No abstract

The accident at the Chernobyl nuclear power plant on April 26, 1986, released approximately 2 EBq of 131I and other radioiodine isotopes that heavily contaminated southern Belarus. An increase in thyroid cancer reported in 1992 and attributed to the Chernobyl accident was challenged as possibly the result of intensive screening. We began a case-control study to test the hypothesis that the Chernobyl accident caused the increase in thyroid cancer. Records of childhood thyroid cancer in the national therapy centers in Minsk in 1992 yielded 107 individuals with confirmed pathology diagnoses and available for interview. Pathways to diagnosis were (1) routine endocrinological screening in 63, (2) presentation with enlarged or nodular thyroid in 25 and (3) an incidental finding in 19. Two sets of controls were chosen, one matched on pathway to diagnosis, the other representing the area of heavy fallout, both matched on age, sex and rural/urban residence in 1986. The 131I dose to the thyroid was estimated from ground deposition of 137Cs, ground deposition of 131I, a data bank of 1986 thyroid radiation measurements, questionnaires and interviews. Highly significant differences were observed between cases and controls (both sets) with respect to dose. The differences persisted within pathway to diagnosis, gender, age and year of diagnosis, and level of iodine in the soil, and were most marked in the southern portion of the Gomel region. The case-control comparisons indicate a strong relationship between thyroid cancer and estimated radiation dose from the Chernobyl accident.

After the Chernobyl accident in 1986, the "liquidators" or clean-up workers were among those who received the highest radiation doses to the thyroid from external radiation. Some were also exposed to radioiodines through inhalation or ingestion. A collaborative case-control study nested within cohorts of Belarusian, Russian and Baltic liquidators was conducted to evaluate the radiation-induced risk of thyroid cancer. The study included 107 cases and 423 controls. Individual doses to the thyroid from external radiation and from iodine-131 ((131)I) were estimated for each subject. Most subjects received low doses (median 69 mGy). A statistically significant dose-response relationship was found with total thyroid dose. The Excess Relative Risk (ERR) per 100 mGy was 0.38 [95% confidence interval (CI): 0.10, 1.09]. The risk estimates were similar when doses from (131)I and external radiation were considered separately, although for external radiation the ERR was not statistically significantly elevated. The ERR was similar for micro carcinomas and larger size tumors, and for tumors with and without lymph node involvement. Although recall bias and uncertainties in doses could have affected the magnitude of the risk estimates, the findings of this study contribute to a better characterization the risk of thyroid cancer after radiation exposure in adulthood.

Significant quantities of long-lived radionuclides were released to the environment during the Chernobyl nuclear power plant accident in 1986. These radionuclides contributed to radiation doses due to ingestion of contaminated foods and external exposure from the ground deposition that resulted. The contributions of these exposure pathways to thyroid doses received by subjects of an epidemiologic study of children from Belarus are evaluated and presented. The analysis shows that ingestion of the long-lived radionuclides, primarily radiocesium, typically contributed a small percentage of the total thyroid dose received by the study subjects. The median and mean fractional contributions were 0.76 and 0.95%, respectively. The contribution of external exposure to the thyroid dose was generally larger and more variable, with median and mean contributions of 1.2 and 1.8% of the total thyroid doses, respectively. For regions close to the reactor site, where radionuclide deposition was highest, the contributions of radiocesium ingestion and external exposure were generally lower than those of the short-lived radioiodine isotopes (132I and 133I) and their precursors (132Te). In other areas, the contributions of these two pathways were comparable to those of the short-lived radioiodines. For all subjects, intakes of 131I were the primary source of dose to the thyroid.

Large amounts of radioiodines were released into the atmosphere during the accident at the Chernobyl nuclear power plant on 26 April 1986. In order to investigate whether the thyroid cancers observed among children in Belarus could have been caused by radiation exposures from the Chernobyl accident, a team of Belarusian, Russian, and American scientists conducted a case-control study to compare cases and controls according to estimated thyroid dose. The primary purpose of this paper is to present detailed information on the estimated thyroid doses, due to intakes of 131I, that were used in the case-control study. The range of the 131I thyroid doses among the 107 cases and the 214 controls was found to extend from 0.00002 to 4.3 Gy, with medians of approximately 0.2 Gy for the cases and 0.07 Gy for the controls. In addition, the thyroid doses resulting from the intakes of short-lived radioiodines (132I, 133I, and 135I) and radiotelluriums (131mTe and 132Te) were estimated and compared to the doses from 131I. The ratios of the estimated thyroid doses from the short-lived radionuclides and from I for the cases and the controls range from 0.003 to 0.1, with median values of approximately 0.02 for both cases and controls.