Atrazine has been studied continuously for decades, for both its agricultural benefits and its human health and environmental impacts. This body of research has been aggregated and analyzed by regulators and researchers over time, generating a host of meta-analyses that continue to influence policy decisions and drive debate.

In 1991, the US EPA established a Maximum Contaminant Level (MCL) for atrazine in drinking water of 3.0 micrograms per liter, or 3 parts per billion. Industrial chemicals are not tested for safety directly on humans for obvious ethical reasons, so EPA contaminant levels are established by investigating toxic doses in animals, and then setting regulatory limits at some fraction of those doses. Human and environmental health advocates criticize this approach for ignoring chronic low-dose and multi-chemical exposures, while chemical producers view the approach as arbitrary and resulting in overly restrictive limits.

The most significant regulatory decision in recent years occurred in 2003, after the EU, US, and other nations decided to re-examine the safety of atrazine in light of new evidence. At that time, research had expanded beyond toxicity studies and was beginning to investigate long-term, low-dose exposures in animals, particularly female and fetal animals, and arrived at conclusions such as the following:

In long-term dietary studies in rats, effects on red blood cell parameters in females, an increased incidence of non-neoplastic lesions in the liver, lung, thyroid and testis and a slight decrease in body weight gain were observed (WHO 2003, p. 5).

A US Department of Health and Human Services toxicology report notes, with regard to fetal and childhood exposures:

Little information is available regarding the effects of atrazine in children. Maternal exposure to atrazine in drinking water has been associated with low fetal weight and heart, urinary, and limb defects in humans. Atrazine has been shown to slow down the development of fetuses in animals, and exposure to high levels of atrazine during pregnancy caused reduced survival of fetuses. It is unclear whether or at what level of exposure this might occur in humans. It is not known whether atrazine or its metabolites can be transferred from a pregnant mother to a developing fetus through the placenta or from a nursing mother to her offspring through breast milk (ATSDR, 2003, p. 99).

In humans, a number of epidemiological studies found evidence linking atrazine exposure to adverse health effects. For example, a study of Iowa farm communities found that increased exposure to atrazine nearly doubled women's risk of having low birth weight and premature deliveries (Munger et al, 1997). More recent studies have found an increase in birth defects, the leading cause of infant mortality, among infants conceived during periods of peak atrazine use (Mattix, et al, 2007; Winchester, et al, 2009).

While epidemiological studies of farming communities are an essential component in evaluating atrazine's potential health effects, evidence gleaned from them is often clouded by their broad focus in a complex setting. For example, farmers use a variety of herbicides and other pesticides throughout the growing season and even in a single application, making it difficult to tease out the effects of any single agent. Consequently, both proponents and opponents of atrazine use find support for their positions in these studies.

EPA Safety Targets Versus Fate of Atrazine in Environment

Atrazine in soil breaks down through interaction with environmental compounds, particularly soil bacteria. Because the metabolizing bacteria are rare to nonexistent in surface water and groundwater, atrazine can persist for months to as long as a year (Rohr and McCoy, 2010, p. 20) once it enters surface or ground water. Approximately 75% of surface water and 40% of all groundwater in agricultural areas tested by the U.S. Geological Survey were contaminated with atrazine (Gilliom, et al, 2006).

Because it is persistent in water, atrazine and its metabolites can accumulate in drinking water reservoirs downstream from farms. Metabolites have been found in groundwater at concentrations much higher than atrazine, yet there is little corresponding safety research on these metabolites themselves (Kolpin, et al, 1996; Kolpin, et al, 1997; Potter and Carpenter, 1995). And, atrazine and its metabolites have been found to accumulate in drinking water reservoirs at higher concentrations than in runoff streams immediately adjacent to cropland (Liu, et al, 1996).

In 1993, the EPA passed revised application guidelines designed to limit atrazine's runoff into surface water (Koskinen and Clay, 1997, p. 151), and these guidelines were strengthened after the EPA reviewed environmental risk studies in 2002. The guidelines include, for example, 50-foot setback zones between the application area and any groundwater wells, streams or rivers, and lakes or reservoirs. A 200-foot setback around lakes or reservoirs is recommended for aerial spraying.²

Yet, drinking water monitoring programs have continued to find levels of atrazine in farm communities in excess of the annual MCL. Beyond farming communities, atrazine is one of the most commonly found drinking water contaminants throughout the US. In 2009, the EPA announced that it would revisit its regulatory position on atrazine yet again, beginning with a review of data on human cancer and non-cancer health effects gathered since 2003. In April 2010, EPA began the process with a series of public hearings.

Atrazine, Endocrine Disruption, and Aromatase

While Syngenta, the manufacturer of atrazine, points to decades of use and study as evidence of atrazine's safety, a growing body of research is pinpointing ways in which atrazine functions as a hormone or as a hormone disruptor, which may spur the growth and proliferation of human cancer cells.

For example, a 2008 study (Lappano, et al.) found that atrazine stimulates aromatase activity in human ovarian cancer cells (Albanito, et al, 2008), confirming an earlier study reporting the same findings (Fan, et al, 2007). Aromatase, an enzyme that converts testosterone into estrogen, is produced by the adrenal glands and by some cancer cells. Cancer patients with estrogen-promoted cancers (primarily breast, prostate, and ovarian cancers) are treated with aromatase inhibitors, a class of drugs designed specifically to block the production of aromatase, thereby decreasing levels of estrogen in patients.

Atrazine's widespread presence in drinking water and its action as a stimulator of cancer-promoting aromatase have lead cancer advocacy organizations to condemn the current regulatory standards (Breast Cancer Action, 2008, noting that Syngenta produces both atrazine and aromatase inhibiting drugs; National Breast Cancer Coalition, 2006). While the 2008 Lappano study demonstrates that atrazine promotes estrogen production by directly interfering with gene expression, epidemiological studies of atrazine exposure and breast or ovarian cancer incidence have been mixed. (See section on regulation below.)

For example, a 1997 study by the University of Kentucky found a small but statistically significant increase in break cancer risk with increasing levels of atrazine exposure, but the study authors did not conclude that atrazine directly promotes breast cancer. A subsequent study, also by the University of Kentucky, failed to confirm the association (Hopenhayn-Rich, et al, 2002). A 2006 study of California farm communities found a link between breast cancer risk and exposure to methoxychlor, another organochlorine herbicide, but not to atrazine (Mills and Yang, 2006).

Currently, neither the US EPA nor the World Health Organization's International Agency for Research on Cancer list atrazine as a human carcinogen.

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2 Full text of label restriction available online via University of Nebraska/Lincoln Cooperative Extension program: http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=2090&context=extensionhist (accessed April 26, 2010).