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      Ambient Air Pollution Is Associated With the Severity of Coronary Atherosclerosis and Incident Myocardial Infarction in Patients Undergoing Elective Cardiac Evaluation

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          Abstract

          Background

          The effect of air pollution exposure on atherosclerosis severity or incident clinical events in patients with coronary artery disease is not known.

          Methods and Results

          We conducted a prospective longitudinal cohort study of 6575 Ohio residents undergoing elective diagnostic coronary angiography. Multinomial regression and Cox proportional hazards models were used to assess the relationship between exposure to fine particulate matter <2.5 μm in diameter ( PM 2.5) and nitrogen dioxide on coronary artery disease severity at baseline and risk of myocardial infarction, stroke, or all‐cause mortality over 3 years of follow‐up. Among participants with coronary artery disease, exposure to PM 2.5 levels was associated with increased likelihood of having coronary atherosclerosis that was mild (odds ratio 1.43, 95% CI 1.11–1.83, P=0.005) and severe (odds ratio 1.63, 95% CI 1.26–2.11, P<0.0001), with the effect on severe coronary artery disease being significantly increased compared with mild disease ( P trend=0.03). Exposure to higher PM 2.5 levels was also significantly associated with increased risk of incident myocardial infarction (hazard ratio 1.33, 95% CI 1.02–1.73, P=0.03) but not stroke or all‐cause mortality. The association of PM 2.5 with incident myocardial infarction was not affected after adjustment for Framingham Adult Treatment Panel III ( ATP III) risk score or statin therapy. In comparison, there were no significant associations between nitrogen dioxide levels and all‐cause mortality or risk of stroke after adjustment for Framingham ATP III risk score.

          Conclusions

          Exposure to PM 2.5 increased the likelihood of having severe coronary artery disease and the risk of incident myocardial infarction among patients undergoing elective cardiac evaluation. These results suggest that ambient air pollution exposure may be a modifiable risk factor for risk of myocardial infarction in a highly susceptible patient population.

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          Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model.

          Qinghua Sun, Aixia Wang, Ximei Jin … (2005)
          Recent studies have suggested a link between inhaled particulate matter exposure in urban areas and susceptibility to cardiovascular events; however, the precise mechanisms remain to be determined. To test the hypothesis that subchronic exposure to environmentally relevant particulate matter, even at low concentrations, potentiates atherosclerosis and alters vasomotor tone in a susceptible disease model. Between July 21, 2004, and January 12, 2005, 28 apolipoprotein E-/- (apoE-/-) mice were, based on randomized assignments, fed with normal chow or high-fat chow and exposed to concentrated ambient particles of less than 2.5 microm (PM2.5) or filtered air (FA) in Tuxedo, NY, for 6 hours per day, 5 days per week for a total of 6 months. Composite atherosclerotic plaque in the thoracic and abdominal aorta and vasomotor tone changes. In the high-fat chow group, the mean (SD) composite plaque area of PM2.5 vs FA was 41.5% (9.8%) vs 26.2% (8.6%), respectively (P<.001); and in the normal chow group, the composite plaque area was 19.2% (13.1%) vs 13.2% (8.1%), respectively (P = .15). Lipid content in the aortic arch measured by oil red-O staining revealed a 1.5-fold increase in mice fed the high-fat chow and exposed to PM2.5 vs FA (30.0 [8.2] vs 20.0 [7.0]; 95% confidence interval [CI], 1.21-1.83; P = .02). Vasoconstrictor responses to phenylephrine and serotonin challenge in the thoracic aorta of mice fed high-fat chow and exposed to PM2.5 were exaggerated compared with exposure to FA (mean [SE], 134.2% [5.2%] vs 100.9% [2.9%], for phenylephrine, and 156.0% [5.6%] vs 125.1% [7.5%], for serotonin; both P = .03); relaxation to the endothelium-dependent agonist acetylcholine was attenuated (mean [SE] of half-maximal dose for dilation, 8.9 [0.2] x 10(-8) vs 4.3 [0.1] x 10(-8), respectively; P = .04). Mice fed high-fat chow and exposed to PM2.5 demonstrated marked increases in macrophage infiltration, expression of the inducible isoform of nitric oxide synthase, increased generation of reactive oxygen species, and greater immunostaining for the protein nitration product 3-nitrotyrosine (all P<.001). In an apoE-/- mouse model, long-term exposure to low concentration of PM2.5 altered vasomotor tone, induced vascular inflammation, and potentiated atherosclerosis.
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            Adverse cardiovascular effects of air pollution.

            Nicholas Mills, Ken Donaldson, Paddy Hadoke … (2009)
            Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular disease in urban communities. Acute exposure has been linked to a range of adverse cardiovascular events including hospital admissions with angina, myocardial infarction, and heart failure. Long-term exposure increases an individual's lifetime risk of death from coronary heart disease. The main arbiter of these adverse health effects seems to be combustion-derived nanoparticles that incorporate reactive organic and transition metal components. Inhalation of this particulate matter leads to pulmonary inflammation with secondary systemic effects or, after translocation from the lung into the circulation, to direct toxic cardiovascular effects. Through the induction of cellular oxidative stress and proinflammatory pathways, particulate matter augments the development and progression of atherosclerosis via detrimental effects on platelets, vascular tissue, and the myocardium. These effects seem to underpin the atherothrombotic consequences of acute and chronic exposure to air pollution. An increased understanding of the mediators and mechanisms of these processes is necessary if we are to develop strategies to protect individuals at risk and reduce the effect of air pollution on cardiovascular disease.
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              Ambient Air Pollution and Atherosclerosis in Los Angeles

              Nino Künzli, Michael Jerrett, Wendy J. Mack … (2004)
              Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 μm in aerodynamic diameter (PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects’ residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 μg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 μg/m3 PM2.5, CIMT increased by 5.9% (95% confidence interval, 1–11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9–4.3% (p-values, 0.05–0.1). Among older subjects (≥60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and CIMT were larger with the strongest associations in women ≥60 years of age (15.7%, 5.7–26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.
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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): 28 July 2016
                Publication date Collection: August 2016
                Volume: 5
                Issue: 8 ( doiID: 10.1002/jah3.2016.5.issue-8 )
                Electronic Location Identifier: e003947
                Affiliations
                [ 1 ] Department of Preventive Medicine Keck School of MedicineUniversity of Southern California Los Angeles CA
                [ 2 ] Institute for Genetic Medicine Keck School of MedicineUniversity of Southern California Los Angeles CA
                [ 3 ] Department of Cardiovascular MedicineCleveland Clinic Cleveland OH
                [ 4 ] Department of Cellular and Molecular MedicineCleveland Clinic Cleveland OH
                [ 5 ]Sonoma Technologies, Inc. Petaluma CA
                Author notes
                [*] [* ] Correspondence to: Hooman Allayee, PhD, Institute for Genetic Medicine, Keck School of Medicine, University of Southern California, 2250 Alcazar Street, CSC202, Los Angeles, CA 90033. E‐mail: hallayee@ 123456usc.edu
                Article
                Publisher ID: JAH31671
                DOI: 10.1161/JAHA.116.003947
                PMC ID: 5015312
                PubMed ID: 27468926
                SO-VID: 2f9d6f19-c327-44e0-99e0-8c94db4852a1
                Copyright © © 2016 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 : 21 June 2016
                Date accepted : 07 July 2016
                Page count
                Pages: 19
                Funding
                Funded by: NIH
                Award ID: P01ES022845
                Award ID: P30ES007048
                Award ID: R01ES021801
                Award ID: R01ES021801‐S3
                Award ID: R01ES025786
                Award ID: R01HL103866
                Award ID: P20HL113452
                Award ID: P01HL098055
                Award ID: P01HL076491
                Award ID: R01HL103931
                Funded by: U.S. EPA
                Award ID: RD83544101
                Funded by: Wright Foundation
                Categories
                Subject: Original Research
                Subject: Original Research
                Subject: Epidemiology
                Custom metadata
                source-schema-version-number 2.0
                component-id jah31671
                cover-date August 2016
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:24.08.2016

                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: air pollution,coronary atherosclerosis,myocardial infarction,epidemiology,coronary artery disease,secondary prevention,quality and outcomes
                Data availability:
                ScienceOpen disciplines: Cardiovascular Medicine
                Keywords: air pollution, coronary atherosclerosis, myocardial infarction, epidemiology, coronary artery disease, secondary prevention, quality and outcomes

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