|| Checking for direct PDF access through Ovid
Indium oxide (In2O3), a raw material from which indium tin oxide (ITO) is produced, causes indium lung disease, and there is a possibility of inhalation exposure during the manufacturing of ITO. It is, however, not known whether indium is more widely distributed throughout the body after In2O3 exposure. The aim of this study was to clarify the tissue distribution of indium in rats after intratracheal instillation or subcutaneous injection of In2O3.Male rats were divided into three groups: an In2O3 intratracheal group (n=25), an In2O3 subcutaneous group (n=25), and a control group (n=30). In both In2O3 groups, rats received a single 10 mg In/kg body weight dose of In2O3. A subset of rats was periodically euthanized throughout the study from 1 day to 36 weeks after treatment. Indium concentrations in the organs were determined using inductively coupled plasma–mass spectrometry.In both In2O3 groups, very low concentrations of indium were detected in the main organs on day 1 after treatment. Although the content of indium in the lungs for the subcutaneous group gradually increased over the 36 week observation periods, that for the intratracheal group deceased slowly with clearance half-life of approximately 22 weeks. In both In2O3 groups, the indium concentration in each intraperitoneal organ gradually increased over time until 36 weeks, with levels being higher in the subcutaneous group than in the intratracheal group at 36 weeks.Although the indium accumulation ratio in each intraperitoneal organ for the total administration doses was very low, indium accumulation in these organs indicated that translocation from the lungs or subcutaneous tissue occurred. This study clarifies that when In2O3 is administered intratracheally or subcutaneously in rats, indium becomes widely distributed in the body and is excreted very slowly.