Is Secondhand Smoke Exposure Associated With Increased Exacerbation Severity Among Children Hospitalized for Asthma?

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Is Secondhand Smoke Exposure Associated With Increased Exacerbation Severity Among Children Hospitalized for Asthma?

Hosp Pediatr. 2015 May;5(5):249-255

Authors: Andrews AL, Shirley N, Ojukwu E, Robinson M, Torok M, Wilson KM

Abstract
OBJECTIVE: To determine the association between secondhand smoke (SHS) exposure and length of stay (LOS) and other exacerbation severity indicators in children hospitalized for asthma.
METHODS: We conducted a retrospective chart review at 2 children’s hospitals. Patients aged 2 to 18 hospitalized for asthma in 2012 were included. Outcome variables included LOS, PICU, magnesium, and intravenous (IV) steroids. Bivariate analysis determined differences between SHS-exposed and non-SHS-exposed groups. Geometric means were used for LOS to account for skewed distribution. Logistic and zero-truncated negative binomial regression models were used to determine the independent association between SHS exposure and hospitalization severity indicators.
RESULTS: A total of 623 patients were included; 41% reported SHS exposure. Mean LOS was 47.5 hours. In the SHS-exposed group, LOS was 50.0 (95% confidence interval [CI] 46.7-54.0) and in the nonexposed group it was 45.8 (95% CI 43.4-48.4) (P = .02). In regression analysis, institution modified the effect of SHS exposure on LOS. At Children’s Hospital Colorado, SHS exposure was associated with a 20% increase in LOS (incidence rate ratio 1.2, 95% CI 1.1-1.3). At the Medical University of South Carolina, there was no significant association. SHS-exposed patients were more likely to receive IV steroids (odds ratio 1.6, 95% CI 1.1-2.3) CONCLUSIONS: Among children hospitalized for asthma, we identified a significant association at 1 institution between SHS exposure and LOS and found that IV steroid use was significantly associated with LOS at both institutions. Eliminating SHS exposure among children with asthma is important.

PMID: 25934808 [PubMed – as supplied by publisher]

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Nearly Half of Older Adults With Asthma, COPD Still Smoke: CDC – U.S. News & World Report

Nearly Half of Older Adults With Asthma, COPD Still Smoke: CDC
U.S. News & World Report
WEDNESDAY, Jan. 7, 2015 (HealthDay News) — Close to half of U.S. adults over 40 who have trouble breathing due to asthma or COPD still continue to smoke, federal health officials reported Wednesday. The findings highlight the difficulty facing many …
About 1 in 7 Older Adults Has Some Form of Lung Disease: CDCDoctors Lounge
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Cigarette Smoke Induces uPAR in Vivo and Isoforms Selectively Contribute to Bronchial Epithelial Phenotype.

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Cigarette Smoke Induces uPAR in Vivo and Isoforms Selectively Contribute to Bronchial Epithelial Phenotype.

Am J Respir Cell Mol Biol. 2014 Dec 9;

Authors: Portelli MA, Stewart CE, Hall IP, Brightling CE, Sayers I

Abstract
The urokinase plasminogen activator receptor (uPAR) gene (PLAUR) has been identified as an asthma susceptibility gene, with polymorphisms within that gene being associated with baseline lung function, lung function decline and lung function in a smoking population. Soluble cleaved uPAR (scuPAR), a molecule identified as a marker of increased morbidity and mortality in a number of diseases, has itself been shown to be elevated in the airways of asthma and COPD patients. However, the functionality of soluble receptor isoforms and their relationship with an important initiator for obstructive lung disease, cigarette smoke, remains undefined. In this study, we set out to determine the effect of cigarette smoke on soluble uPAR isoforms, its regulatory pathway and the resultant effect on bronchial epithelial cell function. We identified a positive association between cigarette pack/years and uPAR expression in the airway bronchial epithelium of biopsies from asthma patients (n=27, P=0.0485). In vitro, cigarette smoke promoted cleavage of uPAR from the surface of bronchial epithelial cells (1.5X induction, P<0.0001) and induced the soluble spliced isoform through changes in mRNA expression (~2X change, P<0.001), driven by loss of endogenous 3`UTR suppression. Elevated expression of the soluble isoforms resulted in a pro-remodelling cell phenotype, characterised by increased proliferation and MMP-9 expression in primary bronchial epithelial cells. This suggests that cigarette smoke elevates soluble receptor isoforms in bronchial epithelial cells through direct (cleavage), and indirect (mRNA expression) means. These findings provide further insight into how cigarette smoke may influence changes in the airways of importance to airway remodelling and obstructive lung disease progression.

PMID: 25490122 [PubMed – as supplied by publisher]

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