Episodic exposure to fine particulate air pollution decreases circulating levels of endothelial progenitor cells.

ABSTRACT:

Rationale

Acute and chronic exposures to airborne particulate matter (PM) have been linked in epidemiological studies to a wide spectrum of cardiovascular disorders that are characterized by a dysfunctional endothelium. The pathophysiological mechanisms underlying these associations are unclear.

Objective

To examine whether exposure to fine PM with an aerodynamic diameter of <2.5 microm (PM(2.5)) affects the circulating levels of endothelial progenitor cell (EPC) populations, systemic inflammation and coagulation.

Methods and results

Phenotypically distinct EPC populations were quantified by flow cytometry in young (18 to 25 years) adult humans exposed to episodic increases in PM(2.5) along the Wasatch Mountain Front in Utah. In addition, Sca-1+/Flk-1+ cells were meas

SUBMITTER: O'Toole TE 

PROVIDER: S-EPMC2943671 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature