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The burden of morbidity and mortality due to TB in the U.S. has long been noted to fall disproportionately on racial/ethnic minorities (1, 2, 4, 6). In our study we found that, even after adjusting for age, sex, and country of birth, TB rates among racial/ethnic minorities were 5–10 times higher than those in whites from 1987–1993. Despite the longstanding nature of the evidence documenting the increased TB risk among racial/ethnic minorities in the U.S., there is currently no satisfactory explanation for these observed differences.

Although most previous studies sought to explain the increased risk of TB among racial/ethnic minorities through intrinsic, genetically related factors, we attempted to determine the interaction with SES, an extrinsic factor long associated with risk of TB. Low SES has frequently been linked to increased risk of TB, especially among those living in crowded settings (2, 5), such as crowded households (7, 8), congregate living facilities, e.g., homeless shelters, long-term nursing facilities, and correctional facilities (9), and more crowded urban versus rural settings (1, 5). Less frequently, other indicators of low SES, such as poverty (8), receipt of public assistance income (8), and unemployment (7), have also been associated with increased TB risk. In our study, we found that risk of TB increased with lower SES for all the SES indicators evaluated, with crowding having the greatest impact. The absolute case rates are not significantly different for the SES indicators, with the exception of crowding. The higher rates of TB associated with crowding has a plausible biologic explanation in that there is a greater degree of shared airspace in crowded living quarters, which would increase exposure to Mycobacterium tuberculosis. Our results suggest that SES influences TB risk by at least two separate mechanisms, the first a strong effect directly attributable to crowding and manifested predominantly in overcrowded settings and the second, evident for all the other SES indicators evaluated, a previously unrecognized SES–health gradient, in which TB risk increases at a relatively constant rate with decreasing SES across the entire SES spectrum. Similar SES–health gradients have been described for aggregate mortality and other specific diseases, such as coronary heart disease, hypertension, cancer, and many chronic diseases (10).

Several early studies suggested that low SES was an important contributor to the increased risk of TB among blacks in the U.S. (2, 11). Our study is the first to examine this connection using national surveillance data and multivariate methods to explore the relationships between demographic characteristics and SES indicators. We found that adjusting for the six SES indicators accounted for approximately half the increased risk of TB previously ascribed to race/ethnicity among U.S.-born blacks, Hispanics, and Native Americans. Adjusting for SES had relatively less effect among foreign-born blacks and Asians, suggesting that other factors, such as increased TB exposure, either overseas or in the U.S. as a result of contact with TB cases arising from reactivation of infection acquired overseas, are relatively more important TB risk factors in these groups. Rates of TB in Asian countries are several-fold higher than in other parts of the world and the tendency of immigrants to the U.S. to settle in or be resettled in areas with other immigrants increases exposure to M. tuberculosis above that in other areas of the U.S. (13).

Early studies had suggested that the magnitude and pattern of the increased TB risk associated with decreasing SES was similar between racial/ethnic groups (2, 12). Our study corroborated this finding for all the SES indicators evaluated except crowding, where the impact on TB risk was relatively greater among blacks, especially those younger than 45 yr of age. The higher prevalence of multiple known risk factors for TB among younger blacks living in crowded conditions, such as homelessness, alcoholism, incarceration, intravenous drug use, and infection with human immunodeficiency virus (HIV), most likely accounted for much of the accentuated effect of crowding in this population (14). Additional adjustment for interaction between race/ethnicity and crowding in the final model further increased the proportion of TB risk accounted for by SES, especially among U.S.-born blacks. Among U.S.-born individuals in the final model, TB risk among blacks, Hispanics, and Native Americans in the highest (least crowded) quartile was only approximately twice that of whites, dramatically lower than the 5–10 times higher risk demonstrated in these groups prior to adjusting for SES. Many social components of racial and ethnic categories other than genetically determined susceptibility to tuberculous infection probably explain the residual twofold increased risk in the highest SES group (15). Increased exposure to TB in minorities could result from preferential association with persons of similar racial and ethnic backgrounds who are at increased risk of this disease (e.g., homeless, substance abusers, etc.) regardless of the SES status of the minority subgroup. Other factors, especially HIV, which are not equally distributed between racial/ethnic groups, could increase the risk of progression to active disease. The methodology we used to assign SES values to TB cases, which will be discussed below, could also result in some residual confounding. Finally, the three-way interaction between white versus black race, age, and crowding suggest that such time related effects are important. An individual's risk of active disease is dependent on a lifetime history of exposure, not just their current SES status as was measured in our study. Hence, the greater upward socioeconomic mobility of minority groups since the civil rights movement will mean that a larger portion of blacks in a high SES category will have experienced poverty, and a greater risk of TB exposure, in their earlier lives.

Previous studies linking TB and SES frequently did not control for the impact of demographic characteristics and the potential for confounding between SES indicators. While our current study used multivariate modeling to avoid these limitations, it still shares two other important methodological limitations with previous studies. The first is that, since all these studies are ecological analyses, they may erroneously assign group-based measures of disease-exposure association to individuals within the group, i.e., the ecological fallacy, and/or tend to inherently overestimate the strength of the exposure-disease association (16). The second shared limitation is the potential for error introduced by assigning SES values to persons with TB based on median values for their demographic counterparts within a given geographic area, e.g., ZIP code. Given the high rates of TB among various subpopulations commonly associated with low SES, e.g., the homeless, alcoholics, intravenous drug users, persons who have been incarcerated, and persons living in medically-underserved urban area (5, 9), persons with TB have long been assumed to be of relatively lower SES than their demographic and geographic counterparts. Assigning SES values to persons with TB based on median/mean values for their demographic and geographic counterparts, therefore, would tend to, perhaps markedly, underestimate the true magnitude of the association between SES and TB.