iodoprotein levels, leading to a false interpretation of protein-bound iodine
(PBI) determinations.
It became apparent only then that low serum thyroxine
(Ty) levels in’some of the children had probably been masked by high levels of
iodoprotein. Several children with slight growth retardation had lowered T,

levels.
The hypothyroidism appeared to be from primary thyroid damage and not
secondary to pituitary damage, since tests for growth hormone in several

growth-retarded children were normal, and their serum thyroid-stimulating hormone (TSH) levels were elevated.

In 1963, 9 years after exposure, a 12-year-old exposed Rongelap girl was
found to have an asymptomatic nodule of the thyroid gland.
Development of thyroid nodules has continued in other exposed Rongelap and Ailingnae people and
in the past decade in the Utirik group.
Two of three Rongelap children ex~

posed in utero developed thyroid nodules during the past 6 years. At this
time (1981) a total of 46 exposed Marshallese (29 in the Rongelap/Ailingnae
group and 17 in the Utirik group) have developed nodules, and 42 of these have

undergone surgery.
In the unexposed comparison population 35 of 600 people in
the age-matched control group have been found to have nodules and 14 of these

have undergone surgery (see Section IX.C. and Appendix IV, Table 1).

In 1965 the seriousness of the development of thyroid lesions in the
Rongelap people became more evident, and preventive treatment with thyroid hormone was instituted in the Rongelap group.
Later (1969) the Ailingnae group

was also included.

The difficulties in carrying out the treatment regimen

will be referred to in Section IX.C.4.
With increasing development of thyroid abnormalities it has become apparent that the original control group of unexposed Rongelap people was numeri-

cally inadequate for proper evaluation of the thyroid findings in the exposed

people.
Therefore, during the past decade thyroid surveys have included all
available unexposed Rongelap and Utirik people as well as some people at
Likiep and Wotje atolls.
More than 1200 of these people have been examined.
About half of them were in the same age range as the exposed people, and the
others were in the younger age group (born after 1954).
During the last seven years, specific radioimmunoassay techniques for
measurement of serum Ty, and TSH have been employed to monitor the population

for evidence of hypothyroidism (1,36,110).

Results have shown that at least

one-half of those who had thyroid surgery, and supposedly were taking thyroid

replacement medication, had significant elevations in serum TSH on one or more
occasions, indicating lack of compliance with the thyroxine replacement schedule and also indicating the inadequacy of residual thyroid tissue in patients

with subtotal thyroidectomies to maintain the euthyroid state without compensatory increases in TSH secretion.
These observations led to attempts to determine the degree of thyroid function in exposed populations of both Rongelap
and Utirik,-which necessitated temporary discontinuation of the thyroid hor-

mone in the Rongelap group.
(The Utirik group was not routinely receiving
such treatment.)
In earlier studies, discussed in detail in the 20-year report (1), a number of individuals with apparently normal

thyroid glands were found to have

subnormal increments in plasma T, 24 hours after receiving 10 units of TSH

intramuscularly.
The mean increment in Ty, in 25 exposed Marshallese was 2.35
ug/dl (SD = 1.2), whereas the increment in a control group of unexposed euthy-

roid Rongelap and Utirik individuals was 4.2 lig/dl (SD = 1.3).

nificantly greater than in the exposed subjects (p > 0.001).

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