METHODS Available biochemical and toxicological data on some pesticides, particularly on paraquat, are discussed to help in the evaluation of epidemiological data.
RESULTS The nigrostriatal system is particularly sensitive to oxidative damage, caused by different mechanisms and agents. Thus the epidemiological evidence that Parkinson’s disease is an environmental disease is biologically plausible. Experimental animal studies have been conducted with a high single or a few doses of pesticide, and have been followed up for days or weeks after treatment. Experimental data indicate additive/synergistic effects of different pesticides that act on different targets within the dopaminergic system, and other brain areas. In these conditions and to a different extent, certain pesticides cause neurotoxic effects that may suggest a possible role in the development of a PD-like syndrome in animals. Although no single chemical can reproduce all the characteristics of PD, these data can be of help for understanding the role of pesticide exposure in human PD development. It should be noted that farmers are exposed for days or weeks during several years to much lower doses than those used in experimental studies.
DISCUSSION Consequently, a firm conclusion on the role of pesticide exposure on the increased risk of developing PD cannot be drawn. Useful information may be obtained by close follow up of survivors of acute poisonings by these pesticides, or identification in epidemiological studies of such subjects or of those reporting episodes of accidentally high exposure. Evaluation of exposure to multiple pesticides, not necessarily at the same time, in epidemiological studies, might also provided additional relevant information.