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Association of short-term exposure to fine particulate air pollution and mortality: effect modification by oxidant gases.

ABSTRACT: Short term changes in exposure to outdoor fine particulate matter (PM_2.5) concentrations are associated with an increased risk of mortality. However, less is known about how oxidant gases may modify the acute health effects of PM_2.5. Our objective was to investigate whether associations between acute exposure to PM_2.5 and mortality were modified by the oxidant gases O₃ and NO₂ using their redox-weighted average (O_x). We conducted a multi-city case-crossover study in 24 cities across Canada between 1998-2011 including 1,179,491 nonaccidental mortality events. Interquartile increases in lag-0 and 3-day mean PM_2.5 and O_x concentrations were each associated with small increases in nonaccidental and cardiovascular mortality. In stratified analyses, associations between PM_2.5 and nonaccidental and cardiovascular mortality tended to be greatest in the highest tertile of O_x with a significant interaction observed between lag 0 PM_2.5 and 3-day mean O_x (interaction p-value?=?0.04). There was no evidence of effect modification by O_x in the relationship between PM_2.5 and respiratory mortality. Overall, the relationship between short-term changes in outdoor PM_2.5 and nonaccidental mortality may be greater when oxidant gas concentrations are also elevated. In some regions, reductions in oxidant gas concentrations may also reduce the acute health impacts of PM_2.5.

SUBMITTER: Lavigne E

PROVIDER: S-EPMC6208424 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature

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Association of short-term exposure to fine particulate air pollution and mortality: effect modification by oxidant gases.

Lavigne Eric E Burnett Richard T RT Weichenthal Scott S

Scientific reports 20181031 1

Short term changes in exposure to outdoor fine particulate matter (PM2.5) concentrations are associated with an increased risk of mortality. However, less is known about how oxidant gases may modify the acute health effects of PM2.5. Our objective was to investigate whether associations between acute exposure to PM2.5 and mortality were modified by the oxidant gases O3 and NO2 using their redox-weighted average (Ox). We conducted ...[more]

PMID: 30382168

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Project description:Epidemiological evidence indicates that exposures to fine particulate matter air pollution (PM2.5) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM2.5 exposure induces cardiovascular injury remain unclear. PM2.5-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM2.5 exposure was associated with the elevated levels of endothelial microparticles (annexin V+/CD41-/CD31+), including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62+. These changes were accompanied by suppressed circulating levels of proangiogenic growth factors (EGF [epidermal growth factor], sCD40L [soluble CD40 ligand], PDGF [platelet-derived growth factor], RANTES [regulated on activation, normal T-cell-expressed and secreted], GRO? [growth-regulated protein ?], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNF? [tumor necrosis factor ?], IP-10 [interferon ?-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1?/? [macrophage inflammatory protein 1?/?], IL-6 [interleukin 6], and IL-1? [interleukin 1?]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an antiangiogenic plasma profile, and elevated levels of circulating monocytes and T, but not B, lymphocytes. These changes could contribute to the pathogenic sequelae of atherogenesis and acute coronary events.

Dataset Information

Association of short-term exposure to fine particulate air pollution and mortality: effect modification by oxidant gases.

Publications

Association of short-term exposure to fine particulate air pollution and mortality: effect modification by oxidant gases.

Similar Datasets

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