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Plutonium ingestion toxicity

Figure 8.9 Principal contributions to the long-term ingestion toxicity of high-level waste from reprocessing uranium fuel (fuel from uranium-fueled PWR, 33 MWd/kg, 0.5 percent of uranium and plutonium appear in waste). Figure 8.9 Principal contributions to the long-term ingestion toxicity of high-level waste from reprocessing uranium fuel (fuel from uranium-fueled PWR, 33 MWd/kg, 0.5 percent of uranium and plutonium appear in waste).
Figure 8.10 Relative ingestion toxicity of solid residuals from LWR fuel cycle (uranitun fuel, 0.5 percent of uranium and plutonium in high-level wastes). Figure 8.10 Relative ingestion toxicity of solid residuals from LWR fuel cycle (uranitun fuel, 0.5 percent of uranium and plutonium in high-level wastes).
Relatively little Pu, Pu, Pu, americium and curium are formed in the irradiation of thorium-uranium fuel with fissUe makeup. However, when plutonium is used as fissile makeup for a thorium fuel cycle, considerable quantities of americium and curium are formed. As discussed in Sec. 2.4, these are the radionuclides that are the greatest contributors to radioactivity and ingestion toxicity after about 600 years of waste isolation, when the fission products have decayed. [Pg.379]

Alpha particles from plutonium cannot penetrate the epidermis, so toxicity is limited to conditions where the substance is present within the body. The primary routes of entry are inhalation, ingestion, or through wounds, cuts, or abrasions. The potential for adverse health effects caused by plutonium isotopes depends on the route of entry and subsequent deposition, redistribution, and retention, which in turn is highly influenced by the physical (e.g., particle size) and chemical forms of the isotope. [Pg.2035]

A further possible reason for separating plutonium from uranium and the fission products relates to the extreme toxicity of Pu. Plutonium(IV) mimics iron(lll) (the aqueous E° and charge-to-radius ratios of the two ions are very similar), so that cancers are likely to result from the absorption of even microgram amounts of ingested radioactive Pu into organs of the human body (bone marrow, spleen, liver) that store iron(III). It may therefore be considered desirable to remove Pu, a long-lived health hazard, from spent nuclear fuels before disposal of the latter in repositories that may not remain inviolate for thousands of years into the uncertain future (most of the fission products decay away to negligible levels of activity in an acceptable time). [Pg.364]

It is is the third most toxic substance known after plutonium and botulism it is a protein toxin that is extracted from the castor bean (Ricinus communis). The USA Centers for Disease Control (CDC) considers 500 pg to be the lethal dose of ricin in humans if exposure is from injection or inhalation. Ricin is poisonous if inhaled, injected, or ingested, acting by the inhibition of protein synthesis. While there is no known antidote, the US military has developed a vaccine. [Pg.12]

The toxicity of the actinide elements which requires an absolute barrier between the experiment and the experimenter is dictated to only a small extent by external radiation hazards. Plutonium-239 is intensely radioactive, emitting 1.4 X 10 a particles per milligram per minute. However, the alpha radiation from plutonium-239 can easily be shielded by even a thin sheet of paper. It is the consequences of ingestion that make plutonium-239 and the other actinide elements such toxic substances. Plutonium-239, inhaled into the lungs as fine particulate matter, is translocated to the bone, and, over a period of time, may give rise to bone neoplasms (cf. Section 14.10). The biological properties of the actinide elements are discussed in more detail in Sections 14.9 and 14.10. [Pg.253]

The toxic properties of plutonium have attracted interest to such an extent that it has become one of the best understood toxic substances known. Although plutonium has been known since 1940 and has been manufactured and handled on a large scale, no unquestionable direct relationship, 40 years later has been established between its toxicity and human death [65]. Everything known about the toxicity of plutonium has been learned from animal experimentation, as there is no known case of ingestion by a human of a suffidently large amount of plutonium to produce symptoms of acute toxicity. The application of information acquired in this way to humans can only be by extrapolation, which raises questions of species specificity that cannot be answered at this time. The information available about the other actinide elements is fragmentary and much less abundant, and generalizations must be accepted with reservations. [Pg.307]


See other pages where Plutonium ingestion toxicity is mentioned: [Pg.368]    [Pg.387]    [Pg.216]    [Pg.828]    [Pg.1729]    [Pg.1775]    [Pg.364]    [Pg.959]    [Pg.216]    [Pg.161]    [Pg.216]    [Pg.510]    [Pg.2609]    [Pg.864]    [Pg.82]    [Pg.82]    [Pg.723]    [Pg.309]    [Pg.182]    [Pg.12]   
See also in sourсe #XX -- [ Pg.373 , Pg.376 ]




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