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

Circ Res. 2010 Jul 23;107(2):200-3. doi: 10.1161/CIRCRESAHA.110.222679. Epub 2010 Jul 1.


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 measured in the peripheral blood of mice exposed to concentrated particles from ambient air in Louisville, Ky. In both studies, PM exposure was negatively correlated with circulating EPC levels. In humans, statistically significant associations between PM(2.5) exposure and the plasma levels of platelet-monocyte aggregates, high-density lipoprotein, and nonalbumin protein were also observed. Episodic increases in PM(2.5) did not change plasma levels of C-reactive protein, interleukin-1beta, interleukin-6, fibrinogen, or serum amyloid A.

Conclusions: Episodic exposure to PM(2.5) induces reversible vascular injury, reflected in part by depletion of circulating EPC levels, and increases in platelet activation and the plasma level of high-density lipoprotein. These changes were also accompanied by an increase in nonalbumin protein and may be related to mechanisms by which exposure to particulate air pollution increases the risk of cardiovascular disease and adverse cardiovascular events.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Adolescent
  • Adult
  • Air Pollutants / adverse effects*
  • Animals
  • Antigens, CD / blood
  • Biomarkers / blood
  • Blood Platelets / drug effects
  • Blood Platelets / metabolism
  • Cardiovascular Diseases / blood
  • Cardiovascular Diseases / chemically induced*
  • Cardiovascular Diseases / immunology
  • Cholesterol, HDL / blood
  • Down-Regulation
  • Endothelial Cells / drug effects*
  • Endothelial Cells / immunology
  • Endothelial Cells / metabolism
  • Female
  • Flow Cytometry
  • Humans
  • Inflammation Mediators / blood
  • Kentucky
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Monocytes / drug effects
  • Particulate Matter / adverse effects*
  • Phenotype
  • Platelet Adhesiveness / drug effects
  • Serum Albumin / metabolism
  • Stem Cells / drug effects*
  • Stem Cells / immunology
  • Stem Cells / metabolism
  • Time Factors
  • Utah
  • Young Adult


  • Air Pollutants
  • Antigens, CD
  • Biomarkers
  • Cholesterol, HDL
  • Inflammation Mediators
  • Particulate Matter
  • Serum Albumin