Hanford radiation study III: a cohort study of the cancer risks from radiation to workers at Hanford (1944-77 deaths) by the method of regression models in life-tables.

This paper reports on results from the study initiated by Mancuso into the health risks from low-level radiation in workers engaged in plutonium manufacture at Hanford Works, Washington State, USA, and attempts to answer criticisms of previous reports by an in-depth study. Previous reports have aroused much controversy because the reported risk per unit radiation dose for cancers of radiosensitive tissues was much greater than the risk generally accepted on the basis of other studies and widely used in setting safety levels for exposure to low-level radiation. The method of regression models in life-tables isolates the effect of radiation after statistically controlling for a wide range of possible interfering factors. Like the risk of lung cancer for uranium miners the dose-response relation showed a significant downward curve at about 10 rem. There may, therefore, be better agreement with other studies, conduct at higher doses, than is widely assumed. The findings on cancer latency (of about 25 years) and the effect of exposure age (increasing age increases the risk) are in general agreement with other studies. An unexplained finding is a significantly higher dose for all workers who developed cancers in tissues that are supposed to have low sensitivity to cancer induction by radiation.     

Cancer risk modelling and radiological protection

Statistical models describing how the radiation-related risks of particular types of cancer vary with the doses of radiation received by specific tissues are derived from data gathered in epidemiological studies of exposed groups of people, guided by an incomplete understanding of radiobiological mechanisms gleaned from experimental studies. Cancer risk models have been developed for a dozen or so different types of cancer, and take account of the effect of important risk modifying factors such as age at exposure and time since exposure. Of primary importance in the development of cancer risk models is the experience of the Japanese atomic bomb survivors, but other exposed groups contribute information, including those exposed to radiation from internally deposited radioactive material, such as inhaled radon. Cancer risk models predict that at low doses or low dose rates the excess risk of cancer is directly proportional to the dose of radiation received, with no threshold dose--the linear no threshold (LNT) dose-response model--and the inferred summary estimate of the overall average lifetime excess risk of developing a serious cancer is ～ 5%/Sv. It is these cancer risk models and this inferred nominal risk estimate that provide the technical basis of radiological protection. Although it is difficult to definitively test the LNT model at low doses or low dose rates, because the predicted excess risk is small compared with fluctuations in the baseline risk, evidence exists that a small risk of cancer results from low-level exposure to radiation and that the excess risk is around that predicted by current risk models.     

A method to detect low-level 63Ni activity for estimating fast neutron fluence from the Hiroshima atomic bomb.

The Hiroshima and Nagasaki atomic bombs resulted in the worst reported exposure of radiation to the human body. The data of survivors have provided the basis for the risk estimation for ionizing radiation, and thus are widely used as the basis of radiation safety. In this report we have studied a new method to detect the low-level 63Ni activity in copper samples in order to estimate the fast neutron fluence from the Hiroshima atomic bomb. Only 0.8 x 10(-3) Bq g(-1) of 63Ni is expected to be produced by the atomic bomb in a copper sample with the 63Cu(n, p)63Ni reaction at a distance of 500 m from the hypocenter. Our method has the required level of sensitivity for determination of the fast neutron fluence out to distances of at least 500 m, and perhaps as far as 1,000 m. We have already investigated and collected some bomb-irradiated copper samples for further study.     

Radar commentary: Use of linear no-threshold hypothesis in radiation protection regulation in the United States

Radiation protection recommendations advanced by the International Commission on Radiological Protection and National Council on Radiation Protection and Measurements, and many times adopted into regulations by the United States Nuclear Regulatory Commission, need to be based on scientifically justified assumptions and conclusions. The linear no-threshold model assigns risk to every radiation exposure above zero dose and is the current basis for setting radiation protection standards worldwide. This hypothesis is vigorously challenged by many individuals but just as vigorously defended in spite of the uncertainties surrounding health effects at low dose levels. It is clear that at radiation doses below 100 mSv, the effects, if any, are so low as to be unobservable and perhaps, therefore, unknowable. However, the linear no-threshold hypothesis is used routinely to formulate regulatory dose limits for workers and the general public and to derive stochastic radiogenic risk estimates at low doses. This note will show that while the linear no-threshold hypothesis may play a legitimate role in setting radiation protection standards and operating policies, such as establishing dose limits or as part of an operational "as low as is reasonably achievable" (ALARA) policy, it is inappropriate for use in estimating possible cancer risks associated with low-level radiation exposures. It will also demonstrate that the raising, not lowering, of current regulatory dose limits is more solidly supported by the actual observed data on radiation dose and effects. The authors submit that the misuse of the linear no-threshold model for predicting radiation effects in exposed individuals and populations should be discontinued.     

Multiple myeloma and engine exhausts, fresh wood, and creosote: a case-referent study

The effect of potential risk factors for multiple myeloma was evaluated in a case-referent study encompassing 131 cases and 431 randomized referents, all alive. Information on exposure was obtained with questionnaires mailed to the subjects. An analysis of the material by means of the Miettinen confounder score technique resulted in a few rate ratios significantly exceeding unity--namely, occupational exposure to engine exhausts, creosote, and fresh wood. In view of other studies that suggest ionizing radiation as a risk factor, it was somewhat surprising that low-level gamma radiation from background exposure was less common among the cases than the referents.     

Effects of radiation and chemical exposures on cancer mortality among Rocketdyne workers: a review of three cohort studies

The purpose of the UCLA Rocketdyne Study was to estimate the effects of occupational exposures to low-level ionizing radiation and selected chemicals on cancer mortality among nuclear and aerospace workers who were employed at Rocketdyne/Atomics International between 1950 and 1993. The results of this retrospective cohort study suggest that: (1) exposure to external radiation, especially doses greater than 200 mSv, increased the risk of dying from lymphopoietic cancers, lung cancer, and possibly other solid cancers; (2) exposure to internal radiation increased the risk of dying from lymphopoietic cancers and upper-aerodigestive-tract cancers; and (3) exposure to hydrazine or other chemicals associated with the same jobs at rocket-engine test stands increased the risk of dying from lung cancer and possibly other cancers.     

廊坊市放射工作人员医疗照射频度及受照剂量调查分析

目的 了解廊坊市不同级别医院的各类放射工作人员的医疗照射频度与外照射个人剂量,评估放射工作人员职业健康风险,为放射防护工作提供技术依据。方法 对廊坊市6家不同级别医院2016年全部医疗照射频度、外照射个人剂量开展调查,对调查数据进行统计分析。结果 6家医院中,三级、二级、一级医院放射诊断人员医疗照射人均人次数分别为4 217、3 066、883;三级、二级医院介入放射人员医疗照射人均人次数分别为174、115;一家三级医院的放疗人员医疗照射人均人次数为30;各类放射人员全年有效剂量范围为0.78~1.29 mSv;介入、放射治疗、牙科、放射诊断放射工作人员单次暴露有效剂量分别为0.005 6~0.011、0.038、0.001 3~0.004 2、0.000 27~0.002 3 mSv。结论 从事介入、放射治疗的放射工作人员单次电离辐射暴露的健康损害风险远高于其他放射工作人员;应以介入、放射治疗人员和低级别医院为重点,加强放射防护工作。     

Radiation and mortality of workers at Oak Ridge National Laboratory: positive associations for doses received at older ages.

We examined associations between low-level exposure to ionizing radiation and mortality among 14,095 workers hired at the Oak Ridge National Laboratory between 1943 and 1972. Workers at the facility were individually monitored for external exposure to ionizing radiation and have been followed through 1990 to ascertain cause of death information. Positive associations were observed between low-level exposure to external ionizing radiation and mortality. These associations were larger for doses received after 45 years of age, larger under longer lag assumptions, and primarily due to cancer causes of death. All cancer mortality was estimated to increase 4.98% [standard error (SE) = 1.5] per 10-mSv cumulative dose received after age 45 under a 10-year lag, and 7.31% (SE = 2.2) per 10-mSv cumulative dose received after age 45 under a 20-year lag. Associations between radiation dose and lung cancer were of similar magnitude to associations between radiation dose and all cancers except lung cancer. Nonmalignant respiratory disease exhibited a positive association with cumulative radiation dose received after age 45, whereas ischemic heart disease exhibited no association with radiation dose. These findings suggest increases in cancer mortality associated with low-level external exposure to ionizing radiation and potentially greater sensitivity to the carcinogenic effects of ionizing radiation with older ages at exposure.     

辐射工作者个人受照剂量与淋巴细胞微核的相关研究

目的 分析个人受照剂量对外周血淋巴细胞微核的影响，为采取有效措施，保护放射工作者健康提供科学依据。方法 连续6年对放射工作人员个人受照剂量进行监测，并检验淋巴细胞微核，分析两者相关规律。结果 放射组工作人员淋巴细胞微核细胞率、微核阳性检出率均显著高于对照组。乡镇医院组、工业探伤组显著高于市属医院组、县区医院组。淋巴细胞微核率、微核检出率与放射工龄呈曲线正相关关系（r=0．957，P〈0．01）；与个人年受照剂量呈直线正相关（r=0．996，P〈0．01）；与个人累积受照剂量呈直线正相关（r=0．996，P〈0．01）。结论 低剂量电离辐射对放射工作人员细胞遗传学造成一定损伤，放射防护工作中必须重视减少电离辐射剂量。     

A case-control study of congenital malformations and occupational exposure to low-level ionizing radiation

In a case-control study, the authors investigated the association of parental occupational exposure to low-level external whole-body penetrating ionizing radiation and risk of congenital malformations in their offspring. Cases and controls were ascertained from births in two counties in southeastern Washington State, where the Hanford Site has been a major employer. A unique feature of this study was the linking of quantitative individual measurement of external whole-body penetrating ionizing radiation exposure of employees at the Hanford Site, using personal dosimeters, and the disease outcome, congenital malformations. The study population included 672 malformation cases and 977 matched controls from births occurring from 1957 through 1980. Twelve specific malformation types were analyzed for evidence of association with employment of the parents at Hanford and with occupational exposure to ionizing radiation. Two defects, congenital dislocation of the hip and tracheoesophageal fistula, showed statistically significant associations with employment of the parents at Hanford, but not with parental radiation exposure. Neural tube defects showed a significant association with parental preconception exposure, on the basis of a small number of cases. Eleven other defects, including Down syndrome, for which an association with radiation was considered most likely, showed no evidence of such an association. When all malformations were analyzed as a group, there was no evidence of an association with employment of the parents at Hanford, but the relation of parental exposure to radiation before conception was in the positive direction (one-tailed p value between 0.05 and 0.10). Given the number of statistical tests conducted, some or all of the observed positive correlations are likely to represent false positive findings. In view of strong contradictory evidence, based on no demonstrated effects in genetic studies of atomic bomb survivors in Hiroshima and Nagasaki, it is unlikely that these correlations result from a cause and effect association with parental radiation exposure.     

Evidence on the human health effects of low-level methylmercury exposure

Background: Methylmercury (MeHg) is a known neuro-toxicant. Emerging evidence indicates it may have adverse effects on the neuro-logic and other body systems at common low levels of exposure. Impacts of MeHg exposure could vary by individual susceptibility or be confounded by bene-ficial nutrients in fish containing MeHg. Despite its global relevance, synthesis of the available literature on low-level MeHg exposure has been limited.Objectives: We undertook a synthesis of the current knowledge on the human health effects of low-level MeHg exposure to provide a basis for future research efforts, risk assessment, and exposure remediation policies worldwide.Data sources and extraction: We reviewed the published literature for original human epidemio-logic research articles that reported a direct biomarker of mercury exposure. To focus on high-quality studies and those specifically on low mercury exposure, we excluded case series, as well as studies of populations with unusually high fish consumption (e.g., the Seychelles), marine mammal consumption (e.g., the Faroe Islands, circumpolar, and other indigenous populations), or consumption of highly contaminated fish (e.g., gold-mining regions in the Amazon).Data synthesis: Recent evidence raises the possibility of effects of low-level MeHg exposure on fetal growth among susceptible subgroups and on infant growth in the first 2 years of life. Low-level effects of MeHg on neuro-logic outcomes may differ by age, sex, and timing of exposure. No clear pattern has been observed for cardio-vascular disease (CVD) risk across populations or for specific CVD end points. For the few studies evaluating immunologic effects associated with MeHg, results have been inconsistent.Conclusions: Studies targeted at identifying potential mechanisms of low-level MeHg effects and characterizing individual susceptibility, sexual dimorphism, and non-linearity in dose response would help guide future prevention, policy, and regulatory efforts surrounding MeHg exposure.     

Greater sensitivity to ionizing radiation at older age: follow-up of workers at Oak Ridge National Laboratory through 1990.

BACKGROUND: Workers at Oak Ridge National Laboratory (ORNL) were individually monitored for whole body exposure to ionizing radiation. Studies of these workers may provide valuable information about the long-term effects of occupational exposure to ionizing radiation. Since biological changes occur as adults age, a potentially important question in these investigations is whether sensitivity to the carcinogenic effects of ionizing radiation changes with age at exposure. METHODS: Vital status and cause of death were ascertained through 1990 for 8307 white males hired at ORNL from 1943 through 1972. Associations between whole body ionizing radiation dose and all-cancer mortality were quantified using life table regression methods for time dependent exposures. Analyses focused of differences in radiation-cancer associations with age at exposure. Length of follow-up, period of hire, and age at risk were considered as alternative explanations for effects of age at exposure. RESULTS: Cumulative radiation dose was associated with a 1.8% (SE = 0.9) increase in all-cancer mortality per 10 mSv, assuming a 10-year lag between exposure and mortality. However, radiation doses received at older ages exhibited larger associations with cancer mortality than doses received at younger ages. Doses received after age 45 were associated with a 5.9% (SE = 1.7) increase in cancer mortality per 10 mSv, adjusted for doses received before age 45. Dose-response associations between cancer mortality and doses received after age 45 appeared consistent across periods of follow-up, periods of hire, and ages at risk. CONCLUSIONS: Findings suggest that sensitivity to the carcinogenic effects of ionizing radiation may increase with older ages at exposure. More attention should be given to the role of age at exposure in studies of the health effects of low-level exposure to ionizing radiation, and to efforts to limit exposure to ionizing radiation.     

Genetic susceptibility to radiogenic cancer in humans

The clinical benefits associated with the use of ionizing radiation for diagnostic and therapeutic purposes are well established, particularly in cancer medicine. Unfortunately, it is now clear that prior exposure to radiation is associated with an excess risk of developing malignancy in the exposure field. Indeed, the development of a second primary malignancy is a devastating side effect that can often be attributed to radiotherapy for a first cancer. Research has focused on elucidating the relationship between therapeutic radiation dose and site-specific cancer risk, and how this relationship is affected by host factors such as age, sex, and exposure to other potential carcinogens. By contrast, there is a relative paucity of data on host genetic susceptibility to cancer following cytotoxic and mutagenic radiation exposure. Animal model systems suggest a strong genetic basis underlying susceptibility to radiogenic cancer. In humans, research has focused on investigating loci with relatively rare putative high penetrance risk alleles. However, genetic susceptibility to radiogenic cancer and other late effects of radiation exposure may be determined predominantly by co-inheritance of low penetrance risk alleles, and how these interact with each other (gene-gene interactions), with radiation dose (gene-exposure interactions) and other risk factors.     

低水平辐射对致癌危险的影响研究

本文介绍了BEIR推荐的线性假说——根据高水平辐射效应的数据,线性外推到低水平,作为估计低水平辐射效应的方法,评论了线性假说的各种证据,分析了低水平辐射的癌危险度。同时,阐述了低水平辐射效应的潜伏期、危险持续期,讨论了年龄与辐射剂量及癌症发病的关系。     

An analysis of public-interest group positions on radiation protection

The history of radiation risk management is replete with contentious public debate between public interest groups and the technical community of radiation protection professionals. To promote a deeper understanding of this phenomenon, this paper describes the rationales and values underlying public-interest group positions in one radiation risk domain (low-level waste) and contrasts them with those of the technical community. Public interest group objections to recycling of radioactivity-contaminated materials and to discarding of other low-level wastes are made on fairness, risk assessment, and energy-policy grounds. Concerns about procedural fairness stem from the continuing use of top-down expert-driven, rather than deliberative, systems for low-level waste policy-making. Concerns about distributional fairness arise because the benefits and risks of alterative low-level waste policies accrue to different stakeholders. Risk assessment is faulted for failure to acknowledge hidden subjective assumptions (e.g., on screening vigilance in materials recycling, on integrity of disposal facilities in the far future). Skepticism of technological risk management arises from a history peppered with unexpected untoward events that lay outside the design bases of protection systems. Finally, public interest groups view low-level waste issues as part of a larger debate on wise and legitimate energy policy, and are reluctant to support measures that provide relief to a nuclear industry that, in their view, established itself outside the democratic process.     

Physiology of the hormetic effect

Beneficial (hormetic) effects of ionizing radiation have been largely ignored in developing radiobiological theory, chiefly because a suitable explanatory hypothesis is lacking. Examination of the relevant literature has revealed that food restriction effects in animals resemble those of low-level, low-LET, whole-body ionizing radiation exposure (without food restriction) in two major respects: increased longevity and change in the variance of longevity. These physiological changes can be interpreted as resulting from alteration of the "steady-state" flux of oxygen radicals which affect the endocrine balance. Oxy-radical-producing, low-level ionizing radiation exposure (whole body) is interpreted by the body as excess food intake, thus lowering the appetite and reducing caloric intake which, in turn, increases longevity. The greater variance in longevity accompanying increases in the median age at death with food restriction alters the ratio of long-lived to short-lived descendants and hastens the population's adaptation to semi-permanently diminished rates of food supply. Less variance and earlier mean ages at death result from an increased rate of food supply. Whole-body ionizing radiation exposure results in a mixed response, because it reduces caloric intake while signaling that an increase has occurred.     

Radiation risk in the context of liability for injury.

It is perceived by the man in the street that low-level radiation from a nuclear facility is more dangerous than that from other practices. The radiation protection system, in particular the ALARA principle, leads to concerns that even the smallest exposure to radiation is abnormal and dangerous. Public perception of the radiation risk leads to fear in the minds of the public. A consequence of this fear itself may be damage to health in the form of psychological damage or nervous shock. The paper draws attention to the liability for damages by radiation, in particular under the common law of the UK and US, and how liability, determined by the court, is not necessarily influenced by scientific rationality. A natural conclusion may be that a claimant suffering injury of the type caused by radiation and who had been exposed to radiation, no matter how small a dose, that could be shown to come from a nuclear installation would be awarded damages against the licensee of the site of the installation unless it could be shown that the injury was predominantly caused by another source (radioactive or otherwise).     

基于生物监测指标评估的低浓度苯暴露职业健康风险

目的通过流行病学调查资料和苯接触生物标志物的检测资料,初步建立基于生物监测指标的低浓度苯暴露致癌风险评价方法。方法根据苯的流行病学调查资料,基于多阶模型推导出低浓度苯职业暴露下的致癌风险模型。利用贝叶斯线性回归和马尔科夫链蒙特卡洛方法,采用R语言、JARG软件包和水晶球软件建立苯空气浓度与苯代谢物浓度函数关系并进行不确定性分析,并利用尿中苯巯基尿酸(S-phenylmercapturic acid,S-PMA)和反-反式黏糠酸(trans,trans-muconic acid,tt-MA)的浓度预测苯的致癌风险。结果考虑适用低浓度苯暴露的情况,建立了二项式的多阶模型用于表征致癌风险。基于建立的致癌风险模型,我国现行的职业接触限值[空气中苯的时间加权平均容许浓度6 mg/m^(3),工作班后尿S-PMA浓度100μg/g(以Cr校正),班后尿tt-MA浓度3.0 mg/g(以Cr校正)]下的致癌风险分别为5.64×10^(-4)、2.31×10^(-4)、1.52×10^(-4),均高于美国环境保护署(EPA)和疾病预防控制中心(CDC)提出的职业人群致癌风险可接受水平(10^(-4))。结论利用苯的代谢产物预测致癌风险,显示在空气中苯浓度低于职业接触限值的情况下,苯的致癌影响仍然存在。需要采取工程控制及个体防护等措施,尽可能降低苯的致癌风险。目前我国苯职业接触限值存在尽可能降低的必要性。     

The promise of molecular epidemiology in defining the association between radiation and cancer

Molecular epidemiology involves the inclusion in epidemiologic studies of biologic measurements made at a genetic and molecular level and aims to improve the current knowledge of disease etiology and risk. One of the goals of molecular epidemiology studies of cancer is to determine the role of environmental and genetic factors in initiation and progression of malignancies and to use this knowledge to develop preventive strategies. This approach promises extraordinary opportunities for revolutionizing the practice of medicine and reducing risk. However, this will be accompanied by the need to address and resolve many challenges, such as ensuring the appropriate interpretation of molecular testing and resolving associated ethical, legal, and social issues. Traditional epidemiologic approaches determined that exposure to ionizing radiation poses significantly increased risk of leukemia and several other types of cancer. Such studies provided the basis for setting exposure standards to protect the public and the workforce from potentially adverse effects of ionizing radiation. These standards were set by using modeling approaches to extrapolate from the biological effects observed in high-dose radiation studies to predicted, but mostly unmeasurable, effects at low radiation doses. It is anticipated that the addition of the molecular parameters to the population-based studies will help identify the genes and pathways characteristic of cancers due to radiation exposure of individuals, as well as identify susceptible or resistant subpopulations. In turn, the information about the molecular mechanisms should aid to improve risk assessment. While studies on radiogenic cancers are currently limited to only a few candidate genes, the exponential growth of scientific knowledge and technology promises expansion of knowledge about identity of participating genes and pathways in the future. This article is meant to provide an introductory overview of recent advances in understanding of carcinogenesis at the molecular level, with an emphasis of the aspects that may be of use in establishing the association between radiation and cancer.     

用热释光剂量计测定计算机视频终端的电离辐射剂量

目的:测定计算机视频终端的X射线剂量水平。方法:采用高灵敏LiF(Mg,Cu,P)热释光剂量计对计算机视频终端表面及其附加防护屏(网)后的辐射剂量进行累积剂量监测。结果:计算机视频终端表面的平均照射量率为2.40×10^-7C·kg^-1/d(0.93mR/d),在防护屏(网)外的平均照射量率是0.62×10^-7C·kg^-1/d(0.24mR/d)。结论:监测结果表明,计算机产生的低能和低水平电离辐射剂量未超过有关规定标准。