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Clinical Investigations: SMOKING |

Smoking and Airway Inflammation in Patients With Mild Asthma*

George W. Chalmers, MD; Kirsten J. MacLeod, BSc; Lorna Thomson, BA; Stuart A. Little, MB, ChB:; Charles McSharry, PhD; Neil C. Thomson, MD
Author and Funding Information

*From the Departments of Respiratory Medicine (Drs. Chalmers, Little, and Thomson, and Ms. Thomson) and Immunology (Ms. MacLeod and Dr. McSharrry), Western Infirmary, Glasgow, UK.

Correspondence to: Neil C. Thomson, MD, Department of Respiratory Medicine, Western Infirmary/Gartnavel General Hospital, 1053 Great Western Rd, Glasgow G12 0YN, UK; e-mail nct1f@clinmed.gla.ac.uk



Chest. 2001;120(6):1917-1922. doi:10.1378/chest.120.6.1917
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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.

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