Controlled Exposure of Healthy Young Volunteers to Ozone Causes Cardiovascular Effects
Background—Recent epidemiology studies have reported associations between acute ozone exposure and mortality. Such studies have previously reported associations between airborne particulate matter pollution (PM) and mortality and support for a causal relationship has come from controlled exposure studies which describe pathophysiological mechanisms by which PM could induce acute mortality. In contrast, for ozone, there are almost no controlled human exposure studies which have tested whether ozone exposure can modulate the cardiovascular system.
Methods and Results—Twenty three young healthy individuals were exposed in a randomized crossover fashion to clean air and 0.3 ppm ozone for two hours while undergoing intermittent exercise. Blood was obtained immediately prior to exposure, immediately afterward, and the next morning. Continuous Holter monitoring began immediately prior to exposure and continued for 24 hours. Lung function was performed immediately prior to and immediately after post exposure and bronchoalveolar lavage was performed 24 hours after exposure. Immediately following ozone exposure we observed a 98.9% increase in IL-8, a 21.4% decrease in plasminogen activator inhibitor 1 (PAI-1), a 51.3% decrease in the high frequency component of HRV, and a 1.2 % increase in QT duration. Changes in IL-1B, and PAI-1 were apparent 24 hours after exposure. In agreement with previous studies, we also observed ozone-induced drops in lung function and an increase in pulmonary inflammation.
Conclusions—This controlled human exposure study shows that ozone can cause an increase in vascular markers of inflammation, changes in markers of fibrinolysis, as well markers that affect autonomic control of heart rate and repolarization. We believe these findings provide biologic plausibility for the epidemiology studies that associate ozone exposure with mortality.
Clinical Trial Registration Information—clinicaltrials.gov; Identifier: NCT01492517.
- Received January 20, 2012.
- Accepted May 8, 2012.
- Copyright © 2012, American Heart Association, Inc. All rights reserved. Unauthorized use prohibited