Exposure to Fine Particulate Air Pollution Is Associated with Endothelial Injury and Systemic Inflammation
Rationale: Epidemiologic 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.
Objective: To examine whether acute exposure to PM2.5 is associated with endothelial injury and systemic inflammation.
Methods and Results: Blood was collected from healthy, non-smoking, young adults over three 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 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 pro-angiogenic growth factors (EGF, sCD40L, PDGF, RANTES, GROα, and VEGF), and an increase in the levels of anti-angiogenic (TNFα, IP-10) and proinflammatory cytokines (MCP-1, MIP-1α/β, IL-6, and IL-1β), and markers of endothelial adhesion (sICAM-1 and sVCAM-1). PM2.5 exposure also was associated with an inflammatory response characterized by elevated levels of circulating CD14+, CD16+, CD4+, and CD8+, but not CD19+ cells.
Conclusions: Episodic PM2.5 exposures are associated with increased endothelial cell apoptosis, an anti-angiogenic 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.
- Endothelial microparticles
- air pollution
- endothelial dysfunction
- vascular disease
- particulate matter
- cardiovascular disease
- Received September 13, 2016.
- Revision received October 3, 2016.
- Accepted October 4, 2016.