Towards a new dose and dose-rate effectiveness factor (DDREF)? Some comments
Towards a new dose and dose-rate effectiveness factor (DDREF)? Some comments
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DOI：
10.1088/1361-6498/aa6722
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发表时间：
2017-06-01
影响因子：
1.5
通讯作者：
Chadwick, K. H.
中科院分区：
文献类型：
--
作者：
Chadwick, K. H.
本文的目的是提供一种比（Ruhm et al 2016 Ann. ICRP 45 262-79）用于解释癌症诱导关系的更广泛的基于机制的分析工具。文章解释了这种更广泛的分析工具的局限性及其使用的影响，鉴于Leuraud等人2015年的出版物（Lancet Haematol. 2 e276-81）和Richardson等人2015（Br. J. 351 h5359）。Ruhm等人2016年发表的出版物（Ann. ICRP 45 262-79）显然是正在进行的工作，审查了ICRP建议的剂量和剂量率有效性因子（DDREF）的现状。它还考虑了可能影响DDREF的价值及其在辐射防护中的应用的重新评估的问题。在这篇文章中，从不同的角度来探讨这个问题，并从评论Ruhm等人2016年（Ann. ICRP 45 262-79）用于开发其分析的有限科学数据开始，最终导致他们使用线性二次剂量效应关系来拟合日本原子弹幸存者寿命研究的固体癌症死亡率数据。这里采取的方法包括更多的数据，诱导DNA双链断裂，并使用从文献中获得的实验数据，直接涉及到细胞杀伤，染色体畸变和体细胞突变的断裂。这些关系被扩展以描述癌症的诱导，因为癌症突变细胞必须存活以表达其恶性性质，所以癌症的诱导是由辐射诱导的细胞学损伤与细胞杀伤相结合引起的。方程推导出急性和慢性暴露于稀疏电离辐射后的癌症诱导。将方程拟合至小鼠中的癌症诱导，以说明总剂量范围内的剂量效应关系。从这两个方程推导出的“DDREF”随剂量而变化，DDREF概念受到质疑。虽然急性照射方程可用于分析原子弹爆炸幸存者数据，但拟合受二次剂量分量的支配。因此，很少有有用的信息可以推导出的线性剂量分量，这是重要的推导低剂量率的风险。建议辐射防护委员会从流行病学研究（例如，对工人群体的研究）以及细胞辐射生物学研究的资料中得出低剂量率下的风险。
The aim of this article is to offer a broader, mechanism-based, analytical tool than that used by (Ruhm et al 2016 Ann. ICRP 45 262-79) for the interpretation of cancer induction relationships. The article explains the limitations of this broader analytical tool and the implications of its use in view of the publications by Leuraud et al 2015 (Lancet Haematol. 2 e276-81) and Richardson et al 2015 (Br. Med. J. 351 h5359). The publication by Ruhm et al 2016 (Ann. ICRP 45 262-79), which is clearly work in progress, reviews the current status of the dose and dose-rate effectiveness factor (DDREF) as recommended by the ICRP. It also considers the issues which might influence a reassessment of both the value of the DDREF as well as its application in radiological protection. In this article, the problem is approached from a different perspective and starts by commenting on the limited scientific data used by Ruhm et al 2016 (Ann. ICRP 45 262-79) to develop their analysis which ultimately leads them to use a linear-quadratic dose effect relationship to fit solid cancer mortality data from the Japanese life span study of atomic bomb survivors. The approach taken here includes more data on the induction of DNA double strand breaks and, using experimental data taken from the literature, directly relates the breaks to cell killing, chromosomal aberrations and somatic mutations. The relationships are expanded to describe the induction of cancer as arising from radiation induced cytological damage coupled to cell killing since the cancer mutated cell has to survive to express its malignant nature. Equations are derived for the induction of cancer after both acute and chronic exposure to sparsely ionising radiation. The equations are fitted to the induction of cancer in mice to illustrate a dose effect relationship over the total dose range. The 'DDREF' derived from the two equations varies with dose and the DDREF concept is called into question. Although the equation for acute exposure can be used to analyse atomic bomb survivor data, the fitting is dominated by the quadratic dose component. Thus, little useful information can be derived about the linear dose component which is important for the derivation of low dose rate risk. The ICRP are advised to derive the risk at low dose rates from epidemiological studies of, for example, worker populations, together with information from cellular radiation biological research.