller, Franz; Carpy, Serge (2001). "Weed Control". Ullmann's Encyclopedia of Industrial Chemistry. doi:10.1002/14356007.a28_165. ISBN 3-527-30673-0. 
  15. ^ Interim Reregistration Eligibility Decision for Atrazine, U.S. EPA, January, 2003.
  16. ^ Zeng Y, Sweeney CL, Stephens S, Kotharu P. (2004). Atrazine Pathway Map. Wackett LP. Biodegredation Database.
  17. ^ a b c Wackett, L. P.; Sadowsky, M. J.; Martinez, B.; Shapir, N. (January 2002). "Biodegradation of atrazine and related s-triazine compounds: from enzymes to field studies". Applied Microbiology and Biotechnology 58 (1): 39–45. doi:10.1007/s00253-001-0862-y. PMID 11831474. 
  18. ^ Crawford, J. J., G.K. Sims, R.L. Mulvaney, and M. Radosevich (1998). "Biodegradation of atrazine under denitrifying conditions". Appl. Microbiol. Biotechnol. 49 (5): 618–623. doi:10.1007/s002530051223. PMID 9650260. 
  19. ^ Bichat, F., G.K. Sims, and R.L. Mulvaney (1999). "Microbial utilization of heterocyclic nitrogen from atrazine". Soil Science Society of America Journal 63: 100–110. doi:10.2136/sssaj1999.03615995006300010016x. 
  20. ^ Ralebitso TK, Senior E, van Verseveld HW (2002). "Microbial aspects of atrazine degradation in natural environments". Biodegradation 13: 11–19. doi:10.1023/A:1016329628618. 
  21. ^ Cai B, Han Y, Liu B, Ren Y, Jiang S. (2003). "Isolation and characterization of an atrazine-degrading bacterium from industrial wastewater in China". Letters in Applied Microbiology 36 (5): 272–276. doi:10.1046/j.1472-765X.2003.01307.x. PMID 12680937. 
  22. ^ Krutz, L.J., D.L. Shaner, C. Accinelli, R.M. Zablotowicz, and W.B. Henry (2008). "Atrazine dissipation in s-triazine-adapted and non-adapted soil from Colorado and Mississippi: Implications of enhanced degradation on atrazine fate and transport parameters". Journal of Environmental Quality 37 (3): 848–857. doi:10.2134/jeq2007.0448. PMID 18453406. 
  23. ^ Xu, J., J. W. Stucki, J. Wu, J. Kostka, and G. K. Sims (2001). "Fate of atrazine and alachlor in redox-treated ferruginous smectite". Environmental Toxicology & Chemistry 20 (12): 2717–2724. doi:10.1002/etc.5620201210. 
  24. ^ 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.
  25. ^ USGS Pesticide Use Maps
  26. ^ Walsh, Edward (2003-02-01). "EPA Stops Short of Banning Herbicide". Washington Post. pp. A14. Retrieved 2007-04-27. 
  27. ^ "Restricted Use Products (RUP) Report: Six Month Summary List". Environmental Protection Agency. Archived from the original on 11 January 2010. Retrieved 1 December 2009. 
  28. ^ City of Greenville v. Syngenta Crop Protection, Inc., and Syngenta AG Case No. 3:10-cv-00188-JPG-PMF, accessed August 23, 2013
  29. ^ Dalton, Rex (2010). "E-mails spark ethics row". Nature 466 (7309): 913. doi:10.1038/466913a. PMID 20725013. 
  30. ^ Tillery planning to file new litigation involving atrazine, Madison County Record, June 19, 2013, accessed August 23, 2013
  31. ^ Kopsell, Dean A.; Armel, Gregory R.; Mueller, Thomas C.; Sams, Carl E.; Deyton, Dennis E.; McElroy, J. Scott; Kopsell, David E. (2009). "Increase in Nutritionally Important Sweet Corn Kernel Carotenoids following Mesotrione and Atrazine Applications". Journal of Agricultural and Food Chemistry 57 (14): 6362–8. doi:10.1021/jf9013313. PMID 19537793. 
  32. ^ "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. 
  33. ^ Beane Freeman, Laura E. (2011) Atrazine and Cancer Incidence Among Pesticide Applicators in the Agricultural Health Study (1994–2007). Environmental Health Perspetives.
  34. ^ Interim Reregistration Eligibility Decision for Atrazine, U.S. EPA, January, 2003.
  35. ^ Study: Exposure to herbicide may increase risk of rare disorder
  36. ^ a b Forbes: Berkeley Anti-Atrazine Crusader Blames 'Big Ag', Set To Sue, After University Dispute Freezes Research. August 19, 2013.
  37. ^ 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. 
  38. ^ Jennifer Lee (2003-06-19). "Popular Pesticide Faulted for Frogs' Sexual Abnormalities". The New York Times. 
  39. ^ 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. 
  40. ^ 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. 
  41. ^ Briggs, Helen. (April 15, 2002), Pesticide 'causes frogs to change sex'. BBC News. Retrieved on 2007-10-16.
  42. ^ Jooste et al.; Du Preez, LH; Carr, JA; Giesy, JP; Gross, TS; Kendall, RJ; Smith, EE; Van Der Kraak, GL et al. (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. 
  43. ^ 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. 
  44. ^ Environmental Protection Agency: Atrazine Updates. Current as of January 2013, URL accessed August 24, 2013.
  45. ^ Weedkiller 'threatens frogs', BBC News. 31 October 2002
  46. ^ 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. 
  47. ^ Renner, Rebecca (May 2008). "Atrazine Effects in Xenopus Aren't Reproducible (Perspective)". Environmental Science & Technology 42 (10): 3491–3493. doi:10.1021/es087113j. 
  48. ^ 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. 
  49. ^ Early Exposure To Common Weed Killer Impairs Amphibian Development
  50. ^ "Pesticide atrazine can turn male frogs into females" (Press release). University of California. Retrieved March 5, 2010. 
  51. ^ a b 'Chemicals in the News: Atrazine', Australian Pesticides and Veterinary Medicines Authority, June 30, 2010
  52. ^ 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. 

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