37

children born to an exposed parent or parents
have shown, on the basis of incidence of gross
anomalies, no evidence of inherited radiation-

induced mutations.
The principal aberrations noted in Marshallese
adults and children have been bilateral shortening
of the fifth finger, prominent headof ulna,dislocated wrist, enlarged cornea, tortuosity of retinal
vessels, asymmetry of face, congenital nystagmus,
and pigmentation of the cornea. Studies offamilial
patterns of such defects have not been done; they
are not related to exposure.
The possible increase in miscarriages andstillbirths among the exposed women during thefirst
5 years maylead to speculations that radiation in-

duced lethal mutations in germ cells of the ovary
or, less likely, in sperm cells.* The presence of
chromosomeaberrations in peripheral blood lym-

phocytes in the Marshallese 10 years post expo-.

sure, and the possible somatic mutation in the
hemoglobin, described above, support speculations
that mutations in the germ plasm occurred and
might be detected in the offspring by moresensitive tests. However, in view of the relatively small
dose of radiation and the small size of the population, on a priort grounds a clear-cut demonstration

of a genetic effect of radiation in the children born
to exposed parents would seem unlikely. Never-

theless, given the nature of the circumstances, it

has been deemeddesirable to make every effort to
collect such data. Since recessive combinations
*About one-half the miscarriages occurred in exposed women
married to unexposed men.

may take several generations to affect the pheno-

type, recognition of their radiation etiology may
be extremely difficult. Neel et al. are at present
carrying out more sophisticated studies in the Japanese, concerned with the occurrence of variant

forms of 24 serum proteins and erythrocyte enzymes. He and Dr. R.E. Ferrell kindly consented
to examine blood samples collected in 1974 from
187 Marshallese children and parents (exposed
and unexposed). Theresults, summarized below,
included nosignificant findings indicating radiation-induced mutations.
b. The Frequency of “Rare’’ Protein Variants.

The blood samples mentioned above were sub-

jected to electrophoretic analyses for polymor-

phisms andrare variants of proteins and erythrocyte enzymes.8?2 The findings were summarized by
Neelet al.8? as follows.
‘Blood specimens from a sample of 187 Marshall Islanders were studied with reference to variants of 24 serum proteins and erythrocyte enzymes.
Six of the traits studied exhibited genetic polymorphisms (adenosine deaminase, phosphoglucomutase;, acid phosphatase, 6-phosphogluconate
dehydrogenase, haptoglobin, group specific component). There was in addition one ‘rare’ variant
(of albumin) in 4047 determinations. These results

on rare variants have been combinedwith those of
others on Micronesians, and the frequency ofrare
variants in Micronesians compared withthe frequencies in West European Caucasians, Japanese.
and Amerindians. There are manydifficulties in
such comparisons, and, although the observed values for the four ethnic groups differ by a factor of

Table 22

o.

-

-

Ne

Gene Frequencie#for Six Genetic Polymorphismsint the Marshail Islands®?
a Phenotype
System

Adenosine deaminase
Groupspecific component

Haptoglobin*

7

.

oo
"167
°
-.
116

Phosphoglucomutase;**
Acid phosphatase

“~

6-Phosphogluconate dehydrogenase

:

_

56

156

_A
101

164

2-1

18
50

93

26

AB
73

21

2

Total

Gene frequency

0
2,

185
168

ADA!
Gel

= 0.951
= 0.839

f

184

PGM,!

= 0.912

32

B

Ul

0

177

485

185

Hp!

APA

= 0.579

= 0.743

6-PGDA = 0.943

*The Hp® type was observed in 4 individuals.
**Two examples of the PGM phenotype 2-7 and a single phenotype 1-7 were observed (PGM,7 =0.008).

Select target paragraph3