Chest
Volume 120, Issue 6, December 2001, Pages 1917-1922
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Clinical Investigations
SMOKING
Smoking and Airway Inflammation in Patients With Mild Asthma

https://doi.org/10.1378/chest.120.6.1917Get rights and content

Study objectives

Cigarette smoking is common in asthmatic patients, and we investigated the impact of cigarette smoking on airway inflammation in asthma.

Design

Single-center observational study of airway inflammation in asthmatic and healthy smokers and nonsmokers.

Setting

Asthma research unit in a university hospital.

Patients or participants

Sixty-seven asthmatic and 30 nonasthmatic subjects classified as smokers or nonsmokers. Asthmatics had chronic, stable asthma and were not receiving inhaled or oral steroids at the time of the study.

Interventions

We examined induced-sputum cell counts and levels of interleukin (IL)-8 and eosinophilic cationic protein (ECP). Bronchial hyperreactivity was assessed using methacholine challenge.

Measurements and results

Asthmatic smokers had higher total sputum cell counts than nonsmoking asthmatics and both smoking and nonsmoking healthy subjects. Smoking was associated with sputum neutrophilia in both asthmatics and nonasthmatics (median, 47% and 41%, respectively) compared with nonsmokers (median, 23% and 22%, respectively), and sputum IL-8 was increased in smokers compared with nonsmokers, both in subjects with asthma (median, 945 pg/mL vs 660 pg/mL, respectively) and in healthy subjects (median, 1,310 pg/mL vs 561 pg/mL, respectively). Sputum eosinophils and ECP levels were higher in both nonsmoking and smoking asthmatics than in healthy nonsmokers. In smoking asthmatics, lung function (FEV1 percent predicted) was negatively related to both sputum IL-8 (r = − 0.52) and sputum neutrophil proportion (r = − 0.38), and sputum IL-8 correlated positively with smoking pack-years (r = 0.57) and percent neutrophil count (r = 0.51).

Conclusions

In addition to the eosinophilic airway inflammation observed in patients with asthma, smoking induces neutrophilic airway inflammation; a relationship is apparent between smoking history, airway inflammation, and lung function in smoking asthmatics.

Section snippets

Subjects

Thirty nonasthmatic and 67 asthmatic subjects were further classified according to their smoking habits. Asthmatic subjects had stable symptoms at the time of study, and no history within the preceding 2 months of respiratory infection, or antibiotic or oral corticosteroid use, and were treated only with inhaled bronchodilators as required. Asthma was defined according to the American Thoracic Society definition,13 baseline lung function was recorded and, in asthmatic subjects, nonspecific

Patients

There were no significant differences between the groups in terms of age or smoking history (Table 1). The mean (SD) resting prebronchodilator FEV1 percent predicted was lower in asthmatic smokers (83 [15]%), asthmatic nonsmokers (85 [16]%) and healthy smokers (91 [15]%) than the healthy nonsmokers (103.9 [14]%) [p < 0.05 in each case; Table 1]. All asthmatic patients had hyperreactive airways at screening, although one asthmatic smoker had a PC20 of 16 mg/mL at the study visit (geometric mean

Discussion

Studies examining airway inflammation in asthma have concentrated mainly on nonsmoking subjects, presumably to avoid the known effects of smoking confounding the pathogenic mechanisms under investigation, and there is therefore little direct information about the effect of smoking on asthmatic airway inflammation. We have demonstrated that cigarette smoking has an impact on asthmatic airway inflammation, with evidence of an increase in sputum WBC count, relative and absolute neutrophilia, and

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    Dr. Chalmers was Chest Heart and Stroke Scotland Research Fellow, and Ms. Thomson and Dr. Little were funded by grants from the Scottish Home and Health Department, and the National Asthma Campaign, respectively.

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