Racial disparities in health have been long noted in the United States. In describing these differences, we will be attentive to the role of gender and present gender differences whenever the data are available. It has recently been argued that although black women lag behind other social groups on some societal indicators, they are nonetheless rapidly becoming a “model minority” on a broad range of indicators.6 For example, black women have a higher rate of college enrollment than black males but also than whites and Hispanics. In addition, they also have lower suicide rates than black males and whites and low rates of crime, cigarette smoking, alcohol use, and the use of illegal drugs.
The routine reports of the National Center for Health Statistics (NCHS) provide life expectancy data only for blacks and whites. In 2004, the life expectancy at birth for blacks was 73.1 years compared to 78.3 years for whites.7 If blacks could improve their life expectancy at the rate at which overall life expectancy increased in the United States between 1980 and 2000 (an average of 0.2 years annually), it would take them 26 years to close the current 5.2-year gap in life expectancy!Table 1 presents life expectancy at birth and at specific ages for blacks and whites of both sexes.7 These data illustrate the complex ways in which multiple statuses combine to affect health risks. First, life expectancy differences by race, for both men and women, are large during early and mid adulthood and decline with increasing age. Second, at every age except the eldest, the racial differences in life expectancy are larger for men than for women. Third, factors linked to both race and sex likely contribute to life expectancy such that, at every age, black women have higher levels of life expectancy than white men. Fourth, gender differences in life expectancy are consistently larger for blacks than for whites. Finally, the gap in life expectancy between black men and women is consistently larger, at every age, than the racial gap in life expectancy.
National mortality data provide another window on racial disparities in health. Table 2 presents the overall mortality rates for whites by age in the United States in 2005 and the minority/white mortality ratios.8,9 The data reveal that African Americans and American Indians have a consistent pattern of elevated mortality risk compared to whites. This pattern is evident in early childhood, and persists until advanced age. In contrast, Latinos have rates that are roughly equivalent at the youngest ages but are lower than those of whites at older ages. Asians, a diverse group with an even higher proportion of immigrants than Hispanics, have mortality rates that are markedly lower than those of whites, throughout the life course. The disparities in mortality are generally similar for men and women although there is a consistent trend for the health advantage of Hispanics over whites to be slightly larger for women than for men.
National data on mortality are more accurate for blacks and whites than for Hispanics, Asians and Native Americans. A major problem affecting the quality of mortality data is related to the undercount in the number of deaths because of the misclassification of nontrivial proportions of Hispanics, Asians, and especially American Indians as white on death certificates.10 This error leads to an undercount in the numerator for death rates for these groups that underestimates their actual death rates. Challenges of population coverage and/or inadequate sample size for small racial populations and ethnic subgroups within the larger racial categories continue to obscure population patterns of health risks. For example, aggregation of the Native Hawaiian and other Pacific Islander (NHOPI) group with the Asian category obscures the reality that the NHOPIs are one of the highest risk populations in the United States in terms of CVD, diabetes, and obesity risk.11 Similarly, Arab Americans are masked under the white population of the United States and although they have relatively high levels of SES, they have elevated risk of some diseases such as diabetes and certain cancers.12
First and worse
One of the characteristics of the elevated rates of disease for minorities compared to whites is the earlier onset of illness, greater severity of disease and poorer survival. For example, a 20-year follow-up of the CARDIA study's cohort of young adults found that incident heart failure before the age of 50 was 20 times more common in blacks than whites with the average age of onset being 39 years old.13 National data from the NHANES study also shows that hypertension occurs earlier in blacks than in whites.14 During the 1999–2002 period of this study, 63% of black adults with hypertension were younger than 60 years of age compared to 45% of their white counterparts. Moreover, for both racial groups the proportions with hypertension under age 60 in 1999–2002 was higher than during the earlier 1988–1994 data collection period (59 and 41%, respectively).
An unexpected patterning of neonatal mortality rates by mother's race and age can be viewed as evidence of premature aging. National data on first births for white and Mexican American women reveal that, as expected, infant mortality rates are lower for mothers who give birth in their twenties compared to those in their teens.15 The opposite pattern is evident for black and Puerto Rican women, where the lowest rates of neonatal mortality are evident for births during the 15–19 age group, with rates increasing as childbearing is delayed to ages 20–29 or later. Geronimus15“weathering hypothesis” argues that for groups residing in unhealthy contexts, chronological age reflects higher levels of exposure to adverse conditions in social and physical environments and greater wear and tear on physiological systems.
A striking example of a racial difference in the early onset of disease is evident for breast cancer. It is well documented that white women have an overall incidence of breast cancer that is higher than that of blacks. However, the opposite pattern exists under the age of 40, with African American women having a higher incidence of breast cancer than their white counterparts.16 Thus, despite having a lower overall incidence rate of breast cancer compared to their white peers, black women have a higher risk of early onset, severe types of breast cancer and a reduced risk of late-onset types.16 The association of some risk factors with breast cancer varies by age: parity is associated with an increased risk of breast cancer incidence in younger women but a reduced risk in older women.16 Similarly, while obesity is associated with reduced risk in younger women, it is associated with increased risk in older women. Importantly, the crossover in breast cancer incidence by race persists even after adjustment for risk factors.16 In addition to being more likely to get breast cancer when young, black women are more likely than whites to be diagnosed at an advanced stage, have aggressive forms of the disease that are resistant to treatment, and to have poorer outcomes.17
Major depression is another disease for which blacks have a lower rate of illness but a prognosis that is considerably worse than whites. A recent national study found that although blacks have lower current and lifetime rates of major depression than whites, the cases of depression among blacks were more likely to be persistent, severe, disabling, and untreated.18 National data also reveal that whites are more likely than blacks (but not Hispanics) to develop alcohol dependence.19 However, once dependence existed, both blacks and Latinos were more likely than whites to persist in alcohol dependence.
Other evidence indicates that the increased risk of disease for minorities is evident very early in life. A study of 23-year-old young men found that compared to whites of similar BMI, body fat, fitness, renal function, blood lipids and glucose levels, black men had comparable brachial blood pressure (BP), but greater central blood pressure, greater augmentation of central BP from wave reflections, and greater macrovascular and microvascular dysfunction reflected in increased central artery stiffness and reduced peripheral endothelial function.20 A recent report from a longitudinal birth cohort study of 8,550 children in the United States provided further evidence that racial differences in risk factors are established early.21 By age 4, 13% of Asians and 16% of whites were obese, compared to 21% of blacks, 22% of Hispanics and 31% of American Indians. Neither of these studies included adjustment for SES.
Further evidence of the early health deterioration of African Americans compared to whites comes from analyses of a 10-item measure of allostatic load that was attempting to capture the physiologic burden on multiple biological systems in the NHANES data, due to the wear and tear of exposure to stressors and other environmental adversity.22 This study found that blacks had higher scores than whites at all ages, with the racial differences being most marked between 35 and 64 years. Moreover, the racial differences persisted after adjustment for poverty with nonpoor blacks having higher scores than poor whites. In addition, black women consistently had higher allostatic load scores than black men.22 These differences could be due to the double jeopardy of racial and gender discrimination that women face, and/or to stressors linked to the central role that black women often play as economic providers to their families.
Research also reveals that some risk factors have a more adverse impact on blacks than on whites even when their overall levels are lower than or similar to those of whites. This is evident for both tobacco and alcohol. For example, the risks of lung cancer do not mirror variations in smoking behavior with a given level of smoking associated with an elevated risk of lung cancer for African Americans and Native Hawaiians compared to whites, Japanese Americans and Latinos.23 In a similar vein, alcohol-related mortality is more than twice as high for black males than for their white counterparts and almost twice as high for females.24 A general population sample in New York State also found evidence of greater susceptibility to liver damage in blacks compared to whites.25 Compared to whites, blacks had higher levels of common biomarkers of liver damage at every level of alcohol consumption with the differences being largest at the highest level of alcohol use. This pattern persisted after adjustment for age, sex, education, BMI, and pack years of smoking. We are currently unaware of the extent to which these patterns reflect group variation in the specific types of substance used (compared to whites, blacks are more likely than whites to use menthol cigarettes and to use hard liquor), differential exposure to unmeasured physical and chemical agents in occupational and residential environments, or interactions between health practices and stressors that markedly exacerbate health risks.
Relatedly, several studies find that moderate alcohol consumption is not associated with better health outcomes among African Americans, as it is for whites. In the NHANES Epidemiologic Follow-up Study (NHEFS) there was no beneficial effect of moderate alcohol consumption on all-cause mortality for black men or women.26 Moreover, although moderate alcohol consumption tends to be cardio-protective in middle-aged adults, in the Atherosclerosis Risk in Communities (ARIC) study, opposite to the pattern for whites and black females, it was positively related to incident coronary heart disease27 and incident hypertension for black men.28 Similarly, the CARDIA study found a positive association between alcohol consumption and the development of coronary calcification with the absence of a beneficial effect of moderate alcohol consumption being clearest among black males.29 The factors underlying these patterns are not well understood, but it is possible that SES is a contributor. There is considerable evidence that at least some of the reported protective effects of moderate drinking are likely due to residual confounding of moderate alcohol consumption with high SES and good health practices,30–32 and limited evidence that when controls are introduced for multiple measures of SES, the inverse association between moderate consumption and mortality is no longer evident.33
Research is also needed to identify the mechanisms and processes that give rise to those situations where whites are more adversely affected by risk factors than racial minorities. In one national study, for example, persistent poverty was unrelated to stunting and wasting for blacks, but positively related for whites and Hispanics.34 Similarly, black newborns are twice as likely as white ones to be low birth weight, but low birth weight is more strongly linked to neonatal mortality for whites than for blacks.35 Although the prevalence of obesity is higher for black than for white women, obesity is more strongly related to mortality for white than for black women.36,37 Future research could profitably explore the extent to which these patterns could reflect weaker, habituation effects for blacks due to earlier exposure and elevated levels of exposure, and/or the conditions under which the presence of cultural, SES, psychosocial, religious and other resources can weaken the health effects of certain risk factors. Research should also examine the extent to which observed racial variations in the effects of risk factors are similar to SES differences. Earlier research on stress and health found that although both blacks and low SES persons were more exposed to stress than whites and high SES individuals, comparable stressors had a more adverse effect on the mental health of both socially disadvantaged groups.38 More generally, these patterns of findings highlight the importance of attending not only to variations in exposure to risk factors but also to variations in vulnerability as reflected in both differential preparedness for coping with adversity and differential ability to recover.39