南乌拉尔的辐射危险研究进展

20 0 2年 6月 9～ 1 1日在德国巴伐利亚州的Chiemsee,召开了“南乌拉尔的辐射危险研究研讨会”。南乌拉尔的玛雅克生产联合企业 ,曾经大规模地生产和加工核材料 ,其中包括前苏联制造核武器所用的核材料。玛雅克工厂的工作人员及工厂所在的捷恰河下游沿岸人群均受到辐射照射和摄入放射性核素的照射 ,尤其是在 2 0世纪 40年代末、5 0年代初。这些受照群体的集体剂量与日本广岛和长崎原子弹爆炸幸存者的剂量相当。1 0年来 ,来自美国、欧盟和日本的研究团体 ,与苏联的科学家合作 ,建立并分析了玛雅克工作人员和捷恰河受照群体的数据库。这些数…     

原子弹轰炸幸存者：有关早期死亡有后期效应的进一步证据

重新对原子弹轰炸幸存者的资料进行的分析已显示出如下两点：ａ）在受到终生观察的５年幸存者队列的高剂量（＞１Ｇｙ）亚群中，明显缺少轰炸时年龄小于１０岁和年龄大于５０岁的个体；ｂ）在子宫内受照儿童的队列内，又明显缺少受照时胎龄小于８周的个体。本文就这一淘汰过程造成的偏差是如何影响到对原子弹辐射的３种效应（骨髓损伤、致瘤作用及第二代效应）的识别进行了讨论。     

辐射致癌效应与机制

电离辐射是已确定的物理致癌因子.辐射致癌效应的发现要追溯到上世纪初,当时,从事超量放射性物质操作却未做有效防护的职业研究人员中,有不少后来身患癌症,随后大量的动物实验也证实辐射的致癌性.在对日本原爆幸存者、有关矿工等受照人群的癌症发生率和死亡率的流行病学研究的基础上,建立了癌症危险估算模型.辐射致癌的细胞和分子机理的研究,近年来取得了重要进展,包括辐射致DNA集簇性损伤与基因突变的启动事件、基因组不稳定性、细胞增殖调控的信号转导机制、旁效应引申出的辐射非靶效应等.对辐射致癌相关基因的分离鉴定和功能研究,也取得了重要进展.     

放射线影响研究所(RERF)简介之一——概况及主要科研任务

该所过去名为原爆伤害调查委员会(Atomic Bomb Casualty Cornmission,简称ABCC),成立于1947年。1975年4月改名为放射线影响研究所(Radiation Effects Research Foundation,简称RERF)。位于日本西南部的广岛。广岛是第一个受原子弹袭击的地方,不仅有必要对原子弹爆炸(以后简称原爆)受照者的急性辐射效应进行研究;而且也认为有必要对原爆受照者进行长期的医学观察,了     

国际放射防护委员会(ICRP)第91任务组介绍

正国际放射防护委员会(ICRP)第91任务组(TG 91)是第1分委员会下设的一个任务组。它的任务是研究"为辐射防护目的的低剂量和低剂量率照射的辐射危险推断"。ICRP推荐的危害调节标称危险系数在很大程度上依据的是从日本原子弹爆炸幸存者得到的数据。因为他们的照射是单一的急性照射,并且剂量响应关系的最合理的生物模型应当是线性二次型(意味着高剂量时的斜率大于低剂量时),所以许多国际和国家组织,例如UNSCEAR、BEIR和ICRP,     

欧洲核能机构详细说明低剂量的影响

【英国《国际核工程》 1 999年 4月号报道】　线性无阈 (L NT)剂量—效应关系的假说是支持核工业工作人员和一般公众设定辐射防护限值的基本科学原理 ,这一理论设想 ,任何辐射剂量水平都会增加患癌症的危险。虽然不可能证明低辐射剂量下射线照射量和癌症之间的直接关系 ,但动物实验和对受照人群 (像广岛和长崎原子弹爆炸幸存者和切尔诺贝利及切尔雅宾斯克周围居民 )的流行病学研究证明了这种影响。如果低辐射剂量对健康有影响 ,那么影响多大 ,这在科学上仍有很大的不确定性。欧洲核能机构的报告对公认情况归纳如下 :　　 ● 低剂量电离辐…     

放射性核素在核医学应用中的辐射剂量估算

采用一种估算方法来研究放射性核素在核医学应用中的辐射剂量水平。选取临床上常用的几种诊疗用放射性核素,分别采用剂量系数法和点源模型估算内照射与外照射剂量。并对比其他估算方法,分析受照剂量存在差异的原因。结果发现,单次核医学诊断所致患者的全身待积有效剂量最高可达1.63 Sv,对A、B类医护人员造成的单次有效剂量分别为1.48 μSv和1.15 μSv。本研究估算结果稍大于实测有效剂量,小于其他估算结果。该估算模型可作为核医学放射性核素辐射剂量水平的一种有效估算方法。     

辐射致癌的遗传学易感性

在辐射致癌危险估计中,假定受照群体内每个相同性别、相同年龄的成员在接受相同剂量照射后具有相同的致癌易感性,亦即假定这时辐射致癌效应的随机性只依赖于受照后发生的电离事件的随机性。实际上决定辐射致癌效应的宿主因素不只是性别和年龄以及与此有关联的免疫能力和激素水平的不同,还有遗传和环境因素的影响,这些影响构成人群内部在辐射致癌易感性上的进一步差别。认识这种差别,从受照人群中找出易     

空勤人员辐射剂量的估算与测定

1991年,ICRP建议将空勤人员列入职业受照人群;2002年,我国颁布实施了《空勤人员宇宙辐射控制标准》。本文介绍航空飞行高度上的辐射环境及空勤人员辐射剂量的估算方法和常用的测量手段,并比较了不同方法的计算和测量结果。     

“从生物学观点探讨辐射防护政策的新思路”研讨会简介

介绍了 2 0 0 0年 5月 1 7日在日本广岛举行的“从生物学观点探讨辐射防护政策的新思路”研讨会上 ,由 D.Preston,Y.Ishikawa,P.Duport,C.Streffer,M.Ohtaki,M.N.Mohankumar和 X.A.Chen等 7位专家所作的发言 ,内容包括 :广岛和长崎原子弹爆炸幸存者的辐射效应 ;二氧化钍造影剂病人肝和肺的致癌 ;受到低剂量电离辐射照射的动物的癌的危险 ;辐射诱发癌的致癌机制 ;把诱发遗传不稳定性假说作为依据的辐射致癌的数学含义 ;对电离辐射的适应性响应及其在影响放射防护标准中的作用以及长期吸入钍尘对健康影响的 1 4年追踪。     

Monte Carlo simulation for internal radiation dosimetry based on the high resolution Visible Chinese Human

The internal radiation dose calculations based on Chinese models is important in nuclear medicine. Most of the existing models are based on the physical and anatomical data of Caucasian, whose anatomical structure and physiological parameters are quite different from the Chinese, may lead significant effect on internal radiation.Therefore, it is necessary to establish the model based on the Chinese ethnic characteristics, and applied to radiation dosimetry calculation. In this study, a voxel model was established based on the high resolution Visible Chinese Human(VCH). The transport procedure of photon and electron was simulated using the MCNPX Monte Carlo code.Absorbed fraction(A.F) and specific absorbed fraction(SAF) were calculated and S-factors and mean absorbed doses for organs with 99roTe located in liver were also obtained. In comparison with those of VIP-Man and MIRD models,discrepancies were found to be correlated with the racial and anatomical differences in organ mass and inter-organ distance. The internal dosimetry data based on other models that were used to apply to Chinese adult population are replaced with Chinese specific data. The obtained results provide a reference for nuclear medicine, such as dose verification after surgery and potential radiation evaluation for radionuclides in preclinical research, etc.     

国际放射防护委员会的剂量系数的可靠性

在评价公众成员摄入放射性核素的辐射危害时，需估算每单位摄入量所致的剂量。摄入放射性素后器官或民受到的剂量是受到的剂量是通过生物学模型和剂量学模型来确定的，因此剂量也必须根据模型来确定。文中初步探讨了国际放射防护委员会给出的剂量系数的可靠性问题。文中首先说明了估算剂量系数的概念和方法，然后分析了剂量系数估算中，采用胃肠道模型，呼吸道模型，系统生物动力学模型和剂量学模型所遇到的不确定度的各种主要来源。     

Dose field in hiroshima and the risk of radiation-induced cancer

The dose distribution of γ-neutron radiation over the earth's surface as a result of the atomic explosion in Hiroshima is of decisive value for establishing the risk coefficients for death from radiation-induced cancer. At the same time, this radiation field is unique, since the ratio of its components varies both with distance from the hypocenter and with dose. For the DS 86 dosimetric system, the relation between mortality from solid cancer and dose has a linear, zero-threshold character. For this reason, the linear zero-threshold dependence is used as a basis for the entire system of radiation protection. However, the DS 86 results depend strongly on the choice of the coefficients of relative biological effectiveness of neutrons, which have not been established adequately. New data, which could change the dosimetric system and lead to a reexamination of the risk coefficients at low dose, are analyzed. 3 figures, 1 table, 7 references. State Science Center of, the Russian Federation-Institute of Biophysics. Translated from Atomnaya énergiya, Vol. 87, No. 4, pp. 294–297, October, 1999.     

Genetic susceptibility to cancer: ICRP Publication 79

A Task Group of the ICRP Committee 1 (Radiation Effects) has reviewed relevant data with the objective of advising the Main Commission of the ICRP on the possible implications for radiological protection of emerging views on genetic susceptibility to cancer (Chapter 1).Chapter 2 considers DNA damage and its processing/repair after ionising radiation and serves principally to demonstrate that a few rare cancer-prone, human recessive genetic disorders show DNA repair deficiency and profound increases in radiosensitivity. Less dramatic changes in radiosensitivity are also apparent in a wider range of such disorders. The cellular mechanisms that underly the association between DNA damage processing and tumorigenesis are discussed.Chapter 3 reviews the mechanisms and genetics of solid tumours illustrating the ways in which mutations in proto-oncogenes, tumour suppressor genes together with those in DNA repair and cell cycle control genes can contribute to tumour development. Specific examples are given of how germ line mutation of such genes can predispose to familial cancer. It is judged that up to 5% of all solid tumours have a recognisable genetic component. Heritable organ-specific effects are most usual and cancers of the breast and colon tend to show the most obvious genetic components. Clearly discernible genetic effects are seen when rare dominant germ line mutations express strongly as familial cancer (high penetrance mutations), but the existence of perhaps less rare low penetrance mutations and gene–gene interactions are recognised but not well understood.Chapter 4 considers the mechanisms and genetics of lympho-haemopoietic tumours. Specific chromosomal translocations and proto-oncogene activation events are much more frequent in human leukaemia/lymphoma than in solid tumours. Genetic predisposition to leukaemia/lymphoma is found in a number of non-familial recessive genetic disorders of DNA processing and/or chromosomal instability. Familial manifestation of susceptibility to these tumours is, however, extremely rare. The genetic component, although poorly defined, is judged to be less than that of solid tumours and expressed largely in childhood.Chapter 5 reviews and discusses limited data that comment upon tumorigenic radiosensitivity in cancer-prone genetic conditions. From knowledge of the fundamental processes involved it is judged that in most, but not all, cases genetic susceptibility to spontaneous tumours will be accompanied by a greater-than-normal risk after radiation. A review of epidemiological, clinical and experimental data relevant to this issue suggests that although a wide range of different sensitivities may be involved, a factor of 10 increase in sensitivity broadly accords with the limited human data available. This interim judgement of a factor of 10 increase in radiation risk in such human genetic disorders is made for the purposes of illustrative modelling and calculation. In addition, specific attention is given to breast cancer risk in heterozygotes for the radiosensitive human disorder, ataxia-telangiectasia; this association, while in no way discounted, is judged to be less strong than that claimed by some.Chapter 6 discusses and develops computational modelling procedures that aim to describe the impact of genetic factors on radiation-tumorigenesis in human populations. Estimates of the prevalence of known cancer-prone genetic disorders are made but breast cancer susceptibility is used to illustrate the application of the model developed. The most important message to emerge from this work is that, even at an assumed high level of radiation sensitivity, the prevalence of familial (high penetrance) genetic disorders in the population is too low (<1%) for there to be a significant impact on risk in typical human populations. In principle, however, there is the potential for such impact in atypical inbred sub-populations where these mutations can be more common. These modelling procedures are also used to illustrate how incomplete penetrance of these mutations will dilute any impact on population risk.In conjunction with the Main Commission of the ICRP, in Chapter 7 the Task Group discusses the potential implications of the main report for radiological protection. Their principal conclusions are: (i) That current estimates of radiation cancer risk already include an unknown contribution from genetically radiosensitive sub-populations. (ii) Using the data cited, the likely contribution to radiation risk from familial cancer disorders is too low to generate an unacceptable distortion of current estimates of cancer risk in the vast majority of human populations. (iii) There is insufficient knowledge to judge the contribution to risk from mutations of low penetrance that do not express as familial cancer. (iv) Because of the high risk of spontaneous cancer in familial disorders, low doses of radiation (say 100 mSv) are most unlikely to impact significantly on life-time cancer risk in an affected individual; at high doses, such as those experienced in radiotherapy, this relative risk may however become important. (v) Because organ-specific cancer risk is predicted in most familial disorders, the absolute increase overall in risk to an affected individual will be diluted, ie. comparing normal and affected individuals. (vi) The utility of genetic testing for cancer predisposition in the context of radiological protection is currently limited by technical factors and concerns on predictive power. In the future genetic testing may find selected use prior to certain medical exposures to radiation, but the value of such procedures, as applied to low-dose occupationally exposed individuals, is open to doubt; it would also be subject to major ethical scrutiny outside the remit of the ICRP.The Task Group and the Main Commission of the ICRP stress that, because of the current lack of knowledge, the above judgements should be regarded as preliminary. The report serves principally to provide a framework on which to develop further views in this rapidly advancing area of human genetics.     

Risk estimation for multifactorial diseases. A report of the International Commission on Radiological Protection

This report reviews data on naturally-occurring multifactorial diseases and develops a mathematical model to predict the impact of radiation-induced mutations on the frequencies of these diseases in the population. It provides an outline of the aetiological features and examples of multifactorial diseases, interpreted to arise as a result of the joint action of genetic and environmental factors. Examples include common congenital abnormalities (such as neural tube defects, cardiovascular malformations, cleft lip+/-palate etc.) and chronic diseases (such as coronary heart disease, essential hypertension, diabetes mellitus etc.). These diseases are not readily explained on the basis of simple mendelian patterns of inheritance. The report considers the concepts and models used to explain the inheritance patterns of multifactorial diseases with particular emphasis on the multifactorial threshold model (MTM) of disease liability. The MTM is useful for predicting risk to relatives of those affected from information on their population frequencies. In these predictions, the heritability (h(2)) provides a measure of the relative importance of transmissible genetic effects in the overall phenotypic variation. Conceptual differences between mendelian and multifactorial diseases are discussed. The genetic basis of a multifactorial disease is that a genetically susceptible individual may or may not develop the disease depending on the interaction of a number of risk factors, both genetic and environmental. Three chronic multifactorial disease entities are reviewed in depth, viz. diabetes mellitus, essential hypertension, and coronary heart disease. The report considers briefly mechanistic population genetic models developed to explain polygenic variation. The basic conclusion is that the concepts of liability and threshold (underlying the MTM model) and that of mutation-selection balance (from population genetic models) together provide a basis for developing a model for assessing the impact of radiation-induced mutations on the frequencies of multifactorial diseases in the population.The mutation component (MC) of genetic diseases quantifies the responsiveness of the genetic component of a disease to an increase in mutation rate (e.g. after radiation exposure). This report integrates the concepts of liability and threshold (from the MTM model) and of mutation-selection equilibrium (from mechanistic population genetic models) into the 'Finite Locus Threshold Model' (FLTM) for estimating MC for multifactorial diseases and the relationship between MC and h(2) of these diseases. Computer simulation studies illustrate the effects of one-time or a permanent increase in mutation rate on MC for multifactorial diseases.Finally, the report addresses the estimation of the radiation risk of multifactorial diseases. A formal revision of the estimates of risk of multifactorial diseases (and also of mendelian diseases) contained in the 1990 Recommendations of ICRP, Publication 60, must await the results of studies currently underway. While future genetic risk estimates are likely to be lower than those in current use, until the new ones become available, those provided in Publication 60 may be regarded as being adequate for use in radiological protection- they are unlikely to underestimate risk.     

Risk estimation for multifactorial diseases: ICRP Publication 83

This report reviews data on naturally-occurring multifactorial diseases and develops a mathematical model to predict the impact of radiation-induced mutations on the frequencies of these diseases in the population. It provides an outline of the aetiological features and examples of multifactorial diseases, interpreted to arise as a result of the joint action of genetic and environmental factors. Examples include common congenital abnormalities (such as neural tube defects, cardiovascular malformations, cleft lip±palate etc.) and chronic diseases (such as coronary heart disease, essential hypertension, diabetes mellitus etc.).These diseases are not readily explained on the basis of simple mendelian patterns of inheritance. The report considers the concepts and models used to explain the inheritance patterns of multifactorial diseases with particular emphasis on the multifactorial threshold model (MTM) of disease liability. The MTM is useful for predicting risk to relatives of those affected from information on their population frequencies. In these predictions, the heritability (h²) provides a measure of the relative importance of transmissible genetic effects in the overall phenotypic variation.Conceptual differences between mendelian and multifactorial diseases are discussed. The genetic basis of a multifactorial disease is that a genetically susceptible individual may or may not develop the disease depending on the interaction of a number of risk factors, both genetic and environmental. Three chronic multifactorial disease entities are reviewed in depth, viz. diabetes mellitus, essential hypertension, and coronary heart disease. The report considers briefly mechanistic population genetic models developed to explain polygenic variation. The basic conclusion is that the concepts of liability and threshold (underlying the MTM model) and that of mutation-selection balance (from population genetic models) together provide a basis for developing a model for assessing the impact of radiation-induced mutations on the frequencies of multifactorial diseases in the population.The mutation component (MC) of genetic diseases quantifies the responsiveness of the genetic component of a disease to an increase in mutation rate (e.g. after radiation exposure). This report integrates the concepts of liability and threshold (from the MTM model) and of mutation-selection equilibrium (from mechanistic population genetic models) into the ‘Finite Locus Threshold Model' (FLTM) for estimating MC for multifactorial diseases and the relationship between MC and h² of these diseases. Computer simulation studies illustrate the effects of one-time or a permanent increase in mutation rate on MC for multifactorial diseases.Finally, the report addresses the estimation of the radiation risk of multifactorial diseases. A formal revision of the estimates of risk of multifactorial diseases (and also of mendelian diseases) contained in the 1990 Recommendations of ICRP, Publication 60, must await the results of studies currently underway. While future genetic risk estimates are likely to be lower than those in current use, until the new ones become available, those provided in Publication 60 may be regarded as being adequate for use in radiological protection- they are unlikely to underestimate risk.     

Possible Approach to Modifying the Formula for Calculating the Effective Dose

The purpose of this work is to provide justification for introducing a dependence on the age of an individual at the moment of irradiation into the definition of the effective dose and to estimate the numerical values of the age-weighting coefficients. A modified approach to defining the effective dose, taking account of the age at the moment of irradiation, is proposed. The numerical values of the age-weighting coefficients are determined using the basic models for extrapolating radiation risk for two different populations: the Russian population and part of the US population.     

The development and validation of a thermal hydraulic code in rolling motion

An advanced thermal hydraulic code is established on the basis of RELAP5/MOD3.3 code for the investigation of the thermal hydraulic behavior of nuclear power systems. The RELAP5 code is modified by adding a module calculating the effect of rolling motion and introducing new flow and heat transfer models. The experimental data are used to validate the theoretical models and calculation results. It is shown that the advanced flow and heat transfer models could correctly predict the frictional resistance and heat transfer coefficients in rolling motion. The thermal hydraulic code is used to simulate the operation of a natural circulation system in rolling motion. The calculation results are in good agreement with experimental data. The relative discrepancies between calculation results and experimental data are less than 5%.     

Semiempirical transport in tokamaks

A class of semiempirical transport models is proposed for testing against confinement data from tokamaks and for use in operations planning and machine design. A reference model is proposed to be compatible with published confinement data. Theoretical considerations are used to express the anomalous transport coefficients in terms of appropriate dimensionless parameters. The reference model is applied to heating of an advanced tokamak experiment.