Risk of all-cause mortality and cardiovascular disease associated with secondhand smoke exposure: A systematic review and meta-analysis
Introduction
Cardiovascular disease (CVD) remains the leading cause of death worldwide [1]. Among various modifiable risk factors of CVD, smoking is one of the most significant. Secondhand smoke (SHS), also known as passive smoking, was associated with 25% to 30% increased risk of coronary heart disease (CHD), as suggested by previous systematic reviews and meta-analyses [2], [3], [4], [5]. With over 30% of the world's non-smokers exposed to SHS [6], the worldwide burden of deaths from CVD attributable to SHS is immense.
A number of new studies assessing the association between SHS and CVD have been published following the last comprehensive meta-analysis in 1999 [2]. Most of these studies demonstrated an increased risk of CVD associated with SHS, while others found little or no relationship, presumably due to the heterogeneity of study characteristics (e.g. gender distribution, ethnicity, or source of exposure). For example, Gallo et al. reported a significantly increased risk of CVD mortality related to SHS exposure at home but not to exposure at workplaces [7]. In a large prospective study in Norway, Iversen et al. found that the risk of myocardial infarction was increased in passive smoking women but not in passive smoking men [8]. Additionally, by analyzing data from the American Cancer Society's Cancer Prevention Study I, Enstrom et al. failed to detect a significant association of exposure to SHS with CHD mortality [9], while in a cohort study in China, He et al. showed that never smokers exposed to SHS had a 2-fold risk of CHD death [10]. Therefore, the question as to what extent SHS is associated with CVD risk and whether the association varied by important study characteristics warrants an in-depth reassessment of the relationship between SHS exposure and CVD.
Early studies investigating the relationship between SHS and CVD mainly relied on participants' self-reported SHS exposure at home or workplaces. However, this questionnaire-based assessment of SHS might be subject to misclassification. In 2004, for the first time, Whincup et al. evaluated the risk of CHD associated with SHS using an objective assessment of SHS exposure by measuring concentrations of serum cotinine, showing that the risk of CHD might be increased by 54% to 89% in never smokers with different levels of SHS exposure [11]. Since the objective measurement was able to capture the total SHS exposure from all sources, researchers argued that the cardiovascular impact of SHS exposure may be as large as that of active smoking and that previous assessment of SHS by self-reported exposure could have underestimated the impact of SHS [3]. Following Whincup, three studies were conducted using this objective cotinine-based measurement to examine the risk of CVD related with SHS. Available evidence needs to be synthesized to generate a more precise risk estimate of CVD associated with objectively assessed SHS exposure and to determine whether self-reported measurement of SHS did bias the risk of CVD downward.
SHS exposure was not only related to risk of cardiovascular morbidity and mortality, but also increased the risk of other causes of death, such as death due to breast cancer, lung cancer, or chronic obstructive pulmonary disease [12], [13], [14], [15]. Literatures have suggested an association between SHS and all-cause mortality. However, the magnitude of the association has not been systematically assessed.
Therefore, we conducted the current meta-analysis to 1) estimate the relative risk (RR) of CVD associated with self-reported SHS exposure as well as objectively measured SHS exposure, and find out whether the association varied by important study characteristics, and 2) estimate the RR of all-cause mortality associated with SHS exposure.
Section snippets
Search strategy
We performed this meta-analysis following the proposed MOOSE (Meta-Analysis of Observational Studies in Epidemiology) statement.
Two qualified investigators (X.L. and J.S.) conducted database search and discrepancies were resolved by discussion and consensus with a senior investigator (Y.X.). We searched PubMed and Embase for prospective cohort and case–control studies published from inception date to May 2014, which investigated the association between SHS exposure and the risk of all-cause
Identification of studies
Our initial electronic database search yielded 752 publications: 521 from PubMed and 231 from Embase. After screening titles and abstracts, we identified 58 articles for further full-text review. Among those, we identified two studies which met our inclusion criteria but the required data were not reported [19], [20]. However, contact with the authors was not successful because the two studies were conducted three decades ago. Additional 4 articles were obtained from reference lists of
Discussion
This meta-analysis is the most comprehensive study that evaluated the effect of SHS exposure on all-cause mortality and CVD. The number of studies included in our analysis was almost doubled compared with that of previous ones [2], [3], [4]. Our analysis indicated that never smokers exposed to SHS, compared with those unexposed, had a significantly increased risk of 18% for all-cause mortality, 23% for CVD, 23% for CHD, and 29% for stroke. Various study characteristics, such as gender and age
Conclusion
Our study provides sufficient evidence that exposure to SHS significantly increased the risk for all-cause mortality and CVD. In addition, the risk associated with SHS exposure was large in China while the risk was only modest in the US. Studies using objectively measured SHS exposure may yield a higher risk of CVD than those using self-reported SHS exposure.
The following are the supplementary data related to this article.
Funding
This work is supported by the National Natural Science Foundation of China (81100564), the Shanghai Shen-Kang Hospital Development Center Foundation (shdc12012301), and the Chinese Society of Endocrinology Foundation (12020250315).
Conflicts of interest
No potential conflicts of interest relevant to this article were reported.
Author contributions
XL, JS, and YX proposed the study protocol. YB contributed to the interpretation of data and edited the manuscript. XL and JS performed database searching, data extraction, statistical analyses, and wrote the first manuscript. MX, JL, and LZ provided critical suggestions. YX reviewed and edited the manuscript. All authors approved the final version.
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X.L. and J.S. contributed equally to this work. All authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.