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  Vol. 292 No. 21, December 1, 2004 TABLE OF CONTENTS
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Thyroid Neoplasia, Autoimmune Thyroiditis, and Hypothyroidism in Persons Exposed to Iodine 131 From the Hanford Nuclear Site

Scott Davis, PhD; Kenneth J. Kopecky, PhD; Thomas E. Hamilton, MD, PhD; Lynn Onstad, ScM; and the Hanford Thyroid Disease Study Team

JAMA. 2004;292:2600-2613.

Context  Approximately 740 000 Ci (2.73 x 1016 Bq) of iodine 131 (131I) were released to the atmosphere from the Hanford Nuclear Site in Washington State from 1944 through 1957. The risk of thyroid disease resulting from prolonged environmental 131I exposure is poorly understood.

Objective  The Hanford Thyroid Disease Study (HTDS) was conducted to determine if thyroid disease is increased among persons exposed as children to atmospheric releases of 131I from Hanford.

Design  Retrospective cohort study. Exposure could have occurred from December 1944 through 1957. Follow-up occurred until the time of the HTDS examination (December 1992–September 1997). Participants’ thyroid radiation doses from Hanford’s 131I releases were estimated from interview data regarding residence and dietary histories.

Setting  The cohort included a sample of all births from 1940 through 1946 to mothers with usual residence in 1 of 7 counties in eastern Washington State.

Participants  Of 5199 individuals identified, 4350 were located alive and 3440 were evaluable; ie, had sufficient data for dose estimation and received an HTDS evaluation for thyroid disease, including a thyroid ultrasound, physical examination, and fine needle biopsy if required to evaluate thyroid nodularity.

Main Outcome Measures  Thyroid cancer, benign thyroid nodules, total neoplasia, any thyroid nodules, autoimmune thyroiditis, and hypothyroidism.

Results  There was no evidence of a relationship between Hanford radiation dose and the cumulative incidence of any of the outcomes. These results remained unchanged after taking into account several factors that might confound the relationship between radiation dose and the outcomes of interest.

Conclusion  These results do not support the hypothesis that exposure during infancy and childhood to 131I at the dose levels (median, 97 mGy; mean, 174 mGy) and exposure circumstances experienced by our study participants increases the risk of the forms of thyroid disease evaluated in this study.


Author Affiliations: Programs in Epidemiology (Drs Davis and Hamilton and Ms Onstad) and Cancer Prevention (Dr Kopecky), Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, and Departments of Epidemiology (Dr Davis) and Biostatistics (Dr Kopecky), School of Public Health and Community Medicine, and Division of Endocrinology and Metabolism, School of Medicine (Dr Hamilton), University of Washington, Seattle.



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