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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.

Indoor dining is one of the potential drivers of COVID-19 transmission. We used the heterogeneity among state government preemption of city indoor dining closures to estimate the impact of keeping indoor dining closed on COVID-19 incidence.We obtained case rates and city or state reopening dates from March to October 2020 in 11 US cities. We categorized cities as treatment cities that were allowed by the state to reopen but kept indoor dining closed or comparison cities that would have kept indoor dining closed but that were preempted by their state and had to reopen indoor dining. We modeled associations using a difference-in-difference approach and an event study specification. We ran negative binomial regression models, with city-day as the unit of analysis, city population as an offset, and controlling for time-varying nonpharmaceutical interventions, as well as city and time fixed effects in sensitivity analysis and the event study specification.Keeping indoor dining closed was associated with a 55% (IRR = 0.45; 95% confidence intervals = 0.21, 0.99) decline in the new COVID-19 case rate over 6 weeks compared with cities that reopened indoor dining, and these results were consistent after testing alternative modeling strategies.Keeping indoor dining closed may be directly or indirectly associated with reductions in COVID-19 spread. Evidence of the relationship between indoor dining and COVID-19 case rates can inform policies to restrict indoor dining as a tailored strategy to reduce COVID-19 incidence. See video abstract at, http://links.lww.com/EDE/B902.

Background Understanding the magnitude of cardiovascular disease (CVD) inequalities is the first step toward addressing them. The linkage of socioeconomic and clinical data in universal health care settings provides critical information to characterize CVD inequalities. Methods and Results We employed a prospective cohort design using electronic health records data from all residents of Catalonia aged 18+ between January and December of 2019 (N=6 332 228). We calculated age‐adjusted sex‐specific prevalence of 5 CVD risk factors (diabetes, hypertension, hyperlipidemia, obesity, and smoking), and 4 CVDs (coronary heart disease, cerebrovascular disease, atrial fibrillation, and heart failure). We categorized income into high, moderate, low, and very low according to individual income (tied to prescription copayments) and receipt of welfare support. We found large inequalities in CVD and CVD risk factors among men and women. CVD risk factors with the largest inequalities were diabetes, smoking, and obesity, with prevalence rates 2‐ or 3‐fold higher for those with very low (versus high) income. CVDs with the largest inequalities were cerebrovascular disease and heart failure, with prevalence rates 2 to 4 times higher for men and women with very low (versus high) income. Inequalities varied by age, peaking at midlife (30–50 years) for most diseases, while decreasing gradually with age for smoking. Conclusions We found wide and heterogeneous inequalities by income in 5 CVD risk factors and 4 CVD. Our findings in a region with a high‐quality public health care system and universal coverage stress that strong equity‐promoting policies are necessary to reduce disparities in CVD.

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.

Research linking characteristics of the neighborhood environment to health has relied on traditional regression methods where prespecified distances from participant's locations or areas are used to operationalize neighborhood-level measures. Because the relevant spatial scale of neighborhood environment measures may differ across places or individuals, using prespecified distances could result in biased association estimates or efficiency losses. We use novel hierarchical distributed lag models and data from the Multi-Ethnic Study of Atherosclerosis (MESA) to (1) examine whether and how the association between the availability of favorable food stores and body mass index (BMI) depends on continuous distance from participant locations (instead of traditional buffers), thus allowing us to indirectly infer the spatial scale at which this association operates; (2) examine if the spatial scale and magnitude of the association differs across six MESA sites, and (3) across individuals. As expected, we found that the association between higher availability of favorable food stores within closer distances from participant's residential location was stronger than at farther distances, and that the magnitude of the adjusted association declined quickly from zero to two miles. Furthermore, between-individual heterogeneity in the scale and magnitude of the association was present; the extent of this heterogeneity was different across the MESA sites. Individual heterogeneity was partially explained by sex. This study illustrated novel methods to examine how neighborhood environmental factors may be differentially associated with health at different scales, providing nuance to previous research that ignored the heterogeneity found across individuals and contexts.

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.

This report presents findings of an ad hoc working group assembled by the National Heart, Lung, and Blood Institute (NHLBI) to assess research needs to improve prevention, treatment, and control of hypertension among African Americans. Non-Hispanic Blacks (African American and Black will be used for US and international studies, respectively) tend to have an earlier onset, higher prevalence, and disproportionately high risk of complications for hypertension compared with non-Hispanic Whites and Mexican Americans.1 Surveys identify substantial variation in mean blood pressure (BP) among populations of African origin.2 In high-income countries, including the United States, mean BP and prevalence of hypertension are higher in adults self-described,3–6 observer reported,7,8 or otherwise identified9,10 as being black or having darker skin color.11 However, the relationship between African origin and BP is absent or only minimally apparent in reports from middle-income countries.12–14 Research to clarify reasons for this variability may contribute to understanding of hypertension-related racial disparities in the United States. In US National Health and Nutrition Examination Survey (NHANES) reports, crude and age-adjusted prevalence of hypertension (systolic BP [SBP] ≥140 mm Hg, diastolic BP ≥90 mm Hg, or taking antihypertensive medication) in adults has remained fairly constant at ≈30% since 1999 to 2000.3,4 The corresponding prevalence estimate for African Americans is ≈40% and has also remained reasonably stable. In African Americans, hypertension awareness and treatment rates are higher but control rates lower compared with non-Hispanic Whites (85.7% versus 82.7% for awareness, 77.4% versus 76.7% for treatment, and 49.5% versus 53.9% for control in NHANES 2011–2012).4 The lower prevalence of BP control is present despite use of more BP-lowering medications, including thiazide diuretics.15 This contrasts with clinical trial experience, where differences in BP control rates by race/ethnicity …

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 Current literature examining the prospective relationship between depression and other measures of negative affect with atrial fibrillation (AF) are limited. We determined the relationships of depression, anger, anxiety, and chronic stress with incident AF in a multiethnic cohort of middle‐ and older‐aged adults. Methods and Results This analysis included 6644 MESA (Multi‐Ethnic Study of Atherosclerosis) study participants who were free of AF at baseline. Depressive symptoms were assessed at baseline and defined as either a 20‐item Center for Epidemiologic Studies Depression Scale score ≥16 or use of antidepressant medications. The Spielberger Trait Anger Scale, Spielberger Trait Anxiety Scale, and Chronic Burden Scale were also administered at baseline to assess anger, anxiety, and chronic stress, respectively. The primary outcome was incident AF , identified by follow‐up study visit ECGs, hospital discharge diagnoses, or Medicare claims data. A total of 875 (13%) incident AF cases were detected over a median follow‐up of nearly 13 years. A Center for Epidemiologic Studies Depression Scale score ≥16 (referent, Center for Epidemiologic Studies Depression Scale score AF , respectively, in separate adjusted Cox proportional hazards analyses (hazard ratio, 1.34; 95% CI 1.04–1.74 for Center for Epidemiologic Studies Depression Scale ≥16; hazard ratio, 1.36; 95% CI , 1.04–1.77 for antidepressant use). No significant associations were observed for anger, anxiety, or chronic stress with development of AF . Conclusions Depressive symptoms are associated with an increased risk of incident AF . Further study into whether improving depressive symptoms reduces AF incidence is important.

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.

Background Social factors may enhance health effects of air pollution, yet empirical support is inconsistent. The interaction of social and environmental factors may only be evident with long-term exposures and outcomes that reflect long-term disease development. Methods We used cardiac magnetic resonance imaging data from the Multi-Ethnic Study of Atherosclerosis to assess left-ventricular mass index (LVMI) and left-ventricular ejection fraction (LVEF). We assigned residential concentrations of fine particulate matter (PM2.5), oxides of nitrogen, and nitrogen dioxide in the year 2000 to each participant in 2000 using prediction models. We examined modifying roles of four measures of adversity: race/ethnicity, racial/ethnic residential segregation, and socioeconomic status and psychosocial adversity as composite indices on the association between air pollution and LVMI or LVEF. Results Compared with whites, blacks showed a stronger adjusted association between air pollution and LVMI. For example, for each 5 µg/m greater PM2.5 level, whites showed a 1.0 g/m greater LVMI (95% confidence interval = -1.3, 3.1), while blacks showed an additional 4.0 g/m greater LVMI (95% confidence interval = 0.3, 8.2). Results were similar for oxides of nitrogen and nitrogen dioxide with regard to black race and LVMI. However, we found no evidence of a modifying role of other social factors or ethnic groups. Furthermore, we found no evidence of a modifying role for any social factors or racial/ethnic groups on the association between air pollution and LVEF. Conclusions Our results suggest that racial group membership may modify the association between air pollution and cardiovascular disease.

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.

To investigate associations of work hours, job control, job demands, job strain, and occupational category with brachial artery flow-mediated dilation (FMD) in 1499 Multi-Ethnic Study of Atherosclerosis participants.Flow-mediated dilation was obtained using high-resolution ultrasound. Mean values of FMD were examined across categories of occupation, work hours, and the other exposures using regression analyses.Occupational category was significantly associated with FMD overall, with blue-collar workers showing the lowest mean values-management/professional = 4.97 ± 0.22%; sales/office = 5.19 ± 0.28%; services = 4.73 ± 0.29%; and blue-collar workers = 4.01 ± 0.26% (adjusted P0.001). There was evidence of effect modification by sex (interaction P = 0.031)-significant associations were observed among women (adjusted P = 0.002) and nearly significant results among men (adjusted P = 0.087). Other exposures were not significantly associated with FMD.Differences in endothelial function may account for some of the variation in cardiovascular disease across occupational groups.

Background and Purpose— This study investigated chronic stress, depressive symptoms, anger, and hostility in relation to incident stroke and transient ischemic attacks in middle-aged and older adults. Methods— Data were from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based cohort study of 6749 adults, aged 45 to 84 years and free of clinical cardiovascular disease at baseline, conducted at 6 US sites. Chronic stress, depressive symptoms, trait anger, and hostility were assessed with standard questionnaires. The primary outcome was clinically adjudicated incident stroke or transient ischemic attacks during a median follow-up of 8.5 years. Results— One hundred ninety-five incident events (147 strokes; 48 transient ischemic attacks) occurred during follow-up. A gradient of increasing risk was observed for depressive symptoms, chronic stress, and hostility (all P for trend ≤0.02) but not for trait anger ( P >0.10). Hazard ratios (HRs) and 95% confidence intervals indicated significantly elevated risk for the highest-scoring relative to the lowest-scoring group for depressive symptoms (HR, 1.86; 95% confidence interval, 1.16–2.96), chronic stress (HR, 1.59; 95% confidence interval, 1.11–2.27), and hostility (HR, 2.22; 95% confidence interval, 1.29–3.81) adjusting for age, demographics, and site. HRs were attenuated but remained significant in risk factor–adjusted models. Associations were similar in models limited to stroke and in secondary analyses using time-varying variables. Conclusions— Higher levels of stress, hostility, and depressive symptoms are associated with significantly increased risk of incident stroke or transient ischemic attacks in middle-aged and older adults. Associations are not explained by known stroke risk factors.

Background— The concept of cardiovascular health (CVH) was introduced as a global measure of one's burden of cardiovsacular risk factors. Previous studies established the relationship between neighborhood characteristics and individual cardiovascular risk factors. However, the relationship between neighborhood environment and overall CVH remains unknown. Methods and Results— We analyzed data from the Multi-Ethnic Study of Atherosclerosis baseline examination (2000–2002). Mean age was 61.6 years, and 52% were women. Ideal, intermediate, and poor categories of cholesterol, body mass index, diet, physical activity, fasting glucose, blood pressure, and smoking were defined according to the American Heart Association 2020 Strategic Goals, assigned an individual score, and summed to create an overall score. CVH scores were categorized into ideal (11–14 points), intermediate (9–10), and poor (0–8). Neighborhood exposures included favorable food store and physical activity resources densities (by 1-mile buffer), reported healthy food availability, walking/physical activity environment, safety, and social cohesion (by census tract). Multinomial logistic regression was used to determine the association of each characteristic with ideal and intermediate CVH, adjusted for demographics and neighborhood socioeconomic status. Over 20% of Multi-Ethnic Study of Atherosclerosis participants had an ideal CVH score at baseline. In fully adjusted models, favorable food stores (odds ratio=1.22; 1.06–1.40), physical activity resources (odds ratio=1.19; 1.08–1.31), walking/physical activity environment (odds ratio=1.20; 1.05–1.37), and neighborhood socioeconomic status (odds ratio=1.22; 1.11–1.33) were associated with higher odds of having an ideal CVH score. Conclusions— Neighborhood environment including favorable food stores, physical activity resources, walking/physical activity environment, and neighborhood socioeconomic status are associated with ideal CVH. Further research is needed to investigate the longitudinal associations between neighborhood environment and CVH.

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.

Carotid arterial wall thickness, measured as intima-media thickness (IMT), is an early subclinical indicator of cardiovascular disease. Few studies have investigated the association of psychological factors with IMT across multiple ethnic groups and by sex.We included 6561 men and women (2541 whites, 1790 African Americans, 1436 Hispanics, and 794 Chinese) aged 45 to 84 years who took part in the first examination of the Multi-Ethnic Study of Atherosclerosis. Associations of trait anger, trait anxiety, and depressive symptoms with mean values of common carotid artery (CCA) and internal carotid artery (ICA) IMTs were investigated using multivariable regression and logistic models.In age-, sex-, and race/ethnicity-adjusted analyses, the trait anger score was positively associated with CCA and ICA IMTs (mean differences per 1-standard deviation increment of trait anger score were 0.014 [95% confidence interval {CI} = 0.003-0.025, p = .01] and 0.054 [95% CI = 0.017-0.090, p = .004] for CCA and ICA IMTs, respectively). Anger was also associated with the presence of carotid plaque (age-, sex-, and race/ethnicity-adjusted odds ratio per 1-standard deviation increase in trait anger = 1.27 [95% CI = 1.06-1.52]). The associations of the anger score with thicker IMT were attenuated after adjustment for covariates but remained statistically significant. Associations were stronger in men than in women and in whites than in other race/ethnic groups, but heterogeneity was only marginally statistically significant by race/ethnicity. There was no association of depressive symptoms or trait anxiety with IMT.Only one of the three measures examined was associated with IMT, and the patterns seemed to be heterogeneous across race/ethnic groups.

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.

Several studies have linked life-orientation, as reflected by levels of optimism and pessimism, to cardiovascular disease risk (1–8). Optimism is generally defined as the tendency to believe that future expectations and goals will be met, and is different than simply the absence of depression. Although prior studies have conceptualized optimism and pessimism as opposing poles of a continuum, recent studies show they may be better characterized as distinct, negatively related factors (9–12). Optimism has been linked to lower cardiovascular disease (CVD) and coronary heart disease (CHD) mortality (5), lower rates of nonfatal myocardial infarction (MI), slower progression of carotid atherosclerosis (4, 7, 8), better outcomes after coronary artery bypass graft procedures and fewer re-stenoses after percutaneous transluminal coronary angioplasty (13). The related construct of pessimism, defined as the general tendency to expect negative outcomes, has been shown to be associated with increased adverse cardiac events, including MI and death from CHD (6), and interacts with socioeconomic status in increasing rates of hypertension (14). There are several mechanisms through which optimism and pessimism may affect cardiovascular disease and its progression, but these mechanisms have not been well established in empirical studies. Elucidating these mechanisms is important for strengthening causal inferences regarding the health consequences of life orientation and will also enhance our understanding of the etiology of cardiovascular disease generally. One possible mechanistic pathway involves health behaviors. Life orientation may affect the adoption and maintenance of behaviors such as diet and physical activity, which are known risk factors for cardiovascular disease. Dispositional optimism has been reported to be associated with nonsmoking, increased physical activity, moderate alcohol consumption, and more fruits, vegetables and whole grains in the diet (15–17). This finding may result from optimistic persons being more likely to anticipate benefits of behavioral change and hence may be more likely to adopt and maintain these changes over time. It is also plausible that optimism and pessimism affect health through biological mechanisms independent of health behaviors that have been linked to chronic inflammation and CVD. For example, dispositional optimism may downregulate the autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal (HPA) axis (18–20). In contrast, a pessimistic disposition may stimulate chronically increased sympathetic tone and stimulation of the HPA axis (20–21), which in turn may induce chronic inflammation and hemostasis. Constructs related to optimism and pessimism, such as positive affect and cynical distrust, have been shown to be associated with IL-6 and CRP (22–23). However, to our knowledge, the relationship between optimism and pessimism and markers of inflammation and hemostasis has not yet been investigated. In this study, we explore the relationship between life-orientation and seven circulating inflammation and hemostasis markers that have been previously associated with increased CVD risk: IL-6, CRP, homocysteine, fibrinogen, D-dimer, factor VIII, and plasmin antiplasmin (24). We use data from the Multi-Ethnic Study of Atherosclerosis (MESA), a large and diverse cohort of individuals from 45 to 84 years of age. We hypothesized that increased optimism and decreased pessimism would be inversely related to levels of inflammation and hemostatic markers, and these associations would be attenuated but remain significant after adjustment for traditional CVD risk factors, behaviors, depression, and cynical distrust. We investigated life orientation as a single bipolar scale, as well as differentiated into two distinct but negatively related constructs (optimism and pessimism). We hypothesized that stronger associations would be observed with the two-factor approach.

To determine if cynical hostility is associated with alterations in diurnal profiles of cortisol. Hostility has been linked to cardiovascular disease but the biological mechanisms mediating this association remain unknown.Up to 18 measures of salivary cortisol taken over 3 days were obtained from each of 936 participants in the Multi-Ethnic Study of Atherosclerosis (MESA). Cynical hostility was measured using an eight-item subscale of the Cook-Medley Hostility Scale. Cortisol profiles were modeled using regression spline models that incorporated random parameters for subject-specific effects. Models were adjusted for race, sex, age, socioeconomic position, and lifestyle factors. The association of cynical hostility with key features of the cortisol diurnal profile, both in the full sample and important subsamples, was examined.Waking cortisol levels as well as the extent of the morning surge in cortisol levels did not differ significantly across tertiles of cynical hostility. Respondents in the lowest tertile of cynical hostility experienced a 22% sharper decline in salivary cortisol (age- and sex-adjusted slope of -0.49 microg/dL per hour) than respondents in the highest tertile (-0.40 microg/dL per hour, p for difference = .0004). Intertertile differences in these parameters remained unaltered after further adjustment for potential confounders. This pattern of differences in cortisol diurnal profile tended to be related in a dose-response way to level of cynical hostility, and persisted in stratified analyses.Cynical hostility is associated with the declining phase of the awakening cortisol response. The implications of this for cardiovascular and other health outcomes remain to be determined.

The objective of this study was to examine the association of individual socioeconomic status (iSES) and neighborhood SES (nSES) on the prevalence of metabolic syndrome (MetS) in the Atherosclerosis Risk in Communities Study (1987-1999).Participants included 2932 black and 9777 white men and women aged 45 to 64 years without diabetes at baseline. Total combined family income for the past 12 months and six census tract socioeconomic measures combined into a composite index were used to quantify iSES and nSES, respectively. Poisson regression was used to assess associations of the joint contribution of iSES and nSES on the MetS, stratified by gender and race and adjusting for multiple covariates. For analyses that included nSES, hierarchical modeling techniques were used.Using 2005 Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults criteria, MetS was identified in 40% of black women, 30% of white women, 28% of black men, and 35% of white men. Among black and white men, there was no association between MetS and iSES or nSES. In contrast, after adjustment for risk factors, black and white women with low (L)-iSES and medium (M)-iSES were more likely to have MetS than those with high (H)-iSES. Similar but weaker patterns were noted for L-nSES and M-nSES.In summary, both iSES and nSES were independently associated with an increased prevalence of MetS among women but not men. Efforts aimed at understanding the causes of these gender differences may offer insight into avenues for reducing the prevalence of the MetS and its chronic disease sequelae.

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.

To assess the cross-sectional association between depression and glucose tolerance status.We conducted a study of 6754 White, Black, Hispanic, and Chinese men and women aged 45 to 84 years in the Multiethnic Study of Atherosclerosis (MESA). Depression was defined as Center for Epidemiologic Studies Depression scale score ofor =16 and/or antidepressant use. Glucose tolerance status was defined as normal, impaired fasting glucose (IFG) or Type 2 diabetes mellitus (untreated and treated).In the minimally adjusted model, although depression was not associated with a greater odds of IFG (odds ratio (OR) = 1.01; 95% confidence interval (CI): 0.87-1.18) or untreated diabetes (OR = 1.03; 95% CI: 0.74-1.45), it was associated with a greater odds of treated diabetes (OR = 1.57; 95% CI: 1.27-1.96). This persisted following adjustment for body mass index (OR = 1.52; 95% CI: 1.22-1.90), metabolic (OR = 1.54; 95% CI: 1.23-1.93), and inflammatory (OR=1.53; 95% CI: 1.21-1.92) factors, daily caloric intake and smoking (OR = 1.48; 95% CI: 1.16-1.88), and socioeconomic markers (OR = 1.47; 95% CI: 1.17-1.85). Among individuals with treated diabetes, median depression scores were higher in those with microalbuminuria compared with those without microalbuminuria (median = 7; interquartile range: 3-13 versus median = 6; interquartile range: 2-11; p = .046). Depression scores were not associated with homeostatic model assessment of insulin resistance among individuals without diabetes.In MESA, depression was significantly associated with treated diabetes. Further studies are needed to determine the temporality of this association.

Background Improving cardiovascular health ( CVH ) of all Americans by 2020 is a strategic goal of the American Heart Association. Understanding the sources of variation and identifying contextual factors associated with poor CVH may suggest important avenues for prevention. Methods and Results Cross‐sectional data from the Behavioral Risk Factor Surveillance System for the year 2011 were linked to state‐level coronary heart disease and stroke mortality data from the National Vital Statistics System and to state‐level measures of median household income, income inequality, taxes on soda drinks and cigarettes, and food and physical activity environments from various administrative sources. Poor CVH was defined according to the American Heart Association definition using 7 self‐reported CVH metrics (current smoking, physical inactivity, obesity, poor diet, hypertension, diabetes, and high cholesterol). Linked micromap plots and multilevel logistic models were used to examine state variation in poor CVH and to investigate the contributions of individual‐ and state‐level factors to this variation. We found significant state‐level variation in the prevalence of poor CVH (median odds ratio 1.32, P CVH and cardiovascular disease mortality were clustered in the southern states. Minority and low socioeconomic groups were strongly associated with poor CVH and explained 51% of the state‐level variation in poor CVH ; state‐level factors explained an additional 28%. State‐level median household income (odds ratio 0.89; 95% CI 0.84–0.94), taxes on soda drinks (odds ratio 0.94; 95% CI 0.89–0.99), farmers markets (odds ratio 0.91; 95% CI 0.85–0.98), and convenience stores (odds ratio 1.09; 95% CI 1.01–1.17) were predictive of poor CVH even after accounting for individual‐level factors. Conclusions There is significant state‐level variation in poor CVH that is partly explained by individual‐ and state‐level factors. Additional longitudinal research is warranted to examine the influence of state‐level policies and food and physical activity environments on poor CVH .

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.

Increased left ventricular mass (LVM) and lower socioeconomic status (SES) are predictors of cardiovascular morbidity and mortality. Blacks and Hispanics are more likely to have higher LVM and lower SES. The relation between SES, race–ethnicity, and LVM has not been fully explored. Data were used from the NOMAS population-based sample of 1916 subjects living in Northern Manhattan. SES was characterized on the basis of educational attainment and divided into 4 categories. Echocardiography-defined LVM was indexed according to height at the allometric power of 2.7 and analyzed as a continuous variable. LVM varied by race in our cohort (blacks 48.9 g/m 2.7 , Hispanics 48.4 g/m 2.7 , whites 45.6 g/m 2.7 ; P =0.004). Using ANCOVA, there was a significant inverse and graded association between mean LVM and SES for the total cohort. Mean LVM was 48.4 g/m 2.7 , 48.6 g/m 2.7 , 47.1 g/m 2.7 , and 45.3 g/m 2.7 for the lowest to the highest educational level category ( P trend=0.0004). This relationship remained among normotensives ( P trend=0.0005) and was present for blacks ( P trend=0.009), but not for whites ( P trend=0.86) or Hispanics ( P trend=0.47). The difference in mean LVM between the highest and lowest categories of education was 5.3 g/m 2.7 for blacks, 0.0 g/m 2.7 for whites, and 1.0 g/m 2.7 for Hispanics. Lower SES is an independent predictor of increased LVM among hypertensive and normotensive blacks.

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.

Background: Over 65 million Americans live in Primary Care Health Professional Shortage Areas (HPSAs) which are associated with less preventive care, poorer general health and an increased risk for hospitalizations. However, little is known about how living in a HPSA impacts primary prevention for CVD. Methods: We used data from CARDIA, a multi-center cohort study of black and white men and women. Participants who had risk factor data and geocoded addresses available at year 20 (2005) were included in this analysis (n=3479). Primary care HPSAs were defined using data from US HRSA. Diabetes, hypertension and hyperlipidemia prevalence and control were defined according to ADA Guidelines 2000, JNC VI, and ATP III, respectively. Individuals who reported being diagnosed or reported use of medications were considered aware of the risk factor. The prevalence of smoking and obesity was also examined. Neighborhood (census block) characteristics were derived from Census 2000 and ACCRA. Multivariable Poisson models were used to examine the independent association of HPSA residence with each outcome. Results: Over 11% of CARDIA participants live in a HPSA. Residents of HPSAs were more likely to be female (64% vs 56%), African American (81% vs 43%), have low education, and low income. HPSA residents had more difficulty paying for food/basics and medical care, had poorer access to medical care and lived in areas with a higher cost of healthcare and low neighborhood SES. HPSA residents had a higher prevalence of hypertension (PR 1.39, 95% CI 1.18-1.65), obesity (1.30, 1.16-1.45) and smoking (1.72, 1.46-2.03) and were less likely to have their hypertension (0.79, 0.66-0.95) or hyperlipidemia (0.66, 0.44-0.99) controlled as compared to non-residents. The association between HPSA and risk factors prevalence was explained by race and neighborhood SES. The cost of medical care and having a usual source of care were the largest mediators of the association between HPSA residence and risk factor control. Conclusion: The increased prevalence and poorer control of CVD risk factors in HPSAs, can be explained by the demographic and neighborhood characteristics of their residents. Future interventions should be targeted to these high-risk populations found within HPSAs.

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 …