Received date: July 10, 2012; Accepted date: July 10, 2012; Published date: July 15, 2012
Citation: Katoh H, Watanabe M, Adachi M (2012) Secondary Thyroid Cancer after Exposure to Radioactive Iodine from the Fukushima Daiichi Nuclear Power Plant accident. Otolaryngology 2:e104. doi:10.4172/2161-119X.1000e104
Copyright: © 2012 Katoh H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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The catastrophic great east Japan earthquake on March 11, 2011 triggered the explosion of Fukushima Daiichi Nuclear Power Plants. As a result, high volatility fission products including 129mTe, 131I, 134Cs, 136Cs, and 137Cs were released into the air and deposited on the ground. Moreover, highly radioactive contaminated water continued to escape from the nuclear plant after 1 year after the accident. Although the impacts of radiation exposure on rates of non-thyroid solid cancers and leukemia in the exposed population is still unclear, strong evidence of an increased risk of developing secondary thyroid cancer was found among children who were exposed to radioactive iodine after the Chernobyl Nuclear Power Plant accident on 26 April 1986 in Ukraine. Ideally, potassium iodide should be prophylactically administered before or within several hours after 131I exposure. Administration of potassium iodide more than 1 day after exposure has a limited effect and is not recommended unless further exposure is expected . In the case of Fukushima, children were not given prophylactic potassium iodide immediately. Thyroid screening for children who are among the evacuees was started in October 2011 and has gradually increased, and screening for the all citizens who are younger than 18 years will be started in Fukushima prefecture after 2014.
Thyroid screening should be started immediately after a nuclear disaster both for early detection of disease in the affected population and to estimate the incidence of secondary thyroid cancer as accurately as possible. It is difficult to determine the most appropriate level of screening because the efficacy of screening relies on the level (i.e. Screening more people is costly but has limited benefits). Some increase in the reported incidence of secondary thyroid cancer after the Fukushima accident may be observed because of the screening effect, no matter how carefully data are collected. However, even though the screening effect may decrease over time, the eligibility of citizens for screening should not be geographically narrowed considering the scattered hot spots of radioactive agents in prefectures outside of Fukushima. Precise information from individuals and the radiation level in each area should be tracked.
As the number of examined individuals rises, the need for Fine- Needle Aspiration Cytology (FNAC) will increase. The diagnostic accuracy of FNAC reaches more than 95% for papillary thyroid cancer in adolescence, although the diagnostic accuracy of FNAC for follicular cancer is still low. Additionally, increasing the diagnostic accuracy of FNAC in children is very important, as it is increasing the specificity of ultrasound screening.
Other diagnostic and prognostic markers are needed to refine the accuracy of FNAC and to estimate the aggressiveness of each tumor. The revised management guidelines of the American Thyroid Association recommend the use of an appropriate mutational panel for thyroid nodules with indeterminate FNAC to assist clinical management . Most sporadic thyroid cancers are caused by either a point mutation or chromosomal rearrangement. A point mutation is a single nucleotide change, often in the RAS and BRAF genes. Chromosomal rearrangement can be a deletion, duplication, inversion, and translocation, caused by breakage and fusion of parts of chromosomes .
Chromosomal rearrangements of the tyrosine kinase protooncogene RET, specifically RET/PTC rearrangements, are considered a hallmark of radiation-induced thyroid cancer and are found in approximately 80% of patients with papillary thyroid cancer who were exposed to either accidental radiation or therapeutic radiation during childhood or adolescence [4,5]. The two most common types of rearrangements are RET/PTC1 (fusion with CCDC6) and RET/PTC3 (fusion with NCOA4) [6,7]. RET/PTC3 rearrangements was the most common mutation observed after the Chernobyl accident, followed by the RET/PTC1 rearrangements with delay . Indeed, radioactive induction of RET/PTC rearrangements was confirmed by animal and in vitro experiments [9-11]. However, high incidence of RET/ PTC rearrangements is also reported in sporadic childhood papillary thyroid cancer in patients with no history of exposure to radiation . Therefore, discovery of more sensitive and specific markers of thyroid cancer is greatly needed to improve early detection, prognostication, and determination of the most appropriate treatment. It is also important for determination of governmental compensation.
In 2005, nearly 20 years after the Chernobyl accident, researchers finally reached a consensus on the causal relationship of radiation exposure with thyroid cancer. Accumulation of a sufficient number of patients with a disease to show statistical evidence of a cause takes a long time, often resulting in insufficient governmental provision of resources to address the problem. Thus, it is important to pay more attention to individual cases and not to overlook specific signs of a cause that may be proven with more evidence in the future.
Hiroshi Katoh was supported by the Uehara Memorial Foundation Research Fellowship. Makoto Adachi was supported by the Uehara Memorial Foundation Postdoctoral Fellowship and the Japan Society for the Promotion of Science Postdoctoral Fellowship for Research Abroad. None of the study sponsors had any role in the decision to submit this manuscript for publication. We particularly thank the Otolaryngology editorial team.
The authors declare no conflict of interest.