Smokers Do Not Have Less Functional Alpha1-Protease Inhibitor in Their Lower Respiratory Tracts Than Nonsmokers

Abstract

Cigarette smoking is the major risk factor in the development of pulmonary emphysema, a condition thought to result from an imbalance between the elastase and antielastase levels in the lungs. An increased number of neutrophils and alveolar macrophages in the lungs of smokers could account for an elevation of their elastase burden. A decreased level of functional alpha1-protease inhibitor (alpha1-PI) has been reported in the bronchoalveolar lavage (BAL) fluid from smokers as compared with nonsmokers. 1 Gadek JE Fells GA Crystal RG Cigarette smoking induces functional antiprotease deficiency in the lower respiratory tract of humans. Science. 1979; 206: 1315-1316 Crossref PubMed Scopus (264) Google Scholar , 2 Carp H Miller F Hoidal JR Janoff A Potential mechanism of emphysema: α1-proteinase inhibitor recovered from lungs of cigarette smokers contains oxidized methionine and has decreased elastase inhibitory capacity. Proc Natl Acad Sci USA. 1982; 79: 2041-2045 Crossref PubMed Scopus (268) Google Scholar We determined binding and inactivation of 3H-porcine pancreatic elastase and 125I-human neutrophil elastase by alpha1-PI in BAL from volunteers; we also measured the inhibition by BAL of porcine pancreatic elastase-catalyzed solubilization of 3H-elastin. The mean levels of functional alpha1-PI in the BAL of smokers were comparable to those of nonsmokers.