Racial disparities in sexually transmitted diseases (STDs) are a persistent and important public health problem in the United States. With an estimated 19 million new STDs every year, blacks, especially adolescents, bear a disproportionate burden.1–5 For example, among 15- to 19-year-olds, rates of gonorrhea are more than 20 times higher for blacks compared with whites.1 Although many STDs are treatable, if left undiagnosed or untreated, they can have serious sequelae including the facilitation of HIV transmission, infertility, organ damage, cancer, and adverse outcomes for babies born to mothers with a prevalent infection.1 Moreover, STDs cost an estimated US$17 billion to the US health care system annually.1 It is imperative that we understand the causes of these truly astonishing disparities to eliminate them.
Because differences in sexual behaviors such as condom use do not seem to explain the large disparities in STD risk,3,6,7 there has been a call for a greater examination of potential contextual or structural causes—such as, barriers to testing, neighborhood socioeconomic status, and rates of imprisonment.4,8–12 Accordingly, research on potential structural causes of these disparities has been growing. Adding to this increasing body of research, in this issue, Pugsley et al.13 examined the association between residential racial segregation and rates of gonorrhea in the United States.
Residential racial segregation describes the separation of racial groups (e.g., blacks and whites) in metropolitan areas in the United States. Residential racial segregation has been conceptualized in 5 dimensions. Metropolitan areas are as follows: isolated if black and whites do not often share neighborhoods; concentrated if blacks occupy less physical space relative to whites, centralized if blacks are more likely than whites to live in neighborhoods around an urban center, clustered if blacks live in neighborhoods that are grouped together, and uneven if blacks are overrepresented in some neighborhoods and underrepresented in other neighborhoods.14
Residential racial segregation has decreased over the last few decades; however, the magnitude of change has been small.15 In fact, residential segregation remains the norm for many metropolitan areas in the United States.8,15–17 Even with the overall decrease in segregation, census tracts historically occupied overwhelmingly by blacks have not become more integrated.8,16 Moreover, about two thirds of blacks lived in highly segregated metropolitan areas,8 and blacks at all income levels remain more segregated than any other racial/ethnic group.17,18
Historically, residential segregation of blacks from whites was legislated in the United States and supported and upheld by practices of economic, judicial, and social institutions and systems. Although segregation is no longer legislated, this long-standing systemic and systematic separation of blacks in the United States is likely an important explanation for the persistence of health and economic disparities through its impact on determining interpersonal contact patterns, access to services, and social environment.4,8,9,11,19 Empirical research examining the health impacts of this social structure is relatively new. Most studies have used characteristics of an individual’s neighborhood to describe differences in risk. However, residential racial segregation may be more conceptually relevant to understanding racial disparities than neighborhood characteristics because it captures the unequal structure for blacks and whites across an entire residential market.20 Galea et al.21 performed a meta-analysis to estimate the number of deaths that were attributable to a variety of social factors. They estimated that nearly 176,000 deaths were caused by residential racial segregation in 2000, compared with 39,000 for area-level poverty and 133,000 for individual-level poverty.
Very limited research has been done to examine the potential impact of residential racial segregation on disparities in STDs specifically. It is hypothesized that residential racial segregation may lead to differential exposure to STDs through its impact on sexual network patterns, by imposing barriers to testing and care, and by fostering environments that are conducive to behaviors that put individuals at increased STD risk.9 To the best of my knowledge, the study by Pugsley et al. in this issue is only the second study to examine the association between residential racial segregation and STDs in the United States.22
In their study, Pugsley et al. conducted an ecological analysis to examine the association between black isolation (a measure of residential racial segregation) and income inequality (a measure of economic segregation) on average rates of gonorrhea in 277 large metropolitan statistical areas (MSAs) in the United States from 2005 to 2009. Using Centers for Disease Control and Prevention (CDC) surveillance data and the US Census Bureau’s American Community Survey, they found that MSAs with high levels of residential racial segregation had more than 3 times higher odds of having high rates of gonorrhea compared with areas with low levels of segregation, even after adjustment for multiple area-level confounders. A significant association was not seen for income equality and gonorrhea rates.
Notably, the findings reported in this issue by Pugsley et al. are similar to those described previously by Biello et al.,22 although there were differences in data, measures, and statistical techniques. Using 2003–2007 CDC surveillance data and 2000 US Census Bureau data, Biello et al. found that the high level of isolation was associated with 1.3 times higher gonorrhea rates among blacks. Although the effect sizes are substantially different, this is mainly caused by differences in regression procedures. Biello et al. directly modeled the rates of gonorrhea using Poisson regression, whereas Pugsley et al. used logistic regression to model MSAs with high versus low rates of gonorrhea. In fact, in post hoc analyses, Pugsley et al. found that higher isolation was associated with 1.2 times increase in gonorrhea rates when directly modeling gonorrhea rates using Poisson regression.
Importantly, Pugsley et al. included a measure of income inequality, thus broadening the narrative regarding structural determinants of STD risk to include economic segregation. Given that economic segregation affects residential patterns, this is an important addition to this area of research. One limitation of their study was that they only analyzed one dimension of residential racial segregation, that is, black isolation. Although they assert that isolation may be best suited to capture patterns of infectious disease risk, each dimension of segregation may have varying degrees of salience in describing distinct mechanisms that impact sexual risk and STD transmission.9,10,19 By ignoring the other dimensions, they were limited in their ability to test their assertion and to indirectly explore potential mechanisms of the segregation-gonorrhea association. In their examination of segregation and gonorrhea rates, Biello et al. used multiple measures to represent distinct dimensions of segregation. These results painted a more complex picture—some of the dimensions predicted to be associated with gonorrhea rates were not (e.g., concentration), whereas others that were not predicted were (e.g., unevenness).10
One reason that research regarding population-level determinants such as residential racial segregation remains underdeveloped is that design and analysis of these research questions are complex.19,23–25 These studies require a sufficient number of cases spread across a large geographic area so that most MSAs are represented. To this end, Pugsley et al. used an ecological design to examine the association between MSA-level segregation and MSA gonorrhea rates. Further nuance could be garnered from a multilevel design, which can also be used to study population-level determinants and disease rates and, in fact, may provide additional insight into the association. With this design, potential mechanisms may be elucidated because factors at other levels can be included. For example, a multilevel strategy allows for examination of potential race, age, and sex differences in the association between segregation and gonorrhea rates. In addition, although not possible with the CDC surveillance data used by Pugsley et al., by using a multilevel design, one could explore more deeply whether MSA-level segregation is associated with sexual risk at the individual level. Two separate studies have examined the association of MSA-level segregation and individual sexual risk behaviors among adolescents.26,27 In one study, segregation explained the racial disparity in age at first sex26—an outcome marked by racial disparities.3 However, in the other study, segregation was not associated with condom use and number of partners27—outcomes for which evidence of racial disparities does not exist.3,6,7 In summary, although it is important to document that residential racial segregation is associated with STD rates, describing how segregation ultimately leads to increased STD risk for individuals is critical for reducing risk.
The important study by Pugsley et al. published in this issue augments the limited research indicating that residential racial segregation is associated with STD risk. There is also evidence that residential racial segregation is linked to increased burden of a multitude of health outcomes for blacks in the United States.8,10,19,28–31 Therefore, although the actual mechanisms are still untested and should be studied, structural interventions and policy changes aimed at reducing segregation may be key to reducing or even eliminating disparities in STDs and other health outcomes.
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