Basis For Radiation Protection Standards Research Articles

Low-level radon exposure and lung cancer in the Pooled Uranium Miners Analysis (PUMA)

BACKGROUND AND AIM: Radon, a ubiquitous gas, and its progeny are a leading environmental and occupational cause of lung cancer. To better inform radiation protection standards by estimating risk, we assembled an international cohort study of workers employed in uranium mining in Canada, the Czech Republic, France, Germany, and the United States. METHODS: We focus on miners employed during the more contemporary period of the uranium mining industry when radon exposures tended to be comparatively low, and individual exposure data are available. A cohort of 56,614 male uranium miners first employed in 1960 or later was assembled and followed to ascertain causes of death. Estimates of excess relative rate (ERR) per working level month (WLM) of cumulative radon progeny exposure for mortality from lung cancer were derived by internal Poisson regression. RESULTS:In the follow-up period a total of 1217 lung cancer deaths occurred, accumulating 1.9 million person-years at risk. The relative rate of lung cancer increased in a linear fashion with cumulative exposure to radon progeny, lagged 5 years (ERR/100 WLM=1.34; 95% CI: 0.89, 1.89). Attained age was a clear modifier of this association, showing a decrease in ERR/WLM with increasing attained age. Further potential modifiers are age at exposure or time since exposure and exposure rate. CONCLUSIONS:PUMA provides the most precise and informative estimates to-date of the association between low-level exposure to radon progeny and lung cancer mortality. The results strengthen the basis for radiation protection standards for radon and its progeny. KEYWORDS: Ionizing radiation, Occupational exposures, Risk assessment,International collaboration

Estimates of Radiation Effects on Cancer Risks in the Mayak Worker, Techa River and Atomic Bomb Survivor Studies.

For almost 50 y, the Life Span Study cohort of atomic bomb survivor studies has been the primary source of the quantitative estimates of cancer and non-cancer risks that form the basis of international radiation protection standards. However, the long-term follow-up and extensive individual dose reconstruction for the Russian Mayak worker cohort (MWC) and Techa River cohort (TRC) are providing quantitative information about radiation effects on cancer risks that complement the atomic bomb survivor-based risk estimates. The MWC, which includes ~26 000 men and women who began working at Mayak between 1948 and 1982, is the primary source for estimates of the effects of plutonium on cancer risks and also provides information on the effects of low-dose rate external gamma exposures. The TRC consists of ~30 000 men and women of all ages who received low-dose-rate, low-dose exposures as a consequence of Mayak's release of radioactive material into the Techa River. The TRC data are of interest because the exposures are broadly similar to those experienced by populations exposed as a consequence of nuclear accidents such as Chernobyl. In this presentation, it is described the strengths and limitations of these three cohorts, outline and compare recent solid cancer and leukemia risk estimates and discussed why information from the Mayak and Techa River studies might play a role in the development and refinement of the radiation risk estimates that form the basis for radiation protection standards.

TH‐A‐BRD‐01: Radiation Biology for Radiation Therapy Physicists

Mechanisms by which radiation kills cells and ways cell damage can be repaired will be reviewed. The radiobiological parameters of dose, fractionation, delivery time, dose rate, and LET will be discussed. The linear‐quadratic model for cell survival for high and low dose rate treatments and the effect of repopulation will be presented and discussed. The rationale for various radiotherapy techniques such as conventional fractionation, hyperfractionation, hypofractionation, and low and high dose rate brachytherapy, including permanent implants, will be presented.The radiobiological principles underlying radiation protection guidelines and the different radiation dosimetry terms used in radiation biology and in radiation protection will be reviewed. Human data on radiation induced cancer, including increases in the risk of second cancers following radiation therapy, as well as data on radiation induced tissue reactions, such as cardiovascular effects, for follow up times up to 20–40 years, published by ICRP, NCRP and BEIR Committees, will be examined. The latest risk estimates per unit dose will be presented. Their adoption in recent radiation protection standards and guidelines and their impact on patient and workers safety in radiotherapy will be discussed.Biologically‐guided radiotherapy (BGRT) provides a systematic method to derive prescription doses that integrate patient‐specific information about tumor and normal tissue biology. Treatment individualization based on patient‐specific biology requires the identification of biological objective functions to facilitate the design and comparison of competing treatment modalities. Biological objectives provide a more direct approach to plan optimization instead of relying solely on dose‐based surrogates and can incorporate factors that alter radiation response, such as DNA repair, tumor hypoxia, and relative biological effectiveness. We review concepts motivating biological objectives and provide examples of how they might be used to address clinically relevant problems. Underlying assumptions and limitations of existing models and their proper application will be discussed.This multidisciplinary educational session combines the fundamentals of radiobiology for radiation therapy and radiation protection with the practical application of biophysical models for treatment planning and evaluation.Learning Objectives: To understand fractionation in teletherapy and dose rate techniques in brachytherapy. To understand how the linear‐quadratic models the effect of radiobiological parameters for radiotherapy. To understand the radiobiological basis of radiation protection standards applied to radiotherapy. To distinguish between stochastic effects and tissue reactions. To learn how to apply concepts of biological effective dose and RBE‐weighted dose and to incorporate biological factors that alter radiation response. To discuss clinical strategies to increase therapeutic ratio, i.e., maximize local control while minimizing the risk of acute and late normal tissue effects.

A reanalysis of cancer mortality in Canadian nuclear workers (1956–1994) based on revised exposure and cohort data

Background:A 15-country study of nuclear workers reported significantly increased radiation-related risks of all cancers excluding leukaemia, with Canadian data a major factor behind the pooled results. We analysed mortality (1956–1994) in the updated Canadian cohort and provided revised risk estimates.Methods:Employment records were searched to verify and revise exposure data and to restore missing socioeconomic status. Excess relative risks per sievert (ERR/Sv) of recorded radiation dose and 95% confidence intervals (CIs) were estimated using Poisson regression.Results:A significant heterogeneity of the dose–response for solid cancer was identified (P=0.02), with 3088 early (1956–1964) Atomic Energy of Canada Limited (AECL) workers having a significant increase (ERR/Sv=7.87, 95% CI: 1.88, 19.5), and no evidence of radiation risk for 42 228 workers employed by three nuclear power plant companies and post-1964 AECL (ERR/Sv=−1.20, 95% CI: <−1.47, 2.39). Radiation risks of leukaemia were negative in early AECL workers and non-significantly increased in other workers. In analyses with separate terms for tritium and gamma doses, there was no evidence of increased risk from tritium exposure. All workers had mortality lower than the general population.Conclusion:Significantly increased risks for early AECL workers are most likely due to incomplete transfer of AECL dose records to the National Dose Registry. Analyses of the remainder of the Canadian nuclear workers (93.2%) provided no evidence of increased risk, but the risk estimate was compatible with estimates that form the basis of radiation protection standards. Study findings suggest that the revised Canadian cohort, with the exclusion of early AECL workers, would likely have an important effect on the 15-country pooled risk estimate of radiation-related risks of all cancer excluding leukaemia by substantially reducing the size of the point estimate and its significance.

TH‐E‐213AB‐01: Review of Radiobiological Principles of Radiotherapy and Radiation Protection

Mechanisms by which radiation kills cells and ways cell damage can be repaired will be reviewed. The effect of radiobiological parameters which we can control for radiotherapy will be discussed including dose/fraction, number of fractions, time between fractions, overall treatment time, and the LET of the radiation. Reasons why we fractionate the way we do will be discussed, along with how sparing of normal tissues using conformal techniques might affect optimal fractionation. The linear‐quadratic model for cell survival for high and low dose rate treatments and the effect of repopulation will be presented and discussed. Radiation protection and the dose response of normal tissues will be reviewed, including effects on the developing embryo/fetus. The concepts of equivalent dose and effective dose in medical radiation protection, the Sv unit, and radiation and tissue‐weighting factors will be presented. The latest information on human data on radiation‐induced cancer, genetic effects and harmful tissue effects, especially cerebrovascular and cardiovascular diseases as well as cataract formation, published by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR), the Biological Effects of Ionizing Radiation (BEIR) Committee and the International Commission on Radiological Protection (ICRP) will be examined. Estimates of risk per unit exposure will be presented. Their use in the development of radiation protection guidelines and standards will be discussed.Learning Objectives1. To understand the radiobiological basis of radiation protection standards.2. To define the radiation protection magnitudes and units, their values and their practical measurement.3. To distinguish between stochastic and deterministic effects.

TH-A-BRA-02: Review of the Radiobiological Principles of Radiotherapy and Radiation Protection

The radiobiological principles underlying radiation protection guidelines will be reviewed, analyzing the published results of the effects of ionizing radiation at the cellular level, in animal experiments and, especially,in epidemiological studies. Human data on radiation induced cancer and genetic effects published by the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) and the Biological Effects of Ionizing Radiation (BEIR) Committee,with their latest estimates of risk per unit dose, will be presented. The dose response of normal tissues will be discussed, including effects on the developing embryo and fetus. The recent draft of the International Commission on Radiological Protection (ICRP) on Early and late effects of radiation in normal tissues and organs: threshold doses for tissue reactions and other non‐cancer effects of radiation in a radiation protectioncontext,which includes follow up times much longer than those common in radiotherapy (up to 20 to 40 versus 5 to 10 years) for some tissues, will be introduced. In particular, the current information on acute and chronic radiation syndromes, as well as the newly proposed threshold doseof 0.5 Gy for cataract induction and cardiovascular effects, will be examined. The impact of these newly proposed threshold values on the development of radiation protection guidelines and standards, especially in the forthcoming International Basic Safety Standards on Protection against Ionizing Radiation and for the Safety of RadiationSources(BSS),will be evaluated. The units and their values used in radiation protection, and the operational units used for measurements, will be presented. The concepts of equivalent dose vs dose equivalent as well as the term effective dose, the Sv unit, and the radiation and tissue weighting factors will be explained and illustrated. Learning Objectives: 1. To understand the radiobiological basis of radiation protection standards. 2. To distinguish between stochastic and deterministic effects. 3. To define the radiation protection magnitudes and units, their values and their practical measurement.

LAURISTON S. TAYLOR LECTURE: RADIATION EPIDEMIOLOGY—THE GOLDEN AGE AND FUTURE CHALLENGES

Epidemiology is the study of the distribution and causes of disease in humans. Studies of human populations exposed to ionizing radiation have been conducted for nearly 100 y during the "Golden Age of Radiation Epidemiology." Radiation epidemiology is now so sophisticated that human studies are the basis for radiation protection standards and for compensation schemes in response to claims of ill health from prior exposures. The studies of exposed human populations are very broad and include not only the Japanese atomic bomb survivors, but also patients given radiotherapy for cancer, patients treated with radiation for nonmalignant disease, patients given diagnostic radiation, persons with intakes of radionuclides, workers exposed to occupational radiation, and communities exposed to environmental sources of radiation. But there is more to be learned, and future knowledge may be advanced from new and continued occupational studies of the early radiation workers, atomic veterans, medically exposed patients, and populations living in areas of high natural background radiation. The interaction between radiation and underlying genetic susceptibilities is an important emerging area of research. It is indeed an honor to be included among the Lauriston S. Taylor Lecturers.

TH-B-I-611-02: The Science Behind The ICRP 2005 Recommendations: Biological and Epidemiological Information

The ICRP 2005 Recommendations are stated to be “based on a simple, but widely applicable, general system of protection that will clarify its objectives and will provide a basis for the more formal systems needed by operating managements and regulators”. Underlying each of the broad areas of recommendation is a series of Foundation Documents that provide details of the most recent and/or appropriate scientific research in support of the recommendations. This presentation will focus on the approaches for quantitating health effects attributable to radiation exposure and the biological mechanisms that underlie these effects. The adverse health effects are grouped as (1) tissue reactions (2) cancer development in exposed individuals and heritable disease in their offspring. For considerations of tissue injury, ICRP has conducted a comprehensive review of experimental and epidemiological studies to revisit current estimates of thresholds for tissue reactions (deterministic effects) and consider revising these. For hereditary risks, ICRP has significantly modified its approach by using spontaneous human mutation rates in conjunction with radiation‐induced mutation rates from mouse studies. In addition, hereditary risks are considered up to the second generation only. The overall result is a reduction in the genetic risk that will tend to reduce the value of tissue weighting factor for gonads. New epidemiological data on cancer mortality and incidence have been considered by ICRP and the broad conclusion is that the linear no threshold model remains as the best overall fit to the data. An important component of such a conclusion is that extensive data on cancer incidence are available from the A‐bomb Life Span Study (LSS); these provide more accurate diagnosis and take account of relatively high prevalence but low mortality tumors. In addition, models were developed to facilitate transport of risk across populations, particularly based on data from the LSS population. The risk models also incorporated the concept of quality of life detriment, which is a departure from the detriment based on mortality alone. The recent data that impacted the value of DDREF were reviewed, but it was concluded that the current value of 2 was compatible with both human and laboratory animal data. A review of data for the production of non‐cancer diseases after radiation was conducted, particularly for the LSS. While it is clear that there is an increase in several such diseases, the data available are not sufficient for their inclusion in the estimation of detriment at doses in the range of a few tens of mSv. Some of these judgments will be considered in greater detail during the presentation. Educational Objectives: 1. To understand the biological data that for the basis for radiation risk assessments. 2. To understand how new data have necessitated a reconsideration of the basis for radiation protection standards. This abstract has been reviewed in accordance with EPA guidelines but it does not necessarily reflect EPA policy.

Accounting for errors in dose estimates used in studies of workers exposed to external radiation.

This paper discusses approaches for accounting for errors in dose estimates used in dose-response analyses of data from epidemiologic studies of workers exposed to external radiation and illustrates these approaches with analyses of data on workers at the Hanford site. In these analyses, estimates of the excess relative risk are corrected for bias in recorded doses as estimates of organ dose, and confidence intervals reflect uncertainty in the correction factors. For the Hanford data, these procedures did not greatly modify results for all cancer excluding leukemia, but the upper confidence limit for leukemia was increased by about 40%, a difference that is of some importance in comparing worker-based estimates and confidence intervals with estimates that serve as the basis of radiation protection standards. It is argued that aside from taking account of uncertainty in correction factors, no additional corrections are needed to address random errors resulting from variation in exposure energies and geometries. In addition, it is shown that because the larger cumulative doses, which are most influential in dose-response analyses, are the sums of large numbers of independent dosimeter readings, random errors resulting from variation in laboratory measurements are unlikely to be important for epidemiologic purposes. It is hoped that the approaches illustrated in this paper will be applied to future analyses of data from worker studies, especially combined analyses of data from several countries. Taking account of uncertainty in factors that correct for systematic bias will be especially important as uncertainty resulting from sampling variation decreases.