Abstract
BackgroundShort-term exposure to ambient air pollution has been associated with acute increases in cardiovascular hospitalization and mortality. However, causative chemical components and underlying pathophysiological mechanisms remain to be clarified. We hypothesized that endothelial dysfunction would be associated with mobile-source (traffic) air pollution and that pollutant components with higher oxidative potential to generate reactive oxygen species (ROS) would have stronger associations.MethodsWe carried out a cohort panel study in 93 elderly non-smoking adults living in the Los Angeles metropolitan area, during July 2012-February 2014. Microvascular function, represented by reactive hyperemia index (RHI), was measured weekly for up to 12 weeks (N = 845). Air pollutant data included daily data from regional air-monitoring stations, five-day average PM chemical components and oxidative potential in three PM size-fractions, and weekly personal nitrogen oxides (NOx). Linear mixed-effect models estimated adjusted changes in microvascular function with exposure.ResultsRHI was inversely associated with traffic-related pollutants such as ambient PM2.5 black carbon (BC), NOx, and carbon monoxide (CO). An interquartile range change increase (1.06 μg/m3) in 5-day average BC was associated with decreased RHI, −0.093 (95 % CI: −0.151, −0.035). RHI was inversely associated with other mobile-source components/tracers (polycyclic aromatic hydrocarbons, elemental carbon, and hopanes), and PM oxidative potential as quantified in two independent assays (dithiothreitol and in vitro macrophage ROS) in accumulation and ultrafine PM, and transition metals.ConclusionsOur findings suggest that short-term exposures to traffic-related air pollutants with high oxidative potential are major components contributing to microvascular dysfunction.Electronic supplementary materialThe online version of this article (doi:10.1186/s12940-016-0157-5) contains supplementary material, which is available to authorized users.
Highlights
Short-term exposure to ambient air pollution has been associated with acute increases in cardiovascular hospitalization and mortality
In a follow-up panel study with organic components measured in the accumulation mode size fraction (PM0.25–2.5), we found that exposure markers of combustion-related air pollutants including PM0.25–2.5 polycyclic hydrocarbons (PAHs) and/or PM0.25 PAHs were positively associated with expression of genes in inflammatory and oxidative stress pathways, including NFE2L2, Nrf2-mediated genes (HMOX1, NQO1, and SOD2), CYP1B1, IL1B, and SELP [35]
We found that decreased reactive hyperemia index (RHI) was significantly associated with Cr, Mn, Ni, Cu and Fe in PM2.5–10 with the strongest association observed with Ni (−0.156, 95 % confidence interval (CI):-238, −0.074, Fig. 2)
Summary
Short-term exposure to ambient air pollution has been associated with acute increases in cardiovascular hospitalization and mortality. Previous studies have reported positive associations of cardiovascular morbidity and mortality with short-term exposure to air pollutions [1,2,3]. A recent cross-sectional study investigated microvascular function using peripheral arterial tonometry and reported associations between baseline pulse amplitude and short-term exposure to ambient air pollutants, including particulate matter with aerodynamic diameter < 2.5 μm (PM2.5), black carbon (BC), and particle number concentrations, but not with vasodilator response [7]. A cohort panel study examined microvascular function in the retinal blood vessels and suggested that short-term exposure to higher levels of particulate matter with aerodynamic diameter < 10 μm (PM10) and BC may be associated with damage to the retinal microvasculature [8]. No cohort panel studies have evaluated relationships between peripheral microvascular function and air pollution, and there are no data on the importance of particle oxidative potential or specific particle components on microvascular function
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