These studies were conducted to investigate the mechanism of indium phosphide (InP) induced pulmonary carcinogenesis and pleural hyperplasia in B6C3F1 mice. InP is a particulate or brittle metal used predominantly in the microelectronics industry. Chronic inhalation exposure of mice to InP particles caused alveolar/bronchiolar adenomas and carcinomas, and hyperplasia of the pleural mesothelium (NTP, 2000). The mechanisms by which InP causes lung tumors and mesothelial hyperplasia are not known. Although fibers are known to cause lesions in the pleural mesothelium, pleural effects are uncommon after inhalation of a non-fibrous particulate. Inhaled indium phosphide (InP) particulates were recently shown to cause pleural adhesions and fibrosis in mice. These types of lesions of the pleural mesothelium are uncommon following exposure to a non-fibrous particle. An objective of initial studies was to determine if pleural lesions observed after inhalation exposure can be replicated by a single intratracheal instillation of InP. Intratracheal instillation is a much simpler procedure and allows more accurate control of dosing than does inhalation exposure. However, unlike inhalation exposure, intratracheal instillation results in a bolus dose of chemical. If intratracheal administration can be used to reproduce the pleural lesions, then this method will be used to investigate the mechanism and progression of InP induced pleural lesions.
