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Introduction: Epidemiologic studies have documented the associations between experiences of discrimination and adverse health outcomes. However, the relationship between discrimination and mortality, and the factors that may moderate this relationship are not well understood. This study examined whether lifetime and everyday discrimination were associated with all-cause and cardiovascular mortality, and whether these associations differed by race/ethnicity, gender, and racial/ethnic residential segregation. Hypothesis: We hypothesized that greater exposure to lifetime and everyday discrimination would be associated with increased risk of cardiovascular mortality, and that these associations would be modified by race/ethnicity, gender, and racial/ethnic residential segregation. Methods: The study included 1,633 Black, 1,403 Hispanic/Latino, and 2,473 White participants aged 45 to 84 years from the Multi-Ethnic Study of Atherosclerosis, enrolled from 2000-2002 and followed across 5 exams (2002-2018). In addition to exams, follow-up for mortality involved phone calls and linkage with the National Death Index. Discrimination was measured using the lifetime discrimination (major experiences of unfair treatment) and everyday discrimination (day-to-day experiences of unfair treatment) scales. Racial/ethnic residential segregation was measured using the Gi* statistic. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (95%CIs), adjusting for sociodemographic characteristics, health behaviors, and clinical risk factors. Results: Each increase in reports of lifetime discrimination was associated with increased all-cause (HR=1.06; 95%CI 1.00,1.11,) and cardiovascular (HR=1.15; 95%CI 1.04, 1.27) mortality, adjusting for sociodemographic factors, health behaviors, and clinical risk factors. Associations between lifetime discrimination and cardiovascular mortality were observed across all racial/ethnic groups but were strongest and only statistically significant among Black participants (HR=1.18; 95%CI 1.02, 1.37). Additionally, in the fully adjusted model, each increase in reports of everyday discrimination was marginally associated with increased all-cause mortality (HR=1.07; 95%CI 0.98-1.17) and strongly associated with increased cardiovascular mortality (HR=1.21; 95%CI 1.03, 1.43). Associations for lifetime and everyday discrimination with all-cause and cardiovascular mortality were not modified by race/ethnicity, gender, or racial/ethnic residential segregation. Conclusion: These findings suggest that experiences of discrimination are associated with increased all-cause and cardiovascular mortality. Our results underscore the need for interventions aimed at preventing and mitigating the adverse health effects of discrimination.

Background: Despite improvements in population health, marked racial and ethnic disparities in longevity and cardiovascular disease (CVD) mortality persist. This study aimed to describe risks for all-cause and CVD mortality by race and ethnicity, before and after accounting for socioeconomic status (SES) and other factors, in the MESA study (Multi-Ethnic Study of Atherosclerosis). Methods: MESA recruited 6814 US adults, 45 to 84 years of age, free of clinical CVD at baseline, including Black, White, Hispanic, and Chinese individuals (2000–2002). Using Cox proportional hazards modeling with time-updated covariates, we evaluated the association of self-reported race and ethnicity with all-cause and adjudicated CVD mortality, with progressive adjustments for age and sex, SES (neighborhood SES, income, education, and health insurance), lifestyle and psychosocial risk factors, clinical risk factors, and immigration history. Results: During a median of 15.8 years of follow-up, 22.8% of participants (n=1552) died, of which 5.3% (n=364) died of CVD. After adjusting for age and sex, Black participants had a 34% higher mortality hazard (hazard ratio [HR], 1.34 [95% CI, 1.19–1.51]), Chinese participants had a 21% lower mortality hazard (HR, 0.79 [95% CI, 0.66–0.95]), and there was no mortality difference in Hispanic participants (HR, 0.99 [95% CI, 0.86–1.14]) compared with White participants. After adjusting for SES, the mortality HR for Black participants compared with White participants was reduced (HR, 1.16 [95% CI, 1.01–1.34]) but still statistically significant. With adjustment for SES, the mortality hazards for Chinese and Hispanic participants also decreased in comparison with White participants. After further adjustment for additional risk factors and immigration history, Hispanic participants (HR, 0.77 [95% CI, 0.63–0.94]) had a lower mortality risk than White participants, and hazard ratios for Black participants (HR, 1.08 [95% CI, 0.92–1.26]) and Chinese participants (HR, 0.81 [95% CI, 0.60–1.08]) were not significantly different from those of White participants. Similar trends were seen for CVD mortality, although the age- and sex-adjusted HR for CVD mortality for Black participants compared with White participants was greater than all-cause mortality (HR, 1.72 [95% CI, 1.34–2.21] compared with HR, 1.34 [95% CI, 1.19–1.51]). Conclusions: These results highlight persistent racial and ethnic differences in overall and CVD mortality, largely attributable to social determinants of health, and support the need to identify and act on systemic factors that shape differences in health across racial and ethnic groups.

Background: African Americans have a higher risk for hypertension compared to other racial or ethnic groups in the United States. One possible explanation for this health disparity is perceived discrimination. Few studies have prospectively examined the association between discrimination and the incidence of hypertension. Methods: We examined the associations of everyday, lifetime, and stress from lifetime discrimination with incident hypertension and whether these associations differed by sex, discrimination attribution (i.e. the main reason for the discrimination event), and coping responses to discrimination among African Americans enrolled in the Jackson Heart Study. Discrimination was self-reported by 1845 African Americans aged 21 to 85 years without hypertension at baseline (2000-2004). Participants completed two follow-up study visits from 2005-2008 and 2009-2013. We used interval-censored Cox regression to estimate associations of discrimination with incident hypertension (antihypertensive medication use; and/or systolic blood pressure ≥ 140 mm Hg and diastolic blood pressure ≥ 90 mm Hg at follow-up visits 2 or 3) after adjustment for confounding variables. Results: Overall, 52% (954 of 1845) of participants developed hypertension over the follow-up period. After adjustment for age, sex, education and hypertension risk factors (body mass index, alcohol use, smoking, diet and physical activity), medium versus low levels of lifetime discrimination (hazard ratio-HR: 1.45, 95% confidence interval-CI: 1.15-1.82) and high versus low levels of lifetime discrimination (HR: 1.35, CI: 1.08-1.68) were associated with a higher incidence of hypertension. High versus low stress from lifetime discrimination was associated with hypertension risk after adjustment for demographics (HR: 1.20, CI: 1.02-1.41), but the association was attenuated after adjustment for hypertension risk factors (HR: 1.14, CI: 0.97-1.35). Lifetime discrimination and stress from discrimination were associated with an increased hypertension risk among females, but not males. No interactions with age, attribution or coping were present for any type of discrimination. Conclusions: Findings from this study support an association between lifetime discrimination and incident hypertension in African Americans.

Introduction: The prevalence of type-2 diabetes is increasing globally with the sharpest increases occurring in low and middle-income countries. Residential segregation results in increased exposure to adverse neighborhood environments that may inhibit the successful management of diabetes. Moreover, due to historical and contemporary forms of structural racism, marginalized racial groups are more likely to live in these environments. Using a spatial measure of neighborhood-level economic residential segregation (hereafter, segregation) we examined the association between segregation and uncontrolled diabetes in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Methods: The sample included 828 Black, Brown/Mixed-Race, and White participants ages 35-74 with diagnosed diabetes and complete, geocoded information from the baseline examination of ELSA-Brasil (2008-2010). Residential segregation was based on data from the 2010 IBGE demographic census and calculated for study-defined neighborhoods using the local G i * statistic— a spatially weighted z-score that represents how much a neighborhood’s income composition deviates from the larger metropolitan area. Uncontrolled diabetes was based on 2017 ADA criteria and defined as HbA1c ≥ 7%. Multivariable logistic regression models were used to test cross-sectional associations between segregation and uncontrolled diabetes. Results: Black and Brown participants were more likely than Whites to live in highly segregated neighborhoods. The prevalence of uncontrolled diabetes increased across low, medium, and high levels of segregation (23.1% vs. 37.8% vs. 47.7%, respectively). In multivariable models adjusting for age, gender, race, education, income, and study site, segregation was positively associated with uncontrolled diabetes (OR: 1.20, 95% CI: 1.07-1.56). The association was attenuated but remained statistically significant in models adjusting for neighborhood characteristics, behavioral risk factors and time since diabetes diagnosis. (OR: 1.16; 95% CI: 1.05-1.28). In models that included segregation as a categorical variable, individuals living in highly segregated neighborhoods had a 2-fold higher risk of uncontrolled diabetes compared to individuals living in less segregated neighborhoods (High Segregation, OR: 2.20, 95% CI: 1.35-3.58; Medium Segregation, OR: 1.65, 95% CI: 1.08-2.51). Conclusions: Residential segregation may lead to disparate diabetes-related morbidity among urban-dwelling adults in Brazil. Moreover, the disproportionate clustering of Blacks and Browns within segregated neighborhoods implicates segregation as a potential driver of racial inequalities in these outcomes. Policies and/or structural interventions designed to improve neighborhood conditions may be viable strategies to improve the management of diabetes in this setting.

Introduction: Obesity and obesity-related diseases are increasing globally with the sharpest increases occurring in low and middle-income countries. Economic residential segregation results in increased exposure to adverse neighborhood environments; however, the impact of segregation on markers of obesity have been mostly investigated in US-based samples. Using a novel spatial measure of neighborhood-level economic residential segregation (hereafter, segregation) we examined the association between segregation, obesity and visceral adiposity in the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Methods: The sample included 6,104 women and 4,789 men ages 35-74 with complete geocoded information from the baseline examination of ELSA-Brasil (2008-2010). Segregation was based on data from the 2010 IBGE demographic census and calculated for study-defined neighborhoods using the local Gi* statistic— a spatially weighted z-score that represents how much a neighborhood’s income composition deviates from the larger metropolitan area. Body mass index (BMI) was calculated by dividing the participants’ measured weight in kilograms by their measured height in meters squared. Participants were considered “obese” if they had a BMI greater than 30 kg/m 2 . Visceral adiposity was assessed using measured waist circumference (in cm) as a proxy. Based on statistically significant interactions between gender and segregation, gender-stratified multivariable logistic and linear regression models were used to test associations between segregation and obesity status and visceral adiposity, respectively. Results: Approximately 14% of the sample resided in segregated neighborhoods. Blacks and Browns were more likely to reside in segregated neighborhoods than Whites (Blacks: 25.9%; Browns: 20.2%; Whites: 8.2%). The prevalence of obesity in the sample was 24% among women and 20% among men and was highest among Black women living in the most economically segregated neighborhood environments (35%). After adjusting for age, sex, race, education, income, and study site, segregation was positively associated with obesity among women (OR: 1.29, 95% CI: 1.07-1.56). Associations for men were not statistically significant (OR: 1.07; 95% CI: 0.85-1.34). Similar patterns were found for visceral adiposity among women (High Segregation, β=1.94 ± 0.51, p=0.0002; Medium Segregation, β=0.90 ± 0.39, p=0.0192) with no statistically significant findings among men. Conclusion: Women residing in economically segregated neighborhoods in Brazil appear to be at an increased risk of obesity and have higher levels of visceral adiposity. Black women may be at highest risk in these settings. Policies and/or structural interventions designed to improve neighborhood conditions may be viable strategies to mitigate the burden of obesity in this setting.

Background: Although some evidence shows that neighborhood deprivation is associated with greater subclinical atherosclerosis, prior studies have not identified what aspects of deprived neighborhoods were driving the association. Methods: We investigated whether social and physical neighborhood characteristics are related to the progression of subclinical atherosclerosis in 5950 adult participants of the MESA (Multi-Ethnic Study of Atherosclerosis) during a 12-year follow-up period. We assessed subclinical disease using coronary artery calcium (CAC). Neighborhood features examined included density of recreational facilities, density of healthy food stores, and survey-based measures of availability of healthy foods, walking environment, and social environment. We used econometric fixed-effects models to investigate how change in a given neighborhood exposure is related to simultaneous change in subclinical atherosclerosis. Results: Increases in density of neighborhood healthy food stores were associated with decreases in CAC (mean changes in CAC Agatston units per 1-SD increase in neighborhood exposures, −19.99; 95% confidence interval, −35.21 to −4.78) after adjustment for time-varying demographic confounders and computed tomography scanner type. This association remained similar in magnitude after additional adjustment for time-varying behavioral risk factors and depression. The addition of time-varying biomedical factors attenuated associations with CAC slightly (mean changes in CAC per 1-SD increase in neighborhood exposures, −17.60; 95% confidence interval, −32.71 to −2.49). Changes across time in other neighborhood measures were not significantly associated with within-person change in CAC. Conclusions: Results from this longitudinal study provide suggestive evidence that greater access to neighborhood healthy food resources may slow the development of coronary atherosclerosis in middle-aged and older adults.

Background: Depression has been suggested as a potential risk factor for atrial fibrillation (AF) through effects on the autonomic nervous system and hypothalamus-pituitary-adrenal axis. Current literature examining the prospective relationship between depression and AF is inconsistent and limited to studies performed in predominantly white populations. We determined the relationship of both depressive symptoms and anti-depressant use with incident AF in a multi-ethnic cohort. Methods: The Multi-Ethnic Study of Atherosclerosis is a prospective study of 6,814 individuals without clinical cardiovascular disease. Depressive symptoms were assessed at baseline by the 20-item Center for Epidemiologic Studies Depression Scale (CES-D) and use of anti-depressant medications. Five CES-D groups were created based on the score distribution in approximate quartiles, and the top quartile split in 2 such that the top group represented persons with a score ≥16, a value commonly used to identify clinically relevant symptoms. Incident AF was identified from study ECGs verified for AF, ICD-9 hospital discharge diagnoses consistent with AF, and, for participants enrolled in fee-for-service Medicare, inpatient and outpatient AF claims data. Results: 6,644 participants (mean age=62; 53% women; 38% white; 28% black; 22% Hispanic; 12% Chinese-American) were included and followed for a median of 13 years. In separate adjusted Cox proportional hazards analyses, a CES-D≥16 (referent=CES-D Conclusions: Depressive symptoms are associated with an increased risk of incident AF. Further study into whether improving depressive symptoms reduces AF incidence is important.

Introduction: Racial residential segregation results in increased exposure to adverse neighborhood environments for African Americans; however, the impact of segregation on ideal cardiovascular health (CVH) has not been examined in large, socioeconomically diverse African American samples. Using a novel spatial measure of neighborhood-level racial residential segregation, we examined the association between segregation and ideal CVH in the Jackson Heart Study (JHS). Hypothesis: Racial residential segregation will be associated with worse cardiovascular health among African American adults. Methods: The sample included 4,354 men and women ages 21-93 from the baseline exam of the JHS (2000-2004). Racial residential segregation was assessed at the census-tract level. Data on racial composition (% African American) from the 2000 US Census was used to calculate the local G i * statistic- a spatially-weighted z-score that represents how much a neighborhood’s racial/ethnic composition deviates from the larger metropolitan area. Ideal CVH was assessed using the AHA Life’s Simple Seven (LS7) index which includes 3 behavioral (nutrition, physical activity, and smoking) and 4 biological (systolic BP, glucose, BMI, and cholesterol) metrics of CVH. Multivariable regression models were used to test associations between segregation and the LS7 index continuously (range: 0-14) and categorically (Inadequate: 0-4; Average: 5-9; and Optimal: 10-14). Covariates included age, sex, income, education, and insurance status. Results: The average LS7 summary score was 7.03 (±2.1) and was lowest in the most racially segregated neighborhood environments (High Segregation: 6.88 ±2.1 vs. Low Segregation: 7.55 ±2.1). The prevalence of inadequate CVH was higher in racially segregated neighborhoods (12.3%) compared to neighborhoods that were the least segregated (6.9%). After adjusting for key socio-demographic characteristics, racial residential segregation was inversely associated with ideal CVH (B=-0.041 ±0.02, p=0.0146). Moreover, a 1-SD unit increase in segregation was associated with a 6% increased odds of having inadequate CVH (OR: 1.06, 95% CI: 1.00-1.12, p=0.0461). Conclusion: In conclusion, African Americans in racially segregated neighborhoods are less likely to achieve ideal CVH even after accounting for individual-level factors. Policies aimed at restricting housing segregation/discrimination and/or structural interventions designed to improve neighborhood environments may be viable strategies to improving CVH in this at-risk population.

Introduction: Individual and area-level socioeconomic status (SES) are associated with hypertension incidence and blood pressure changes in midlife. However, examination of the relationship between SES and late-life hypertension incidence are limited. Methods: ARIC Study participants free of hypertension at visit 4 (1996-1998) were followed by annual and semi-annual calls through December 31, 2013 for incidence of hypertension, defined as a self-reported diagnosis or use of antihypertensive medications. Individual and neighborhood SES indicators were assessed at study baseline (using criteria listed in the Table). Among individuals with follow-up and complete data (N=3,374) associations were examined using Cox regression models. Results: Among men and women with a median baseline blood pressure of 118/68 mg Hg, mean age was 61 years (SD ± 5.5), 45% were female, 12% were Black, and 21.7% had an annual household income of Conclusion: Both neighborhood and individual SES are related to late life incidence of hypertension, at least among Whites. Understanding the mechanisms, such as the role of access to care, for these associations can guide prevention strategies.

Introduction: Perceived discrimination is associated with risk factors for type 2 diabetes, including measures of adiposity. However, the relationship between perceived discrimination and incident diabetes is unknown. Objectives: To determine whether perceived discrimination is related to incident diabetes, and whether this association varies by race/ethnicity, age or sex. Methods: Included in this analysis were 5,310 MESA participants aged 45-84 years, without a history of diabetes at baseline. Perceived discrimination was measured using the Lifetime Discrimination scale, which assessed experiences of unfair treatment in 6 life domains (e.g. fired or denied a promotion, unfair treatment by police, not hired for a job, having life made difficult by neighbors). Participants were also asked to attribute their experiences of discrimination to various factors (e.g. race/ethnicity, age, sex, religion). Incident diabetes was identified at four follow-up examinations as fasting glucose ≥126 mg/dL or use of diabetes medications. Multivariable-adjusted Cox proportional hazard regression was used to model lifetime discrimination as a continuous and categorical variable (0, 1, ≥2 domains). Results: A total of 654 incident diabetes cases accrued over a median follow-up of 9.4 years (range 0.9-11.4). Lifetime discrimination reported in ≥ 2 domains (versus none) was associated with a 34% increased risk of incident diabetes, after adjustment for potential confounders or mediators (Table). Similar patterns were observed when we evaluated discrimination attributed to race/ethnicity only, or to a combination of other sources. There were no differences in the strength of association by race/ethnicity, age or sex. Conclusions: Lifetime discrimination was associated with increased risk of incident diabetes, regardless of attribution. These associations were independent of obesity, behavioral and psychosocial factors. Future research is needed to explore the mechanisms of the discrimination-diabetes relationship.

In 2004, the first American Heart Association scientific statement on “Air Pollution and Cardiovascular Disease” concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM 2.5 ) over a few hours to weeks can trigger cardiovascular disease–related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM 2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM 2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality.

Background— Low socioeconomic position is known to be associated with cardiovascular events and atherosclerosis. Reasons for these associations remain a topic of research. Inflammation could be an important mediating mechanism linking socioeconomic position to cardiovascular risk. Methods and Results— This cross-sectional study used data from the baseline examination of the Multi-Ethnic Study of Atherosclerosis (MESA), a study of 6814 men and women 45 to 84 years of age. Race- and ethnicity-stratified regression analyses were used to estimate associations of household income and education with C-reactive protein and interleukin-6 before and after adjustment for infection and medication use, psychosocial factors, behaviors, adiposity, and diabetes mellitus. Low income was associated with higher concentrations of interleukin-6 in all race/ethnic groups. Percent differences associated with 1-SD–lower income were 9% (95% confidence interval [CI], 7 to 11), 6% (95% CI, 1 to 10), 8% (95% CI, 4 to 11), and 8% (95% CI, 3 to 13) for whites, Chinese, blacks, and Hispanics. Low levels of education were associated with higher levels of interleukin-6 only among whites and blacks (percent difference in interleukin-6 associated with 1-SD–lower education: 9% [95% CI, 6 to 12] among Whites, and 7% [95% CI, 3 to 10] among blacks). Similar patterns were observed for C-reactive protein. Adiposity was the single most important factor explaining socioeconomic position associations, especially among blacks and whites. A smaller effect was seen for psychosocial factors and behaviors in all race groups. Conclusions— Both household income and education are associated with inflammation, but associations vary across race/ethnic groups. Associations likely result from socioeconomic position patterning of adiposity and other factors.

Introduction: Research on the association between neighborhood environments and systolic blood pressure (SBP) is limited, predominantly cross-sectional, and has produced mixed results. Investigating specific aspects of neighborhood environments in relation to changes in SBP may help to identify the most important interventions for reducing the population burden of hypertension. Hypothesis: Better neighborhood food, physical activity, and social environments will be associated with lower baseline levels of SBP and smaller increases in SBP over time. Methods: The Multi-Ethnic Study of Atherosclerosis recruited participants from six sites in the U.S., aged 45-84 (mean 59) and free of clinical cardiovascular disease at baseline. Those with non-missing data for key variables were included (N=5,997); the analytic sample was 52.5% female, 39.1% White, 27.3% Hispanic, 11.9% Black, and 21.7% Chinese, with median follow-up time of 9.2 years (IQR 4.5) and SBP measured at three or more exams for 91.3% of participants. SBP in subjects taking anti-hypertensive medication were replaced with multiply imputed estimates of unmedicated SBP, imputed at each exam. Summary measures of neighborhood food and physical activity environments incorporated survey-based scales (healthy food availability and walking environment) and GIS-based measures (density of favorable food stores and recreational resources). The summary measure of the social environment combined survey-based measures of social cohesion and safety. Neighborhoods were defined by a one-mile buffer around each participant’s home address. Linear mixed models were used to model associations of time-varying cumulative average neighborhood environmental summary measures with SBP over time, adjusting for individual-level covariates (demographics, individual- and neighborhood-level SES); models with and without adjustment for baseline SBP were used to evaluate associations of neighborhood environments with SBP trajectories. Results: In models mutually adjusted for all three neighborhood domains and covariates, living in a better physical activity environment was associated with lower SBP at baseline (-1.34 mmHg [95% CI: -2.24, -0.45] per standard deviation higher cumulative average physical activity summary score), while living in a better social environment was associated with higher SBP at baseline (1.00 mmHg [0.39, 1.63] per standard deviation higher); food environment scores were not associated with baseline SBP. After adjustment for baseline SBP, there was no association between any neighborhood environments and trajectories of SBP. Conclusions: Better food and physical activity environments were associated with lower baseline SBP, while better social environments were associated with higher baseline SBP. Neighborhood environments appear to have minimal direct effect on SBP trajectories.

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 G i * 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.

Background — Few studies have examined how the longitudinal change in blood pressure associated with aging differs across social groups within industrialized countries. Methods and Results — Data from the Atherosclerosis Risk In Communities Study were used to investigate differences in the incidence of hypertension and in aging-related changes in blood pressure by neighborhood and individual socioeconomic factors over a 9-year follow-up. Disadvantage in multiple socioeconomic dimensions was associated with the greatest risk of developing hypertension (age- and sex-adjusted hazard ratio [HR] and 95% CI: HR 1.95, 95% CI 1.38 to 2.75 in whites and HR 1.43, 95% CI 0.96 to 2.13 in blacks). Aging-related increases in systolic blood pressure were inversely associated with socioeconomic position in whites (mean [SEM] 5-year increase in systolic blood pressure 7 [0.7] mm Hg in the most disadvantaged category and 5.4 [0.4] mm Hg in the most advantaged category). In whites, low socioeconomic position was also associated with more rapid declines in diastolic blood pressure after 50 years of age. Socioeconomic differences in hypertension incidence and changes in systolic blood pressure were reduced after adjustment for baseline blood pressure. Conclusion — The change in blood pressure associated with aging varies by social groups within the United States.

Background: Several individual-level measures of stress have been linked to incident CHD in prospective studies, but less attention has focused on the influence of neighborhood-level stressors. We assessed prospective associations of individual- and neighborhood-level stressors with incident CHD. Methods: MESA participants were aged 45-84 years at baseline (2000-2002). Analyses were conducted separately for those with complete data on individual- (n=6678) and neighborhood-level stressors (n=6105). Missing values on covariates were imputed with multiple imputation. Baseline individual-level sources of stress were assessed using the chronic burden scale, a measure of the presence and perceived stressfulness of ongoing health, job, relationship, and financial problems lasting over 6 months. Survey-based neighborhood safety (3 items) and neighborhood social cohesion (5 items) were examined as neighborhood-level sources of chronic stress. Each participant’s neighborhood safety and neighborhood social cohesion scores were constructed using Empirical Bayes estimation techniques that incorporated the responses of other MESA participants and a sample of non-participants living within a mile of that participant. Scores for each individual- and neighborhood-level stress measures were categorized into approximate tertiles (low, medium, and high) for analyses. CHD was defined as nonfatal myocardial infarction, resuscitated cardiac arrest, or CHD death. Median follow-up time was 8.5 years. Multivariable Cox proportional hazard models were used to estimate associations of high chronic burden, low neighborhood cohesion, and low neighborhood safety with incident CHD after adjusting for sociodemographic characteristics as well as behavioral and biological risk factors. Results: Participants in the high chronic burden category had 55% higher risk of incident CHD (hazard ratio (HR): 1.55; 95% confidence interval (CI): 1.11, 2.15) than those in the low category after adjusting for age, race/ethnicity, gender, education, income, marital status and field center. Findings attenuated slightly but remained significant with further adjustment for hypercholesterolemia, hypertension, diabetes, body mass index, physical activity, current smoking, and current alcohol use (HR: 1.47; 95% CI: 1.03, 2.00). Neither low (vs. high) neighborhood cohesion (HR: 1.23; 95% CI: 0.74, 2.06) nor low (vs. high) neighborhood safety (HR: 1.12; 95% CI: 0.68, 1.84) was associated with CHD in sociodemographic-adjusted models. Conclusions: Individual-level sources of stress were more strongly associated with incident CHD than neighborhood-level stressors.

Air pollution is associated with CVD and systemic inflammation is posited to mediate this effect. Animal, experimental and epidemiologic studies suggest that increases in short-term air pollution cause an inflammatory response. Few studies, however, have assessed the contribution of long-term exposure to pollutants even though chronic inflammation may be more relevant to the observed risk of atherosclerotic disease. We assessed the hypothesis that long-term exposure to pollutants is associated with markers of inflammation, coagulation and endothelial activation. We studied participants from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort with repeat measures of serum C-reactive protein (CRP), fibrinogen, D-dimer, soluble E-selectin and soluble Intercellular Adhesion Molecule-1 (sICAM-1). We estimated associations of these markers with outdoor PM2.5, individual-level ambient PM2.5 (integrating indoor concentrations and time-location data) and oxides of nitrogen (NOX). Pollutant concentrations were predicted from likelihood based models from cohort-specific monitoring and were averaged over the year prior to blood draw. CRP and D-Dimer were log-transformed for analysis. A random effects model controlling for relevant covariates was used to account for within person clustering. Participants with a recent history of acute infection were excluded from analysis. A total of 713 participants contributed 1736 observations (mean 1.8 observations per person over 3 visits). After excluding those with a recent infection we were left with 1233 observations among 491 participants. In multivariable models, both D-dimer and E-selectin were associated with pollutants, specifically PM2.5 and NOx (see table). There was no association between pollutants and CRP, fibrinogen or sICAM-1. In conclusion, these data are consistent with the hypothesis that associations between long-term exposure to particulate and traffic-related air pollution and CVD may be related to endothelial activation and fibrinolysis.

Although social engagement is important to health behaviors, prior studies mostly considered only one of multiple different dimensions of it, with inconsistent results. Presence of countervailing or interacting influences of different types of social engagement may account for prior conflicting findings. This study identifies which dimensions of social engagement are associated with risk behaviors of smoking, low levels of physical activity, and a diet poor of fruit and vegetable intake. Cross-sectional data from 5004 participants, aged 45-84 from the Multi-Ethnic Study of Atherosclerosis was used. Social support was measured using the ENRICHD Social Support Instrument, loneliness with a three item instrument derived from the revised University of California at Los Angeles Loneliness Scale, and neighborhood social cohesion with the instrument from the Project on Human Development in Chicago Neighborhoods. Prevalence ratios of behaviors associated with standardized social engagement variables were modeled with Poisson regression, using robust standard errors. In unadjusted analyses, higher social support and neighborhood social cohesion were associated with slightly lower prevalence of smoking (prevalence ratio, PR=0.82, 95% CI: 0.77-0.87, and PR=0.91, 95% CI: 0.84-0.98, respectively) and slightly higher likelihood of achieving recommended levels of physical activity (PR=1.04, 95% CI: 1.02-1.07, and PR=1.05, 95% CI: 1.03-1.07, respectively). Higher loneliness was associated with slightly higher prevalence of smoking (PR=1.17, 95% CI: 1.10-1.24) and slightly less physical activity (PR=0.95, 95% CI: 0.93-0.98 ) . Associations of social support and loneliness with smoking, and associations of social support and neighborhood cohesion with physical activity, persisted after adjusting for individual characteristics. After further adjusting for all dimensions of social engagement, only neighborhood social cohesion remained associated with very slightly higher probability of achieving recommended physical activity levels (PR=1.03, 95% CI: 1.01, 1.05), and only social support remained associated with lower prevalence of smoking (PR=0.87, 95% CI: 0.81, 0.94) and higher probability of quitting, amongst those who had ever smoked (PR=1.03, 95% CI: 1.01, 1.06). Social support interacted with loneliness (p for interaction=0.001), such that these associations were present only amongst non-lonely individuals (PR=0.77, 95% CI: 0.69, 0.86). In fully adjusted models, no associations were found for fruit and vegetable intake. This study is among the first to simultaneously investigate several dimensions of social engagement and their interactions in relation to risk behaviors. Social support is more consistently associated with smoking than other dimensions of social engagement and this association appears to be modified by loneliness.

Objective: To determine whether long-term exposure to oxides of nitrogen (NO x ) is associated with left ventricular mass index (LVMI) in adults without known cardiovascular disease (CVD). Background: An association between very close (x , a specific, gaseous traffic related pollutant and more reliable surrogate for traffic-related pollution, has not been examined. Methods: This study included 4125 participants free of clinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis (MESA) who underwent cardiac MRI, cardiac computed tomography (CT), and an extensive air pollution exposure assessment campaign to determine long-term individual residential exposure to NO x . This study used year 2000 average exposure to estimate long term exposure to NO x . LVMI was calculated by indexing cardiac MRI measures of left ventricular mass to body surface area measured at the exam. Agatston score was calculated based on cardiac CT. Multiple linear regression was used to examine the association between long-term exposure to NO x and LVMI, adjusted for multiple potential confounders including study site. To examine whether such relationships may be mediated by atherosclerosis or blood pressure, additional adjustment for Agatston score and blood pressure was performed. Results: An interquartile range (44 ppb) increase in estimated residential NO x was associated with significantly higher LVMI (1.6 g/m 2 , 95% CI: 0.1 to 3.1, p=0.03). Such estimates were comparable to prior associations observed for the relationship between close residential proximity to major roadways and LVMI (comparing individuals living 150m away). Additional adjustment for Agatston score and blood pressure had no effect on estimates of association. Stratified analyses suggested interactions with age, with younger individuals demonstrating larger associations than older individuals (p for interaction = 0.05). No significant evidence of effect modification by race, gender, other cardiovascular risk factors, or study site was observed. Conclusions: This study further supports the observation that long-term exposure to traffic-related air pollution is associated with higher left ventricular mass, and suggests that such associations may be independent of effects on blood pressure or atherosclerotic disease.

Cardiovascular disease (CVD) epidemiology is often presented as the paradigm for an approach to prevention that focuses on identifying individual-level risk factors and intervening on them through behavioral change (eg, diet and physical activity interventions) or through the early detection and treatment of biomedical risk factors (such as high blood pressure or dyslipidemias). At times, this approach has been criticized for failing to consider the more distal causes of these individual-level risk factors (many times of a social or economic nature) that drive the distributions of the proximal risks factors, shape population-level differences in cardiovascular risk, and present large potential opportunities for CVD prevention. Article see p 2262 In parallel to the risk factor approach, a long tradition in CVD epidemiology has documented the social patterning of CVD and the impact of a number of distal factors, including social class, work environments, and neighborhood environments, on cardiovascular events and risk factors. The article by Arcaya et al1 in this issue of Circulation on the links between foreclosures and blood pressure falls squarely within the latter tradition that aims to place CVD within social and economic contexts. Spurred perhaps in part by recent economic circumstances in the United States and worldwide, a growing body of work has attempted to document the health consequences of economic recessions or exposures to specific conditions (such as job loss, financial stress, or experiences of losing a home) that may be more common during recessions. As in other areas of health research, clearly specifying the causal question of interest is key. Precisely specifying the causal question is particularly important in investigating the health effects of distal economic processes because the total population health impact of economic recessions (which may involve unfavorable effects for those experiencing unemployment counterbalanced or even exceeded by favorable effects associated with …

Background— Coronary calcium has recently emerged as a marker of subclinical coronary heart disease. Although there has been much interest in race differences in calcification, heterogeneity within race or ethnic groups has not been investigated. Methods and Results— Data from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based study of coronary calcification, were used to investigate acculturation and socioeconomic position as predictors of coronary calcification within 2553 non-Hispanic whites, 1734 non-Hispanic blacks, 1457 Hispanics, and 797 Chinese residing in the United States. Coronary calcium was assessed by chest CT. Relative risk regression and linear regression were used to estimate adjusted associations of sociodemographic variables with the presence and amount of calcium. Not being born in the United States was associated with a lower prevalence of calcification in blacks (relative prevalence [RP], 0.75; 95% confidence limit [CL], 0.61 to 0.94) and Hispanics (RP, 0.89; 95% CL, 0.81 to 0.98) after adjustment for age, sex, income, and education. Years in the United States was positively associated with prevalence of calcification in non–US-born Chinese (adjusted RP per 10 years in United States, 1.06; 95% CL, 1.01 to 1.11) and non–US-born blacks (RP, 1.59; 95% CL, 1.22 to 2.06). Low education was associated with a higher prevalence of calcification in whites (adjusted RP for no high school versus complete college, 1.17; 95% CL, 1.05 to 1.32) but with lower prevalence of calcification in Hispanics (RP, 0.91; 95% CL, 0.77 to 1.09) ( P for interaction=0.02). US birth and time in the United States were also positively associated with the extent of calcification in persons with detectable calcium. These differences did not appear to be accounted for by smoking, body mass index, LDL and HDL cholesterol, hypertension, and diabetes. Conclusions— Acculturation and socioeconomic factors are associated with differences in the prevalence and amount of coronary calcification within whites, Chinese, blacks, and Hispanics. The presence of this heterogeneity needs to be acknowledged in the quantification and investigation of race/ethnic differences.