Volume 18, Issue S11 e067071
PUBLIC HEALTH
Free Access

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

Liuhua Shi

Corresponding Author

Liuhua Shi

Emory University, Atlanta, GA, USA

Correspondence

Liuhua Shi, Emory University, Atlanta, GA, USA.

Email: [email protected]

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First published: 20 December 2022

Abstract

Background

Growing evidence suggests 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 emission reductions of specific sources with the greatest health protection.

Method

We conducted a nationwide population-based cohort study (2000-2017), by integrating 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). 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.

Results

Of the 18.5 million dementia and 19.2 million AD individuals within these 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 6-7% using two exposure datasets. For different PM2.5 constituents, associations remained significant in black carbon (BC), organic matter (OM), sulfate (SO4 2−), and ammonium (NH4 +). Incident dementia was observed to have the strongest association with increases in exposure to SO4 2− and BC (10-11% increase and 4-6% per IQR increase, respectively). Effect estimates for AD were even larger. For both endpoints, all constituents had largely linear concentration-response relationships in the low exposure range, but most tailed off at high exposure concentrations, particularly for AD.

Conclusion

Our study suggests that long-term exposure to PM2.5 is significantly associated with increased incident dementia and AD, and that the different PM2.5 constituents may elicit differential neurotoxicity. Reduction of PM2.5 emissions, especially for the main sources of BC and SO4 2−, may reduce the burden of dementia or AD in the aging US population.