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      Longitudinal Associations of Smoke-Free Policies and Incident Cardiovascular Disease : CARDIA Study

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          Abstract

          <div class="section"> <a class="named-anchor" id="S1"> <!-- named anchor --> </a> <h5 class="section-title" id="d6915268e173">Background</h5> <p id="P1">Smoke-free legislation has been associated with lower rates of cardiovascular disease hospital admissions in ecologic studies. However, prior studies lacked detailed information on individual-level factors (e.g. socio-demographic and clinical characteristics) that could potentially confound associations. Our objective was to estimate associations of smoke-free policies with incident cardiovascular disease in a longitudinal cohort after controlling for socio-demographics, cardiovascular disease risk factors, and policy covariates. </p> </div><div class="section"> <a class="named-anchor" id="S2"> <!-- named anchor --> </a> <h5 class="section-title" id="d6915268e178">Methods</h5> <p id="P2">Longitudinal data from 3,783 black and white adults in the Coronary Artery Risk Development in Young Adults (CARDIA) study (1995-2015) were linked to state, county and local 100% smoke-free policies in bars, restaurants, and non-hospitality workplaces by census tract. Extended Cox regression estimated hazard ratios (HRs) of incident cardiovascular disease associated with time-dependent smoke-free policy exposures. Models were adjusted for socio-demographic characteristics, cardiovascular disease risk factors, state cigarette tax, participant-reported presence of a smoking ban at their workplace, field center, and metropolitan statistical area poverty. </p> </div><div class="section"> <a class="named-anchor" id="S3"> <!-- named anchor --> </a> <h5 class="section-title" id="d6915268e183">Results</h5> <p id="P3">During a median follow-up of 20 years (68,332 total person-years), 172 participants had an incident cardiovascular disease event (2.5 per 1,000 person-years). Over the follow-up period, 80% of participants lived in areas with smoke-free policies in restaurants, 67% in bars, and 65% in non-hospitality workplaces. In fully adjusted models, participants living in an area with a restaurant, bar, or workplace smoke-free policy had lower risk of incident cardiovascular disease compared to those in areas without smoke-free policies (HR: 0.75, 95% CI: 0.49, 1.15; HR: 0.76, 95% CI: 0.47, 1.24; HR: 0.54, 95% CI: 0.34, 0.86, respectively; HR 0.58, 95% CI: 0.33, 1.00 for living in an area with all 3 types of policies compared to none). The estimated preventive fraction was 25% for restaurant policies, 24% for bar policies, and 46% for workplace policies. </p> </div><div class="section"> <a class="named-anchor" id="S4"> <!-- named anchor --> </a> <h5 class="section-title" id="d6915268e188">Conclusions</h5> <p id="P4">Consistent with prior ecologic studies, these individual-based data add to the evidence that 100% smoke-free policies are associated with lower risk of cardiovascular disease among middle-aged adults. </p> </div>

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          Most cited references40

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          Global and regional patterns in cardiovascular mortality from 1990 to 2013.

          There is a global commitment to reduce premature cardiovascular diseases (CVDs) 25% by 2025. CVD mortality rates have declined dramatically over the past 2 decades, yet the number of life years lost to premature CVD deaths is increasing in low- and middle-income regions. Ischemic heart disease and stroke remain the leading causes of premature death in the world; however, there is wide regional variation in these patterns. Some regions, led by Central Asia, face particularly high rates of premature death from ischemic heart disease. Sub-Saharan Africa and Asia suffer disproportionately from death from stroke. The purpose of the present report is to (1) describe global trends and regional variation in premature mortality attributable to CVD, (2) review past and current approaches to the measurement of these trends, and (3) describe the limitations of existing models of epidemiological transitions for explaining the observed distribution and trends of CVD mortality. We describe extensive variation both between and within regions even while CVD remains a dominant cause of death. Policies and health interventions will need to be tailored and scaled for a broad range of local conditions to achieve global goals for the improvement of cardiovascular health.
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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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              Cardiovascular mortality and exposure to airborne fine particulate matter and cigarette smoke: shape of the exposure-response relationship.

              Fine particulate matter exposure from both ambient air pollution and secondhand cigarette smoke has been associated with larger risks of cardiovascular mortality than would be expected on the basis of linear extrapolations of the relative risks from active smoking. This study directly assessed the shape of the exposure-response relationship between cardiovascular mortality and fine particulates from cigarette smoke and ambient air pollution. Prospective cohort data for >1 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II in 1982. Cox proportional hazards regression models that included variables for increments of cigarette smoking and variables to control for education, marital status, body mass, alcohol consumption, occupational exposures, and diet were used to describe the mortality experience of the cohort. Adjusted relative risks of mortality were plotted against estimated average daily dose of fine particulate matter from cigarette smoke along with comparison estimates for secondhand cigarette smoke and air pollution. There were substantially increased cardiovascular mortality risks at very low levels of active cigarette smoking and smaller but significant excess risks even at the much lower exposure levels associated with secondhand cigarette smoke and ambient air pollution. Relatively low levels of fine particulate exposure from either air pollution or secondhand cigarette smoke are sufficient to induce adverse biological responses increasing the risk of cardiovascular disease mortality. The exposure-response relationship between cardiovascular disease mortality and fine particulate matter is relatively steep at low levels of exposure and flattens out at higher exposures.
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                Author and article information

                Journal
                Circulation
                Circulation
                Ovid Technologies (Wolters Kluwer Health)
                0009-7322
                1524-4539
                August 07 2018
                August 07 2018
                : 138
                : 6
                : 557-566
                Affiliations
                [1 ]Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL (S.L.M., A.J.C., K.N.K.).
                [2 ]Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneap-olis (R.W., P.J.S., D.R.J.).
                [3 ]Department of Nutrition, University of North Carolina Gillings School of Public Health, Chapel Hill (P.G.-L.).
                Article
                10.1161/CIRCULATIONAHA.117.032302
                6202173
                29735485
                24af7db0-eb87-41b5-adab-516544349a5f
                © 2018
                History

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