Speciation 98: Abstracts

The past half century there has seen wide interest in the development of safe methods for accelerating the naturally slow rate of removal of plutonium from the human body. This interest has been focused on the treatment of workers in the nuclear industry who may have accidentally acquired a systemic burden of plutonium. However, recent concerns about the 1200 tonne stockpile of now largely unwanted plutonium which has been accumulated world-wide may mean that there is a need to consider emergency procedures for decorporation of plutonium from members of the public should this material fall into the hands of terrorists, or unscrupulous scrap dealers.

For many years the agent of choice for the treatment of plutonium contamination has been the polyaminopolycarboxylate ligand, diethylenetriaminepentaacetate (DTPA). But while this ligand can produce significant reductions in the body burden of plutonium when it is administered within a few hours of contamination, it is much less effective at longer time after exposure. There has been a great deal of research into the design of ligands with a higher affinity, and greater specificity towards plutonium and related actinides and some interesting ligands have emerged. However, this strategy ignores the fact that plutonium is deposited within the body not only in several different chemical forms, but in locations which may be separated from the blood and extracellular fluids by one or more membrane barriers which my be nearly impermeable to the ligand.

Knowledge of the chemical speciation of plutonium in the human body is far from complete. In blood plutonium is protein bound, mainly to the iron-transport protein transferrin, from which it can be quite readily released by DTPA, providing that an effective molar ligand:metal ratio can be achieved. In liver, one the two main deposition sites, plutonium rapidly deposits within intracellular membrane-bounded lysosomal structures. The chemical form of this plutonium is not yet clear but it appears to be associated with ferritin in an insoluble form. Similarly, in bone, the second major deposition site, plutonium becomes associated with the bone matrix in an, as yet, poorly defined chemical form. In vitro studies with liver lysosomes, or bone powder, indicate that plutonium is not readily mobilised from these structures by DTPA. The available evidence from in vivo-, in vitro, and computer speciation modelling studies of plutonium mobilisation suggests that the chemical speciation of plutonium in the cells and tissues, and the biokinetics of the ligand are two very important factors which, together with ligand affinity/specificity, must be given full consideration in any search for improved and safe treatment regimes.

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