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Directly measured secondhand smoke exposure and COPD health outcomes

BACKGROUND: 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 out...

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Autores principales: Eisner, Mark D, Balmes, John, Yelin, Edward H, Katz, Patricia P, Hammond, S Katherine, Benowitz, Neal, Blanc, Paul D
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1524811/
https://www.ncbi.nlm.nih.gov/pubmed/16756671
http://dx.doi.org/10.1186/1471-2466-6-12
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author Eisner, Mark D
Balmes, John
Yelin, Edward H
Katz, Patricia P
Hammond, S Katherine
Benowitz, Neal
Blanc, Paul D
author_facet Eisner, Mark D
Balmes, John
Yelin, Edward H
Katz, Patricia P
Hammond, S Katherine
Benowitz, Neal
Blanc, Paul D
author_sort Eisner, Mark D
collection PubMed
description BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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spelling pubmed-15248112006-07-29 Directly measured secondhand smoke exposure and COPD health outcomes Eisner, Mark D Balmes, John Yelin, Edward H Katz, Patricia P Hammond, S Katherine Benowitz, Neal Blanc, Paul D BMC Pulm Med Research Article BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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. BioMed Central 2006-06-06 /pmc/articles/PMC1524811/ /pubmed/16756671 http://dx.doi.org/10.1186/1471-2466-6-12 Text en Copyright © 2006 Eisner et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Eisner, Mark D
Balmes, John
Yelin, Edward H
Katz, Patricia P
Hammond, S Katherine
Benowitz, Neal
Blanc, Paul D
Directly measured secondhand smoke exposure and COPD health outcomes
title Directly measured secondhand smoke exposure and COPD health outcomes
title_full Directly measured secondhand smoke exposure and COPD health outcomes
title_fullStr Directly measured secondhand smoke exposure and COPD health outcomes
title_full_unstemmed Directly measured secondhand smoke exposure and COPD health outcomes
title_short Directly measured secondhand smoke exposure and COPD health outcomes
title_sort directly measured secondhand smoke exposure and copd health outcomes
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1524811/
https://www.ncbi.nlm.nih.gov/pubmed/16756671
http://dx.doi.org/10.1186/1471-2466-6-12
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