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dc.contributor.authorLi, Wenyuan
dc.contributor.authorKeaney, John F. Jr.
dc.contributor.authorMittleman, Murray A.
dc.date2022-08-11T08:09:45.000
dc.date.accessioned2022-08-23T16:42:12Z
dc.date.available2022-08-23T16:42:12Z
dc.date.issued2016-04-28
dc.date.submitted2016-08-16
dc.identifier.citation<p>J Am Heart Assoc. 2016 Apr 28;5(5). pii: e002742. doi: 10.1161/JAHA.115.002742. <a href="http://dx.doi.org/10.1161/JAHA.115.002742">Link to article on publisher's site</a></p>
dc.identifier.issn2047-9980 (Linking)
dc.identifier.doi10.1161/JAHA.115.002742
dc.identifier.pmid27126478
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40042
dc.description<p>Full author list omitted for brevity. For full list of authors see article.</p>
dc.description.abstractBACKGROUND: Short-term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community-based studies have assessed this association. METHODS AND RESULTS: Two thousand thirty-five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998-2001) and urinary creatinine-indexed 8-epi-prostaglandin F2alpha (8-epi-PGF2alpha) at the seventh and eighth (2005-2008) examinations. We measured fine particulate matter (PM2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1-, 2-, 3-, 5-, and 7-day moving averages of each pollutant. Measured myeloperoxidase and 8-epi-PGF2alpha were loge transformed. We used linear regression models and linear mixed-effects models with random intercepts for myeloperoxidase and indexed 8-epi-PGF2alpha, respectively. Models were adjusted for demographic variables, individual- and area-level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2- to 7-day moving averages of PM2.5 and sulfate were consistently positively associated with 8-epi-PGF2alpha. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without. CONCLUSIONS: Our community-based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=27126478&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/
dc.subjectair pollution
dc.subjectisoprostanes
dc.subjectmyeloperoxidase
dc.subjectCardiology
dc.subjectCardiovascular Diseases
dc.titleShort-Term Exposure to Air Pollution and Biomarkers of Oxidative Stress: The Framingham Heart Study
dc.typeJournal Article
dc.source.journaltitleJournal of the American Heart Association
dc.source.volume5
dc.source.issue5
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3853&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2848
dc.identifier.contextkey8985385
refterms.dateFOA2022-08-23T16:42:12Z
html.description.abstract<p>BACKGROUND: Short-term exposure to elevated air pollution has been associated with higher risk of acute cardiovascular diseases, with systemic oxidative stress induced by air pollution hypothesized as an important underlying mechanism. However, few community-based studies have assessed this association.</p> <p>METHODS AND RESULTS: Two thousand thirty-five Framingham Offspring Cohort participants living within 50 km of the Harvard Boston Supersite who were not current smokers were included. We assessed circulating biomarkers of oxidative stress including blood myeloperoxidase at the seventh examination (1998-2001) and urinary creatinine-indexed 8-epi-prostaglandin F2alpha (8-epi-PGF2alpha) at the seventh and eighth (2005-2008) examinations. We measured fine particulate matter (PM2.5), black carbon, sulfate, nitrogen oxides, and ozone at the Supersite and calculated 1-, 2-, 3-, 5-, and 7-day moving averages of each pollutant. Measured myeloperoxidase and 8-epi-PGF2alpha were loge transformed. We used linear regression models and linear mixed-effects models with random intercepts for myeloperoxidase and indexed 8-epi-PGF2alpha, respectively. Models were adjusted for demographic variables, individual- and area-level measures of socioeconomic position, clinical and lifestyle factors, weather, and temporal trend. We found positive associations of PM2.5 and black carbon with myeloperoxidase across multiple moving averages. Additionally, 2- to 7-day moving averages of PM2.5 and sulfate were consistently positively associated with 8-epi-PGF2alpha. Stronger positive associations of black carbon and sulfate with myeloperoxidase were observed among participants with diabetes than in those without.</p> <p>CONCLUSIONS: Our community-based investigation supports an association of select markers of ambient air pollution with circulating biomarkers of oxidative stress.</p>
dc.identifier.submissionpathoapubs/2848
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Medicine, Division of Cardiovascular Medicine


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Copyright © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Except where otherwise noted, this item's license is described as Copyright © 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.