Associated with the use of 238Pu in thermoelectric power sources for space probes is the potential for human exposure, primarily by inhalation and most likely as 238PuO2. Several models have been developed for assessing the level of intake and predicting the resulting radiation dose following human exposure to 239Pu. However, there are indications that existing models do not adequately describe the disposition and dosimetry of 238Pu following human exposure. In this study, a canine model that accounts for these differences has been adapted for use with human excretion data. The model is based on existing knowledge about organ retention of plutonium. An analysis of the sensitivity of the model to changes in aerosol-associated properties indicated that predictions of urinary excretion are most sensitive to changes in particle solubility and diameter and in the ratio of fragment:particle surface area. Application of the model to urinary excretion data from seven workers exposed to a 238Pu ceramic aerosol gave estimated intakes of 390-8,200 Bq and associated initial pulmonary burdens of 80-1,700 Bq. The resulting 50-y dose commitments to critical organs per Bq of 238Pu intake were estimated to be 0.5 mSv for the thoracic region, 0.2 mSv for the liver, and 1 mSv for the bone surfaces.

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.

The lung retention of uranium was determined in rats that inhaled aerosols of commercial yellowcake powders obtained from two mills (Mill A and Mill D) and whose chemical composition and solubilities in vitro were significantly different. Analysis by IR absorption indicated Mill A yellowcake contained 82% ammonium diuranate (ADU) and 18% U3O8. The Mill D powder contained 25% ADU and 75% U3O8. In vitro dissolution studies indicated for the Mill A sample, approximately 85% of the uranium had a dissolution half-time (T 1/2) of less than one day, with the remainder dissolving with a half-time of 500 days. For the Mill D sample, 25% had T 1/2 less than one day and 75% had T 1/2 of 300 days. Groups of 50 rats were exposed by nose-only inhalation to aerosols of either the Mill A or the Mill D yellowcake. Rats were sacrificed in groups of five at intervals through six months after exposure. Selected tissues and excreta samples were assayed by fluorometry to determine their uranium contents. For the Mill A yellowcake, 78% initial lung (broncho-alveolar) burden cleared with T 1/2 of 0.5 days, and 22% with T 1/2 of 240 days. For the Mill D yellowcake, 25% initial lung burden cleared with T 1/2 of 3.5 days and 75% with T 1/2 of 110 days. Thus, the lung clearance of uranium in the rat mimicked the in vitro dissolution data and supported the contention that ADU should be considered as a Class D compound (T 1/2 = 0.5 days) and U3O8 behaves in the lung as a Class Y (T 1/2 greater than 100 days) material.

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.

Beagle dogs received a single inhalation exposure to a monodisperse or a polydisperse aerosol of 241AmO2 to determine the radiation dose to internal organs. Three monodisperse aerosol sizes (0.75, 1.5 and 3.0 micrometer activity median aerodynamic diameter) and one polydisperse aerosol (1.8 micrometer activity median aerodynamic diameter) were used to assess the role of particle size in clearance of 241AmO2 from the lung and the rate of translocation of 241Am to other tissues. Dogs were sacrificed in groups of two or three at 8, 32, 64, 128, 256, 365 and 730 days after exposure. The clearance rate of 241Am from lung was particle size dependent; this resulted in an increased radiation dose to lung at 2 yr by 70% as particle size increased from 0.75 to 3.0 micrometer aerodynamic diameter. Conversely, the radiation dose to liver and skeleton decreased by 20 and 35% respectively as particle size increased from 0.75 to 3.0 micrometer activity median aerodynamic diameter. When the radiation doses absorbed by lung, liver and skeleton were compared to those predicted by the ICRP 30 model, differences were noted.