Pesticides and Parkinson's disease--is there a link?

Abstract

Parkinson's disease (PD) is an idiopathic disease of the nervous system characterized by progressive tremor, bradykinesia, rigidity, and postural instability. It has been postulated that exogenous toxicants, including pesticides, might be involved in the etiology of PD. In this article we present a comprehensive review of the published epidemiologic and toxicologic literature and critically evaluate whether a relationship exists between pesticide exposure and PD. From the epidemiologic literature, there does appear to be a relatively consistent relationship between pesticide exposure and PD. This relationship appears strongest for exposure to herbicides and insecticides, and after long durations of exposure. Toxicologic data suggest that paraquat and rotenone may have neurotoxic actions that potentially play a role in the development of PD, with limited data for other pesticides. However, both the epidemiology and toxicology studies were limited by methodologic weaknesses. Particular issues of current and future interest include multiple exposures (both pesticides and other exogenous toxicants), developmental exposures, and gene-environment interactions. At present, the weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists but is insufficient for concluding that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined pesticide and other exogenous toxicant exposure.

Figure 1

Forest plot of case–control studies examining pesticide exposure and the risk of developing PD. (a) Results taken from meta-analysis of Priyadarshi et al. (2000). (b) Unmatched calculation; figures unavailable for matched analysis. (c) Adjusted OR. (d) Assuming no missing responses and using cardiovascular patient control group. (e) Exposure to pesticides and fertilizers.

Figure 2

Forest plot of case—control studies looking at exposure to specific groups of pesticides or individual pesticide compounds and the risk of developing PD. (a) Adjusted OR. (b) Results taken from the meta-analysis of Priyadarshi et al. (2000). (c) Men only; cases compared with control group of patients with chronic cardiovascular disease. (d) Cases compared with regional controls. (e) OR recalculated from data presented.

Figure 3

Potential mechanisms involved in the development of PD. Pathways are considered interdependent and are not necessarily mutually exclusive. Adapted from Betarbet et al. (2002).