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


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.
O'Toole
Timothy E
TE
Diabetes and Obesity Center, University of Louisville, Louisville, KY 40202, USA. teotoo01@louisville.edu
Hellmann
Jason
J
Wheat
Laura
L
Haberzettl
Petra
P
Lee
Jongmin
J
Conklin
Daniel J
DJ
Bhatnagar
Aruni
A
Pope
C Arden
CA
D000293:Adolescent; D000328:Adult; D000393:Air Pollutants / Q000009:adverse effects*; D000818:Animals; D015703:Antigens, CD / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000097:blood / Q000139:chemically induced* / Q000276:immunology; D008076:Cholesterol, HDL / Q000097:blood; D015536:Down-Regulation; D042783:Endothelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007629:Kentucky; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000187:drug effects; D052638:Particulate Matter / Q000009:adverse effects*; D010641:Phenotype; D010973:Platelet Adhesiveness / Q000187:drug effects; D012709:Serum Albumin / Q000378:metabolism; D013234:Stem Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D013997:Time Factors; D014589:Utah; D055815:Young Adult
D000393:Air Pollutants; D015703:Antigens, CD; D015415:Biomarkers; D008076:Cholesterol, HDL; D018836:Inflammation Mediators; D052638:Particulate Matter; D012709:Serum Albumin