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1. RISK OVERVIEW 1.1 Recent Developments in Radiation Dosimetry Estimates of health risks to exposed cohorts in the HRSA program have historically been obtained from dose assessment or retrospective dosimetry because many of the people did not have personal dosimeters and there was a lack of comprehensive workplace or environmental monitoring. The doses from external radiation were estimated using conversion factors similar to those compiled by Unger and Truby (1981), International Commission on Radiological Protection (ICRP) Publication 74 (ICRP, 1996), and International Commission on Radiation Units and Measurements Report 68 (ICRU, 2002). Doses from internally deposited radionuclides were estimated using physiologically-based pharmacokinetic (PBPK) models, such as those developed by ICRP (1979), and these methods are continually updated. There have been changes in tissue weighting factors, wT, which are defined as the fraction of stochastic risk for carcinogenesis or hereditary effects resulting from radiation exposure of organ T, relative to the risk from uniform exposure of the entire body (ICRP, 1991). Changes in wT based on incidence as a measure of health detriment are being planned by ICRP and will increase the estimated risk of several cancers (particularly cancers of the thyroid and breast), without a major effect on the estimated risk of respiratory cancers. There has been complete revision of the model for the human respiratory tract (ICRP, 1994) and of basic anatomic data on the skeleton (ICRP, 1995). Although the recent revisions can reduce uncertainty, they will not substantially change the general assessment of risk to cohorts in the HRSA program. The revised PBPK model for the human respiratory tract does not include dosimetry for inhalation of radon or the short-lived descendants of radon that are referred to as radon daughters. Historically, the risks posed by radon have been related to the time-integrated concentration of potential alpha energy from short-lived radon daughters, usually expressed in Working Level Month (WLM, or J s m−3). The committee does not expect that this practice will be revised. Any changes in risk estimates from radon will be related to biology or observed cancer incidence, rather than dosimetry. The most comprehensive database of risks associated with external exposure from ionizing radiation is the Life Span Study of Japanese atomic-bomb survivors conducted by the Radiation Effects Research Foundation. Current estimates of risk are related to dose assessments for each person according to a system called DS86 (NRC, 1987). In 2001, a National Research Council report made recommendations regarding revisions to DS86 to reduce uncertainty in dose assessments (NRC, 2001). The revisions have been completed and will be published as DS02 (Roessler, 2003). The protocol will be used to obtain an updated estimate of dose for each person. Initial indications are that changes in dose are expected to be small and will not substantially affect cancer mortality risk factors (for example, risk per sievert) for low linear energy transfer radiations such as from gamma rays and beta particles as stated in this interim report. The committee will provide more specific evaluation of these changes in the final report after reviewing the published results from DS02.
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1.2. Recent Developments in Radiation Biology Recent studies in cellular radiation biology are providing new insights as to the mechanisms whereby radiation interacts with the components of a mammalian cell and how signals can be transferred from one cell to another. That information should improve our understanding of the basic cellular changes after radiation exposure that might be involved in inducing mutations and of how the mutations are related to a risk of cancer or hereditary disorders. However, it is not necessary at this time to reassess human cancer or heritable risk in light of the new observations because radiation cancer and hereditary risk estimates are derived from results of epidemiologic studies of exposed human populations and experimental studies of irradiated laboratory animals. Basic mechanisms are empirically accounted for in those results even if they are not identified or understood. Furthermore, they are supported by information on dose-response relationships for a variety of mutational end points of the type known to be associated with carcinogenesis and hereditary effects. New knowledge of biologic mechanisms has been included in the reviews by various authoritative international and national scientific groups that summarized the risks to health arising from exposure to low doses of radiation (NCRP, 2001, UNSCEAR, 2000a). None of the reviews has led to a conclusion that suggests that modifications of the linear-nonthreshold dose-response model that forms the basis of current risk estimates are required at this time. 1.3. Recent Developments in Radiation Epidemiology Current risk estimates for radiogenic cancers of interest among the populations covered by RECA, specifically uranium miners, millers and ore transporters, and downwinders and onsite nuclear-test participants, are based primarily on the results of epidemiologic studies of uranium and other miners who were exposed to radon underground, the Japanese atomic-bomb survivors exposed primarily to external gamma rays, and populations exposed internally to radioiodine; they have been reviewed in detail (NRC, 1990; ICRP, 1991; NRC, 1999a; UNSCEAR, 2000b; IARC, 2000; 2001). Radiation protection organizations generally have based their risk estimates for radiogenic cancers on linear-nonthreshold dose response models for all but skin cancers. In so doing, they assumed that even small increases in dose above natural background radiation levels result in a proportional increase in risk. Risk to Uranium Miners, Millers and Ore Transporters The studies of miners have identified an increased risk of lung cancer associated with exposure to alpha-particle radiation from decay products of inhaled radon. The epidemiologic studies of miners generally employed relative risk models, the estimates of which are discussed below. It should be noted that a decrease in excess relative risk could occur even if absolute risk (number of cancers per 100,000 persons) stays constant
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or slightly increases. While absolute risk is very important from a public health perspective, we chose to discuss relative risk because of its use in the cited literature, as well as the ease of understanding by an individual person in the RECA population. The most recent and widely recognized lung-cancer risk estimates associated with that exposure were reported in the BEIR VI report (NRC, 1999a). An important finding of the BEIR VI committee relevant to some of the RECA populations—identified as uranium miners, uranium millers, and ore transporters—is that the excess relative risk of radiogenic lung cancer decreases with increasing age and time since exposure. Accordingly, the populations now alive and seeking compensation, who are generally over 60 years old and who have been out of the mines for 30 years or more, are at much lower relative risk now than they were shortly after retiring from mining uranium. For example, using data from 11 international cohorts, the BEIR VI committee estimated that uranium miners of 65–74 years old have about 25% of the excess relative risk of radon-induced lung cancer that miners in their 50s have, and the most recent analysis of the Colorado Plateau uranium-miner data (Hornung et al., 1998) estimated that the excess relative risk for miners in their 70s is less than 10% of that of miners in their 50s. Similarly, the BEIR VI committee estimated that miners who have been out of the mines for more than 25 years have less than half the lung-cancer risk of recently retired miners, and the analysis of the Colorado Plateau miner data indicated a 65% reduction in excess relative risk for miners who have been out of the mines for more than 25 years. The RECA population should also be informed that these analyses also have shown a synergistic relationship between exposure to radon and cigarette smoking. That is, the excess relative risk of radiogenic lung cancer for smoking miners is greater than the sum of the excess relative risks of smoking alone and radon alone. Risks to uranium millers and ore transporters have not been nearly as well characterized as risks to miners. A small mortality study of 662 millers from the Colorado Plateau published in 1973 (Archer et al., 1973) found a significantly elevated relative risk for lymphatic and hematopoietic cancers based upon only 4 observed deaths. A later study of millers expanded to 2002 millers in the same area was published in 1983 (Waxweiler et al., 1983). This more powerful study found no statistically significant increase in the mortality risks among the millers for any malignant neoplasms when compared with the risks among the general population. The only statistically significant increased risk for nonmalignant disease was for respiratory diseases but there was no significant trend with duration of employment in the mills. The committee is unaware of any epidemiological studies of ore transporters who would likely have very low exposures to ionizing radiation. Risks to Downwinders and Onsite Nuclear-Test Participants Estimates of the cancer risks associated with external exposure to gamma radiation generally are influenced by age at exposure and time since exposure; the risks are highest for those exposed in childhood and are relatively higher for the radiogenic leukemias than for other cancer types. For leukemias, except chronic lymphocytic leukemia (CLL), and for thyroid (nonmedullary) and lung cancer, the highest risks occur
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about 10 and 25 years, respectively, after exposure, and they appear to remain elevated thereafter though they gradually decrease (NRC, 1990; UNSCEAR, 2000a, b). The studies’ results also suggest that the risk of thyroid cancer is only about 10% of the risk of benign thyroid nodules. The excess risk of thyroid cancer in exposed children declined by a factor of 2 for each 5-year age-at-exposure group under the age of 15 years (Ron et al., 1995). This suggests that excess relative risks to the surviving RECA populations (identified as downwinders and onsite nuclear-test participants) associated with their radiation exposure may now be substantially reduced compared to excess relative risks observed 10 to 25 years after radiation exposure occurred. The risks of most other types of solid cancers appear to reach a peak 20–25 years after exposure and then decrease but remain elevated for at least an additional 25 years. Risks posed by chronic exposure to low doses of sparsely ionizing radiation such as gamma rays, are estimated to be 1/3–1/2 of the risk following acute exposure to high doses, and this has been taken into account in estimating the risk of low doses of such radiation. This finding, however, is in contrast to the inverse dose rate effect found in the Colorado miners where exposure for long periods of time to low doses of densely ionizing radiation, specifically, alpha-particle radiation from radon decay products, was more harmful than exposure to high doses of this type of radiation for short periods of time (Hornung et al., 1998, NRC, 1999a). Estimates of the magnitude of the risk of all solid cancers combined, based on data from a low-dose group (less than 0.5 Sv) of atomic-bomb survivors, are consistent with the estimates derived from data obtained from survivors exposed to wider dose ranges (0–2 Sv; 0–4 Sv) (Pierce and Preston, 2000). Evidence of associations between radiation exposure and increased risks of some cancers (Hodgkin’s disease, non-Hodgkin’s lymphoma, multiple myeloma, and prostatic cancer) is weak or absent (chronic lymphocytic leukemia). Increased risk of thyroid cancer from external radiation to the head and neck has been observed in persons who received x-ray therapy (especially in childhood) and Japanese atomic-bomb survivors who received high whole-body doses. No increase was observed in adults who received even higher doses from the large amounts of 131I given in therapy. Children exposed to fallout from weapons testing at the Marshall Islands and from the Chornobyl accident have had a high incidence of thyroid cancer, but studies of downwinders who received much lower doses from the Nevada Test Site and from releases from Hanford (NRC, 1999b) have not revealed an increased incidence of thyroid cancer or of leukemia. The downwinders and onsite nuclear-test participants also were at risk of exposure to radiation internally from inhaled or ingested radioactive iodines, particularly 131I. Increased incidence of radiation-induced thyroid cancer and leukemia was anticipated based on the experience of other populations exposed externally to gamma radiation. However, epidemiologic studies of populations, mostly adults treated medically, with 131I, have shown no increased risk of leukemia and evidence is equivocal for thyroid cancer. Reports of increases in thyroid cancer incidence among populations less than 20 years old when exposed to radioactive fallout from the 1986 Chornobyl
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accident suggest that the risk is significantly greater among those who were less than 6 years old and resident in heavily contaminated areas of the former Soviet Union at the time of the accident. Uncertainties in individual dose estimates and about the influence of iodine deficiency on the induction of radiogenic thyroid cancer are among the factors that currently preclude reliable risk estimates for thyroid cancer in these populations (Ivanov et al., 2003). An unexplained statistically significant increase in the risk of nonmalignant disease mortality (in 1950–1985) with increasing dose was identified among atomic-bomb survivors. Analysis of updated data (1950–1990) has strengthened but still not explained the association with respect to nonmalignant circulatory, respiratory, and digestive system diseases. The increase in relative risk is about 10% of that for radiogenic cancer and appears not to be influenced by age at exposure or attained age. The data further suggest that the risk is negligible below 0.5 Sv (Shimizu et al., 1999). Thus, even if the association eventually proves to be causal, the likelihood that nonmalignant diseases in the RECA populations will be associated with radiation probably will be small in light of the high natural incidence of these diseases. Reviews by the National Research Council (Committee on Health Risks from Exposure to Low Levels of Ionizing Radiation, BEIR VII) of updated and new data from epidemiologic studies of exposed populations are in progress. Those studies might contribute to refinements in existing risk estimates, but they are not expected to identify new radiogenic diseases. In addition, an update of the National Institute for Occupational Safety and Health (NIOSH) mortality study of uranium millers has recently been completed and is under review. Publication of the results of the National Research Council and NIOSH studies is expected in 2004. On the basis of the above discussion, the committee’s preliminary assessment is that At this time, there is no new physical, biologic, or epidemiologic evidence to suggest a need to revise the estimates of risk for radiogenic cancers among populations previously exposed to ionizing radiation as identified in relation to RECA or the fundamental procedures used to estimate them (UNSCEAR 2000a, b; NCRP, 2001, NRC, 1999a). The excess relative risk of lung cancer from exposure to radon decay products decreases with age and time after the last exposure. Similarly, excess relative risks for most of the cancers associated with onsite participants’ and downwinders’ exposure decrease with age and time since exposure. Thus, the excess relative risks among the surviving population for developing cancers that may be attributed to radiation are lower today than they were when the exposures occurred several decades ago.
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