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      Short-term effects of air pollution on a range of cardiovascular events in England and Wales: case-crossover analysis of the MINAP database, hospital admissions and mortality

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          Abstract

          Objective

          To inform potential pathophysiological mechanisms of air pollution effects on cardiovascular disease (CVD), we investigated short-term associations between ambient air pollution and a range of cardiovascular events from three national databases in England and Wales.

          Methods

          Using a time-stratified case-crossover design, over 400 000 myocardial infarction (MI) events from the Myocardial Ischaemia National Audit Project (MINAP) database, over 2 million CVD emergency hospital admissions and over 600 000 CVD deaths were linked with daily mean concentrations of carbon monoxide (CO), nitrogen dioxide (NO 2), particulate matter less than 10 μm in aerodynamic diameter (PM 10), particulate matter less than 2.5 μm in aerodynamic diameter (PM 2.5) and sulfur dioxide (SO 2), and daily maximum of 8-hourly running mean of O 3 measured at the nearest air pollution monitoring site to the place of residence. Pollutant effects were modelled using lags up to 4 days and adjusted for ambient temperature and day of week.

          Results

          For mortality, no CVD outcome analysed was clearly associated with any pollutant, except for PM 2.5 with arrhythmias, atrial fibrillation and pulmonary embolism. With hospital admissions, only NO 2 was associated with a raised risk: CVD 1.7% (95% CI 0.9 to 2.6), non-MI CVD 2.0% (1.1 to 2.9), arrhythmias 2.9% (0.6 to 5.2), atrial fibrillation 2.8% (0.3 to 5.4) and heart failure 4.4% (2.0 to 6.8) for a 10th–90th centile increase. With MINAP, only NO 2 was associated with an increased risk of MI, which was specific to non-ST-elevation myocardial infarction (non-STEMIs): 3.6% (95% CI 0.4 to 6.9).

          Conclusions

          This study found no clear evidence for pollution effects on STEMIs and stroke, which ultimately represent thrombogenic processes, though it did for pulmonary embolism. The strongest associations with air pollution were observed with selected non-MI outcomes.

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          Most cited references18

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          Fine particulate air pollution and mortality in 20 U.S. cities, 1987-1994.

          Air pollution in cities has been linked to increased rates of mortality and morbidity in developed and developing countries. Although these findings have helped lead to a tightening of air-quality standards, their validity with respect to public health has been questioned. We assessed the effects of five major outdoor-air pollutants on daily mortality rates in 20 of the largest cities and metropolitan areas in the United States from 1987 to 1994. The pollutants were particulate matter that is less than 10 microm in aerodynamic diameter (PM10), ozone, carbon monoxide, sulfur dioxide, and nitrogen dioxide. We used a two-stage analytic approach that pooled data from multiple locations. After taking into account potential confounding by other pollutants, we found consistent evidence that the level of PM10 is associated with the rate of death from all causes and from cardiovascular and respiratory illnesses. The estimated increase in the relative rate of death from all causes was 0.51 percent (95 percent posterior interval, 0.07 to 0.93 percent) for each increase in the PM10 level of 10 microg per cubic meter. The estimated increase in the relative rate of death from cardiovascular and respiratory causes was 0.68 percent (95 percent posterior interval, 0.20 to 1.16 percent) for each increase in the PM10 level of 10 microg per cubic meter. There was weaker evidence that increases in ozone levels increased the relative rates of death during the summer, when ozone levels are highest, but not during the winter. Levels of the other pollutants were not significantly related to the mortality rate. There is consistent evidence that the levels of fine particulate matter in the air are associated with the risk of death from all causes and from cardiovascular and respiratory illnesses. These findings strengthen the rationale for controlling the levels of respirable particles in outdoor air.
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            Case-crossover analyses of air pollution exposure data: referent selection strategies and their implications for bias.

            The case-crossover design has been widely used to study the association between short-term air pollution exposure and the risk of an acute adverse health event. The design uses cases only; for each individual case, exposure just before the event is compared with exposure at other control (or "referent") times. Time-invariant confounders are controlled by making within-subject comparisons. Even more important in the air pollution setting is that time-varying confounders can also be controlled by design by matching referents to the index time. The referent selection strategy is important for reasons in addition to control of confounding. The case-crossover design makes the implicit assumption that there is no trend in exposure across the referent times. In addition, the statistical method that is used-conditional logistic regression-is unbiased only with certain referent strategies. We review here the case-crossover literature in the air pollution context, focusing on key issues regarding referent selection. We conclude with a set of recommendations for choosing a referent strategy with air pollution exposure data. Specifically, we advocate the time-stratified approach to referent selection because it ensures unbiased conditional logistic regression estimates, avoids bias resulting from time trend in the exposure series, and can be tailored to match on specific time-varying confounders.
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              Particulate air pollution and acute health effects.

              Epidemiological studies have consistently shown an association between particulate air pollution and not only exacerbations of illness in people with respiratory disease but also rises in the numbers of deaths from cardiovascular and respiratory disease among older people. Meta-analyses of these studies indicate that the associations are unlikely to be explained by any confounder, and suggest that they represent cause and effect. We propose that the explanation lies in the nature of the urban particulate cloud, which may contain up to 100000 nanometer-sized particles per mL, in what may be a gravimetric concentration of only 100-200 micrograms/m3 of pollutant. We suggest that such ultra-fine particles are able to provoke alveolar inflammation, with release of mediators capable, in susceptible individuals, of causing exacerbations of lung disease and of increasing blood coagulability, thus also explaining the observed increases in cardiovascular deaths associated with urban pollution episodes. This hypothesis is testable both experimentally and epidemiologically.
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                Author and article information

                Journal
                Heart
                Heart
                heartjnl
                heart
                Heart
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                1355-6037
                1468-201X
                15 July 2014
                4 June 2014
                : 100
                : 14
                : 1093-1098
                Affiliations
                [1 ]Department of Social and Environmental Health Research, London School of Hygiene and Tropical Medicine , London, UK
                [2 ]Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine , London, UK
                Author notes
                [Correspondence to ] Dr Ai Milojevic, Department of Social and Environmental Health Research, London School of Hygiene & Tropical Medicine, 15-17 Tavistock Place, London, WC1H 9SH, UK; ai.milojevic@ 123456lshtm.ac.uk
                Article
                heartjnl-2013-304963
                10.1136/heartjnl-2013-304963
                4078678
                24952943
                a8088e68-d886-4aa9-b483-e7d605b21d5d
                Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions

                This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 3.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/3.0/

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                Categories
                1506
                Cardiac Risk Factors and Prevention
                Original article
                Custom metadata
                unlocked

                Cardiovascular Medicine
                myocardial ischaemia and infarction (ihd),arrhythmias
                Cardiovascular Medicine
                myocardial ischaemia and infarction (ihd), arrhythmias

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