Metabolic modeling for the deposition of transuranic nuclides on bone surfaces

Due to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.Includes bibliographical references.Issued also on microfiche from Lange Micrographics.The study of toxic effects of plutonium was begun by Dr. Glenn Seaborg in 1950 with a twenty year project. Although many effects of plutonium have been previously discovered during various studies, an accurate metabolic model for the transport of plutonium throughout the body has still not been developed. It was determined that the majority of these nuclides are deposited on bone surfaces and are removed with a specific biological half-life, [ ],. ICRP Publication 2 addressed the dosimetry of the skeletal system, but based most of their assumptions on data from radium exposures. ICRP Publication 30 refined this simple model by differentiating between the types of radiation and the deposition mechanisms in the skeletal system. However, this approach still lacked inclusion of the actual mechanisms of biologic removal of the nuclides. In order to get an accurate representation of the dose to target cells in the bone, a new model was needed which included the actual biologic systems such as bone remodeling and reabsorption of nuclides into the blood stream and was flexible enough to allow expansion. A single comprehensive model has been developed using the STELLA 11 software which further refined the ICRP-30 bone model and included the lung, GI tract and blood compartmental models. This new model based the removal of nuclides from the bone surfaces of the skeletal system on the metabolic mechanisms involved instead of excretion data alone. This model included both types of bone, but only the cortical system ( haversian canals ) was actually modified in this research. However, the model allows the inclusion of cancellous remodeling as well as expansion to include any other biological or radiological aspects of dosimetry. This model was used to recalculate integrated activity over fifty years, U, values, as a function of intake for use in dose calculations for plutonium deposit on bone surfaces. These values were compared with those in ICRP-30 and showed a substantial decrease in the estimated dose to bone surfaces. Although only plutonium was used in the evaluation of this model, any bone surface-seeking, alpha-emitting nuclide, and any class compound, can be used with this model