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      Risk of Thyroid Cancer After Exposure to 131 I in Childhood

      , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , ,
      JNCI: Journal of the National Cancer Institute
      Oxford University Press (OUP)

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          Abstract

          After the Chernobyl nuclear power plant accident in April 1986, a large increase in the incidence of childhood thyroid cancer was reported in contaminated areas. Most of the radiation exposure to the thyroid was from iodine isotopes, especially 131I. We carried out a population-based case-control study of thyroid cancer in Belarus and the Russian Federation to evaluate the risk of thyroid cancer after exposure to radioactive iodine in childhood and to investigate environmental and host factors that may modify this risk. We studied 276 case patients with thyroid cancer through 1998 and 1300 matched control subjects, all aged younger than 15 years at the time of the accident. Individual doses were estimated for each subject based on their whereabouts and dietary habits at the time of the accident and in following days, weeks, and years; their likely stable iodine status at the time of the accident was also evaluated. Data were analyzed by conditional logistic regression using several different models. All statistical tests were two-sided. A strong dose-response relationship was observed between radiation dose to the thyroid received in childhood and thyroid cancer risk (P<.001). For a dose of 1 Gy, the estimated odds ratio of thyroid cancer varied from 5.5 (95% confidence interval [CI] = 3.1 to 9.5) to 8.4 (95% CI = 4.1 to 17.3), depending on the risk model. A linear dose-response relationship was observed up to 1.5-2 Gy. The risk of radiation-related thyroid cancer was three times higher in iodine-deficient 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). Exposure to (131)I in childhood is associated with an increased risk of thyroid cancer. Both iodine deficiency and iodine supplementation appear to modify this risk. These results have important public health implications: stable iodine supplementation in iodine-deficient 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.

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          Most cited references17

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          Thyroid Cancer after Exposure to External Radiation: A Pooled Analysis of Seven Studies

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            Thyroid cancer after Chernobyl.

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              Cancer risks from medical radiation.

              Elaine Ron (2003)
              About 15% of the ionizing radiation exposure to the general public comes from artificial sources, and almost all of this exposure is due to medical radiation, largely from diagnostic procedures. Of the approximately 3 mSv annual global per caput effective dose estimated for the year 2000, 2.4 mSv is from natural background and 0.4 mSv from diagnostic medical exams. Diagnostic and therapeutic radiation was used in patients as early as 1896. Since then, continual improvements in diagnostic imaging and radiotherapy as well as the aging of our population have led to greater use of medical radiation. Temporal trends indicate that worldwide population exposure from medical radiation is increasing. In the United States, there has been a steady rise in the use of diagnostic radiologic procedures, especially x rays. Radiotherapy also has increased so that today about 40% of cancer patients receive some treatment with radiation. Epidemiologic data on medically irradiated populations are an important complement to the atomic-bomb survivors' studies. Significant improvement in cancer treatment over the last few decades has resulted in longer survival and a growing number of radiation-related second cancers. Following high-dose radiotherapy for malignant diseases, elevated risks of a variety of radiation-related second cancers have been observed. Risks have been particularly high following treatment for childhood cancer. Radiation treatment for benign disease was relatively common from the 1940's to the 1960's. While these treatments generally were effective, some resulted in enhanced cancer risks. As more was learned about radiation-associated cancer risks and new treatments became available, the use of radiotherapy for benign disease has declined. At moderate doses, such as those used to treat benign diseases, radiation-related cancers occur in or near the radiation field. Cancers of the thyroid, salivary gland, central nervous system, skin, and breast as well as leukemia have been associated with radiotherapy for tinea capitis, enlarged tonsils or thymus gland, other benign conditions of the head and neck, or benign breast diseases. Because doses from diagnostic examinations typically are low, they are difficult to study using epidemiologic methods, unless multiple examinations are performed. An excess risk of breast cancer has been reported among women with tuberculosis who had multiple chest fluoroscopies as well as among scoliosis patients who had frequent diagnostic x rays during late childhood and adolescence. Dental and medical diagnostic x rays performed many years ago, when doses were presumed to be high, also have been linked to increased cancer risks. The carcinogenic effects of diagnostic and therapeutic radionuclides are less well characterized. High risks of liver cancer and leukemia have been demonstrated following thorotrast injections, and patients treated with radium appear to have an elevated risk of bone sarcomas and possibly cancers of the breast, liver, kidney, thyroid, and bladder.
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                Author and article information

                Journal
                JNCI: Journal of the National Cancer Institute
                Oxford University Press (OUP)
                1460-2105
                0027-8874
                May 18 2005
                May 18 2005
                May 18 2005
                May 18 2005
                May 18 2005
                May 18 2005
                : 97
                : 10
                : 724-732
                Article
                10.1093/jnci/dji129
                15900042
                6b1b324f-a340-45a2-a13e-372212f036b1
                © 2005
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