Pesticide exposure could increase risk of early onset of Parkinson's disease (press release)

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Low-level exposure to a banned but lingering pesticide appears to accelerate changes in the brain that can potentially lead to the onset of Parkinson's disease symptoms years or even decades before they might naturally develop. This finding, by researchers at Emory University and the Georgia Institute of Technology in Atlanta, was presented today at the 232nd national meeting of the American Chemical Society, the world's largest scientific society.

The concept of an accelerated disease process is a new twist in the investigation of the long-suspected link between the use of pesticides and Parkinson's disease, according to the researchers.

"Our current study clearly shows that pesticides such as dieldrin appear to accelerate or exacerbate the already underlying disease," said Gary Miller, Ph.D., an associate professor of environmental and occupational health at Emory University. "Pesticides aren't necessarily the causative agents, but they do promote Parkinson's. So it appears the more you are exposed to pesticides, the greater your risk of developing the disease earlier in life."

In their pilot study, Miller and his co-researchers -- Emory graduate student Jaime Hatcher and Georgia Tech Professor Kurt Pennell, Ph.D. -- found that levels of dieldrin, an organochlorine pesticide developed in the 1940s as an alternative to DDT, were three times higher in the brains of 14 people who had Parkinson's disease than in the brains of 12 people who didn't.

Based on this finding, the researchers estimated the lifetime exposure levels of these people and extrapolated these levels to mice. They then exposed laboratory mice to low, but "environmentally relevant" dosages of dieldrin - about 1 to 3 milligrams per kilogram. After one month, although none of the mice showed symptoms of Parkinson's disease, the researchers did detect increased levels of oxidative stress in the brain and significantly reduced uptake of dopamine, the neurotransmitter that plays a key role in the development of Parkinson's.

This latest work adds more evidence establishing a link between pesticides and Parkinson's. Earlier this year, a Harvard School of Public Health study of more than 140,000 adults found that those exposed to long-term, low levels of pesticides had a 70 percent higher incidence of Parkinson's disease. Another recent study, by the same Emory/Georgia Tech team, found that fetal rodents exposed to dieldrin had brain alterations that made them more susceptible to Parkinson's-inducing toxins.

"All of the evidence that has been accumulating suggests that exposure to pesticides increases the risk of Parkinson's disease," Miller said. "We believe that a person who is destined to get Parkinson's because of genetics or other factors at age 80 might develop symptoms when they're 65 or 70 if they have been exposed to pesticides."

Dieldrin, which was most commonly used to control agricultural pests and termites, was banned for most uses by the Environmental Protection Agency in 1974 after it was found to be harmful to fish and other wildlife. It was totally banned in 1987. Although no longer used, dieldrin can persist in the environment for decades and move up through the food chain, particularly in dairy products and meats, to humans, Pennell said.

Over the next few decades, however, dieldrin and other banned pesticides should dissipate in the environment and become less of a factor in the development of Parkinson's disease, according to Miller.

"Today, people are being exposed to much lower levels of pesticides than people were 30 or 40 years ago," Miller said. "I would predict that over the course of the next several decades that we will see a decrease in the incidence of Parkinson's disease."

At least 500,000 Americans have Parkinson's disease and about 50,000 new cases are diagnosed each year, according to the National Institute of Neurological Disorders and Stroke. The disease occurs when certain nerve cells die or become impaired and can no longer produce dopamine.

Contact: Michael Bernstein m_bernstein@acs.org 415-978-3532 (San Francisco, CA, Sept. 10-14, 2006) 202-872-4400 (Washington, DC) American Chemical Society

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