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 alpha₁-antitrypsin. The ability of the smoke of a brand to inactivate alpha₁-antitrypsin correlates well with the known tar and nicotine and with the amount of oxidants as measured using o-dianisidine. Filters were found to remove about 73% of the oxidants from smoke. Smoke from a commercial nontobacco cigarette was also found to contain a significant amount of oxidants and to also destroy alpha₁- antitrypsin.

Catatase and superoxide dismutase reduce the effect of solutions containing smoke on the EIC of alpha₁-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 hydrogen peroxide to the smoke solution increases both its oxidant content and its ability to inactivate alpha₁-antitrypsin.

These data suggest that occurrence of hydrogen peroxide caused by secretion from macrophages found in the small airways of smokers may contribute to a locally damaging environment for alpha₁ antitrypsin in the presence of cigarette smoke that could promote the development of centrilobular emphysema.