Meta-analysis of the Association Between Second-hand Smoke Exposure and Ischaemic Heart Diseases, COPD and Stroke

Florian Fischer; Alexander Kraemer

Disclosures

BMC Public Health. 2015;15(1202) 

In This Article

Background

Second-hand smoke (SHS) still remains the most important contaminant of indoor air in first world countries.[1] Despite significant reductions within the past decades, a considerable part of the global population is regularly, and usually involuntarily, exposed to SHS. Therefore, it is a highly important risk factor for the total population. SHS exposure may lead to several chronic conditions, which are highly relevant in terms of morbidity and mortality for a population's health.[2] There is a broad scientific consensus that SHS exposure is linked to carcinogenesis, in particular lung cancer. Furthermore, SHS has been linked to most diseases which are caused by active smoking.[3–7] This association is comprehensible due to the more than 50 carcinogens that have been identified in SHS.[8]

Several mechanisms may lead to an increased likelihood of adverse effects in the cardiovascular and respiratory system. These mechanisms may cause a reduction in vascular flow and therefore the development of atherosclerosis.[8,9] The mechanisms by which SHS exposure increases the risk of heart disease are multiple and interact with each other.[10] In comparison with lung cancer, there is one important difference in the association between SHS exposure and ischaemic heart diseases (IHD): for lung cancer, adverse health effects result from long-term exposure, whereas for other diseases, such as IHD, these effects are not merely long-term and chronic but also acute.[11–15] The effects of even brief passive smoking are often nearly as great as (chronic) active smoking.[10,16,17]

Evidence of Adverse Health Effects Attributable to SHS Exposure

Research focused on the associations between SHS exposure and lung cancer first.[18] But subsequently other outcomes, such as IHD,[19–21] respiratory diseases[22,23] and stroke[24–26] were also included in the research. Beginning in 1984, observational studies started to point out the association between SHS exposure and IHD. This seems to be the most important outcome attributable to SHS exposure, because the effects on cardiovascular diseases are obvious even at low doses of SHS exposure[19,27] and because IHDs are much more frequent than lung disease. Because IHD is so prevalent, even a small increase in risk associated with SHS exposure will have a substantial public health impact.[28] Extensive epidemiological research spanning a period of 25 years has indicated that SHS exposure increases the risk of IHD by 25–30 %,[2,10,17,19–21,29] and this was also concluded by the Institute of Medicine.[30] The effects still remain if other factors such as dietary intake, socio-economic status, and health-care use are included in the analysis.[31]

Furthermore, a dose–response relationship between the level of SHS exposure and the occurrence of IHD was observed.[32] The reported RR of 1.3 (indicating a 30 % excess risk) for the association between SHS exposure and IHD that has been described in several meta-analyses,[12,19,20,33,34] is quite large compared to active smoking. The excess risk for regular SHS exposure is about one third of that smoking 20 cigarettes per day, although the total exposure to tobacco smoke is only 1 % of that from 20 cigarettes per day.[4,32] Assuming a linear dose–response relationship would lead to an expected excess risk associated with SHS exposure of only 0.8 % (1 % of the 80 % excess risk from smoking 20 cigarettes per day).[35]

Active smoking is the most important risk factor for chronic obstructive pulmonary diseases (COPD). Almost 85–90 % of COPD related mortality is attributable to active cigarette smoking. However, it is also suggested that 10–15 % of COPD cases are attributable to other risk factors such as SHS exposure, occupational exposures, and genetic factors.[22,36] Since environmental tobacco smoke contains potent airway irritants, SHS exposure could lead to chronic airway irritation, inflammation, and obstruction.[37,38] Nevertheless, up to now the causal association between SHS exposure and COPD has received limited attention in epidemiological studies. The first studies focusing on the association between SHS exposure and COPD faced several limitations. First of all, most studies are based on self-reports and secondly, different methods for defining COPD were used. Therefore, the reported effects of passive smoking on lung function are small and partially inconsistent.[22,39–41]

Comparable to COPD, the relationship between SHS exposure and stroke was not verified for a long time.[8,42,43] In 2014, stroke was included as a condition that is causally linked to SHS exposure in the Surgeon General's Report.[44] After several studies provided overall inconsistent results regarding the association between SHS exposure and stroke,[25,26,43,45–48] a meta-analysis of 20 studies indicated a strong dose-dependent association between SHS exposure and stroke.[49]

Study Objective and Research Question

Tobacco use is one of the most important modifiable risk factors for several adverse health effects. Nevertheless, the effects of SHS exposure on health have not yet been fully recognized in public health policies.[31,50] Although several studies have accounted for the (causal) associations between SHS exposure and disease conditions, some results are still inconsistent. In order to implement demand-actuated and successful strategies to protect the public from adverse health effects attributable to SHS exposure, it is necessary to provide evidence-based information about the magnitude and reliability of associations between SHS exposure and health outcomes. Therefore, this study aims to quantify the effect sizes of SHS exposure for three major outcomes: IHD, COPD, and stroke. Based on the results of a systematic review, a meta-analysis was performed to summarize the results of single studies in one effect size for each of the three outcomes. The main goals of the meta-analysis were: 1) to test whether the study results are homogeneous and, if so, 2) to obtain a combined estimator of the effect magnitude for the association between SHS exposure and the outcomes IHD, COPD and stroke. Although some meta-analyses have dealt with the association between SHS exposure and IHD as well as stroke, this is the first meta-analysis on the association between SHS exposure and COPD. Furthermore, it is the first study that allows a comparison of the effects for the selected outcomes, because the same methodology was used for the systematic literature review and meta-analysis.

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