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Hyperparathyroidism in Persons Exposed to Iodine-131 from the Hanford Nuclear Site

Programs in Epidemiology (T.E.H., S.D., L.O.) and Cancer Prevention (K.J.K.), Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98195; Division of Endocrinology and Metabolism (T.E.H.), University of Washington School of Medicine, Seattle, Washington 98195; and Departments of Epidemiology (S.D.) and Biostatistics (K.J.K.), University of Washington School of Public Health and Community Medicine, Seattle, Washington 98195

Address all correspondence and requests for reprints to: Dr. Thomas Hamilton, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, M4-A830, P.O. Box 19024, Seattle, Washington 98109-1024. E-mail: tehamilton{at}aol.com.

Context: The risk of primary hyperparathyroidism from exposure to external radiation has been well documented in the last 20 yr. However, it remains unclear whether hyperparathyroidism might also be caused by internal exposure to radioactive iodine.

Objective: The objective of this study was to determine whether exposure to ¹³¹I from the Hanford Nuclear Site during 1944–1957 increased the risk of hyperparathyroidism among people living in the area.

Design: The Hanford Thyroid Disease Study was conducted as a retrospective cohort study.

Setting: The study setting was the general community in Washington State.

Participants: The participants were 5199 persons born to mothers with usual residence in one of seven counties in eastern Washington State, randomly selected from birth records for the years 1940–1946.

Intervention: Of the 5199 selected, 3440 underwent a Hanford Thyroid Disease Study clinical evaluation, including an evaluation for hyperparathyroidism. Individual thyroid radiation dose, which could be estimated for 3191 study participants, ranged from 0.0029–2823 mGy (mean, 174 mGy).

Main Outcome Measure: Hyperparathyroidism was the main outcome measure.

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 the doses and exposure conditions experienced by this cohort, increased the risk of primary hyperparathyroidism. However, the effects of different doses and conditions of exposure to ¹³¹I on the risk of hyperparathyroidism remain to be defined.