39 These data also mav be useful as a base line, should - genetic changes appear in later generations, pos- sibly related to radiation exposure. IV. Thyroid Findings A. EARLY FINDINGS Examinations for 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 most seriouslate result of the fallout ex- posure in the Marshallese people. A chronological review of events leading to the development of thyroid abnormalities follows. Beginning several years after exposure it was noted that 5 of 19 children exposed at <10 years of age showedretardation of growth.8-16 This was particularly notable in the boys exposed at <5 years of age (Figure 26). The cause ofthis retardation was not immediately apparent. It was recog- nized that thyroid hormonedeficiency from thyroid injury could result in such growth retardation. 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). However, examinations duringthis early period did not reveal any thyroid abnormalities, and the PBI levels in these children as well asin all Marshallese were in the normal to high range. The growthretardation gradually became more apparent, and at po EET 165+ so} = 135 2 = 120-F a = = 105-- 90F ° omm—ee Exposed at age 1-5 75 e+-=- Control group 4 4 ee 1 3 5 7 9 1k 613 13 7 Age Figure 26. Staturai growth in Rongelap boys exposed at <5 years of age, 1958-1967. SOGb13b Figure 28. Bone dysgenesis of heads of humeri in subject No.5, typical of hypothyroid disease (1965).