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