Neighborhood-Level Racial/Ethnic Residential Segregation and Incident Cardiovascular DiseaseCLINICAL PERSPECTIVE
The Multi-Ethnic Study of Atherosclerosis
Background—Previous research suggests that neighborhood-level racial/ethnic residential segregation is linked to health, but it has not been studied prospectively in relation to cardiovascular disease (CVD).
Methods and Results—Participants were 1595 non-Hispanic black, 2345 non-Hispanic white, and 1289 Hispanic adults from the Multi-Ethnic Study of Atherosclerosis free of CVD at baseline (aged 45–84 years). Own-group racial/ethnic residential segregation was assessed by using the Gi* statistic, a measure of how the neighborhood racial/ethnic composition deviates from surrounding counties’ racial/ethnic composition. Multivariable Cox proportional hazards modeling was used to estimate hazard ratios for incident CVD (first definite angina, probable angina followed by revascularization, myocardial infarction, resuscitated cardiac arrest, coronary heart disease death, stroke, or stroke death) over 10.2 median years of follow-up. Among blacks, each standard deviation increase in black segregation was associated with a 12% higher hazard of developing CVD after adjusting for demographics (95% confidence interval, 1.02–1.22). This association persisted after adjustment for neighborhood-level characteristics, individual socioeconomic position, and CVD risk factors (hazard ratio, 1.12; 95% confidence interval, 1.02–1.23). For whites, higher white segregation was associated with lower CVD risk after adjusting for demographics (hazard ratio, 0.88; 95% confidence interval, 0.81–0.96), but not after further adjustment for neighborhood characteristics. Segregation was not associated with CVD risk among Hispanics. Similar results were obtained after adjusting for time-varying segregation and covariates.
Conclusions—The association of residential segregation with cardiovascular risk varies according to race/ethnicity. Further work is needed to better characterize the individual- and neighborhood-level pathways linking segregation to CVD risk.
- cardiovascular diseases
- continental population groups
- ethnic groups
- residence characteristics
The spatial distribution of racial/ethnic groups in US metropolitan areas is highly patterned as a consequence of a complex set of social, cultural, and economic forces that also lead to the differential distribution of and exposure to resources and opportunities across space by race/ethnicity.1,2 Despite discrimination and other exclusionary housing practices having been outlawed for >50 years, racial/ethnic residential segregation in US metropolitan areas remains high; the average white individual lives in a neighborhood that is 75% white, whereas the average black and Hispanic individuals, who make up ≈13% and 16% of the US population, respectively,3 live in neighborhoods that are only 35% white.4 Predominantly minority neighborhoods are disproportionately higher in poverty than predominantly white neighborhoods.5 It has been proposed that racial/ethnic residential segregation may lead to adverse cardiovascular (cardiovascular disease [CVD]) outcomes for minorities through multiple mechanisms, including limiting opportunities for socioeconomic mobility, access to health-promoting resources, exposure to safe areas, and access to quality health care.2,6 However, as the ethnic density hypothesis posits, segregation may also confer beneficial health outcomes for minorities by fostering strong social networks, reinforcing social control, and shielding minorities from exposure to prejudice and discrimination.7
Editorial see p 124
Clinical Perspective on p 148
Although studies examining associations of metropolitan-level segregation with mortality have largely found that higher metropolitan area segregation is associated with worse outcomes among blacks,8–12 the findings from studies investigating the relationship between segregation and mortality across neighborhoods within cities (herein referred to as neighborhood-level segregation) are less clear.13–19 The existing studies of neighborhood-level segregation and cardiovascular outcomes have largely used death certificate data to examine associations of racial composition with CVD mortality rates, and findings generally indicate that higher segregation is related to lower mortality, particularly among older blacks.13–15 However, these studies are limited by their inability to capture nonfatal cardiovascular outcomes and minimal adjustment for individual-level confounders.
Moreover, studies of segregation and health have largely focused on blacks.20 Few have examined the impact of segregation on health for other minority groups, and none, to our knowledge, have examined the associations of segregation with cardiovascular outcomes. Given that the Hispanic population is projected to double, to constitute almost one-third of the US population by 2060,21 there is a strong imperative to also investigate the impact of residential segregation in Hispanics.
Using data from the Multi-Ethnic Study of Atherosclerosis (MESA), we prospectively examined associations of own-group neighborhood-level racial/ethnic residential segregation with incident cardiovascular disease in non-Hispanic black, non-Hispanic white, and Hispanic adults. We then assessed whether these relationships were explained by individual socioeconomic position (SEP), neighborhood characteristics, and traditional individual behavioral and biological CVD risk factors.
MESA is an observational prospective cohort study designed to examine the determinants of subclinical cardiovascular disease in adults aged 45 to 84 years. Self-identified black, Chinese, Hispanic, and white participants free of clinical CVD at baseline were recruited from 6 sites (New York, New York; Baltimore City and County, Maryland; Forsyth County, North Carolina; St. Paul, Minnesota; Chicago, Illinois; and Los Angeles County, California) between 2000 and 2002. Random population samples were selected at each site by using various population-based approaches. Additional details are provided elsewhere.22 Of the selected persons deemed eligible after screening, 59.8% participated in the study. Institutional review board approval was obtained at each site and all participants gave informed consent. Four additional examinations have been completed since baseline: examination 2 (2002–2004), examination 3 (2004–2005), examination 4 (2005–2007), and examination 5 (2010–2012). Because of the small number of cardiovascular events among Chinese participants, our analyses were restricted to blacks, Hispanics, and whites.
Racial/Ethnic Residential Segregation
Neighborhood-level racial/ethnic residential segregation was measured separately for blacks, whites, and Hispanics by using the local Gi* statistic,23 based on the geocoded addresses of MESA participants linked to US Census data. The Gi* statistic returns a Z score for each neighborhood (census tract), indicating the extent to which the racial/ethnic composition in the focal tract and neighboring tracts deviates from the mean racial composition of some larger areal unit surrounding the tract (in our case, the set of counties represented in each MESA site). Higher positive Gi* Z scores indicate higher racial/ethnic segregation or clustering (overrepresentation), scores near 0 indicate racial integration, and lower negative scores suggest lower racial/ethnic representation (underrepresentation), in comparison with the racial composition of the larger areal unit.
Most studies of neighborhood-level racial/ethnic residential segregation use racial/ethnic composition, or the proportion of a race/ethnic group in a neighborhood, as a proxy for segregation.24 However, this measure is limited in that it does not incorporate any information on the racial composition of the larger area in which the neighborhood is embedded or on the distribution of groups in space.1 The Gi* statistic, in contrast, better reflects both the contextual and spatial aspects of segregation. A given neighborhood will have a higher Gi* statistic the larger the difference between its racial composition and the composition of the larger areal unit. In addition, a neighborhood surrounded by similarly segregated areas will have a higher Gi* statistic than those surrounded by less segregated areas. Further details on the Gi* statistic are available in the Methods in the online-only Data Supplement.
Fatal and Nonfatal Incident CVD
Incident CVD was defined as first definite angina, probable angina followed by revascularization, myocardial infarction, resuscitated cardiac arrest, coronary heart disease (CHD) death, stroke, or stroke death. Incident CHD, defined as first myocardial infarction, resuscitated cardiac arrest, or CHD death, was also assessed as a secondary outcome. MESA uses a standard adjudication protocol to classify events.22 Every 9 to 12 months, participants (or, when necessary, their proxies) are contacted to inquire about hospital admissions, cardiovascular diagnoses, and deaths. Possible vascular events are abstracted from hospital records and sent for review and classification by an independent adjudication committee. Outcome follow-up data were available for events occurring on or before and adjudicated through December 31, 2011 (median follow-up of 10.2 years).
Sociodemographic covariates included age, sex, education (categorized as less than high school graduate, high school graduate, some college, and college degree or higher), health insurance status, and income (specified in quartiles). Baseline income was available and used for 80.0% of black participants, 85.0% of Hispanic participants, and 88.3% of white participants. When baseline income was missing, data from examination 2 were used (4.4% of black participants, 1.2% of Hispanic participants, and 1.2% of white participants).
Neighborhood (census tract) characteristics were adjusted for included neighborhood poverty, the neighborhood social environment, and the neighborhood physical environment. Neighborhood poverty was defined as the percentage of neighborhood residents who were below the US Census Bureau–defined poverty threshold, based on baseline address linked to Census 2000 data.25 Survey-based information on the neighborhood social and physical environments was collected as part of the MESA Neighborhood study, an ancillary study designed to assess neighborhood conditions of potential relevance to CVD. In addition to MESA participants, a sample of 5988 individuals (recruited between January and August 2004) residing in the same neighborhoods as MESA participants were asked to rate several aspects of their neighborhood via a telephone survey. Supplementing the neighborhood survey with participants other than those in MESA reduced the potential for same source bias, increased the within-neighborhood sample size for constructing more reliable subjective neighborhood variables, and provided a more representative measure of neighborhood conditions.26
The neighborhood social environment measure was generated by summing 3 scales, including neighborhood safety (a composite of 3 self-reported questions of safety and violence), neighborhood social cohesion (a composite of 5 self-reported questions on feelings of mutual trust and solidarity with neighbors), and esthetic quality (a composite of 3 self-reported questions relating to noise, presence of trash and litter, and overall neighborhood attractiveness). Possible scores ranged from 3 to 15, with higher scores indicating a better social environment (Cronbach α, 0.89). The neighborhood physical environment measure was constructed by summing responses of neighborhood walking environment (4 items) and neighborhood food environment (2 items) scales. Possible scores ranged from 2 to 10 (Cronbach α, 0.75). For each neighborhood scale, conditional empirical Bayes estimates were derived to increase the reliability of the measures. Additional details on the development of the scales are provided elsewhere.26 Both the neighborhood social and physical environment measures were categorized into tertiles.
We also adjusted for traditional behavioral and biological CVD risk factors, including cigarette smoking, physical activity, diabetes mellitus, systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, and body mass index. Physical activity was categorized as high (≥1000 MET-minutes per week of energy expenditure from recreational activity), intermediate (>0 and <1000 MET-minutes per week), or physically inactive based on the 2008 Physical Activity Guidelines for Americans.27 Cigarette smoking was categorized as current, former, and never; alcohol use was categorized as heavy (>14 drinks per week for men and >7 drinks per week for women), moderate, or none. Diabetes mellitus was defined as having a fasting glucose of ≥126 mg/dL or being on insulin or oral hypoglycemic medications.28 Resting seated blood pressure was measured 3 times at a single visit by trained and certified clinic staff using a Dinamap PRO 100 automated oscillometric device (Critikon, Tampa, FL), and the average of the last 2 measurements was used.29 Plasma high-density lipoprotein and total cholesterol were measured by the cholesterol-oxidase method.30
All analyses were stratified by race/ethnicity. Descriptive analyses compared baseline participant characteristics by levels of residential segregation score (high: Gi*>1.96; medium: Gi* 0–1.96; and low: Gi*<0). The high category corresponds to statistically significant clustering at the α=0.05 level, and the low category corresponds to both the absence of any clustering or areas in which the group is significantly underrepresented (Gi* < –1.96). These categories were combined because the number of blacks and Hispanics living in areas where they were significantly underrepresented was very small. Baseline characteristics were also compared in those who did and did not develop incident CVD/CHD.
A series of marginal Cox proportional hazards regression modeling were estimated by using a robust sandwich estimator to examine the relationship between baseline continuous segregation and CVD/CHD event while accounting for any residual correlations among individuals residing in the same census tract.31,32 Time was measured from the date of the baseline examination, and subjects were censored at the last contact date for outcome information if a CVD/CHD event was not observed. The proportional hazards assumption was tested by evaluating interactions of analysis time with the full complement of covariates; there was no evidence of violation. Model 1 adjusted for demographics including age, sex, and MESA study site (nativity was adjusted for as well for the analysis of Hispanics). We did not find evidence suggesting that the associations of segregation with incident CVD varied by MESA study site (P for interaction≥0.5), so findings are presented pooled across the sites. Model 2 additionally adjusted for neighborhood-level characteristics through which segregation may impact CVD/CHD, including neighborhood poverty, the neighborhood physical environment, and the neighborhood social environment. The black (r=0.31), Hispanic (r=0.31), and white (r=–0.59) segregation scores were correlated with neighborhood poverty, but not strongly enough to preclude us from assessing their independent associations. Model 3 further adjusted for individual factors that may have been influenced by segregation: education and income. Model 4 additionally adjusted for baseline CVD risk factors including hypercholesterolemia, hypertension, diabetes mellitus, body mass index, physical activity, current alcohol use, and current cigarette smoking as potential individual-level mediators.
We estimated 3 additional models to leverage our longitudinal data structure and more precisely operationalize our constructs. We first modeled the behavioral and biological CVD risk factors as time-varying covariates (model 5), and then we specified both residential segregation and CVD risk factors as time varying (model 6). As a secondary analysis, we also examined associations of change in segregation score with incident CVD. This was done by calculating the difference in the segregation score between each examination and baseline and including this variable as a time-varying covariate in the Cox regression.
For analyses of Hispanic segregation, we also tested whether the association between segregation and incident CVD varied between those of Mexican origin and those not of Mexican origin (including Dominican, Puerto Rican, Cuban, and other Hispanics) by incorporating a segregation–Mexican origin interaction term. This was motivated by prior research that had found associations between residential environment and health to differ by Hispanic subgroup.33,34 Small sample sizes precluded assessing this relationship separately in the other Hispanic subgroups. Based on previous research,35 we also tested for effect modification by nativity and acculturation. Nativity was dichotomized as foreign-born versus US-born. Acculturation was assessed by using a summary score based on length of time lived in the United States (3=US born; 2=foreign born and lived in the United States ≥20 years; 1=foreign-born and lived in the United States 10–19 years; and 0=foreign born and lived in the United States <10 years) and language spoken at home (2=English; 1=English and Spanish; and 0=Spanish).36 Scores ranged from 0 (least acculturated) to 5 (most acculturated) and were categorized into 3 groups (0–1, 2, and 3–5).
Analyses were based on the 5227 participants free of CVD with complete data on all covariates at baseline. Of the total 6011 black, Hispanic, and white MESA participants, 576 were excluded for missing address data and 4 were excluded for having prevalent CVD at baseline (as determined after recruitment via surveillance for events that occurred before baseline). Another 204 were missing data on ≥1 of the other study covariates measured at baseline. All analyses were conducted by using SAS 9.4 (SAS Institute, Inc, Cary, NC).
Baseline black segregation scores ranged from –2.85 to 11.58 for blacks (median, 2.47; interquartile range, 0.63–3.92). Median segregation scores remained similar across the follow-up examinations. The distribution of baseline Hispanic segregation for Hispanics was similar, with scores from –3.20 to 12.12 (median, 3.16; interquartile range, 0.67–4.82). Median scores decreased steadily across the follow-up examinations. For whites, baseline white segregation scores ranged from –4.86 to 5.02 (median, 0.44; interquartile range, –1.34 to 1.26). Median segregation scores over the follow-up examinations for all groups (not shown).
Overall, the patterning of individual- and neighborhood-level characteristics by level of segregation was similar in black and Hispanic participants (Table 1). With few exceptions, black and Hispanic participants living in less segregated tracts had higher SEP and better neighborhood conditions than their counterparts in more segregated areas. However, there were few significant differences in behavioral or biological CVD risk factors by level of segregation. In contrast, in whites, higher white segregation was generally associated with higher individual and neighborhood SEP, better neighborhood physical and social environments, and lower current smoking, physical inactivity, and body mass index.
Table 2 presents baseline characteristics by race/ethnicity and incident CVD status. Among all race/ethnic groups, those who developed CVD were older, and more likely to be male, hypertensive, and diabetic. Participants who developed CVD were more likely to have low education and income, although this difference was only significant for whites. There were no significant differences in neighborhood poverty by CVD status for blacks and Hispanics. In contrast, whites who developed CVD lived in higher-poverty neighborhoods. Blacks who developed CVD were less likely to live in poor (lowest tertile) social environments but more likely to live in poor physical environments. Mean segregation scores were higher for blacks who developed CVD than for those who did not, but this difference was not statistically significant (P=0.07). Segregation scores were lower for Hispanics and whites who developed CVD, but again these differences were not statistically significant (P=0.45 and 0.1, respectively). Patterns were similar when the outcome was restricted to CHD (not shown).
In blacks, higher segregation was significantly associated with higher incident CVD (Table 3). Each unit increase in black segregation was associated with a 12% increase (model 1 hazard ratio [HR], 1.12; 95% confidence interval [CI], 1.02–1.22) in the hazard of developing CVD after adjusting for age, sex, and study site. This association remained unchanged with further adjustment for individual- and neighborhood-level SEP, and measures of the neighborhood physical and social environments (models 2 and 3). Adjustment for potential mediating behavioral and biological CVD risk factors (model 4) had no effect on this association (model 4 HR, 1.12; 95% CI, 1.02–1.23). Point estimates for HRs associated with segregation were slightly larger among blacks when the outcome was restricted to CHD (model 1 HR, 1.18; 95% CI, 1.05–1.33); associations remained essentially unchanged in fully adjusted models (model 4 HR, 1.17; 95% CI, 1.03–1.32).
Hispanic segregation levels were not associated with CVD incidence for Hispanics across all adjusted models (eg, model 1 HR, 1.00; 95% CI, 0.95–1.05). There was some evidence suggesting that higher segregation was related to higher CVD incidence among foreign-born and less acculturated Hispanics, but the tests for interaction were not statistically significant (Table I in the online-only Data Supplement; P for interaction in demographic-adjusted models=0.09 and 0.1, respectively). The association between segregation and incident CVD did not vary significantly by country of origin (P for interaction in demographic-adjusted models=0.14). Findings were similar when analyses were restricted to CHD (model 1 HR, 1.03; 95% CI, 0.95–1.12).
Higher white segregation among whites was associated with 12% lower CVD incidence in demographic-adjusted models (Table 3; model 1 HR, 0.88; 95% CI, 0.81–0.96). This association was attenuated slightly and lost statistical significance with adjustment for neighborhood characteristics (model 2 HR, 0.91; 95% CI, 0.80–1.02). This association remained unchanged with further adjustment for individual SEP and CVD risk factors. As with incident CVD, segregation was inversely associated with incident CHD for whites in models adjusted for demographics (model 1 HR, 0.88; 95% CI, 0.79–0.99) but was attenuated after adjusting for neighborhood characteristics (model 2 HR, 0.94; 95% CI, 0.80–1.10).
All associations between segregation and CVD were essentially unchanged when CVD behavioral and biological risk factors were modeled as time-varying covariates, and when both segregation and risk factors were modeled as time varying, as well (not shown). In secondary analyses, change in segregation score was not significantly associated with incident CVD among whites (HR, 0.85; 95% CI, 0.69–1.05), blacks (HR, 1.01; 95% CI, 0.84–1.22), or Hispanics (HR, 0.99; 95% CI, 0.86–1.14).
We found that higher neighborhood-level own-group racial residential segregation was associated with higher CVD incidence among blacks and with lower CVD incidence among whites after adjusting for individual-level demographic characteristics. The magnitude of these associations persisted for blacks with further adjustment for individual SEP, neighborhood characteristics, and traditional CVD risk factors. Associations were attenuated for whites with adjustment for neighborhood characteristics. We found no evidence linking segregation to CVD incidence for Hispanics. All findings were similar when the outcome was restricted to CHD and when segregation and risk factors were modeled as time varying.
Our results for whites are consistent with previous research, which has shown that CVD mortality rates are lower for whites living in predominantly white neighborhoods in comparison with those living in predominantly minority neighborhoods.15 In our study, the association for whites was attenuated after adjusting for neighborhood characteristics, suggesting this was a key pathway linking segregation to cardiovascular risk. This is consistent with the segregation literature which suggests that neighborhood poverty is a predominant pathway by which racial/ethnic segregation influences health and health disparities, especially because exposure to high neighborhood poverty for black and Hispanic Americans is so much higher than for white Americans.2,5 In addition, neighborhood poverty and neighborhood racial/ethnic composition are correlated, particularly for blacks and whites.2,37 The correlations between own-group segregation and poverty were higher in whites than in blacks, which may explain why adjusting for neighborhood characteristics attenuated associations of segregation with CHD more for whites than for blacks.
Prior work on the relationship between neighborhood-level segregation and CVD in blacks has been less consistent. In contrast to our results, a Texas study found that blacks living in predominantly black areas lost fewer years of life to heart disease,13 and studies in New York City and Atlanta showed that older blacks (≥65 years) living in predominantly black neighborhoods had lower mortality rates (CHD and stroke, respectively) than those living in predominantly white neighborhoods.14,15 However, consistent with our findings, stroke mortality rates in the Atlanta study were higher for younger blacks living in predominantly black versus predominantly white neighborhoods.14 Differences across these studies may be attributable to a variety of factors including the cities included in the analyses, the way segregation was measured (tract racial composition in other studies versus Gi* statistic in our study, the latter which incorporates spatial dependence of neighboring tracts), and the type of events included (eg, fatal in other studies versus a combination of fatal and nonfatal in our study). Age differences across studies may also play a role, particularly if, among older populations, mortality selection is operating to cull blacks such that only hearty blacks had survived to participate in the sample. Because mortality selection may be especially operative in predominantly black neighborhoods,9,11 this could explain the apparent protective effect of racial composition with CVD mortality seen in previous studies of adults ages 65 and older.
Although we did not directly examine the contribution of segregation to black-white differences in CVD, our finding that higher segregation is associated with higher CVD risk in blacks is consistent with the notion that racial residential segregation may be a fundamental cause of black-white health disparities.2,38 Segregation has been called a fundamental cause of disparities because it determines access to opportunities for socioeconomic attainment and influences exposure to other health-harming and health-promoting conditions in the social and physical environment.2 In our study, adjusting for socioeconomic conditions and characteristics of the neighborhood social and physical environments did not attenuate associations of segregation with incident CVD for blacks. Our findings also persisted with adjustment for several mediating behavioral and biological risk factors. One reason for this may be that the other pathways we did not test, such as stress-related neuroendocrine and sympathetic nervous system pathways, or experiences of prejudice and discrimination39,40 may link segregation to increased CVD risk.29 Differences in access to quality health care may be another unmeasured pathway linking segregation to increased CVD risk. For example, a study using national Medicare data found that black patients are significantly more likely to undergo coronary artery bypass grafting and abdominal aortic aneurysm repair procedures in low-quality hospitals than whites living in medium- and high-segregation areas, but they found no significant black-white differences in low-segregation areas.6
It may also be that persistent associations of segregation with CVD among blacks may be attributable to residual confounding. For example, our baseline neighborhood measures may not adequately reflect the life course neighborhood-level exposures that influence CVD risk. However, MESA participants were asked in the study at baseline how long they lived in their current address, and these data show participants lived in their baseline addresses for an average of nearly 20 years (20.9 years for whites, 19.7 years for blacks, and 18.2 years for Hispanics). In addition, when we operationalized segregation as time varying over 10 years of follow-up, we found similar results as a baseline operationalization. Another possibility is that error in the measurement of the behavioral and biological CVD risk factors could have led to an underestimate of the impact of risk factors, even though our time-varying operationalization of CVD risk factors across almost a decade improves on much previous longitudinal CVD evidence.
No studies, to our knowledge, have examined associations of neighborhood-level residential segregation with cardiovascular outcomes among Hispanics. The findings from studies of neighborhood-level segregation and other health outcomes among Hispanics are mixed.19,34,41 As with blacks, research suggests that Hispanics face housing discrimination in rental and sales markets.40 However, the continuous influx of Hispanic immigrants into the United States promotes the development and maintenance of immigrant enclaves that ease the transition into the US labor market and facilitate retention of potentially health-promoting social and cultural ties, which may help to counterbalance the disadvantaged context that Hispanics face.38,39 Our null findings among Hispanics may reflect heterogeneity in the social and economic contexts of Hispanic enclaves.
Because Hispanics reflect a very heterogeneous population, previous research suggests that nativity or Hispanic country of origin may modify the impact of Hispanic segregation on health. For example, an examination of segregation and birthweight among Mexican-origin mothers showed living in ethnic enclaves was associated with lower birthweight for infants born to US-born Mexican-origin mothers but not foreign-born Mexican-origin mothers.35 In addition, a study of Puerto Rican and Mexican American Chicago residents found that higher segregation was associated with more frequent acute physical symptoms (eg, headaches and pains in chest or heart) in Puerto Ricans.34 In contrast, higher segregation in that Chicago study was not associated with physical symptoms in first-generation (foreign-born) Mexican Americans, but it was associated with better health in US-born (second- or higher-generation) Mexican Americans. However, we did not find significant differences in the Hispanic segregation-CVD association by acculturation, nativity, or country of origin. It is possible that the Mexican versus non-Mexican categorization was too broad, but, unfortunately, small sample sizes of other non-Mexican Hispanic subgroups limited our ability to examine neighborhood segregation-CVD associations among those groups. Further work is needed to better characterize the possible differing relationships between segregation and CVD risk among Hispanic subgroups. Studies in larger, more diverse (geographically and ethnically) Hispanic cohorts will help us better disentangle the impact of segregation on CVD risk in this heterogeneous population.
In secondary analyses, we found that a change in segregation was not related to CVD risk. One explanation is that there was not enough change in segregation levels across examinations, because few participants moved and segregation levels did not change substantially over time in the neighborhoods where participants resided. Another explanation is that, because many of the exposures associated with segregation that influence cardiovascular risk are experienced over the life course, later life moves may not be sufficient to mitigate the adverse health effects of living in segregated neighborhoods.42 Further work is needed in younger cohorts to better understand how segregation patterns over the life course impact cardiovascular risk.
The important strengths of our study include the prospective study design over 10 years of follow-up, multi-ethnic study population, adjudicated health outcomes, inclusion of multiple levels of potential confounders and mediators relevant for CVD, and our modeling of time-varying segregation and CVD covariates. One limitation of our study is that we did not have sufficient power to examine cardiovascular outcomes in Chinese MESA participants or to assess the relationships of segregation with specific cardiovascular outcomes other than CHD (eg, stroke). Another limitation is that MESA participants are not necessarily representative of the national population or even the cities in which they reside, which may reduce the generalizability of our findings.
No prospective study, to our knowledge, has investigated the connection between neighborhood-level racial/ethnic residential segregation and incident CVD. Our findings suggest that associations of segregation with CVD risk vary by race/ethnic group, reflecting differences in the processes that lead to segregation across these different groups and in the consequences of segregation for CVD-relevant exposures. One proposed strategy for reducing the adverse impact of segregation on health is to address the characteristics of segregated neighborhoods that are unhealthy.1 Thus, a better understanding of the impact of segregation on CVD risk, and the individual- and neighborhood-level pathways linking segregation to CVD, as well, may help guide the efforts to prevent CVD and reduce racial/ethnic disparities in cardiovascular outcomes.
Sources of Funding
This research was supported by grant R01 HL071759 (Diez Roux) and contracts N01-HC-95159 through N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-RR-024156 and UL1-RR-025005 from NCRR. The authors thank the other investigators, the staff, and the participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org. The information contained herein was derived in part from data provided by the Bureau of Vital Statistics, New York City Department of Health and Mental Hygiene.
The online-only Data Supplement is available with this article at http://circ.ahajournals.org/lookup/suppl/doi:10.1161/CIRCULATIONAHA.114.011345/-/DC1.
- Received May 22, 2014.
- Accepted October 17, 2014.
- © 2014 American Heart Association, Inc.
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Because of a variety of cultural, social, and economic forces, blacks, whites, and, to a lesser extent, Hispanics have persistently been segregated spatially in most US metropolitan areas. The processes that lead to this spatial separation influence the distribution of health-promoting neighborhood resources and opportunities for socioeconomic mobility. As such, racial/ethnic residential segregation may represent an important contributor to racial/ethnic disparities in cardiovascular disease risk. However, no prospective studies have examined this relationship. The goal of this study was to examine whether own-group residential segregation was associated with cardiovascular disease incidence among black, Hispanic, and white participants of the Multi-Ethnic Study of Atherosclerosis. Among blacks, each unit increase in segregation of blacks from other groups was associated with a 12% higher risk of developing cardiovascular disease independent of sociodemographic characteristics, neighborhood characteristics, and traditional cardiovascular disease risk factors. Segregation of Hispanics was not related to cardiovascular disease incidence among Hispanics. For whites, the higher segregation of whites from other groups was associated with lower cardiovascular disease risk in demographic-adjusted models, but this was attenuated with the adjustment for neighborhood characteristics. Our findings suggest that, for blacks, racial residential segregation limits opportunities and resources available to prevent cardiovascular disease and that providing effective care in this often underserved population will require addressing health-related issues beyond treating individual symptoms.