Groups of Beagle dogs received inhalation exposure to one of three sizes of monodisperse or a polydisperse aerosol of 238PuO2. Periodic sacrifice of pairs of dogs through 4 yr after inhalation exposure provided data on the retention, translocation and mode of excretion of 238Pu. Fragmentation of 238PuO2 particles deposited in lung led to enhanced dissolution, translocation and excretion of 238Pu compared to previous studies using 239PuO2. A mechanistic simulation model was formulated to account for particle dissolution and fragmentation. This model provided adequate prediction of the time course of lung retention, uptake and retention in other organs and excretion. Predictions of the model provided more accurate description of the data than the Task Group on Lung Dynamics model incorporated in the ICRP Publication 30. The mechanistic model provided estimates of cumulative radiation dose to liver and bone that are a factor of five greater and to lung that are a factor of two less than predicted by the Task Group Lung Model.

Beagle dogs were exposed by inhalation to monodisperse aerosols of 238PuO2. Autoradiographs of lung sections were studied for nine dogs sacrificed from 4 to 730 days after exposure. Fragmentation of particles in lung was observed autoradiographically. A simple mathematical model fitted to the fragmentation and lung retention data for dogs suggests that lung clearance from intact particles (65%) and particle fragments (32%) were important to the removal of 238PuO2 deposited in the lung by inhalation. The increased surface area resulting from fragmentation should increase dissolution and risk to other organs from irradiation by translocated plutonium.

This study provides information on patterns of radiation dose in laboratory animals after inhalation exposure to an aerosol of one form of mixed uranium and plutonium oxide. The aerosol contained a mixture of UO2 and 750 degrees C heat-treated PuO2 obtained from the ball milling operation in a mixed-oxide fuel fabrication process. Americium-241 from the decay of 241Pu was also present in the PuO2 matrix. Fischer-344 rats, Beagle dogs, and Cynomolgus and Rhesus monkeys inhaled aerosols re-generated from dry mixed oxide powders with particle size distribution characteristics similar to those observed in samples collected at the industrial site. Clearance from the lung and distribution in other tissues of the plutonium from this UO2 + PuO2 admixture was similar to what has been observed for PuO2 from laboratory-produced aerosols. The UO2-PuO2 aerosol was relatively insoluble in the lungs of all species. Monkeys and rats cleared plutonium and americium from their lungs faster than dogs. Very little plutonium or americium translocated within the first 2 yr after exposure to tissues other than tracheobronchial lymph nodes. The greater accumulation of plutonium and americium in the tracheobronchial lymph nodes of dogs as compared to monkeys and rats combined with the more rapid initial clearance of these radionuclides from the lungs of rats and monkeys suggests that errors could result from using data from a single animal species to estimate risk to humans from inhalation of these industrial aerosols.

Curium isotopes are major by-products in irradiated nuclear reactor fuel and comprise a significant fraction of the alpha-emitting radionuclide inventory. Although little use is currently being made of purified Cm sources, such usage is possible if reprocessing of spent fuel becomes feasible. Because little information is available on the biokinetics and dosimetry of inhaled Cm compounds, a study was conducted in which adult beagle dogs received a single inhalation exposure to either a monodisperse aerosol of 244Cm2O3 (1.4 micron activity median aerodynamic diameter [AMAD]; sigma g = 1.16) or a polydisperse aerosol of 244Cm (NO3)3 (1.1 micron AMAD; sigma g = 1.74). At times ranging from 4 h to 2 y after exposure, animals were sacrificed and their tissues analyzed for Cm content. The data describing the uptake and retention of 244Cm in the different organs and tissues and the measured rates of excretion of these dogs formed the basis on which a biokinetic model of Cm metabolism was constructed. This Cm model was based on a previously published model of the biokinetics of 241Am that was shown to be applicable to data from human cases of inhalation exposure to 241Am aerosols. This Cm model was found to be adequate to describe the biological distribution of Cm in dogs and was also applied to the sparse data from humans. Reasonable agreement was found between the model predictions for lung retention of Cm and for urinary excretion patterns in humans.

Two models of the metabolism of inhaled 241AmO2 in Beagles have been formulated. these models differ in their description of lung retention; the empirical dissolution model uses an empirically derived function to describe dissolution of inhaled 241AmO2 while the surface area model uses a dissolution function based on physical and chemical characteristics of the inhaled aerosol. Both models provide more accurate descriptions of retention data for 241Am from several studies in Beagles than does the model published by the ICRP. The surface area model is extended to describe several cases of inhalation of 241Am in humans. This latter model is employed to calculate Annual Limits of Intake for comparison with results based on the current ICRP model.