Online Program

334590
Air Pollution and Tobacco Smoke Differentially Depress Circulating Angiogenic Cells in Humans


Monday, November 2, 2015

Natasha DeJarnett, PhD, MPH, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Ray Yeager II, MPH, School of Public Health and information Sciences, University of Louisville, Louisville, KY
Daniel Conklin, PhD, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Timothy O'Toole, PhD, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
James McCracken, PhD, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Wesley Abplanalp, BS, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Daniel Riggs, MS, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Ihab Hamzeh, MD, Cardiology, Baylor College of Medicine, Houston, TX
Stephen Wagner, MD, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Atul Chugh, MD, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Andrew Defilippis, MD, MSc, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Tiffany Ciszewski, MEd, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Bradley Wyatt, DMD, MPH, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Carrie Becher, MPH, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Deirdre Higdon, APRN, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Jordan Finch, MS, Pharmacology and Toxicology, University of Louisville, Louisville, KY
Imtiaz Ismail, MD, Medicine, Rosalind Franklin University of Medicine and Science, North Chicago, IL
David J. Tollerud, MD, MPH, Environmental and Occupational Health Sciences, University of Louisville School of Public Health and Information Sciences, Louisville, KY
Shesh Rai, PhD, Department of Bioinformatics and Biostatistics, University of Louisville, Louisville, KY
Jasmit Shah, MS, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Nagma Zafar, MD, Division of Cardiovascular Medicine, University of Louisville, Louisville, KY
Sathya Krishnasamy, MD, Endocrinology, University of Louisville, 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

Background: There is considerable epidemiological evidence linking environmental exposures such as fine particulate matter (PM2.5) and tobacco smoke with increased cardiovascular disease (CVD) risk. Although endothelial dysfunction is considered a shared effect of these toxins, it is unclear whether these exposures induce injury by a shared mechanism. Hence, we assessed whether levels of circulating angiogenic cells (CACs), a surrogate marker of endothelium health, were associated with PM2.5 and tobacco smoke exposure.

 

Methods: CACs were identified by the presence of stem cell-related antigens (CD34 and AC133) using flow cytometry. In a cross-sectional analysis, we measured 15 antigenically-distinct CACs in 316 participants. Daily mean PM2.5 data at the community level were acquired from EPA-validated monitors, and tobacco smoke exposure was assessed via self-report. Generalized linear models were used to assess the association between PM2.5 and/or tobacco smoke exposure and CAC levels.

 

Results: Study participants were 50±10 years old, 40% African American, 49% female, and 35% smokers. Regression analyses were adjusted for potential confounders: age, gender, ethnicity, body mass index, diabetes, myocardial infarction, and socioeconomic status. In general, CAC (CD34+) levels were inversely associated with either PM2.5 or tobacco smoke exposure such that PM2.5 suppressed early/immature (AC133+) cells while current smokers had significantly fewer mature (AC133-) CACs in peripheral blood.

Conclusions: Exposure to PM2.5 appears to suppress an immature CAC phenotype, implying a mechanism targeting bone marrow development of CACs, whereas tobacco smoke appears to deplete more mature CACs, which are important for vascular injury repair. Although both exposures induce endothelial dysfunction and increase CVD risk, herein we demonstrate that these pollutants induce vascular injury via different mechanisms. These findings suggest that CACs are sensitive markers of environmental exposures, and thus, this relationship between vascular health, tobacco smoke exposure, and ambient PM2.5 may further facilitate the development and promulgation of environmental pollutant standards.

Learning Areas:

Environmental health sciences
Public health biology

Learning Objectives:
Assess the relationship between exposure to fine particulate matter (PM2.5) and circulating angiogenic cells (CAC) in humans. Assess the relationship between exposure to tobacco smoke and CAC levels in humans. Evaluate the potential contribution of air pollution-induced changes in CAC levels in humans with elevated CVD risk.

Keyword(s): Heart Disease, Environmental Health

Presenting author's disclosure statement:

Qualified on the content I am responsible for because: I have been involved with the planning, coordinating, and organizing as well as analysis 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.