35 25).71 No two-hit aberrations were found in the unexposed group, but both groups had an unusual numberof acentric fragments, the cause of which is not known, Paradoxically, Rongelap peopie with the lower exposure had more aberrations than those with the higher exposure. These studies indicate that a small but significant number of . chromosomeaberrations persisted in blood lym- phocytes in some Marshallese as late as 10 vears after exposure. The results are consistent with those of similar studies on the exposed Japanese fishermen," on victims of other radiation acci- dents,73 and on Japanese bombsurvivors. ’4 2. Samatic Mutations In 1974, studies* were madeof the frequency of amino acid substitution in the hemoglobin ofthe Marshallese on blood samples sent to Oak Ridge. *5 Since there is no codedisoleucine“¢ in aduit human hemoglobin A,its presence must be due to errors in transcription or translation or to somatic mutations arising during DNAreplication. Errors in transcription, which occur infrequently, form altered mRNA, tRNA, and rRNA; they change the coding in the mRNA and may reduce the fidelity of the tRNA with regard to both the kind of aminoacid it accepts and the mRNA codons it recognizes.?? Errors in translation’? arise through the attachment of wrong amino acids totRNA (aminoacyl synthetase errors) and the imprecise recognition of mRNAcodons by tRNAanticodons (translauonal variation). Somatic mutations result from mistakes in replication of DNA; manysingle- base-substitution mutations change nonisoleucine Figure 25. Two-hit chromosomeaberrations in exposed Marshailese. Top: arrow points to dicentric form; bottom: arrow points to ring form. }2 > 20) and 8 unexposed Rongelap people.* Chromosome aberrations were noted in 23 of the exposed andin 5 of the unexposed Marshallese, but the exposed group had a number of two-break ab- errations (represented by dicentric chromosomes, _ translocations, and a ring form) that are thought into isoleucine codons,’® and the resulting mutant cells could have hemoglobin mRNA withisoleucine codons. For this reason, an increase in the isoleucine content of hemoglobin A would be expected in humans exposedto agents causing basesubstitution mutations. Possibly radiation may cause base-substitution mutations in human somatic cells, but this has never been established. Theisoleucine content of the hemoglobin A was determined in blood from 13 exposed Marshallese and 12 unexposed. The frequencyof isoleucine substitution for other amino acids in hemoglobin was calculated by dividing the nanomoles ofiso- ~ leucine by the total nanomoles ofall other amino to be associated with radiation exposure (Figure acids in each sample. The frequencies are listed in Table 21. "These analyses were done by Drs. H. Lisco, New England Deaconess Hospital, and R.A. Conard, BNL. *These studies were done by Drs. R.A. Popp, G. P. Hirsch, and E.G, Bailiff at Oak Ridge National Laboratory. 900b132