The effect of acute exposure to coarse particulate matter air pollution in a rural location on circulating endothelial progenitor cells: results from a randomized controlled study

Authors: Brook, Robert D.1; Bard, Robert L.1; Kaplan, Mariana J.1; Yalavarthi, Srilakshmi1; Morishita, Masako2; Dvonch, J. Timothy2; Wang, Lu2; Yang, Hui-yu2; Spino, Catherine2; Mukherjee, Bhramar2; Oral, Elif A.1; Sun, Qinghua3; Brook, Jeffrey R.4; Harkema, Jack5; Rajagopalan, Sanjay3

Source: Inhalation Toxicology, Volume 25, Number 10, August 2013 , pp. 587-592(6)

Publisher: Informa Healthcare

Buy & download fulltext article:


Price: $35.96 plus tax (Refund Policy)



Context: Fine particulate matter (PM) air pollution has been associated with alterations in circulating endothelial progenitor cell (EPC) levels, which may be one mechanism whereby exposures promote cardiovascular diseases. However, the impact of coarse PM on EPCs is unknown.

Objective: We aimed to determine the effect of acute exposure to coarse concentrated ambient particles (CAP) on circulating EPC levels.

Methods: Thirty-two adults (25.9 ± 6.6 years) were exposed to coarse CAP (76.2 ± 51.5 μg m−3) in a rural location and filtered air (FA) for 2 h in a randomized double-blind crossover study. Peripheral venous blood was collected 2 and 20 h post-exposures for circulating EPC (n = 21), white blood cell (n = 24) and vascular endothelial growth factor (VEGF) (n = 16–19) levels. The changes between exposures were compared by matched Wilcoxon signed-rank tests.

Results: Circulating EPC levels were elevated 2 [108.29 (6.24–249.71) EPC mL−1; median (25th–75th percentiles), p = 0.052] and 20 h [106.86 (52.91–278.35) EPC mL−1, p = 0.008] post-CAP exposure compared to the same time points following FA [38.47 (0.00–84.83) and 50.16 (0.00–104.79) EPC mL−1]. VEGF and white blood cell (WBC) levels did not differ between exposures.

Conclusions: Brief inhalation of coarse PM from a rural location elicited an increase in EPCs that persisted for at least 20 h. The underlying mechanism responsible may reflect a systemic reaction to an acute “endothelial injury” and/or a circulating EPC response to sympathetic nervous system activation.

Keywords: Air pollution; endothelial function; endothelial progenitor cells; inflammation

Document Type: Research Article


Affiliations: 1: 1Division of Cardiovascular Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA, 2: 2School of Public Health, University of Michigan, Ann Arbor, MI, USA, 3: 3Dorothy M. Davis Heart Lung Research Institute, College of Medicine, Ohio State University Medical Center, Columbus, OH, USA, 4: 4School of the Environment, University of Toronto, Toronto, Ontario, Canada, and 5: 5College of Veterinary Medicine, Michigan State University, East Lansing, MI, USA

Publication date: August 1, 2013

More about this publication?


Free Content
Free content
New Content
New content
Open Access Content
Open access content
Subscribed Content
Subscribed content
Free Trial Content
Free trial content

Text size:

A | A | A | A
Share this item with others: These icons link to social bookmarking sites where readers can share and discover new web pages. print icon Print this page