Professor Kristien Boelaert

There have been a number of alarming media reports in recent weeks, citing significant increases in the number of children in Fukushima diagnosed with thyroid cancer. Three years after the Daiichi nuclear power plant suffered a triple meltdown, releasing huge quantities of radiation into the atmosphere, the latest figures from the Fukushima Health Management Survey have been released. The surveillance programme includes regular thyroid ultrasound evaluation of people aged 18 years or younger and living in the Fukushima prefecture at the time of the accident. Thus far, 81% of the target population has been screened and 254,280 tests have been performed, identifying 1,490 children with suspicious lesions that have undergone biopsy. Since screening started in 2011, there have been 33 confirmed and 42 suspected diagnoses of thyroid cancer. 

Thyroid cancer generally has a good prognosis, with ten-year survival rates of 95-98% both in adults and children. The incidence of thyroid cancer is increasing significantly worldwide, although this is largely due to significant improvements in imaging procedures and the incidental detection of very small, low-risk malignancies. At first glance the Fukushima figures are concerning, since they indicate a significantly higher incidence of thyroid cancer than the expected one to two per million cases in 10 to 14-year old Japanese children. The carcinogenic effect of radioactive iodine, the main form of environmental radiation released following nuclear accidents, is particularly evident in those aged younger than five years at the time of exposure. The thyroid is the only organ in the body to take up and store iodine - which is required for the synthesis of thyroid hormones - and the childhood thyroid gland seems exquisitely sensitive to radiation-induced carcinogenesis. 

Most of our knowledge regarding the epidemiological consequences of man-made environmental radiation is derived from the intensively studied population cohort living in northern Ukraine around the Chernobyl power plant. The whole-body doses accumulated by those exposed to radiation from Chernobyl over a 19-year period (1986–2005) are estimated to be in the region of 50 millisieverts (mSv) for those in the 50 km exclusion zone closest to the power plant and five times lower for those living further from the reactor site. The doses of radioiodine received to the thyroid were, in fact, relatively small considering that worldwide the estimated average effective dose from natural radiation in the environment is around 200 mSv over a lifetime. In Chernobyl, a clear dose-response relationship was observed, with the greatest risk of developing thyroid cancer observed in those exposed to the highest doses. 

Numerous studies have investigated the molecular biology of radiation-induced thyroid cancer and a raft of genetic mutations and gene-rearrangements have been identified in post-Chernobyl thyroid cancers. However, careful analysis of all available data suggests that, whilst the molecular biology of childhood thyroid cancer is different from that in older subjects, radiation-induced thyroid cancer is not different from non-radiation-induced childhood thyroid malignancy at a molecular level. Moreover, based on the limited available evidence, the clinical outcomes in young people with post-Chernobyl thyroid cancer are similar to the outcomes for those who develop sporadic thyroid malignancy. Young people generally respond extremely well to treatment and are less likely to suffer a relapse than adults. It is still too early to tell if these low recurrence rates will persist since thyroid cancer has a risk of relapse up to 30 years after initial diagnosis. 

It is notable that the first recorded cases of thyroid cancer after the Chernobyl accident occurred three to four years after exposure and in people exposed to higher radiation. In the Fukushima children diagnosed with thyroid cancer, the estimated radiation dose exposure in the four months following the accident was below one mSv. Moreover, the majority of children with suspected or confirmed thyroid cancer were older than ten years at the time of the accident; the current figures indicate no clear dose–response relationship; the total radiation exposure was much lower than in Chernobyl; and increased rates of thyroid cancer diagnosis were evident as early as one year after the accident, suggesting that the increased incidence may not be related to molecular alterations. To reach any valid conclusions about the increase in cancer rates related to the disaster, a screening control group in an unaffected area is required, and it is unfortunate that this has not been set up in Japan. 

Efforts are currently underway to study the molecular biology of the tumours found in children from Fukushima and an internationally accessible biobank of tissues from people potentially affected by radiation is being set up to enhance our understanding of the effects of accidental radiation exposure. At present, a direct link between the Fukushima accident and the increased incidence of thyroid cancer in Japanese children is unconfirmed. 

Professor Kristien Boelaert
Reader in Endocrinology, School of Clinical and Experimental Medicine, College of Medical and Dental Sciences