Secondhand Smoke Exposure, Pulmonary Function, and Cardiovascular Mortality
Introduction
Secondhand smoke (SHS) exposure has been linked to an increased risk of cardiovascular disease and stroke in epidemiologic studies 1, 2, 3, 4, 5, 6. Many of these studies controlled for the traditional cardiovascular risk factors, such as age, sex, direct smoking, blood pressure, and serum lipids (1). Mechanistically, SHS has been assumed to increase the risk of cardiovascular disease by its deleterious effects on platelet aggregation, endothelial function, serum lipids, and heart rate variability 5, 7, 8, 9, 10, 11. This traditional view of SHS exposure and cardiovascular disease, however, may oversimplify the causal pathway and result in biased estimates of its effects.
Forced expiratory volume in 1 second (FEV1) has been established as an important predictor of cardiovascular mortality 12, 13, 14, 15, 16, 17, 18, 19, 20, 21. Although the exact mechanism for this association is unknown, FEV1 is likely to capture important biological processes that are unaccounted for by traditional cardiovascular risk factors. These factors, which potentially include fat distribution, insulin resistance, and chronic inflammation, may contribute to causation of cardiovascular disease and mortality 14, 22, 23, 24.
Secondhand smoke exposure has been associated with reduced FEV1 in some epidemiologic studies of adults, but the evidence has not been consistent 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45. Many of these studies are cross-sectional, which precludes establishment of a clear temporal relation between SHS exposure and pulmonary function. To better assess this relation, we examined the prospective impact of SHS exposure on FEV1 among never-smoking older adults over an 8-year period.
The effect of SHS exposure on cardiovascular mortality may be mediated, in part, by its influence on FEV1 and those biological processes captured by measurement of FEV1. To correctly estimate the effect of SHS on cardiovascular mortality requires consideration of the possible mediating effect of FEV1 on the causal pathway, because it is well known that inclusion of factors on the causal pathway in conventional statistical analysis may bias the effect estimates in unpredictable ways (46). Consequently, we used marginal structural models (MSM) to study the impact of SHS exposure on cardiovascular mortality in older adults, taking into account its intervening effect on FEV1.
To assess the extent to which FEV1 is a surrogate for underlying risk factors for cardiovascular mortality, we repeated the above MSM analysis to directly assess the effects of traditional cardiovascular risk factors on the association between SHS exposure and cardiovascular mortality. This approach provides a less biased estimate of the impact of SHS exposure cardiovascular mortality in persons without any known history of cardiovascular disease than would be expected with more conventional statistical approaches.
Section snippets
Overview
We used data from a longitudinal cohort study of older adults collected at baseline and over three subsequent examinations spanning nearly a decade. As described below, mortality ascertainment was complete for the cohort. We used baseline and longitudinal data to examine the relation between SHS exposure and pulmonary function, the first step in our hypothesized causal pathway for the effects of SHS on cardiovascular mortality (Figure 1). In subsequent analysis, we evaluated the impact of SHS
Subject Characteristics and SHS Exposure
The cohort was predominately elderly (mean age, 70.7 years), female (68%), and white (96%) (Table 1). The median duration of cumulative lifetime home SHS exposure was 5 years (25th to 75th interquartile range, 2 to 20 years), whereas the median duration work exposure was 10 years (25th to 75th interquartile range, 0 to 25 years). Older age, female sex, and white race ethnicity were associated with higher lifetime home SHS exposure; male sex, higher educational attainment, and higher household
Discussion
Findings of this study advance our understanding of the causal inter-relations between SHS exposure, pulmonary function, and cardiovascular mortality. SHS exposure was associated with a greater longitudinal decline in pulmonary function over nearly a decade of follow-up. This observation clarifies the previously published mixed results that are based mostly on cross-sectional or small studies that have lacked the prospective design, control for confounding, or statistical power to definitively
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2019, Respiratory MedicineCitation Excerpt :ETS exposure in non-smokers has also increased mortality from lung cancer and COPD [33,34]. Additionally, ETS has been associated with a greater burden of cardiovascular risk factors [35], such as higher BMI and fasting glucose [36], and with endothelial dysfunction and increased plasma fibrinogen levels [37]. The strength of our study was a large study population and a long follow-up.