Toxicology of high-fired beryllium oxide inhaled by rodents. II. Metabolism and early effects.
Several groups of male and female rats and hamsters were exposed by inhalation to an aerosol of BeO particles calcined at 1000 C. Initial alveolar depositions ranged from 12 mug to 160mug Be. The alveolar retention half-life for BeO was approximately six months. Only the pulmonary lymph nodes accumulated detectable amounts of translocated BeO. Early alterations were seen in the alveolar macrophages, which were subsequently converted to histiocytic cells that accumulated in subpleural and peribronchiolar granulomatous lesions within eight months after the exposure. The alveolar clearance of a test aerosol, radioactive plutonium dioxide (239PuO2), was decreased to 60% of the normal rate when the radioactive material was given at 1, 30, or 60 days after exposure to BeO. These results demonstrate the important function of the alveolar macrophage in Be-induced granulomatous disease, as well as the rapid impairment of alveolar macrophage function by phagocytized BeO.
D000818:Animals; D001608:Beryllium / Q000378:metabolism / Q000633:toxicity*; D006224:Cricetinae; D005243:Feces / Q000032:analysis; D005260:Female; D008168:Lung / Q000378:metabolism; D008171:Lung Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D008198:Lymph Nodes / Q000378:metabolism; D008264:Macrophages / Q000473:pathology; D008297:Male; D011650:Pulmonary Alveoli / Q000378:metabolism / Q000473:pathology; D051381:Rats
D001608:Beryllium