tetano
Editor, Senior Moderator
[h=1]Exposure to Fine Particulate Air Pollution Is Associated with Endothelial Injury and Systemic Inflammation[/h] C A Pope, Aruni Bhatnagar, James McCracken, Wesley T Abplanalp, Daniel J Conklin and Timothy E O'Toole
http://dx.doi.org/10.1161/CIRCRESAHA.116.309279 Circulation Research. 2016;CIRCRESAHA.116.309279
Originally published October 25, 2016
[h=2]Abstract[/h] Rationale: Epidemiologic evidence indicates that exposures to fine particulate matter air pollution (PM[SUB]2.5[/SUB]) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM[SUB]2.5[/SUB] exposure induces cardiovascular injury remain unclear. PM[SUB]2.5[/SUB]-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.
Objective: To examine whether acute exposure to PM[SUB]2.5[/SUB] 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 PM[SUB]2.5[/SUB] levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM[SUB]2.5[/SUB] exposure was associated with elevated levels of endothelial microparticles (annexin V[SUP]+[/SUP]/CD41-/CD31[SUP]+[/SUP]) including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62[SUP]+[/SUP]. 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). PM[SUB]2.5[/SUB] exposure also was associated with an inflammatory response characterized by elevated levels of circulating CD14[SUP]+[/SUP], CD16[SUP]+[/SUP], CD4[SUP]+[/SUP], and CD8[SUP]+[/SUP], but not CD19[SUP]+[/SUP] cells.
Conclusions: Episodic PM[SUB]2.5[/SUB] 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.
http://circres.ahajournals.org/content/early/2016/10/19/CIRCRESAHA.116.309279
http://dx.doi.org/10.1161/CIRCRESAHA.116.309279 Circulation Research. 2016;CIRCRESAHA.116.309279
Originally published October 25, 2016
[h=2]Abstract[/h] Rationale: Epidemiologic evidence indicates that exposures to fine particulate matter air pollution (PM[SUB]2.5[/SUB]) contribute to global burden of disease, primarily as a result of increased risk of cardiovascular morbidity and mortality. However, mechanisms by which PM[SUB]2.5[/SUB] exposure induces cardiovascular injury remain unclear. PM[SUB]2.5[/SUB]-induced endothelial dysfunction and systemic inflammation have been implicated, but direct evidence is lacking.
Objective: To examine whether acute exposure to PM[SUB]2.5[/SUB] 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 PM[SUB]2.5[/SUB] levels. Microparticles and immune cells in blood were measured by flow cytometry, and plasma cytokine/growth factors were measured using multiplexing laser beads. PM[SUB]2.5[/SUB] exposure was associated with elevated levels of endothelial microparticles (annexin V[SUP]+[/SUP]/CD41-/CD31[SUP]+[/SUP]) including subtypes expressing arterial-, venous-, and lung-specific markers, but not microparticles expressing CD62[SUP]+[/SUP]. 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). PM[SUB]2.5[/SUB] exposure also was associated with an inflammatory response characterized by elevated levels of circulating CD14[SUP]+[/SUP], CD16[SUP]+[/SUP], CD4[SUP]+[/SUP], and CD8[SUP]+[/SUP], but not CD19[SUP]+[/SUP] cells.
Conclusions: Episodic PM[SUB]2.5[/SUB] 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.
http://circres.ahajournals.org/content/early/2016/10/19/CIRCRESAHA.116.309279