Increased exposure to PM2.5 resulted in higher blood levels of the inflammation markers IL-6, Tumor Necrosis Factor (TNF) and IL-1β. An increase in the death of cells lining blood vessels was also noted. Researchers stated higher PM2.5 decreased levels of important and highly beneficial growth factors that typically repair and regenerate cells lining blood vessels and arteries. The study was conducted using 72 healthy non-smokers. Participants had blood drawn at three different times over a one year period that coincided with different levels of air pollution and PM2.5. More details and concluding remarks of scientists can be viewed in 'Read More.'
Results showed the inflammatory marker TNF increased 25% with each 10 μg/m3 incremental increase in PM2.5. While higher PM2.5 is known to increase heart disease and stroke, this study is one of the first to provide an explanation of why this is occurring. The following is the concluding statements by the authors in the introductory paragraph - "We found robust evidence of endothelial injury and systemic inflammation upon exposure to increased PM2.5 levels even in young healthy individuals. These findings lend support to the view that PM2.5 causes endothelial injury, potentially by establishing a mild inflammatory state. Our results are also consistent with the possibility that aberrant immune responses and endothelial injury may be early causes of endothelial dysfunction and CVD attributable to PM2.5 exposure in susceptible individuals." ...................................................
ABSTRACT
Rationale: 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.
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, 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], 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]). 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.
Conclusions: 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.