Distribution and toxicity of 230 Pu in bone.

Abstract

Abstract The deposition of 239Pu the classical transuranium element upon bone surfaces is governed by the route of administration, physicochemical state of the plutonium, and the age of the animal. The effectiveness of the various routes of administration in delivering plutonium tobone, indecreasingorder, is: intravenous = intraperitoneal > subcutaneous > intramuscular > intratracheal > inhalation > oral > direct application upon skin. Reticuloendothelial cells in the marrow compete with bone for polymeric plutonium and thus decreases the plutonium available for bone surfaces. The uptake in young and adult bones differed by a factor of 2. The fate of the plutonium surface deposits is modified by bone growth, modeling and remodeling in growing animals and remodeling in adults. These age-related processes remove the plutonium from bone surfaces and/or bury the surface deposits with new bone. The endpoints of low dose plutonium skeletal toxicity are bone necrosis and the induction of osteogenic sarcoma. The factors involved in bone tumor production is believed to be the delivery of sufficient radiation to bone surfaces (the sensitive site), the volume of cells at risk and, most important, the proliferative activity of the osteogenic tissue.