Traffic-related air toxics and Parkinson's disease in California's Central Valley.

Growing evidence links air pollution to Parkinson's disease (PD), yet most research focuses on criteria pollutants like nitrogen dioxide (NO2) and fine particulate matter (PM2.5), which cannot pinpoint specific toxic constituents driving the association. This population-based case-control study from the counties of Fresno, Tulare, and Kern in central California (764 patients, 798 controls) investigated whether specific air toxics - metals with mobile-source/industrial contributions (nickel, zinc), vehicle-exhaust volatile organic compounds (benzene, 1,3-butadiene), and industrial/urban metals (lead, chromium) - are associated with PD. Using land-use regression models linked to participants' full residential and workplace address histories, we estimated 10-year, 5-year, and 1-year average pollutant exposures preceding diagnosis (patients) or interview year (controls). Associations were assessed via logistic regression, adjusting for sociodemographics and pesticide exposure. For nickel we estimated the strongest and most consistent effect across all averaging periods, with a 10-year residential odds ratio (OR) of 1.63 (95% CI = 1.04-2.55) and a nearly three-fold increase in the odds of PD due to ambient exposure at the workplace (OR = 2.89, 95% CI = 1.48-5.80) per interquartile range increase. Zinc showed a positive 10-year residential address association (OR = 1.42, 95% CI = 0.98-2.10). The volatile organic compounds benzene (5-year workplace OR = 1.83, 95% CI = 1.16-2.93) and 1,3-butadiene (1-year workplace OR = 4.56, 95% CI = 2.86-7.49) exhibited stronger associations at shorter averaging windows, particularly at workplace addresses. In co-pollutant models, air toxics associations persisted after adjustment for NO2 or PM2.5, while criteria pollutant associations attenuated. No associations were observed for lead or chromium in these predominantly agricultural counties. Our findings highlight that traffic-related and industrial air toxics from both non-exhaust and exhaust sources may contribute to PD risk, underscoring the importance of evaluating pollutant sources and components when assessing environmental determinants of PD.