[2] It is used to prevent pre-emergence broadleaf weeds in crops such as maize (corn),[3] soybean[3] and sugarcane and on turf, such as golf courses and residential lawns.

[4] As of 2001[update], atrazine was the most commonly detected pesticide contaminating drinking water in the U.S.[8]: 44  Studies suggest it is an endocrine disruptor, an agent that can alter the natural hormonal system.

[9] However, in 2006 the U.S. Environmental Protection Agency (EPA) had stated that under the Food Quality Protection Act "the risks associated with the pesticide residues pose a reasonable certainty of no harm",[10] and in 2007, the EPA said that atrazine does not adversely affect amphibian sexual development and that no additional testing was warranted.

[11] The EPA's 2009 review[12] 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".

"[2] 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 canola.

Like other triazine herbicides, atrazine functions by binding to the plastoquinone-binding protein in photosystem II, which animals lack.

[29] Atrazine contamination of surface water (lakes, rivers, and streams) in the U.S. has been monitored by the EPA and has consistently exceeded levels of concern in two Missouri watersheds and one in Nebraska.

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.

In pure cultures of atrazine-degrading bacteria, as well as active soil communities, atrazine ring nitrogen, but not carbon are assimilated into microbial biomass.

[34] 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.

[39] In 2016, photolytic degradation with 254 nm ultraviolet was seen by the authors of a particular study as an efficient process, which could be used in pilot plants to reduce or eliminate compounds of the atrazine class or similar emerging contaminants, in effluents.

[40] 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.

Little information is available regarding the risks to children, however "[m]aternal exposure to atrazine in drinking water has been associated with low fetal weight and heart, urinary, and limb defects in humans".

[9] EPA opened a new review in 2009[12] 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.

"[16] A Natural Resources Defense Council report from 2009 said that the EPA is ignoring atrazine contamination in surface and drinking water in the central United States.

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.

[49] Atrazine has been a suspected teratogen, with some studies reporting causing demasculinization in male northern leopard frogs even at low concentrations.

[55] In 2010, the Australian Pesticides and Veterinary Medicines Authority (APVMA) tentatively concluded that environmental atrazine "at existing levels of exposure" was not affecting amphibian populations in Australia consistent with the 2007 EPA findings.

[56] APVMA responded to Hayes' 2010 published paper,[57] that his findings "do not provide sufficient evidence to justify a reconsideration of current regulations which are based on a very extensive dataset.

As required by the EPA, two experiments were conducted under Good Laboratory Practices (GLP) and were inspected by EPA and German regulatory authorities, concluding 2009 that "long-term exposure of larval X. laevis to atrazine at concentrations ranging from 0.01 to 100 μg/L does not affect growth, larval development, or sexual differentiation".

This was done because while the EU's ban was based on a legislated pollutant level of 0.1 μg/L, the Canadian regulations call for a home-grown "risk-based scientific approach in determining the risk to human health from pesticides in drinking water."