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In a review published in
Endocrine, researchers from the Laboratory of Experimental Oncology (IRCM/CEA-Jacob) compared the consequences of exposure to ionizing radiation in the populations living close to the Chernobyl and Fukushima nuclear power plants at the times of their respective accidents. They discussed thyroid cancer risks following radioactive iodine exposure as a function of recent dosimetry data, population management, the presence or absence of dietary iodine deficiency, and potassium iodine prophylaxis.
The two large nuclear power plant accidents, the first in Chernobyl in 1986 and the second in Fukushima in 2011, projected enormous quantities of radioactive iodine into the atmosphere. All radioactive iodine isotopes have short half-lives ranging from several hours to several days, but the risk of contamination does remain for several weeks after the accident.
After a nuclear accident, contamination of the surrounding populations occurs either through inhalation of radioactive iodine or by ingestion of locally-produced foods (e.g., vegetables and particularly milk). Normally, the thyroid gland takes up dietary iodine and uses it to synthesize hormones. However, any radioactive iodine will also be taken up by the thyroid, thus causing exposure to ionizing radiation. Relative concentrations of radioactive iodine can become particularly high in children, who have small thyroids, and in people with iodine deficiencies, which increases the thyroid's uptake of the radioactive iodine. In childhood, the thyroid is also highly sensitive to radiation because of the proliferation of thyrocytes, the cells that produce and secrete thyroid hormones. Thus, in children, the risk of developing radiation-induced thyroid cancer in the five to ten years following exposure to doses ≥50 milligrays (mGy) is greatly increased. Any effects of exposure to ionizing radiation after this childhood period of high thyroid radiosensitivity have not been demonstrated.
In a review published in Endocrine, researchers from the Laboratory of Experimental Oncology (IRCM) and Gustave Roussy teamed with a specialist in radioprotection (EDF) to compare the consequences of exposure to ionizing radiation in the populations living close to the Chernobyl and Fukushima nuclear power plants at the times of their respective accidents.
In Chernobyl, radiation doses to the thyroid ranged from several mGy to 100–500 mGy for the majority of exposed people. In Fukushima, they ranged from 1–2 to 20 mGy. Thus, at least a part of the children in Chernobyl and the near entirety of those in Fukushima were exposed to low radiation doses (<50 mGy). However, conventional epidemiological statistical methods are ill suited for estimating the risk of radiation-induced thyroid cancer in such low doses. Indeed, as radiation doses go down so does the frequency of radiation-induced (R) cancers. If these low doses do cause thyroid cancers, the number of these latter is insignificant compared to the number of spontaneous (S) thyroid cancers occurring with age. Less pronounced increases in thyroid cancer incidence were reported in adults after the accidents, but they were in all likelihood due to increased post-accident screening rather than the ejected ionizing radiation itself.
To determine thyroid cancer etiology and define risks following low-dose radiation exposure, researchers and healthcare providers must be able to differentiate R and S thyroid cancers. That task is difficult however, because the two forms present the same clinical, anatomical, pathological and mutational characteristics. In their review, the IRCM/Roussy team discussed robust and promising molecular signatures* for R and S thyroid tumor discrimination.
The researchers also reemphasized the preventive measures that must be deployed after nuclear accidents, underlining particularly the importance of providing the affected populations with potassium iodide (KI), which floods the thyroid, thus preventing the fixation of radioactive iodine. KI can be administered in the form of tablets, with priority given to the highly radiosensitive children and furthermore pregnant women to protect fetuses. KI administration and other measures such as population evacuation and dietary restrictions effectively reduce the dose of radiation received by the thyroid in the presence of radioactive iodine.
The consequences of the Chernobyl accident illustrate clearly that shelters and plans for dietary restrictions and KI thyroid prophylactics must be available and deployable to protect the people living close to nuclear power plants should accidents occur. Children, adolescents and pregnant women should have priority for these effective and safe countermeasures.
* Between 2011 and 2013, a partnership between CEA–Fontenay-aux-Roses, the Gustave Roussy campus and the Pasteur Hospital in Nice, identified a number of molecular markers able to distinguish the causes of certain thyroid cancers. Specifically, these "signatures" differentiate tumors that occur spontaneously from those caused by exposure to radiation (via radiation therapy, nuclear accidents, etc.).
Comparison of Transcriptomic Signature of Post-Chernobyl and Postradiotherapy Thyroid Tumors I Thyroid
Consequences of atmospheric contamination by radioiodine: the Chernobyl and Fukushima accidents I Endocrine
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