Ruthenium-106 is a fission product radionuclide present in nuclear fuel cycles and has potential for release as ruthenium tetroxide. Ruthenium tetroxide is a vapor, diffuses rapidly in air and through porous barriers and is rapidly reduced to the dioxide form when in contact with organic compounds. The current ICRP model for inhaled particles does not predict respiratory tract deposition and clearance for inhaled vapors. This study provides data needed to assess radiation doses to humans exposed to IMRu tetroxide. Rats were given a nose-only exposure to IMRuO4 vapor to determine the subsequent distribution and retention. Initial whole-body activity ranged from 4.1 to 15 pCi of IMRu. Fifty-four per cent was in the upper respiratory tract, less than 1% was in the pulmonary region, the remaining 45% was external contamination. Clearance of l ' Ru from the body was predominately through the gastrointestinal tract to feces. A simulation model was developed to describe retention and translocation of inhaled IMRu04 and to provide estimates of radiation doses to internal organs. Current ICRP recommendations consider lung and gastrointestinal tract as critical organs for inhaled particles of radioactive ruthenium. This study indicated that the nasopharynx should be considered a critical region for vapor forms of radioactive ruthenium in human inhalation exposures.

Whole-body retention and tissue distribution of inhaled 140Ba-leoLa and wholebody retention of ingested lSBa were studied in Beagle dogs after administration in soluble chloride forms. The resulting data were used to formulate a biological retention model which was executed with both analog and digital computer methods. This model was then used to estimate radiation protection guidelines for human exposure to soluble and relatively insoluble aerosols of 140Ba and l=Ba. The biological tissues receiving the most significant radiation doses were predicted to be the skeleton after inhalation of 140BaCIz and 133BaC12 and the lung after inhalation of l4OBaSO,. The influence of species differences, age, dietary state at the time of inhalation exposure and aerosol particle size upon the calculation of (MPC), guidelines was also discussed.

Chronic inhalation of insoluble particles of low toxicity that produce substantial lung burdens of particles, or inhalation of particles that are highly toxic to the lung, can impair clearance. This report describes model calculations of accumulations in lung of inhaled low-toxicity diesel exhaust soot and high-toxicity Ga2O3 particles. Lung burdens of diesel soot were measured periodically during a 24-mo exposure to inhaled diesel exhaust at soot concentrations of 0, 0.35, 3.5, and 7 mg m-3, 7 h d-1, 5 d wk-1. Lung burdens of Ga2O3 were measured for 1 y after a 4-wk exposure to 23 mg Ga2O3 m-3, 2 h d-1, 5 d wk-1. Lung burdens of Ga2O3 were measured for 1 y both studies using inhaled radiolabeled tracer particles. Simulation models fit the observed lung burdens of diesel soot in rats exposed to the 3.5- and 7-mg m-3 concentrations of soot only if it was assumed that clearance remained normal for several months, then virtually stopped. Impaired clearance from high-toxicity particles occurred early after accumulations of a low burden, but that from low-toxicity particles was evident only after months of exposure, when high burdens had accumulated in lung. The impairment in clearances of Ga2O3 particles and radiolabeled tracers was similar, but the impairment in clearance of diesel soot and radiolabeled tracers differed in magnitude. This might have been related to differences in particle size and composition between the tracers and diesel soot. Particle clearance impairment should be considered both in the design of chronic exposures of laboratory animals to inhaled particles and in extrapolating the results to people.

Intravenously administered diethylenetriaminepentaacetic acid (DTPA) was beneficial in removing 144Ce from dogs after inhalation of a 144CeC13 aerosol; however, the effectiveness depended upon early treatment. I n dogs given DTPA 1 hr after the inhalation exposure, the lung, liver and skeletal burdens after 28 days were reduced to 40, 36 and 27%, respectively, of the initial lung burden of the exposed untreated control group. DTPA treatment initiated at 5 days post-inhalation 0 f~~~C e C 1 , resulted in a 50 % reduction in the lung burden with very little effect on the liver and skeletal burdens. The urinary excretion of lUCe increased to 8 times the control level in the animals treated with DTPA on day 0 but in the animal treated on day 5 the urinary excretion was only 2 times that of the control. An animal injected intravenously with sterile isotonic saline 1 hr after an exposure to a 144CeCl, aerosol had lung, liver and skeletal burdens and a urinary excretion pattern not significantly different from the exposed untreated control dogs. Comparisons of the data are made with those from a study in which DTPA was added to the fluid used for bronchopulmonary lavage.