This paper reports on an enriched uranium dioxide (UO2) mass clearance study undertaken with Fischer-344 rats. The UO2 had a uranium (U) isotopic composition of 0.79% 234U, 92.8% 235U, 0.34% 236U and 6.06% 238U, by mass, with an alpha-particle activity of 1.91 Bq micrograms-1. Forty-six rats were exposed to an enriched UO2 aerosol that had an activity median particle aerodynamic diameter ranging from 2.7 to 3.2 microns. The rats were killed from 1 to 720 d post-inhalation (PI). The mass of enriched UO2 present in the trachea, lung lobes, thoracic lymph nodes, kidneys, liver, spleen, gut, and the remainder of the carcass was assessed at death. At 720 d after exposure, 82% of the total body burden of enriched UO2 was in the lung, with a further 10% in the thoracic lymph nodes. This represented 17% and 2% of the original (5 d PI) lung burden. The mass clearance of enriched UO2 from the lung was fitted to a single exponential function, normalized to 100% at 5 d PI. The rate constant (k) was 2.8 X 10(-3) d-1, giving a clearance half-time of 247 d. Although statistical comparisons with the majority of published data were not possible, it appeared that both enriched UO2 and natural UO2 particles cleared at rates that were broadly similar, with a t1/2 in the rat lung of 150 to 300 d over the 5- to 720-d PI period. As a consequence of the 234U component in the inhaled UO2 particles, the rats killed at 720 d PI received a total mean accumulated alpha-particle dose averaged over the whole lung of 5.7 Gy. Histologic investigations of the rat lungs found that widespread lung disease was only observed in animals killed at 720 d PI.
Mice were exposed to weakly penetrating beta-particles from an external source, using 12 different surface doses ranging from 5.4 to 260 Gy and given at four different dose rates from 200 to 1.7 cGy/min. As in previous investigations, both epidermal and dermal tumours occurred with the latter predominating. The lowest surface dose to produce a statistically significant increase in skin tumours was 21.7 Gy, no effect being detected with doses of 5.4-16.3 Gy. The dose-response curves rose steeply when obvious increases occurred. Consideration of these findings and the fact that radiation-induced skin tumours can have an exceptionally long latent period leads to the suggestion that there is some relatively radioresistant factor which normally restrains potential radiation-induced cancer cells in the skin from becoming tumours until the skin is subjected to high local doses. Tumour-induction was unaffected by reducing the highest dose rate by a factor of 10 and the dose-response curves were almost identical. Further reductions of dose rate, encompassing a further factor of 10, in general resulted in fewer tumours.
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