The prevalence of hepatitis B virus (HBV) infection in the United States and associated demographic and behavioral risk factors have been estimated from studies of the blood donor population and other selected populations (1-4). However, blood donors are not characteristic of the general U.S. population (4) and do not adequately estimate demographic risk factors associated with HBV infection. This report presents results from a seroprevalence study of HBV infection in a population that is representative of the general U.S. population (5) and describes racial differences in rates of HBV infection.

Serum collected in the Second National Health and Nutrition Examination Survey (NHANES II), conducted by CDC's National Center for Health Statistics during 1976-1980, was used to estimate the prevalence of HBV markers in the United States. NHANES II was a representative sample of the noninstitutionalized civilian U.S. population aged 6 months to 74 years. Demographic, socioeconomic, and morbidity data, as well as related medical and nutritional information, were collected by interview and physical examination (6). Serum was available from 14,488 (71.3%) of the 20,322 persons interviewed and examined. The distribution of age, sex, race, and region of the country was similar in adults tested and not tested for HBV markers. Of the 5843 children aged 6 months to 12 years, serum was available for testing for 2591 (44.3%). Serum was tested by enzyme immunoassay for hepatitis B surface antigen (HBsAg), antibody to hepatitis B core antigen (anti-HBc), and antibody to HBsAg (anti-HBs).

The prevalence of serologic markers for HBV infection (HBsAg, anti-HBs, or anti-HBc) in this population was 4.8%. Serologic markers were found in 3.2% of white participants and 13.7% of black participants. Among persons aged 65-74 years, 6.9% of whites and 39.6% of blacks were seropositive (p less than 0.001) (Figure 1). For children less than 12 years of age, rates of HBV infection for both races were low (black=1.6%, white=0.8%) (not statistically significant, p=0.147). For all age groups from 12 to 74 years, rates of seropositivity were lower for whites than for blacks (statistically significant differences for all groups). Within each race, the distribution of HBV markers was similar for males and females--for whites, 3.7% of males and 3.0% of females; for blacks, 13.9% of both males and females.

Of the 13,811 white and black participants tested for HBsAg, 40 (0.3%) were positive (Table 1). The prevalence of HBV carriers (i.e., persons who test positive for HBsAg) per 1000 was 1.9 for whites and 8.5 for blacks (not statistically significant).

The race-adjusted prevalences of all HBV markers were lower in the Midwest than in other regions (p less than 0.001): 3.2% in the Midwest, compared with 5.2% in the North east, 5.5% in the South, and 5.9% in the West. Reported by: TR Townsend, MD, Johns Hopkins Univ Hospital, Baltimore, Maryland. Div of Health Examination Statistics, National Center for Health Statistics; Hepatitis Br, Div of Viral and Rickettsial Diseases, Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: A difference in the prevalence of HBV infection by race in the United States has been suggested previously (7); however, this difference has not been studied using a statistically valid population-based sample. The availability of serum from NHANES II provided an opportunity to examine the distribution of HBV markers in the general U.S. population. However, because only 313 persons were classified as other than black or white in NHANES II, and ethnicity data were unknown for this group, prevalence estimates can be determined only for the black and white population. Since this survey represents 1976-1980, when the incidence of HBV infection began to increase, the results provide a baseline estimate of the prevalence of HBV infection (8). The change in prevalence over time can be assessed by determining the seroprevalence of HBV markers in NHANES III.

Because an estimated 50% of clinical HBV infections are not reported by existing passive surveillance systems (9), population-based prevalence estimates of HBV seropositivity are useful in developing prevention strategies. Moreover, for each clinically apparent case of acute icteric hepatitis, two to three persons have disease so mild either they do not seek medical attention or HBV is not considered in the diagnosis.

Hepatitis B (HB) immunization programs have focused primarily on selected groups at high risk for infection, e.g., persons at occupational risk for exposure to blood and body fluids, staff and residents in institutions for the developmentally disabled, and staff and patients in hemodialysis units (10). Data from surveillance in four sentinel counties suggest that those who are at the greatest risk of infection--intravenous-drug users, persons acquiring disease through heterosexual exposure, and homosexual men--are not served by HB vaccine programs (11). In addition, approximately 30% of hepatitis patients have no known source of infection (11).

Analysis of the NHANES II data also showed that a positive serologic test for syphilis was associated with HBV infection in both races (5) and reinforced that HBV infection is also a sexually transmitted disease (11,12). The higher prevalence of HBV infection in the black population and the increasing prevalence of infection during adolescence suggest that immunization of the traditionally targeted risk groups will not markedly affect the spread of infection in the United States. The NHANES II data suggest that, to prevent a substantial proportion of HBV infections, HB immunization programs need to include adolescents and young adults.

References

1. Szmuness W, Prince AM, Brothman B, et al. Hepatitis B antigen

and antibody in blood donors: an epidemiologic study. J Infect Dis 1973;127:17-25.

2. Basstiaans MJ, Dodd RY, Nath N, et al. Hepatitis associated markers in the American Red Cross volunteer blood donor population: trends in HBsAg detection, 1975-1978. Vox Sang 1980;39:1-8.

3. Ling CM, Overby LR. Prevalence of hepatitis B virus antigen as revealed by direct radio immunoassay with ((125))I antibody. J Immunol 1972;109:834-41.

4. Moss AJ. Blood donor characteristics and types of donations: United States 1973. Vital Health Stat 1973;10(106).

5. McQuillan GM, Townsend TR, Fields HA, et al. The seroepidemiology of hepatitis B virus in the United States, 1976-80. Am J Med 1989;87(suppl 3A):5-10.

6. NCHS. Plan and operation of the Second National Health and Nutrition Examination Survey 1976-80. Vital Health Stat 1981;1(15).

7. Szmuness W, Hirsch RL, Prince AM. Hepatitis B surface antigen in blood donors: further observations. J Infect Dis 1975;131:111-8.

8. CDC. Hepatitis surveillance report no. 51. Atlanta: US Department of Health and Human Services, Public Health Service, 1987:9-23.

9. Alter MJ, Mares A, Hadler SC, Maynard JE. The effect of underreporting on the apparent incidence and epidemiology of acute viral hepatitis. Am J Epidemiol 1987;125:133-9. 10. ACIP. Update on hepatitis B prevention. MMWR 1987;36:353-60,366. 11. CDC. Changing patterns of groups at high risk for hepatitis B in the United States. MMWR 1988;37:429-32,437. 12. Alter MJ, Coleman PJ, Alexander WJ, et al. Importance of heterosexual activity in the transmission of hepatitis B and non-A, non-B hepatitis. JAMA 1989;262:1201-5.

Disclaimer   All MMWR HTML documents published before January 1993 electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

**Questions or messages regarding errors in formatting should be addressed to mmwrq@cdc.gov.

Page converted: 08/05/98

This page last reviewed 5/2/01