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Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease

BACKGROUND: Exposure to environmental tobacco smoke (ETS), which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiolo...

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Autores principales: Eisner, Mark D, Balmes, John, Katz, Patricia P, Trupin, Laura, Yelin, Edward H, Blanc, Paul D
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1145187/
https://www.ncbi.nlm.nih.gov/pubmed/15890079
http://dx.doi.org/10.1186/1476-069X-4-7
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author Eisner, Mark D
Balmes, John
Katz, Patricia P
Trupin, Laura
Yelin, Edward H
Blanc, Paul D
author_facet Eisner, Mark D
Balmes, John
Katz, Patricia P
Trupin, Laura
Yelin, Edward H
Blanc, Paul D
author_sort Eisner, Mark D
collection PubMed
description BACKGROUND: Exposure to environmental tobacco smoke (ETS), which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiologic studies. METHODS: Using data from a population-based sample of 2,113 U.S. adults aged 55 to 75 years, we examined the association between lifetime ETS exposure and the risk of developing COPD. Participants were recruited from all 48 contiguous U.S. states by random digit dialing. Lifetime ETS exposure was ascertained by structured telephone interview. We used a standard epidemiologic approach to define COPD based on a self-reported physician diagnosis of chronic bronchitis, emphysema, or COPD. RESULTS: Higher cumulative lifetime home and work exposure were associated with a greater risk of COPD. The highest quartile of lifetime home ETS exposure was associated with a greater risk of COPD, controlling for age, sex, race, personal smoking history, educational attainment, marital status, and occupational exposure to vapors, gas, dusts, or fumes during the longest held job (OR 1.55; 95% CI 1.09 to 2.21). The highest quartile of lifetime workplace ETS exposure was also related to a greater risk of COPD (OR 1.36; 95% CI 1.002 to 1.84). The population attributable fraction was 11% for the highest quartile of home ETS exposure and 7% for work exposure. CONCLUSION: ETS exposure may be an important cause of COPD. Consequently, public policies aimed at preventing public smoking may reduce the burden of COPD-related death and disability, both by reducing direct smoking and ETS exposure.
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spelling pubmed-11451872005-06-09 Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease Eisner, Mark D Balmes, John Katz, Patricia P Trupin, Laura Yelin, Edward H Blanc, Paul D Environ Health Research BACKGROUND: Exposure to environmental tobacco smoke (ETS), which contains potent respiratory irritants, may lead to chronic airway inflammation and obstruction. Although ETS exposure appears to cause asthma in children and adults, its role in causing COPD has received limited attention in epidemiologic studies. METHODS: Using data from a population-based sample of 2,113 U.S. adults aged 55 to 75 years, we examined the association between lifetime ETS exposure and the risk of developing COPD. Participants were recruited from all 48 contiguous U.S. states by random digit dialing. Lifetime ETS exposure was ascertained by structured telephone interview. We used a standard epidemiologic approach to define COPD based on a self-reported physician diagnosis of chronic bronchitis, emphysema, or COPD. RESULTS: Higher cumulative lifetime home and work exposure were associated with a greater risk of COPD. The highest quartile of lifetime home ETS exposure was associated with a greater risk of COPD, controlling for age, sex, race, personal smoking history, educational attainment, marital status, and occupational exposure to vapors, gas, dusts, or fumes during the longest held job (OR 1.55; 95% CI 1.09 to 2.21). The highest quartile of lifetime workplace ETS exposure was also related to a greater risk of COPD (OR 1.36; 95% CI 1.002 to 1.84). The population attributable fraction was 11% for the highest quartile of home ETS exposure and 7% for work exposure. CONCLUSION: ETS exposure may be an important cause of COPD. Consequently, public policies aimed at preventing public smoking may reduce the burden of COPD-related death and disability, both by reducing direct smoking and ETS exposure. BioMed Central 2005-05-12 /pmc/articles/PMC1145187/ /pubmed/15890079 http://dx.doi.org/10.1186/1476-069X-4-7 Text en Copyright © 2005 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
Eisner, Mark D
Balmes, John
Katz, Patricia P
Trupin, Laura
Yelin, Edward H
Blanc, Paul D
Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
title Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
title_full Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
title_fullStr Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
title_full_unstemmed Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
title_short Lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
title_sort lifetime environmental tobacco smoke exposure and the risk of chronic obstructive pulmonary disease
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1145187/
https://www.ncbi.nlm.nih.gov/pubmed/15890079
http://dx.doi.org/10.1186/1476-069X-4-7
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