BRONCHIAL REACTIVITY, SMOKING, AND ALPHA1-ANTITRYPSIN - A POPULATION-BASED STUDY OF MIDDLE-AGED MEN

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Abstract
Bronchial reactivity to increasing doses of inhaled methacholine (MCH) was assessed in a population-based study on .alpha.1-antitrypsin. Consecutive 48-50 yr-old heterozygous (Pi-MZ) men (34) were compared with 31 men of the same age with normal Pi phenotype (Pi-M) matched for smoking habits. There was no significant difference between control FEV1 [1-s forced expiratory volume] or in MCH reactivity between the Pi-MZ and the Pi-M group. Twelve Pi-MZ subjects and 11 Pi-M subjects showed a fall of .gtoreq. 15% of FEV1 (PC 15%). Smokers showed increased sensitivity to MCH in both phenotype groups, although there was no significant difference in control FEV1 between the smoking and nonsmoking groups. Eleven smokers and ex-smokers, 5 with histories of asthma or sputum production showed bronchial hyperreactivity, i.e., PC 15% FEV1 to 0.1% MCH or lower concentrations. Among nonsmokers there was 1 reactor and 1 hyperreactor. Heterozygous .alpha.1-antitrypsin deficiency (Pi-MZ) does not increase bronchial reactivity; smoking does.