Cigarette smoking is the most common factor responsible for the development of chronic obstructive pulmonary disease (COPD) leading to oxidant overload in the lower airways because of the presence of oxidants in cigarette smoke and recruitment and activation of pulmonary phagocytes. In this study we intended to determine whether: 1) patients with stable COPD have higher H2O2 levels in expired breath condensate than healthy nonsmoking subjects and 2) whether cigarette smoking increases H2O2 exhalation in patients with stable COPD. The H2O2 content of the expired breath condensate of 17 healthy nonsmoking subjects and 38 patients (10 current smokers, 17 exsmokers and 11 who have never smoked) with stable COPD (forced expiratory volume in one second (FEV1) 63.3 +/- 15.5% of predicted value) was measured spectrofluorimetrically (homovanillic acid method). The mean H2O2 concentration in the expired breath condensate of COPD subjects was 10-times higher than that found in healthy controls (0.55 +/- 0.69 microM versus 0.05 +/- 0.07 microM, p < 0.005). There were no significant differences between H2O2 levels found in current smokers with COPD (0.44 +/- 0.56 microM) and COPD subjects who have never smoked (0.49 +/- 0.70 microM). No correlation was found between expired H2O2 and daily cigarette consumption or cumulative cigarette consumption in current smokers or exsmokers with COPD. These findings demonstrate that subjects with stable chronic obstructive pulmonary disease exhibit increased H2O2 generation in the airways and that cigarette smoking does not increase H2O2 production.