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Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients
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 acros...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5697214/ https://www.ncbi.nlm.nih.gov/pubmed/29157250 http://dx.doi.org/10.1186/s12940-017-0335-0 |
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author | Mirowsky, Jaime E. Carraway, Martha Sue Dhingra, Radhika Tong, Haiyan Neas, Lucas Diaz-Sanchez, David Cascio, Wayne Case, Martin Crooks, James Hauser, Elizabeth R. Elaine Dowdy, Z. Kraus, William E. Devlin, Robert B. |
author_facet | Mirowsky, Jaime E. Carraway, Martha Sue Dhingra, Radhika Tong, Haiyan Neas, Lucas Diaz-Sanchez, David Cascio, Wayne Case, Martin Crooks, James Hauser, Elizabeth R. Elaine Dowdy, Z. Kraus, William E. Devlin, Robert B. |
author_sort | Mirowsky, Jaime E. |
collection | PubMed |
description | 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 (PM(2.5)) were obtained from central monitoring stations. Single (ozone) and two-pollutant (ozone and PM(2.5)) 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 PM(2.5). 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 PM(2.5). ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12940-017-0335-0) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5697214 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-56972142017-12-01 Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients Mirowsky, Jaime E. Carraway, Martha Sue Dhingra, Radhika Tong, Haiyan Neas, Lucas Diaz-Sanchez, David Cascio, Wayne Case, Martin Crooks, James Hauser, Elizabeth R. Elaine Dowdy, Z. Kraus, William E. Devlin, Robert B. Environ Health Research 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 (PM(2.5)) were obtained from central monitoring stations. Single (ozone) and two-pollutant (ozone and PM(2.5)) 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 PM(2.5). 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 PM(2.5). ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12940-017-0335-0) contains supplementary material, which is available to authorized users. BioMed Central 2017-11-21 /pmc/articles/PMC5697214/ /pubmed/29157250 http://dx.doi.org/10.1186/s12940-017-0335-0 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Mirowsky, Jaime E. Carraway, Martha Sue Dhingra, Radhika Tong, Haiyan Neas, Lucas Diaz-Sanchez, David Cascio, Wayne Case, Martin Crooks, James Hauser, Elizabeth R. Elaine Dowdy, Z. Kraus, William E. Devlin, Robert B. Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
title | Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
title_full | Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
title_fullStr | Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
title_full_unstemmed | Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
title_short | Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
title_sort | ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5697214/ https://www.ncbi.nlm.nih.gov/pubmed/29157250 http://dx.doi.org/10.1186/s12940-017-0335-0 |
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