National Academies Press: OpenBook

Review of the Hanford Thyroid Disease Study Draft Final Report (2000)

Chapter: Appendix B: Responses to Selected Comments by the Public

« Previous: Appendix A: Subcommittee Activities
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
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Page 168
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
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Page 169
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
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Page 170
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
×
Page 171
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
×
Page 172
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
×
Page 173
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
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Page 174
Suggested Citation:"Appendix B: Responses to Selected Comments by the Public." National Academy of Sciences. 2000. Review of the Hanford Thyroid Disease Study Draft Final Report. Washington, DC: The National Academies Press. doi: 10.17226/9738.
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Page 175

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AppendE~c B Responses to Selected Comments by the Public This section provides responses to various questions and comments posed to the subcommittee at the public meeting held in Spokane, Washington, in June 1999. Comment: Differences in terrain were not included in the fallout model, and there were great differences in mountains and plains in that area. Response: Major terrain effects are indirectly accounted for in the HEDR dose mode! even though the computer code assumed a flat terrain for the entire area being modeled. The terrain was implicitly taken into account in the meteorologic projections of where the ]3~{ pane went and to a lesser extent in a "surface roughness parameter". The hourly meteorologic data from the 16 stations in the geographic area roughly reflect the effects of the Cascade range, the Blue Mountains south of WalIa Walla, and the Bitterroot Mountain range east of Spokane, Coeur d'A1ene, and Lewiston. The modeling of terrain effects in a more detailed manner is impeded by the severe limitations of the meteorologic data that are available for the mode] for 1944-1947, the period of greatest interest. 168

Append['x B 169 Comment: The Spokane area has had a historically high thyroid disease incidence due to lack of iodized salt or other sources of iodine. Were the data corrected for the high incidence in the Spokane area in the 1940s and 1950s? Response: iodized salt was widely available by the 1940s, so low dietary iodine might have been an issue only in some unidentified and probably small subset of children in that era. Development of thyroid disease related to iodine deficiency typically takes a number of years of low iodine intake. The children in this study, born when iodized salt had already been introduced, were probably much less subject to iodine- deficiency disease than were their parents and grandparents. However, one potential impact of low iodine in a subset of the children might have been to increase the uptake of |3~}, that is, to give iodine-deficient children more radioactive iodine than they otherwise would have received. In the absence of knowledge of which children were iodine-def~cient, it would be impossible to factor this into the individual dose estimates. Comment: The cohort studied should have been far larger, at least 10,000 persons. More higher doses should have been included in the cohort. Response: The calculations of HTDS investigators performed initial statistical power that showed excellent statistical power for the set of assumptions that they used, which at the time appeared plausible; and that made them think that they did not need any more subjects. However, the NRC subcommittee believes that their assumption that dose- measurement errors were of a type ("Berkson error") that did not adversely affect statistical power is unlikely to be valid. There are several reasons to believe that the dose-measurement errors did reduce statistical power. Hence, we agree that in principle a larger study would have been very desirable.

170 Review of the HTDS Draft Final Report Nevertheless, it seems unlikely that the number of high-dose study subjects could have been increased appreciably. it is preferable to study those who were young children (less than 10 years old and preferably less than 5) at the time of AT exposure, in that children, adolescents, and adults are markedly less sensitive to radiation effects on the thyroid than young children are. The HTDS investigators apparently studied all possible young children in the high-dose counties (Adams, Franklin, and Benton) unless there are other high-dose counties that the subcommittee is unaware of. The only other possibility would have been to increase the numbers somewhat in the intermediate-dose category (for example, WalIa Walla County), but this would probably have increased the statistical power by only a small amount, and adding more subjects from low-dose counties would likewise have only a small effect on statistical power. Comment: Increases in mortality and birth defects were high in the area before and after the Hanford exposure period with no explanation. Response: Perinatal mortality (death rate during the first month of life) and mortality due to birth defects (congenital anomalies) were somewhat higher than national rates. However, as the comment noted, they were higher in the area both before and during the period of Hanford fallout exposures. Therefore, it seems not very likely that the higher rates were caused by the fallout. A more detailed study of birth defects in Hanford downwinders found no increase in birth-defect rates, except for a possible increase in neural-tube defects (Sever and others, 1988~. Comment: Risk analyses from other ]3~{ thyroid studies appear different than this study.

Appendix B 171 Response: The Utah study of thyroid disease after Nevada Test Site ~3~! fallout showed marginal excesses of thyroid cancer, thyroid nodules, and both combined; but when dose uncertainties were properly included in the risk estimates, the results were not statistically significant. Furthermore, our subcommittee shows in its report that the thyroid-cancer risk estimates from the Utah and Hanford studies are probably statistically compatible with each other. A comparison with the Marshall islanders is questionable because the doses were very high for children on the islands studied and were mostly from short-lived forms of radioactive iodine and gamma rays, rather than from Mar. Two studies of ~3~T administered to young people for diagnostic medical purposes have not shown statistically significant excesses of thyroid cancer (Holm, 1991; Hamilton and others, 1989~. The average thyroid doses in the two studies were about 800 and 1500 mGy. However, most ofthe subjects were adolescents at the time of }3~{ exposure, and the atomic- bomb study and other studies show that radiation exposure in adolescence causes much less thyroid cancer than the same exposure in early childhood. Therefore, it is difficult to interpret the negative results. the Chernobyl studies In Ukraine and Belarus have shown increases in thyroid cancer after the Chernobyl 13~} releases. The risk per mGy is not well quantified at this point, so it is not clear whether the Chernobyl and Hanford results are statistically compatible. a. a. . . . ~ . . Comment: The study should have investigated synergism with other environmental insults. . Response: The study did make some attempt to do so with regard to radiation, the main known environmental risk factor for thyroid disease. The HTDS investigators obtained a history of diagnostic and therapeutic medical irradiation and

172 Review of the HTDS Draft Final Report information on occupational radiation exposure, and they found no synergism. Other studies have found little evidence of synergism of radiation and other environmental exposures in causing thyroid cancer. For instance, one study that has investigated this found no synergism of oral contraceptive use, hormone-replacement therapy, and smoking (Shore and others, 19931. Comment: A study of "clusters" should be done, particularly in families in which no previous thyroid disease had been found. Families with thyroid problems should be studied. Response: At the various public-comment meetings, a number of people who lived in downwind areas stated their belief that they and their families had experienced more frequent thyroid diseases than would have been expected in the population at large. They could be right, and their disease could have been the result of unusual fallout or ingestion patterns. However, it is also true that thyroid disease tends to run in families, and the particular occurrences could be related to genetic factors in the families, chance, or even mistaken diagnoses. A compilation and study of such clusters could have been undertaken, but that would have been a special study and was not part of the HTDS design. Comment: Screening effects are a major unresolved issue that needs evaluation. Response: The HTDS investigators wanted to compare the rate of thyroid cancer among the Hanford downwinders with that found in an unirradiated general population. But to do so they knew that they needed to take account of the fact that their study population all had sensitive thyroid screening with ultrasonography and palpation of the thyroid by expert thyroid

Appendix B 173 physicians. It is well known that many more thyroid cancers and nodules are detected when there is intensive screening. To address the inequity in thyroid-cancer or nodule detection between the intensively screened population and the general US population, the investigators chose an increase by a factor of 3 in thyroid-disease rates due to screening on the basis of an estimate in a 1985 publication (NCRP, 19851. However, two studies since then have suggested different screening factors, from 2.5 to about 7 for thyroid cancer and 17 for thyroid nodules (Thompson and others, ~ 994~. Hence, we have much uncertainty about the size of screening effects. That is one of the reasons that it was more appropriate to compare disease rates within the study population, in which everyone underwent screening, than between this study population and some other, mostly unscreened population. Comment: Other health problems that could possibly result from IT exposure should be included and not just thyroid disease alone. Response: IT concentrates in the thyroid, where it remains for several weeks. The concentration and long residence time lead to potentially large doses to the thyroid. Other organs receive only about one-thousandth of the dose received by the thyroid, and retain IT or its because they do not concentrate and retain CAST radioactive metabolites. Except for the parathyroid glands, no other organs could have received biologically significant doses from the environmental releases from Hanford. The parathyroid glands are intimately attached to the thyroid and receive fairly high doses because of their proximity. Changes in parathyroid function were screened for, and no changes related to radiation injury were found; because no effects were seen in the parathyroid glands, it is most unlikely that radiation effects in other organs would have occurred and gone undetected.

174 Review of the HTDS Draft Final Report Comment: Doses were too low to detect any thyroid changes. Only about 2 dozen in the study had estimated doses over 100 red. Response: Many scientists believe that the bulk of evidence suggests that even quite small doses can cause thyroid cancer. For instance, a study in Israel of children who received x-ray thyroid exposure of about 100 mGy (10 red) had clear excesses of thyroid cancer and thyroid nodules (Ron and others, 19951. In comparison, the average thyroid dose in the HTDS was about I80 mGy (~8 red). However, it is generally believed that nit is less effective in causing thyroid disease than are x-rays, and this might be especially true when the 13~{ doses are spread out over several years (dose protraction tends to reduce the amount of cell damage that cells cannot repair). Comment: Effects of 13~ and x-rays should be considered equivalent. Comment: The AT dose-response relationship for thyroid disease is not linear. There is a threshold for radiation effects on the thyroid. Response: Human data on thyroid cancer after gamma-ray exposures (in the Japanese atomic-bomb study) or medical studies of x-ray exposure are best fitted as a linear dose- response association (Ron and others, 1989), although a threshold at some low dose under 0.! Gy (10 red) cannot be conclusively ruled out. There are no compelling biologic reasons for the shape of the dose-response curve to differ greatly for ]3~} exposure. in fact, the best study comparing the effect of x-ray and HI exposure in rats found essentially the

Appendix B 175 same dose-response relationships for both (Lee and others, 1 982~. Furthermore, the largest body of data on thyroid cancer after childhood exposure to IT the Chernobyl data-also show a substantial excess of thyroid cancer in the estimated dose ranges of 0.~-0.5 Gy (10-50 red) and 0.5-~.0 Gy (50-100 red), although there is a suggestion that ill} is only about 50°/0 as effective as gamma rays in inducing thyroid cancer (Jacob and others, 1998~.

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In 1986, officials of the US Department of Energy revealed that the Hanford Atomic Products Operations in Richland, Washington, had been releasing radioactive material, in particular iodine-131, into the environment over a period of years. This information, which confirmed the suspicions of some people in the Pacific Northwest about what they called the Hanford Reservation or just Hanford, created quite a stir. Both the US Congress and citizens of the Northwest became keenly interested in knowing whether these radiation releases had caused human health effects. They were particularly concerned about whether Hanford releases of iodine-131 had led to an increase in thyroid disease among the population of the area.

In 1988, Congress ordered a study of the human health effects of exposure to the iodine-131 released from Hanford. Funded by the Centers for Disease Control and Prevention (CDC), the study was carried out by the Seattle-based Fred Hutchinson Cancer Research Center over the last decade. The study examined estimate of exposure of the thyroid and rates of thyroid disease because iodine-131 concentrates in the thyroid and that organ would be the best indicator of radiation damage in the population. The Centers for Disease Control and Prevention (CDC) asked the National Academy of Sciences-National Research Council (NAS-NRC) to give an independent appraisal of the study methodology, results, and interpretation and of the communication of the study results to the public.

Review of the Hanford Thyroid Disease Study Draft Final Report constitutes the response of the NRC subcommittee to that request. To respond to the charge, the NRC subcommittee felt that it needed to go beyond the specific questions addressed to it by CDC and develop a broad understanding and critique of the HTDS and the Draft Final Report. As part of those activities, the subcommittee solicited comments from outside experts and members of the public primarily in a public meeting held in Spokane, Washington, in June 1999, where 14 scientists and members of the public made formal presentations to the subcommittee about various aspects of the Draft Final Report. Other members of the public also spoke during four open-comment sessions at the meeting. In addition, efforts were made to evaluate all information materials prepared for the public and additional CDC communication plans. Information was gathered through interviews with journalists, members of concerned citizen groups in the Hanford region, members of the CDC scientific and media staff in Atlanta, and the HTDS investigators.

In this summary, the main points follow the structure of our report and are presented under several headings: epidemiologic and clinical methods and data collection, dosimetry, statistical analyses, statistical power and interpretation of the study, and communication of the study results to the public. We then provide a brief synopsis of our response to the questions raised by CDC.

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