Ambient air pollution and the progression of atherosclerosis in adults
Cross-sectional studies suggest an association between exposure to ambient air pollution and atherosclerosis. We investigated the association between outdoor air quality and progression of subclinical atherosclerosis (common carotid artery intima-media thickness, CIMT). We examined data from five do...
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description | Cross-sectional studies suggest an association between exposure to ambient air pollution and atherosclerosis. We investigated the association between outdoor air quality and progression of subclinical atherosclerosis (common carotid artery intima-media thickness, CIMT).
We examined data from five double-blind randomized trials that assessed effects of various treatments on the change in CIMT. The trials were conducted in the Los Angeles area. Spatial models and land-use data were used to estimate the home outdoor mean concentration of particulate matter up to 2.5 micrometer in diameter (PM2.5), and to classify residence by proximity to traffic-related pollution (within 100 m of highways). PM2.5 and traffic proximity were positively associated with CIMT progression. Adjusted coefficients were larger than crude associations, not sensitive to modelling specifications, and statistically significant for highway proximity while of borderline significance for PM2.5 (P = 0.08). Annual CIMT progression among those living within 100 m of a highway was accelerated (5.5 micrometers/yr [95%CI: 0.13-10.79; p = 0.04]) or more than twice the population mean progression. For PM2.5, coefficients were positive as well, reaching statistical significance in the socially disadvantaged; in subjects reporting lipid lowering treatment at baseline; among participants receiving on-trial treatments; and among the pool of four out of the five trials.
Consistent with cross-sectional findings and animal studies, this is the first study to report an association between exposure to air pollution and the progression of atherosclerosis--indicated with CIMT change--in humans. Ostensibly, our results suggest that air pollution may contribute to the acceleration of cardiovascular disease development--the main causes of morbidity and mortality in many countries. However, the heterogeneity of the volunteering populations across the five trials, the limited sample size within trials and other relevant subgroups, and the fact that some key findings reached statistical significance in subgroups rather than the sample precludes generalizations to the general population. |
doi_str_mv | 10.1371/journal.pone.0009096 |
format | Article |
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We examined data from five double-blind randomized trials that assessed effects of various treatments on the change in CIMT. The trials were conducted in the Los Angeles area. Spatial models and land-use data were used to estimate the home outdoor mean concentration of particulate matter up to 2.5 micrometer in diameter (PM2.5), and to classify residence by proximity to traffic-related pollution (within 100 m of highways). PM2.5 and traffic proximity were positively associated with CIMT progression. Adjusted coefficients were larger than crude associations, not sensitive to modelling specifications, and statistically significant for highway proximity while of borderline significance for PM2.5 (P = 0.08). Annual CIMT progression among those living within 100 m of a highway was accelerated (5.5 micrometers/yr [95%CI: 0.13-10.79; p = 0.04]) or more than twice the population mean progression. For PM2.5, coefficients were positive as well, reaching statistical significance in the socially disadvantaged; in subjects reporting lipid lowering treatment at baseline; among participants receiving on-trial treatments; and among the pool of four out of the five trials.
Consistent with cross-sectional findings and animal studies, this is the first study to report an association between exposure to air pollution and the progression of atherosclerosis--indicated with CIMT change--in humans. Ostensibly, our results suggest that air pollution may contribute to the acceleration of cardiovascular disease development--the main causes of morbidity and mortality in many countries. However, the heterogeneity of the volunteering populations across the five trials, the limited sample size within trials and other relevant subgroups, and the fact that some key findings reached statistical significance in subgroups rather than the sample precludes generalizations to the general population.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0009096</identifier><identifier>PMID: 20161713</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Adults ; Air Pollutants - chemistry ; Air Pollutants - poisoning ; Air pollution ; Air Pollution - adverse effects ; Air Pollution - analysis ; Air Pollution, Indoor - adverse effects ; Air Pollution, Indoor - analysis ; Air quality ; Analysis ; Animals ; Anticholesteremic agents ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - etiology ; Cardiovascular diseases ; Cardiovascular Disorders ; Carotid Arteries - drug effects ; Carotid Arteries - pathology ; Carotid artery ; Disease Progression ; Environmental Exposure - adverse effects ; Environmental Exposure - analysis ; Exposure ; Health risk assessment ; Highways ; Humans ; Land use ; Los Angeles ; Micrometers ; Morbidity ; Mortality ; Outdoor air quality ; Particle Size ; Particulate emissions ; Particulate matter ; Particulate Matter - chemistry ; Particulate Matter - poisoning ; Pollution ; Population (statistical) ; Preventive medicine ; Proximity ; Public Health and Epidemiology ; Public Health and Epidemiology/Environmental Health ; Public Health and Epidemiology/Epidemiology ; Public Health and Epidemiology/Global Health ; Public Health and Epidemiology/Preventive Medicine ; Randomized Controlled Trials as Topic ; Risk Assessment ; Spatial data ; Statistical analysis ; Statistical significance ; Statistics ; Studies ; Subgroups ; Traffic models ; Tunica Intima - drug effects ; Tunica Intima - pathology ; Tunica Media - drug effects ; Tunica Media - pathology</subject><ispartof>PloS one, 2010-02, Vol.5 (2), p.e9096</ispartof><rights>COPYRIGHT 2010 Public Library of Science</rights><rights>2010 Kuenzli et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Kuenzli et al. 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c757t-d559f975a2cc7842c0cfe88c2bafebf53c28121dfb0edb7715b19040a05d1a3a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817007/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2817007/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2106,2932,23875,27933,27934,53800,53802</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20161713$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Myer, Landon</contributor><creatorcontrib>Künzli, Nino</creatorcontrib><creatorcontrib>Jerrett, Michael</creatorcontrib><creatorcontrib>Garcia-Esteban, Raquel</creatorcontrib><creatorcontrib>Basagaña, Xavier</creatorcontrib><creatorcontrib>Beckermann, Bernardo</creatorcontrib><creatorcontrib>Gilliland, Frank</creatorcontrib><creatorcontrib>Medina, Merce</creatorcontrib><creatorcontrib>Peters, John</creatorcontrib><creatorcontrib>Hodis, Howard N</creatorcontrib><creatorcontrib>Mack, Wendy J</creatorcontrib><title>Ambient air pollution and the progression of atherosclerosis in adults</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cross-sectional studies suggest an association between exposure to ambient air pollution and atherosclerosis. We investigated the association between outdoor air quality and progression of subclinical atherosclerosis (common carotid artery intima-media thickness, CIMT).
We examined data from five double-blind randomized trials that assessed effects of various treatments on the change in CIMT. The trials were conducted in the Los Angeles area. Spatial models and land-use data were used to estimate the home outdoor mean concentration of particulate matter up to 2.5 micrometer in diameter (PM2.5), and to classify residence by proximity to traffic-related pollution (within 100 m of highways). PM2.5 and traffic proximity were positively associated with CIMT progression. Adjusted coefficients were larger than crude associations, not sensitive to modelling specifications, and statistically significant for highway proximity while of borderline significance for PM2.5 (P = 0.08). Annual CIMT progression among those living within 100 m of a highway was accelerated (5.5 micrometers/yr [95%CI: 0.13-10.79; p = 0.04]) or more than twice the population mean progression. For PM2.5, coefficients were positive as well, reaching statistical significance in the socially disadvantaged; in subjects reporting lipid lowering treatment at baseline; among participants receiving on-trial treatments; and among the pool of four out of the five trials.
Consistent with cross-sectional findings and animal studies, this is the first study to report an association between exposure to air pollution and the progression of atherosclerosis--indicated with CIMT change--in humans. Ostensibly, our results suggest that air pollution may contribute to the acceleration of cardiovascular disease development--the main causes of morbidity and mortality in many countries. 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We investigated the association between outdoor air quality and progression of subclinical atherosclerosis (common carotid artery intima-media thickness, CIMT).
We examined data from five double-blind randomized trials that assessed effects of various treatments on the change in CIMT. The trials were conducted in the Los Angeles area. Spatial models and land-use data were used to estimate the home outdoor mean concentration of particulate matter up to 2.5 micrometer in diameter (PM2.5), and to classify residence by proximity to traffic-related pollution (within 100 m of highways). PM2.5 and traffic proximity were positively associated with CIMT progression. Adjusted coefficients were larger than crude associations, not sensitive to modelling specifications, and statistically significant for highway proximity while of borderline significance for PM2.5 (P = 0.08). Annual CIMT progression among those living within 100 m of a highway was accelerated (5.5 micrometers/yr [95%CI: 0.13-10.79; p = 0.04]) or more than twice the population mean progression. For PM2.5, coefficients were positive as well, reaching statistical significance in the socially disadvantaged; in subjects reporting lipid lowering treatment at baseline; among participants receiving on-trial treatments; and among the pool of four out of the five trials.
Consistent with cross-sectional findings and animal studies, this is the first study to report an association between exposure to air pollution and the progression of atherosclerosis--indicated with CIMT change--in humans. Ostensibly, our results suggest that air pollution may contribute to the acceleration of cardiovascular disease development--the main causes of morbidity and mortality in many countries. However, the heterogeneity of the volunteering populations across the five trials, the limited sample size within trials and other relevant subgroups, and the fact that some key findings reached statistical significance in subgroups rather than the sample precludes generalizations to the general population.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>20161713</pmid><doi>10.1371/journal.pone.0009096</doi><tpages>e9096</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2010-02, Vol.5 (2), p.e9096 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_1289251183 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Adult Adults Air Pollutants - chemistry Air Pollutants - poisoning Air pollution Air Pollution - adverse effects Air Pollution - analysis Air Pollution, Indoor - adverse effects Air Pollution, Indoor - analysis Air quality Analysis Animals Anticholesteremic agents Arteriosclerosis Atherosclerosis Atherosclerosis - etiology Cardiovascular diseases Cardiovascular Disorders Carotid Arteries - drug effects Carotid Arteries - pathology Carotid artery Disease Progression Environmental Exposure - adverse effects Environmental Exposure - analysis Exposure Health risk assessment Highways Humans Land use Los Angeles Micrometers Morbidity Mortality Outdoor air quality Particle Size Particulate emissions Particulate matter Particulate Matter - chemistry Particulate Matter - poisoning Pollution Population (statistical) Preventive medicine Proximity Public Health and Epidemiology Public Health and Epidemiology/Environmental Health Public Health and Epidemiology/Epidemiology Public Health and Epidemiology/Global Health Public Health and Epidemiology/Preventive Medicine Randomized Controlled Trials as Topic Risk Assessment Spatial data Statistical analysis Statistical significance Statistics Studies Subgroups Traffic models Tunica Intima - drug effects Tunica Intima - pathology Tunica Media - drug effects Tunica Media - pathology |
title | Ambient air pollution and the progression of atherosclerosis in adults |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-02T21%3A51%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Ambient%20air%20pollution%20and%20the%20progression%20of%20atherosclerosis%20in%20adults&rft.jtitle=PloS%20one&rft.au=K%C3%BCnzli,%20Nino&rft.date=2010-02-08&rft.volume=5&rft.issue=2&rft.spage=e9096&rft.pages=e9096-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0009096&rft_dat=%3Cgale_plos_%3EA473917013%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1289251183&rft_id=info:pmid/20161713&rft_galeid=A473917013&rft_doaj_id=oai_doaj_org_article_67745466a0b1417ab48d6c46b75d72ab&rfr_iscdi=true |