Histopathologic evidence of lung involvement in subjects with diabetes mellitus has included thickened alveolar epithelial and pulmonary capillary basal laminae, the latter being suggestive of existing pulmonary microangiopathy. Abnormal pulmonary function has been detected in some diabetic patients; the most consistent abnormalities are reduced lung volumes in young (aged less than 25 years) insulin-dependent diabetic subjects, reduced pulmonary elastic recoil in both young and adult (aged greater than 25 years) diabetic subjects, and impaired diffusion due to a reduced pulmonary capillary blood volume in the adult group. Nonenzymatic glycosylation-induced alteration of lung connective tissue is the most likely pathogenetic mechanism underlying mechanical pulmonary dysfunction in diabetic subjects, while the most tenable explanation for impaired pulmonary microangiopathy. these patients is the presence of underlying pulmonary microangiopathy. The finding of abnormal lung function in some diabetic subjects suggests that the lung should be considered a "target organ" in diabetes mellitus; however, the clinical implications of these findings in terms of respiratory disease are at present unknown.