Alterations in cardiometabolic markers associated with Canada-wide and sector-specific multiple air pollutant
Jessica Evans1, Robert Dales2, Kimberly Mitchell2
1Environmental Health Science & Research Bureau, Health Canada, 251 Sir Frederic Banting Driveway, Ottawa, Ontario, K1A 0K9, Canada; University of Ottawa, 451 Smyth Road, Ottawa, Ontario, K1H 8M5, Canada.
Abstract:
Existing evidence on air pollution exposure and cardiometabolic biomarker associations does not consider pollution mixtures and sector-specific pollution contributions. Participants from the cross-sectional Canadian Health Measures Survey (2007-2019) were included. Annual average concentrations of ambient PM2.5, SO2, NO2, and O3 (2006-2019) were modeled using the Global Environmental Multi-scale - Modelling Air quality and Chemistry (GEM-MACH) chemical transport model at a 10 km by 10 km surface resolution from all sources combined as well as from eight specific sectors. The quantile g-computation model was used to estimate changes in lipid and glucose metabolic markers associated with interquartile increases in air pollution. A total of 30,781 participants aged 3-79 years were included in the study. Exposure to PM2.5, O3, NO2, and SO2 from all sectors was associated with increases in the ratio of total cholesterol to HDL (0.039, 95 % CI: 0.017,0.060), apolipoprotein B (0.011, 95 % CI: 0.006,0.017), fasting glucose (0.076, 95 % CI: 0.010,0.142), and insulin (3.159, 95 % CI: 1.180,5.138), as well as decreases in the cardioprotective lipids, HDL (-0.015, 95 % CI: 0.023,-0.008) and apolipoprotein A1 (-0.010, 95 % CI: 0.020,-0.000). Lipid and apolipoprotein levels as well as markers of insulin resistance were predominantly altered in children and younger adults, although there was no significant effect modification by age. On- and off-road transportation sectors were most frequently associated with adverse lipid biomarker effects. The joint effects of mean annual PM2.5, O3, NO2, and SO2 exposures were associated with worsening cardiometabolic markers. Further research is required to better understand the mechanisms by which specific air pollution components disrupt metabolic pathways.
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