• F Hoffmeyer, V Harth, J Bunger, T Bruning, and M Raulf-Heimsoth.
• BGFA, Research Institute of Occupational Medicine, German Social Accident Insurance, Ruhr-University Bochum, Germany. hoffmeyer@bgfa.de
• J. Physiol. Pharmacol. 2009 Nov 1;60 Suppl 5:57-60.

AbstractLong-term cigarette smoking is the major etiological factor for the development of chronic obstructive pulmonary disease (COPD). Airway inflammation and oxidative stress are implicated in the pathogenesis. Biomarkers reflecting these responses could be analyzed in exhaled breath condensate (EBC). Recently, it became obvious that mediator concentrations in EBC could be influenced by age of the subjects, equipment, sampling properties, and the analytical assays applied. In the present study we evaluated 8 smokers (20-56 yr) and 16 non-smoking adults (18-60 yr) with normal spirometry and no episode of airway infection during 6 weeks prior to the study. EBC samples were obtained with the commercial device ECoScreen2 at a controlled temperature of -20 degrees C. Leukotriene B(4) (LTB(4), marker of inflammation), 8-iso-prostaglandin F(2 alpha) (8-iso-PGF(2 alpha)/8-isoprostane, oxidative stress) concentrations, and pH were measured. With 10 min of tidal breathing, a lower EBC volume was collected in smokers (median 1.22 ml; interquantil range 1.06-1.74 ml) than in non-smokers (1.6 ml; 1.16-2.21 ml; P=0.06). Significant differences were found in pH in smokers compared with non-smokers (7.14 (5.70-7.43) vs. 7.59 (7.28-7.73); P<0.01). No significant differences were observed in EBC concentrations of LTB(4) or 8-iso-PGF(2 alpha). The study demonstrates that acidopnea is detectable in otherwise asymptomatic smokers and might precede changes in the level of arachidonic acid metabolites. For pH is considered to be the most validated marker determined in EBC samples, it may be useful for screening asymptomatic individuals for smoking-induced early airway damage.

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