title: Smoking and airway inflammation in patients with mild asthma.
abstract: OBJECTIVE
  Cigarette smoking is common in asthmatic patients, and we investigated the impact of cigarette smoking on airway inflammation in asthma.
  
  
  METHODS
  Single-center observational study of airway inflammation in asthmatic and healthy smokers and nonsmokers.
  
  
  METHODS
  Asthma research unit in a university hospital.
  
  
  METHODS
  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.
  
  
  METHODS
  We examined induced-sputum cell counts and levels of interleukin (IL)-8 and eosinophilic cationic protein (ECP). Bronchial hyperreactivity was assessed using methacholine challenge.
  
  
  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 (FEV(1) 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.
authors.affiliation: Department of Respiratory Medicine, Western Infirmary, Glasgow, UK.
authors.forename: G W
authors.initials: GW
authors.lastname: Chalmers
authors.forename: K J
authors.initials: KJ
authors.lastname: MacLeod
authors.forename: L
authors.initials: L
authors.lastname: Thomson
authors.forename: S A
authors.initials: SA
authors.lastname: Little
authors.forename: C
authors.initials: C
authors.lastname: McSharry
authors.forename: N C
authors.initials: NC
authors.lastname: Thomson
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology*; D001798:Blood Proteins / Q000378:metabolism*; D047091:Eosinophil Granule Proteins; D004804:Eosinophils / Q000276:immunology*; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism*; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology*; D012016:Reference Values; D012260:Ribonucleases; D012907:Smoking / Q000009:adverse effects* / Q000276:immunology; D013183:Sputum / Q000276:immunology*
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D016209:Interleukin-8; D012260:Ribonucleases