We report the first study to assess the impact of objectively measured SHS exposure on a substantial cohort of adults with COPD. Despite the fact that they have chronic respiratory disease, SHS exposure was common among non-smoking adults with COPD. Although the results varied by measurement technique and type of analysis, SHS exposure was generally associated with greater COPD severity and poorer health status. The effect was observed in both cross-sectional and prospective analysis and appeared to be clinically meaningful, as judged against the criterion of the minimally important difference in health status indicators. Taking inter-individual differences in nicotine metabolism into account did not influence the estimates of SHS effect. These data suggest that passive smoking, in addition to direct personal cigarette smoking, may exert an important influence on outcomes in COPD.
Although the literature is small, previous studies suggest that SHS exposure may be a cause of new-onset COPD or impaired pulmonary function.[2
] The effect of SHS exposure on persons with established COPD, however, has received very little study.[5
] In a cohort of adults hospitalized for COPD, self-reported SHS exposure was a risk factor for re-hospitalization.[6
] In another study based on the U.S. National Health Interview Survey, self-reported ETS 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. The present findings add substantive additional evidence that SHS exposure is deleterious for patients with COPD.
The results differed somewhat depending on the method used to measure SHS exposure. For self-reported exposure, the overall pattern of results suggested a deleterious effect of SHS exposure on COPD-related health status, but the estimates were imprecise in many cases. This is probably attributable to the lower accuracy of self-reported SHS exposure. When urine cotinine was examined, which is an objective and specific measure of SHS exposure, the association between higher SHS exposure and poorer COPD-related health status was most clearly demonstrated. Personal badge nicotine levels, in contrast, were not associated with any health status variable. The different results for urine cotinine and personal badge nicotine levels may indicate that peak SHS exposure, rather than average SHS exposure, is more relevant to disease severity and health status in COPD. Personal badge data represent an integrated average exposure to nicotine during the time period that the badge is worn, whereas urinary cotinine data are more reflective of recent peak exposures. Alternatively, the personal nicotine badge measurements may have been subject to greater exposure misclassification than urine cotinine, because correct measurement depended on subjects reliably wearing the badge during all their daily activities (whereas urine cotinine was not). These methodologic differences likely also account for the low correlation among measures.
We used the standard epidemiologic definition of COPD, based on a self-reported physician diagnosis of chronic bronchitis, emphysema, or COPD [12
]. This survey-based approach, supplemented by a mail-based sample acquisition strategy, allowed us to study a population-based sample of adults who resided throughout the United States, enhancing the generalizability of our findings. On logistical grounds, conducting spirometry among subjects who reside thousands of miles apart would be highly difficult, if not impossible. The use of self-reported physician-diagnosis, however, may have resulted in some misclassification of disease status. Previous work indicated that a similar survey-based definition of COPD had a high positive predictive value (78%) when validated using a blinded medical record review that included spirometry and radiographic studies. [42
] Other work confirmed that a self-reported history of COPD is a strong predictor of airflow obstruction [43
]. Our previous validation study indicated that nearly 9 out of 10 participants who had available spirometry data had objective evidence of airflow obstruction.[2
] In sum, misclassification of COPD is not likely to bias our results; if present, such bias would likely be non-differential with respect to SHS exposure and reduce effect estimates towards the null value.
Although direct SHS exposure measurement is a more accurate method than self-report, it is more labor intensive and required a greater degree of commitment from study subjects. Reflecting these facts, not all eligible subjects participated in direct monitoring, which could have introduced selection bias. However, the similarity of participants and non-participants reduced the likelihood of this potential bias. In addition, incorporating sample weights that account for non-response into the analysis had a negligible impact on study results (data not shown). The other consequence of lower study participation is diminished statistical power, which resulted in decreased precision of effect estimates. In some cases, there appeared to be a negative effect of SHS exposure, but the 95% confidence intervals were wide and included no association. A larger sample size might have resulted in clearer evidence of SHS effects in these cases and would be required to detect smaller effects
Other limitations include the potential confounding effects of direct cigarette smoking. We attempted to reduce this confounding effect by limiting the analysis to persons who indicated no current smoking and had urine cotinine levels below a cut-point usually associated with active smoking. We also statistically controlled for a past history of cigarette smoking in multivariate analysis. Nonetheless, we cannot fully exclude confounding by active smoking. And finally, although direct SHS exposure measurement eliminated the bias inherent in self-reported exposure, a bias termed the "healthy passive smoker effect" can still occur, meaning that more severely affected COPD patients may selectively avoid SHS exposure, attenuating the observed association between exposure and asthma health outcomes.