Mechanisms of plutonium toxicity may be attributed to its chemical and/or radioactive properties, although to date, no thorough distinction between the two has been made because the chemical toxicity is thought to be unimportant relative to the radiological toxicity. The toxicologically relevant decay products of plutonium isotopes are alpha emissions. This highly ionizing radiation usually causes the greatest effects in the immediate vicinity of plutonium contamination due to the short penetration distance of alpha particles.
Important factors concerning toxicity in different exposure scenarios include the route of exposure and the age of the organism. Other factors that relate to the exposure level are the contaminant concentration, the half-life of the particular isotope, and its biological retention time. An isotope with a long half-life (e.g., Pu-239) that is retained in target organs will result in a prolonged exposure of those tissues to alpha radiation. On the other hand, at the same concentration, isotopes with shorter half-lives will result in more emissions of alpha radiation over short time frames.
In humans and animals, the route of exposure and the chemical speciation will determine the target organ. Inhalation of less-soluble chemical species will result in localized effects on lung tissue. Plutonium that is absorbed (whether by ingestion or by inhalation of a soluble Pu species) and transported systemically via transferrin, an iron carrier protein, can be stored in the bone. Other target organs include the liver and the lymph nodes.
Depending on the exposure scenario, the resulting effects of the ionizing radiation include cytotoxicity and tissue necrosis (at higher doses) or genotoxicity (at lower doses), with cancer being the best documented in animal studies. In inhalation studies conducted with beagles, in order of frequency, bone, lung, and liver tumors were identified and determined to be the cause of death in many cases, with liver tumors being the least likely to result in death. The mechanisms of action for tumor development (and other non-tumor-forming mutations) are either direct radiation damage of DNA strands or indirect toxicity with strand damage after free radical generation. Other documented effects of plutonium exposure in (nonhuman) mammals include altered immune system structure and function, and reproductive effects.
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