Background: Exposure to metals has been implicated in the pathogenesis of Parkinson disease (PD). 157503-18-9 manufacture to 1 1.33 (95% CI: 0.98, 1.79) for mercury. Conclusions: Overall, we found limited evidence for the association between adulthood ambient exposure to metals and risk of PD. The results for mercury need to be confirmed in long term studies. Citation: Palacios N, Fitzgerald K, Roberts AL, Hart JE, Weisskopf MG, Schwarzschild MA, Ascherio A, Laden F. 2014. A prospective analysis of airborne metallic exposures and risk of Parkinson disease in the Nurses Health Study Cohort. Environ Health Perspect 122:933C938;?http://dx.doi.org/10.1289/ehp.1307218 Introduction Parkinson disease (PD) is the second most prevalent neurodegenerative disorder, after Alzheimer disease (Lang and Lozano 1998). Exposure to metals has been implicated in the pathogenesis of PD. Manganese intoxication is recognized as a cause of parkinsonism at high levels of exposure (Guilarte 2010; Jankovic 2005). However, the pathology of manganese intoxication is definitely unique from that of PD (Jankovic 2005), and the causal association of exposure to manganese with PD continues to be debated (Fored et al. 2006; Fryzek et al. 2005; Mortimer et al. 2012). For example, a study that compared the food practices of 250 individuals and 388 settings found that a high manganese intake combined with a high intake of iron was significantly associated with PD (Capabilities et al. 2003). In another study in Quebec, Canada, a slightly higher although not statistically significant risk of PD was observed among participants with occupational exposure to manganese, iron, and aluminium (Zayed et al. 1990). At the same time, many studies of manganese and PD have been null (Hertzman et al. 1994; Seidler et al. 1996; Semchuk et al. 1993; Vieregge et al. 1995). There has also been some evidence 157503-18-9 manufacture of onset of PD following occupational (Coon et al. 2006; Kuhn et al. 1998) as well as nonoccupational (Weisskopf et al. 2010) exposure to high levels of lead. Improved brain iron levels have been found in PD individuals by some investigators, although this has not been confirmed in all studies (Logroscino et al. 1998, 2006, 2008). Some but not all studies possess reported positive associations between PD and exposure to copper (e.g., Gorell et al. 1997). Furthermore, mercury measured in blood, urine, and hair has been positively associated with PD (Ngim and Devathasan 1989). Cops5 To our knowledge, to day only two epidemiologic studies possess assessed exposure to airborne metals and PD in nonoccupational cohorts. A caseCcontrol study in Canada by Finkelstein and Jerrett (2007) reported a moderate association between airborne manganese and PD. In a study of U.S. Medicare beneficiaries, Willis et al. (2010) used county-level data from your U.S. Environmental Safety Agency (EPA) Toxic Launch Inventory (TRI) (U.S. EPA 2010b) on copper, lead, and manganese and found significant associations between residence in urban counties with high levels of launch of manganese and PD. In this study, we examined the association between census tractClevel air flow emissions of antimony, arsenic, cadmium, chromium, lead, manganese, mercury, and nickel, and risk of PD in a large prospective cohort of woman nurses. Methods and risk of PD among participants within the NHS (and risk of PD among participants within the NHS (and risk of PD among participants within the NHS (n?=?97,430) follow-up, 1990C2008, by quartile (Q) of each metal exposure stratified by county-level human population density low (250,000 ... Conversation With this prospective cohort study of woman nurses, we did not 157503-18-9 manufacture observe a statistically significant association between U.S. EPA HAP-modeled concentrations overall and risk of PD. In modified models, the HR for the highest compared with the lowest quartiles of each metallic ranged from 0.78 (95% CI: 0.59,.