A student of environmental science would be hard pressed to find a more contentious topic than the environmental effects of atrazine. On the one hand, atrazine's manufacturer, Syngenta, can point to a body of research finding no significant correlations between low-level atrazine exposure and disease in humans or animals. On the other hand, there is a significant and growing body of evidence that atrazine is an endocrine disrupter and causes both disease and developmental injury in aquatic fauna.

Atrazine is known to be immediately toxic to most of the animals studied (rats, mice, birds, and rabbits) only at relatively high doses (e.g. over 1000 mg/kg of body weight), with the exception of ruminants (cows and sheep), which succumb at far lower doses (EXTOXNET profile). These were laboratory toxicity tests designed to discover lethal doses. It wasn't until researchers began to examine the effects of atrazine at the much lower concentrations likely to exist in the vicinity of croplands, and on aquatic animals likely to be exposed, that the connection between atrazine and endocrine disruption in amphibians was noted. This effect received widespread media attention when a few widely publicized studies reported evidence that atrazine was causing male tadpoles to develop into female frogs (for example, Hayes, et al., 2003), an effect branded "chemical castration." Subsequent studies have been mixed, some failing to reproduce the original findings, while others confirmed the results, or confirmed them only at exposures many times the EPA limit, or only within limited populations.
 
A 2008 meta-analysis set out to resolve the inconsistencies by reviewing all relevant field and laboratory studies and weighting the studies by selected quality criteria (Solomon, et al., 2008). That paper concluded that the "vast majority" of the evidence failed to support a conclusion that environmentally typical atrazine exposures were harming fish or amphibians, or that atrazine is an aromatase promoter. The analysis was immediately attacked by scientists involved in the research on two grounds: first, that the meta-analysis itself was funded by Syngenta (and the researchers cited recent studies demonstrating that industry-financed scientific studies tend to understate negative research and overstate favorable results). Second, they discovered numerous mischaracterizations in the report's summary of existing research (Rohr and McCoy, 2010, pp. 21-22), noting that the mis-statements followed the trend described in the industry bias studies: namely, that the vast majority of misleading statements favored Syngenta (Raloff, 2010).

In 2010, a fresh meta-analysis was performed, this time enumerating a host of demonstrated adverse effects on amphibians, including immune suppression and sex organ abnormalities. It also reviewed research on the biochemical mechanisms believed to underlie the effects (Rohr and McCoy, 2010). Among the misleading statements identified by the 2010 authors was a study concluding that atrazine caused no harmful changes below 100 parts per billion, although the study data itself showed harmful effects at concentrations as low as 10 parts per billion (Raloff, May 6, 2010). But the 2010 analysis also found only weak or preliminary evidence of a chemical castration effect (Rohr and McCoy, 2010, p. 27).

What accounts for the discrepant results of these two meta-analyses? Both studies reviewed hundreds of peer-reviewed research articles and related reports, but used different criteria in arriving at their conclusions. The 2008 analysis, when evaluating studies showing harmful effects of atrazine, discounted studies that lacked independent support for the observational conclusions, such as a proposed mechanism of action, or evidence of a dose-dependent response (in which higher doses result in more severe effects). The 2010 analysis, in contrast, reviewed the data underlying the studies more closely, but weighted outcomes based on statistical significance, without regard to whether a mechanism of action had been investigated or proposed.

The 2010 analysis also contained a persuasive explanation for conflicting results, based on amphibian physiology and the varying effects of hormonal disturbance at different life cycle stages (i.e., that exposure to a given chemical can produce an effect, or its opposite, depending on the time of exposure). For example, their report explained that exposure to toxic chemicals at one stage of tadpole development can retard its physical transition to frog, while exposure at a later point where body mass is higher can actually speed maturation. Consequently, the result of the exposure can have opposing effects depending on the timing, and therefore studies showing opposing effects don't "cancel" one another out, as suggested by the 2008 analysis.

It would be fair to say that neither analysis resolved the controversy, an outcome to be expected in a body of research that may not be funded as well as, for example, pharmaceutical and biotechnology research, and consequently where studies may be disproportionately affected by the sources of funding. If anything, the 2008 and 2010 analyses underscore that the debate remains in the political realm, as a matter of risk tolerance in the face of conflicting data.

(Photo: American Leopard Frog, Rana pipiens. This is the species used in the 2003 study by Hayes, et al.)

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