"It was noteworthy that the prostate inflammation decreased over time, suggesting the effects may not be permanent," said David Malarkey, D.V.M., Ph.D., an NIEHS pathologist and co-author on the paper.
Fenton points out that these findings may extend beyond atrazine alone, and may be relevant to other herbicides found in the same chlorotriazine family, including propazine and simazine. All three of the herbicides create the same set of breakdown products.
Fenton says more research is needed to understand the mechanism of action of the chlorotriazines and their metabolites on mammary and prostate tissue. "These tissues seem to be particularly sensitive to the effects of atrazine and its breakdown products," Fenton added. "The effects may be due to the stage of fetal development at the time the animals were exposed."
"We hope that this information will be useful to the EPA, as it completes its risk assessment of atrazine," said Linda Birnbaum, Ph.D., director of NIEHS and the National Toxicology Program.
Fenton will be presenting her research findings in September to the EPA, as part of its reassessment of atrazine. EPA announced in 2009 that it had begun a comprehensive new evaluation of atrazine to determine its effects on humans. At the end of this process, the agency will decide whether to revise its current risk assessment of atrazine and whether new restrictions are necessary to better protect public health. For more information about the EPA risk assessment, please visit http://www.epa.gov/pesticides/reregistration/atrazine/atrazine_update.htm.
|Contact: Robin Mackar|
NIH/National Institute of Environmental Health Sciences