Epidemiologic Studies of Secondhand-Smoke Exposure and Cardiovascular Disease
This chapter presents the epidemiologic studies that address following two sets of relationships:
The association between secondhand-smoke exposure and cardiovascular disease, especially coronary heart disease and not stroke (Question 1, see Box 1-1).
The association between secondhand-smoke exposure and acute coronary events (Questions 2, 3, and 5, see Box 1-1).
The chapter begins with background information on risk factors for cardiovascular diseases and events. Next is a discussion of the epidemiologic studies of secondhand-smoke exposure and chronic cardiovascular disease. Two other studies conducted following the implementation of smoking bans that address the association between secondhand smoke exposure and acute coronary events are discussed in Chapter 6. This chapter is relevant to Question 1 in the committee’s charge (see Box 1-1).
There has been much research on the carcinogenic effects of tobacco smoke and its constituents, but given the typical dose–response relationships for cancer end points and the difference in latency periods between cancer and secondhand-smoke–related cardiovascular effects, the modes of action underlying cancer and cardiovascular effects are likely to be different. In keeping with its charge, the committee focuses on research relevant to the cardiovascular system and does not review the data related to cancer. The 2006 surgeon general’s report summarized the literature on the relation of secondhand smoke to the cardiovascular system (HHS, 2006). The com-
mittee reviewed that report, and this chapter alone should not be considered a comprehensive review of the published literature. For that, the reader is referred to the surgeon general’s report or other recent reports (Cal EPA, 2005; HHS, 2006; IARC, 2004). Recommendations for further research on the matter are presented in Chapter 7.
RISK FACTORS FOR ACUTE CORONARY EVENTS
Clinically manifest cardiovascular disease develops progressively. Extensive analyses of large cohorts show that the major risk factors for heart disease are smoking, diabetes, total cholesterol concentration, and hypertension (Wilson et al., 1998). Additional factors—such as obesity, left ventricular hypertrophy, C-reactive protein (CRP), and family history of heart disease at an early age—have been suggested as contributing to cardiovascular disease risk (Wilson et al., 1998). Data on three large prospective U.S. cohorts followed for 21–30 years indicate that exposure to at least one clinically increased major risk factor underlies 87–100% of cases of fatal coronary heart disease. For nonfatal coronary heart disease, the range was 87–92% (Greenland et al., 2003). An etiologic role of the major risk factors in the development of cardiovascular disease is indicated by extensive studies showing that treating or reducing exposure to risk factors lowers the rate of coronary heart disease events (Chobanian et al., 2003). That smoking is a major independent risk factor for coronary heart disease indicates that its effects cannot be entirely explained by changes in other risk factors and that it increases the incidence, development, and manifestation of cardiovascular disease by pathophysiologic mechanisms that are unique and relatively independent of dyslipidemia, hypertension, sex, or diabetes. Like active smoking, exposure to secondhand smoke could be considered an independent risk factor for cardiovascular disease.
EPIDEMIOLOGY OF CHRONIC EXPOSURE TO SECONDHAND-TOBACCO SMOKE IN RELATION TO CORONARY HEART DISEASE AND ACUTE CORONARY EVENTS
The surgeon general’s 2006 report concluded that “the evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and increased risks of coronary heart disease morbidity and mortality among both men and women” and that “pooled relative risks from meta-analyses indicate a 25 to 30 percent increase in the risk of coronary heart disease from exposure to secondhand smoke” (HHS, 2006). This section provides an overview of the relationship between exposure to secondhand smoke and coronary events summarized in that report, not limited to acute coronary events. Much research has been conducted on secondhand-smoke
exposure and coronary heart disease and was the precursor to work on the effects of secondhand smoke on acute coronary events. The epidemiologic studies that investigated the relationship are discussed briefly here and then what is known regarding the dose–response relationship and the potential biases and confounding effects that could affect the relationship.
Many prospective cohort studies and case–control studies have examined the association between exposure to secondhand smoke and the risk of coronary heart disease (Butler, 1988; Chen et al., 2004; Ciruzzi et al., 1998; Dobson et al., 1991; Garland et al., 1985; He, 1989; He et al., 1994; Helsing et al., 1988; Hole et al., 1989; Humble et al., 1990; Jackson, 1989; Kawachi et al., 1997; La Vecchia et al., 1993; Layard, 1995; Lee et al., 1986; LeVois and Layard, 1995; McElduff et al., 1998; Muscat and Wynder, 1995; Pitsavos et al., 2002; Rosenlund et al., 2001; Sandler et al., 1989; Steenland et al., 1996; Svendsen et al., 1987; Tunstall-Pedoe et al., 1995; Whincup et al., 2004). They all showed a trend toward increased risk of coronary heart disease associated with secondhand smoke; most but not all of the relative risk (RR) estimates in individual studies were statistically significant. Several published meta-analyses of the epidemiologic studies pooled RR estimates from individual studies and showed a significant 25–30% increase in the risk of coronary heart disease associated with various exposures to secondhand smoke (Barnoya and Glantz, 2005; He et al., 1999; HHS, 2006; Law et al., 1997; Thun et al., 1999; Wells, 1994, 1998). Two recent and comprehensive meta-analyses are particularly worthy of mention (He et al., 1999; HHS, 2006).
He et al. (1999) conducted a meta-analysis of secondhand smoke and the risk of coronary heart disease in nonsmokers. A total of 10 prospective cohort studies and 8 case–control studies were included (Butler, 1988; Ciruzzi et al., 1998; Dobson et al., 1991; Garland et al., 1985; He, 1989; He et al., 1994; Hirayama, 1990; Hole et al., 1989; Humble et al., 1990; Jackson, 1989; Kawachi et al., 1997; La Vecchia et al., 1993; Lee et al., 1986; Muscat and Wynder, 1995; Sandler et al., 1989; Steenland et al., 1996; Svendsen et al., 1987). In all the cohort studies, the outcome was myocardial infarction (MI) or death due to coronary heart disease. Secondhand-smoke exposure at home was measured in all the cohort studies, but only four measured workplace exposure. In four case–control studies, secondhand-smoke exposure was assessed both at home and in the workplace; in the other four, it was assessed only at home. Such incomplete exposure assessment biases results towards the null. Overall, nonsmokers exposed to secondhand smoke had an RR of coronary heart disease of 1.25 (95% confidence interval [CI], 1.17–1.32) compared with nonsmokers not
exposed to secondhand smoke. Secondhand smoke was consistently associated with an increased RR of coronary heart disease in cohort studies (RR, 1.21; 95% CI, 1.14–1.30), in case–control studies (RR, 1.51; 95% CI, 1.26–1.81), in men (RR, 1.22; 95% CI, 1.10–1.35), in women (RR, 1.24; 95% CI, 1.15–1.34), and in those exposed to secondhand smoke at home (RR, 1.17; 95% CI, 1.11–1.24) or in the workplace (RR, 1.11; 95% CI, 1.00–1.23). In a separate meta-analysis, Wells reported that the combined RR of coronary heart disease associated with secondhand-smoke exposure at work and not at home was 1.18 (95% CI, 1.04–1.34) in eight epidemiologic studies (Wells, 1998).
The surgeon general’s 2006 report (HHS, 2006) updated the meta-analysis of He et al. (1999). The updated meta-analysis included nine cohort studies and seven case–control studies (Butler, 1988; Ciruzzi et al., 1998; Garland et al., 1985; He et al., 1994; Hirayama, 1990; Hole et al., 1989; Humble et al., 1990; Kawachi et al., 1997; La Vecchia et al., 1993; Lee et al., 1986; McElduff et al., 1998; Muscat and Wynder, 1995; Sandler et al., 1989; Steenland et al., 1996; Svendsen et al., 1987). Two of the more recently published studies, by McElduff (1998) and Rosenlund et al. (2001), were identified and included, whereas the articles by Jackson (1989) and Dobson et al. (1991) were excluded because they reported data that were reanalyzed in the paper by McElduff et al. (1998). In addition, the updated meta-analysis did not include one of the two unpublished studies by Butler (1988) or a case–control study published in Chinese (He, 1989). The overall pooled estimate of the RR of coronary heart disease associated with secondhand smoke was 1.27 (95% CI, 1.19–1.36) in the meta-analysis (HHS, 2006). Furthermore, the RR point estimates were similar for men and women and in various exposure venues. The stringent adjustment for potential confounding had little effect on the estimates. The pooled estimate based on the case–control studies was somewhat higher than that based on the cohort studies (HHS, 2006). Most observational studies have adjusted for major coronary heart disease risk factors (He et al., 1999; HHS, 2006).
Five published epidemiologic studies were not included in the updated meta-analysis in the surgeon general’s 2006 report (Chen et al., 2004; Panagiotakos et al., 2002; Stranges et al., 2006; Teo et al., 2006; Whincup et al., 2004). Of those, the Scottish MONICA survey is a cross-sectional study (Chen et al., 2004) and so will not be discussed here.
Panagiotakos et al. (2002) investigated the association between secondhand smoke and the risk of developing a first event of acute coronary syndrome (ACS, that is, acute MI or unstable angina) in nonsmokers in the Greek population. A detailed questionnaire regarding exposure to secondhand smoke was completed by 848 patients with a first ACS event and 1,078 coronary heart disease-free matched controls. When age, sex,
hypertension, hypercholesterolemia, diabetes mellitus, physical inactivity, family history of premature coronary heart disease, education level, annual income, and depression status were controlled for, nonsmokers who were exposed to secondhand cigarette smoke occasionally (fewer than three times per week) had a 26% higher risk of ACS (odds ratio [OR], 1.26; p < 0.01) than nonsmokers not exposed to secondhand smoke, and nonsmokers who were exposed regularly (three or more times per week) had a 99% higher risk (OR, 1.99; p < 0.001) (Panagiotakos et al., 2002).
Whincup et al. (2004) examined the association between serum concentration of cotinine (a biomarker of exposure to secondhand smoke; see Chapter 2 for further discussion) and risk of coronary heart disease in a prospective epidemiologic study, the British Regional Heart Study. A total of 4,729 men who provided baseline blood samples (for cotinine assay) and a detailed smoking history in 1978–1980 were followed for major coronary heart disease (fatal and nonfatal) over 20 years. The 2,105 men who reported that they did not smoke and who had cotinine concentrations under 14.1 ng/mL were divided equally into four groups on the basis of cotinine concentrations. Compared with the first quartile of cotinine concentration (no more than 0.7 ng/mL), the RRs (and 95% CIs) for coronary heart disease in the second quartile of cotinine concentration (0.8–1.4 ng/mL), the third quartile (1.5–2.7 ng/mL), and the fourth (2.8–14 ng/mL) were 1.45 (1.01–2.08), 1.49 (1.03–2.14), and 1.57 (1.08–2.28), respectively, after adjustment for residential area, age, diabetes, physical activity, alcohol intake, blood pressure, body mass index, total cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides, white-cell count, forced expiratory volume, and preexisting coronary heart disease (Whincup et al., 2004). RRs for coronary heart disease (for cotinine of 0.8–14 ng/mL versus under 0.6 ng/mL) were particularly increased during the first 5-year followup period (3.73; 1.32–10.58) and the second 5-year followup period (1.95; 1.09–3.48). This study used a biomarker of secondhand-smoke exposure, which is more objective than self-reporting, and found a greater excess risk of coronary heart disease than studies that used self-reported exposure. It is possible, therefore, that the effects of secondhand smoke may have been underestimated in earlier studies that relied on self-reporting.
The INTERHEART study examined the relationship between secondhand smoke exposure and acute MI (Teo et al., 2006). The INTERHEART study is a standardized case–control study of 15,152 cases of first acute MI and 14,820 age- and sex-matched controls. Cases and controls were from 262 centers in 52 countries in Asia, Europe, Middle East Crescent, Africa, Australia, North America, and South America. After exclusions (individuals with unstable angina alone, unconfirmed acute MI, previous acute MI, missing data on tobacco use, or other missing information), there were a total of 12,133 cases and 14,435 controls. Secondhand-smoke exposure
was self-reported during interviews with trained staff as times per day, average number of hours per week over the previous 12 months, and smoking habits of spouses; no cotinine measurements were presented. Other factors recorded include: serum apo-lipoprotein B and A1 concentrations, height, weight, waist and hip circumference, blood pressure, heart rate, dietary patterns, physical activity, alcohol consumption, education, income, psychosocial factors, personal and family history of cardiovascular disease, hypertension, and diabetes mellitus. Exposure to secondhand smoke increased the risk of a nonfatal acute MI in a graded manner, with an adjusted odds ratio (OR; adjusted for age, sex, region, physical activity, and consumption of fruits, vegetables, and alcohol) of 1.24 (95% CI, 1.17–1.32) and 1.62 (95% CI, 1.45–1.81) in those least exposed (1–7 h of exposure per week) and most exposed (≥22 h of exposure per week), respectively, compared to never-smokers who were not exposed to secondhand smoke. The overall population attributable risk for never-smokers who were exposed to secondhand smoke for 1 hour per week or longer was 15.4% (95% CI, 12.1–19.3). Those ORs for secondhand smoke compare to an overall OR for current smokers compared to never-smokers of 2.95 (95% CI, 2.77–3.14). The risks increased with the number of cigarettes smoked, from an OR of 1.63 (95% CI, 1.45–1.82) for individuals smoking one to nine cigarettes a day to an OR of 4.59 (95% CI, 4.21–5.00) for individuals smoking 20 or more cigarettes a day. Regression analysis demonstrated a dose response in current smokers with the risk of acute MI increasing by 1.056 (95% CI, 1.05–1.06) for every additional cigarette smoked per day.
Stranges et al. (2006) examined lifetime cumulative exposure to secondhand smoke and risk of acute MI in never-smokers. The authors used data from the Western New York Health Study collected from 1995 to 2001 to examine risk factors for coronary heart disease. Cases were recruited from hospitals in Erie and Niagara counties, New York, after discharge for an acute MI incident (ICD-9 410). Controls were randomly selected from residents of those two counties who were ages 35 to 70 years using driver’s license lists (65 years of age or under) and Medicaid and Medicare lists (>65). A total of 1,197 cases (64.3% of identified and eligible cases) and 2,850 controls (59.5% of identified and eligible controls) were interviewed. Of those, Stranges et al. (2006) analyzed 284 nonsmoking cases and 1,257 nonsmoking controls, with smoking status determined by self report during interviews. Interviews included medical history and lifestyle habits, and personal lifetime exposure to secondhand smoke in the home, workplace and other public settings. Information was asked according to exposures younger than 21 years of age, and for each decade of adult life (21–30, 31–40, etc.). Information included the number of people living with the participant who smoked (cigarettes, cigars, or pipes) and the number of years the smoker resided with the participant. From that, cumulative
exposure at home was calculated by adding the person-years across each age period. Similarly, the number of years working near coworkers who smoked was also calculated. For other public exposures, the number of times per week in a typical month the participant visited bars, restaurants, or other settings in which smokers were present was calculated for each age period. Complete smoke exposure histories were available for 1,478 participants (254 cases and 1,224 controls). ORs were calculated based on tertiles of exposure, both overall and by sex; no range of exposures or cotinine concentrations were presented. Data were not adjusted or analyzed with regard to how recent exposures had occurred. Consistent with other data presented in Chapter 3, data in Stranges et al. (2006) indicate that exposures have decreased over time, especially in the home and workplace. After adjusting for age, sex, education, body mass index, race, alcohol intake, physical activity, hypertension, diabetes mellitus, and hypercholesterolemia, exposure to secondhand smoke was not significantly associated with increased risk for MI, with an OR for those in the highest tertile of exposure relative to those in the lowest tertile of exposure of 1.19 (95% CI, 0.78–1.82). This study does differ from others in that it assessed lifetime cumulative exposures, not recent exposures. To the extent that the effects of secondhand-smoke exposure on CVD are due to recent exposures, cumulative exposure is an inappropriate exposure metric.
A dose–response association between secondhand smoke and the risk of coronary heart disease was reported in several epidemiologic studies and meta-analyses (He et al., 1999; HHS, 2006). In the meta-analysis by He et al. (1999) studies that provided RR estimates of association stratified by the intensity of exposure to secondhand smoke, determined by the number of cigarettes smoked per day by a cohabitant or duration of living with a smoker cohabitant (typically measured in years), were used to generate pooled estimates for the dose–response analysis. The RRs of coronary heart disease increased significantly with exposure to a higher level or a longer duration of secondhand smoke (He et al., 1999). For example, as compared with nonsmokers who were not exposed to smoke, nonsmokers who were exposed to 1 to 19 cigarettes per day and to 20 or more cigarettes per day had RRs of coronary heart disease of 1.23 (95% CI, 1.13–1.34) and 1.31 (95% CI, 1.21–1.42), respectively (p = 0.006 for linear trend). Likewise, as compared with nonsmokers who were not exposed to cigarette smoke, nonsmokers who were exposed to a spouse’s smoke for 1 to 9 years, 10 to 19 years, and 20 or more years had RRs of coronary heart disease of 1.18 (95% CI, 0.98–1.42), 1.31 (95% CI, 1.11–1.55), and 1.29 (95% CI, 1.16–1.43), respectively (p = 0.01 for linear trend). A similar dose–response as-
sociation between secondhand smoke and the risk of coronary heart disease was reported in the 2006 surgeon general’s report (HHS, 2006). Compared with unexposed nonsmokers, nonsmokers exposed to levels of secondhand smoke ranging from low to moderate (1 to 14 or 1 to 19 cigarettes per day) had an RR of 1.16 (95% CI, 1.03–1.32). Nonsmokers exposed to levels ranging from moderate to high (≥15 or ≥20 cigarettes per day) had an RR of 1.44 (95% CI, 1.13–1.82) compared with unexposed nonsmokers (HHS, 2006). The results from Whincup et al. (2004), presented earlier in this chapter, support a dose response between intensity of secondhand smoke exposure and cardiovascular disease risk. In that study hazard ratios with the simplest adjustment (stratified by town and adjusted for age) were 1.50 (95% CI, 1.06–2.12), 1.56 (95% CI, 1.11–2.2), and 1.61 (95% CI, 1.15–2.27) for the three highest exposure quartiles (serum cotinine concentrations of 0.8–1.4, 1.5–2.7, and 2.8–14 ng/mL, respectively) relative to the lowest exposure quartile (serum cotinine concentration of ≤0.7 ng/mL). The hazard ratio for the highest exposure quartile was similar to that seen in light active smokers in that same study (1.65; 95% CI, 1.08–2.54).
It should be noted, however, that in all those cases an increased risk is seen even at the lowest levels of exposure compared to unexposed non-smokers. As has been seen with active smoking, even smoking fewer than five cigarettes per day is associated with an elevated risk of heart disease, with risks increasing with increased smoking, but at a lower rate compared to the initial increase (Law and Wald, 2003).
Bias and Confounding Effects
Some methodologic issues—including the possibility of misclassification of secondhand-smoke exposure, the potential for uncontrolled confounding effects, and publication bias—have been raised in the literature (Kawachi and Colditz, 1996).
Several potential sources of misclassification of secondhand-smoke exposure have been suggested (Bailar, 1999; Hackshaw et al., 1997; He et al., 1999; Howard and Thun, 1999; Kawachi and Colditz, 1996; Law et al., 1997; Lee and Forey, 1996; Thun et al., 1999; Wells, 1986, 1998). Some self-reported lifetime nonsmokers may have been smokers in the past, and persons more exposed to secondhand smoke may be more likely to have been active smokers in the past (Kawachi and Colditz, 1996; Lee and Forey, 1996; Wells, 1986). However, that potential bias was unlikely to have a substantial effect on studies of secondhand smoke and coronary heart disease because the extent of such misclassification was minor and the RR of coronary heart disease in former smokers was not high (Hackshaw et al., 1997; Howard and Thun, 1999; Kawachi and Colditz, 1996). In addition, recall bias has been suggested because nonsmokers who develop coronary
heart disease may have selectively recalled their exposures to secondhand smoke (Bailar, 1999). However, the pooled estimates of RR of coronary heart disease associated with secondhand smoke from the prospective cohort studies were significantly increased and would not be subject to this form of bias (He et al., 1999; HHS, 2006). Furthermore, a failure to correct for background exposure to secondhand smoke in most epidemiologic studies (because truly unexposed populations were essentially unavailable) might bias the associations with disease toward the null (Ong and Glantz, 2000). Although many of these studies use self-report of exposures to secondhand smoke, a number of studies have concluded that self-report can be a valid method to assess exposure to secondhand smoke (Emmons et al., 1994; Tunstall-Pedoe et al., 1995; Willemsen et al., 1997). Measurement errors due to failure to assess total secondhand-smoke exposures from different sources, failure to obtain repeated exposure data over time, or underreporting of exposures of nonsmokers would bias the association between secondhand smoke and coronary heart disease toward the null (Kawachi and Colditz, 1996). Furthermore, the one study that looked at coronary heart disease risk in nonsmokers that used serum cotinine concentrations as a measure of exposure rather than self-reported smoking history had a higher relative risk (hazard ratio, 1.61; 95% CI, 1.15–2.27) than those that used self-reports, suggesting that misclassification of secondhand smoke exposure is not responsible for the increased risk (Whincup et al., 2004).
Several cross-sectional surveys found that nonsmokers who were exposed to secondhand smoke were more likely to report low socioeconomic status and unhealthy lifestyle (low physical activity and poor diet) than nonsmokers who were not exposed to secondhand smoke (Emmons et al., 1995; Koo et al., 1997; Matanoski et al., 1995; Thornton et al., 1994), but the differences between the two groups in cardiovascular risk factors could not explain the observed associations between secondhand smoke and risk of coronary heart disease. For example, the overall RR of coronary heart disease associated with secondhand smoke was 1.26 (95% CI, 1.16–1.38) when the analysis was confined to studies that adjusted for important risk factors for coronary heart disease, such as age, sex, blood pressure, body weight, and serum cholesterol in the meta-analysis by He et al. (1999). Whincup et al. (2004) also conducted analyses with various adjustments. The risk of coronary heart disease was not greatly affected by the adjustments. For example, the hazard ratio in the highest exposure group was 1.61 (95% CI, 1.15–2.27) with the simplest adjustments (stratified by town and adjusted for age), 1.46 (95% CI, 1.02–2.07) with more adjustments (also adjusted for systolic and diastolic blood pressure, total cholesterol and HDL cholesterol, forced expiratory volume in 1 second, height, and preexisting coronary heart disease), and 1.57 (95% CI, 1.08–2.28) with even more adjustments (in addition to all previous adjustments, adjusted
for body mass index, triglycerides, white blood cell count, diabetes, physical activity, alcohol intake, and social class).
Another potential bias might be due to the tendency for investigators to submit manuscripts and for editors to accept them on the basis of the statistical significance and direction of the association (positive rather than negative) of study results (publication bias). Overall, there is no evidence to suggest that publication bias attributable to the omission of unpublished data substantially affected the conclusions of the published meta-analyses of the evidence on secondhand smoke and coronary heart disease. For example, unpublished studies were included in the meta-analysis by He et al. (1999). In their meta-analysis, they summarized 18 cohort and case–control studies and performed a rank-correlation analysis of the association between the standard error and the logarithm of RR. If small studies with negative results were less likely to be published, the correlation between the standard error and log RR would be high and would suggest publication bias. The Kendall tau correlation coefficient for the standard error and the standardized log RR was 0.24 (p = 0.16) for all 18 studies and provided little evidence of publication bias. When the study by Garland et al. (1985), which had a relative risk that could be considered an outlier, was excluded from the analysis the Kendall tau correlation coefficient for the standard error and the standardized log RR was further reduced to 0.19 (p = 0.28) (He et al., 1999). We cannot exclude the possibility of publication bias, but there is little reason to believe that it substantially affected the conclusions of the published reviews or meta-analyses of the evidence on coronary heart disease (HHS, 2006).
The results of case–control and cohort studies carried out in multiple populations consistently indicate exposure to secondhand smoke poses about a 25–30% increase in risk of coronary heart disease.
A few epidemiologic studies using serum cotinine concentration, an objective measure of individual exposure to secondhand smoke, indicated that the RR of coronary heart disease associated with secondhand smoke was even greater than those estimates based on self-reported secondhand-smoke exposure.
The excess risk is unlikely to be explained by misclassification bias, uncontrolled confounding effects, or publication bias.
Although few studies have addressed coronary heart disease risk posed by exposure to secondhand smoke in the workplace, there is no reason to suppose that the effect of exposure at work differs from the effect of exposure in the home environment.
A positive dose–response relationship between secondhand-smoke exposure, either self-reported or shown by the presence of biomarkers, supports the conclusion of causality.
Given those findings, the high prevalence of secondhand smoke in the U.S. general population has important implications for public health.
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