ALTERATIONS IN LEUKOCYTE OXIDATIVE-METABOLISM IN CIGARETTE SMOKERS

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Abstract
The polymorphonuclear leukocyte (PMN) may play an important role in the pathogenesis of lung disease associated with cigarette smoking. To investigate its potential for oxidant-mediated lung injury in cigarette smokers, PMN oxidative metabolism was studied in asymptomatic cigarette smokers and nonsmoking control subjects. A marked increase in oxidant release in a group of cigarette smokers was found. After stimulation by phorbol myristate acetate, release of superoxide anion (O2-) by PMN in smokers with white blood counts (WBC) > 9000 was 50% greater than in nonsmokers with similar WBC, or smokers and nonsmokers with WBC < 9,000. Abstinence from smoking did affect the alterations in O2- release nor did a serum factor appear responsible. The changes were part of a generalized increase in oxidative metabolism, as there was greater oxidation of glucose (1-14C) and chemiluminescence by PMN from smokers with WBC > 9000. A further estimate of lung oxidant load was determined by evaluating the marginated pool of PMN. Smokers with WBC > 9000 showed a 70% increase in WBC after epinephrine, and PMN oxidative metabolism remained increased in this group. Cigarette smokers with elevated WBC had increased release of potentially toxic oxygen metabolites. These cigarette smokers also demonstrated increased oxidant release from the marginated PMN pool. Because leukocyte-generated O2 metabolites were highly reactive and cause tissue injury, these findings may have important implications in the pathogenesis of smoking-related lung disease.