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p.M. Dobyns and B.A. Hyrmer: Thyroid Neoplasms and Hydrogen Bomb Fallout
Fig. 5. A second small! lesion (2 mm) in the same individual illustrated in Figure 4. A. Low magnification showing a papillary lesion. This lesion
was enclosed by a very thin intact capsule. The parenchymaof this thyroid did not show microscopic evidence of radiation effect. as was seen in
some thyroids from Rongelap where the dose was higher than on this atoll, Ailingnae. (x75). B. The same lesion shown in A. This lesion was
considered an atypical adenoma (255).
carcinomas were found among 19 cases operated. Eight of the 9
patients had been exposed and 6 of these were amongthe less
exposed Utirik people. Thus the sequence of findings suggests
that benign neoplasms begin to appearfirst and after a longer
interval carcinomas were more frequently found. Thus, the
interval between exposure and the development of carcinoma
was longer particularly in the lower dose group. The peak
occurrence has now clearly passed.
Hypothyroidism was not detected in the exposed Rongelap
people for almost a decade following the accident[1, 5, 6]. More
sophisticated studies on the stored blood samples (taken before
any thyroid supplement wasstarted) revealed that a few individuals had mild biochemical hypothyroidism but without the
clinical signs, except for the 2 boys irradiated in infancy that
developed myxedema {8]. Thus the mild hypothyroidism may
"ave been a factor in producing the early hyperplasia. This
rarses the question whether a modicum of thyroid deficiency
Ra, related to the initiation of neoplasms. The majority of the
this weap People took the thyroxine supplementregularly after
ine therapy was started in 1965. Although short inter-
vals of non-compliance may have occurred in some individuals,
the thyroid masses continued to develop in spite of the medication.
There are perhaps twofactors operating in these people: one
which initiates formation of neoplasms and another which
promotes their growth. The radiation appearsto be theinitiator.
A low thyroid hormone level in a few individuals might be the
stimulant for growth. Thus the clinical appearance of lesions
may have been delayed by giving supplemental thyroid hor-
mone. Ultimately gross neoplasms appeared. This might explain why the lesions continued to become palpable. It might
also explain the abundance of small atypical lesions and small
carcinomas, some of which had already metastasized but had
not become palpabie.
It has been pointed out that the amount of exposure in the
Rongelap group slowly produced frank thyroid failure in the 2
individuals who had been exposed at f year of age. Although 18
of 20 children exposed under the age of 10 developed neoplasms, the 2 individuals who ultimately displayed myxedema
have not developed growths as of 1989. Thus, the masses