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
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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).