31
Aug
Study Shows Atrazine Causes Prostate Inflammation and Delays Puberty
(Beyond Pesticides, August 31, 2010) As the Environmental Protection Agency (EPA) continues its review of the popular herbicide atrazine, a new study shows that male rats prenatally exposed to low doses of the gender-bending chemical are more likely to develop prostate inflammation and to go through puberty later than non-exposed animals. The research adds to a growing body of literature on atrazine, an herbicide used in agriculture, especially in corn and sugar cane production, and on golf courses and residential lawns. Atrazine and its byproducts are known to be relatively persistent in the environment, potentially finding their way into water supplies. It has been linked to a myriad of health problems in humans including disruption of hormone activity, birth defects, and cancer.
The research, “Effects of prenatal exposure to a low dose atrazine metabolite mixture on pubertal timing and prostate development of male Long-Evans rats,” which is available online and will be featured on the cover of Reproductive Toxicology (Vol. 30, # 4), found that the incidence of prostate inflammation went from 48 percent in the control group to 81 percent in the male offspring who were exposed to a mixture of atrazine and its breakdown products prenatally. The severity of the inflammation increased with the strength of the doses. Puberty was also delayed in the animals who received atrazine.
The doses of atrazine mixture given to the rats during the last five days of their pregnancy are close to the regulated levels in drinking water sources. The current maximum contamination level of atrazine allowed in drinking water is 3 parts per billion. The doses given to the animals were 0.09, 0.87 or 8.73 milligrams per kilogram body weight.
The research was led by Suzanne Fenton, PhD, and Jason Stanko, PhD, of the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. “We didn’t expect to see these kinds of effects at such low levels,” Dr. Fenton said. She adds that this is the second paper to show low dose effects of atrazine metabolite mixtures. Dr. Fenton was the senior author on a 2007 paper that demonstrated low doses of the atrazine mix delayed mammary development in female siblings from the same litters used in this current study.
“It was noteworthy that the prostate inflammation decreased over time suggesting the effects may not be permanent,” said David Malarkey, DVM, PHD, an NIEHS pathologist and co-author on the paper.
Dr. 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. The researchers say 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,” Dr. Fenton added. “The effects may be due to the stage of fetal development at the time the animals were exposed.”
In October 2009, EPA announced that it was launching a 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 the pesticide and whether new restrictions are necessary to better protect public health. The announcement followed recent scrutiny and findings that the current EPA regulation of atrazine in water is inadequate. Dr. Fenton will be presenting her research findings in September 2010 to EPA, as part of its reassessment of atrazine.
“We hope that this information will be useful to the EPA as it completes its risk assessment of atrazine,” said Linda Birnbaum, PhD, director of the NIEHS and National Toxicology Program.
For more information on atrazine, see the Pesticide Gateway. For more information on diseases linked to pesticide exposure, see the Pesticide-Induced Diseases Database.
