CHRONIC AIR-FLOW LIMITATION DOES NOT INCREASE RESPIRATORY EPITHELIAL PERMEABILITY ASSESSED BY AEROSOLIZED SOLUTE, BUT SMOKING DOES

Abstract

To determine the separate influences of smoking and severe air-flow limitation on aerosol deposition and respiratory epithelial permeability, 26 normal nonsmokers, 12 smokers without airway obstruction, 12 nonsmokers with chronic obstructive pulmonary disease (COPD) and 11 smokers with COPD were studied. They were aerosolized with 99m-Tc-labeled diethylene triamine pentacetic acid to particles approximately 1 .mu.m activity median aerodynamic diameter. Levels of radioactivity were plotted semilogarithmically against time to calculate clearance as %/min. The distribution of radioactivity was homogeneous in control subjects and in smokers, but patchy in both groups with COPD. No difference was found between clearances of the control group (1.18 .+-. 0.31% min-1), and nonsmoker COPD group (1.37 .+-. 0.82% min-1), whereas values in smokers without COPD (4.00 .+-. 70% min-1) and smokers with COPD (3.62 .+-. 2.88% min-1) were significantly greater than in both nonsmoking groups. Small particles appear to deposit peripherally, even with severe COPD. Respiratory epithelial permeability is normal in nonsmokers with COPD and smoking increases permeability by a mechanism unrelated to air-flow limitation.