Impaired Cough Sensitivity in Children of Smokers (original) (raw)
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Effect of smoking cessation on cough reflex sensitivity
European Respiratory Journal, 2006
Recent studies have shown that cigarette smokers have diminished cough reflex sensitivity compared with nonsmokers. The current authors proposed a mechanism of chronic cigarette smoke-induced desensitisation of airway cough receptors. To investigate this hypothesis, cough sensitivity to inhaled capsaicin (C 5) in chronic smokers was measured both while they were actively smoking and 2, 6, 12 and 24 weeks after smoking cessation. In total, 29 subjects underwent baseline capsaicin challenge while smoking and 2 weeks after smoking cessation. Mean¡SEM log C 5 fell from 1.86¡0.12 to 1.60¡0.12, demonstrating significant enhancement of cough reflex sensitivity. Of the total, 20, 18 and 14 subjects successfully abstained from smoking for 6, 12 and 24 weeks, respectively. Mean log C 5 values after 12 and 24 weeks of smoking cessation were significantly diminished from baseline. In a control group of smokers, mean log C 5 did not decrease from baseline after 6, 12 and 24 weeks. Overall, the log C 5 profile of the smoking cessation group showed a clear, linearly decreasing trend over time compared with the control group. Even after many years of smoking, cough sensitivity is enhanced as early as 2 weeks after smoking cessation. Given the importance of an intact cough reflex, these changes may provide clinical benefit.
Changes in cough reflex sensitivity after cessation and resumption of cigarette smoking
Pulmonary Pharmacology & Therapeutics, 2007
Previous studies have shown that healthy cigarette smokers have diminished cough reflex sensitivity compared to healthy nonsmokers. We have recently demonstrated that cough reflex sensitivity is enhanced soon after smoking cessation, suggesting that diminished cough sensitivity in smokers results from chronic cigarette smoke-induced desensitization of airway cough receptors. In this study, we evaluated cough reflex sensitivity to capsaicin (C 5 ) in 11 chronic smokers who had discontinued smoking for at least 2 weeks, and then resumed smoking.
Capsaicin cough sensitivity in smokers with and without airflow obstruction
Respiratory Medicine, 2009
Background: Cough is a frequent symptom of cigarette smokers that often precedes the development of airflow obstruction. We determined whether chronic cigarette smoking is associated with an increase in capsaicin cough response in the absence of cough. Methods: We examined this in asymptomatic smokers with normal lung function (n Z 68, FEV 1 99.3 AE 2.1% predicted) and in patients with established COPD without cough symptoms (n Z 42; FEV 1 57.0 AE 2.6% predicted), using healthy non-smoking volunteers as control (n Z 92; FEV 1 100.6 AE 1.7% predicted). Using an incremental capsaicin concentration challenge protocol, we recorded the concentrations that induced 2 (C2) and 5 or more coughs (C5). Results: Because females have a lower C2 and C5 than males in the control group, we analysed the data in each group according to gender. Log C5 was decreased both in asymptomatic smokers (1.56 AE 0.11 mmol/L, p < 0.05) and in COPD patients (1.44 AE 0.14 mmol/L, p < 0.01) when compared to non-smokers (1.90 AE 0.09 mmol/L). Log C2 did not differ between groups. Log C2 and log C5 were decreased in women (0.772 AE 0.071 mmol/L and 1.481 AE 0.094 mmol/ L, respectively) when compared to men (1.045 AE 0.088 mmol/L and 1.923 AE 0.087 mmol/L, respectively) (p < 0.05 for log C2; p < 0.001 for log C5). Conclusion: We conclude that chronic cigarette smoking increases capsaicin cough reflex and that this remains so with the development of COPD. ª
Influence of Smoking Status on Cough Reflex Sensitivity in Subjects with COPD
Lung, 2009
Cough reflex sensitivity has not been studied extensively in patients with chronic obstructive pulmonary disease (COPD). The aim of the study was to evaluate cough reflex sensitivity to capsaicin in current and former smokers with COPD and examine its association with potentially protussive mediators. Fifteen active smokers and 18 ex-smokers with moderate to severe COPD, 14 healthy active smokers, and 13 healthy never smokers were enrolled. Capsaicin aerosol was administered in order of ascending concentration until the concentrations inducing two or more coughs (C 2 ) and five or more coughs (C 5 ) were attained. The concentrations of leukotriene E 4 (LTE 4 ), leukotriene B 4 (LTB 4 ), and interleukin-8 (IL-8) in bronchoalveolar lavage (BAL) fluid were analyzed by ELISA. Cough reflex sensitivity in COPD smokers [mean log C 2 = 1.20 ± 0.23 (SEM) lM; log C 5 = 1.85 ± 0.21 lM] did not differ from that in COPD ex-smokers (log C 2 = 1.15 ± 0.14 lM; log C 5 = 2.10 ± 0.19 lM; p [ 0.05). Mean C 2 and C 5 in both COPD groups were significantly lower than in healthy active smokers, but higher compared with the healthy never-smokers. BAL fluid concentrations of LTE 4 and LTB 4 were similar in all groups. IL-8 concentrations did not differ between COPD smokers, COPD ex-smokers, and healthy active smokers, but were significantly higher in all three groups compared with healthy never smokers. Cough reflex sensitivity to capsaicin does not differ between smokers and ex-smokers with COPD.
Cough (London, England), 2006
The relationships between chronic productive cough (CPC), environmental tobacco smoke (ETS) exposure, and asthma are not clearly established in children. Therefore, we wished to determine the prevalence of CPC and examine the relationships between CPC, ETS exposure, and asthma in young teenagers. We performed a cross sectional survey of 2397 Seattle middle school students, 11-15 years old, using written and video respiratory-symptom questionnaires. We defined CPC as--daily cough productive of phlegm for at least 3 months out of the year; current asthma as--yes to "Have you had wheezing or whistling in your chest in the past 12 months?" and yes in the past year to any of the four video wheezing/asthma video scenarios; and ETS exposure as exposed to tobacco smoke at least several hours each day. We used multilogistic regression to examine relationships between CPC, asthma, and ETS exposure and included in the model the potentially confounding variables race, gender, and alle...
Journal of Allergy and Clinical Immunology, 2014
Exposure to environmental tobacco smoke (ETS) has been established as a significant risk factor for respiratory symptoms and diseases in children. However, it is unclear whether the effects of childhood exposure to ETS track into adult life. By using data from the long-term populationbased cohort of the TESAOD study, this study found that parental ETS exposure in childhood significantly increases the risk of persistent cough, chronic cough, and wheeze into young adult life.
Analysis and evaluation of environmental tobacco smoke exposure as a risk factor for chronic cough
2007
Abstract Exposure to environmental tobacco smoke (ETS) and active tobacco smoking has been shown to increase symptoms of bronchial asthma such as bronchoconstriction but effects on other respiratory symptoms remain poorly assessed. Current levels of exposure to tobacco smoke may also be responsible for the development of chronic cough in both children and adults. The present study analyses the effects of tobacco smoke exposure as potential causes of chronic cough.
Parental Smoking and Airway Reactivity in Healthy Infants
Parental tobacco smoking is associated with lower airway function and an increased incidence of wheezy respiratory illnesses in infants. We evaluated in 76 healthy infants whether exposure to parental tobacco smoking was associated with airway hyperreactivity, which could contribute to lower airway function and the increased wheezy illnesses. Airway function was measured using the raised-volume rapid thoracic compression technique, and airway reactivity was assessed by methacholine challenge (0.015-10 mg/ml), which was stopped for a more than 30% decrease in forced expiratory flow (FEF) 75 or the final dose with a less than 30% decrease. Parental tobacco smoking was associated with lower baseline airway function (FEF 50 , 600 vs. 676 ml/second, p Ͻ 0.04; FEF 25-75 , 531 vs. 597 ml/second, p Ͻ 0.05). Infants exposed to tobacco smoking were approximately half as likely to develop a more than 30% decline in FEF 75 at any given methacholine dose (hazard ratio ϭ 0.4, p ϭ 0.001). In addition, a history of asthma in an extended family member increased the likelihood that an infant would develop a more than 30% decline in FEF 75 (hazard ratio ϭ 1.7, p ϭ 0.04). We conclude that exposure to parental smoking is associated with lower airway function but not increased airway reactivity; however, family history of asthma is associated with heightened airway reactivity.
Effects of parental smoking and indoor tobacco smoke exposure on respiratory outcomes in children
Scientific Reports, 2020
The extensive literature has reported adverse effects on environmental tobacco smoke (ETS) on children’s health. We aim to analyze associations of ETS with dry night cough, croup, pneumonia, and frequent common cold and to disentangle the effects of prenatal, infancy and childhood exposure by multilevel logistic regression. A cross-sectional study was conducted among 41,176 children aged 3–8 years in 8 major cities of China during 2010–2011, and obtained demographic information, smoke exposure information, and respiratory outcomes. Parents’ smoking habit and indoor tobacco smoke odor were considered as two indicators of ETS. The prevalences of respiratory outcomes were 6.0% for croup, 9.5% for frequency common cold, 17.1% for dry night cough and 32.3% for pneumonia respectively in the study. The associations between respiratory outcomes and parental smoking were not obvious, while indoor tobacco smoke odor was clearly and strongly associated with most respiratory outcomes, with adju...