Ambient air pollution and incident dementia: exploration of relevant exposure windows

Melinda C. Power, Department of Epidemiology, Milken Institute School of Public Health, George Washington University, 950 New Hampshire Ave NW, Washington, DC, 20052, USA. Electronic address: power@gwu.edu.
Katie M. Lynch, Department of Epidemiology, Milken Institute School of Public Health, George Washington University, 950 New Hampshire Ave NW, Washington, DC, 20052, USA. Electronic address: kmlynch@gwu.edu.
Vixey Fang, Department of Epidemiology & Biostatistics, Texas A&M Health Science Center School of Public Health, 212 Adriance Lab Rd, College Station, TX, 77843, USA. Electronic address: vf91@tamu.edu.
Qi Ying, Zachry Department of Civil & Environmental Engineering, Texas A&M University, 400 Bizzell Street, College Station, TX, 77843, USA. Electronic address: qi.ying@gmail.com.
Eun Sug Park, Texas A&M Transportation Institute, Texas A&M University System, 3135 TAMU, College Station, TX, 77843, USA. Electronic address: e-park@tti.tamu.edu.
Richard L. Smith, Department of Statistics and Operations Research, University of North Carolina at Chapel Hill, 318 Hanes Hall, CB #3260, Chapel Hill, NC, 27599, USA; Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 135 Dauer Drive, 170 Rosenau Hall, CB #7400, Chapel Hill, NC, 27599, USA. Electronic address: rls@email.unc.edu.
James D. Stewart, Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 135 Dauer Drive, 2101 McGavran-Greenberg Hall, CB #7435, Chapel Hill, NC, 27599, USA. Electronic address: j.stewart@unc.edu.
Jeff D. Yanosky, Department of Public Health Sciences, College of Medicine, The Pennsylvania State University, 700 HMC Crescent Road, Hershey, PA, 17033, USA. Electronic address: jyanosky@pennstatehealth.psu.edu.
Eric A. Whitsel, Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 135 Dauer Drive, 2101 McGavran-Greenberg Hall, CB #7435, Chapel Hill, NC, 27599, USA; Department of Medicine, School of Medicine, University of North Carolina at Chapel Hill, 125 MacNider Hall, CB #7005, Chapel Hill, NC, 27599, USA. Electronic address: eric_whitsel@med.unc.edu.
Xiaohui Xu, Department of Epidemiology & Biostatistics, Texas A&M Health Science Center School of Public Health, 212 Adriance Lab Rd, College Station, TX, 77843, USA. Electronic address: xiaohui.xu@tamu.edu.

Document Type

Journal Article

Publication Date

9-12-2025

Journal

Environmental research

Volume

286

Issue

Pt 2

DOI

10.1016/j.envres.2025.122850

Keywords

Air pollution; Cognition; Dementia; Exposure windows

Abstract

BACKGROUND: As dementia has a decades-long preclinical phase, earlier air pollution exposures may be more etiologically relevant to dementia risk than more recent exposures. METHODS: We estimated exposures at Atherosclerosis Risk in Communities (ARIC) study participant addresses to criteria air pollutants, PM components, and trace metals in several exposure windows (1990-1994, 1995-1999, 2000-2004, 2005-2009, and 1990-2009) using a chemical transport model with observation data fusing at two resolutions, 4 km (CTM-4k) and finest available resolution (CTM-FR), and to PM, ozone, and NO using universal kriging with land-use regression and partial least squares regression (UK-LUR-PLSR). We estimated the association between each exposure/exposure window and incident dementia from ARIC Visit 5 (2011-2013) to Visit 7 (2018-2019). RESULTS: During follow-up (mean: 6.1 years) of 5,621 participants (mean baseline age: 76 years), 828 (14.7 %) developed dementia. Analyses did not support an association between most air pollutant exposures in any exposure window and incident dementia. However, we observed stronger associations in later time periods for PM, with significant associations in the latest time period with one exposure estimation approach: (HR (95 % CI) per 1 ug/m higher 2005-2009 p.m. exposure for CTM-FR: 1.11 (0.99, 1.25); CTM-4k: 1.07 (0.89, 1.22), UK-LUR-PLSR: 1.13 (1.03, 1.24). We saw similar patterns for NO, elemental carbon, Ni, and V. DISCUSSION: We found little evidence supporting the hypothesized greater etiologic relevance of earlier exposures on incident dementia. Spatial confounding or acceleration of pathologic processes may explain the stronger associations observed with later exposure windows.

Department

Epidemiology

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