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Under conditions of acute administration, the lethal effect of either X-ray or plutonium is markedly increased by their combined application. If X-irradiation is delayed for 14 days after plutonium administration, the combined lethal effect is reduced. Under conditions of chronic X-irradiation, survival time is substantially shortened by a plutonium burden of 5 µc/kg. Plutonium retention and distribution is not affected by concurrent X-irradiation. The lethal effect of combined radiation is not influenced by the sequence of radiation application; however, it may be significantly altered by prompt DTPA treatment.

Dogs administered oral, intravenous or inhaled 239Pu citrate were sacrificed from 1 to 100 days after exposure to compare distribution and retention kinetics. Approximately 0.08 of the oral dose was retained after 3 days, distributed mainly between skeleton (50) and liver (25). After intravenous administration 239Pu was retained principally in the liver (32–45 of the dose) and skeleton (29 of the dose) during the 100 day post injection period. Inhaled 239Pu reached a peak concentration in blood after 6 hr and then decreased with clearance kinetics similar to those described by others for dogs and humans administered intravenous 239Pu citrate. The lung, skeleton, liver, blood and intestines retained most of the inhaled 239Pu 1 day after exposure. After 100 days 36 of the initial deposit was retained; 33 of that retained was in the lung, 44 in the skeleton and 17 in the liver. Plutonium was concentrated by lymphatic tissue following all methods of administration at all time intervals. Although the concentration in specific lymph nodes (hepatic, splenic and tracheobronchial) was among the highest of any tissue analyzed, the total amount deposited in a selection of 12 lymph nodes (about 10 g tissue) was always less than 0.6 of the body burden.

Rats were administered 253Es by intragastric, intratracheal, intravenous, intra-peritoneal, transplacental and transcutaneous routes. Early results from these studies are reported. Data are also reported on the intragastric and intravenous administration of 249Bk. Results are consistent in general form with what would have been predicted from the known behavior of lighter actinides.

Breath thoron was measured in dogs following inhalation or injection of 228Th enriched ThO2. Immediatedy after exposure, thoron release to the breath was less efficient from inhaled ThO2than from ThO2injected intravenously. After approximately 2 weeks, when the inhaled burden was localized in the lungs, the efficiency of thoron release to the breath was increased by one-half and exceeded that following other modes of administration. The lowest release values were found following intramuscular injection. The ratio relating thoron in the lung space to 228Th in the lung remained fairly constant for a period of 150 days after inhalation exposure. Applying this ratio to periodic breath thoron measurements, the half time for clearance of ThO2from the lung was estimated to be 350 days.

The enhanced acute toxicity of 239Pu as compared on an equivalent microcurie basis with 238Pu was evidenced by mortality data, by weight loss, by hematological and by histopathological observations. This difference in toxicity would seem to be most reasonably explained in terms of the different patterns of internal deposition of the two isotopes, which, in turn, may be explained by differences in physical state of the isotopes resulting from the 270-fold greater mass associated with an equal-microcurie quantity of 239Pu. No evidence was seen of direct chemical toxicity of 239Pu.