ChiroACCESS Article

Second Hand Smoke and Coronary Disease

This information is provided to you for use in conjunction with your clinical judgment and the specific needs of the patient.

ChiroACCESS Editorial Staff



Published on

May 19, 2010

Text Size:   (-) Decrease the text size for the main body of this article    (+) Increase the text size for the main body of this article
Share this:  Add to TwitterAdd to DiggAdd to del.icio.usAdd to FacebookAdd to GoogleAdd to LinkedInAdd to MixxAdd to MySpaceAdd to NewsvineAdd to RedditAdd to StumbleUponAdd to Yahoo

CigarettesA series of 2010 scientific publications highlight the cardiovascular risks associated with second hand smoke (SHS) to infants, children, and other adults.  In one study the crude rates of admissions to area hospitals were compared in regions with smoking bans and those without.  The areas with restaurant smoking bans had a 39% decrease in hospital admissions from cardiovascular disease (CDV) and a 33% reduction in admissions from respiratory conditions.  There was no decrease in the admissions in areas that did not impose a smoking ban.  A Cochrane review also concluded that “There is an increase in support for and compliance with smoking bans after the legislation.” A third study noted that “Sufficient evidence is reported in epidemiological research to support a causal association between SHS exposure and increased risks of CVD morbidity and mortality among both men and women. The risk of developing an acute cardiac syndrome or chronic lifetime coronary events is at least 30%. Similarly, reduction in the incidence of a myocardial infarction decreases by nearly 50% in the absence of SHS.”  Other studies below reflect the same serious risk of second hand smoke.

Second-hand smoke, cotinine levels, and risk of circulatory mortality in a large cohort study of never-smokers.  [LINK]

Epidemiology. 2010 Mar;21(2):207-14.

Gallo V, Neasham D, Airoldi L, Ferrari P, Jenab M, Boffetta P, Overvad K, Tjønneland A, Clavel-Chapelon F, Boeing H, Pala V, Palli D, Panico S, Tumino R, Arriola L, Lund E, Bueno-De-Mesquita B, Peeters PH, Melander O, Hallmans G, Riboli E, Saracci R, Vineis P.
Division of Epidemiology, Public Health and Primary Care, Imperial College, London W2 1PG, United Kingdom.

BACKGROUND: Exposure to second-hand smoke has been shown to be associated with increased cardiovascular mortality in several, but not all, epidemiologic studies. Our aim was to investigate the risk of circulatory death associated with exposure to second-hand smoke in never-smokers in a very large prospective study, the European Prospective Investigation into Cancer and Nutrition. A secondary aim was to use cotinine levels for cross-validating self-reported second-hand smoke exposure.

METHODS: Cox proportional hazard models were used to investigate the risk of death due to circulatory causes associated with second-hand smoke exposure in 135,233 never-smokers. Exposure to second-hand smoke was assessed through a questionnaire at enrollment and then validated against plasma cotinine measurements in a subsample.

RESULTS: Study participants who reported second-hand smoke exposure at home had higher cotinine levels (median plasma cotinine concentration in exposed = 0.82 microg/L; in those unexposed 0.02 microg/L). Second-hand smoke exposure at home was associated with an increased risk of dying from cardiovascular diseases (hazard ratio [HR] = 1.38 [95% confidence interval = 1.01-1.90]), all circulatory diseases (1.28 [0.98-1.69]), and coronary heart disease (1.31 [0.83-2.08]) after adjustment for age, sex, education, physical activity, and body mass index. Dose-response relationships were observed between exposure to second-hand smoke at home and risk of circulatory death (HR per each additional hour/d = 1.25 [1.04-1.50]). Having a partner who smokes more than 30 cigarettes per day considerably increased the risk of a circulatory death (2.94 [1.11-7.78]). Second-hand smoke exposure at home was not associated with total mortality (1.03 [0.93-1.13]).

DISCUSSION: Exposure to second-hand smoke at home (as confirmed by plasma cotinine levels) increases the risk of cardiovascular mortality.

Cotinine-assessed second-hand smoke exposure and risk of cardiovascular disease in older adults.  [LINK]

Heart. 2010 Jun;96(11):854-9.

Jefferis BJ, Lawlor DA, Ebrahim S, Wannamethee SG, Feyerabend C, Doig M, McMeekin L, Cook DG, Whincup PH.
UCL Department of Primary Care and Population Health, UCL Medical School, Rowland Hill Street, London NW3 2PF, UK;

Objectives: To examine whether second-hand smoke (SHS) exposure measured by serum cotinine is associated with increased coronary heart disease (CHD) and stroke risk among contemporary older British adults.

Design: Prospective population-based study with self-reported medical history and health behaviours. Fasting blood samples were analysed for serum cotinine and cardiovascular disease (CVD) risk markers.

Setting: Primary care centres in 25 British towns in 1998-2001. Patients 8512 60-79-year-old men and women selected from primary care registers.

Main outcome measures: Fatal and non-fatal myocardial infarction (MI; n=445) and stroke (n=386) during median 7.8-year follow-up.

Main exposure: Observational study of serum cotinine assayed from fasting blood sample using liquid chromatography tandem mass spectrometry method, and self-reported smoking history.

Results: Among 5374 non-smokers without pre-existing CVD, geometric mean cotinine was 0.15 ng/ml (IQR 0.05-0.30). Compared with non-smokers with cotinine </=0.05 ng/ml, higher cotinine levels (0.06-0.19, 0.2-0.7 and 0.71-15.0 ng/ml) showed little association with MI; adjusted HRs were 0.92 (95% CI 0.63 to 1.35), 1.07 (0.73 to 1.55) and 1.09 (0.69 to 1.72), p(trend)=0.69. Equivalent HRs for stroke were 0.82 (0.55 to 1.23), 0.74 (0.48 to 1.13) and 0.69 (0.41 to 1.17), p(trend)=0.065. The adjustment for sociodemographic, behavioural and CVD risk factors had little effect on the results. The HR of MI for smokers (1-9 cigarettes/day) compared with non-smokers with cotinine </=0.05 ng/ml was 2.14 (1.39 to 3.52) and 1.03 (0.52 to 2.04) for stroke.

Conclusions: In contemporary older men and women, SHS exposure (predominantly at low levels) was not related to CHD or stroke risks, but we cannot rule out the possibility of modest effects at higher exposure levels.

Secondhand smoke (SHS) exposure is associated with circulating markers of inflammation and endothelial function in adult men and women.  [LINK]

Atherosclerosis. 2010 Feb;208(2):550-6. Epub 2009 Jul 30.

Jefferis BJ, Lowe GD, Welsh P, Rumley A, Lawlor DA, Ebrahim S, Carson C, Doig M, Feyerabend C, McMeekin L, Wannamethee SG, Cook DG, Whincup PH.
Department Primary Care & Population Health, UCL Medical School, Rowland Hill St, NW3 2PF, London, UK.

AIMS: Secondhand smoke (SHS) exposure is associated with elevated CHD risks. Yet the pathways through which this may operate have not been investigated in epidemiologic studies with objective SHS exposure measures and a wide range of CHD risk factors associated with active smoking. Therefore we investigate associations between SHS exposure and CHD risk factors, to clarify how SHS exposure may raise risk of CHD.

METHODS: Cross-sectional population-based study of 5029 men and women aged 59-80 years from primary care practices in Great Britain. Smoking, behavioural and demographic information was reported in questionnaires; nurses made physical measurements and took blood samples for analysis of serum cotinine and markers of inflammation, hemostasis and endothelial dysfunction.

RESULTS: Active cigarette smokers had lower albumin and higher triglycerides, CRP, IL-6, white cell count, fibrinogen, blood viscosity, factor VIII, VWF and t-PA than non-smokers. Among non-smokers, serum cotinine levels were independently positively associated with CRP, fibrinogen, factor VIII, VWF and t-PA and inversely associated with albumin, after adjustment for age, gender, social and behavioural factors. The differences in CRP, fibrinogen and albumin between cotinine < or =0.05 and >0.7 ng/ml were one-third to one half the size of differences between cotinine < or =0.05 ng/ml and current smokers, but were of similar magnitude for VWF and t-PA.

CONCLUSIONS: Endothelial, inflammatory and haemostatic markers related to CHD risk showed independent associations with SHS exposure in the same direction as those for active smoking. Results aid understanding of the associations between SHS exposure and elevated CHD risks. Copyright 2009 Elsevier Ireland Ltd. All rights reserved.

Epidemiological evidence associating secondhand smoke exposure with cardiovascular disease.  [LINK]

Inflamm Allergy Drug Targets. 2009 Dec;8(5):321-7.

Faught BE, Flouris AD, Cairney J.
Faculty of Applied Health Sciences, Brock University, Ontario, L2S 3A1, Canada.

The objective of this paper was to review the epidemiological literature examining the association between secondhand smoke (SHS) and cardiovascular disease (CVD). Specifically, we examined the various screening methods available in assessing smoking behaviour and quantifying nicotine absorption. Further, we considered the natural history of those exposed to SHS and the associated risk of CVD. We reviewed routine methods used to assess exposure to SHS; evaluated the utility of subjective screening questions regarding smoking behaviour and examined the efficacy of nicotine and cotinine biomarkers used to quantify SHS exposure in epidemiological and clinical-based research. Self-reporting is practical and cost-effective in identifying smoking behaviour patterns, but is subject to recall bias and underestimation of exposure, especially in the presence of children. Nicotine and cotinine biomarkers have proven valuable in quantifying tobacco smoke absorption and establishing biological plausibility. A combination of SHS self-reported and biomarker evaluation provide the most stringent method of establishing exposure. Sufficient evidence is reported in epidemiological research to support a causal association between SHS exposure and increased risks of CVD morbidity and mortality among both men and women. The risk of developing an acute cardiac syndrome or chronic lifetime coronary events is at least 30%. Similarly, reduction in the incidence of a myocardial infarction decreases by nearly 50% in the absence of SHS. Considering the biological plausibility and dose-response relationship between SHS and CVD, effective interventions that incorporate a comprehensive screening method of behavioral and biological measures of exposure coupled with efficacious treatment should elicit favorable change for at-risk populations.

Association of anti-smoking legislation with rates of hospital admission for cardiovascular and respiratory conditions.  [LINK]

CMAJ. 2010 May 18;182(8):761-7. Epub 2010 Apr 12.

Naiman A, Glazier RH, Moineddin R.

BACKGROUND: Few studies have examined the impact of anti-smoking legislation on respiratory or cardiovascular conditions other than acute myocardial infarction. We studied rates of hospital admission attributable to three cardiovascular conditions (acute myocardial infarction, angina, and stroke) and three respiratory conditions (asthma, chronic obstructive pulmonary disease, and pneumonia or bronchitis) after the implementation of smoking bans.

METHODS: We calculated crude rates of admission to hospital in Toronto, Ontario, from January 1996 (three years before the first phase of a smoking ban was implemented) to March 2006 (two years after the last phase was implemented. We used an autoregressive integrated moving-average (ARIMA) model to test for a relation between smoking bans and admission rates. We compared our results with similar data from two Ontario municipalities that did not have smoking bans and with conditions (acute cholecystitis, bowel obstruction and appendicitis) that are not known to be related to second-hand smoke.

RESULTS: Crude rates of admission to hospital because of cardiovascular conditions decreased by 39% (95% CI 38%-40%) and admissions because of respiratory conditions decreased by 33% (95% CI 32%-34%) during the ban period affecting restaurant settings. No consistent reductions in these rates were evident after smoking bans affecting other settings. No significant reductions were observed in control cities or for control conditions.

INTERPRETATION: Our results serve to expand the list of health outcomes that may be ameliorated by smoking bans. Further research is needed to establish the types of settings in which smoking bans are most effective. Our results lend legitimacy to efforts to further reduce public exposure to tobacco smoke.

Legislative smoking bans for reducing secondhand smoke exposure, smoking prevalence and tobacco consumption.  [LINK]

Cochrane Database Syst Rev. 2010 Apr 14;4:CD005992.

Callinan JE, Clarke A, Doherty K, Kelleher C.
Milford Care Centre, Plassey Park Road, Castletroy, Limerick, Ireland.

BACKGROUND: Smoking bans have been implemented in a variety of settings, as well as being part of policy in many jurisdictions to protect the public and employees from the harmful effects of secondhand smoke (SHS). They also offer the potential to influence social norms and smoking behaviour of those populations they affect.

OBJECTIVES: To assess the extent to which legislation-based smoking bans or restrictions reduce exposure to SHS, help people who smoke to reduce tobacco consumption or lower smoking prevalence and affect the health of those in areas which have a ban or restriction in place.

SEARCH STRATEGY: We searched the Cochrane Tobacco Addiction Group Specialised Register, MEDLINE, EMBASE, PsycINFO, CINAHL, Conference Paper Index, and reference lists and bibliographies of included studies. We also checked websites of various organisations. Date of most recent search; July 1st 2009.

SELECTION CRITERIA: We considered studies that reported legislative smoking bans and restrictions affecting populations. The minimum standard was having a ban explicitly in the study and a minimum of six months follow-up for measures of smoking behaviour. We included randomized controlled trials, quasi-experimental studies (i.e. non-randomized controlled studies), controlled before and after studies, interrupted-time series as defined by the Cochrane Effective Practice and Organization of Care Group, and uncontrolled pre- and post-ban data.

DATA COLLECTION AND ANALYSIS: Characteristics and content of the interventions, participants, outcomes and methods of the included studies were extracted by one author and checked by a second. Because of heterogeneity in the design and content of the studies, we did not attempt a meta-analysis. We evaluated the studies using qualitative narrative synthesis.

MAIN RESULTS: There were 50 studies included in this review. Thirty-one studies reported exposure to secondhand smoke (SHS) with 19 studies measuring it using biomarkers. There was consistent evidence that smoking bans reduced exposure to SHS in workplaces, restaurants, pubs and in public places. There was a greater reduction in exposure to SHS in hospitality workers compared to the general population. We failed to detect any difference in self-reported exposure to SHS in cars. There was no change in either the prevalence or duration of reported exposure to SHS in the home as a result of implementing legislative bans. Twenty-three studies reported measures of active smoking, often as a co-variable rather than an end-point in itself, with no consistent evidence of a reduction in smoking prevalence attributable to the ban. Total tobacco consumption was reduced in studies where prevalence declined. Twenty-five studies reported health indicators as an outcome. Self-reported respiratory and sensory symptoms were measured in 12 studies, with lung function measured in five of them. There was consistent evidence of a reduction in hospital admissions for cardiac events as well as an improvement in some health indicators after the ban.

AUTHORS' CONCLUSIONS: Introduction of a legislative smoking ban does lead to a reduction in exposure to passive smoking. Hospitality workers experienced a greater reduction in exposure to SHS after implementing the ban compared to the general population. There is limited evidence about the impact on active smoking but the trend is downwards. There is some evidence of an improvement in health outcomes. The strongest evidence is the reduction seen in admissions for acute coronary syndrome. There is an increase in support for and compliance with smoking bans after the legislation.

Long-term reprogramming of cardiovascular function in infants of active smokers.  [LINK]

Hypertension. 2010 Mar;55(3):722-8. Epub 2010 Jan 25.

Cohen G, Jeffery H, Lagercrantz H, Katz-Salamon M.
Department of Women and Child Health, Neonatal Unit, Karolinska Institute, Elevhemmet H1-02, S-171 76 Stockholm, Sweden.

Newborn infants of smokers show symptoms of cardiovascular stress hyperreactivity. Persistent hyperreactivity could increase the risk of short- and/or long-term complications, such as hypertension. Here we determined whether incipient dysfunction in a smoker's infant persists or worsens with age, by comparing cardiovascular reflex function of control and tobacco-exposed infants longitudinally from birth to 1 year. We compared infants born at term to nonsmoking couples (controls; n=19) and mothers who smoked moderately (average consumption=15 cigarettes per day; n=17). All were tested at 1 to 3 weeks, 3 months, and 1 year during sleep. We recorded blood pressure and heart rate noninvasively during passive repositioning (60 degrees head-up tilt). Tilting control infants raised blood pressure slightly above baseline at 1 week (+2%) and much more at 1 year (+10%). This trend was reversed in the tobacco-exposed cohort (+10% at 1 week but only +4% at 1 year). At 3 months and 1 year, the heart rate response of tobacco-exposed infants to tilt was also abnormal (highly exaggerated). Our study reveals that maternal smoking leads to long-lasting "reprogramming" of infant blood pressure control mechanisms. The underlying dysfunction in a smoker's infant could plausibly be a precursor or early marker of long-term susceptibility to complications, such as raised blood pressure.
Share this:  Add to TwitterAdd to DiggAdd to del.icio.usAdd to FacebookAdd to GoogleAdd to LinkedInAdd to MixxAdd to MySpaceAdd to NewsvineAdd to RedditAdd to StumbleUponAdd to Yahoo