REDUCTION OF THE ELASTASE INHIBITORY CAPACITY OF ALPHA1-ANTITRYPSIN BY PEROXIDES IN CIGARETTE-SMOKE - AN ANALYSIS OF BRANDS AND FILTERS

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Abstract
A procedure for measuring the oxidant content of aqueous condensates of tobacco cigarette smoke is described. The procedure was used in conjunction with analysis of the ability of the smoke solutions to inactivate the elastase inhibitory capacity (EIC) of .alpha.1-antitrypsin. The ability of the smoke of a brand to inactivate .alpha.1-antitrypsin correlates well with the known tar and nicotine and with the amount of oxidants as measured with o-dianisidine. Filters removed .apprx. 73% of the oxidants from smoke. Smoke from a commercial nontobacco cigarette also contained a significant amount of oxidants and also destroyed .alpha.1-antitrypsin. Catalase and superoxide dismutase reduce the effect of solutions containing smoke on the EIC of .alpha.1-antitrypsin, suggesting that peroxides and superoxide anions in smoke contribute to the oxidant capacity of the smoke. The extent of apparent oxidation by a given quantity of smoke condensate increases for as long as an hour from the time the condensate is collected. The addition of H2O2 to the smoke solution increases its oxidant content and its ability to inactivate .alpha.1-antitrypsin. Apparently, occurrence of H2O2 caused by secretion from macrophages found in the small airways of smokers may contribute to a locally damaging environment for .alpha.1-antitrypsin in the presence of cigarette smoke that could promote the development of centrilobular emphysema.

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