Biological effects after prenatal irradiation (embryo and fetus). A report of the International Commission on Radiological Protection

In its 1990 recommendations, the ICRP considered the radiation risks after exposure during prenatal development. This report is a critical review of new experimental animal data on biological effects and evaluations of human studies after prenatal radiation published since the 1990 recommendations.Thus, the report discusses the effects after radiation exposure during pre-implantation, organogenesis, and fetogenesis. The aetiology of long-term effects on brain development is discussed, as well as evidence from studies in man on the effects of in-utero radiation exposure on neurological and mental processes. Animal studies of carcinogenic risk from in-utero radiation and the epidemiology of childhood cancer are discussed, and the carcinogenic risk to man from in-utero radiation is assessed. Open questions and needs for future research are elaborated.The report reiterates that the mammalian embryo and fetus are highly radiosensitive. The nature and sensitivity of induced biological effects depend upon dose and developmental stage at irradiation. The various effects, as studied in experimental systems and in man, are discussed in detail. It is concluded that the findings in the report strengthen and supplement the 1990 recommendations of the ICRP.     

Radiation Exposure Normalization Taking Account of Specific Effects at Low Doses and Dose Rates

Epidemiological studies of the consequences of radiation exposure of humans already prove that at low dose rates 85% of radiation-induced cancer arises only above a threshold dose from 0.3 to 30 Sv, and sometimes radiation hormesis occurs. In this question, the ICRP and the RNCRP rely on unreliable information and an incorrect linear zero-threshold dose–effect relation model. Two new principles of radiation safety are proposed and a model for normalizing radiation exposure on the basis of the new facts is also proposed. The model retains the adopted maximum lifetime individual risk of death due to radiation-induced cancer, but the dose in organs determines this risk. For uniform whole body radiation exposure, the dose creating the indicated limit can be taken as the equivalent dose. It will equal 150 mSv/yr. According to the model, during the initial years of radiation exposure there is no carcinogenic risk at all. The need for normalizing the content of radionuclides in the human body and introducing other changes in the norms is substantiated.     

Relative biological effectiveness of neutron radiation and its implications for quality factor and dose limitation

The biological effectiveness of fission neutrons relative to low dose rate photon radiations with energies in excess of 400 keV lies in the range from 10 to possibly in excess of 100 depending upon the effect studied; in contrast to the quality factor used in radiological protection for those neutrons of about 10. However, for the majority of genetic effects, tumour induction and life shortening in rodents, the value would appear to lie in the region of 20 to 30. One consistent biological observation is that the effectiveness of photon radiation is decreased at low dose rates. Bearing in mind that human risk estimates have almost all been derived from high dose, high dose rate exposures, it does not seem likely that the current risks to humans from either photon or neutron radiation at low doses and low dose rates have been grossly underestimated. This conclusion is reached after making allowances for the possible effects of a revision of the dosimetry of the Japanese atomic bomb survivors.The recent ICRP recommendation that the quality factor for neutrons should be increased by a factor of two has to be seen in a context in which the concept used in the measurement and control of individual exposures to neutron radiation overestimates the dose limiting quantity also by a factor of about two or three. Therefore, there does not appear to be any urgency in altering the current techniques of controlling exposures to neutron radiation to accommodate the ICRP recommendation, particularly since the ICRP may revise the physical basis for the specification of quality factor in the not too distant future.     

Comparative Operation Risk Assessment for the No. 4 Unit of the Beloyarsk Nuclear Power Plant with a BN-800 Reactor

A quantitative assessment is made of the collective cancer risk for the population in Sverdlovsk oblast due to exposure to radiation during the 30-yr period of normal operation of the No. 4 unit in the Beloyarsk nuclear power plant with a BN-800 reactor and for possible accidents. The estimates are made using the linear zero-threshold concept based on ICRP Publication No. 60.The values obtained are compared with the different forms of cancer risk characteristic for Sverdlovsk oblast (due to radiation and chemical contamination of atmospheric air and drinking water) and the morbidity and mortality risk predominantly due to socioeconomic factors. It is shown that the socioeconomic risk factors determine most cases of death from unnatural causes. Against this background, the health risk due to contamination of the environment by natural radionuclides and chemical carcinogens is negligibly small.The desirability of introducing into domestic practice the health risk assessment methodology developed by the US Environmental Protection Agency is discussed in light of the results obtained.     

Radiation and your patient: a guide for medical practitioners

This didactic text is devoted to the protection of patients against unnecessary exposure to ionising radiation. It is organised in a questions-and-answers format. There are obvious benefits to health from medical uses of radiation, in x-ray diagnostics, interventional radiology, nuclear medicine, and radiotherapy. However, there are well-established risks from high doses of radiation (radiotherapy, interventional radiology), particularly if improperly applied, and possible deleterious effects from small radiation doses (such as those used in diagnostics). Appropriate use of large doses in radiotherapy prevents serious harm, but even low doses carry a risk that cannot be eliminated entirely. Diagnostic use of radiation requires therefore such methodology that would secure high diagnostic gains while minimising the possible harm. For assessment of the risk, a quantitative measure of exposure is a necessary prerequisite. Therefore, dosimetric quantities are explained and defined (absorbed dose, effective dose). Basic facts are presented on mechanisms of action of ionising radiations on living matter. Undesired deleterious effects in man are categorised into two categories. The first one comprises sequelae resulting from massive cell killing (the so-called deterministic effects), requiring a high dose for their manifestation (exceeding the threshold dose). The second category includes those effects originating from mutational changes in the cellular DNA. These may eventually lead to development of radiation-induced cancer and to hereditary changes, transmitted to descendants of exposed individuals after irradiation of their gonads. Data on the magnitude of threshold doses for cell killing effects are presented. On the basis of experimental, clinical, and epidemiological evidence, assessment is also given of the probability with which cancers and hereditary mutations may be induced by doses of various magnitudes, most likely without a threshold dose (below which no effect would obtain). The text provides ample information on opportunities to minimise doses, and therefore the risk from diagnostic uses of radiation. This objective may be reached by avoiding unnecessary (unjustified) examinations, and by optimising the procedures applied both from the standpoint of diagnostic quality and in terms of reduction of the excessive doses to patients. Optimisation of patient protection in radiotherapy must depend on maintaining sufficiently high doses to irradiated tumours, securing a high cure rate, while protecting the healthy tissues to the largest extent possible. Problems related to special protection of the embryo and fetus in the course of diagnostic and therapeutic uses of radiation are presented and practical solutions are recommended. This issue of the Annals of the ICRP also includes a brief report concerning Diagnostic Reference Levels in medical imaging: Review and additional advice.     

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.     

ICRP94年人类呼吸道模型介绍

本文简要介绍了国际放射防护委员会（ＩＣＲＰ）１９９４年发表的用于辐射防护目的的人类呼吸道模型，与ＩＣＲＰ以往的模型进行了比较，还讨论了ＩＣＲＰ９４年人类呼吸道模型在实际中的应用。     

A framework for assessing the impact of ionising radiation on non-human species. ICRP Publication 91

In its 1990 Recommendations, the ICRP indicated that it believed that the standards of environmental control needed to protect man to the degree currently thought desirable would ensure that other species are not put at risk. The ICRP considers that its system of radiological protection has provided a fairly good indirect protection of the human habitat. However, no internationally agreed criteria or policies explicitly address protection of the environment from ionising radiation, and it is difficult to determine or demonstrate whether or not the environment is adequately protected from potential impacts of radiation under different circumstances. The present report suggests a framework, based on scientific and ethical-philosophical principles, by which a policy for the protection of non-human species could be achieved. The primary purpose of developing such a framework is to fill a conceptual gap in radiological protection; it does not reflect any particular concern over environmental radiation hazards. The proposed framework is designed to harmonise with the ICRP's approach to the protection of human beings, but does not intend to set regulatory standards. Instead, the proposed framework is intended to be a practical tool to provide high-level advice and guidance for regulators and operators. An agreed set of quantities and units, a set of reference dose models, reference dose-per-unit-intake (or unit exposure), and reference fauna and flora are required to serve as a basis for the more fundamental understanding and interpretation of the relationships between exposure and dose and between dose and certain categories of effect, for a few, clearly defined types of animals and plants. As a first step, a small set of reference fauna and flora with supporting databases will be developed by the ICRP. Others can then develop more area- and situation-specific approaches to assess and manage risks to non-human species.     

ICRP Publication 115. Lung cancer risk from radon and progeny and statement on radon

Recent epidemiological studies of the association between lung cancer and exposure to radon and its decay products are reviewed. Particular emphasis is given to pooled case-control studies of residential exposures, and to cohorts of underground miners exposed to relatively low levels of radon. The residential and miner epidemiological studies provide consistent estimates of the risk of lung cancer, with significant associations observed at average annual concentrations of approximately 200 Bq/m3 and cumulative occupational levels of approximately 50 working level months (WLM), respectively. Based on recent results from combined analyses of epidemiological studies of miners, a lifetime excess absolute risk of 5 × 10?? per WLM [14 × 10?? per (mJh/m3)] should now be used as the nominal probability coefficient for radon- and radon-progeny-induced lung cancer, replacing the previous Publication 65 (ICRP, 1993) value of 2.8 × 10?? per WLM [8 × 10?? per (mJh/m3)]. Current knowledge of radon-associated risks for organs other than the lungs does not justify the selection of a detriment coefficient different from the fatality coefficient for radon-induced lung cancer. Publication 65 (ICRP, 2003) recommended that doses from radon and its progeny should be calculated using a dose conversion convention based on epidemiological data. It is now concluded that radon and its progeny should be treated in the same way as other radionuclides within the ICRP system of protection; that is, doses from radon and its progeny should be calculated using ICRP biokinetic and dosimetric models. ICRP will provide dose coefficients per unit exposure to radon and its progeny for different reference conditions of domestic and occupational exposure, with specified equilibrium factors and aerosol characteristics.     

Radiation safety aspects of brachytherapy for prostate cancer using permanently implanted sources. A report of ICRP Publication 98

The use of permanent radioactive implants (125I or 103Pd seeds) to treat selected localised prostate cancer patients has been increasing rapidly all over the world for the last 15 years. It is estimated that more than 50,000 patients are treated this way every year in the world, and this number is anticipated to increase in the near future. Although no accidents or adverse effects involving medical staff and/or members of the patient's family have been reported to date, this brachytherapy technique raises a number of radiation safety issues that need specific recommendations from the ICRP. All data concerning the dose received by people approaching patients after implantation have been reviewed. Those doses have been either been measured directly or calculated. The available data show that, in the vast majority of cases, the dose to comforters and carers remains well below the recommended limit of 1 mSv/year. Only the (rare) case where the patient's partner is pregnant at the time of implantation may need specific precautions. Expulsion of sources through urine, semen, or the gastro-intestinal tract is rare. Specific recommendations should be given to patients to allow them to deal adequately with this event. Of note, due to the low activity of an isolated seed and its low photon energy, no incident/accident linked to seed loss has ever been recorded. When performed in the first few months after implantation, cremation of bodies (frequent in some countries) raises several issues related to: (1) the activity that remains in the patient's ashes; and (2) the airborne dose, potentially inhaled by crematorium staff or members of the public. Review of available data shows that cremation can be allowed if 12 months have elapsed since implantation with 125I (3 months for 103Pd). If the patient dies before this delay has elapsed, specific measures must be undertaken. Specific recommendations have to be given to the patient to warn his surgeon in case of subsequent pelvic or abdominal surgery. A 'wallet card' with all relevant information about the implant is useful. In most cases, brachytherapy does make the patient infertile. However, although the therapy-related modifications of the semen reduce fertility, patients must be aware of the possibility of fathering children after such a permanent implantation, with a limited risk of genetic effects for the child. Patients with permanent implants must be aware of the possibility of triggering certain types of security radiation monitors. The 'wallet card' including the main information about the implant (see above) may prove to be helpful in such a case. Considering the available experience after brachytherapy and external irradiation of prostate cancer, the risk of radio-induced secondary tumours appears to be extremely low. The demonstrated benefit of brachytherapy clearly outweighs, by far, the very limited (mainly theoretical)increase in the radiation-induced cancer risk.     

非人类物种的辐射生物效应及其评价

简要介绍了非人类物种的辐射生物效应,并将其与人类的生物效应进行了比较。根据ICRP的有关出版物和其他资料,对防护人类和非人类物种的共同方法、已选定的参考动植物和参考剂量模式作了概要论述。     

Estimating internal dose coefficients of short-lived radionuclides in accordance with ICRP 2007 recommendations

For radiation protection in high-energy accelerator facilities, internal dose coefficients of short-lived radionuclides were estimated using the dosimetric methodology in accordance with the International Commission on Radiological Protection (ICRP) 2007 Recommendations. A computational program was developed for estimating the dose coefficients. The program was verified by confirming whether it could reproduce the dose coefficients provided by ICRP for intakes of representative radionuclides. In addition, the estimated dose coefficients of short-lived radionuclides were compared to the values generated by Dose and risk CALculation software (DCAL), which is based on a dosimetric methodology that is in accordance with the ICRP 1990 Recommendations, to discuss the reasons why the dose coefficients were changed by the revision of the dosimetric methodologies. The comparison revealed a decreasing trend of dose coefficients in the case of inhalation upon revision of the dosimetric methodologies. By contrast, in the case of ingestion, the dose coefficients tended to increase.     

Human alimentary tract model for radiological protection. ICRP Publication 100. A report of The International Commission on Radiological Protection

In this report, the ICRP provides a new biokinetic and dosimetric model of the human alimentary tract to replace the Publication 30 (ICRP, 1979) model. The new human alimentary tract model (HATM) will be used together with the human respiratory tract model (HRTM; ICRP, 1994a,b) in future ICRP publications on doses from ingested and inhaled radionuclides. The HATM is applicable to all situations of radionuclide intake by children and adults. It provides age-dependent parameter values for the dimensions of the alimentary tract regions, and associated transit times for the movement of materials through these regions. For adults, gender-dependent parameter values are given for dimensions and transit times. The default assumption is that radionuclide absorption takes place in the small intestine, but the model allows for absorption in other regions and for retention in or on tissues within the alimentary tract when information is available. Doses are calculated to target cells for cancer induction in the oral cavity, oesophagus, stomach, small intestine, and colon. This report provides reviews of information on the transit of materials through the alimentary tract and on radionuclide retention and absorption. It considers data on health effects, principally in order to specify the target cells for cancer induction within the mucosal lining of the tract and to justify approaches taken to dose averaging within regions. Comparisons are made between doses calculated using the HATM and the Publication 30 model for examples of radionuclide ingestion for which absorption is assumed to occur in the small intestine alone. Examples are also given of the effects on doses of considering absorption from other regions and the effect of possible retention in the alimentary tract. This report also considers uncertainties in model assumptions and their effect on doses, including alimentary tract dimensions, transit times, radionuclide absorption values, and the location of targets for cancer induction.     

外照射情况下有效剂量（E）与有效剂量当量（HE）的比较

ＩＣＲＰ第６０号出版物引入了对外照射辐射剂量学的几个重大变化,６０号出版物推荐的辐射加权方法和基本防护量的技术规格与２６号出版的推荐有很大的不同,本文依据ＩＣＲＰ第７４号出版物给出的数据和讨论,对在各种照射几何条件下对不同能量的光子,中子及电子辐射场计算的有效剂量（Ｅ）与有效剂量当量（ＨＥ）的数值差别作了评述。     

空间质子辐射有效剂量测量的闪烁探测器理论设计

有效剂量可解决航天员在空间飞行中所受质子辐射的危害比较与评价问题,在空间辐射危害评价中具有重要应用。为实现空间质子辐射有效剂量监测,针对空间各向同性质子辐射,利用蒙特卡罗程序设计了一种闪烁探测器。通过对探测器结构的特殊设计,在20-400 Me V能量范围内,各向同性质子在该探测器内沉积的能量与国际辐射防护委员会(International Commission on Radiological Protection,ICRP)116号报告提供的质子有效剂量基本成正比。通过探测质子沉积能量来监测质子辐射有效剂量,克服了直接测量有效剂量所存在的困难。对AP8MIN模型地球俘获带质子能谱与随机抽样质子辐射能谱,经数值计算,探测器给出的有效剂量与ICRP116号报告给出的有效剂量的相对偏差均小于±8%。     

Annals of the ICRP. A report of: doses to infants from ingestion of radionuclides in mothers' milk

In the present report, ICRP provides information on radiation doses to the infant due to intakes of radionuclides in maternal milk. As in Publication 88 (ICRP, 2001) on doses to the embryo and fetus following intakes of radionuclides by the mother, intakes by female members of the public and female workers are addressed. Acute and chronic intakes are considered at various times before and during pregnancy as well as during the period of breastfeeding. Dose coefficients per unit intake by the mother (Sv/Bq) are given for the selected radionuclides of the same 31 elements for which age-specific biokinetic models were given in Publications 56, 67, 69, and 71 (ICRP, 1989, 1993, 1995a,b). For these elements, doses were calculated for the most radiologically significant natural or artificial radionuclides that might be released into the environment due to various human activities. Dose coefficients are also given in this report for radionuclides of an additional four elements: sodium, magnesium,phosphorus, and potassium. Relevant human and animal data on elemental and radionuclide transfer to milk are reviewed. The biokinetic models for adults given in earlier ICRP publications are adapted to include transfer to milk. Model predictions of fractional transfer of ingested or inhaled activity to milk are discussed in the report, and the corresponding dose coefficients for the infant are compared with dose coefficients for in utero exposure, as given in Publication 88 (ICRP, 2001). Illustrative information is also given on doses to the female breast from radionuclides in breastmilk, and external doses received by the child from radionuclides retained in the tissues of the mother. For the additional elements considered in this report, but not in Publication 88 (ICRP,2001), information is also given on doses to the embryo and fetus following maternal intakes of radioisotopes during or before pregnancy. A CD-ROM is to be issued giving data that will supplement the information given in this report. In addition to the dose coefficients given here, committed equivalent doses to the various organs and tissues of the offspring will be given. Dose coefficients will also be given for inhalation of a range of aerosol sizes for the selected radionuclides of the elements covered by this report.     

Setting radiation safety standards from a modern perspective

The basic ideas published more than 50 years ago in A. D. Sakharov’s article “Radioactive Carbon from Nuclear Explosions and Zero-Threshold Biological Effects” are examined from the standpoint of the scientific knowledge accumulated up to 1958 in the field of radiobiology and the effect of radiation on the human body at ultralow doses. The present state of radiological risk regulation is examined in the light of the problems which Sakharov touched upon. The need for improving the normative-legal foundation of radiological safety and protection in connection with the publication of new ICRP recommendations and the development of new safety standards started under IAEA aegis is discussed.     

公众成员某些放射性核素的吸入有效剂量系数

本文根据ＩＣＲＰ７１号出版物，给出了３１个元素的７４个放射性核素对公众的吸入有效剂量系数，并对它们的应用进行了简要讨论。这些核素是由于各种人类活动可能释放环境中去的并在环境辐射防护方面有重要意义的核素。     

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