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BACKGROUND: Genetic factors may influence an individual's sensitivity to ionising radiation and therefore modify his/her risk of developing papillary thyroid carcinoma (PTC). Previously, we reported that common single nucleotide polymorphisms (SNPs) within the DNA damage recognition gene ATM contribute to PTC risk in Belarusian children exposed to fallout from the Chernobyl power plant accident. Here we explored in the same population the contribution of a panel of DNA repair-related SNPs in genes acting downstream of ATM. METHODS: The association of 141 SNPs located in 43 DNA repair genes was examined in 75 PTC cases and 254 controls from the Gomel region in Belarus. All subjects were younger than 15 years at the time of the Chernobyl accident. Conditional logistic regressions accounting for radiation dose were performed with PLINK using the additive allelic inheritance model, and a linkage disequilibrium (LD)-based Bonferroni correction was used for correction for multiple testing. RESULTS: The intronic SNP rs2296675 in MGMT was associated with an increased PTC risk [per minor allele odds ratio (OR) 2.54 95% CI 1.50, 4.30, P per allele = 0.0006, P corr.= 0.05], and gene-wide association testing highlighted a possible role for ERCC5 (P Gene = 0.01) and PCNA (P Gene = 0.05) in addition to MGMT (P Gene = 0.008). CONCLUSIONS: These findings indicate that several genes acting in distinct DNA repair mechanisms contribute to PTC risk. Further investigation is needed to decipher the functional properties of the methyltransferase encoded by MGMT and to understand how alteration of such functions may lead to the development of the most common type of thyroid cancer.

relationship was observed up to 1.5 – 2 Gy. The risk of radiation-related thyroid cancer was three times higher in iodine-defi cient 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). Conclusion: Exposure to 131 I in childhood is associated with an increased risk of thyroid cancer. Both iodine defi ciency and iodine supplementation appear to modify this risk. These results have important public health implications: stable iodine supplementation in iodine-defi cient 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. [J Natl Cancer Inst 2005;97:724 – 32]

A study aimed at comparing the prevalence of thyroid diseases between children born before and after the accident was outlined with emphasis on rationale and design of the study. In the study, a total of 21 601 children in Gomel city and four districts in the neighborhood of Gomel city were examined from February 1998 to December 2000. There were 9720 children born from January 1, 1983 to April 26, 1986 (Group I), 2409 children born from April 27, 1986 to December 31, 1986 and 9472 children born from January 1, 1987 to December 31, 1989 (Group III). Out of the examined children, 32 (0.15%) thyroid cancers were found, among whom 31 were in Group I and one was in Group II, while no cases in Group III. Our findings demonstrate the likelihood that short-lived radioactive fallout due to the Chernobyl accident induced thyroid cancer in children living near Chernobyl.

We measured the radioactivity in the soil and child food samples from farms near Mogilev (56-270 GBq km(-2) 137Cs), Gomel (36-810 GBq km(-2) 137Cs), and Klincy (59-270 GBq km(-2) 137Cs), who had whole-body 137Cs counting results measured as part of a health examination in the Chernobyl Sasakawa Health and Medical Cooperation Project. Soil contamination on the family farm seems to be the main source of human contamination because most of the people in the area live on small farms and they and their domestic animals eat crops from the farms. A clear correlation was found between the children's whole-body 137Cs counting results and the radioactivity in their food (correlation coefficient: 0.76; confidence level of correlation: 3.2 x 10(-9)). There were also significant correlations between the whole-body 137Cs counting results and both the radioactivity of the soil samples (correlation coefficient: 0.22; confidence level of correlation: 0.0107) and the average contamination level of their current residence (correlation coefficient: 0.20; confidence level of correlation: 0.0174).

A dramatic increase in the incidence of papillary thyroid carcinoma (PTC) after childhood exposure to ionizing radiation from the Chernobyl nuclear accident has been described as the largest number of tumors of one type due to one cause that have ever occurred. inter-individual variations in response to radiation have been documented and the role of genetics in sporadic PTC is well established, suggesting that genetic factors may also affect the risk of radiation-related PTC. To investigate how environmental and host factors interplay to modify PTC risk, we genotyped 83 cases and 324 matched controls sampled from children living in the area contaminated by fallout from the Chernobyl power plant accident for 19 polymorphisms previously associated with PTC, thyroid biology or radiation-induced second primary tumors. Significant association with PTC was found for rs1801516 (D1853N) in ATM (odds ratio (OR) = 0.34, 95% confidence interval (CI) 0.16, 0.73) and rs1867277 in the promoter region of FOXE1 (OR = 1.55, 95% CI 1.03, 2.34). Analysis of additional polymorphisms confirmed the association between these two genes and PTC. Our findings suggest that both DNA double-strand break repair pathway and thyroid morphogenesis pathway or dysregulation of thyroid differentiated state maintenance are involved in the etiology of PTC, and that the studied genetic polymorphisms and radiation dose appear to act as independent multiplicative risk factors for PTC.

We collected bricks from buildings in the heavily contaminated evacuated area of Belarus in a 30-km zone around the Chernobyl nuclear power station and the Gomel-Bryansk area of 150-250 km from Chernobyl and estimated the cumulative radiation dose caused by the reactor accident by measuring the thermoluminescence (TL) of the bricks. The annual dose at each location was measured using glass dosimeters and thermoluminescence dosimeters (TLD). The dose rate was measured using an energy-compensated NaI scintillation survey meter. The soil contamination near the location of each brick was measured using a germanium semiconductor detector. The main purpose of the project was to extrapolate the relation between the cumulative external dose and the present dose rate or contamination level to the lower contaminated areas. The results of the glass dosimeter, TLD, and survey meter determinations were almost identical. For a determination of the annual dose higher than 10 mGy y(-1), the cumulative dose by TL (TL dose) was roughly proportional to the annual dose and about 1.5 times larger than the cumulative dose calculated from the annual dose and 137Cs half life. The difference is expected due to the contribution of short-lived nuclides immediately after the accident or localized heavy contamination of the ground surface with 137Cs that migrated afterwards. For annual dose smaller than 10 mGy y(-1), the proportionality was not observed and most of the locations facing indoors showed TL doses very much larger than that expected from the proportionality. The cumulative dose outdoors by TL was also roughly proportional to the regional 137Cs contamination level and the proportional constant is about 10(-1) mGy per GBq km(-2), and is about 250 times larger than the present annual internal dose derived from published results. The correlation between the present dose rate where the brick was sampled and the average 137Cs concentration in the ground soil near the point is not clear, possibly because of the large spatial fluctuation in the 137Cs concentration in the soil.

The Chernobyl nuclear power plant accident happened on April 26, 1986. We investigated the cause of the striking increase in frequency of thyroid cancer in children who lived within a 150 km radius of Chernobyl and who were born before and after the accident. No thyroid cancer was seen in 9472 children born in 1987-89, whereas one and 31 thyroid cancers were recorded in 2409 children born April 27, 1986, to Dec 31, 1986, and 9720 born Jan 1, 1983, to April 26, 1986, respectively. Short-lived radioactive fallout caused by the Chernobyl accident probably induced thyroid cancer in children living near Chernobyl.