Directly measured secondhand smoke exposure and COPD health outcomes
1 Department of Medicine, University of California, San Francisco, UCSF Box 0924, San Francisco, CA, 94113-0924, USA
2 Division of Occupational and Environmental Medicine, Department of Medicine, University of California, San Francisco, UCSF Box 0924, San Francisco, CA, 94113-0924, USA
3 Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, San Francisco, UCSF Box 0924, San Francisco, CA, 94113-0924, USA
4 Institute for Health Policy Studies, University of California, San Francisco, UCSF Box 0920, San Francisco, CA, 94113-0920, USA
5 School of Public Health, University of California, Berkeley, USA
6 Division of Clinical Pharmacology and Experimental Therapeutics, Department of Medicine, University of California San Francisco, UCSF Box 1220, San Francisco, CA, 94143-1220, USA
BMC Pulmonary Medicine 2006, 6:12 doi:10.1186/1471-2466-6-12Published: 6 June 2006
Although personal cigarette smoking is the most important cause and modulator of chronic obstructive pulmonary disease (COPD), secondhand smoke (SHS) exposure could influence the course of the disease. Despite the importance of this question, the impact of SHS exposure on COPD health outcomes remains unknown.
We used data from two waves of a population-based multiwave U.S. cohort study of adults with COPD. 77 non-smoking respondents with a diagnosis of COPD completed direct SHS monitoring based on urine cotinine and a personal badge that measures nicotine. We evaluated the longitudinal impact of SHS exposure on validated measures of COPD severity, physical health status, quality of life (QOL), and dyspnea measured at one year follow-up.
The highest level of SHS exposure, as measured by urine cotinine, was cross-sectionally associated with poorer COPD severity (mean score increment 4.7 pts; 95% CI 0.6 to 8.9) and dyspnea (1.0 pts; 95% CI 0.4 to 1.7) after controlling for covariates. In longitudinal analysis, the highest level of baseline cotinine was associated with worse COPD severity (4.7 points; 95% CI -0.1 to 9.4; p = 0.054), disease-specific QOL (2.9 pts; -0.16 to 5.9; p = 0.063), and dyspnea (0.9 pts; 95% CI 0.2 to 1.6 pts; p < 0.05), although the confidence intervals did not always exclude the no effect level.
Directly measured SHS exposure appears to adversely influence health outcomes in COPD, independent of personal smoking. Because SHS is a modifiable risk factor, clinicians should assess SHS exposure in their patients and counsel its avoidance. In public health terms, the effects of SHS exposure on this vulnerable subpopulation provide a further rationale for laws prohibiting public smoking.