American Review of Respiratory Disease

The obstruction to airflow that develops in some cigarette smokers is thought to be related to inflammation of small airways. However, the mechanism by which inflammation leads to obstruction has not been elucidated. We performed morphometry to determine if the airways of patients with obstruction were thicker than normal. Sixty smokers were selected from those undergoing resectional lung surgery. They were grouped according to their FEV1/FVC ratio (FEV1% control = 77%, FEV1 obstructed = 55%) and matched for age, sex, and height. Wall area (mm2), perimeter (mm), and diameter (mm) were measured by a modification of the technique of James and coworkers (7). The relaxed luminal diameter (mm) and wall thickness (mm) were calculated from these values. A pathology score for inflammation and fibrosis was assigned to each patient, and the percentage of the wall made up of muscle, epithelium, and connective tissue was determined by point counting. Two hundred airways, 90% of which were membranous bronchioles, were measured in each group. The mean-measured luminal diameter in the controls was 0.81 mm and in the obstructed patients 0.70 mm (p ⩽ 0.05). The regression lines relating wall thickness to calculated luminal diameter showed that the airways of the obstructed patients were thicker throughout the size range measured (p ⩽ 0.005). The muscle, epithelium, and connective tissue were all increased in the obstructed patients (p ⩽ 0.001). In addition, the wall thickness correlated with the pathology score (r = 0.6074, p ⩽ 0.002). We conclude that part of the increased resistance to airflow that is found in smokers is related to narrowed small airways that have thickened walls.


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