Dataset Information

Exploration of the composition and sources of urban fine particulate matter associated with same-day cardiovascular health effects in Dearborn, Michigan.

ABSTRACT: The objective was to explore associations of chemical components and source factors of ambient fine particulate matter (aerodynamic diameter ? 2.5 ?m; PM2.5) with cardiovascular (CV) changes following same-day exposure to ambient PM2.5. Twenty-five healthy adults living in rural Michigan were exposed to ambient air in an urban/industrial community for 4 to 5 h daily for five consecutive days. CV health outcomes were measured 1-2 h post exposure. Contributing emission sources were identified via positive matrix factorization. We examined associations between PM2.5 mass, composition and source factors, and same-day changes in CV outcomes using mixed-model analyses. PM2.5 mass (10.8 ± 6.8 ?g/m(3)), even at low ambient levels, was significantly associated with increased heart rate (HR). Trace elements as well as secondary aerosol, diesel/urban dust and iron/steel manufacturing factors potentially explained the HR changes. However, trace element analysis demonstrated additional associations with other CV responses including changes in blood pressure (BP), arterial compliance, autonomic balance and trends toward reductions in endothelial function. Two factors were related to BP changes (diesel/urban dust, motor vehicle) and trends toward impaired endothelial function (diesel/urban dust). This study indicates composition of PM2.5 and its sources may contribute to CV health effects independently of PM2.5 mass.

SUBMITTER: Morishita M

PROVIDER: S-EPMC4560954 | biostudies-literature | 2015 Mar-Apr

REPOSITORIES: biostudies-literature

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Exploration of the composition and sources of urban fine particulate matter associated with same-day cardiovascular health effects in Dearborn, Michigan.

Morishita Masako M Bard Robert L RL Kaciroti Niko N Fitzner Craig A CA Dvonch Timothy T Harkema Jack R JR Rajagopalan Sanjay S Brook Robert D RD

Journal of exposure science & environmental epidemiology 20140528 2

The objective was to explore associations of chemical components and source factors of ambient fine particulate matter (aerodynamic diameter ≤ 2.5 μm; PM2.5) with cardiovascular (CV) changes following same-day exposure to ambient PM2.5. Twenty-five healthy adults living in rural Michigan were exposed to ambient air in an urban/industrial community for 4 to 5 h daily for five consecutive days. CV health outcomes were measured 1-2 h post exposure. Contributing emission sources were identified via ...[more]

PMID: 24866265

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Project description:Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality. We aimed to determine whether brief exposures to PM2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM2.5 targeted at 150 μg/m(3), ozone targeted at 240 μg/m(3) (120 ppb), PM2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.There was a trend towards bigger ΔHOI between PM2.5 and FA 1 h after exposures (p = 0.18) but not 20 h after. This trend became significant (p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM2.5 on the change in HOI at both time points. The change in HOI due to PM2.5 showed a positive trend with particle mass concentration (p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures (p = 0.005).Brief exposures to concentrated PM2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Project description:Traffic is a significant pollution source in cities and has caused various health and environmental concerns worldwide. Therefore, an improved understanding of traffic impacts on particle concentrations and their components could help mitigate air pollution. In this study, the characteristics and sources of trace elements in PM2.5 (fine), and PM10-2.5 (coarse), were investigated in dense traffic areas in Toronto and Vancouver, Canada, from 2015-2017. At nearby urban background sites, 24-h integrated PM samples were also concurrently collected. The PM2.5 and PM10-2.5 masses, and a number of elements (i.e., Fe, Ba, Cu, Sb, Zn, Cr), showed clear increases at each near-road site, related to the traffic emissions resulting from resuspension and/or abrasion sources. The trace elements showed a clear partitioning trend between PM2.5 and PM10-2.5, thus reflecting the origin of some of these elements. The application of positive matrix factorization (PMF) to the combined fine and coarse metal data (86 total), with 24 observations at each site, was used to determine the contribution of different sources to the total metal concentrations in fine and coarse PM. Four major sources were identified by the PMF model, including two traffic non-exhaust (crustal/road dust, brake/tire wear) sources, along with regional and local industrial sources. Source apportionment indicated that the resuspended crustal/road dust factor was the dominant contributor to the total coarse-bound trace element (i.e., Fe, Ti, Ba, Cu, Zn, Sb, Cr) concentrations produced by vehicular exhaust and non-exhaust traffic-related processes that have been deposited onto the surface. The second non-exhaust factor related to brake/tire wear abrasion accounted for a considerable portion of the fine and coarse elemental (i.e., Ba, Fe, Cu, Zn, Sb) mass at both near-road sites. Regional and local industry contributed mostly to the fine elemental (i.e., S, As, Se, Cd, Pb) concentrations. Overall, the results show that non-exhaust traffic-related processes were major contributors to the various redox-active metal species (i.e., Fe, Cu) in both PM fractions. In addition, a substantial proportion of these metals in PM2.5 was water-soluble, which is an important contributor to the formation of reactive oxygen species and, thus, may lead to oxidative damage to cells in the human body. It appears that controlling traffic non-exhaust-related metals emissions, in the absence of significant point sources in the area, could have a pronounced effect on the redox activity of PM, with broad implications for the protection of public health.

Dataset Information

Exploration of the composition and sources of urban fine particulate matter associated with same-day cardiovascular health effects in Dearborn, Michigan.

Publications

Exploration of the composition and sources of urban fine particulate matter associated with same-day cardiovascular health effects in Dearborn, Michigan.

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