Risk of Thyroid Cancer After Exposure to 131I in Childhood

Elisabeth Cardis, Ausrele Kesminiene, Victor Ivanov, Irina Malakhova, Yoshisada Shibata, Valeryi Khrouch, Vladimir Drozdovitch, Evaldas Maceika, Irina Zvonova, Oleg Vlassov, André Bouville, Guennadi Goulko, Masaharu Hoshi, Alexander Abrosimov, Jadvyga Anoshko, Larisa Astakhova, Sergey Chekin, Evgenyi Demidchik, Rosaria Galanti, Masahiro Ito, Elena Korobova, Evgenyi Lushnikov, Marat Maksioutov, Vladimir Masyakin, Alexander Nerovnia, Vladimir Parshin, Evgenyi Parshkov, Nikolay Piliptsevich, Aldo Pinchera, Semyon Polyakov, Nina Shabeka, Eero Suonio, Vanessa Tenet, Anatoli Tsyb, Shunichi Yamashita and Dillwyn Williams

Received September 24, 2004.
Revision received January 19, 2005.
Accepted April 5, 2005.

Background: After the Chernobyl nuclear power plant accident in April 1986, a large increase in the incidence of childhood thyroid cancer was reported in contaminated areas. Most of the radiation exposure to the thyroid was from iodine isotopes, especially 131I. We carried out a population-based case–control study of thyroid cancer in Belarus and the Russian Federation to evaluate the risk of thyroid cancer after exposure to radioactive iodine in childhood and to investigate environmental and host factors that may modify this risk. Methods: We studied 276 case patients with thyroid cancer through 1998 and 1300 matched control subjects, all aged younger than 15 years at the time of the accident. Individual doses were estimated for each subject based on their whereabouts and dietary habits at the time of the accident and in following days, weeks, and years; their likely stable iodine status at the time of the accident was also evaluated. Data were analyzed by conditional logistic regression using several different models. All statistical tests were two-sided. Results: A strong dose–response relationship was observed between radiation dose to the thyroid received in childhood and thyroid cancer risk (P<.001). For a dose of 1 Gy, the estimated odds ratio of thyroid cancer varied from 5.5 (95% confidence interval [CI] = 3.1 to 9.5) to 8.4 (95% CI = 4.1 to 17.3), depending on the risk model. A linear dose–response relationship was observed up to 1.5–2 Gy. The risk of radiation-related thyroid cancer was three times higher in iodine-deficient areas (relative risk [RR]= 3.2, 95% CI = 1.9 to 5.5) than elsewhere. Administration of potassium iodide as a dietary supplement reduced this risk of radiation-related thyroid cancer by a factor of 3 (RR = 0.34, 95% CI = 0.1 to 0.9, for consumption of potassium iodide versus no consumption). Conclusion: Exposure to 131I in childhood is associated with an increased risk of thyroid cancer. Both iodine deficiency and iodine supplementation appear to modify this risk. These results have important public health implications: stable iodine supplementation in iodine-deficient populations may substantially reduce the risk of thyroid cancer related to radioactive iodines in case of exposure to radioactive iodines in childhood that may occur after radiation accidents or during medical diagnostic and therapeutic procedures.
Until the Chernobyl accident, the carcinogenic effect of exposure to 131I was considered to be small compared with that of external photon exposure (1,2). In fact, little information about the effects of exposure of the child’s thyroid to radioactive iodine isotopes was then available, because most studies on the risk of cancer associated with exposure to131I had been conducted in adult populations with underlying thyroid disease. It was, however, well known that the child’s thyroid was sensitive to external x-rays (3,4).

The accident that occurred in reactor 4 of the Chernobyl nuclear power plant in the Ukraine in April 1986 resulted in widespread radioactive contamination, particularly of the territories of Belarus, the Russian Federation, and the Ukraine. For most persons living in these territories, the main contribution to the radiation dose to the thyroid was from radioactive isotopes of iodine, mainly 131I. It is estimated that, in Belarus, the thyroids of several thousand children received 131I doses of at least 2 Gy (5).

A very large increase in the incidence of thyroid cancer in young people was observed as early as 5 years after the accident in Belarus (6,7) and slightly later in the Ukraine and the Russian Federation (8–10). Before the accident, incidence rates in children were, as in most countries in the world, less than one case per million per year; this rate increased to more than 90 per million in Gomel, the most contaminated region of Belarus, in the period from 1991 through 1994 (10). By the end of 2003, a total of 740 cases of childhood thyroid cancer had been observed in Belarus alone among those who were exposed as children (i.e., aged 0–14 years); about half of these were residents of Gomel region at the time of the accident (E. Demidchik, personal communication). An increased incidence of thyroid cancer continues to be observed in this population as it ages into adolescence and young adulthood. The evidence that this increase is related to the fallout of radioactive iodine from the Chernobyl accident is compelling (11–16). Questions remain, however, concerning the magnitude of the risk of thyroid cancer associated with these exposures(5) and the role of iodine deficiency, which was present in most of the affected areas at the time of the accident (17) and which has been postulated as a possible modifier of radiation-related thyroid cancer risk(18,19).

The Chernobyl experience provides the most important source of information for the quantification of risks to young people from exposure to 131I and shorter-lived radioactive isotopes and for the study of factors—both environmental and host factors—that may play a role in the risk of radiation-related thyroid cancer in these areas (18,20,21). We carried out a case–control study of thyroid cancer in young people to evaluate the risk of thyroid cancer related to exposure to 131I in childhood and to study environmental and host factors that may modify this risk, in particular iodine deficiency and stable (nonradioactive) iodine intake.