Comparison of Smoker and Nonsmoker Lavage Fluid for the Rate of Association with Neutrophil Elastase

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Abstract
Cigarette smoking may impair the lung antiprotease screen. To test this hypothesis, the lung lining fluid from 10 smoking and 9 nonsmoking individuals was evaluated for its ability to inhibit neutrophil elastase and porcine pancreatic elastase. To eliminate the possibility of concentration- or purification-induced artifact, unconcentrated bronchoalveolar lavage fluid was used for all experiments. Smokers did not differ significantly from nonsmokers in the antigenic alpha-1-antitrypsin (alpha 1AT) concentrations (0.67 +/- 0.04 versus 0.73 +/- 0.09 nmol alpha 1AT/mg protein), in the neutrophil elastase inhibitory capacity (NEIC) (0.59 +/- 0.03 versus 0.52 +/- 0.05 nmol NEIC/mg protein), or in the porcine pancreatic elastase inhibitory capacity (PPEIC) (0.36 +/- 0.03 versus 0.42 +/- 0.05 nmol PPEIC/mg protein). In contrast, when the PPEIC/NEIC ratio was evaluated, smoker lung lining fluid exhibited a relative defect (0.64 +/- 0.06 smokers versus 0.80 +/- 0.05 nonsmokers, P less than 0.05). In agreement with the smokers' defect in the PPEIC/NEIC ratio, the kinetics of association (Ka) of lung lining fluid for neutrophil elastase was 0.38 +/- 0.3 x 10(7) M-1 s-1 from smokers and 0.58 +/- 0.05 x 10(7) M-1 s-1 from nonsmokers (P less than 0.002). Thus for a given amount of neutrophil elastase, smoker lung lining fluid took approximately 1.5 times longer to inhibit neutrophil elastase. These findings suggest that cigarette smoking is associated with a subtle defect in the antiprotease screen of the lower respiratory tract, recognizable by time-dependent measures of anti-neutrophil elastase function.