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      Short term impact of smoke-free legislation in England: retrospective analysis of hospital admissions for myocardial infarction

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          Abstract

          Objective To measure the short term impact on hospital admissions for myocardial infarction of the introduction of smoke-free legislation in England on 1 July 2007.

          Design An interrupted time series design with routinely collected hospital episode statistics data. Analysis of admissions from July 2002 to September 2008 (providing five years’ data from before the legislation and 15 months’ data from after) using segmented Poisson regression.

          Setting England.

          Population All patients aged 18 or older living in England with an emergency admission coded with a primary diagnosis of myocardial infarction.

          Main outcome measures Weekly number of completed hospital admissions.

          Results After adjustment for secular and seasonal trends and variation in population size, there was a small but significant reduction in the number of emergency admissions for myocardial infarction after the implementation of smoke-free legislation (−2.4%, 95% confidence interval −4.06% to −0.66%, P=0.007). This equates to 1200 fewer emergency admissions for myocardial infarction (1600 including readmissions) in the first year after legislation. The reduction in admissions was significant in men (3.1%, P=0.001) and women (3.8%, P=0.007) aged 60 and over, and men (3.5%, P<0.01) but not women (2.5% P=0.38) aged under 60.

          Conclusion This study adds to a growing body of evidence that smoke-free legislation leads to reductions in myocardial infarctions. It builds on previous work by showing that such declines are observed even when underlying reductions in admissions and potential confounders are controlled for. The considerably smaller decline in admissions observed in England compared with many other jurisdictions probably reflects aspects of the study design and the relatively low levels of exposure to secondhand smoke in England before the legislation.

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          Most cited references66

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          Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

          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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            Increased particulate air pollution and the triggering of myocardial infarction.

            Elevated concentrations of ambient particulate air pollution have been associated with increased hospital admissions for cardiovascular disease. Whether high concentrations of ambient particles can trigger the onset of acute myocardial infarction (MI), however, remains unknown. We interviewed 772 patients with MI in the greater Boston area between January 1995 and May 1996 as part of the Determinants of Myocardial Infarction Onset Study. Hourly concentrations of particle mass <2.5 microm (PM(2.5)), carbon black, and gaseous air pollutants were measured. A case-crossover approach was used to analyze the data for evidence of triggering. The risk of MI onset increased in association with elevated concentrations of fine particles in the previous 2-hour period. In addition, a delayed response associated with 24-hour average exposure 1 day before the onset of symptoms was observed. Multivariate analyses considering both time windows jointly revealed an estimated odds ratio of 1.48 associated with an increase of 25 microg/m(3) PM(2.5) during a 2-hour period before the onset and an odds ratio of 1.69 for an increase of 20 microg/m(3) PM(2.5) in the 24-hour period 1 day before the onset (95% CIs 1.09, 2.02 and 1.13, 2.34, respectively). The present study suggests that elevated concentrations of fine particles in the air may transiently elevate the risk of MIs within a few hours and 1 day after exposure. Further studies in other locations are needed to clarify the importance of this potentially preventable trigger of MI.
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              Cardiovascular effects of secondhand smoke: nearly as large as smoking.

              Secondhand smoke increases the risk of coronary heart disease by approximately 30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system--platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size--is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.
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                Author and article information

                Contributors
                Role: research officer
                Role: senior analyst
                Role: professor of social policy
                Role: clinical reader in public health, Role: clinical senior lecturer
                Journal
                BMJ
                bmj
                BMJ : British Medical Journal
                BMJ Publishing Group Ltd.
                0959-8138
                1468-5833
                2010
                2010
                08 June 2010
                : 340
                : c2161
                Affiliations
                [1 ]School for Health, University of Bath, Bath BA2 7AY
                [2 ]UK Centre for Tobacco Control Studies, University of Bath, Bath
                [3 ]South West Public Health Observatory, Bristol BS8 2RA
                [4 ]Department of Social and Policy Sciences, University of Bath, Bath
                [5 ]London School of Hygiene and Tropical Medicine, London WC1E 7HT
                Author notes
                Correspondence to: A Gilmore, School for Health, University of Bath, Bath BA2 7AY a.gilmore@ 123456bath.ac.uk
                Article
                simm707158
                10.1136/bmj.c2161
                2882555
                20530563
                e5202e10-a849-4a48-bc67-d77c4af6f906
                © Sims et al 2010

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode.

                History
                : 11 February 2010
                Categories
                Research
                Smoking and tobacco
                Drugs: cardiovascular system
                Ischaemic heart disease
                Health education
                Health promotion
                Smoking

                Medicine
                Medicine

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