Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients.

Published online

Journal Article

BACKGROUND: Air 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. METHODS: Using 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. RESULTS: Per 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. CONCLUSIONS: We 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.

Full Text

Duke Authors

Cited Authors

  • Mirowsky, JE; Carraway, MS; Dhingra, R; Tong, H; Neas, L; Diaz-Sanchez, D; Cascio, W; Case, M; Crooks, J; Hauser, ER; Elaine Dowdy, Z; Kraus, WE; Devlin, RB

Published Date

  • November 21, 2017

Published In

Volume / Issue

  • 16 / 1

Start / End Page

  • 126 -

PubMed ID

  • 29157250

Pubmed Central ID

  • 29157250

Electronic International Standard Serial Number (EISSN)

  • 1476-069X

Digital Object Identifier (DOI)

  • 10.1186/s12940-017-0335-0

Language

  • eng

Conference Location

  • England