Lower Respiratory Illnesses Promote FEV₁ Decline in Current Smokers But Not Ex-Smokers with Mild Chronic Obstructive Pulmonary Disease

Abstract

We analyzed Lung Health Study (LHS) data to assess the effect of self-reported lower respiratory illnesses resulting in physician visits (LRI) on lung function. Participants were 5,887 smokers aged 35-60 yr, FEV(1)/FVC < 0.70 and FEV(1) of 55-90% predicted. Two-thirds were randomized into an intensive smoking cessation program (SI); one-third were advised only to stop smoking (UC). For 5 yr participants had annual spirometry and questioning regarding LRI. SI had greater rates of smoking cessation than usual care (UC) with fewer LRI (p = 0.0008). Sustained quitters had fewer LRI than continuing smokers (p = 0.0003). In the year LRI occurred, FEV(1) did not change in sustained quitters, but decreased significantly in smokers (p = 0.0001) with some recovery the following year if no LRI occurred. Over 5 yr, LRI had a significant effect on rate of decline of FEV(1) only in smokers. In smokers averaging one LRI/yr over 5 yr there were additional declines in FEV(1) of 7 ml /yr (p = 0.001). Smokers with more than one LRI/yr had greater declines. Chronic bronchitis was associated with increased frequencies of LRI, but did not affect their influence on lung function. Smoking and LRI had an interactive effect on FEV(1) in people with mild COPD, and in smokers frequent LRI may influence the long-term course of the disease.

Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

“…Additionally, enhanced activation of primed NK cells following infection may activate the adaptive immune response. supported by observations that COPD patients who stop smoking have significantly reduced frequency of exacerbations (32,33), which we hypothesize to be due to loss of NK cell priming.…”

“…Several reports indicate that the numbers of COPD exacerbations in patients are reduced following cigarette smoking cessation (32,33). We therefore examined whether NK cell priming persisted after smoking cessation.…”

Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections

“…5 Although still contentious, 17,18 it has been postulated that repeated respiratory infections are involved in the pathogenesis of COPD, by promoting airway and parenchymal inflammation. 3,4 Hence, genes involved in innate immunity against infection are plausible candidate modifying genes in COPD.…”

“…Repeated respiratory infections have been implicated in the pathogenesis of COPD, 4 including accelerated decline in lung function. 5 Mannose-binding lectin (MBL) is a key component of host defence against infection. 6 MBL is a patternrecognition receptor that binds to surface carbohydrates on microorganisms, which in turn activates the complement system.…”

Influences of patient education on exacerbations and hospital admissions in patients with COPD – a longitudinal national register study

“…Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of decline in Forced Expiratory Volume (FEV 1 )%, increased exacerbations rate [14], and a greater COPD mortality rate than non-smokers [15]. Participation in a smoking cessation program compared to non-participation was shown to significantly decrease self-reported phlegm and significantly less number of days hospitalized for COPD [16].…”