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 Overall, there is no evidence to suggest that publication bias attributable to the omission of unpublished data substantially affected the conclusions of the published meta-analyses of the evidence on secondhand smoke and coronary heart disease. For example, unpublished studies were included in the meta-analysis by He et al.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.