The Effect of Smoking Intervention and an Inhaled Bronchodilator on Airways Reactivity in COPD*

CHEST Journal ◽  
2003 ◽  
Vol 124 (2) ◽  
pp. 449-458 ◽  
Author(s):  
Robert A. Wise ◽  
Richard E. Kanner ◽  
Paula Lindgren ◽  
John E. Connett ◽  
Murray D. Altose ◽  
...  
2021 ◽  
pp. 140349482110076
Author(s):  
Lotus S. Bast ◽  
Lisbeth Lund ◽  
Stine G. LauemØller ◽  
Simone G. Kjeld ◽  
Pernille Due ◽  
...  

Aims: Socio-economic inequalities in health behaviour may be influenced by health interventions. We examined whether the X:IT II intervention, aiming at preventing smoking in adolescence, was equally effective among students from different occupational social classes (OSC). Methods: We used data from the multi-component school-based smoking preventive intervention X:IT II, targeting 13- to 15-year-olds in Denmark. The intervention was tested in 46 schools with 2307 eligible students at baseline (response rate=86.6%) and had three main intervention components: smoke-free school time, smoke-free curriculum and parental involvement. We used a difference-in-difference design and estimated the change in current smoking after the first year of implementation in high versus low OSC. Analyses were based on available cases ( N=1190) and imputation of missing data at follow-up ( N=1967). Results: We found that 1% of the students from high OSC and 4.9% from low OSC were smokers at baseline (imputed data), and 8.2% of the students from high OSC and 12.2% from low OSC were smokers at follow-up. Difference-in-difference estimates were close to zero, indicating no differential trajectory. Conclusions: As intended, the X:IT II intervention, designed to apply equally to students from all socio-economic groups, did not seem to create different trajectories in current smoking among adolescents in high and low socio-economic groups. To diminish social inequality in health, future studies should carefully consider the ability to affect all socio-economic groups equally, or even to appeal mainly to participants from lower socio-economic groups, as they are often the ones most in need of intervention.


2009 ◽  
Vol 11 (4) ◽  
pp. 394-403 ◽  
Author(s):  
Jennifer B. McClure ◽  
Evette Ludman ◽  
Lou Grothaus ◽  
Chester Pabiniak ◽  
Julie Richards ◽  
...  

1999 ◽  
Vol 23 (3) ◽  
pp. 259-280 ◽  
Author(s):  
Frances Stillman ◽  
Anne Hartman ◽  
Barry Graubard ◽  
Elizabeth Gilpin ◽  
David Chavis ◽  
...  

1992 ◽  
Vol 13 (11) ◽  
pp. 403-412
Author(s):  
Gail G. Shapiro

Definition and Pathophysiology Asthma is a reversible airways disease characterized by both smooth muscle hyperreactivity and airway inflammation. During the 1970s and early 1980s the focus was on smooth muscle constriction, and it was believed that better bronchodilators would greatly diminish our difficulties in controlling this condition. This, unfortunately, was not the case. The emphasis of therapy today has turned to airway inflammation. Lung biopsies from patients who have asthma show destruction of respiratory epithelium, basement membrane thickening, and inflammatory cellular infiltrate. Among the infiltrating cells are eosinophils, macrophages, and neutrophils that are called to the site of inflammation by the chemotactic products released by activated mast cells. Upon their arrival, these cells release their own products of inflammation, which amplify this immunologic response. A variety of neuropeptides also play a role, some serving to stabilize and others to destabilize the airway. One result of this airway inflammation is airways reactivity, also known as bronchial hyperresponsiveness. A common example of this scenario is the child who has allergic asthma and encounters a problematic allergen. This child has immunoglobulin E (IgE) to this allergen bound to mast cells in his or her airway. Upon exposure to the allergen, the binding of IgE and antigen triggers mast cell mediator release within minutes.


1986 ◽  
Vol 61 (2) ◽  
pp. 640-646
Author(s):  
A. N. Freed ◽  
U. A. Scheffel ◽  
L. J. Kelly ◽  
B. Bromberger-Barnea ◽  
H. A. Menkes

Following ozone (O3) exposure, airways reactivity increases. We investigated the possibility that exposure to O3 causes a decrease in pulmonary perfusion, and that this decrease is associated with the increase in reactivity. Perfusion was measured with radiolabeled microspheres. A wedged bronchoscope was used to isolate sublobar segments in the middle and lower lobes of anesthetized dogs. Isolated segments were exposed to either O3 or an elevated alveolar pressure. Although increased alveolar pressure decreased microsphere density, exposure to 1 ppm O3 did not. Collateral system resistance rose significantly following exposure to O3 and to high pressure. These studies do not support the hypothesis that pulmonary perfusion is decreased following O3 exposure and is associated with subsequent increases in reactivity.


CHEST Journal ◽  
1984 ◽  
Vol 85 (4) ◽  
pp. 465-470 ◽  
Author(s):  
W.C. Hodgson ◽  
D.J. Cotton ◽  
G.D. Werner ◽  
D.W. Cockcroft ◽  
J. A Dosman

1995 ◽  
pp. 665-667
Author(s):  
C. L. Betson ◽  
T. H. Lam ◽  
J. Peters ◽  
A. J. Hedley ◽  
C. M. Wong

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