Associations of Ozone and PM2.5 Concentrations with Parkinson’s Disease Among Participants in the Agricultural Health Study

Background: Evidence from experimental studies suggests that exposure to air pollution may be associated with risk of Parkinson’s disease (PD). Objective: To evaluate associations of ambient ozone and fine particulate matter (PM2.5 – particulate matter with an aerodynamic diameter ≤2.5 microns) with PD. Methods: We used data from the Agricultural Health Study, a cohort of pesticide applicators and their spouses enrolled from 1993-1997 in Iowa and North Carolina. Cases reported physician-diagnosed PD at enrollment or through follow-up ending in 2010 (n=301). PD cases were compared to participants who did not report PD (n=83,042), using logistic regression models adjusted for age, sex and smoking. We used daily predicted concentrations that were estimated using both modeled and measured PM2.5 and ozone concentration data to derive several surrogates of long-term exposure. Cohort members’ geocoded addresses were linked to annual average (2005) or 4-year average (2002-2005) pollutant concentrations. Warm season average concentrations (April – October) were also computed for ozone. Results: Both the concentrations and the spatial variability of PM2.5 and ozone were greater in North Carolina than in Iowa. In North Carolina we observed positive associations of PD with ozone (e.g., adjusted Odds Ratio [OR] =1.7; 95% Confidence Interval [CI]: 1.0, 3.2, comparing highest quartile 4-year warm season average ozone concentration to the lowest) and PM2.5 (e.g., adjusted OR=1.8; 95% CI: 1.0, 3.3, comparing the highest quartile annual average PM2.5 concentration to the lowest). In Iowa, we observed null associations of PD with both ozone and PM2.5. Conclusions: The results for North Carolina provide limited evidence for an association between air pollution and PD risk in humans. These findings are consistent with experimental data demonstrating that exposure to air pollution damages the substantia nigra, one of the regions of the brain involved in PD pathogenesis. Lack of clear concentration-response relationships, however, suggests the need for confirmation in additional populations. Further research should also explore whether modeled pollutant concentrations are adequate surrogates for long-term exposure.


Kirrane, E., C. Bowman, Allen Davis, J. Hoppin, A. Blair, H. Chen, M. Patel, D. Sandler, C. Tanner, L. Vinikoor-Imler, M. Ward, Tom Luben, AND F. Kamel. Associations of Ozone and PM2.5 Concentrations with Parkinson’s Disease Among Participants in the Agricultural Health Study. JOURNAL OF OCCUPATIONAL AND ENVIRONMENTAL MEDICINE. Lippincott Williams & Wilkins, Philadelphia, PA, 57(5):509-517, (2015).