SHS exposure was common among patients with COPD. Nonetheless, exposure intensity was generally low, which likely reflects the low prevalence of current smoking and the statewide workplace smoking ban in California. Despite the relatively low intensity of exposure, SHS was associated with poorer health status and a greater risk of COPD exacerbation. Consequently, patients with COPD appear to be vulnerable to adverse health effects of low-level SHS exposure.
Our study adds to the emerging literature that SHS exposure may adversely affect the clinical course of COPD. We previously reported in another cohort that short-term SHS exposure, as evidenced by urine cotinine, was related to poorer COPD severity and health status measures.6
In a previous cohort study of adults hospitalized for COPD, self-reported SHS exposure was also a risk factor for re-hospitalization.7
Another population-based US study found that self-reported SHS exposure was related to a greater risk of “chronic respiratory disease exacerbation,” defined as activity limitation or a physician visit due to asthma, chronic bronchitis, emphysema, or chronic sinusitis.42
More recently, indoor PM2.5
levels, a proxy measure of home SHS exposure, was associated with poorer disease-specific quality of life among persons with COPD.1
The present findings add significant additional evidence that SHS exposure is deleterious for patients with COPD.
A significant study strength is the large sample of clinically well-characterized COPD patients who manifest a broad spectrum of disease severity, ranging from mild to severe. The cohort is also diverse in terms of gender, raceethnicity, and socioeconomic status. Recruitment from a large health plan that covers a substantive proportion of the regional population helps to ensure generalizability to patients who are being treated for COPD in clinical practice.
Our study is also subject to several limitations. Although the inclusion criteria required health care utilization for COPD, misclassification of COPD could have occurred. To minimize this, our COPD definition required concomitant treatment with COPD medications to increase the specificity of our definition. In addition, all patients had a physician diagnosis of COPD and reported having the condition. The observed lifetime smoking prevalence was similar to that in other population-based epidemiologic studies of COPD, supporting the diagnosis of COPD rather than asthma.39
We also previously demonstrated the validity of our approach using medical record review.12
Nonetheless, we acknowledge this potential misclassification as a study limitation.
We used self-reported SHS exposure which could have resulted in misclassification of exposure. The SHS survey exposure instrument has been previously validated against a direct measurement of exposure.19
Based on our previous work, however, we know that self-reported SHS exposure tends to underestimate actual exposure.5
To the extent that exposure misclassification is nondifferential with respect to respiratory status, the bias would be conservative (ie, “towards the null”). If persons with greater disease severity were more likely to remember or report SHS exposure, the estimates of SHS-related health effects would be inflated. Because we used two complementary methods to control for the effects of disease severity, which included both traditional multivariable regression and propensity scoring, we explicitly controlled for this possible bias.
In addition, some subjects could have inaccurately reported their current personal smoking status. We observed no relationship between past smoking and reported SHS exposure, which is reassuring that there is no confounding by direct personal smoking. We cannot, however, fully exclude the possibility of residual confounding.
Selection bias could have been introduced by nonparticipation in the study. There were some differences among subjects who did and did not participate in the interviews and clinic visits, but they were modest in scope and not likely to affect the relation between SHS exposure and health outcomes. Even so, we acknowledge the potential for selection bias as a limitation of our study.
In sum, SHS exposure appears to increase the risk of adverse health outcomes, including poorer physical health status, HRQL, exercise capacity, and disease exacerbation resulting in emergency health care utilization. These poor health outcomes were observed at low levels of SHS exposure. Patients with COPD may comprise a vulnerable population who are at especially high risk of the respiratory health effects of SHS exposure. Promotion of smoke-free indoor environments, including the home and public places, will likely benefit persons with COPD and other chronic respiratory diseases.