Dose And Dose-rate Effectiveness Factor Research Articles

Molecular and cellular basis of the dose-rate-dependent adverse effects of radiation exposure in animal models. Part II: Hematopoietic system, lung and liver.

While epidemiological data have greatly contributed to the estimation of the dose and dose-rate effectiveness factor (DDREF) for human populations, studies using animal models have made significant contributions to provide quantitative data with mechanistic insights. The current article aims at compiling the animal studies, specific to rodents, with reference to the dose-rate effects of cancer development. This review focuses specifically on the results that explain the biological mechanisms underlying dose-rate effects and their potential involvement in radiation-induced carcinogenic processes. Since the adverse outcome pathway (AOP) concept together with the key events holds promise for improving the estimation of radiation risk at low doses and low dose-rates, the review intends to scrutinize dose-rate dependency of the key events in animal models and to consider novel key events involved in the dose-rate effects, which enables identification of important underlying mechanisms for linking animal experimental and human epidemiological studies in a unified manner.

Low-Dose Extrapolation Factors Implied by Mortality and Incidence Data from the Japanese Atomic Bomb Survivor Life Span Study Data.

Assessment of the effect of low dose and low-dose-rate exposure depends critically on extrapolation from groups exposed at high dose and high-dose rates such as the Japanese atomic bomb survivor data, and has often been achieved via application of a dose and dose-rate effectiveness factor (DDREF). An important component of DDREF is the factor determining the effect of extrapolation of dose, the so-called low-dose extrapolation factor (LDEF). To assess LDEF models linear (or linear quadratic) in dose are often fitted. In this report LDEF is assessed via fitting relative rate models that are linear or linear quadratic in dose to the latest Japanese atomic bomb survivor data on solid cancer, leukemia and circulatory disease mortality (followed from 1950 through 2003) and to data on solid cancer, lung cancer and urinary tract cancer incidence. The uncertainties in LDEF are assessed using parametric bootstrap techniques. Analysis is restricted to survivors with <3 Gy dose. There is modest evidence for upward curvature in dose response in the mortality data. For leukemia and for all solid cancer excluding lung, stomach and breast cancer there is significant curvature (P < 0.05). There is no evidence of curvature for circulatory disease (P > 0.5). The estimate of LDEF for all solid cancer mortality is 1.273 [95% confidence intervals (CI) 0.913, 2.182], for all solid cancer mortality excluding lung cancer, stomach cancer and breast cancer is 2.183 (95% CI 1.090, >100) and for leukemia mortality is 11.447 (95% CI 2.390, >100). For stomach cancer mortality LDEF is modestly raised, 1.077 (95% CI 0.526, >100), while for lung cancer, female breast cancer and circulatory disease mortality the LDEF does not much exceed 1. LDEF for solid cancer incidence is 1.186 (95% CI 0.942, 1.626) and for urinary tract cancer is 1.298 (95% CI <0, 7.723), although for lung cancer LDEF is not elevated, 0.842 (95% CI 0.344, >100).

Radiation cancer risk at different dose rates: new dose-rate effectiveness factors derived from revised A-bomb radiation dosimetry data and non-tumor doses.

The dose rate of atomic bomb (A-bomb) radiation to the survivors has still remained unclear, although the dose–response data of A-bomb cancers has been taken as a standard in estimating the cancer risk of radiation and the dose and dose-rate effectiveness factor (DDREF). Since the applicability of the currently used DDREF of 2 derived from A-bomb data is limited in a narrow dose-rate range, 0.25-75 Gy/min as estimated from analysis of DS86 dosimetry data in the present study, a non-tumor dose (Dnt) was applied in an attempt to gain a more universal dose-rate effectiveness factor (DREF), where Dnt is an empirical parameter defined as the highest dose at which no statistically significant tumor increase is observed above the control level and its magnitude depends on the dose rate. The new DREF values were expressed as a function of the dose rate at four exposure categories, i.e. partial body low LET, whole body low linear energy transfer (LET), partial body high LET and whole body high LET and provided a value of 14 for environmental level radiation at a dose rate of 10−9 Gy/min for whole body low LET.

Conclusions and Suggestions on Low-Dose and Low-Dose Rate Radiation Risk Estimation Methodology

Background: For radiological protection and control, the International Commission on Radiological Protection (ICRP) provides the nominal risk coefficients related to radiation exposure, which can be extrapolated using the excess relative risk and excess absolute risk obtained from the Life Span Study of atomic bomb survivors in Hiroshima and Nagasaki with the dose and dose-rate effectiveness factor (DDREF). Materials and Methods: Since it is impossible to directly estimate the radiation risk at doses less than approximately 100 mSv only from epidemiological knowledge and data, support from radiation biology is absolutely imperative, and thus, several national and international bodies have advocated the importance of bridging knowledge between biology and epidemiology. Because of the accident at the Tokyo Electric Power Company (TEPCO)’s Fukushima Daiichi Nuclear Power Station in 2011, the exposure of the public to radiation has become a major concern and it was considered that the estimation of radiation risk should be more realistic to cope with the prevailing radiation exposure situation. Results and Discussion: To discuss the issues from wide aspects related to radiological protection, and to realize bridging knowledge between biology and epidemiology, we have established a research group to develop low-dose and low-dose-rate radiation risk estimation methodology, with the permission of the Japan Health Physics Society. Conclusion: The aim of the research group was to clarify the current situation and issues related to the risk estimation of low-dose and low-dose-rate radiation exposure from the viewpoints of different research fields, such as epidemiology, biology, modeling, and dosimetry, to identify a future strategy and roadmap to elucidate a more realistic estimation of risk against low-dose and low-dose-rate radiation exposure.

Sensitivity analysis of parameters and methodological choices used in calculation of radiation detriment for solid cancer

Purpose: Radiation detriment is a concept used by the International Commission on Radiological Protection (ICRP) to quantify the harmful health effects of radiation exposure in humans. The current approach of radiation detriment calculation has been defined in ICRP Publication 103 in 2007. It is determined from lifetime risk of cancer and heritable effects for a composite reference population, taking into account the severity of the disease in terms of lethality, quality of life and years of life lost. Many parameters are used in the calculations and the variation of these parameters can have effects on the cancer detriment, which needs to be investigated.Materials and methods: In this paper, we conducted a sensitivity analysis for examining the impact of 12 different parameters or methodological choices on the calculation of solid cancer detriment, such as the lifetime risk calculation method, survival curve, dose and dose-rate effectiveness factor (DDREF), age-at-exposure, sex, reference population, risk transfer model, latency, attained age, lethality, minimum quality of life factor and relative cancer-free life lost. Sensitivity calculations have been performed systematically for each of 10 solid cancer sites, by changing each one of the parameters in turn.Results: This sensitivity analysis demonstrated a large impact on estimated detriment from DDREF, age-at-exposure, sex and lethality, a noticeable impact of risk transfer model associated to variation of baseline rates, and a limited impact of risk calculation method, survival curve, latency, attained age, quality of life and relative years of life lost.Conclusion: These results could have implications for radiation protection standards, and they should help define priorities for future research in the field of low radiation dose and dose rate research. The present sensitivity analysis is part of a global effort of ICRP to review the bases of radiation detriment calculation and assess potential evolutions to improve the radiation protection system.

Nuclear epidemiologic studies and the estimation of DREF

Purpose: Estimating cancer risks for continuous radiation exposures based upon data from acute exposures has been an important public health problem. A dose and dose rate effectiveness factor (DDREF) is typically used to estimate cancer risks for chronic exposures based upon risk estimates from acute exposures. A value of 2 for a DDREF has most often been used as proposed by the ICRP in ICRP60; however, an influential analysis of several cohorts concluded that there is no risk difference between acute and chronic exposures. It is the purpose of this article to analyze the recent nuclear worker studies and estimate the dose rate effectiveness factor, DREF, for solid cancers.Materials and methods: Twelve mortality studies were identified each with at least 100 cancer deaths and a meta-analysis was then carried out using their individual ratio of low dose rate cancer effect (LDR) to the corresponding high dose rate effect from the A-bomb cohort (LSS). The ratio is denoted by Q and its reciprocal is then an estimate of the DREF.Results: The result was Q= 0.36 (95% CI = 0.11, 0.60) and DREF = 2.63 (95% confidence interval [CI] = 1.61, 7.14). Clearly, this estimate is more consistent with a DREF of 2 than with a DREF of 1. The difficulty with the estimate Q = 0.36 is that it is driven by only two large and dissimilar worker studies, the INWORKS study (q1 = 1.14) and the Mayak worker cohort (q3 = 0.30). The higher exposures for these nuclear workers were often in the early years (e.g. before 1960) with exposures from neutrons and internal emitters that are not included in the risk analyses resulting in likely overestimation of cancer effects per dose which would increase the estimate of the DREF. The Mayak study did, however, adjust for plutonium exposures. Finally, consideration is given to other cohort studies where DREF values may possibly be determined, such as the environmental exposures to the Techa River area residents and the Chernobyl cleanup workers as well as medical X-ray workers. Although dissimilar an overall meta-analysis yielded a Q = 0.45 (95% CI = 0.24, 0.66).Conclusions: It is concluded that the best estimate of a DREF is still about 2. However, because of the various problems with the epidemiology studies, especially their dosimetry, it is concluded that a DREF of about 2 should be accepted with considerable caution since it is driven solely by the Mayak study.

Towards a new dose and dose-rate effectiveness factor (DDREF)? Some comments

The aim of this article is to offer a broader, mechanism-based, analytical tool than that used by (Rühm et al 2016 Ann. ICRP 45 262–79) for the interpretation of cancer induction relationships. The article explains the limitations of this broader analytical tool and the implications of its use in view of the publications by Leuraud et al 2015 (Lancet Haematol. 2 e276–81) and Richardson et al 2015 (Br. Med. J. 351 h5359). The publication by Rühm et al 2016 (Ann. ICRP 45 262–79), which is clearly work in progress, reviews the current status of the dose and dose-rate effectiveness factor (DDREF) as recommended by the ICRP. It also considers the issues which might influence a reassessment of both the value of the DDREF as well as its application in radiological protection. In this article, the problem is approached from a different perspective and starts by commenting on the limited scientific data used by Rühm et al 2016 (Ann. ICRP 45 262–79) to develop their analysis which ultimately leads them to use a linear-quadratic dose effect relationship to fit solid cancer mortality data from the Japanese life span study of atomic bomb survivors. The approach taken here includes more data on the induction of DNA double strand breaks and, using experimental data taken from the literature, directly relates the breaks to cell killing, chromosomal aberrations and somatic mutations. The relationships are expanded to describe the induction of cancer as arising from radiation induced cytological damage coupled to cell killing since the cancer mutated cell has to survive to express its malignant nature. Equations are derived for the induction of cancer after both acute and chronic exposure to sparsely ionising radiation. The equations are fitted to the induction of cancer in mice to illustrate a dose effect relationship over the total dose range. The ‘DDREF’ derived from the two equations varies with dose and the DDREF concept is called into question. Although the equation for acute exposure can be used to analyse atomic bomb survivor data, the fitting is dominated by the quadratic dose component. Thus, little useful information can be derived about the linear dose component which is important for the derivation of low dose rate risk. The ICRP are advised to derive the risk at low dose rates from epidemiological studies of, for example, worker populations, together with information from cellular radiation biological research.

Cardiovascular effects of fission neutron or 60Co γ exposure in the B6CF1 mouse

In this study, the B6CF1 mice from the JANUS program at the Argonne National Laboratory were analyzed for increased cardiovascular disease (CVD) mortality from 60Co γ ray or fission neutron exposures administered in either a single dose or protracted weekly doses. The data used for this study represent the last studies conducted at Argonne and have been archived for at least 15 years. CVD mortality increased in a dose-dependent manner from γ rays as well as from neutron exposures. The relative biological effectiveness (RBE) for neutrons is about 4 or 5. CVD mortality appeared to be enhanced when the dose was protracted, with a DDREF (dose and dose rate effectiveness factor) in the range of 0.4–0.45 for neutron and gamma ray exposure, respectively.

Dose and dose-rate dependence of mutation frequency under long-term exposure – a new look at DDREF from WAM model

ABSTRACTWe have investigated the dependence of the mutation frequency on the dose and dose rate of artificial radiation using the Whack-A-Mole (WAM) model that we recently proposed. In particular, we pay special attention to the case of long-term and low-dose-rate exposure. Our results indicate that the WAM model successfully describes the dose-rate dependence, and it can replace the so-called dose and dose-rate effectiveness factor (DDREF), which has been used for long, to account for the differences between high-dose-rate and low-dose-rate data. The basic properties of the WAM model are discussed with special emphasis on the dose-rate dependence in order to demonstrate how the dose-rate dependence, which is built into the model explicitly, plays a key role. Biological effects of long-term exposure to extremely low-dose-rate radiation are discussed in light of analysis of mega-mouse experiments using the WAM model. In the WAM model, the effects of long-term exposure show a saturation property, thus making it distinctly different from the ‘linear no threshold (LNT)’ hypothesis that predicts a linear increase of the effects with time.

Dose-rate effects in radiation biology and radiation protection.

Quantification of biological effects (cancer, other diseases, and cell damage) associated with exposure to ionising radiation has been a major issue for the International Commission on Radiological Protection (ICRP) since its foundation in 1928. While there is a wealth of information on the effects on human health for whole-body doses above approximately 100 mGy, the effects associated with doses below 100 mGy are still being investigated and debated intensively. The current radiological protection approach, proposed by ICRP for workers and the public, is largely based on risks obtained from high-dose and high-dose-rate studies, such as the Japanese Life Span Study on atomic bomb survivors. The risk coefficients obtained from these studies can be reduced by the dose and dose-rate effectiveness factor (DDREF) to account for the assumed lower effectiveness of low-dose and low-dose-rate exposures. The 2007 ICRP Recommendations continue to propose a value of 2 for DDREF, while other international organisations suggest either application of different values or abandonment of the factor. This paper summarises the current status of discussions, and highlights issues that are relevant to reassessing the magnitude and application of DDREF.

Tremendous Human, Social, and Economic Losses Caused by Obstinate Application of the Failed Linear No-threshold Model

The linear no-threshold model (LNT) was recommended in 1956, with abandonment of the traditional threshold dose-response for genetic risk assessment. Adoption of LNT by the International Commission on Radiological Protection (ICRP) became the standard for radiation regulation worldwide. The ICRP recommends a dose limit of 1 mSv/year for the public, which is too low and which terrorizes innocent people. Indeed, LNT arose mainly from the lifespan survivor study (LSS) of atomic bomb survivors. The LSS, which asserts linear dose-response and no threshold, is challenged mainly on three points. 1) Radiation doses were underestimated by half because of disregard for major residual radiation, resulting in cancer risk overestimation. 2) The dose and dose-rate effectiveness factor (DDREF) of 2 is used, but the actual DDREF is estimated as 16, resulting in cancer risk overestimation by several times. 3) Adaptive response (hormesis) is observed in leukemia and solid cancer cases, consistently contradicting the linearity of LNT. Drastic reduction of cancer risk moves the dose-response curve close to the control line, allowing the setting of a threshold. Living organisms have been evolving for 3.8 billion years under radiation exposure, naturally acquiring various defense mechanisms such as DNA repair mechanisms, apoptosis, and immune response. The failure of LNT lies in the neglect of carcinogenesis and these biological mechanisms. Obstinate application of LNT continues to cause tremendous human, social, and economic losses. The 60-year-old LNT must be rejected to establish a new scientific knowledge-based system.

Dose and dose-rate effects of ionizing radiation: a discussion in the light of radiological protection.

The biological effects on humans of low-dose and low-dose-rate exposures to ionizing radiation have always been of major interest. The most recent concept as suggested by the International Commission on Radiological Protection (ICRP) is to extrapolate existing epidemiological data at high doses and dose rates down to low doses and low dose rates relevant to radiological protection, using the so-called dose and dose-rate effectiveness factor (DDREF). The present paper summarizes what was presented and discussed by experts from ICRP and Japan at a dedicated workshop on this topic held in May 2015 in Kyoto, Japan. This paper describes the historical development of the DDREF concept in light of emerging scientific evidence on dose and dose-rate effects, summarizes the conclusions recently drawn by a number of international organizations (e.g., BEIR VII, ICRP, SSK, UNSCEAR, and WHO), mentions current scientific efforts to obtain more data on low-dose and low-dose-rate effects at molecular, cellular, animal and human levels, and discusses future options that could be useful to improve and optimize the DDREF concept for the purpose of radiological protection.

Comments on the DDREF estimate of the BEIR VII Committee.

Radiation cancer risk estimates have been based primarily on the atomic bomb survivor cohorts, which involve an acute exposure. To adjust for lower dose and continuous exposures, a dose and dose rate effectiveness factor (DDREF) is applied to the acute risk estimates. The commonly accepted value for the DDREF at 1 Gy by the ICRP and the NCRP has been 2. BEIR VII changed this by estimating the value to be 1.5 including an uncertainty distribution. The BEIR VII committee used the atomic bomb solid cancer incidence data to make this estimation, and they chose to truncate the data at 1.5 Gy. The Committee also used the Oak Ridge mouse studies and estimated a DDREF based on these data. Finally they used the animal data-derived DDREF distribution as a Bayesian prior distribution for the atomic bomb survivor DDREF distribution and used the posterior distribution as their DDREF result. The resulting distribution had a maximum likelihood estimate of 1.4, and the Committee chose 1.5 as their best estimate. The purpose of this paper is to reexamine the BEIR VII analysis of both the atomic bomb survivor data and the mouse data. Based upon this analysis, the author concludes that changing the DDREF from 2 to 1.5 is not justified.

The risk of radiation-induced breast cancers due to biennial mammographic screening in women aged 50–69 years is minimal

The main aim of mammographic screening is to reduce the mortality from breast cancer. However, use of ionizing radiation is considered a potential harm due to the possible risk of inducing cancer in healthy women. To estimate the potential number of radiation-induced breast cancers, radiation-induced breast cancer deaths, and lives saved due to implementation of organized mammographic screening as performed in Norway. We used a previously published excess absolute risk model which assumes a linear no-threshold dose-response. The estimates were calculated for 100,000 women aged 50-69 years, a screening interval of 2 years, and with an assumed follow-up until the age of 85 or 105 years. Radiation doses of 0.7, 2.5, and 5.7 mGy per screening examination, a latency time of 5 or 10 years, and a dose and dose-rate effectiveness factor (DDREF) of 1 or 2 were applied. The total lifetime risk of radiation-induced breast cancers per 100,000 women was 10 (95% CI: 4-25) if the women were followed from the ages of 50 to 85 years, for a dose of 2.5 mGy, a latency time of 10 years, and a DDREF of 1. For the same parameter values the number of radiation-induced breast cancer death was 1 (95% CI: 0-2). The assumed number of lives saved is approximately 350. The risk of radiation-induced breast cancer and breast cancer death due to mammographic screening is minimal. Women should not be discouraged from attending screening due to fear of radiation-induced breast cancer death.

Current discussions of DDREF, cataracts, circulatory diseases and dose limits.

Although more than a century of radiation research has provided a lot of insight into radiation risk, there are still fields that need clarification. This is particularly true for the low dose range, meaning doses up to ∼100 mSv. One can detect biological effects in that dose range, but it is unclear whether these biological effects like mutations or chromosomal aberrations translate into health effects like cancer, cataracts or circulatory diseases. Thus, for radiation protection purposes, assumptions have to made that must be reappraised on the basis of new findings from time to time. Affected by new insights are currently the DDREF (dose and dose-rate effectiveness factor), cataracts and circulatory diseases. If the new findings are very convincing, dose limits have to be changed at short notice. If there are only weak indications, stability of the radiation protection system is more important than changing limits all the time.

How to incorporate the dose-rate effect into evaluation of cancer risk for radiation protection

The current radiation rules, based on epidemiological data obtained from the cancer risk of A-bomb survivors, were formulated in the context of extremely high dose rates. The International Commission for Radiological Protection (ICRP) proposed a dose and dose-rate effectiveness factor (DDREF) of 2 based on two high and low dose-rate categories of A-bomb data for an extremely high dose-rate range (ICRP Publication 60, 1991). From a scientific point of view, this value is valid only for the A-bomb dose-rate range, i.e. an extremely high dose rate, and cannot be applied at an environmental level. Nevertheless, this dose-rate factor is currently widely applied in estimating the cancer risk of low dose and low dose-rate radiation and creates an overestimation of cancer risk from radiation at the environmental level, such as in the Fukushima region following the accident at the nuclear power plant. Overestimation of radiation risk results in unnecessary psychological and economical burden on our society. There is a need to reassess the validity of the currently adopted understanding of the dose-rate effect of radiation on cancer risk. This paper is a report of a symposium organized for that purpose under the sponsorship of the Health Research Foundation, Kyoto, at the 56th Annual Meeting of the Japan Radiation Research Society, held in Aomori, Japan, on 18 October 2013. The program for the symposium included the following presentations.

Global and local cancer risks after the Fukushima Nuclear Power Plant accident as seen from Chernobyl: A modeling study for radiocaesium (134Cs &137Cs)

The accident at the Fukushima Daiichi Nuclear Power Plant (NPP) in Japan resulted in the release of a large number of fission products that were transported worldwide. We study the effects of two of the most dangerous radionuclides emitted, 137Cs (half-life: 30.2years) and 134Cs (half-life: 2.06years), which were transported across the world constituting the global fallout (together with iodine isotopes and noble gasses) after nuclear releases. The main purpose is to provide preliminary cancer risk estimates after the Fukushima NPP accident, in terms of excess lifetime incident and death risks, prior to epidemiology, and compare them with those occurred after the Chernobyl accident. Moreover, cancer risks are presented for the local population in the form of high-resolution risk maps for 3 population classes and for both sexes. The atmospheric transport model LMDZORINCA was used to simulate the global dispersion of radiocaesium after the accident. Air and ground activity concentrations have been incorporated with monitoring data as input to the LNT-model (Linear Non-Threshold) frequently used in risk assessments of all solid cancers. Cancer risks were estimated to be small for the global population in regions outside Japan. Women are more sensitive to radiation than men, although the largest risks were recorded for infants; the risk is not depended on the sex at the age-at-exposure. Radiation risks from Fukushima were more enhanced near the plant, while the evacuation measures were crucial for its reduction. According to our estimations, 730–1700 excess cancer incidents are expected of which around 65% may be fatal, which are very close to what has been already published (see references therein). Finally, we applied the same calculations using the DDREF (Dose and Dose Rate Effectiveness Factor), which is recommended by the ICRP, UNSCEAR and EPA as an alternative reduction factor instead of using a threshold value (which is still unknown). Excess lifetime cancer incidents were estimated to be between 360 and 850, whereas 220–520 of them will be fatal. Nevertheless, these numbers are expected to be even smaller, as the response of the Japanese official authorities to the accident was rapid. The projected cancer incidents are much lower than the casualties occurred from the earthquake itself (>20,000) and also smaller than the accident of Chernobyl.

Dose-rate effects and dose and dose-rate effectiveness factor on frequencies of chromosome aberrations in splenic lymphocytes from mice continuously exposed to low-dose-rate gamma-radiation

Dose-rate effects on chromosome aberrations in the low-dose-rate range have not been evaluated previously. The incidences of chromosome aberrations were analysed in splenic lymphocytes from female specific pathogen-free (SPF) C3H mice that were continuously irradiated with low- or medium-dose-rate (LDR, MDR) 137Cs γ rays from 56 days of age to evaluate the dose-rate effects. The dose–response relationship for the frequency of dicentric chromosome aberration at each dose rate (400 mGy/22h/day, 20 mGy/22h/day and 1 mGy/22h/day) was obtained using age-adjusted multiple linear regression analysis assuming that the relationship can be represented by a linear or linear quadratic model and a test for the difference between the irradiated group and the non-irradiated group. Values of the linear term, shown as the slope, decreased as the dose rate was reduced from 400 mGy/22h/day (18.2 mGy h−1) to 1 mGy/22h/day (0.045 mGy h−1), indicating a positive dose-rate effect in the dose-rate region. The incidences of dicentric chromosomes and translocation for LDR (20 mGy day−1) were compared with those for HDR (890 mGy min−1) irradiation at each total dose to obtain the dose and dose-rate effectiveness factor (DDREF). The DDREFs were 4.5 for dicentrics and 2.3 for translocations at a total dose of 100 mGy based on the chromosome aberration rate. These results will be useful for estimating the risk of LDR radiation exposure and radiation protection.

A Mathematical Model for Estimating Biological Damage Caused by Radiation

We propose a mathematical model for estimating biological damage caused by low-dose irradiation. We understand that the Linear Non Threshold (LNT) hypothesis is realized only in the case of no recovery effects. In order to treat the realistic living objects, our model takes into account various types of recovery as well as proliferation mechanism, which may change the resultant damage, especially for the case of lower dose rate irradiation. It turns out that the lower the radiation dose rate, the safer the irradiated system of living object (which is called symbolically "tissue" hereafter) can have chances to survive, which can reproduce the so-called dose and dose-rate effectiveness factor (DDREF).

WE‐A‐211‐03: BEIR VII: What It Does and Doesnˈt Say

Background: Over the last 2 years, there has been considerable attention focused on the potential cancer risks from medical imaging procedures, particularly with the widespread use of multislice CT. Almost all studies rely upon the BEIR VII report (Biological Effects of Ionizing Radiation panel formed under the auspices of the National Academy of Sciences) to generate an estimate of the risk of cancer from a given procedure. In doing so, most studies treat the BEIR VII report as a solid basis of scientific evidence for estimation of cancer risk. In reality, a close reading of this report shows that there are a large number of assumptions inherent in all aspects of the estimates of cancer risk — a fact that is often and clearly stated in the report.This presentation will review some of the assumptions used by the BEIR panel to calculate cancer risk, including the impact of different models (excess absolute risk vs. excess relative risk), the dose and dose rate effectiveness factor (DDREF) and relative biological effectiveness (RBE), on cancer estimates.Often lost in the discussion on medical exposure is a reference level by which exposure levels can be compared to something that unavoidable and impacts everyone on earth — background radiation. This presentation will review the consequences of applying the BEIR model to background radiation and known variations in levels of background radiation throughout the U.S., and how the cancer rate from background compares with that from medical imaging.Learning Objectives1. Understand the assumptions underlying the BEIR VII report2. Be able to compare the relative risks of medical imaging procedures to that from background radiation