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Science News

Lingering Pesticides Linked to Parkinson's

Past exposure to low levels of pesticides that linger in the environment might accelerate the development of Parkinson's, which would put baby boomers and millions of other aging Americans at risk of developing the brain disease earlier in life.

At the American Chemical Society meeting in San Francisco last week, researchers presented new findings that link Parkinson's to exposure to the pesticides dieldrin and DDT. The federal government banned the toxins in the 1970s, but low levels still linger in the soil, says lead researcher Gary Miller of Emory University in Atlanta. Miller's research focused on how exposure to the pesticides from years ago affected the later development of Parkinson's.

"If you're exposed to a pesticide like dieldrin, you might be diagnosed (with Parkinson's) at age 70 instead of at 80," Miller says.

The preliminary report at the ACS meeting fits with evidence from a large study published in July that suggests that exposure to pesticides might increase the risk of developing the degenerative brain disease, which often is diagnosed after age 60. That report didn't zero in on a specific pesticide, but Miller and his colleague Kurt Pennell at the Georgia Institute of Technology did.

The team examined brain tissue taken from 14 Parkinson's patients and 12 people who did not have the disease. They found that levels of dieldrin were three times higher in the brain tissue taken from the Parkinson's patients. That tissue also had the same high levels of a breakdown product of DDT.

A second report by the same team helps explain how pesticides might injure the brain. Miller and Pennell gave small doses of dieldrin to laboratory mice. After only a month, the team found that the pesticide increased the amount of brain damage done by free radicals, highly reactive molecules that are a byproduct of metabolism.

The team found evidence that free radicals had damaged certain brain cells that produce dopamine, a neurotransmitter that plays a key role in Parkinson's disease. People who sustain damage to these same brain cells start to develop the symptoms of Parkinson's, such as a shuffling walk, Miller says.

He believes Parkinson's is kicked off by a combination of factors, including genes, but then the disease speeds up as a result of exposure to pesticides such as dieldrin.

The findings add to others that have linked pesticides to Parkinson's, including a study of more than 143,000 people conducted by researcher Alberto Ascherio of the Harvard School of Public Health and published in the July issue of the Annals of Neurology. He found that people who had reported exposure to pesticides had a 70% greater risk of Parkinson's.

Ascherio says pesticides still in use, such as those for a home garden, also might pose some risk to these sensitive brain cells. To be safe, he says, "people should limit their exposure."

Source: USA Today www.usatoday.com/news/health/2006-09-17-parkinsons_x.htm

Commentary from the Parkinson's Disease Foundation (PDF)

Pesticides and Parkinsonís Disease: Focus on Dieldrin

Over the past two decades, several studies have shown associations between pesticide use or industrialized farming and Parkinsonís disease. In most studies, the prevalence of pesticide exposure was low overall, and most scientists have not proposed that pesticides cause Parkinson's disease by themselves. Rather, most studies suggest that pesticides may increase an individualís vulnerability to earlier disease onset or add an extra risk factor to a patient who is already vulnerable to loss of dopamine in the brain from factors such as genetic predisposition or other environmental exposures. MPTP, the classic toxin used to induce experimental parkinsonism in the laboratory, was originally developed as a potential pesticide, but never marketed.

A recent, more focused effort to study different types of pesticides has led to several evaluations of an compound called dieldrin, an organochloride developed in the 1940s and widely used in the mid-20th century. This chemical is no longer utilized in the United States, but it is very slowly removed from the body and the environment, making it a potential long-term toxin that could contaminate food products and eventually affect humans. This year, JR Richardson and investigators at Emory University published a report in which they documented that early life exposure to dieldrin in animals increased the toxicity of MPTP, the chemical utilized in the laboratory to induce chemical changes typical of Parkinson's disease. The authors suggested that low-level exposure early in life to dieldrin alters the dopamine system in the brain and renders the dopamine cells more vulnerable to later damage in life. The exact mechanism of this vulnerability is yet to be defined, but may involve inhibition of the importance proteasome system, as demonstrated by XF Wang and workers at University of California, Los Angeles. The background of concern for dieldrin and other pesticides in relation to Parkinson's disease has recently been summarized in a 2005 review article by AG Kanthasamy and colleagues in the journal Neurotoxicology.

Most recently, PDF received a press release related to the annual meeting of the American Chemical Society in San Francisco (September 2006). G. Miller and Emory University colleagues report that patients who died with Parkinsonís disease had dieldrin brain levels three times higher than in people without Parkinson's disease. Because this report directly relates to dieldrin and Parkinson's disease in humans, PDF shares this new information with our patients, families and physicians, but recognizes that the information has not yet been reviewed officially for scientific merit by our medical experts. Nonetheless, the report is particularly interesting because it deals with Parkinson's disease itself and not simply animal models of Parkinson's disease and it fits well with the findings of many of the cited scientific papers. Most importantly, the findings may be contribute to the overall theory that environmental exposures and influences can increase the vulnerability of individuals to Parkinson's disease and help understand the question of how some people become afflicted with the disease whereas others do not.

Christopher G. Goetz, MD, Chicago Chair, PDF Medical Policy Subcommittee

Suggested readings: Goetz CG, Lewis SL. "Pesticides" (pp. 1531-1538). In: Neurological Therapeutics: Principles and Practice, ed. JH Noseworthy. London, Martin Dunitz, 2003.

Kanthasamy AG, Kitazawa M, Kanthasamy A, Anantharam V. "Dieldrin-induced neurotoxicity: relevance to Parkinson's disease pathogenesis." Neurotoxicology 2005;26:701-719.

Richardson SR, Caudle WM, Wang M, Dean ED, Pennell KD, Miller GW. "Developmental exposure to the pesticide dieldrin alters the dopamine system and increases neurotoxicity in an animal model of Parkinson's disease." FASEB J 2006;20:1695-1697.

Wang XF, Li S, Chou AP, Bronstein JM. "Inhibitory effects of pesticides on proteasome activity: implication in Parkinson's disease." Neurobiol Dis 2006;23:198-205.

Source Date: Sep 17 2006
Source Publication: USA TODAY
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