Secondhand Smoke Exposure, Pulmonary Function, and Cardiovascular Mortality

https://doi.org/10.1016/j.annepidem.2006.10.008Get rights and content

Purpose

Cardiovascular disease and obstructive lung disease are leading global causes of death. Despite this, the impact of secondhand smoke (SHS) exposure on pulmonary function and cardiovascular disease remains uncertain. Our goal was to elucidate the association between baseline SHS exposure and the risk of lung function decline and cardiovascular mortality over a period of nearly a decade.

Methods

We used data from a longitudinal cohort study of 1,057 older adults to study the association between baseline SHS exposure and the risk of lung function decline and cardiovascular mortality. The effect of SHS exposure on cardiovascular mortality may be mediated by its influence on FEV1 and biological processes captured by measurement of FEV1. Alternatively, the effect of SHS may be mediated by baseline cardiovascular disease status, which reflects the combined effects of traditional cardiovascular risk factors. To correctly estimate the effect of SHS and FEV1 on cardiovascular mortality, we used marginal structural models (MSMs) that took into account the mediating effects of FEV1 and baseline cardiovascular disease in the causal pathway.

Results

In longitudinal multivariate analyses, lifetime cumulative home and work SHS exposure were associated with a greater decline of FEV1 (−15 mL/s; 95% CI, −29 to −1.3 mL/s and −41 mL/s; 95% CI, −55 to −28 mL/s per 10-year cumulative exposure, respectively). Lifetime home SHS exposure was associated with a greater risk of cardiovascular mortality in both conventional multivariate analysis (HR, 1.10 per 10 years of exposure; 95% CI, 0.99 to 1.24) and the MSM for FEV1 (HR, 1.06; 95% CI, 0.95 to 1.19) and baseline cardiovascular disease (HR for subjects with no baseline cardiovascular disease, 1.39; 95% CI, 1.17 to 1.66).

Conclusions

Lifetime SHS exposure appears to result in a greater decline in lung function and risk of cardiovascular mortality, taking into account confounders and the mediating effect of FEV1 and baseline cardiovascular disease.

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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