Abstract
Cellular sites of plutonium localization and later redistribution of plutonium in the lung influences the toxicity of inhaled plutonium compounds. The loss of plutonium from macrophages, the death of macrophages, the engulfment of plutonium by the alveolar epithelium and the sequestration of plutonium in foci of fibrosis accounts for the relatively long retention times for PuO2 in the lung. The concentration of plutonium in particles-disproportionately in a few larger particles-in specific cellular elements of the lung, and in subpleural, fibrotic areas of the lung, provides for high radiation dose rates in limited tissue volumes. Such “hot spots” of alpha irradiation may cause epithelial metaplasia and eventually, alveolo-bronchiolar carcinoma. Such factors may be of great importance when determining the acceptable limits of exposure to man to air-borne plutonium and other transuranic elements.

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