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Submitted on May 16, 2005
Accepted on September 27, 2005
Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center and Division of Endocrinology and Metabolism, School of Medicine, University of Washington, Seattle, WA; Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA; Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center and Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle, WA; Program in Cancer Prevention, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center and Department of Biostatistics, School of Public Health and Community Medicine, University of Washington, Seattle, WA
* To whom correspondence should be addressed. E-mail: tehamilton{at}aol.com.
Context The risk of primary hyperparathyroidism from exposure to external radiation has been well documented in the last twenty years. However, it remains unclear whether hyperparathyroidism might also be caused by internal exposure to radioactive iodine.
Objective To determine whether exposure to 131I from the Hanford Nuclear Site during 1944 to 1957 increased the risk of hyperparathyroidism among people living in the area.
Design The Hanford Thyroid Disease Study (HTDS) was conducted as a retrospective cohort study.
Setting General community in Washington State.
Participants 5199 persons born to mothers with usual residence in one of seven counties in eastern Washington State were randomly selected from birth records for the years 1940 through 1946.
Intervention Of the 5199 selected, 3440 underwent an HTDS clinical evaluation, including an evaluation for hyperparathyroidism. Individual thyroid radiation dose, which could be estimated for 3191 study participants ranged from 0.0029 to 2823 mGy (mean 174 mGy).
Main Outcome Measure Hyperparathyroidism
Results Of 3440 evaluable participants, we confirmed 12 cases of primary hyperparathyroidism (0.35%). We found no evidence that the cumulative incidence of hyperparathyroidism increased with increasing radiation dose.
Conclusion In summary, this study shows no evidence that 131I, received at young ages and at doses and exposure conditions experienced by this cohort, increased the risk of primary hyperparathyroidism. However, the effect of different doses and conditions of exposure to 131I on the risk of hyperparathyroidism remains to be defined.
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