IX. THYROID ABNORMALITIES* It has been clearly demonstrated that the most serious late effects of accidental exposure to fallout in the Marshallese residing on Rongelap and Utirik Atolls on March 1, 1954, has been related to radiation injury to the thyroid, as evidenced by development of nodularities and hypofunction of the gland. Such injury was due to exposure to penetrating gamma radiation and internal absorption of radionuclides during the two-day period prior to their evacuation. In this section, thyroid effects are summarized. Emphasis is on the findings during the past seven years. In Appendix II, the estimated thyroid doses are discussed. Since the principal effects of thyroid exposure, development of nodules (benign and malignant) and hypofunction, are dose dependent, the establishment of thyroid dose is most important in order to derive dose-effect relationships. Unfortunately, it must be stated at the outset that the thyroid dose estimates are subject to considerable uncertainty and may, at least in some cases, be considerably higher than estimated. The effect of thyroid injury on growth and development in the children is described in Section IV. A. Background (Chronology of Developments) Beginning several years after exposure it was noted that some children exposed at <10 years of age showed growth retardation, particularly boys exposed at <5 years of age (see Section IV), but the cause was not immediately apparent. It was recognized that thyroid hormone deficiency due to thyroid in- jury could result in such growth retardation, but examinations during this early period did not reveal any thyroid abnormalities, and the PBI levels in these children as well as in all Marshallese were in the normal to high range. The growth retardation gradually became more apparent, and at 8 years post ex- nosure two boys were recognized to be stunted in growth. They had been ex- posed at one year of age and gradually developed atrophy of the thyroid gland and signs of myxedema with puffy faces, dry skin, sluggish reflexes, and bony dysgenesis of the humerus and femur. In 1965 a satisfactory method for serum thyroxine analysis by lon ex- change column became available. Studies by this method showed that some of the children did indeed have low serum thyroxine levels. Control observations on unexposed Marshallese revealed that many of them had unusually high *The following persons assisted the senior author in the preparation of this report or were actively involved in some of the special studies: Surgical findings--Dr. B. Dobyns (Cleveland Metropolitan General Hospital, Cleveland, OH); Histopathology--Dr. D.E. Paglia (U. of California, Los Angeles); Hypothyroidism--Dr. B.R. Larsen (Peter Bent Brigham Hospital, Boston, MA); Clinical--Drs. J.B. Rall, J. Robbins, and J. Wolff (NIH, Bethesda, MD); Dr. J.T. Nicoloff (U. of Southern California, Los Angeles); Dr. B. Colcock (Lahey Clinic, Boston, MA, Ret.): Drs. H. Pratt, K. Knudsen, and W. Adams (BNL); Dr. C.S. Hill, Jr. (M.D. Anderson Hospital, Houston, TX); Dr. D.D. Becker (Cornell Medical Center, New York, NY). See p. 55 for list of pathologists. -53-