By Brian Bienkowski and Marla Cone
Environmental Health News
Atrazine, one of the most widely used farm pesticides in the United States, has feminized frogs and other animals in some scientific studies. But research examining potential effects in people is relatively sparse.
A few studies have found possible connections between atrazine and higher rates of some birth defects and poor semen quality in men. Yet scientists say more human research is needed to reach any conclusions. “It pales in comparison to the animal research,” said Dr. Paul Winchester, an Indiana University professor of clinical pediatrics who studies the pesticide.
For more than half a century, U.S. farmers have used large volumes of atrazine to kill weeds, particularly in cornfields. The herbicide has been found in waterways and aquifers that supply drinking water. Syngenta, its manufacturer, says that the chemical is safe for both humans and wildlife at levels found in the environment.
But about a decade ago, researchers at University of California, Berkeley, found that low concentrations — the amount expected near farms — caused male tadpoles to turn into female frogs.
Follow-up studies in the wild found that atrazine either turned male tadpoles into females or “demasculinized” them, causing eggs to grow in their testes and rendering them unable to reproduce, said Tyrone Hayes, a UC Berkeley professor of biology who led the research.
The chemical can disrupt hormones and alter male reproductive tissues when an animal is exposed during development. Other impacts include a reduction in size at birth, according to 2005 and 2008 studies of amphibians and fish by University of Texas researchers.
And it’s not just frogs that might be at risk of being feminized — recent research has found that atrazine has similar hormonal effects on salmon, caimans and lab rats.
In addition, “it’s been shown to cause erratic behavior, like weird swimming patterns,” Hayes said. “Fish and frogs start swimming improperly, which has consequences — they can’t escape predators, they can’t find food.”
Syngenta disputes all these findings. The Swiss-based company particularly took issue with Hayes’ research, and cited follow-up studies that could not replicate his work and reported no feminizing effects on frogs. Peer-reviewed and published, the industry studies were conducted at two labs, and were funded by Syngenta after the U.S. Environmental Protection Agency asked the company in 2003 to perform more frog tests.
Hayes in 2004 wrote a paper slamming Syngenta’s studies, saying there were errors, such as high mortality of frogs and inappropriate measurements of hormone levels. He said due to those factors, their research cannot be compared with his. “All of the studies that say [atrazine] doesn’t have any effect come from industry. We’re all finding reproductive effects, except those who are getting paid [by Syngenta],” he said.
The field studies of frogs that couldn’t replicate Hayes’ findings used different, less-accurate methods, said Krista McCoy, a professor of biology at East Carolina University and co-author of a 2010 analysis of atrazine and wildlife research.
McCoy said the studies that didn’t find a link assumed that some ponds were clean and could be used as a reference site. When the researchers found similar abnormalities in frogs from the so-called “clean” site and polluted site, they reported no link to atrazine.
But “there’s no such thing as a clean control site where there’s no manmade chemicals,” McCoy said. “If you collect samples from a pond in an agricultural area and then go across the street to someone’s yard, well, the animals [in the non-agricultural pond] are probably exposed to the same chemicals due to runoff.”
McCoy’s analysis of previous research concluded that atrazine consistently affected reproductive development of male frogs in studies. But it’s unclear whether any animal populations are dropping due to possible effects from the herbicide.
Jason Rohr, a biology professor at the University of South Florida and co-author of that analysis, has some concerns about all of the atrazine research. “There are problems with some of Tyrone’s [Hayes] work, some of it is fantastic,” Rohr said. He wondered whether any variables were introduced in the Syngenta-funded studies that may skew the results.
In a 2007 review of the chemical, the EPA agreed with Syngenta and renewed the registration of atrazine, concluding that it was not harming frogs and other wildlife at levels found in the environment. “Based on the negative results of these studies, the Agency concludes that it is reasonable to reject the hypothesis that atrazine exposure can affect amphibian gonadal development,” the EPA said in its review.
Under federal law, “a pesticide must be found not to cause unreasonable risks to people or the environment” in order for the EPA to allow continued use. But the law also allows the EPA to take into “account the economic, social, and environmental costs and benefits of the use of the pesticide” when assessing “unreasonable risks.” Pesticides are reviewed every 15 years.
Europe banned atrazine in 2003 because of its widespread discovery in water supplies. But the EPA concluded that water containing atrazine at 3 parts per billion is safe to drink. The agency, however, has initiated another review of data collected since 2007 on both human and wildlife health.
One recent study offers clues to the mechanisms through which atrazine can harm animals and possibly humans.
Purdue University researchers found that zebrafish embryos exposed to atrazine at environmental levels showed changes in their genes. “The genes that were altered were associated with neuroendocrine, reproductive function in the fish,” said Jennifer Freeman, a toxicology professor at Purdue University who was the study’s senior author.
While the study didn’t examine whether these gene changes led to health problems, Freeman said it’s plausible that they could be behind some developmental and reproductive effects seen in wildlife. She said these genes work in similar ways in fish and humans.
The strongest evidence of a possible human effect is a study comparing men in a rural area of Missouri to men in three urban areas. The Missouri men with higher atrazine exposures were more likely to have poor semen quality, perhaps due to the chemical’s ability to alter sex hormones, according to the study published a decade ago. Similar effects were reported on the sperm of lab animals.
Another large study, conducted in France, showed babies exposed in the womb to atrazine are born weighing slightly less, by an average of five ounces.
The herbicide also has been linked to changes in breast tissue and birth defects in exposed lab rats, which are used to determine if the chemicals are a danger to humans.
Toxicologist Suzanne Fenton, a leading atrazine researcher at the National Institute of Environmental Health Sciences, said when mother rats are exposed to high doses of atrazine, their pups have developmental delays in mammary glands, which may increase susceptibility to breast cancer.
But the International Agency for Research on Cancer has concluded that there is “inadequate evidence” to say that atrazine causes cancer in humans, and the EPA reported in 2006 that it is “not likely to be carcinogenic to humans.”
“All of the human studies I know of have some issues,” Fenton said. “The hard part about atrazine work is that it has a really short half-life in humans/animals. Hard to measure accurately.”
Similar to rat studies, atrazine has been linked to some birth defects in humans. A study published this year that reviewed birth defect records in Texas found “modest, but consistent, associations” between boys’ genital defects and mothers who live near areas with atrazine. A 2007 study in Indiana found an increased rate of abdominal defects in children born in areas with higher atrazine levels in surface waters. Also, U.S. babies conceived in April through August, when farm chemicals including atrazine were at their highest amounts in water, had more birth defects, according to research by Winchester and colleagues.
However, all three of these birth defect studies had to estimate atrazine exposure, making it questionable whether the health impact was from the chemical and not from some other factor. For example, the scientists don’t know how much atrazine the mothers were actually exposed to; they just know they lived in areas where it was found in streams. Also, the study in France that did measure atrazine in mothers found no increase in birth defects in their children.
Winchester said his research linking agricultural months to birth defects “certainly doesn’t prove that atrazine causes birth defects…but we simply can’t rule it out as a cause.”
“We’re not looking for a fight [with Syngenta],” he said. “We’re just looking for answers.”
Diana Jean Schemo
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