Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25-29, 2009: Symposium Abstracts: Symposia Presentations
*National Institute of Environmental Health Sciences, Research Triangle Park NC, United States; †Parkinson's Institute, Sunnyvale CA, United States; ‡National Cancer Institute, Rockville MD, United States; §Westat Inc, Durham NC, United States; and ¶Pacific Health Research Institute, Honolulu HI, United States.
Abstracts published in Epidemiology have been reviewed by the organizations of Epidemiology. Affliate Societies at whose meetings the abstracts have been accepted for presentation. These abstracts have not undergone review by the Editorial Board of Epidemiology.
Background and Objective:
Pesticide exposure may increase PD risk, but detailed data are lacking. Using data from the AHS, an ∼89,000 member cohort of licensed pesticide applicators and their spouses enrolled in Iowa and North Carolina in 1993–1997, we found that self-reported PD was associated with cumulative lifetime use of pesticides and with factors affecting pesticide exposure, including high-intensity exposures and inadequate use of personal protective equipment. Because this study was limited by reliance on self-reported PD, we conducted a further study based on confirmed diagnoses.
The Farming and Movement Evaluation (FAME) study is a case-control study of PD nested within the AHS. PD diagnoses were confirmed by movement disorder specialists. We enrolled 115 confirmed PD cases and 383 age-, sex-, and state-matched controls. Using structured interviews, we collected information on lifetime use of pesticides implicated in PD by prior human studies or by experimental models or mechanistic hypotheses. We collected additional information on other factors affecting exposure, including application methods and use of personal protective equipment. Data were analyzed by unconditional logistic regression with adjustment for age, sex, state, and cigarette smoking.
We found that PD risk was associated with exposure to specific pesticides and confirmed and extended our earlier work on factors affecting exposure.
These results add to evidence supporting an association between pesticide exposure and PD risk. They recapitulate experimental models and may shed light on mechanisms involved in PD pathophysiology.