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Thyroid Disease Associated With Exposure to the Nevada Nuclear Weapons Test Site Radiation: A Reevaluation Based on Corrected Dosimetry and Examination Data

Lyon, Joseph L.*; Alder, Stephen C.*; Stone, Mary Bishop*; Scholl, Alan*; Reading, James C.*; Holubkov, Richard*; Sheng, Xiaoming*; White, George L. Jr*; Hegmann, Kurt T.*; Anspaugh, Lynn†; Hoffman, F Owen§; Simon, Steven L.∥; Thomas, Brian§; Carroll, Raymond¶; Meikle, A Wayne‡

doi: 10.1097/01.ede.0000240540.79983.7f
Original Article

Background: A study was begun in 1965 to 1966 to determine whether children exposed to radioactive iodine from nuclear weapons testing at the Nevada Test Site from 1951 through 1962 were at higher risk of thyroid disease. In 1993, we reported that among those examined in 1985 to 1986 (Phase II) there was an association between radiation from the Nevada Test Site and thyroid neoplasms.

Methods: We reevaluated the relationship between exposure to Nevada Test Site fallout and thyroid disease using newly corrected dose estimates and disease outcomes from the Phase II study. A prospective cohort of school children 12 to 18 years old living in Utah, Nevada, and Arizona was first examined for thyroid disease in 1965 to 1966 and reexamined in 1985 to 1986. In the Phase II report, 2497 subjects formed the basis for this analysis. Thyroid disease, including thyroid neoplasms and thyroiditis, was expressed as cumulative incidence and risk ratios (RRs) with a dose–response expressed as excess risk ratio (ERR/Gy).

Results: The RR between thyroid radiation dose in the highest dose group and thyroid neoplasms increased from 3.4 (in the earlier analysis) to 7.5. The RR for thyroiditis increased from 1.1 to 2.7 with an ERR/Gy of 4.9 (95% confidence interval = 2.0 to 10.0). There were too few malignant thyroid neoplasms to estimate risk.

Conclusions: Persons exposed to radioactive iodine as children have an increased risk of thyroid neoplasms and autoimmune thyroiditis up to 30 years after exposure.

From the Departments of *Family and Preventive Medicine, †Radiobiology, and ‡Internal Medicine; School of Medicine, University of Utah, Salt Lake City, UT; §SENES Oak Ridge, Inc., Oak Ridge, TN; the ∥Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD; and the ¶Department of Statistics, Texas A&M University, College Station, TX.

Editors’ note: A commentary on this article appears on page 599.

Submitted 17 October 2005; accepted 12 April 2006.

This study was supported by Cooperative Agreement # U50/CCU816245 and CDC Grant # 1 R01 EH000055 from the U.S. Centers for Disease Control and Prevention, Atlanta, GA.

Correspondence: Joseph L. Lyon, Department of Family and Preventive Medicine, University of Utah School of Medicine, 375 Chipeta Way, Suite A, Salt Lake City, UT 84108. E-mail: jlyon@dfpm.utah.edu

© 2006 Lippincott Williams & Wilkins, Inc.