Extracellular release of hydrogen peroxide by human alveolar macrophages: the relationship to cigarette smoking and lower respiratory tract infections.

It has been suggested that oxidants from pulmonary inflammatory cells may contribute to the development of emphysema by (i) direct tissue toxicity and (ii) inhibition of alpha 1-antitrypsin, thus diminishing protection of the lung from proteolytic damage. The extracellular release of hydrogen peroxide (H2O2) by human alveolar macrophages (AM) has been measured. AM were obtained by bronchoalveolar lavage and adherence from 24 smokers and 17 non-smokers. Smokers' AM released significantly more H2O2 (3.83 nmol h-1 micrograms-1 of DNA; SEM 0.44) than those of non-smokers' (2.33 nmol h-1 microgram-1 of DNA; SEM 0.40) (P less than 0.05). AM from donors with a recent lower respiratory tract infection released increased quantities of H2O2 (5.22 nmol h-1 microgram-1 of DNA; SEM 0.72; P less than 0.01) even when allowance was made for smoking habits. These findings are consistent with the hypothesis that H2O2 of AM origin contributes to the development of emphysema in smokers.