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A voluntary partial-body donor (US Transuranium and Uranium Registries case 0785) was accidentally exposed to Pu via inhalation and wounds. This individual underwent medical treatment including wound excision and extensive chelation treatment with calcium ethylenediaminetetraacetic acid and calcium diethylenetriaminepentaacetic acid. Approximately 2.2 kBq of Pu was measured in the wound site 44 y after the accident. Major soft tissues and selected bones were collected at autopsy and radiochemically analyzed for Pu, Pu, and Am. Postmortem systemic retention of Pu, Pu, and Am was estimated to be 32.0 ± 1.4 Bq, 2,172 ± 70 Bq, and 394 ± 15 Bq, respectively. Approximately 3% of Pu whole-body activity was still retained in the lungs 51 y after the accident indicating exposure to insoluble plutonium material. To estimate the intake and calculate radiation dose, urine measurements not affected by chelation treatment, in vivo chest counts, and postmortem radiochemical analysis data were simultaneously fitted using Integrated Modules for Bioassay Analysis Professional Plus software. The currently recommended International Commission on Radiological Protection Publication 130 human respiratory tract model and National Council on Radiation Protection and Measurements Report 156 wound model were used with default parameters. The intake, adjusted for Pu removed by chelation treatment, was estimated at approximately 79.5 kBq with 68% resulting from inhalation and 32% from the wound. Inhaled plutonium was predominantly insoluble type S material (74%) with insoluble plutonium fragments deposited in the wound. Only 1.3% reduction in radiation dose was achieved by chelation treatment. The committed effective dose was calculated to be 1.49 Sv. Using urine data available for this case, the effect of chelation therapy was evaluated. Urinary excretion enhancement factors were calculated as 83 ± 52 and 38 ± 17 for initial and delayed calcium ethylenediaminetetraacetic acid treatments, respectively, and as 18 ± 5 for delayed calcium diethylenetriaminepentaacetic acid. The enhancement factor decreases proportionally to an inverse cubic root of time after intake. For delayed calcium ethylenediaminetetraacetic acid treatment, with five consecutive daily administrations, the enhancement factor increased from day 1 to 4, followed by approximately a 50% drop on day 5. The half-time of plutonium ethylenediaminetetraacetic acid complex removal in urine was evaluated to be 1.4 d.

Decorporation therapy with salts of diethylenetriamine-pentaacetic acid binds actinides, thereby limiting uptake to organs and enhancing the rate at which actinides are excreted in urine. International Commission on Radiological Protection reference biokinetic models cannot be used to fit this enhanced exertion simultaneously with the baseline actinide excretion rate that is observed prior to the start of therapy and/or after the effects of therapy have ceased. In this study, the Coordinated Network on Radiation Dosimetry approach, which was initially developed for modeling decorporation of plutonium, was applied to model decorporation of americium using data from a former radiation worker who agreed to donate his body to the US Transuranium and Uranium Registries for research. This individual was exposed to airborne Am, resulting in a total-body activity of 66.6 kBq. He was treated with calcium-diethylenetriamine-pentaacetic acid for 7 y. The time and duration of intakes are unknown as no incident reports are available. Modeling of different assumptions showed that an acute intake of 5-μm activity median aerodynamic diameter type M aerosols provides the most reasonable description of the available pretherapeutic data; however, the observed Am activity in the lungs at the time of death was higher than the one predicted for type M material. The Coordinated Network on Radiation Dosimetry approach for decorporation modeling was used to model the in vivo chelation process directly. It was found that the Coordinated Network on Radiation Dosimetry approach, which only considered chelation in blood and extracellular fluids, underestimated the urinary excretion of Am during diethylenetriamine-pentaacetic acid treatment; therefore, the approach was extended to include chelation in the liver. Both urinary excretion and whole-body retention could be described when it was assumed that 25% of chelation occurred in the liver, 75% occurred in the blood and ST0 compartment, and the chelation rate constant was 1 × 10 pmol d. It was observed that enhancement of urinary excretion of Am after injection of diethylenetriamine-pentaacetic acid exponentially decreased to the baseline level with an average half-time of 2.2 ± 0.7 d.

A recently proposed system of models for plutonium decorporation (SPD) was developed using data from an individual occupationally exposed to plutonium via a wound [from United States Transuranium and Uranium Registries (USTUR) Case 0212]. The present study evaluated the SPD using chelation treatment data, urine measurements, and post-mortem plutonium activities in the skeleton and liver from USTUR Case 0269. This individual was occupationally exposed to moderately soluble plutonium via inhalation and extensively treated with chelating agents. The SPD was linked to the International Commission on Radiological Protection (ICRP) Publication 66 Human Respiratory Tract Model (HRTM) and the ICRP Publication 30 Gastrointestinal Tract model to evaluate the goodness-of-fit to the urinary excretion data and the predictions of post-mortem plutonium retention in the skeleton and liver. The goodness-of-fit was also evaluated when the SPD was linked to the ICRP Publication 130 HRTM and the ICRP Publication 100 Human Alimentary Tract Model. The present study showed that the proposed SPD was useful for fitting the entire, chelation-affected and non-affected, urine bioassay data, and for predicting the post-mortem plutonium retention in the skeleton and liver at time of death, 38.5 years after the accident. The results of this work are consistent with the conclusion that Ca-EDTA is less effective than Ca-DTPA for enhancing urinary excretion of plutonium.

Individuals with significant intakes of plutonium (Pu) are typically treated with chelating agents, such as the trisodium salt form of calcium diethylenetriaminepentaacetate (CaNa 3 -DTPA, referred to hereafter as Ca-DTPA). Currently, there is no recommended approach for simultaneously modeling plutonium biokinetics during and after chelation therapy. In this study, an improved modeling system for plutonium decorporation was developed. The system comprises three individual model structures describing, separately, the distinct biokinetic behaviors of systemic plutonium, intravenously injected Ca-DTPA and in vivo-formed Pu-DTPA chelate. The system was linked to ICRP Publication 100, "Human Alimentary Tract Model for Radiological Protection" and NCRP Report 156, Development of a Biokinetic Model for Radionuclide-Contaminated Wounds and Procedures for Their Assessment, Dosimetry and Treatment." Urine bioassay and chelation treatment data from an occupationally-exposed individual were used for model development. Chelation was assumed to occur in the blood, soft tissues, liver and skeleton. The coordinated network for radiation dosimetry approach to decorporation modeling was applied using a chelation constant describing the secondorder, time-dependent kinetics of the in vivo chelation reaction. When using the proposed system of models for plutonium decorporation, a significant improvement of the goodness-of-fit to the urinary excretion data was observed and more accurate predictions of postmortem plutonium retention in the skeleton, liver and wound site were achieved., (© 2019 by Radiation Research Society.)