• R A Stolarek, M Kasielski, J Rysz, P Bialasiewicz, and D Nowak.
• Department of Experimental and Clinical Physiology and Biochemistry, Medical University of Lodz, Poland.
• Monaldi Arch Chest Dis. 2006 Mar 1;65(1):19-25.

BackgroundThis study was designed to investigate the effect of cigarette smoking on hydrogen peroxide (H2O2) and thiobarbituric reactive substances (TBARs) concentrations in exhaled breath condensate (EBC) in patients with community acquired pneumonia (CAP).MethodsH2O2 and TBARs concentrations in EBC were determined with spectrofluorimetrical assays.ResultsNon-smoking CAP patients (n = 24) exhaled 1.4, 1.8 and 1.7 times more H2O2 than the smoking patients with CAP (n = 19) as assessed one (0.73 +/- 0.32 microM v. 0.51 +/- 0.36 microM), three (0.84 +/- 0.31 microM v. 0.47 +/- 0.24 microM) and five (0.66 +/- 0.28 microM v. 0.40 +/- 0.35 microM) days after admission (p < 0.05 in each case). Over 10 days of hospital treatment, mean level of exhaled H2O2 0.45 +/- 0.22 microM in CAP patients with smoking history was decreased if compared with 0.71 +/- 0.19 microM exhaled H2O2 in CAP group (p = 0.005). On the contrary, TBARs concentration evaluated over entire study period was increased in smoking CAP patients (median 0.02 microM, range 0-0.32 microM) compared with non-smoking group (median 0.01 microM, range 0-0.21 microM, p < 0.05). Concurrent, active smoking status was related with the decreased levels of H2O2 exhaled in breath condensate within the course of CAP but it appeared to increase levels of TBARs.ConclusionsThe differential alternations of oxidative parameters in EBC with respect to the smoking status might provide evidence of increased H2O2 decomposition and enhanced generation of reactive species in airways of CAP patients.

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