Pesticides and Parkinson’s Disease in Rats

A new study released at a meeting of the Society for Neuroscience on Monday, Nov. 6, shows that a certain species of rat develops a clinical and neurological syndrome almost identical to human Parkinson’s disease when exposed intravenously to a “natural” pesticide called rotenone.

Parkinson’s disease is one of the more common neurological diseases in Americans, affecting perhaps 1 million people, and a large majority is over age 60. However, the disease can strike at a younger age, as it has actor Michael J. Fox and former boxing champion Muhammad Ali. Genetic factors account for a small portion of affected patients, but in general the disease strikes unpredictably.

The new study’s authors, a group from Emory University, administered modest doses of rotenone, a natural or “organic” pesticide derived from plant roots, intravenously to rats, continuously over a period of four to five weeks. About half of the study rodents developed traits similar to humans with Parkinson’s: tremors, slow and unstable gait, and muscle rigidity. On autopsy, the rats’ brains also showed characteristic changes compatible with those seen in the post-mortem exams of Parkinson’s patients.

Some scientists and environmentalists used this report to attack pesticides, and environmental chemicals in general, as a cause of Parkinson’s. The facts do not so indicate, by any means. The substance involved, rotenone, was given intravenously and continuously — an exposure not related to human exposure in any meaningful way. And while the doses given were “modest” by rodent-testing standards, they were still far beyond any conceivable human exposure level. A different rat species proved not to be susceptible to the disease-producing effects of the rotenone, despite a much higher exposure dose. The authors themselves acknowledge there have never been any test animals that have developed Parkinson’s disease on oral exposure to pesticides at any dose.

So, what is the lesson to be learned? For one thing, while the production of this animal model for Parkinson’s may well prove to be a tremendous accomplishment, as it may allow testing for possible therapies to treat or even prevent the condition, to extrapolate an association between all human Parkinson’s disease and pesticide exposure from this data is completely unwarranted.

There is currently no proof, or even a basis for speculation, that a cause-effect relationship exists between pesticides and human Parkinson’s. Even if further study were to implicate rotenone in the causation of some Parkinson’s cases, there would be no reason to generalize from that to a widespread effect of all pesticides. The plants themselves produce the large majority of pesticides, while those under attack by “environmental” groups tend to be synthetic. But as this study reiterates that natural does not equal safe, just as synthetic does not equal toxic.

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