Rabbit alveolar macrophages were exposed in culture medium to asbestos, beryllium sulfate, and beryllium oxide. The specific activities of the lysosomal hydrolases, acid phosphatase beta-N-acetylglucosaminidase and beta-glucuronidase plus the glycolytic enzyme, phosphohexose isomerase were determined in the medium, whole-cell homogenates, mitochondrial fractions, and supernatant. These hydrolases increased significantly in the medium but not in the mitochondrial fraction of cells exposed to dusts. Asbestos and beryllium sulfate were highly cytotoxic for alveolar macrophages in vitro and the data suggested that these agents were not associated with an increase in enzyme synthesis but rather a direct cytotoxic effect at the macrophage membrane level. For induction of enzyme release in vitro, a higher concentration of beryllium oxide was needed when compared with asbestos and beryllium sulfate. The cytotoxicity and enzyme release induced by these agents may represent an important nonspecific mechanism by which they induce inflammation and perhaps local proliferation of fibroblasts.

Acetylglucosaminidase↗

PubMedDate not supplied

Pulmonary function in sandblasters' silicosis.

Lung function was examined in 55 patients with sandblasters' silicosis. In this type of silicosis, patients with simple nodular disease had normal function. Restrictive and obstructive impairment was present in patients with large opacities, and was more marked in patients with radiographic evidence of contraction or cavitation. In the last group, striking average annual declines in ventilatory function occurred. Compared to patients with classical silicosis, these patients were younger and had intense, short exposures to free crystalline silica. The pattern of functional abnormalities suggested that restriction of lung volumes is a fundamental abnormality in this form of silicosis.

Adult↗