37 children born to an exposed parent or parents have shown, on the basis of incidence of gross may take several generationsto affect the pheno- type, recognition of their radiation etiology may be extremely difficult. Neel et al. are at present anomalies, no evidence of inherited radiation- carrying out more sophisticated studies in the Jap- induced mutations. The principal aberrations noted in Marshailese anese, concerned with the occurrenceof variant forms of 24 serum proteins and erythrocyte en- 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 of familial patterns of such defects have not been done; they are not related to exposure. The possible increase in miscarriages andstillbirths among the exposed women duringthefirst zymes. He and Dr. R.E. Ferrell kindly consented to examine blood samples collected in 1974 from 187 Marshallese children and parents (exposed and unexposed). The results, summarized below, included nosignificant findings indicating radiadon-induced mutations. b. The Frequency of ‘“‘Rare”’ Protein Variants. duced lethal mutations in germ cells of the ovary The blood samples mentioned above were subjected to electrophoretic analyses for polymorphisms and rare variants of proteins and erythro- chromosome aberrationsin peripheral blood lym- Neel et al.82 as follows. 5 years may lead to speculations that radiationin- or, less likely, in sperm cells.* The presence of phocytes in the Marshallese 10 years post exposure, 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 populaton, on 4 prior: grounds a clear-cut demonstration of a genetic effect of radiation in the children born to exposed parents would seem unlikely. Nevertheless, given the nature of the circumstances,it cyte enzymes.82 The findings were summarized by ‘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. Theseresuits on rare variants have been combined with those of others on Micronesians, and the frequency ofrare collect such data. Since recessive combinations variants in Micronesians compared withthefrequencies in West European Caucasians, Japanese, *About one-half the miscarriages occurred in exposed women miasried to unexposed men. such comparisons, and, although the observed values for the four ethnic groups differ by a factor of has been deemed desirable to make every effort to and Amerindians. There are manydifficulties in Table 22 Gene Frequencies for Six Genetic Polymorphisms in the Marshall Isiands®? Phenotype System Adenosine deaminase Groupspecific component Haptogiobin* Phosphogiucomutase,** Acid phosphatase 6-Phosphogiuconate dehydrogenase 1 2-1 2 Total 167 116 56 156 18 50 © 93 26 0 2 32 1 185 168 177 184 ADA! Gel Hp? PGM,' = = = = 185 APA = 0.743 A AB B 164 21 0 101 *The Hp® type was observed in 4 individuals. 73 11 185 Genefrequency 0.951 0.839 0.579 0.912 6-PGDA = 0,943 **Two examples of the PGM phenotype 2-7 and a single phenotype |-7 were observed (PGM,7 = 0.008).