PULMONARY TOXICITY TO INTRATRACHEALLY ADMINISTERED INDIUM TRICHLORIDEIN FISCHER-344 RATS

The use of indium by the semiconductor industry has risen sharply in r ecent years with the discovery that the electrical properties of compo unds such as indium phosphide and indium arsenide are better than thos e of silicon. However, relatively little is known about its potential to induce lung damage. These studies examined the effect of indium tri chloride (InCl3) on the lung. To examine the disposition and removal o f InCl3 from the lung, groups of female Fischer 344 rats received a si ngle intratracheal dose of 1.3 mg In/kg as InCl3 and were euthanized a fter 1, 2, 4, 7, 14, 28, and 56 days at which time lung samples were a nalyzed for metal content. Furthermore, the histology, hydroxyproline levels, and bronchoalveolar lavage (BAL) fluid cellularity of the lung were studied. In addition, the effect of 0.00016, 0.00325, 0.065, and 1.3 mg In/kg on inflammatory response and BAL fluid cellularity was c ompared. While a dose as low as 0.00325 mg In/kg was capable of initia ting an influx of inflammatory cells, instillation of 1.3 mg In/kg res ulted in an inflammatory response that was still evident 56 days later . After 28 days, the lung weight of the InCl3-treated animals was 2.5 times greater than that of the controls. The total cell number in the BAL fluid of the treated animals after 28 days was 32 times higher tha n that in the control rats. Sixty-seven percent of these cells were gr anulocytes. Compared to the controls, the hydroxyproline content of th e lungs from the InCl3-treated animals were twofold greater after 28 a nd 56 days. Furthermore, the levels of fibronectin and TNF alpha prese nt in the BAL fluid of InCl3-treated rats increased sharply during the first 24 hr and remained elevated 56 days later. These data and the h istological examination of the lung following InCl3 treatment suggest that InCl3 is capable of causing severe lung damage and the developmen t of fibrosis. (C) 1994 Society of Toxicology.