metabolic function of the thyroids of young children (237). It was observed,
however, that the risk for carcinoma was greater in the older exposed groups
than in the children.
(See Table 4, Appendix IV.) This may be related to the
higher doses in the children ("overkill effect").
(See Appendix II.)
The finding of thyroid nodules in two children who were exposed in utero
on Rongelap indicates the importance of fetal irradiation of the thyroid gland
by radioiodines absorbed by the mother. Since there were only three children
exposed in utero on Rongelap, this finding seems significant.
Though thyroidal hypofunction had been noted earlier in some exposed
Rongelap children,
this finding has been more recently noted in adults of this
population who had received lower thyroid doses and who had not exhibited thyroid nodularity. The appearance of hypothyroidism following accidental exposure to radioactive iodines contained in fallout has not been previously reported except in this Marshallese population.
Studies of Rallison et al. did
not show an increased number of cases of overt hypothyroidism in children exposed to low levels of fallout in Utah (181). Most previous studies of the effects of radioiodine on human thyroid function have consisted of evaluations
of the risk of hypothyroidism developing after various quantities of 131y administered for the treatment of hyperthyroidism (173,209). Such treatment generally results in thyroidal doses >5000 rads.
The most severe thyroidal hypofunction was noted in 6 of 22 Rongelap
children exposed at age <l10 years (Table 8). As pointed out, this group had
received thyroid doses about three times as great as that of the adults be-~
cause of the smaller size of their thyroid glands. While the thyroidal hypofunction in the prospectively studied, older-age group (Table 7), was generally less pronounced,
the plasma TSH concentrations were considerably greater
than those found in the control Marshallese population and the FT,I results
were reduced.
It is pertinent to note that, using the same TSH assay as em-
ployed in these studies, a plasma TSH of 6 WU/ml maintained for 6 hr by TRH infusion results in significant stimulation of the thyroid glands in normal individuals (132). Further evidence of decreased thyroid reserve in this prospective study was a decreased response to TSH and enhanced TRH responsiveness.
Thyroidal hypofunction was noted in only one individual exposed on Ailingnae,
none in the groups exposed on Utirik Atoll, and only one in the unexposed
group.
The abnormal plasma TSH concentrations were not found in a comparably
aged, euthyroid, unexposed population, which indicated that this finding was
not a manifestation of age alone. No individuals were found to have elevated
titres of antimicrosomal or ant ithyroglobulin antibodies.
On the basis of studies of 13! treatment of primary hypothyroidism, it
has been estimated that 4 to 5 cases of hypothyroidism/10
persons/year/rad
would appear from thyroidal exposures to
li in excess of 2500 rem (163,
173,174). This risk factor was used to estimate the number of hypothyroid
cases that might be expected in the more heavily exposed Rongelap population
at 25 years after exposure.
In the 22 Rongelap individuals who were <10 years
of age at the time of exposure (using a mean estimated dose of 1200 rads),
only 3 hypothyroid cases would be expected, whereas 7 of these children were
hypothyroid within 14 years of exposure. Among 45 Rongelap individuals who
were >10 years of age at the time of exposure (average thyroidal dose of about
387 rads), two cases of hypothyroidism would be expected whereas four were
noted in this group. These numbers are considerably higher than expected on
the basis of 1511 risk data.
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