Respiratory health consequences of environmental tobacco smoke

Dhala, Atiya; Pinsker, Kenneth L.; Prezant, David J.

doi:10.1016/j.mcna.2004.06.005

Cited by 33 publications

(23 citation statements)

References 84 publications

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“…The existing epidemiologic data suggest that chronic airway inflammation caused by microbial infection or noninfective irritants, such as tobacco smoke, promote lung carcinogenesis (41,42), and that lung cancer risk is positively associated with the severity and duration of inflammation (43). However, although these data underline the relationships, they do not establish causal links.…”

Section: Promotion Of Lung Cancer By Exogenous Copd-like Airway Inflamentioning

confidence: 99%

Promotion of Lung Carcinogenesis by Chronic Obstructive Pulmonary Disease–Like Airway Inflammation in a K-ras–Induced Mouse Model

Moghaddam

Li²,

Cho³

et al. 2009

Am J Respir Cell Mol Biol

129

146

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Lung cancer is the leading cause of cancer deaths in the United States. In addition to genetic abnormalities induced by cigarette smoke, several epidemiologic studies have found that smokers with chronic obstructive pulmonary disease (COPD), an inflammatory disease of the lungs, have an increased risk of lung cancer (1.3-to 4.9-fold) compared to smokers without COPD. This suggests a link between chronic airway inflammation and lung carcinogenesis, independent of tobacco smoke exposure. We studied this association by assaying the inflammatory impact of products of nontypeable Haemophilus influenzae, which colonizes the airways of patients with COPD, on lung cancer promotion in mice with an activated Kras mutation in their airway epithelium. Two new mouse models of lung cancer were generated by crossing mice harboring the LSL-Kras G12D allele with mice containing Cre recombinase inserted into the Clara cell secretory protein (CCSP) locus, with or without the neomycin cassette excised (CCSP Cre and CCSP Cre-Neo , respectively). Lung lesions in CCSP Cre-Neo /LSL-K-ras G12D and CCSP Cre /LSL-Kras G12D mice appeared at 4 and 1 month of age, respectively, and were classified as epithelial hyperplasia of the bronchioles, adenoma, and adenocarcinoma. Weekly exposure of CCSP Cre /LSL-Kras G12D mice to aerosolized nontypeable Haemophilus influenzae lysate from age 6-14 weeks resulted in neutrophil/macrophage/ CD8 T-cell-associated COPD-like airway inflammation, a 3.2-fold increase in lung surface tumor number (156 6 9 versus 45 6 7), and an increase in total lung tumor burden. We conclude that COPD-like airway inflammation promotes lung carcinogenesis in a background of a G12D-activated K-ras allele in airway secretory cells.

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Section: Promotion Of Lung Cancer By Exogenous Copd-like Airway Inflamentioning

confidence: 99%

Promotion of Lung Carcinogenesis by Chronic Obstructive Pulmonary Disease–Like Airway Inflammation in a K-ras–Induced Mouse Model

Moghaddam

Li²,

Cho³

et al. 2009

Am J Respir Cell Mol Biol

129

146

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“…30 Exposure to ETS is unequivocally associated with exacerbation of asthma and is a notable contributing factor to disease severity and pathogenesis, with numerous reviews outlining the effect of ETS on asthma exacerbation and sensitization to allergens. 1,25,29,[31][32][33][34][35][36][37][38] Experimental exposure to ETS augments nasal responses to allergen in atopic human subjects, with investigators reporting increased allergen-induced specific IgE and IgG4 levels; increased IL-4, IL-5, and IL-13 levels; decreased IFN-g levels; and increased amounts of postallergen histamine in nasal lavage fluid. 39 Taken together, these studies provide initial mechanistic support to the epidemiologic reports suggesting that ETS exposure enhances the development of atopy and asthma.…”

Section: Pathogenesis: Nonallergensmentioning

confidence: 99%

Environmental and occupational allergies

Peden

Reed

2010

Journal of Allergy and Clinical Immunology

161

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“…It is estimated that environmental tobacco smoke exposure results in 50,000 excess deaths annually, of which ,3,000 are lung cancer deaths in nonsmokers [30]. There is less conclusive support to substantiate a causal relationship in adults between environmental tobacco smoke exposure and acute or chronic respiratory symptoms or as a cause of COPD or asthma.…”

Section: Discussionmentioning

confidence: 99%

Clinical determinants of exacerbations in severe, early-onset COPD

Foreman¹,

DeMeo²,

Hersh³

et al. 2007

European Respiratory Journal

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Chronic obstructive pulmonary disease (COPD) exacerbations impair health. The present authors analysed participants in the Boston Early-Onset COPD Study for familial aggregation and propensity for COPD exacerbations.In the present study, two exacerbation outcomes, episodes of cough and phlegm, and frequent exacerbations were analysed with multivariable modelling and generalised estimating equations.In early-onset COPD probands, passive tobacco smoke exposure within the home was strongly associated with episodes of cough and phlegm. Chronic phlegm production was associated with both exacerbation phenotypes in probands. In first-degree relatives of early-onset COPD probands, chronic bronchitis, episodic wheezing, pneumonia and active smoking were associated with the episodes of cough and phlegm phenotype. In relatives, identical characteristics plus exertional dyspnoea were associated with frequent exacerbations. Exacerbation risk increased with declining lung function. Familial aggregation for episodes of cough and phlegm was observed in relatives with severe obstruction.In conclusion, passive smoke exposure increases morbidity in severe early-onset chronic obstructive pulmonary disease probands, and chronic obstructive pulmonary disease exacerbations correlate with chronic sputum production in probands and relatives. The familial aggregation of exacerbations suggests a genetic basis for susceptibility to chronic obstructive pulmonary disease exacerbations.KEYWORDS: Chronic obstructive pulmonary disease, exacerbation, familial aggregation, passive smoking I ndividuals with chronic obstructive pulmonary disease (COPD), a progressive and irreversible illness, manifest symptoms of cough, phlegm, dyspnoea and exercise limitation. A proportion of individuals experience exacerbations during which these symptoms are acutely intensified. These episodes reduce quality of life, alter activities of daily living and commonly compel additional medical therapy. COPD exacerbations result in substantive morbidity, increased resource utilisation and significant financial burden [1][2][3][4]. Unfortunately, some individuals experience COPD exacerbations frequently. Other individuals have longer periods of relative stability. Frequent exacerbations are associated with increased morbidity and mortality [5]. The magnitude of this effect is highlighted by reports linking exacerbation frequency to acceleration in loss of lung function [6], reduction in quality of life [7,8], and risk for increased hospitalisations [9,10]. The fundamental reasons underlying the propensity to frequent exacerbations have not been determined. SILVERMAN et al. [11] previously demonstrated that current or former smoking relatives of severe, early-onset COPD probands in the Boston Early-Onset COPD Study had lower lung function and a higher relative risk of chronic bronchitis than controls who smoked. DEMEO et al. [12] demonstrated that both smoking and nonsmoking first-degree relatives of severe earlyonset COPD probands have significantly lower s...

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Respiratory health consequences of environmental tobacco smoke

Cited by 33 publications

References 84 publications

Promotion of Lung Carcinogenesis by Chronic Obstructive Pulmonary Disease–Like Airway Inflammation in a K-ras–Induced Mouse Model

Promotion of Lung Carcinogenesis by Chronic Obstructive Pulmonary Disease–Like Airway Inflammation in a K-ras–Induced Mouse Model

Environmental and occupational allergies

Clinical determinants of exacerbations in severe, early-onset COPD

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