Ozone and PM2.5 in the air pollution mixture differentially impact cardiopulmonary pathophysiologic mechanisms

Abstract

Introduction: The relative contributions of ozone (O3) and PM2.5 in air pollution mixtures to cardiopulmonary outcomes remain poorly understood. This study examines whether and how O3 and PM2.5 may differentially impact mechanisms of cardiopulmonary pathophysiology. Methods: Exposures to each pollutant were manipulated for 89 office workers living together on a work campus in China with various combinations of an O3-generating electrostatic precipitator (ESP) and a high efficiency particulate air (HEPA) filter. Subjects were measured for biomarkers of cardiopulmonary pathophysiology at four time points each separated by 2-3 week intervals. Results: Mean 24-hour exposure concentrations during the study were 37 ± 1.5 µg/m3 for PM2.5 and 6.4 ± 0.2 ppb for O3, and they were significantly negatively correlated. Contrary to previous literature showing these biomarkers all being associated with PM2.5 exposure, this study shows that lung inflammation (fractional exhaled nitric oxide and exhaled breath condensate (EBC) nitrite and nitrate), systolic and diastolic blood pressure, and platelet activation (soluble P-selectin (sP-sel)) were tightly associated with short-term and chronic O3 exposure. In contrast, pulmonary oxidative stress (EBC malondialdehyde), arterial stiffness (augmentation index), and endothelial cell dysfunction (von Willebrand factor (VWF)) were significantly associated with chronic PM2.5 exposure. For example, an interquartile range (IQR) increase in 24-hour O3 exposure concentration (4.1 ppb) and 2-week mean ambient O3 (11.0 ppb) was significantly associated with a 12.5% and 27.4% increase in sP-sel, respectively. An IQR increase in 2-week mean ambient PM2.5 (41.4 µg/m3) was associated with a significant 11.2% increase in VWF. Conclusions: These findings have provided insights into biological mechanisms by which O3 and PM2.5 can differentially enhance cardiopulmonary disease risk.