39 These data also may be useful as a baseline, should genetic changes appear in later generations, possibly related to radiation exposure. IV. Thyroid Findings A. EARLY FINDINGS Examinationsfor possible thyroid abnormalities were an importantpart of the program from the beginning. At the time of the accident it was not considered likely that the thyroid had received a sufficient dose of radioiodine to result in abnormalities. In retrospect this proved to be quite wrong, since thyroid injury and its sequelae have been the mostseriouslate result of the fallout exposure in the Marshallese people. A chronological review of events leading to the development of thyroid abnormalities follows. Beginningseveral years after exposure it was noted that 5 of 19 children exposed at < 10 years of age showedretardation of growth.8-16 This was we U yy kad u * particularly notable in the boys exposed at <5 years of age (Figure 26). The cause ofthis retardation was not immediately apparent. It was recognized that thyroid hormonedeficiency from thyroid injury could result in such growth retardation. However, examinationsduringthis early period did not reveal any thyroid abnormalities, and the PBI levels in these children as well as in all Marshallese were in the normalto high range. The growth retardation gradually became mre apparent, and at Figure 27. Growth-retarded boys exposed at age | year (No.3, left, and No. 5), 6 months after start of treatment at age 11 (1966). & Height(cm) 180 105Fr 75 60+ Figure 26. Statural growth in Rongelap boys exposed at <5 years of age, 1958-1967. Figure 28. Bone dysgenesis of heads of humeni in subject No.5, typical of hypothyroid disease (1965).