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A Population-Based Case-Control Study

Jordan A. Firestone, MD, PhD, MPH; Terri Smith-Weller, MN, COHN; Gary Franklin, MD, MPH; Phillip Swanson, MD, PhD; W. T. Longstreth, Jr, MD, MPH; Harvey Checkoway, PhD

Arch Neurol. 2005;62:91-95.

Background  Pesticide exposures are suspected risk factors for Parkinson disease (PD), but epidemiological observations have been inconsistent.

Objective  To investigate associations between pesticide exposures and idiopathic PD.

Design  Population-based case-control study.

Setting  Group Health Cooperative, a health care system in western Washington State, and the University of Washington.

Participants  Two hundred fifty incident PD case patients and 388 healthy control subjects (age- and sex-matched). We assessed self-reported pesticide exposures using a structured interview. Odds ratios (ORs) and 95% confidence intervals (CIs) were determined using logistic regression models, controlling for age, sex, and smoking.

Results  Odds ratios for occupational exposures were not significant but suggested a gradient that paralleled occupational exposures (pesticide worker: OR, 2.07; 95% CI, 0.67-6.38; crop farmer: OR, 1.65; 95% CI, 0.84-3.27; animal and crop farmer: OR, 1.10; 95% CI, 0.60-2.00; and dairy farmer: OR, 0.88; 95% CI, 0.46-1.70). Odds ratios for organophosphates paralleled the World Health Organization hazard classifications, with parathion much higher than diazinon or malathion. We also found elevated ORs from herbicides (OR, 1.41; 95% CI, 0.51-3.88) and paraquat (OR, 1.67; 95% CI, 0.22-12.76). We found no evidence of risk from home-based pesticide exposures. We found significantly increased ORs from lifelong well water consumption (OR, 1.81; 95% CI, 1.02-3.21).

Conclusions  The findings for occupational pesticide exposures are consistent with a growing body of information linking pesticide exposures with PD. However, the lack of significant associations, absence of associations with home-based exposures, and weak associations with rural exposures suggest that pesticides did not play a substantial etiologic role in this population.

Author Affiliations: Departments of Neurology (Drs Firestone, Franklin, Swanson, and Longstreth), Environmental and Occupational Health Sciences (Ms Smith-Weller and Drs Franklin and Checkoway), and Epidemiology (Drs Longstreth and Checkoway), University of Washington, Seattle.

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