Incident Dementia and Long-Term Exposure to Constituents of U.S. Fine Particle Air Pollution: A National Cohort Study

LIUHUA SHI, Qiao Zhu, Yifan Wang, Hua Hao, Haisu Zhang, Aaron van Donkelaar, Randall Martin, Heresh Amini, Kyle Steenland, Jeremy A. Sarnat, Howard Chang, Jeremiah Liu, Tszshan Ma, Haomin Li, William M. Caudle, Rodney J. Weber, Pengfei Liu, Emory University

     Abstract Number: 47
     Working Group: Health-Related Aerosols

Abstract
Background: Growing evidence has suggested that PM2.5 likely increases the risks of neurological disorders, yet little is known about the relative contributions of different constituents. Understanding constituent-specific effects are critical to targeting emissions reductions of specific sources with the greatest health protection.

Method: We conducted a nationwide population-based cohort study (2000-2017), by leveraging the Medicare Chronic Conditions Warehouse database and two sets of high-resolution, multiple-species, air pollution datasets to investigate the impact of long-term exposure to PM2.5 constituents on incident dementia and Alzheimer’s disease (AD). Incident dementia and AD were identified from Medicare claims (2000-2017), including inpatient and outpatient claims, carrier file (primarily doctor visits), skilled nursing facility, and home health-care claims. Hazard ratios for dementia and AD were estimated using single- and multi-constituent Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration-response relationships. We further tested effect modifications by individual- and community-level characteristics.

Results: Of the 18.5 million dementia and 19.2 million AD cohorts, 31.5% and 14.6% developed dementia and AD events, respectively. From the single-pollutant models, an interquartile range (IQR) increase in PM2.5 mass was associated with an increase in dementia incidence ranging between 6.3 (95% CI: 5.8%-6.7%) to 6.6% (95% CI: 6.2%-7.1%) by using two exposure datasets. For different PM2.5 constituents, associations remained significant in black carbon (BC), organic matter (OM), sulfate (SO42−), and ammonium (NH4+) for both endpoints. Increases in exposure to SO42− and BC per IQR, and increase in exposure to BC per 1 µg/m3, had the strongest associations with incident dementia or AD. There was linearity in the concentration-response (C-R) relationship for BC, SO42−, and NH4+ with both endpoints. The C-R relationships for OM, DUST, and NO3− also show an essentially linear association with both endpoints until high, and less frequently occurring concentrations.

Conclusion: Our study suggests that long-term exposure to PM2.5 is significantly associated with increased incident dementia and AD, and that different constituents have different neurotoxicity. Reduction of PM2.5 emissions, especially for main sources of black carbon and sulfate, may reduce the burden of dementia or AD in the aging United States population.