Park J F, Buschbom R L, Dagle G E, James A C, Watson C R, Weller R E
Pacific Northwest National Laboratory, Richland, Washington 99352, USA.
Radiat Res. 1997 Oct;148(4):365-81.
Beagle dogs exposed to 238PuO2 aerosols (136 dogs, 13-22 per group, mean initial lung depositions of 0.0, 0.13, 0.68, 3.1, 13, 52 and 210 kBq) were observed throughout life to determine tissues at risk and dose-effect relationships. The pulmonary retention of 238Pu was represented by the sum of two exponentially decreasing components of the initial lung deposition; about 84% cleared with a 174-day half-time; the half-time of the remainder was 908 days. The average percentages of final body burden found in lung, skeleton, liver and thoracic lymph nodes in the 30 longest-surviving dogs (mean survival 14 years) were 1, 46, 42 and 6%, respectively. Of 116 beagles exposed to plutonium, 34 (29%) developed bone tumors, 31 (27%) developed lung tumors, and 8 (7%) developed liver tumors. Although lungs accumulated a higher average radiation dose than skeleton, more deaths were due to bone tumors than to lung tumors. Deterministic effects included radiation pneumonitis, osteodystrophy, hepatic nodular hyperplasia, lymphopenia, neutropenia and sclerosing tracheobronchial lymphadenitis. Hypoadrenocorticism was also observed in a few dogs. Increased serum alanine aminotransferase, indicative of liver damage, was observed in groups with > or =3.1 kBq initial lung deposition. Estimates of cumulative tissue dose in a human exposed to airborne 238PuO2 for 50 years at a rate of one annual limit on intake each year were derived based on a comparison of the data on metabolism for humans and beagles. The 50-year dose estimates for humans are an order of magnitude lower than doses at which increased incidence of neoplasia was observed in these dogs, whereas the projected doses to humans from 50-year exposure at the annual limit of intake are of similar magnitude to those at which deterministic effects were seen in the beagles.
将比格犬暴露于238PuO2气溶胶中（136只犬，每组13 - 22只，初始肺沉积量的均值分别为0.0、0.13、0.68、3.1、13、52和210 kBq），对其进行终生观察，以确定风险组织和剂量 - 效应关系。238Pu在肺内的滞留情况由初始肺沉积的两个呈指数下降的成分之和表示；约84%以174天的半衰期清除；其余部分的半衰期为908天。在存活时间最长的30只犬（平均存活14年）中，肺、骨骼、肝脏和胸段淋巴结中最终体内负荷的平均百分比分别为1%、46%、42%和6%。在116只暴露于钚的比格犬中，34只（29%）发生了骨肿瘤，31只（27%）发生了肺肿瘤，8只（7%）发生了肝肿瘤。尽管肺累积的平均辐射剂量高于骨骼，但因骨肿瘤导致的死亡多于肺肿瘤。确定性效应包括放射性肺炎、骨营养不良、肝结节性增生、淋巴细胞减少、中性粒细胞减少和硬化性气管支气管淋巴结炎。在少数犬中还观察到肾上腺皮质功能减退。在初始肺沉积量≥3.1 kBq的组中，观察到血清丙氨酸氨基转移酶升高，这表明肝脏受到了损伤。基于对人类和比格犬代谢数据的比较，得出了人类以每年一个摄入年限值的速率暴露于空气中的238PuO2 50年的累积组织剂量估计值。人类50年的剂量估计值比在这些犬中观察到肿瘤发生率增加时的剂量低一个数量级，而人类以摄入年限值暴露50年的预计剂量与在比格犬中观察到确定性效应时的剂量大小相似。
