This multi-center study focused on the effects of ozone in human volunteers, aged 55 to 70 years, who were exposed in chambers to near ambient levels of ozone with intermittent exercise. Effects on the cardiovascular system, along with changes in pulmonary function, inflammation and oxidative stress were studied. Part 1 has been published (see link below). Part 2 of the study is ongoing, to further analyze the participant's prior exposures to ambient air pollutants and conduct additional analyses of the rich dataset.
Abstract for HEI Annual Conference 2017
Multicenter Ozone Study in oldEr Subjects (MOSES). Part 2: Impacts of Personal and Ambient Concentrations of Ozone and Other Pollutants on Cardiovascular and Pulmonary Function.
Balmes J, Arjomandi M, and Ganz P, University of California, San Francisco, CA; Bromberg P, Hazucha M, Hinderliter A, Alexis N, and Mackman N, University of North Carolina at Chapel Hill, NC; Frampton M, Rich D, and Zareba W, University of Rochester Medical Center, Rochester, NY.
Background It is well established that exposure to air pollution contributes to cardiovascular morbidity and mortality and is a significant risk factor for cardiovascular disease. To date, little attention has been paid to acute cardiovascular responses to ozone (O3), in part due to the notion that O3 causes primarily local effects on lung function, which are the basis for the current O3 National Ambient Air Quality Standards (NAAQS). However, several recent epidemiological studies reported stronger associations of ambient exposures to O3 with cardiovascular mortality than with respiratory mortality. Pathways by which ozone could cause cardiovascular dysfunction include: a) systemic inflammation and/or oxidative stress and b) alterations in autonomic balance. These initial responses could lead ultimately to endothelial dysfunction, acute arterial vasoconstriction, arrhythmias, and pro-coagulant activity.
Study Design MOSES is a multi-center study that investigated whether short-term exposure of elderly, healthy volunteers to ambient levels of O3 in a controlled exposure setting induces acute cardiovascular responses (Phase 1). The study is being conducted at three clinical centers and a Data Coordinating and Analysis Center. Healthy volunteers 55 to 70 years of age were exposed for 3 hours in random order to clean air, 70 ppb O3 (near the current NAAQS), and 120 ppm O3 (a level measured in several outdoor locations in the US), while alternating 15 min of moderate exercise with 15 min of rest. In addition, personal exposure to ozone and nitrogen dioxide in the 72 hours prior each exposure was measured using Ogawa personal samplers. Ambient air quality and meteorological data were obtained from a central monitoring station located in the vicinity of each clinical center. A suite of cardiovascular and pulmonary endpoints was measured on the day before, the day of, and up to 22 hours after, each exposure using a common protocol. The primary endpoints include: electrocardiographic changes (heart rate variability and repolarization), blood pressure, endothelial function measured as flow-mediated dilatation (FMD) of the brachial artery, and venous blood markers of platelet activation, thrombosis, inflammation, and microparticle-associated tissue factor activity. Lower airways inflammation (assessed in induced sputum) and pulmonary function (spirometry) were also measured.
Results A total of 87 subjects completed all three chamber exposures in Phase 1. Results of the effects of these exposures were presented previously. Briefly, exposure to ozone caused small but statistically significant changes in lung function and increases in some markers of lung inflammation and injury, but did not cause any significant effects on any of the cardiovascular endpoints. In the second phase of the study, which started in the fall of 2016, we are investigating whether personal and ambient ozone and other pollutant exposures impact the pre- to post-chamber ozone exposure changes in the endpoints measured in Phase 1, whether they modify any biomarker response to chamber ozone, and/or whether they impact the baseline (pre-exposure) biomarker levels. Preliminary results of these analyses will be presented.
Poster by MOSES Investigators' Team, 2017 HEI Annual Conference