Pulmonary macrophages and plutonium particles were removed by washing the lungs of rats that had inhaled plutonium oxide-(239)Pu. A significant amount of plutonium was found in multiple washings of the same lung. The removal of toxic particles by washing is of potential therapeutic value. Particles were phagocytized by macrophages during the first 3 hours and retained within these cells for up to 25 days. Nearly all particles in washings were found in macrophages after the second day. The percent of macrophages with engulfed particles increased with increasing amounts of plutonium deposited in the lungs. The ability of pulmonary macrophages to rapidly phagocytize and retain plutonium particles deposited in the lungs has been shown.

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.

Pulmonary hyalinosis occurred in Beagles exposed to radon daughters with uranium ore dust. The lesion was composed of alveolar cells distended with material positive for periodic acid-Schiff (PAS) and oil red O that ultrastructurally consisted of a whorled arrangement of lamellar membranes suggestive of a storage disease. The high incidence in exposed dogs and the ultrastructural appearance suggested the material originated endogenously as a degenerative response to injury.

No abstract

The distribution of thorium in the liver of a patient 36 y after injection with Thorotrast was examined with autoradiographic and scanning electron microscope backscatter image techniques. Autoradiographic examination of randomly selected histologic sections of the liver showed a total alpha activity calculated at 33.7 Bq g-1, with the highest concentration of alpha activity sequestered in subcapsular scare tissue. Subcapsular scare tissue received 4.8 cGy d-1 of alpha radiation, periportal areas were accumulating 1.4 cGy d-1, and the hepatic cord areas 0.09 cGy d-1 of alpha radiation at the time of death. The concentration of dose in periportal areas correlates with higher incidence of bile duct tumors (than hepatocellular carcinomas) found in patients exposed to Thorotrast. The backscatter technique was demonstrated as useful for identifying thorium in liver specimens.