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Janet Gray, Ph.D.
Janet Gray, Ph.D.

As author of our 2008 and 2010 State of the Evidence reports, Dr. Gray drives the science behind all our work.

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Triazine Herbicides (Atrazine)

CATEGORY*: Endocrine disruptors

FOUND IN: Agricultural and household pest control

THE GIST: It kills weeds, impacts wildlife and may be carcinogenic. The European Union banned Atrazine in 2005, but in the United States more than 75 million pounds of it is applied to corn and sorghum crops each year. The toxic stuff seeps into groundwater and drinking water, and has been associated with an increased risk of breast cancer. (Scientific studies also show that atrazine changes the sex of male frogs.)

State of the Evidence on Atrazine (Triazine Herbicides)

Triazine herbicides are the most heavily used agricultural chemicals in the United States. Triazines include atrazine, simazine, propazine and cyanazine. Although all have been shown to cause mammary cancer in laboratory rats (O'Connor, 2000), there are relatively little scientific data exploring the relationship between simazine or cyanazine and human breast cancer. The literature on atrazine is more substantial.

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Organic produce is grown without harmful man-made pesticides and herbicides. Visit a farmers' market for locally grown organic fruits and vegetables, or ask your grocer to stock organic produce.

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Atrazine was banned in the European Union in 2005 because of its ubiquity in drinking water, its demonstrated harmful effects on wildlife, and its potential health hazards for humans. Atrazine is, however, still approved for use in the United States. More than 75 million pounds of atrazine are applied annually in the United States, primarily to control broadleaf weeds in corn and sorghum crops in the Midwest (EPA, 2008).

Elevated levels of atrazine are found each spring and summer in both drinking water and groundwater in agricultural areas (Hua, 2006; Miller, 2000; Villanuaeva, 2005). Atrazine is a known endocrine disruptor, causing dramatic damage to reproductive structures in frogs, fish and other wildlife  (Hayes, 2003; Rohr, 2009). 

High levels of triazines (primarily atrazine) in contaminated waters have been associated with an increased risk of breast cancer (Kettles, 1997), and application of higher levels of mixed pesticides, including atrazine, was also associated with increased breast cancer in rural communities (Muir, 2004). However, not all ecological studies support these findings (e.g., Hunter, 2008). These studies tend to compare countywide average levels of chemical exposures and cancer incidence, rather than individual exposure levels of atrazine contamination and incidence rates.

Research in rodents has shown that atrazine exposure disrupts pituitary-ovarian function. The resulting decreases in levels of circulating prolactin and luteinizing hormone contribute to the effects of this herbicide on increased incidence of mammary tumors (Cooper, 2000; O’Connor, 2000). Atrazine also exerts endocrine-disrupting effects by increasing the activity of the enzyme aromatase (Fan, 2007; Sanderson, 2001), an enzyme that is critical for the conversion of testosterone and other androgens to estrogens, including estradiol. Androgens are found naturally in women, although at lower levels than in men. The production of estrogens through the aromatase pathway, however, is of sufficient importance as a possible mechanism underlying the development of breast cancer that a current class of breast cancer drugs aims specifically to block the activity of aromatase.

Exposure to atrazine or mixtures of atrazine metabolites during gestation delays development of the rat mammary gland in puberty, expanding the period of time when the developing tissue is particularly sensitive to carcinogens (Enoch, 2007; Raynor, 2005). Similarly, exposure of rats late in pregnancy to a mixture of commonly formed metabolites of atrazine also leads to persistent changes in mammary gland development in pups exposed during gestation. These abnormalities persist into adulthood (Enoch, 2007). The early developmentally induced changes in mammary gland development may reflect an indirect effect of the atrazine-related decreases in the amount of food mothers ate during the time of pesticide exposure (Hovey, 2011). Exposure of rats with existing mammary tumors to atrazine increases the rate of cell proliferation in those tumors (Ueda, 2005).

A recent review of the scientific literature on atrazine was funded by Syngenta, the major industrial producer of the pesticide. This review concluded that evidence did not support a causal relationship between atrazine exposure and development of breast cancer (Simpkins, 2011).

Most of the studies incorporated in this review examined exposures of rodents during adulthood, although it also concluded that there was insufficient evidence to link in utero exposures to atrazine with later development of disease. As several independent scientists have acknowledged, it is critical to develop consistent methods and criteria for assessing early life exposures to chemicals, including atrazine, and to incorporate these procedures regularly and reliably into test guidelines and ongoing risk-assessment protocols. In particular, it will be important to examine endpoints of mammary gland development in these studies in order to understand better the possible connections between early exposures and alterations in mammary tissue development that might predispose an animal to later development of breast cancer (Fenton, 2006, 2012; Rudel, 2011).

*For chemicals that have been shown to be carcinogens, we provide classifications from two authoritative bodies: the International Agency for Research on Cancer (IARC, an international body) and the National Toxicology Program (NTP, a division of the U.S. Department of Health and Human Services). We have categorized endocrine-disrupting compounds where the body of peer-reviewed research indicates a strong foundation for doing so.