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ceived thyroid irradiation in 1954 seems to conform
in a general way to, the concepts outlined above.
Radiation appears to have been the cause of the
thyroid abnormalities seen, since 200 natives of the
same ethnic background and living under identical
conditions showed no thyroid disease. Furthermore,
there is no evidence that these people have been
exposed to other factors that might cause pathologic
changes in the gland: urinalyses indicate that the
iodine intake is adequate, and no dietary goitrogenic factors have been implicated. In addition, the
data in the present study show a much greater incidence of thyroid disease in children than in adults
in accord with the findings cited above. This greater
sensitivity of infants may also be related to the relative magnitudes of the dose of radiation received,
the infant gland probably receiving five to ten times
the radiation dose that an average adult’s gland
received. The dose range of from 700 to 1400 rads
delivered to the children’s thyroid glands is similar
to the doses received during thymic irradiation. The
apparently greater incidence of pathologic changes
in the glands of the Marshallese is not clear. It mav
be related to a greater dose of radiation received by
the Marshallese since the calculations for thyroid

dose in these people is subject, as noted above, to

large uncertainties.
There appears to be an increased incidence of

thyroid carcinoma in inhabitants of Hiroshima and
Nagasaki exposed to radiation from the atomic-bomb

explosions. The numbers are small, however, com-

prising 19 cases in a combined exposed group of

almost 15,000 individuals, as compared to 2 cases in

slightly less than 5000 unexposed individuals.*
These people were exposed to varying doses of
external radiation to the thyroid gland but not to
internal exposure from radioiodine.

The growth retardation previously noted in some
of the exposed children has been assumed to be
due to the radiation, but the mechanism has not
been known. With the recent development of frank
hypothyroidism in 2 of the most retarded boys in
the exposed group hypothyroidism seems the most

likely cause. In 2 otherretarded boys.
and
thyroid nodules have developed. However,it is interesting that the exposed girls have shownverylittle

retardation of growth and development although the

nodules are more prevalent among them. Except for
the 2 boys with hypothyroidism, the rest of the children with growth retardation have shown normal protein-bound iodine and cholesterol values. Minimal
hypothyroidism may have been missed and may be
enoughto account for the growth retardation seen. The
finding of high TSH levels in the 2 most retarded boys
with hypothyroidism and slight elevation in 2 other
retarded children strongly indicates primary hypothyroidism. The growth response of these children after
thyroid feeding will offer an interesting therapeutic
test of the hypothyroid etiology of the growth retardation:

The treatment of the exposed group with levothyroxine deserves some further comment. Bielschowsky?# and Astwood and Cassidy* have reviewed the
favorable effects of thyroid treatment of patients
with nodules of the thyroid gland. The only experimental evidence found directly applicable to the
Marshallese situation is a paper by Nichols et al.
and unpublished data by Godwin®* demonstrating a

reduced incidence of I'!-induced adenomas in rats

treated with thyroid hormone. This form of treatment, therefore, seems reasonable in the Marshallese.
'
The implications of the present findings are twofold. In the first place, contrary to previous concepts, the. quantity of radioisotopes of iodine in
fallout of the close-in type associated with atomicbomb detonations must be regarded as a major longterm hazard. Secondly, the development of hypothyroidism, of thyroid adenomatoid lesions and of a
thyroid carcinoma after doses of radioiodine that
deliver 300 to 1400 rads to the gland makes caution in
the use of radioiodine necessary

SUMMARY AND CONCLUSIONS

Pathologic changes in the thyroid gland were
found in a number of Marshallese people of Rongelap Iskand who were accidentally exposed to radio-

active fallout in 1954. Definite thyroid nodules were

noted in 11 people, minimal changes in 5 others,

and hypothyroidism in 2. All but 1 case occurred in
the more heavily exposed population (55 living of
the original 64 persons), who received about 175
rads of whole-body gamma radiation, burns of the
skin from fallout products and internal absorption of
fission products. One case with a nodule was noted

in an adult woman in the smaller Rongelap group
(16 of the 18 are still alive) that had received less
than half the exposure of the other group. In 200
individuals of a control group not exposed no such
thyroid

abnormalities

were

found.

In

the

more

heavily exposed group, thyroid abnormalities de-

veloped in 55 per cent of children exposed at less

than ten vears of age. Five children were found at
surgerv to have benign adenomatous yoiters. The 1
adult patient had a mixed papillary and follicular
carcinoma,

with

localized

metastasis.

Two

boys

showed marked retardation of growth, apparently
owing to primary hypothvroidism.
The radiation etiology in these cases appears to
be reasonably certain in view of the following facts:
the thyroid glands received a substantial dose of
radiation from radioiodines and external gamma
radiation (adults about 300 rads, and children about
700 to 1400 rads); and the incidence of thyroid abnormalities was high in the exposed group and ab-

sent in an unexposed control population living on
the same island.
The present findings suygvest that the seriousness
of the internal hazard associated with fallout, particularly from radioiodine, must be revised upward.

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