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      Short‐Term Exposure to Fine Particulate Matter Air Pollution Is Preferentially Associated With the Risk of ST‐Segment Elevation Acute Coronary Events

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          Abstract

          Background

          Air pollution is associated with greater cardiovascular event risk, but the types of events and specific persons at risk remain unknown. This analysis evaluates effects of short‐term exposure to fine particulate matter air pollution with risk of acute coronary syndrome events, including ST‐segment elevation myocardial infarction, non– ST‐segment elevation myocardial infarction, unstable angina, and non– ST‐segment elevation acute coronary syndrome.

          Methods and Results

          Acute coronary syndrome events treated at Intermountain Healthcare hospitals in urban areas of Utah's Wasatch Front were collected between September 1993 and May 2014 (N=16 314). A time‐stratified case‐crossover design was performed matching fine particulate matter air pollution exposure at the time of each event with referent periods when the event did not occur. Patients served as their own controls, and odds ratios were estimated using nonthreshold and threshold conditional logistic regression models. In patients with angiographic coronary artery disease, odds ratios for a 10‐μg/m 3 increase in concurrent‐day fine particulate matter air pollution >25 μg/m³ were 1.06 (95% CI 1.02–1.11) for all acute coronary syndrome, 1.15 (95% CI 1.03–1.29) for ST‐segment elevation myocardial infarction, 1.02 (95% CI 0.97–1.08) for non– ST‐segment elevation myocardial infarction, 1.09 (95% CI 1.02–1.17) for unstable angina, and 1.05 (95% CI 1.00–1.10) for non– ST‐segment elevation acute coronary syndrome events. Excess risk from fine particulate matter air pollution exposure was not observed in patients without angiographic coronary artery disease.

          Conclusions

          Elevated fine particulate matter air pollution exposures contribute to triggering acute coronary events, especially ST‐segment elevation myocardial infarction, in those with existing seriously diseased coronary arteries but not in those with nondiseased coronary arteries.

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          A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010

          Stephen S Lim, Theo Vos, Abraham D. Flaxman … (2012)
          The Lancet, 380(9859), 2224-2260
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            Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

            C. Pope, Richard Burnett, George Thurston … (2004)
            Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.
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              Effects of long-term exposure to air pollution on natural-cause mortality: an analysis of 22 European cohorts within the multicentre ESCAPE project

              Rob Beelen, Ole Raaschou-Nielsen, Massimo Stafoggia … (2014)
              Few studies on long-term exposure to air pollution and mortality have been reported from Europe. Within the multicentre European Study of Cohorts for Air Pollution Effects (ESCAPE), we aimed to investigate the association between natural-cause mortality and long-term exposure to several air pollutants. We used data from 22 European cohort studies, which created a total study population of 367,251 participants. All cohorts were general population samples, although some were restricted to one sex only. With a strictly standardised protocol, we assessed residential exposure to air pollutants as annual average concentrations of particulate matter (PM) with diameters of less than 2.5 μm (PM2.5), less than 10 μm (PM10), and between 10 μm and 2.5 μm (PMcoarse), PM2.5 absorbance, and annual average concentrations of nitrogen oxides (NO2 and NOx), with land use regression models. We also investigated two traffic intensity variables-traffic intensity on the nearest road (vehicles per day) and total traffic load on all major roads within a 100 m buffer. We did cohort-specific statistical analyses using confounder models with increasing adjustment for confounder variables, and Cox proportional hazards models with a common protocol. We obtained pooled effect estimates through a random-effects meta-analysis. The total study population consisted of 367,251 participants who contributed 5,118,039 person-years at risk (average follow-up 13.9 years), of whom 29,076 died from a natural cause during follow-up. A significantly increased hazard ratio (HR) for PM2.5 of 1.07 (95% CI 1.02-1.13) per 5 μg/m(3) was recorded. No heterogeneity was noted between individual cohort effect estimates (I(2) p value=0.95). HRs for PM2.5 remained significantly raised even when we included only participants exposed to pollutant concentrations lower than the European annual mean limit value of 25 μg/m(3) (HR 1.06, 95% CI 1.00-1.12) or below 20 μg/m(3) (1.07, 1.01-1.13). Long-term exposure to fine particulate air pollution was associated with natural-cause mortality, even within concentration ranges well below the present European annual mean limit value. European Community's Seventh Framework Program (FP7/2007-2011). Copyright © 2014 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Am Heart Assoc
                Journal ID (iso-abbrev): J Am Heart Assoc
                Journal ID (doi): 10.1002/(ISSN)2047-9980
                Journal ID (publisher-id): JAH3
                Journal ID (hwp): ahaoa
                Title: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2047-9980
                Publication date (Electronic): 08 December 2015
                Publication date Collection: December 2015
                Volume: 4
                Issue: 12 ( doiID: 10.1002/jah3.2015.4.issue-12 )
                Electronic Location Identifier: e002506
                Affiliations
                [ 1 ] Department of EconomicsBrigham Young University Provo UT
                [ 2 ] Intermountain Heart InstituteIntermountain Medical Center Murray UT
                [ 3 ] Department of Internal MedicineUniversity of Utah Salt Lake City UT
                Author notes
                [*] [* ] Correspondence to: C. Arden Pope III, PhD, 142 FOB, Brigham Young University, Provo, UT 84602. E‐mail: cap3@ 123456byu.edu
                Article
                Publisher ID: JAH31228
                DOI: 10.1161/JAHA.115.002506
                PMC ID: 4845284
                PubMed ID: 26645834
                SO-VID: 3421dace-abe6-4524-90a6-14e0c81c23d2
                Copyright © © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
                License:

                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.

                History
                Date received : 24 August 2015
                Date accepted : 21 October 2015
                Page count
                Pages: 10
                Funding
                Funded by: National Institutes of Health
                Award ID: ES019217
                Funded by: Mary Lou Fulton Professorship at Brigham Young University
                Categories
                Subject: Original Research
                Subject: Original Research
                Subject: Epidemiology
                Custom metadata
                source-schema-version-number 2.0
                component-id jah31228
                cover-date December 2015
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.8.4 mode:remove_FC converted:03.03.2016

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: acute coronary syndrome,air pollution,cardiovascular disease,particulate matter,st‐segment elevation myocardial infarction,epidemiology,acute coronary syndromes
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: acute coronary syndrome, air pollution, cardiovascular disease, particulate matter, st‐segment elevation myocardial infarction, epidemiology, acute coronary syndromes

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