Development of Pulmonary Lesions Following Acute Exposure to Diborane in Male ICR Mice

Develompment of Pulmonary Lesions Following Acute Exposure to Diborane in Male ICR Mice: Takamoto U emura . Department of Preventive Medicine and Public Health, School of Medicine, Keio University —In order to investigate the sequential development of respiratory injuries following acute exposure to diborane, male ICR mice were exposed to 15 ppm diborane for four hours and histo‐ pathological, hematological and serum biochemical examinations were conducted immediately, one day, three days and two weeks after exposure. Immediately after exposure, polymorphonuclear neutrophil infiltration of the bronchiolar lumens was observed. On the following day, macrophages had infiltrated into the alveolar and bronchiolar lumen. Multifocal and disseminated inflammatory obstructive changes, edema and congestion diffusely developed at the respiratory bronchiolus, and were diagnosed as diffuse panbronchiolitis (DPB)‐like lesions. These changes progressed most severely on day 3, and lung weight significantly increased with the severity of the pulmonary lesions. Transmission electron microscopy revealed deposition of fine fibrillar materials in the alveoli sacs immediately after exposure and phagocytosis of the materials by macrophages on day 3. At two weeks, few inflammatory cells in the bronchiolar lumen remained, and peribronchiolar thickening was disseminated at almost the same sites where DPB‐like inflammatory foci had been detected. These sequential changes in the histopathological observations from this study corroborated very well with the clinical signs and symptoms of human acute diborane poisoning cases reported in the 1960s. No significant changes in the nasal cavity or major bronchi were detected at any time. No particular trends were identifiable in the blood biochemistry findings. Further studies are necessary to elucidate the pathogenetic mechanism responsible for the respiratory organ damage caused by diborane.