Leukocyte Traits and Exposure to Ambient Particulate Matter Air Pollution in the Women's Health Initiative and Atherosclerosis Risk in Communities Study.

Published

Journal Article

BACKGROUND: Inflammatory effects of ambient particulate matter (PM) air pollution exposures may underlie PM-related increases in cardiovascular disease risk and mortality, although evidence of PM-associated leukocytosis is inconsistent and largely based on small, cross-sectional, and/or unrepresentative study populations. OBJECTIVES: Our objective was to estimate PM-leukocyte associations among U.S. women and men in the Women's Health Initiative and Atherosclerosis Risk in Communities study ( n = 165,675 ). METHODS: We based the PM-leukocyte estimations on up to four study visits per participant, at which peripheral blood leukocytes and geocoded address-specific concentrations of PM ≤ 10 , ≤ 2.5 , and 2.5 - 10 μ m in diameter ( PM 10 , PM 2.5 , and PM 2.5 - 10 , respectively) were available. We multiply imputed missing data using chained equations and estimated PM-leukocyte count associations over daily to yearly PM exposure averaging periods using center-specific, linear, mixed, longitudinal models weighted for attrition and adjusted for sociodemographic, behavioral, meteorological, and geographic covariates. In a subset of participants with available data ( n = 8,457 ), we also estimated PM-leukocyte proportion associations in compositional data analyses. RESULTS: We found a 12   cells / μ L (95% confidence interval: - 9 , 33) higher leukocyte count, a 1.2% (0.6%, 1.8%) higher granulocyte proportion, and a - 1.1 % ( - 1.9 % , - 0.3 % ) lower CD 8 + T-cell proportion per 10 - μ g / m 3 increase in 1-month mean PM 2.5 . However, shorter-duration PM 10 exposures were inversely and only modestly associated with leukocyte count. DISCUSSION: The PM 2.5 -leukocyte estimates, albeit imprecise, suggest that among racially, ethnically, and environmentally diverse U.S. populations, sustained, ambient exposure to fine PM may induce subclinical, but epidemiologically important, inflammatory effects. https://doi.org/10.1289/EHP5360.

Full Text

Duke Authors

Cited Authors

  • Gondalia, R; Holliday, KM; Baldassari, A; Justice, AE; Stewart, JD; Liao, D; Yanosky, JD; Engel, SM; Jordahl, KM; Bhatti, P; Horvath, S; Assimes, TL; Pankow, JS; Demerath, EW; Guan, W; Fornage, M; Bressler, J; North, KE; Conneely, KN; Li, Y; Hou, L; Baccarelli, AA; Whitsel, EA

Published Date

  • January 2020

Published In

Volume / Issue

  • 128 / 1

Start / End Page

  • 17004 -

PubMed ID

  • 31903802

Pubmed Central ID

  • 31903802

Electronic International Standard Serial Number (EISSN)

  • 1552-9924

Digital Object Identifier (DOI)

  • 10.1289/EHP5360

Language

  • eng

Conference Location

  • United States