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Indications for Using Potassium Iodide to Protect the Thyroid from Low Level Internal Irradiation* Jacob Robbins, M.D

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Indications for Using Potassium Iodide to Protect the Thyroid from Low Level Internal Irradiation* Jacob Robbins, M.D 1028 INDICATIONS FOR USING POTASSIUM IODIDE TO PROTECT THE THYROID FROM LOW LEVEL INTERNAL IRRADIATION* JACOB ROBBINS, M.D. Clinical Endocrinology Branch National Institute of Arthritis, Diabetes, and Digestive and Kidney Diseases National Institutes of Health Bethesda, Maryland S INCE Three Mile Island, the possibility that detrimental effects from radioactive fallout might be avoided by appropriate management of an exposed population has been the subject of extensive discussion and debate. Much of this debate has centered on the wisdom of providing potassium iodide to prevent thyroid tumors that might develop after exposure to radioactive iodine. Proponents of the two extreme viewpoints have been heard. Dr. Shleien, reflecting the deliberations at the Food and Drug Administration and the belief that even low doses of radioiodine may be detrimental, proposes that iodide administration should be activated at a low exposure level. Dr. Yalow, supporting the view that the thyroid tumor risk is not life-threatening whereas the dangers of widespread iodide administration are potentially serious, argues against providing iodide to the community at large. I shall attempt to achieve a balance in these two legitimate points of view, and make some proposals that seem to me warranted by our present knowledge of the problem. First, I would make some general observations concerning the type of risks we are considering, based on the analysis by Starr and Whipple.1 I believe we can agree that the probability of fatality from radiation-induced thyroid tumors is extremely low, so that the value of risk avoidance to the individual is not greater than its value to society (Figure 1, Ref. 1). On the other hand, because exposure to accidental radiation does not benefit the individual, even this low risk, if in fact it exists, is unacceptable (Figure 4, Ref. 1) provided that it can be safely and effectively avoided. There- fore, we must consider the cost to society of providing the means for *Presented in a panel, Protective Value of Potassium Iodide, as part of the Symposium on the Health Aspects of Nuclear Power Plant Incidents held by the Committee on Public Health of the New York Academy of Medicine April 7 and 8, 1983. Address for reprint requests: Dr. Jacob Robbins, Building 10, Room 8N315, National Institutes of Health, Bethesda, Maryland 20205 Bull. N.Y. Acad. Med. IMPLICATIONS FOR POTASSIUM IODIDE 1029 TABLE I. THYROID RISK AFTER X-RAY EXPOSURE IN CHILDREN* Mean thyroid dose (rads)t 9 17 119 257 449 715 Persons 10,842 1,485 235 427 206 53 Cancers 23 1 1 6 9 5 Adenomas 9 7 8 1 1 15 3 Relative risk or (observedlexpected) t Cancer 4.6 (3) (15) (50) (117) (217) Adenoma > 9 4.6 24 23 36 39 Excess tumors /106 PY-radt t Cancer 8.3 1.6 1.6 2.6 3.8 5.0 Adenoma 12.7 13.5 4.5 6.2 2.8 *Follow-up period - 20 yrs. t9 rad from Ron and Modan, 1980. > 9 rad from Shore, Woodard, Pasternack and Hempelmann, 1980.: tRelative risk, (Excess + Expected)/Expected, was calculated using the number expected that was derived from control study groups. Observed/Expected (numbers in parentheses) used incidence data from the Connecticut Tumor Registry for the number of expected cancers since none were observed in the control study group. ,ttPY-rad = patient years x rads. avoidance and the cost to the individual if the avoidance mechanism itself carries a risk. The former consideration requires a political decision whereas the latter requires a medical decision. My remarks, as were those of my colleagues on this panel, are directed mainly at the medical question: Is it reasonable to expect that individuals will be put at risk? And can this risk be safely counteracted? Our ability to answer the medical question will simplify the task of those responsible for the political decision. The first question to settle is whether radioiodine is a hazard, particular- ly at a low level of exposure. Fortunately, we have reliable data indicating that exposure of a child's thyroid gland to as little as 9 rad from x-ray irra- diation significantly increases the risk of thyroid cancer (Table I). Al- though this risk, expressed as cancers/10 PY-rads,* appears to be highest at the lower exposure levels, the fact that the data come either from different sources2)3 or from too few cases: suggests that we should use the average risk, which depends mainly on the more reliable higher-dose data, as a first approximation (Table II). Two factors suggest that these values could be underestimates: The numbers of cancers were obtained from *Patient years x rads Vol. 59, No. 10, December 1983 1030 J. ROBBINS TABLE II. THYROID RISK AFTER X-RAY EXPOSURE IN CHILDREN Both sexes Females Males Excess tumors/106 PY-rad (Shore et al., 1980)3 Cancers 3.8 5.2 1.8 Adenomas 4.5 6.8 2.6 Relative risk or (observedlexpected)* Cancers (Shore et al., 1980)3 (29) (60) (Ron and Modan, 1980)2 16 4.5 *Cf Table I TABLE III. THYROID TUMOR LATENCY IN YEARS (SHORE ET AL., 1980)3 Control < 400 rad > 400 rad Cancers 15.8* 27.6 (11. 1, 21.8)t (19.8, 34.4) Adenomas 27.3* 31.9 25.7 (22.7, -----)t (29.4, 36.6) (23.0, 30.9) *Median t90% confidence limits of the estimate hospital surgical records2 or from follow-up, mainly by correspondence,3 and are probably incomplete. The follow-up period averaged about 20 years, and available data show no decrease in appearance of new cases as the exposed cohort ages. Thus, only part of the induced cancers have been detected and the rate of thyroid cancers coming to clinical attention could increase with time. In fact, the latency in the cancer occurrence often exceeds 20 years (Table III). Tables I and II also show that benign thyroid tumors are induced by low-level external irradiation, and, although the numbers of benign tumors exceed the malignant tumors, the relative risk of inducing cancer is greater, at least at the higher dose levels. This reflects the higher likeli- hood that a thyroid nodule induced by irradiation will be a cancer (about 30 to 40%) than in the unexposed population. It is also seen (Table II) that more induced tumors of both kinds were found in women than in men, although the relative risk of developing thyroid cancer was greater in men in the experience of Shore et al. (but not in that of Ron and Modan in Israel). We must emphasize that all these data were obtained when exposure to Bull. N.Y. Acad. Med. IMPLICATIONS FOR POTASSIUM IODIDE 1031 TABLE IV. THYROID RISK AFTER RADIOIODINE OR X-RAY EXPOSURE IN ANIMALS Relative risk 132I 131J X-Ray Mice* (Walinder and Sjdden, 1971)9 4 1 4 (Walinder et al., 1972)" Rats* (Book et al., 1980)" 9 1 Rats (Lee et al., 1982)'7 80 rad: cancer 1 0.7 adenoma 1 0.6 400 rad: cancer 1 1.1 adenoma 1 2.0 *Based on goitrogenesis assay rather than tumor induction. irradiation occurred during early childhood, and that there is little evi- dence that adults are at risk from similar exposures.4 In fact, a recent careful study by Royce et al.,' although purporting to contradict earlier evidence on cancer risk, actually provides evidence that the risk of developing a thyroid tumor may be negligible when the average age at exposure is 18 to 20 years. This report, however, is flawed by the low fraction of the exposed cohort that was examined and the fact that many of the women had received thyroid medication. A key question that needs to be answered is whether internal irradiation of the thyroid from radioiodine is equivalent to external irradiation. That thyroid tumors can be induced by radioiodine is evident not only from animal studies' but also from the experience in the Marshall Islands where 18 of the 29 children on Rongelap exposed to fallout before the age of 10 years developed thryoid nodules.7 The 175 rads of simultaneous external radiation would not have produced this many tumors. The estimate of 275 to 1,150 rads from internal exposure, however, is uncertain and may actually be low,8 and much of this irradiation was derived from short-lived radioiodines which appear to be more effective than 131I in producing thyroid damage (Table IV). Except for one case of leukemia which may have resulted from irradiation, thyroid tumor induction, including cancer, was the major late effect of the exposure in this population. Adults as well as children were affected. There are no other data from which we can derive an accurate risk estimate for radioiodine exposure. Evaluation of the effects of radioiodine fallout in Utah and Nevada,12"13 where no increase in thyroid tumors was Vol. 59, No. 10, December 1983 1032103 J.J.RBBNROBBINS TABLE V. THYROID RISK AFTER DIAGNOSTIC 1311 IN SWEDEN (HOLM ET AL., 1980)15.16 < 20 yr > 20 yr Persons 486 9647 Dose (rad) 159 58 Mean follow-up (yrs) 18 18 Cancers: Observed 0 9 Expected < 1 8.3 Calculated* 5.6 48 *Based on an excess of 4/106 PY-rad (x ray) + expected, as given in Table VII. For the entire group based on UNSCEAR risk figures and corrected for thyroid size, Holm et al.16 calculated 47-124 tumor. observed after exposure estimated at 10 to 600 rads, is also flawed by uncertainty in the dose.14 An important recent follow-up of individuals receiving diagnostic 131I in Sweden also failed to reveal an increased incidence of thyroid cancer after a mean exposure of 159 rad in "chil- dren" and 58 rads in adults.
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