Harrison John, Leggett Rich, Lloyd David, Phipps Alan, Scott Bobby
Health Protection Agency, Radiation Protection Division, Centre for Radiation, Chemicals and Environmental Hazards, Chilton, Didcot, Oxon, UK.
J Radiol Prot. 2007 Mar;27(1):17-40. doi: 10.1088/0952-4746/27/1/001. Epub 2007 Mar 6.
The death of Alexander Litvinenko on 23 November 2006 has brought into focus scientific judgements concerning the radiotoxicity of polonium-210 ((210)Po). This paper does not consider the specific radiological circumstances surrounding the tragic death of Mr Litvinenko; rather, it provides an evaluation of published human and animal data and models developed for the estimation of alpha radiation doses from (210)Po and the induction of potentially fatal damage to different organs and tissues. Although uncertainties have not been addressed comprehensively, the reliability of key assumptions is considered. Concentrating on the possibility of intake by ingestion, the use of biokinetic and dosimetric models to estimate organ and tissue doses from (210)Po is examined and model predictions of the time-course of dose delivery are illustrated. Estimates are made of doses required to cause fatal damage, taking account of the possible effects of dose protraction and the relative biological effectiveness (RBE) of alpha particles compared to gamma and x-rays. Comparison of LD(50) values (dose to cause death for 50% of people) for different tissues with the possible accumulation of dose to these tissues suggests that bone marrow failure is likely to be an important component of multiple contributory causes of death occurring within a few weeks of an intake by ingestion. Animal data on the effects of (210)Po provide good confirmatory evidence of intakes and doses required to cause death within about 3 weeks. The conclusion is reached that 0.1-0.3 GBq or more absorbed to blood of an adult male is likely to be fatal within 1 month. This corresponds to ingestion of 1-3 GBq or more, assuming 10% absorption to blood. Well-characterised reductions in white cell counts would be observed. Bone marrow failure is likely to be compounded by damage caused by higher doses to other organs, including kidneys and liver. Even if the bone marrow could be rescued, damage to other organs can be expected to prove fatal.
亚历山大·利特维年科于2006年11月23日去世,这使有关钋-210(²¹⁰Po)放射毒性的科学判断成为焦点。本文不考虑围绕利特维年科先生悲惨死亡的具体放射学情况;相反,它对已发表的人类和动物数据以及为估算来自²¹⁰Po的α辐射剂量和对不同器官和组织造成潜在致命损伤而开发的模型进行了评估。尽管未全面探讨不确定性,但考虑了关键假设的可靠性。专注于经口摄入的可能性,研究了使用生物动力学和剂量学模型来估算来自²¹⁰Po的器官和组织剂量,并说明了剂量递送时间进程的模型预测。考虑到剂量延长的可能影响以及与γ射线和X射线相比α粒子的相对生物效能(RBE),对造成致命损伤所需的剂量进行了估算。将不同组织的半数致死剂量(LD₅₀)值(导致50%的人死亡的剂量)与这些组织可能的剂量积累进行比较表明,骨髓衰竭可能是经口摄入后几周内发生的多种致死原因的重要组成部分。关于²¹⁰Po影响的动物数据为在约3周内导致死亡所需的摄入量和剂量提供了很好的证实性证据。得出的结论是,成年男性血液吸收0.1 - 0.3 GBq或更多可能在1个月内致命。假设对血液的吸收率为10%,这相当于摄入1 - 3 GBq或更多。会观察到白细胞计数有明确的减少。骨髓衰竭可能会因对包括肾脏和肝脏在内的其他器官的更高剂量损伤而加剧。即使骨髓能够得到挽救,对其他器官的损伤预计也会是致命的。