Serum antiproteases in smokers and nonsmokers. Relationships to smoking status and pulmonary function

In this study of 50 relatively young male smokers and an equal number of age- and race-matched male nonsmokers, smokers had a 13.3% (p = 0.007) increase in mean serum alpha 1-proteinase inhibitor (alpha 1-Pl) concentration. This increase in serum alpha 1-Pl concentration was accompanied by increases in both the serum trypsin inhibitory capacity (TIC) (9.9%, p = 0.002) and the elastase inhibitory capacity (EIC) (12.4%, p = 0.001). That cigarette smoking increases serum alpha 1-Pl concentration and total protease inhibitory capacity was further supported by a significant association of alpha 1-PI, TIC, and EIC with increased pack-years smoking history, plasma nicotine, and plasma cotinine concentrations. Pulmonary function did not correlate with serum alpha 1-PI concentration. However, higher serum TIC and EIC did correlate with tests of small airways dysfunction. Highly significant correlations (r greater than or equal to 0.6, p = 0.001) were observed between TIC (or EIC) and alpha 1-PI concentrations. The linear relationships between TIC (or EIC) and serum alpha 1-PI concentration were not significantly different in smokers and nonsmokers. Further, no significant differential effect of smoking on either the TIC or EIC could be demonstrated. A decreased apparent functional activity of alpha 1-PI (i.e., nanomoles of protease inhibited per nanomole of alpha 1-PI) was associated with its higher serum concentration, a phenomenon observed in both smokers and nonsmokers. Thus, although cigarette smoking increases serum alpha 1-PI concentration and total protease inhibitory capacity, no evidence was obtained to suggest that the functional activity of serum alpha 1-PI (against either trypsin or elastase) was directly affected by smoking.