IT WILL NOT SURPRISE THE reader when we point out that there are glaring health disparities by racial or ethnic identity, including in sexually transmitted disease (STD) rates. For example, the rates of primary and secondary syphilis, HIV/AIDS, chlamydial infection and gonorrhea among blacks range from 5.4 to 17.8 times the rates in whites.1 Prevalence differences among groups can even overwhelm the effects of individual sexual behavior. For example, a recent review of Add Health (National Longitudinal Study of Adolescent Health) data concluded that young black men and women would be at risk even with normative behavior.2 Also, national data reveal little difference in the sexual behaviors of white and black women aged 15 to 44 years in the United States. In 2002, the median number of lifetime sex partners for white women was 3.6 (10.2% have had 15 or more sex partners), compared with 4.1 (8.8%) for black women.3 Our purpose in this article, one in a series of articles in this issue addressing STD racial and ethnic disparities, is to discuss the role of social determinants in such disparities. Specifically, we will present an organizing framework for the social determinants of health underlying STD disparities.
A Model of Social Determinants and STD Outcomes
Figure 1 represents a general organization of the relationship between social determinants of health and actual health outcomes. For STD, the health outcomes are acquisition or transmission, both largely discrete events. Adverse social determinants of health form a destructive environment in which many overlapping conditions lead indirectly to infectious disease. They do so by interacting with characteristics of the pathogen and broad societal norms and patterns of behavior to influence the epidemiology of infectious disease in which people live. The epidemiologic context thus typically mediates the relationships between social determinants and STD outcomes (this logic does not necessarily hold for chronic disease). The epidemiologic context, in turn, interacts with individual behaviors to influence the odds of STD acquisition or transmission. Figure 1 neither shows health outcomes entirely occluded by the epidemiologic context nor the context occluded by social determinants, indicating that there are other factors at work. Nevertheless, the destructive influence of social determinants is shown in a title quote from a study of determinants of STD rates in North Carolina: “This place is killing me.”4 (italics added).
Figure 2 represents this model applied specifically to social determinants relevant to racial and ethnic STD disparities. Note that the actual social determinants have reciprocal patterns of influence among themselves, rather than being independent actors upon the epidemiologic context. We posit below that racial segregation underlies and reinforces other social determinants and acts directly upon the epidemiologic mediators of core areas and sexual networks. We further posit that until underlying social determinants are addressed, the success of interventions to address racial disparities in STD risk and infection will be limited.
In the United States, a key underlying factor is the legacy and continuing effects of segregation, which is a manifestation of institutionalized racism,5 and a previously noted factor in addressing disparities in syphilis rates.6,7 Understanding the underlying factors tied to the social determinants that lead to health disparities is vital to decreasing disparities. It may be easier and more comfortable to talk about the outcomes of segregation such as geographic clustering of disease (i.e., the epidemiologic context instead of the social determinant). But a response that considers only the context–building houses further apart?–will not resolve the problem of STD clustering.
Other social determinants (Fig. 2) include components of the health care environment such as facilities (e.g., hospitals, urgent care centers, primary care practices). We, therefore, include a review of health care among our social determinants. They also include less tangible components such as community-level social organization and economic resources; we reflect these in discussions of economics and migration patterns. These 2 areas are also part of a recently proposed health model with components extending beyond the domain of individual behavior, the gender relations, economics, migration (GEM) model.8 Incarceration among minority communities is so closely tied to STD that is worthy of its own place among social determinants of health. Finally, we address 2 key components of the epidemiologic context, core areas and sexual network, which are more proximate influences upon STD rates and disparities.
Disparities among groups are by definition community-level differences. Communities may be defined by multiple conditions, such as physical proximity (e.g., neighborhoods) or commonality of purpose (e.g., a social club). However, if a disparity is identified by race/ethnicity, the community must be definable by those variables. That, in turn, points to social segregation—the outcome of racism, as a fundamental social determinant of STD disparities5 and an underlying principle for various overlapping social determinants. Given these perspectives, various social determinants of health which produce racial/ethnic disparities are outcomes of social segregation.
Legal segregation by race was formally disbanded with the passage of the Civil Rights Act of 1965, which repudiated racial segregation and invalidated state laws to the contrary. Most notably, this repudiation renounced the previous “separate, but equal” doctrine by defining segregation as an inherent manifestation of inequality.9 But this was not and is not enough to eliminate disparities resulting from legal segregation.
Racial/ethnic segregation pertains to the physical or social separation of persons into largely exclusive groups on the basis of their race/ethnicity. Environmental factors that reinforce segregation have been widely studied and reviewed,10 including the role of the social construction of race and racism (personally mediated, internalized, and institutional).5 Numerous measures exist, including some at the individual level.11,12 The various measures and factors all point to the fact that individuals and groups are more likely to associate with like individuals and groups than with others. Census 2000 data show that more than 60% of all census blocks (approximately 300 households per block) are racially homogeneous.12 For persons of minority races/ethnicities, this means that many are surrounded by households representing well under 20% of the US population (non-Hispanic black and Hispanic persons as groups each make up approximately 14% of the US population; other racial and ethnic groups form smaller proportions).
One need not rely on personally-mediated racism to maintain segregation, nor even deliberate ongoing efforts to maintain institutionalized racism (though this does occur). When group segregation is correlated with previous health disparities, as is the historical case in the United States, it becomes an underlying factor for maintaining disparities, even if previously overt efforts to maintain group disparities no longer exist.
Finally, migration, under certain circumstances, presents a special instance of segregation-based clustering and bridging. Bridging is the phenomenon through which individuals from one community acquire disease from members of another community and then transmit within their own community.13 Migration is a determinant of HIV spread.14 Numerous migrants come to the United States each year (noncitizen migrants numbered approximately 21 million in 2004, or 7% of the total population),15 many of whom have migrated because of economic desperation. Many poor migrants have only rudimentary access to health care and, although mobile, remain segregated from the communities they encounter for long periods of time. (Migrant settlement in groups certainly exists, and such settled groups vary in the extent to which they remain segregated from residents of the communities into which they settle.) The rates for syphilis for Latino migrants are 2 to 4 times the rate for the US population. When migrant populations do not bring sex partners with them, they may seek sex among community members. In these instances, sex may carry high risk of STD transmission and acquisition (e.g., unprotected sex with commercial sex workers), and infected migrants can then act as bridges to others in their own communities.
Health Care Provision and Use.
The presence of, and access to, relevant health care is essential to STD prevention.16,17 Aral and Wasserheit's Person-Time of Infectiousness model centered on factors influencing delays in health care access and provision,18,19 the latter of which constitutes a social determinant of health. Lack of insurance reduces preventive care (it is insurance status that is the social determinant)20 and has been associated with chlamydial infection among adolescents.21 Much of the research related to disparities in the provision of health care has been focused on adolescents, although disparities involving other populations exist.22 Race and low socioeconomic status (SES) are relevant to health care access. Public STD services draw from those who are disproportionately poor, underemployed, uninsured, and of members of minority races/ethnicities.23 Social disorganization in segregated communities may further reduce health care access. For example, gang activity in some cities further constrains movement within and between neighborhoods,24 thus reducing access to health care facilities.
Lack of access to mental health services, combined with the comorbidity between mental health, substance use, and STD,25,26 provides a potent mix that contributes to racial and ethnic disparities. Although a mental health-related diagnosis is technically the property of the individual, the prevalence of mental health problems is high enough to constitute a community-level factor and, therefore, a social determinant. The incidence of mental disorders (i.e., diagnoses found in the Diagnostic and Statistical Manual of the American Psychiatric Association) may be as high as 20% among adults.27 Recent work also shows medication use (as a proxy for health care access) that is substantially lower among black and Mexican Americans than among whites.28
In particular, stress caused by the effects of racism in all forms and its outcomes affects daily life for many blacks and other minority ethnicities4,5,29; as a result, the rates of mental health distress, especially among groups made up of persons of minority races/ethnicities who have relatively few socioeconomic resources (measured as group means), may well be exacerbated.30 Large-scale community efforts designed to account for such stress in multifaceted interventions are unusual, although not unknown, with chronic disease outcomes, such as asthma.31
One of the most important social determinants of sexual health is SES. At the macro level, poverty and unemployment are associated with residential instability, segregation, and migration.32–34 As a result of racism and segregation, populations of minority groups have suffered disproportionate poverty and have had fewer employment and educational opportunities. Institutionalized discrimination and residential segregation reinforce a lack of economic resources for black residents in the United States.34 Residential instability, which can result from poverty, was identified as a key contributor to rising HIV rates in blacks.31 The National Minority AIDS Council recommended that the nation as a whole “support the strengthening of stable black communities by addressing the need for more affordable housing.”
Lack of resources and inequality of resource distribution has been found to lead to risky sexual behavior, lack of health care, and rising STD rates.32,35 For example, STD rates tend to be higher in countries with higher income inequality. The US income ratio for the richest five to the poorest five was 10 to 1 in 1999.32 From 1974 to 2001, the Gini coefficient (measure of income equality) has increased among men in the United States (Fig. 3), suggesting that income distribution in men has become increasingly inequitable.36 Also, factors such as high unemployment rate, low mean income, and low education levels (e.g., less than 9th grade) have been associated with higher STD rates.7,37,38 Finally, poverty and lack of employment can influence migration and sexual networks. The migration of skilled black men to the southeastern United States for better employment opportunities has been associated with rising STD rates in one county in North Carolina.39 In this instance, migration led to a disproportionate sex ratio (i.e., less number of men in the population than women)—a pattern identified as a factor in the rates of syphilis in the southeastern United States38 and of sexual risk factors in general.
Although disparities in incarceration rates have long existed—in 1974, 8.7% of black men had been incarcerated compared to only 1.4% of white men—the disparities increased markedly during the last 2 decades (Fig. 4).40 In the latter part of the 20th century, the United States experienced a crack epidemic. In response, the United States toughened drug legislation and enforcement,41 and rates of incarceration soared to the highest of any nation.34,42 Communities consisting of poor persons of minority races/ethnicities were hit hardest by the crack epidemic—socially, legally, and demographically. Legal enforcement practices led to an especially high rate of incarceration for black men—by 2001, 16.6% of black men had been incarcerated.40 These practices led to what Thomas and Torrone called a “forced migration” that resulted in disproportionate sex ratios, destabilized communities, and disrupted sexual networks.42 Additionally, the crack epidemic led to exchanging sex for money or drugs, which also affected sexual networks.34 Using crack cocaine, having sex at a crack house, and exchanging sex for money or drugs were related to syphilis in a Philadelphia study of heterosexual adults and adolescents, most of whom were black.43 In Brooklyn as well, crack and cocaine use was related to STD infection, especially syphilis, in black women.44 From 1995 through 2003, arrests related to illicit drugs were responsible for almost half of the increase in the number of prison inmates.45
The high rates of incarceration and the disproportionate burden of incarceration rates shouldered by black people persist. In 2005, over 2.2 million persons were in prison.45 Although only 12% of the US population is black, during 2005, 40% of persons in correctional facilities were black.46 In addition to disrupting sexual networks, incarceration contributes to the maintenance of poverty rates and places individuals at a further economic disadvantage.32,34 High incarceration rates in North Carolina counties were significantly correlated with high rates of STD infection, including chlamydial infection, gonorrhea, syphilis, and HIV, which brought about the “unintended consequence of destabilizing communities.”42
At this point, we move from the upper section of Figure 2 to the epidemiologic context in the lower section. Physical proximity is a noted commonality between carriers of gonorrhea and syphilis, given that these STDs have been found in (a) highly concentrated areas and (b) for gonorrhea, at least, even within areas of high endemicity, one infected person lives closer to another than would be expected by chance.47 Persons living in close functional proximity are more likely to form social relationships than those further apart.48 One study in Baltimore found the mean distance between sex partners in geographically defined core areas was lower than in other areas, meaning that people with gonorrhea (past or present) were literally closer to each other than were uninfected people.47 This work was further developed by Bernstein et al., who found that persons with repeat gonorrhea infections clustered more closely than those with single infections.49
Lack of social capital in geographic units may be an indicator of increased prevalence of STDs in populations. When a selection of firehouses in New York was closed for budgetary reasons, the neighborhoods in which they were located experienced increased HIV infection rates; any causal relationship between the closing of firehouses and increases in HIV rates may have been mediated through the factors resulting in neighborhood deterioration.50 Measures of neighborhood disorganization and disruption (i.e., negative indicators of social capital) beyond the effects of poverty correlate with STD rates. In 1 study, indicators of disregard for community (e.g., graffiti, high numbers of abandoned cars, and the broken windows that made up a broken windows index) predicted gonorrhea rates by geographic area, independent of poverty, employment, and educational measures.51 Particularly, neighborhoods with a high level of poverty and high scores on the broken windows index had gonorrhea rates almost twice that of equivalently poor neighborhoods with low index scores. Other negative indicators associated with STD rates include density of alcohol outlets and gonorrhea,52 a connection made plausible by the widely estimated correlations between alcohol use, risky sexual behavior, and disease. These associations are typically ecologic in nature, but in 1 natural case-control study conducted after civil unrest in Los Angeles, gonorrhea rates were lower in areas in which the unrest resulted in lower density of alcohol outlets.53
Finally, we return to the example of bridging.13 Bridging is not confined to racial or ethnic groups. But in large sexually segregated groups, bridging is a source of new STD transmission via concurrency and elevated numbers of partners,54 the effects of which are magnified by inadequate health care and other social determinants. More important, bridging rates do not have to differ by race/ethnicity to produce differential effects on STD rates. Bridging magnifies the effects of other determinants of disparities, acting as a manifestation of the interaction between social determinants and societal behavioral patterns to influence the epidemiologic context (Fig. 1).
Poverty, residential segregation, illicit drugs, and high rates of incarceration are related to higher rates and disparities of STD infection. All of these factors may contribute to the unequal patterns of migration by men and women in mostly black communities and the population composition that has been shown to be related to STD disparities.39 Specifically, migration and low sex ratio are associated with marital patterns including divorce, family stability, and issues related to partner selection.34,55 As noted by Thomas and Thomas, “A relative shortage of men places women at a disadvantage in maintaining a mutually faithful relationship.”55 This inequity between men and women makes it easier for men to maintain concurrent partnerships, and concurrent partnerships have been implicated in STD.33,34,56,57 In fact, studies have found that concurrency is more common in blacks and populations with lower income.33,34,57
In addition to poverty and migration, residential segregation is likely to be related to sexual networks. Data from a national survey demonstrated that black disparities in bacterial STD infection are largely a result of differences in sexual networks.56 Specifically, blacks are more likely to have sex with other blacks (e.g., have segregated partner choices), which is one reason why STDs tend to persist in the black population. Also, a black who had only 1 partner (during the past year) was much more likely than a white counterpart to have a partner who was classified as a core transmitter (e.g., had >4 partners during the past year).56
Conclusions: Implications for STD Prevention and Control
The implications are daunting: typical STD control programs are far more expert at addressing the epidemiologic context than they are at addressing social determinants; yet, our logic requires acting upon these extremely broad measures. One cannot seriously suggest reduction of segregation as a goal of STD prevention alone. However, those interested in STD prevention can at least collaborate with each other and with other health promotion and control entities whose outcomes are also affected by segregation and the other social determinants we have discussed here. In particular, the National Center for HIV, Viral Hepatitis, STD and TB Prevention, has named service integration as a priority and has recently undertaken first steps to promote service integration in all health concern centers. As social determinants are recognized as factors in each of the infectious diseases in the center, leverage through collaboration should be expected. The principle of collaboration needs to be extended further within CDC and beyond, as has happened with CDC's Syphilis Elimination Effort.58
STD prevention programs at various levels should engage communities with ongoing, genuine, and mutual advice and feedback. Wherever possible, STD activities should be then incorporated into community-level intervention projects: let an STD program contribute social capital to community cohesion and constructive organization. This may entail, for example, matching screening with efforts to improve reproductive health, stress reduction, and provision of services—outside clinical environments. If these efforts are explicitly tied to reducing disparities, so much the better.
Specific plans should be generated through, and tailored to, local communities. To chip away at negative social determinants of health in this fashion requires long-term planning, acceptance of innovation, and is not made easier by scarce resources for important traditional STD prevention and control functions (i.e., screening, testing, treatment, partner management). Yet, until disparities in underlying social determinants are addressed, the reduction of STD disparities cannot be guaranteed.
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