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

摘要

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.