J. A. Hayes

Intravascular Bronchioloalveolar Tumor (IV-BAT)

Intravascular bronchioloalveolar tumor (IV-BAT) is a recently described, histologically distinct, malignant, primary lung neoplasm. Originally it was believed to arise from type II alveolar cells which invade blood vessels within the lung, and hence its name. More recent ultrastructural studies suggest an origin from mesenchymal cells, and therefore the tumor may be more appropriately considered a sarcoma. The onset of the disease may be insidious, and its clinical course may vary from slow to rapid progression. A history is present of a young woman with slowly enlarging multiple ill defined pulmonary nodules. Open lung biopsy was diagnostic of IV-BAT. The clinical course, differential diagnosis and pathogenesis of this tumor are briefly discussed.

Lung aryl hydrocarbon hydroxylase: Inhibition following cadmium chloride inhalation

Polycyclic hydrocarbon metabolism in male Sprague-Dawley rats following inhalation of aerosolized cadmium chloride (CdCl2) was examined. Constitutive activity of microsomal aryl hydrocarbon hydroxylase (AHH) (benzo(a)pyrene substrate) was monitored in lung and liver homogenates up to 10 days after exposure. Lung AHH activity was reduced by 85% during the first 2 days following cadmium inhalation, and did not return to normal levels until 7 days after exposure. Enzyme activity in the livers of cadmium-treated animals was similarly depressed (by 65%) within 24 hr. Cadmium inhalation also inhibited (by 50%) 3-methylcholanthrene (MC) induction of lung AHH when compared with MC-treated controls. No significant effect on AHH inducibility by MC was noted in liver homogenates from cadmium-exposed animals. Nonspecific microsomal damage appeared not to occur since glucose-6-phosphatase activity in lung was unaffected by cadmium treatment. Although the mechanism of cadmiums action remains unclear, it appears not to involve a direct interaction of the metal with enzyme. The alteration of AHH activity by cadmium may result from injury to a specific cell type within the lung, which may be a major site of pulmonary AHH activity, or may result from modulation of synthesis and/or degradation of heme proteins in the lung. These results suggest that cadmium, under these conditions, markedly reduces the constitutive and inducible activity of AHH in the lung.