title: Tissue distribution and elimination of indium in male Fischer 344 rats following oral and intratracheal administration of indium phosphide.
abstract: The use of indium phosphide (InP) in the semiconductor industry has raised concerns about potential occupational exposure. The tissue distribution and elimination of indium were investigated in adult male Fischer 344 rats following either a single or 14 consecutive daily oral doses, or following an intratracheal instillation of InP (10 mg/kg). The concentrations of indium ions in blood, urine, feces, and tissues were quantified either using direct acid digestion followed by electrothermal atomic absorption spectrophotometry (ET-AAS) or using an extraction method with methyltricapryl ammonium ions to remove indium from the matrix followed by ET-AAS. Indium was poorly absorbed from the gastrointestinal tract in both single and multiple oral dose studies. Upon its absorption, indium was relatively evenly distributed among the major organs such as liver, kidney, lung, spleen, and testes. By 96 h after oral dose treatment, less than 0.11% of the dose of indium was recovered from tissues in the single- or multiple-dose experiment. At 96 h, retention of indium in the body was about 0.36% of the dose (except for lung) following intratracheal instillation of InP. Following oral dose administration, the majority of indium was recovered from the gastrointestinal tract and its contents. The high recovery of indium (73% of the dose) in the feces after intratracheal instillation presumably reflects mucociliary clearance and/or biliary excretion of indium. Urinary indium accounted only for 0.08-0.23% of the dose during a 240-h collection period in both single- and multiple-dose studies. It seems that fecal excretion serves as the major route for indium elimination, and this results from poor absorption. Because of the poor absorption of indium following multiple oral doses or intratracheal instillation of InP, it seems unlikely that indium will accumulate in the body following InP exposure.
authors.affiliation: Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson.
authors.forename: W
authors.initials: W
authors.lastname: Zheng
authors.forename: S M
authors.initials: SM
authors.lastname: Winter
authors.forename: M J
authors.initials: MJ
authors.lastname: Kattnig
authors.forename: D E
authors.initials: DE
authors.lastname: Carter
authors.forename: I G
authors.initials: IG
authors.lastname: Sipes
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D007204:Indium / Q000008:administration & dosage / Q000378:metabolism / Q000493:pharmacokinetics*; D007408:Intestinal Absorption; D007442:Intubation, Intratracheal; D008297:Male; D010720:Phosphines / Q000008:administration & dosage / Q000378:metabolism / Q000493:pharmacokinetics*; D051381:Rats; D011916:Rats, Inbred F344; D013054:Spectrophotometry, Atomic; D014018:Tissue Distribution
chemical_list: D010720:Phosphines; D007204:Indium; C090882:indium phosphide