Cardis Elisabeth, Kesminiene Ausrele, Ivanov Victor, Malakhova Irina, Shibata Yoshisada, Khrouch Valeryi, Drozdovitch Vladimir, Maceika Evaldas, Zvonova Irina, Vlassov Oleg, Bouville André, Goulko Guennadi, Hoshi Masaharu, Abrosimov Alexander, Anoshko Jadvyga, Astakhova Larisa, Chekin Sergey, Demidchik Evgenyi, Galanti Rosaria, Ito Masahiro, Korobova Elena, Lushnikov Evgenyi, Maksioutov Marat, Masyakin Vladimir, Nerovnia Alexander, Parshin Vladimir, Parshkov Evgenyi, Piliptsevich Nikolay, Pinchera Aldo, Polyakov Semyon, Shabeka Nina, Suonio Eero, Tenet Vanessa, Tsyb Anatoli, Yamashita Shunichi, Williams Dillwyn
International Agency for Research on Cancer, Lyon, France.
J Natl Cancer Inst. 2005 May 18;97(10):724-32. doi: 10.1093/jnci/dji129.
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.
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.
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).
Exposure to (131)I 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.
1986年4月切尔诺贝利核电站事故后，据报道受污染地区儿童甲状腺癌发病率大幅上升。甲状腺所受的大部分辐射来自碘同位素，尤其是131I。我们在白俄罗斯和俄罗斯联邦开展了一项基于人群的甲状腺癌病例对照研究，以评估儿童期接触放射性碘后患甲状腺癌的风险，并调查可能改变这种风险的环境和宿主因素。
我们研究了截至1998年的276例甲状腺癌病例患者和1300例匹配的对照对象，事故发生时他们均未满15岁。根据每个对象在事故发生时及之后数天、数周和数年的行踪及饮食习惯估算其个人剂量；还评估了他们在事故发生时可能的稳定碘状态。使用几种不同模型通过条件逻辑回归分析数据。所有统计检验均为双侧检验。
观察到儿童期甲状腺接受的辐射剂量与甲状腺癌风险之间存在强烈的剂量反应关系（P<0.001）。对于1 Gy的剂量，根据风险模型，甲状腺癌的估计比值比在5.5（95%置信区间[CI]=3.1至9.5）至8.4（95%CI=4.1至17.3）之间变化。在剂量达到1.5 - 2 Gy之前观察到线性剂量反应关系。缺碘地区辐射相关甲状腺癌的风险比其他地区高3倍（相对风险[RR]=3.2，95%CI=1.9至5.5）。作为膳食补充剂服用碘化钾可使这种辐射相关甲状腺癌的风险降低2/3（服用碘化钾与未服用相比，RR=0.34，95%CI=0.1至0.9）。
儿童期接触131I与甲状腺癌风险增加有关。碘缺乏和碘补充似乎都会改变这种风险。这些结果具有重要的公共卫生意义：在缺碘人群中补充稳定碘可能会在儿童期因辐射事故或医疗诊断及治疗程序中可能接触放射性碘的情况下，大幅降低与放射性碘相关的甲状腺癌风险。
