was due to loss of chromosomes. The number of chromatid and isochromatid gaps and breaks, although somewhat higher in the exposed group, was within normal limits. Polyploid cells occurred with equal frequency in the two groups. No aberrations were found in the karyotypes that had been made from the 32 grossly intact cells from the four subjects showing relatively high rates of aberration. Likewise, no abnormalities were seen in 50 cells from the bone marrow of one of the exposed subjects. We pointed out earlier that the proportion of aberration-positive persons in the low-exposure group was twice that amongthe highly exposed. We can“not explain this paradoxical effect, but we should mention that Bloom etal. also failed to detect a relation between chromosomally abnormal survivors in Hiroshima and Nagasaki and their esti- mated doses of radiation (8). Chromosome aberrations did not correlate with: age or sex, nor could any relation be established between the occurrence of thyroid lesions and chromosome abnormalities. We cannot account for the unusually high incidence of acentric fragments in the unexposed andtheir relative deficit in the exposed people. Radiation from ingested radionuclides is not likely to be a factor, since all Marshall Island- ers have been exposed to low levels of residual radionuclides such as Cs}8", Zn*, and Sr®° since their return to Rongelap in 1957, and since body bur- dens of these elements were about the same in both groups. Although viruses fallout (7); the incidence of aberrations, excluding aneuploid ceils, was 2.1 percent and thus identical with our finding; most were two-break aberrations. The- incidence of acentric fragments in a control population of Japanese studied by: the same authors was 0.11 percent -—20 times less than our finding among the eight unexposed Marshall Islanders. In a controlled cytogenetic study of sampled survivors of the atomic bombings of Hiroshima and Nagasaki, this type may play in the pathogenesis of radiation-induced leukemia can only be surmised at present. It is problematical and indeed doubtful whether chromosomeaberrations in lymphocytes can serve to indicate abnormalities in other tissues, except perhaps inferentially. Indeed, of the ten individuals who have developed thyroid lesions since our examinations were made, only three show double-break aberrations. HERMANN LIsco Cancer Research Institute, New England Deaconess Hospital, and Department of Pathology, Harvard Medical School, Boston, Massachusetts 02215 -RoBERT A, CONARD Medical Department, Brookhaven National Laboratory, Upton, Long Island, New York 11973 References and Notes 4.1. M. Tough, K, E. Buckton, A. G. Baikie, W. M. Court-Brown, Lancet 1960-II, 849 Bloom et al. have found exchange-type chromosome aberrations in 33 persons —35 percent of 94 survivors examined 20 years after exposure (8); the incidence of aberrations was 0.6 percent in the exposed group—less than half our finding among the Marshall Islanders, Bloom et al. found only a single acentric fragment in 8847 cells from the 94 controls, an incidence of 0.01 percent; for the 33 aberration-positive individuals, the dose ranged from 237 to 891 rads, and for none of the entire group was it less than 200 rads. All persons examined were 30 years of age or younger at the time of the bombings. The results of our study demonstrate that a small but significant number of chromosome aberrations persists in blood lymphocytes of some Marshall Islanders 10 years after exposure to fallout radiation. The conclusion that at least some of these aberrations were caused by the radiation, and not by other factors, rests on the finding that exchange-type aberrations were found only in the exposed people and not among the controls. The biologic significance of persistent chromosome aberrations in blood lym- 2. . w& not significant; in most cells, aneuploidy phocytes of hematologically normal persons many years after exposure to ionizing radiation is not known. In . particular, any role that aberrations of wb Aberrations ranged from one to four per person. Sixteen of the 23 exposed and two of the five unexposed persons had multiple aberrations. In most instances no more than one aberration was noted per cell. Aneuploidy was higher in the exposed than in the unexposed group, but the difference was ionizing radiations, are known to produce breaks in human chromosomesin vivo and in vitro (/3), the kind and distribution of the fragments seen in the cells of the unexposed group do not suggest this origin. If these agents were implicated, it is not clear why they failed to produce a similar effect in the exposed people who have lived on the sameisland underidentical environmental conditions since 1957. Similar chromosome aberrations have been reported in the Japanese fishermen exposed to radiation from the same . aA level (P < .01). and some chemicals, in addition to . on aberrations either alone or in combination with fragments. The difference between the exposed and unexposed groups in the relative incidence of twobreak aberrations and acentric fragments was significant at the 1-percent (1960); K. E. Buckton, P. A. Jacobs, W. M. Court-Brown, R. A. Doll, idid. 1962-11, 676 (1962). S. Warren and L. Meisner, J. Amer. Med. Assoc, 193, 351 (1965); R. E. Millard, Cytogenetics 4, 277 (1965); P. C. Nowell, Blood 26, 798 (1965); M. Bauchinger and O. Hug, Strahlentherapie 131, 109 (1966). A. D. Bloom and J. H. Tjio, New Eng. J. Med, 270, 1341 (1964), A, Norman, M. Sasaki, R. E. Ottoman, R. C. Veomett, Radiation Res. 23, 282 (1964). M. A. Bender and P. C. Gooch, ibid, 18, 389 (1963); ibid. 29, 568 (1966), ¥Y. Doida, T. Sugahara, M. Horikawa, ibid. 26, 69 (1965). T. Ishihara and T. Kumatori, Acta Haematol. Japon. 28, 291 (1965). . A. D. Bloom, S. Neriishi, N. Kamada, T. wo tions only; all others showed two-break 10. 11. 12, 13. 14. Iseki, R. J. Keehn, Lancet 1966-ET, 672 (1966). R, A. Conard and A, Hicking, J. Amer. Med. Assoc, 192, 457 (1965). R. A. Conard, J. E. Rall, W. W. Sutow, New Eng. J. Med. 274, 1391 (1966). P. S. Moorhead, P. C. Nowell, W. J. Mellman, D. M. Battips, D. A. Hungerford, Exp. Cell Res. 20, 613 (1960). K. E, Buckton and M. C, Pike, Intern, J. Radiation Biol. 8, 439 (1964), C. E. Nasjleti and H. H. Spencer, Cancer Res. 26, 2437 (1966); W. W. Nichols, Amer. J, Human Genet, 18, 81 (1966). Supported by AEC (Brookhaven National Laboratory), the Trust Territory of the Pacific Islands, AEC contract AT(30-1)-3777 with New England Deaconess Hospital, and PHS grant CA-06930. For expert assistance we thank V. Estey, I. Irwin, and W. Merrill of New England Deaconess Hospital, Boston (with the chromosome analysis); and P. Crumrine, R. Hammerstrom, W. A. Scott, and W. Waithe of Brookhaven National Laboratory. We thank S, M. Shea for help with the statistics, and many individuals in AEC and the Trust Territory of the Pacific Islands for their support. 8 May 1967