Thyroid Disease 60 Years After Hiroshima and 20 Years After Chernobyl

Abstract

1 Subsequent surveys found a significant excess of papillary thyroid cancer but not of follicular, medullary, or anaplastic cancer.2,3 A straight line adequately describes the relationship between radiation dose and thyroid cancer incidence, relative risks are similar in males and females, and age at exposure substantively influences risk. Risk is highest for children exposed when younger than 10 years, and there is no significant increase in risk of thyroid cancer for those exposed after age 20 years. Radiation-induced thyroid cancers are rarely fatal, but the risk per unit dose following exposure in childhood is higher than for any other radiation-induced malignancy. 4 Radiation-induced thyroid cancer has been extensively studied in human populations other than atomic bomb survivors. These populations include patients treated with radiation for malignant and nonmalignant conditions, populations exposed to radioactive fallout from nuclear weapons tests, and populations living in the vicinity of nuclear installations such as Chernobyl in the former Soviet Union and Hanford in Washington State. 4,5 The latest research from the Adult Health Survey (AHS) in Japan reported in this issue of JAMA by Imaizumi and colleagues 6 derives from a cross-sectional study of 4091 survivors of the Hiroshima and Nagasaki atomic bombings in 1945 who were invited to a special thyroid examination more than 50 years later. The prevalences of thyroid cancer (n=87), benign nodules (n = 207), and cysts (n = 324) were significantly increased and directly related to radiation dose, and the risk decreased with increasing age at exposure; however, autoimmune thyroid diseases (positive antithyroid antibodies, antithyroid antibody-positive hypothyroidism, or Graves disease) were not linked to radiation exposure.There are several new findings of note. First, it is remarkable that a biological effect from a single brief environmental exposure nearly 60 years in the past is still present and can be detected. The radiation doses (mean, 45 cGy) were related to the distance from the hypocenters, and enormous effort was required to accurately estimate exposures for individuals. 7 The existence of dose-response relationships strongly supports the authors' assertion of a radiationrelated excess of thyroid neoplasms nearly 60 years after exposure. Second, using highly sensitive assays to detect serum levels of antithyroid antibodies and thyroid-stimulating hormone, this study was not able to confirm the findings of a smaller but similar investigation of Nagasaki atomic bomb survivors that purported to show an association between radiation and autoimmune thyroid disease. 8 The absence of a dose-response relationship for any measure of autoimmune disease in the study by Imaizumi et al is consistent with earlier studies of atomic bomb survivors 6 and a recent study of persons exposed as children to iodine 131 releases from the Hanford nuclear site. 9The study of atomic bomb survivors remains the single most important study of radiation effects in huma...

Risk of thyroid cancer in survivors of childhood cancer: Results from the British Childhood Cancer Survivor Study

“…10 Reports from studies of survivors of the Chernobyl accident have reported a high risk of thyroid cancer in children as a consequence of exposure to lowdose radiation. [6][7][8][9] As a result, thyroid carcinoma is a complication of irradiation even when the tissue lies outside the radiation field where the gland is exposed to scatter irradiation. The radiosensitivity of thyroid tissue coupled with the increased vulnerability of the paediatric gland accounts for the high incidence of thyroid carcinoma in childhood cancer survivor cohorts 23 as well as children who were exposed to radioactive contamination after the Chernobyl nuclear accident in 1986.…”

“…The radiosensitivity of thyroid tissue coupled with the increased vulnerability of the paediatric gland accounts for the high incidence of thyroid carcinoma in childhood cancer survivor cohorts 23 as well as children who were exposed to radioactive contamination after the Chernobyl nuclear accident in 1986. [6][7][8][9] Childhood cancer survivors who were under the age of 5 at the time of exposure to radiation therapy are reported to be at greatest risk and the risk remains comparatively higher for those under the age of 10 compared to older age groups. 10 In our study, risk was lowest in those aged more than 10 years when compared to the 5-9 and 0-4 year age groups: RR 1.0 (standard), 1.0 (0.4-2.2) and 0.5 (0.2-1.3), respectively although there was no significant difference.…”

“…The proportion of papillary carcinomas in radiation induced thyroid neoplasia has been reported to be more than 90% in post-Chernobyl studies with the type of differentiation (follicular or papillary) associated with age at exposure to radiation. [6][7][8][9] The genesis of papillary carcinomas in radiation-induced thyroid malignancy is thought to result from mutations in the RET/PTC oncogene. 24 Radiation exposure has been shown to result in activating rearrangements of the RET/PTC oncogene.…”

“…Studies of thyroid cancer following the Chernobyl reactor disaster provide evidence of a doseresponse relationship and a predominance of papillary thyroid cancer in children: thousands of thyroid cancers were reported but only a few deaths. [6][7][8][9] The paediatric thyroid is particularly vulnerable to the oncogenic effects of radiation although there is evidence of cell kill at exposure to radiation doses higher than 3,000 cGy. 10 Thyroid cancer has been frequently reported as a SPN after treatment for childhood cancers including Hodgkin's disease, neuroblastoma and other malignancies that involve radiation to the neck region.…”

Radioiodine therapy of thyrotoxicosis in children and adolescents. Indications, efficacy and safety. Literature review

“…Напом-ним, что для лечения дифференци рованного РЩЖ применяются гораздо более высокие разовые активности 131 I (100-200 мКи и выше) и до суммарной активности 600 мКи нет никаких данных о повышении риска радиа ционно индуцированных карцином и лейкемии, нарушении детородной функ-ции, врожденных аномалиях развития у по-томков [21,22]. Необходимо отметить, что накопленный мировой наукой опыт свиде-тельствует, что риск развития РЩЖ возни-кает после облучения ЩЖ (минимальный латентный период 5 лет, максимальный -30 лет) в малых дозах (0,05-25 Гр; 0,09-30 мкКи/г) и при условии непрерывного (повто ряющегося) облучения ЩЖ [23,24]. Это объяс няется накоплением абберантных и сублетальных повреждений ДНК, которые накапливаются и повышают риск развития РЩЖ.…”