Literature DB >> 15642854

Pesticides and risk of Parkinson disease: a population-based case-control study.

Jordan A Firestone1, Terri Smith-Weller, Gary Franklin, Phillip Swanson, W T Longstreth, Harvey Checkoway.   

Abstract

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.

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Year:  2005        PMID: 15642854     DOI: 10.1001/archneur.62.1.91

Source DB:  PubMed          Journal:  Arch Neurol        ISSN: 0003-9942


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