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Abstract
BackgroundAir pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Several studies have found associations between ozone and cardiovascular morbidity, but the results have been inconclusive. We investigated associations between ozone and changes across biological pathways associated with cardiovascular disease.MethodsUsing a panel study design, 13 participants with coronary artery disease were assessed for markers of systemic inflammation, heart rate variability and repolarization, lipids, blood pressure, and endothelial function. Daily measurements of ozone and particulate matter (PM2.5) were obtained from central monitoring stations. Single (ozone) and two-pollutant (ozone and PM2.5) models were used to assess percent changes in measurements per interquartile ranges of pollutants.ResultsPer interquartile increase in ozone, changes in tissue plasminogen factor (6.6%, 95% confidence intervals (CI) = 0.4, 13.2), plasminogen activator inhibitor-1 (40.5%, 95% CI = 8.7, 81.6), neutrophils (8.7% 95% CI = 1.5, 16.4), monocytes (10.2%, 95% CI = 1.0, 20.1), interleukin-6 (15.9%, 95% CI = 3.6, 29.6), large-artery elasticity index (−19.5%, 95% CI = −34.0, −1.7), and the baseline diameter of the brachial artery (−2.5%, 95% CI = −5.0, 0.1) were observed. These associations were robust in the two-pollutant model.ConclusionsWe observed alterations across several pathways associated with cardiovascular disease in 13 coronary artery disease patients following ozone exposures, independent of PM2.5. The results support the biological plausibility of ozone-induced cardiovascular effects. The effects were found at concentrations below the EPA National Ambient Air Quality Standards for both ozone and PM2.5.
Highlights
Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor
Epidemiological studies suggest that the strongest associations are between particulate matter (PM) and cardiovascular morbidity and mortality [2, 3]; recent work suggests that ozone may be associated with negative
We describe the association of ozone with various cardiovascular outcomes, using both a one- and two-pollutant model
Summary
Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Epidemiological studies suggest that the strongest associations are between particulate matter (PM) and cardiovascular morbidity and mortality [2, 3]; recent work suggests that ozone may be associated with negative. Mirowsky et al Environmental Health (2017) 16:126 in systemic pro-inflammatory markers were observed in 26 healthy human participants following exposures to ozone and clean air [10, 11]. Researchers have found changes in fibrinolysis markers such as plasminogen activator inhibitor-1, plasminogen, and D-dimer, when young healthy participants were exposed to ozone [11, 12]. Researchers have begun looking at changes in cardiovascular biomarkers in larger epidemiological work to support associations between ozone exposure and cardiovascular morbidity and mortality. Additional research of men participating in the Normative Aging Study found changes in heart rate variability parameters with exposures to ambient ozone levels [15]
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