Microdistribution and microdosimetry of thorium deposited in the liver.

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.

Effects of copper on the sabellid polychaete, Eudistylia vancouveri. II. Copper accumulation and tissue injury in the branchial crown.

Copper in seawater caused injury to the radioles (gills) of the sabellid polychaete, Eudistylia vancouveri. Light and electron microscopy showed the loss of cellular adhesion and the structural derangement that lead to cell necrosis and death. The progression of injury was related to the uptake of copper into the tissues. Copper was found by X-ray microanalysis to be localized subcellularly in membrane-bound vesicles that are similar to lysosomes. Cell breakdown may result from lysosomal labilization.

Naturally occurring Tyzzer's disease and intestinal spirochetosis in guinea pigs.

Bacillus piliformis infection (Tyzzer's disease) occurred in two young guinea pigs, causing unthriftiness and diarrhea which resulted in death. There was necrosis and inflammation of the ileum, cecum, and colon. Intestinal epithelial cells contained organisms resembling Bacillus piliformis. Spirochetes were found in the cecum and colon, mainly in crypts. Acute diarrhea occurred in another guinea pig which became cachetic and was killed. Histologically, large numbers of spirochetes were present in the wall of both the cecum and colon, and they were associated with severe necrosis and inflammation. Bacillus pilformis was not found in this animal.

Pulmonary hyalinosis in dogs.

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.

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.

Phagocytosis of inhaled plutonium oxide-239pu particles by pulmonary macrophages.

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.