Exposure to Fine Particulate Air Pollution Is Associated With Endothelial Injury and Systemic Inflammation

To examine whether acute exposure to PM 2.5 is associated with endothelial injury and systemic inflammation. Methods and Results: Blood was collected from healthy, nonsmoking, young adults during 3 study periods that included episodes of elevated PM 2.5 levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM 2.5 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], GROα [growth-regulated protein α], and VEGF [vascular endothelial growth factor]), and an increase in the levels of antiangiogenic (TNFα [tumor necrosis factor α], IP-10 [interferon γ-induced protein 10]), and proinflammatory cytokines (MCP-1 [monocyte chemoattractant protein 1], MIP-1α/β [macrophage inflammatory protein 1α/β], IL-6 [interleukin 6], and IL-1β [interleukin 1β]), and markers of endothelial adhesion (sICAM-1 [soluble intercellular adhesion molecule 1] and sVCAM-1 [soluble vascular cellular adhesion molecule 1]). PM 2.5 exposure was also associated with an inflammatory response characterized by elevated levels of circulating CD14 + , CD16 + , CD4 + , and CD8 + , but not CD19 + cells.

Episodic PM 2.5 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.