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ARTICLE |

Thyroid Hypofunction After Exposure to Fallout From a Hydrogen Bomb Explosion

P. Reed Larsen, MD; Robert A. Conard, MD; Knud D. Knudsen, MD; Jacob Robbins, MD; Jan Wolff, MD, PhD; J. Edward Rall, MD; John T. Nicoloff, MD; Brown M. Dobyns, MD
JAMA. 1982;247(11):1571-1575. doi:10.1001/jama.1982.03320360021024.
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Thyroid function was evaluated in the Marshallese who were accidentally exposed to fallout-containing radioiodine isotopes in 1954. Measurements of thyrotrophin (TSH, thyroid-stimulating hormone) levels and free thyroxine (T4) index (FT4I) have revealed that, among 86 persons exposed on Rongelap and Ailingnae atolls, 14 have shown evidence of thyroid hypofunction. This was first noted in some individuals about ten years after exposure. Only two of these showed clinical evidence of hypothyroidism. The most marked TSH elevations were noted in nine persons exposed when younger than 6 years, with estimated doses to the thyroid from 390 to 2,100 rad. Most of this group subsequently had surgery for removal of thyroid nodules. The remaining five cases have been noted more recently among 36 surviving adults exposed at an older age who showed no other detectable thyroid abnormalities. This group had received estimated thyroid doses ranging from 135 to 335 rad and showed modest elevation of serum TSH levels (6 to 9 μU/mL) and a slightly subnormal FT4I. No abnormalities were found in persons on Utirik who received substantially less radiation, and hypothyroidism was present in less than 1% of the control, unexposed Marshallese. The high prevalence of a thyroid hypofunction in these persons indicates that this condition, as well as thyroid nodularity, can be a delayed complication of exposure to early fallout from a nuclear explosion. The fact that a significant fraction of the radiation to the thyroid was from short-lived radioiodine isotopes (132I,133I,135I), as opposed to131I, may account for the severity of the thyroid damage.

(JAMA 1982;247:1571-1575)

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