Schneider Uwe, Walsh Linda
Division of Medical Physics, Department of Radiation Oncology and Nuclear Medicine, The Triemli Hospital Zürich, 8063 Zürich, Switzerland.
Radiat Environ Biophys. 2008 Apr;47(2):253-63. doi: 10.1007/s00411-007-0151-y. Epub 2007 Dec 21.
Most information on the dose-response of radiation-induced cancer is derived from data on the A-bomb survivors who were exposed to gamma-rays and neutrons. Since, for radiation protection purposes, the dose span of main interest is between 0 and 1 Gy, the analysis of the A-bomb survivors is usually focused on this range. However, estimates of cancer risk for doses above 1 Gy are becoming more important for radiotherapy patients and for long-term manned missions in space research. Therefore in this work, emphasis is placed on doses relevant for radiotherapy with respect to radiation-induced solid cancer. The analysis of the A-bomb survivor's data was extended by including two extra high-dose categories (4-6 Sv and 6-13 Sv) and by an attempted combination with cancer data on patients receiving radiotherapy for Hodgkin's disease. In addition, since there are some recent indications for a high neutron dose contribution, the data were fitted separately for three different values for the relative biological effectiveness (RBE) of the neutrons (10, 35 and 100) and a variable RBE as a function of dose. The data were fitted using a linear, a linear-exponential and a plateau-dose-response relationship. Best agreement was found for the plateau model with a dose-varying RBE. It can be concluded that for doses above 1 Gy there is a tendency for a nonlinear dose-response curve. In addition, there is evidence of a neutron RBE greater than 10 for the A-bomb survivor data. Many problems and uncertainties are involved in combing these two datasets. However, since very little is currently known about the shape of dose-response relationships for radiation-induced cancer in the radiotherapy dose range, this approach could be regarded as a first attempt to acquire more information on this area. The work presented here also provides the first direct evidence that the bending over of the solid cancer excess risk dose response curve for the A-bomb survivors, generally observed above 2 Gy, is due to cell killing effects.
大多数关于辐射诱发癌症剂量反应的信息来自原子弹爆炸幸存者的数据，这些幸存者受到了γ射线和中子的照射。由于出于辐射防护目的，主要关注的剂量范围在0至1 Gy之间，因此对原子弹爆炸幸存者的分析通常集中在这个范围内。然而，对于放射治疗患者和太空研究中的长期载人任务而言，高于1 Gy剂量的癌症风险估计变得越来越重要。因此，在这项工作中，重点放在了与放射治疗相关的辐射诱发实体癌剂量方面。通过纳入两个额外的高剂量类别（4 - 6 Sv和6 - 13 Sv）以及尝试将其与接受霍奇金病放射治疗患者的癌症数据相结合，对原子弹爆炸幸存者的数据进行了扩展分析。此外，由于最近有一些迹象表明中子剂量贡献较高，因此针对中子的相对生物效应（RBE）的三个不同值（10、35和100）以及作为剂量函数的可变RBE，分别对数据进行了拟合。使用线性、线性指数和平坦剂量反应关系对数据进行拟合。发现平坦模型与剂量变化的RBE具有最佳一致性。可以得出结论，对于高于1 Gy的剂量，存在非线性剂量反应曲线的趋势。此外，对于原子弹爆炸幸存者的数据，有证据表明中子RBE大于10。将这两个数据集结合起来涉及许多问题和不确定性。然而，由于目前对于放射治疗剂量范围内辐射诱发癌症的剂量反应关系形状知之甚少，这种方法可被视为在该领域获取更多信息的首次尝试。此处展示的工作还首次直接证明，原子弹爆炸幸存者实体癌超额风险剂量反应曲线通常在2 Gy以上出现的弯曲是由于细胞杀伤效应。
