247266 Contribution of air pollutant combustion product acrolein to circulating endothelial progenitor cell level and cardiovascular disease risk

Monday, October 31, 2011

Natasha DeJarnett, MPH , Environmental and Occupational Health Sciences, University of Louisville School of Public Health and Information Sciences, Louisville, KY
Sumanth Prabhu, MD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Aruni Bhatnagar, PhD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
David J. Tollerud, MD, MPH , Environmental and Occupational Health Sciences, University of Louisville School of Public Health and Information Sciences, Louisville, KY
Stephen Wagner, MD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Ihab Hamzeh, MD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Atul Chugh, MD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Matthew Zahn, MD , Medical Director, Louisville Metro Health Department, Louisville, KY
Adewale Troutman, MD, MPH, MA, CPH , College of Public Health, University of South Florida, Tampa, FL
John A. Myers, PhD , School of Public Health and Information Sciences, University of Louisville, Louisville, KY
Carrie Becher, BA , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Deirdre Higdon, MSN, ANP-BC , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Bradley Wyatt, MPH , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Wesley Abplanalp, BS , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
James McCracken, PhD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Tiffany Ciszewski, BSS , Department of Bioinformatics and Biostatistics, University of Louisville, Louisville, KY
Daniel Riggs, MS , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Daniel Conklin, PhD , Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Background: Fine particulate air pollution exposure is associated with increased cardiovascular morbidity and mortality. Endothelial progenitor cell (EPC) level is a predictor of cardiovascular disease (CVD) risk, and EPCs are decreased by acute exposure to elevated particulate matter and in chronic smokers. Decreased EPC level is a marker of endothelial dysfunction the hallmark of atherosclerosis. The mechanisms whereby air pollution and tobacco smoke contribute to decreased EPCs and elevated CVD risk are unknown. Methods: In a cross-sectional assessment of CVD in Louisville, KY, participants were receiving primary or secondary CVD care from cardiology clinics. Air pollution exposure measures included self-reported data from an interview questionnaire and biological samples (urine and blood). The questionnaire included CVD history and tobacco smoke exposure. Urinary levels of hydroxypropylmercapturic acid (HPMA; major metabolite of acrolein, measured by HPLC/MS) and cotinine (major urinary metabolite of nicotine; measured by ELISA) were used to assess overall exposure. EPC populations in blood were characterized using flow cytometry with established markers: CD34/CD45/CD31/CD133+. Results: The participant mean age was 501 years (n=100; 46% female), ranging from 23-80 years with 50% Caucasian, 46% African American, and 3% Hispanic. Mean HPMA (normalized to creatinine) values for high, low, and no tobacco smoke exposure strata were 421.0393.25 ug/g (n= 49), 78.8227.26 ug/g (n=17), and 50.996.55 ug/g (n=16), respectively. EPCs were regressed against HPMA and cotinine, and the highest EPCs levels were observed in subjects with lowest HPMA levels. Conclusions: HPMA values were correlated with smoking status, with increased HPMA values associated with increased cotinine levels. EPCs appear to inversely correlate with HPMA, where highest EPC levels were observed in subjects with the lowest HPMA levels. The results suggest that tobacco smoke exposure, perhaps as a result of acrolein, may be inversely related to circulating EPC levels and may be predictive of CVD risk.

Learning Areas:
Environmental health sciences
Public health biology

Learning Objectives:
1. To describe the endothelial progenitor cell (EPC) profile among patients with cardiovascular disease (CVD) or at high risk to develop CVD. 2. To assess the relationship between circulating EPC counts and acrolein exposure. 3. To evaluate the link between EPCs and tobacco smoke exposure.

Keywords: Heart Disease, Environmental Exposures

Presenting author's disclosure statement:

Qualified on the content I am responsible for because: I have been involved with the planning, coordinating, and organizing of the project for submission.
Any relevant financial relationships? No

I agree to comply with the American Public Health Association Conflict of Interest and Commercial Support Guidelines, and to disclose to the participants any off-label or experimental uses of a commercial product or service discussed in my presentation.