78 ADAMSETAL. because (i) the 30-year survival curves of the three exposure categories are virtually identical, and (ii) there has been only one exposed person, an 82-year-old Rongelap man, whois known to have died with a diagnosis of possible liver disease (9, /6). Thereis evidence that lethal consequencesof hepatitis B infection may be decreased in immunosuppressed persons, perhaps because cell-mediated immunologic reac- tions are minimized (/7). However, patients who are immunologically suppressed maybeat increased risk for developing a chronic HBsAgcarrierstate (/8). An analysis of hepatitis B serology among the exposed Rongelap population doesnot indicate that they share thatrisk. In addition, the age distribution of exposed Rongelap indi- viduals having no serologic evidence of prior hepatitis B infection did not differ from serologically negative persons in the comparison group. Thesefindings do not suggest a clustering of immunologically impaired persons among those in the exposed Rongelap group who were youngatthe timeoffallout exposure. Since hepatitis B surface antigenemia in the comparison population and unex- posed current inhabitants of Rongelap was notsignificantly different from the exposed Rongelap group,it is likely that the relatively low prevalence of HBsAg in presentor past inhabitants of Rongelap and the high prevalence on Utirikare related to local factors rather than radiation dose. In such small isolated populations the factors affecting maternal-newborn (vertical) transmission, an important mode of hepatitis B virus infection, mayvary significantly from island to island. Inhabitants of Rongelap were removed from their contaminated atoll between 1954 and 1957, andin the early years after the fallout the Rongelap exposed received greater medical attention than those on Utirik. However, no Rongelap individual 20 years of age or older at the time of exposure whowas tested in this survey had HBsAg,thus suggesting that neither the temporary relocation nor the differences in medical attention following exposure accountfor the lower prevalence. ACKNOWLEDGMENT This investigation was supported by the U.S. Department of Energy under Contract DE-AC0276CHO00016. RECEIVED: March4, 1986; REVISED: May 19, 1986 REFERENCES I. D.C. Wona, R. H. PURCELL, and L. ROSEN, Prevalence of antibody to hepatitis A and hepatitis B viruses in selected populationsof the South Pacific. Am. J. Epidemiol. 110, 227-236 (1979). 2. T. KUBERSKI, G. LEGONIDEC, I. D. Gust, M. DIMITRAKAKIS, D. CANTALOUBE, and P. ZIMMET, Hepatitis B virus infections in Melanesians and Polynesians in New Caledonia. Am. J. Epidemiol. 114, 355-361 (1981). 3. R. P. BEASLEY, L. Y. HWANG,C.C. Lin, M. L. Leu, C. E. STEVENS, W. SZMUNESS,and K.P. CHEN, Incidenceof hepatitis B virus in preschool children in Taiwan. J. Infect. Dis. 146, 198-204 (1982). 4. H. ZHUANG,A. G. COULEPIS, P. ZIMMET, R. TAYLOR, P. RAM, S. BANUVE,and I. D. Gust,Seroepi- demiologyof infection with hepatitis B virus in Fiji. Am. J. Epidemiol. 116, 608-616 (1982). 5. S. KASHIWAG, J. HAYASHI, H. IKEMATSU, H. NOMURA, T. KUSABA, T. SHINGU, K. HAYASHIDA, and M. Kan, An epidemiologic study of hepatitis B virus in Okinawa and Kyushu, Japan. Am. J. Epidemiol. 118, 787-794 (1983). “ o a ”, Cc a a 3012953