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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 The available evidence of the health effects of urban regeneration is scarce In Latin America, and there are no studies focused on formal housing that longitudinally evaluate the impact of housing and neighborhood interventions on health. The “Regeneración Urbana, Calidad de Vida y Salud” (Urban Regeneration, Quality of Life, and Health) or RUCAS project is a longitudinal, multi-method study that will evaluate the impact of an intervention focused on dwellings, built environment and community on the health and wellbeing of the population in two social housing neighborhoods in Chile. Methods RUCAS consists of a longitudinal study where inhabitants exposed and unexposed to the intervention will be compared over time within the study neighborhoods (cohorts), capitalizing on interventions as a natural experiment. Researchers have developed a specific conceptual framework and identified potential causal mechanisms. Proximal and more distal intervention effects will be measured with five instruments, implemented pre- and post-interventions between 2018 and 2021: a household survey, an observation tool to evaluate dwelling conditions, hygrochrons for measuring temperature and humidity inside dwellings, systematic observation of recreational areas, and qualitative interviews. Survey baseline data (956 households, 3130 individuals) is presented to describe sociodemographics, housing and health characteristics of both cohorts, noting that neighborhoods studied show worse conditions than the Chilean population. Discussion RUCAS’ design allows for a comprehensive evaluation of the effects that the intervention could have on various dimensions of health and health determinants. RUCAS will face some challenges, like changes in the intervention process due to adjustments of the master plan, exogenous factors –including COVID-19 pandemic and associated lockdowns– and lost to follow-up. Given the stepped wedge design, that the study capitalizes on within household changes over time, the possibility of adjusting data collection process and complementarity of methods, RUCAS has the flexibility to adapt to these circumstances. Also, RUCAS’ outreach and retention strategy has led to high retention rates. RUCAS will provide evidence to inform regeneration processes, highlighting the need to consider potential health effects of regeneration in designing such interventions and, more broadly, health as a key priority in urban and housing policies.

Background Understanding how urban environments influence people’s health, especially as individuals age, can help identify ways to improve health in the rapidly urbanizing and rapidly aging populations. Objectives To investigate the association between age and self-reported health (SRH) in adults living in Latin-American cities and whether gender and city-level socioeconomic characteristics modify this association. Methods Cross-sectional analyses of 71,541 adults aged 25–97 years, from 114 cities in 6 countries (Argentina, Brazil, Colombia, Chile, El Salvador, and Guatemala), as part of the Salud Urbana en America Latina (SALURBAL) Project. We used individual-level age, gender, education, and self-reported health (SRH) data from harmonized health surveys. As proxies for socioeconomic environment we used a city-level socioeconomic index (SEI) calculated from census data, and gross domestic product (GDP) per-capita. Multilevel Poisson models with a robust variance were used to estimate relative risks (RR), with individuals nested in cities and binary SRH (poor SHR vs. good SRH) as the outcome. We examined effect modification by gender and city-level socioeconomic indicators. Results Overall, 31.4% of the sample reported poor SRH. After adjusting for individual-level education, men had a lower risk of poor SRH (RR = 0.76; CI 0.73–0.78) compared to women, and gender modified the association between age and poor SRH (p-value of interaction Conclusions Across cities in Latin America, aging impact on health is significant among middle-aged adults, and among men. In both genders, cities with lower SEI or lower GDP per-capita were associated with poor SRH. More research is needed to better understand gender inequalities and how city socioeconomic environments, represented by different indicators, modify exposures and vulnerabilities associated with aging.

We explored associations between residential preferences and sociodemographic characteristics, the concordance between current neighborhood characteristics and residential preferences, and heterogeneity in concordance by income and race/ethnicity. Data came from a cross-sectional phone and mail survey of 3668 residents of New York City, Baltimore, Chicago, Los Angeles, St. Paul, and Winston Salem in 2011-12. Scales characterized residential preferences and neighborhood characteristics. Stronger preferences were associated with being older, female, non-White/non-Hispanic, and lower education. There was significant positive but weak concordance between current neighborhood characteristics and residential preferences (after controlling sociodemographic characteristics). Concordance was stronger for persons with higher income and for Whites, suggesting that residential self-selection effects are strongest for populations that are more advantaged.

Study Objectives African-Americans have a high burden of poor sleep, yet, psychosocial determinants (e.g. discrimination) are understudied. We investigated longitudinal associations between everyday discrimination and sleep quality and duration among African-Americans (N = 3404) in the Jackson Heart Study. Methods At Exam 1 (2000–2004) and Exam 3 (2008–2013), participants completed the Everyday Discrimination Scale, rated their sleep quality (1 = poor to 5 = excellent), and self-reported hours of sleep. A subset of participants (N = 762) underwent 7-day actigraphy to objectively measure sleep duration and sleep quality (Sleep Exam 2012–2016). Changes in discrimination were defined as low stable (reference), increasing, decreasing, and high stable. Within-person changes in sleep from Exam 1 to Exam 3 were regressed on change in discrimination from Exam 1 to Exam 3 while adjusting for age, sex, education, income, employment, physical activity, smoking, body mass index, social support, and stress. Results At Exam 1, the mean age was 54.1 (12.0) years; 64% were female, mean sleep quality was 3.0 (1.1) and 54% were short sleepers. The distribution of the discrimination change trajectories were 54.1% low stable, 13.5% increasing, 14.6% decreasing, and 17.7% were high stable. Participants who were in the increasing (vs. low stable) discrimination group had greater decrease in sleep quality. There was no association between change in discrimination and change in sleep duration. Among Sleep Exam participants, higher discrimination was cross-sectionally associated with shorter self-reported sleep duration, independent of stress. Conclusion Discrimination is a unique stressor for African-Americans; thus, future research should identify interventions to reduce the burden of discrimination on sleep quality.

Background Black Americans have a higher risk of hypertension compared with White Americans. Perceived discrimination is a plausible explanation for these health disparities. Few studies have examined the impact of perceived discrimination on the incidence of hypertension among a racially diverse sample. Our study examined associations of everyday and lifetime discrimination with incidence of hypertension and whether these associations varied by sex, discrimination attribution, and racial residential segregation. Methods and Results The study included 3297 Black, Hispanic, Chinese, and White participants aged 45 to 84 years from the Multi‐Ethnic Study of Atherosclerosis who were without hypertension at exam 1 (2000–2002) and who completed at least 1 of 5 follow‐up exams (2002–2018). Cox proportional hazards regression was used to estimate associations of perceived discrimination with incident hypertension. Over the follow‐up period, 49% (n=1625) of participants developed hypertension. After adjustment for age, sex, socioeconomic status, hypertension risk factors, and study site, Black participants reporting any lifetime discrimination (compared with none) were more likely to develop hypertension (hazard ratio [HR], 1.35; 95% CI, 1.07–1.69). In fully adjusted models, everyday discrimination (high versus low) was associated with a lower risk for hypertension among Hispanic participants (HR, 0.73; 95% CI, 0.55–0.98). Statistically significant interactions of perceived discrimination (everyday and lifetime) with sex, discrimination attribution, and racial residential segregation were not observed. Conclusions This study suggests that lifetime, but not everyday discrimination is associated with incident hypertension in Black Americans.

Considering that urban environments may affect self-rated health through behavioral and psychosocial mechanisms, the aim of this study was to investigate the association between self-rated health and perceived urban environment characteristics among adults living in four Latin American cities. Data is from a population-based survey by Development Bank of Latin America, encompassing adults between 20 and 60 years old in Buenos Aires, Lima, Mexico City, and Panama City. Self-rated health was measured using a single question and the response options were categorized as poor and good. The explanatory variables were empirical Bayes estimates of self-reported area physical disorder, social disorder, access to services, and access to leisure spaces derived from the survey. The covariates were: individual age, sex, education, wealth index, and length of residency in the neighborhood, and an area social environment index. Multilevel logistic regressions with two levels (individual and sub-city areas) were fitted. Poor self-rated health was reported by 34.73% (95% CI: 33.17 to 36.29) of the participants and was associated with physical disorder (OR = 1.16 per SD, 95% CI: 1.02 to 1.32). Our findings suggest that public policies to promote population health should consider area urban environment factors, especially those associated with disorder.

Background: Current knowledge regarding the relationship between segregation and body weight is derived mainly from cross-sectional data. Longitudinal studies are needed to provide stronger causal inference. Methods: We use longitudinal data from the Multi-Ethnic Study of Atherosclerosis and apply an econometric fixed-effect strategy, which accounts for all time-invariant confounders, and compare results to conventional cross-sectional analyses. We examine the relationship between neighborhood-level racial/ethnic segregation, neighborhood poverty, and body mass index (BMI) separately for blacks, Hispanics, and whites. Segregation*gender interactions are included in all models. Neighborhood segregation was operationalized by the local Gi* statistic, which assesses the extent to which a neighborhood’s racial/ethnic composition is under (Gi* statistic 0) represented, given the composition in the broader (e.g., county) area. For black, Hispanic, and white stratified models, the Gi* statistic reflects the level of black, Hispanic, and white segregation, respectively. The Gi* statistic was scaled such that a unit change represents a 1.96 difference in the score. Results: Cross-sectional models indicated higher segregation to be negatively associated with BMI for white females and positively associated for Hispanic females. No association was found for black females or males in general. In contrast, fixed-effect models adjusting for neighborhood poverty, higher segregation was positively associated with BMI for black females (coeff= 0.25 kg/m2; 95% CI=[0.03, 0.46]; P-value=0.03) but negatively associated for Hispanic females (coeff= −0.17 kg/m2 ; 95% CI=[−0.33, −0.01]; P-value=0.04) and Hispanic males (coeff= −0.20; 95% CI=[−0.39, −0.01]; P-value=0.04.). Further controls for socioeconomic factors fully explained the associations for Hispanics but not for black females. Conclusions: Fixed-effect results suggest that segregation’s impacts might not be universally harmful, with possible null or beneficial impacts, depending on race/ethnicity. The persistent associations after accounting for neighborhood poverty indicate that the segregation-BMI link may operate through different pathways other than neighborhood poverty.

The concept of a so-called urban advantage in health ignores the possibility of heterogeneity in health outcomes across cities. Using a harmonized dataset from the SALURBAL project, we describe variability and predictors of life expectancy and proportionate mortality in 363 cities across nine Latin American countries. Life expectancy differed substantially across cities within the same country. Cause-specific mortality also varied across cities, with some causes of death (unintentional and violent injuries and deaths) showing large variation within countries, whereas other causes of death (communicable, maternal, neonatal and nutritional, cancer, cardiovascular disease and other noncommunicable diseases) varied substantially between countries. In multivariable mixed models, higher levels of education, water access and sanitation and less overcrowding were associated with longer life expectancy, a relatively lower proportion of communicable, maternal, neonatal and nutritional deaths and a higher proportion of deaths from cancer, cardiovascular disease and other noncommunicable diseases. These results highlight considerable heterogeneity in life expectancy and causes of death across cities of Latin America, revealing modifiable factors that could be amenable to urban policies aimed toward improving urban health in Latin America and more generally in other urban environments.

Leukocyte telomere length (LTL) is a biomarker of cellular aging. African Americans report more stress than other groups; however, the association of psychosocial stressors with biological aging among African Americans remains unclear. The current study evaluated the association of psychosocial factors (negative affect and stressors) with LTL in a large sample of African American men and women (n = 2,516) from the Jackson Heart Study. Using multivariable linear regression, we examined the sex-specific associations of psychosocial factors (cynical distrust, anger in and out, depressive symptoms, negative affect summary scores, global stress, weekly stress, major life events, and stress summary scores) with LTL. Model 1 adjusted for demographics and education. Model 2 adjusted for model 1, smoking, alcohol intake, physical activity, diabetes, hypertension, and high-sensitivity C-reactive protein. Among women, high (vs. low) cynical distrust was associated with shorter mean LTL in model 1 (b = -0.12; p = 0.039). Additionally, high (vs. low) anger out and expressed negative affect summary scores were associated with shorter LTL among women after full adjustment (b = -0.13; p = 0.011; b = -0.12, p = 0.031, respectively). High levels of cynical distrust, anger out, and negative affect summary scores may be risk factors for shorter LTL, particularly among African-American women.

BackgroundLow socioeconomic status (SES) is associated with cardiovascular disease (CVD) risk, but its association with different markers of SES may be heterogeneous by sex and race/ethnicity.MethodsWe have examined the relationships of four SES markers (education, family income, occupation and neighborhood SES) to ideal cardiovascular health (ICH), an index formed by seven variables. A total of 6792 cohort participants from six regions in the USA: Baltimore City and Baltimore County, MD; Chicago, IL; Forsyth County, NC; Los Angeles County, CA; New York, NY; and St. Paul, MN of the Multi-Ethnic Study of Atherosclerosis (MESA) (52.8% women) were recruited at baseline (2000–2) and included in the present analysis.ResultsICH was classified as poor, intermediate or ideal. Level of education was significantly and inversely associated with ICH in non-Hispanic White men and women, in Chinese-American and Hispanic American men and African-American women. Family income was inversely and significantly associated with poor ICH in African-American men only.ConclusionsWe conclude that the strength of the associations between some SES markers and ICH differ between sexes and race/ethnic groups.

Residential segregation is the spatial manifestation of entrenched socioeconomic and racial inequities and is considered a fundamental cause of racial inequalities in health. Despite the well-documented racialized spatial inequalities that exist in urban areas throughout Brazil, few empirical investigations have examined the link between residential segregation and health and considered its implications for racial health inequalities in this setting. In the present study, we used data from the Brazilian Longitudinal Study of Adult Health (2008e2010) to examine the association between economic residential segregation and two major cardio-metabolic risk factorsdhypertension and diabetes. We also examined whether associations were stronger for historically marginalized racial groups in Brazil. Residential segregation was calculated for study-defined neighborhoods using the Getis-Ord Local Gi* statistic and was based on household income data from the 2010 IBGE demographic census. Multivariable logistic regression models were used to examine associations. In our sample, Blacks and Browns were more likely to live in economically segregated neighborhoods. After taking into account income, education, and other demographic characteristics we found that individuals living in the most economically segregated neighborhoods were 26% more likely to have hypertension and 50% more likely to have diabetes than individuals living in more affluent areas. Although Blacks and Browns living in highly segregated neighborhoods had higher prevalence of hypertension and diabetes compared to Whites, we observed no statistically significant racial differences in the associations with residential segregation. Our findings suggest that residential segregation may be an important structural determinant of cardio-metabolic risk factors in Brazil. Moreover, the systematic and disproportionate exposure of Blacks and Browns to highly segregated neighborhoods may implicate these settings as potential drivers of racial inequalities in cardio-metabolic risk factors in urban settings in Brazil.

Differences in coping within the African American population are not well understood, yet these differences may be critical to reducing stress, improving health, and reducing racial health disparities. Using a descriptive, exploratory analysis of the Jackson Heart Study (N = 5301), we examine correlations between coping responses and associations between coping and demographic, socioeconomic, psychosocial, and neighborhood factors. Overall, coping responses were not strongly correlated and patterns of associations between covariates and coping responses were largely inconsistent. The results suggest that coping varies substantially within this African American population and is driven mainly by psychosocial factors such as spirituality and interpersonal support. Understanding these complex relationships may inform strategies by which to intervene in the stress process to mitigate the effects of stress on health and to identify vulnerable subgroups of African Americans that might need targeted interventions to reduce exposure to stressors and improve coping capacities.

Risk factors can drive socioeconomic inequalities in cardiovascular disease (CVD) through differential exposure and differential vulnerability. In this paper, we show how econometric decomposition directly enables simultaneous, policy-oriented assessment of these 2 mechanisms. We specifically estimate contributions of neighborhood environment and proximal risk factors to socioeconomic inequality in CVD incidence via these mechanisms. We followed 5,608 participants in the Multi-Ethnic Study of Atherosclerosis (2000-2012) to their first CVD event (median length of follow-up, 12.2 years). We used a summary measure of baseline socioeconomic position (SEP). Covariates included baseline demographics, neighborhood characteristics, and psychosocial, behavioral, and biomedical risk factors. Using Poisson models, we decomposed the difference (inequality) in incidence rates between low- and high-SEP groups into contributions of 1) differences in covariate means (differential exposure) and 2) differences in CVD risk associated with covariates (differential vulnerability). Notwithstanding large uncertainty in neighborhood estimates, our analysis suggested that differential exposure to poorer neighborhood socioeconomic conditions, adverse social environment, diabetes, and hypertension accounted for most of the inequality. Psychosocial and behavioral contributions were negligible. Further, neighborhood SEP, female sex, and white race were more strongly associated with CVD among low-SEP (vs. high-SEP) participants. These differentials in vulnerability also accounted for nontrivial portions of the inequality and could have important implications for intervention.

Self-rated health (SRH) is considered a strong indicator of well-being and clinical health status and has been linked to inflammatory markers. The objective of this work was to examine how self-rated physical health (SRPH) and mental health (SRMH) influence the immune system through the regulation of a stress-related gene expression profile known as the ‘conserved transcriptional response to adversity’ (CTRA), which involves the up-regulation of pro-inflammatory genes and down-regulation of genes involved in type I interferon (IFN) response and antibody synthesis. CTRA expression data were derived from genome-wide transcriptional data on purified monocytes in 1264 adult participants from the multi-ethnic study of atherosclerosis. SRPH and SRMH were assessed through the SF-12 questionnaire. Multiple linear regression models were used to determine the association between the composite score of the CTRA subsets and SRPH and SRMH. Higher scores of SRPH and SRMH were associated with an increased expression of the overall CTRA profile. The individual gene subsets analysis did not reveal an increased expression of pro-inflammatory genes in persons with lower scores of SRH. However, we observed that higher scores of SRPH positively modulate the immune response through the up-regulation of both type I interferon response and antibody synthesis-related genes, while better scores of SRMH were associated with a down-regulation of genes involved in antibody synthesis. The significant association between SRH and a gene expression profile related to type I IFN response and antibody synthesis suggests that SRH may be linked to the immunocompetence status. Impact statement In this work, we evaluated for the first time how self-rated mental (SRMH) and physical health (SRPH) influence the immune response at the molecular level in a large multi-ethnic cohort. We observed that both SRMH and SRPH are related to immunocompetence status. These findings indicated that the link between how we perceive our health and poorer health outcomes could be explained by alterations in the immune response by shifting the expression of genes related to the type I IFN response and antibody synthesis.

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.

Background: Cortisol, a stress hormone released by the activation of the hypothalamic-pituitary-adrenal (HPA) axis, is critical to the body's adaptive response to physiological and psychological stress. Cortisol has also been implicated in the health effects of air pollution through the activation of the sympathetic nervous system. This study evaluates the cross-sectional and longitudinal association between several air pollutants and salivary cortisol. Methods: We used data from the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort of 45–85 years old participants from six US cities. Salivary cortisol was evaluated at two time points between 2004 and 2006 and then again from 2010 to 2012. Cortisol samples were taken several times per day on two or three consecutive days. Particulate matter

Previous studies have demonstrated an inverse association between chronic psychosocial stress and leukocyte telomere length (LTL), a potential marker of cellular aging. However, due to paucity of longitudinal data, responses of LTL and the LTL aging trajectory to changes in chronic stress exposure remain less well understood. Using data from the Stress I and II ancillary studies of the Multi-Ethnic Study of Atherosclerosis, we estimated the 10-year longitudinal (n = 1,158) associations of within-person changes in chronic stress with changes in LTL, as well as the pooled, cross-sectional associations of chronic stress and LTL (total n = 2,231). We measured chronic stress from both individual and neighborhood-environment sources. At the individual level, we calculated a summary score of each participant’s rating of their ongoing (>6 months) material/social problems as moderately/very stressful on the Chronic Burden Scale. Neighborhood-level stress was measured using a summary score of reverse-coded MESA Neighborhood safety, aesthetic quality, and social cohesion scales. Quantiles of these scores were empirically categorized as high, moderate, or low stress. We then summed these individual- and neighborhood-level categorical variables for a total stress measure. Longitudinal within-person associations were estimated with fixed-effects models, which control for all time-invariant confounding, with additional control for time-varying demographics, lagged behaviors and chronic conditions, and specimen storage duration, as well as correction for regression to the mean. Change from low to high total chronic stress was associated with telomere shortening by 0.054 units [95% confidence interval: −0.095, −0.013] over 10 years. This was consistent with, though stronger in magnitude than, cross-sectional estimates. Change in individual-level stress was the primary driver of this effect. We also found suggestive evidence that 1) individuals with persistently high stress experienced the least shortening of telomeres, and 2) changes in individual-level stress were associated with stronger telomere shortening among women, whereas changes in neighborhood stress were associated with stronger shortening among men. Our findings provide longitudinal support to existing evidence, and point to interesting dynamics in telomere attrition across stress levels and genders.

Racial disparities in cardiovascular health (CVH) continue to remain a public health concern in the United States. We use unique population-based data from the Multi-Ethnic Study of Atherosclerosis cohort to explore the black-white differences in optimal CVH. Utilizing geographically weighted regression methods, we assess the spatial heterogeneity in black-white differences in optimal CVH and the impact of both individual- and neighborhood-level risk factors. We found evidence of significant spatial heterogeneity in black-white differences that varied within and between the five sites. Initial models showed decreased odds of optimal CVH for blacks that ranged from 60% to 70% reduced odds - with noticeable variation of these decreased odds within each site. Adjusting for risk factors resulted in reductions in the black-white differences in optimal CVH. Further understanding of the reasons for spatial heterogeneities in black-white differences in nationally representative cohorts may provide important clues regarding the drivers of these differences.

Autonomic nervous system effects have been hypothesized as a mechanism of air pollutant health effects, though scant prior epidemiologic research has examined the association between air pollutants and catecholamines.To examine the association of long-term air pollutants with three urinary catecholamines: dopamine (DA), epinephrine (EPI), and norepinephrine (NE). As a secondary aim, we also examined the association between short-term (or acute) exposure to fine particulate matter [particulate matter with aerodynamic diameter [Formula: see text] ([Formula: see text])] and those catecholamines.We used data from the Multi-Ethnic Study of Atherosclerosis (MESA) and two of its ancillary studies, the MESA Air Pollution Study and the MESA Stress Study, to provide exposure and outcome data. DA, EPI, and NE from urine samples were collected from 2004 to 2006 from 1,002 participants in the New York, New York, and Los Angeles, California, study sites. Spatiotemporal models incorporated cohort-specific monitoring and estimated annual average pollutant concentrations ([Formula: see text], [Formula: see text], [Formula: see text] and black carbon) at participants' homes the year prior to urine collection. Secondarily, short-term [Formula: see text] was evaluated (day of, day prior, and 2- to 5-d lags prior to urine collection). Several covariates were considered confounders (age, race, sex, site, socioeconomic status, cardiovascular disease risk factors, psychosocial stressors, and medication use) in linear regression models.A [Formula: see text] higher annual [Formula: see text] concentration was associated with 6.3% higher mean EPI level [95% confidence interval (CI): 0.3%, 12.6%]. A 2-[Formula: see text] higher annual ambient [Formula: see text] concentration was associated with 9.1% higher mean EPI (95% CI: 3.2%, 15.3%) and 4.4% higher DA level (95% CI: 1%, 7.9%). [Formula: see text], black carbon, and short-term [Formula: see text] exposures were not significantly associated with any of the catecholamines.We found an association between EPI and long-term concentrations of [Formula: see text] and [Formula: see text] and an association between DA and long-term ambient [Formula: see text]. These novel findings provide modest support for the hypothesis that air pollutant exposures are related to sympathetic nervous system activation. https://doi.org/10.1289/EHP3286.

Study ObjectivesSleep disturbances and sleep apnea are associated with increased vulnerability to age-related disease, altering molecular pathways affecting biological aging. Telomere length captures one component of biological aging. We evaluated whether objectively assessed sleep and sleep apnea relate to leukocyte telomere length (LTL) in the Multi-Ethnic Study of Atherosclerosis (MESA).MethodsMen and women aged 44–84 years (n = 672) from the MESA Stress and MESA Sleep studies underwent polysomnography and 7 day actigraphy (at Exam 5) and assessment of LTL (at baseline [Exam 1] and about 10 years later [Exam 5]).ResultsGeneral linear models adjusting for age, sex, race/ethnicity, BMI, physical activity, and smoking found that severe obstructive sleep apnea (OSA; apnea–hypopnea index > 30) was cross-sectionally associated with shorter LTL (p = 0.007). Modest associations of shorter LTL with less rapid eye movement sleep, more stage 1 sleep, wake after sleep onset >30 min, and long sleep duration were found, but these effects were diminished after adjusting for lifestyle and OSA. Exploratory analyses found that higher arousal index at Exam 5 was associated with greater LTL decline over the prior 10 years (p = 0.004).ConclusionsOSA was associated with shorter LTL. Individuals with high-arousal frequency had greater leukocyte telomere attrition over the prior decade. These findings suggest that sleep apnea and sleep fragmentation are associated with accelerated biological aging.

ObjectiveAfrican Americans, especially those in the Southeastern USA, have different dietary behaviours from the general US population, and have the highest prevalence, incidence and mortality of diet-related disease outcomes, such as cardiovascular disease. However, there are scant data regarding factors such as socioeconomic position (SEP) across the life course that influence dietary behaviours in this high-risk population. Our aim was to examine the impact of life course and neighbourhood SEPs on dietary intake among African Americans.Participants and settingData for this cross-sectional analysis came from the community-based Jackson Heart Study (JHS). We analysed a total of 3948 JHS participants (mean age: 55.4±12.5; 63.9% women), who had complete dietary intake and covariate information.MethodsWe examined the associations of childhood SEP (CSEP), adulthood SEP (ASEP) and neighbourhood SEP (NSEP) with 10 selected dietary intake measures, using multilevel log-gamma generalised linear regression models.Outcome measuresDietary intake measures include daily saturated fat, sodium, protein, fibre, fruits and vegetables, whole grains, sugar-sweetened beverage, nuts, fish and processed meat.ResultsIn age, sex and total energy intake adjusted models, most dietary intakes were associated with these three SEP measures. After additional adjustment for other SEP measures, most of the significant associations with CSEP and NSEP were attenuated, except for the associations of fibre with CSEP (relative rate [RR] [95% CI] 1.05 [1.00–1.10]) and whole grains with NSEP (RR [95% CI] 1.28 [1.02–1.61]). The associations (shown as RR [95% CI]) between ASEP and sugar-sweetened beverage: 0.70 (0.59–0.83), processed meat: 0.75 (0.63–0.90), sodium: 0.99 (0.94–1.00), fibre: 1.10 (1.03–1.16), protein: 1.05 (1.01–1.09), fruits and vegetables: 1.21 (1.11–1.32), nuts: 2.13 (1.59–2.87), and fish: 1.57 (1.27–1.95) generally persisted after additional adjustment for both CSEP and NSEP. However, the association between ASEP and whole grains was attenuated.ConclusionsHigh ASEP may have a more beneficial influence on dietary practices in African Americans than CSEP or NSEP.

Home foreclosures can precipitate declines in health among the individuals who lost their homes. Whether home foreclosures can "spillover" to affect the health of other neighborhood residents is largely unknown. Using longitudinal data from the Multi-Ethnic Study of Atherosclerosis that were linked to foreclosure data from 2005 to 2012, we assessed whether greater exposure to neighborhood foreclosures was associated with temporal changes in 3 objectively measured cardiometabolic risk factors: body mass index, systolic blood pressure, and fasting glucose level. We used fixed-effects models to estimate mean changes in cardiometabolic risk factors associated with changes in neighborhood foreclosures over time. In models in which we controlled for time-varying income, working status, medication use, neighborhood poverty, neighborhood unemployment, and interactions of age, sex, race, and state foreclosure laws with time, a standard-deviation increase in neighborhood foreclosures (1.9 foreclosures per quarter mile) was associated with increases in fasting glucose (mean = 0.22 mg/dL, 95% confidence interval: -0.05, 0.50) and decreases in blood pressure (mean = -0.27 mm Hg, 95% confidence interval: -0.49, -0.04). Changes in neighborhood foreclosure rates were not associated with changes in body mass index. Overall, greater exposure to neighborhood foreclosures had mixed associations with cardiometabolic risk factors over time. Given the millions of mortgages still in default, further research clarifying the potential health effects of neighborhood foreclosures is needed.

We investigated the relationships between neighborhood socio-demographic characteristics (socioeconomic status [SES], percentage of Black residents, and percentage of Hispanic residents) and survey-based measures of the social environment (social cohesion, safety) and the physical environment (healthy food environment, walking environment) in six sites from 2000 through 2011. Neighborhood environments were patterned by area SES and racial/ethnic composition, such that higher SES and lower percentage minority neighborhoods had better physical and social environments. Increasing disparities over time were observed for some neighborhood environments. Further research should explore the role of neighborhood environments in maintaining or increasing social disparities in health.

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 …

Purpose: Studies on how the interaction of psychological and environmental characteristics influences walking are limited, and the results are inconsistent. Our aim is to examine how the attitude toward walking and neighborhood environments interacts to influence walking. Design: Cross-sectional phone and mail survey. Setting: Participants randomly sampled from 6 study sites including Los Angeles, Chicago, Baltimore, Minneapolis, Manhattan, and Bronx Counties in New York City, and Forsyth and Davidson Counties in North Carolina. Participants: The final sample consisted of 2621 persons from 2011 to 2012. Measures: Total minutes of walking for travel or leisure, attitude toward walking, and perceptions of the neighborhood environments were self-reported. Street Smart (SS) Walk Score (a measure of walkability derived from a variety of geographic data) was obtained for each residential location. Analysis: Linear regression models adjusting for age, gender, race/ethnicity, education, and income. Results: Attitude toward walking was positively associated with walking for both purposes. Walking for travel was significantly associated with SS Walk Score, whereas walking for leisure was not. The SS Walk Score and selected perceived environment characteristics were associated with walking in people with a very positive attitude toward walking but were not associated with walking in people with a less positive attitude. Conclusion: Attitudes toward walking and neighborhood environments interact to affect walking behavior.

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.

The ways in which a neighborhood environment may affect depression and depressive symptoms have not been thoroughly explored. This study used longitudinal data from 5475 adults in the Multi-Ethnic Study of Atherosclerosis to investigate associations of time-varying depressive symptoms between 2000 and 2012 (measured using the 20-item Center for Epidemiologic Studies Depression Scale (CES-D)) with survey-based measures of neighborhood safety and social cohesion (both individual-level perceptions and neighborhood-level aggregates) and densities of social engagement destinations. Linear mixed models were used to examine associations of baseline cross-sectional associations and cumulative exposures with changes over time in CES-D. Econometric fixed effects models were utilized to investigate associations of within-person changes in neighborhood exposures with within-person changes in CES-D. Adjusting for relevant covariates, higher safety and social cohesion and greater density of social engagement destinations were associated with lower CES-D at baseline. Greater cumulative exposure to these features was not associated with progression of CES-D over 10 years. Within-person increases in safety and in social cohesion were associated with decreases in CES-D, although associations with cohesion were not statistically significant. Social elements of neighborhoods should be considered by community planners and public health practitioners to achieve optimal mental health.

Cross-sectional association has been shown between type 2 diabetes and hypothalamic–pituitary–adrenal (HPA) axis dysregulation; however, the temporality of this association is unknown. Our aim was to determine if type 2 diabetes is associated with longitudinal change in daily cortisol curve features. We hypothesized that the presence of type 2 diabetes may lead to a more blunted and abnormal HPA axis profile over time, suggestive of increased HPA axis dysregulation. This was a longitudinal cohort study, including 580 community-dwelling individuals (mean age 63.7 ± 9.1 years; 52.8 % women) with (n = 90) and without (n = 490) type 2 diabetes who attended two MultiEthnic Study of Atherosclerosis Stress ancillary study exams separated by 6 years. Outcome measures that were collected were wake-up and bedtime cortisol, cortisol awakening response (CAR), total area under the curve (AUC), and early, late, and overall decline slopes. In univariate analyses, wake-up and AUC increased over 6 years more in persons with as compared to those without type 2 diabetes (11 vs. 7 % increase for wake-up and 17 vs. 11 % for AUC). The early decline slope became flatter over time with a greater flattening observed in diabetic compared to non-diabetic individuals (23 vs. 9 % flatter); however, the change was only statistically significant for wake-up cortisol (p-value: 0.03). Over time, while CAR was reduced more, late decline and overall decline became flatter, and bedtime cortisol increased less in those with as compared to those without type 2 diabetes, none of these changes were statistically significant in adjusted models. We did not identify any statistically significant change in cortisol curve features over 6 years by type 2 diabetes status.

Given limited research on the impact of neighborhood environments on accelerated biological aging, we examined whether changes in neighborhood socioeconomic and social conditions were associated with change in leukocyte telomere length using 10 years of longitudinal data from the Multi-Ethnic Study of Atherosclerosis (years 2000–2011; N = 1031; mean age = 61, SD = 9.4). Leukocyte telomere length change was corrected for regression to the mean and neighborhood was defined as census tract. Neighborhood socioeconomic indicators (factor-based score of income, education, occupation, and wealth of neighborhood) and neighborhood social environment indicators (aesthetic quality, social cohesion, safety) were obtained from the U.S Census/American Community Survey and via study questionnaire, respectively. Results of linear mixed-effects models showed that independent of individual sociodemographic characteristics, each unit of improvement in neighborhood socioeconomic status was associated with slower telomere length attrition over 10-years (β = 0.002; 95% Confidence Interval (CI): 0.0001, 0.004); whereas each unit of increase in safety (β = −0.043; 95% CI: -0.069, −0.016) and overall neighborhood social environment score (β = -0.005; 95% CI: -0.009, −0.0004) were associated with more pronounced telomere attrition, after additionally adjusting for neighborhood socioeconomic status. This study provides support for considerations of the broader social and socioeconomic contexts in relation to biological aging. Future research should explore potential psychosocial mechanisms underlying these associations using longitudinal study designs with repeated observations.

Background Exposure to adverse social factors has been associated with an altered inflammatory profile, a risk factor for several acute and chronic diseases. Differential gene expression may be a biological mediator in the relationship. In this study, associations between a range of social factors and expression of inflammation-related genes were investigated. Methods Social factor and gene expression data were collected from 1,264 individuals in the Multi-Ethnic Study of Atherosclerosis (MESA). Inflammation-related genes were identified from the Gene Ontology database. The associations between social factors and gene expression were first assessed using the Global Analysis of Covariance (Global ANCOVA) gene set enrichment test. When the global test was significant, linear regression and elastic net penalized regression were employed to identify the individual gene transcripts within each gene set associated with the social factor. Results Loneliness (p = 0.003), chronic burden (p = 0.002), and major or lifetime discrimination (p = 0.045) were significantly associated with global expression of the chronic inflammatory gene set. Of the 20 transcripts that comprise this gene set, elastic net selected 12 transcripts for loneliness, 8 for chronic burden, and 3 for major or lifetime discrimination. Major or lifetime discrimination was also associated with the inflammatory response (p = 0.029), regulation of the inflammatory response (p = 0.041), and immune response (p = 0.025) gene sets in global analyses, and 53, 136, and 26 transcripts were selected via elastic net for these gene sets respectively. There were no significant associations in linear regression analyses after adjustment for multiple testing. Conclusions This study highlights gene expression as a biological mechanism through which social factors may affect inflammation.

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: With climate change, temperatures are increasing. Heat-associated health events disproportionately affect certain subpopulations. However, prior research has often lacked information on individual-level health and air conditioning and neighborhood stressors/protections. OBJECTIVES: To assess whether 1) heat (2-day mean temperature above local 75(th) percentiles) is associated with increased heart rate and decreased blood pressure, controlling for age, time, season, daily ozone, and daily particulate matter (PM(2.5)), and 2) associations differ by anti-hypertensive-medication use, renal function, fasting glucose, emotional support, air conditioning ownership and use, normalized difference vegetation index, neighborhood safety, and residence-specific oxides of nitrogen and PM(2.5). METHODS: Health and behavioral characteristics were obtained repeatedly on participants of the Multi-Ethnic Study of Atherosclerosis in six U.S. sites (2000–2010). These were linked with airport temperature, air quality, and satellite- and survey-derived neighborhood characteristics. We used a fixed-effects design, regressing health outcomes on linear temperature splines with knots at the 75(th) percentiles, interaction terms for each characteristic, and adjustment for month-of-year, age, PM(2.5), and ozone. RESULTS: Overall, heat was not associated with heart rate. However, for a 2 degree-Celsius increase in heat, systolic blood pressure (SBP) decreased by 1.1 mmHg (95% CI: −1.6, −0.6) and diastolic by 0.3 mmHg (95% CI: −0.6, −0.1). Among non-users of anti-hypertensive medications, heat-associated decreases in SBP were 2.1 mmHg greater among individuals with central air conditioning vs. without. Confidence intervals around the remaining modifiers were wide after multiple-comparisons corrections or sensitivity analyses. CONCLUSIONS: Outdoor heat is associated with decreasing blood pressure, and cardiovascular vulnerability may vary primarily by ownership of central air conditioning.

Air pollution exposures are hypothesized to impact blood pressure, yet few longitudinal studies exist, their findings are inconsistent, and different adjustments have been made for potentially distinct confounding by calendar time and age.We aimed to investigate the associations of long- and short-term [Formula: see text] and [Formula: see text] concentrations with systolic and diastolic blood pressures and incident hypertension while also accounting for potential confounding by age and time.Between 2000 and 2012, Multi-Ethnic Study of Atherosclerosis participants were measured for systolic and diastolic blood pressure at five exams. We estimated annual average and daily [Formula: see text] and [Formula: see text] concentrations for 6,569 participants using spatiotemporal models and measurements, respectively. Associations of exposures with blood pressure corrected for medication were studied using mixed-effects models. Incident hypertension was examined with Cox regression. We adjusted all models for sex, race/ethnicity, socioeconomic status, smoking, physical activity, diet, season, and site. We compared associations from models adjusting for time-varying age with those that adjusted for both time-varying age and calendar time.We observed decreases in pollution and blood pressures (adjusted for age and medication) over time. Strong, positive associations of long- and short-term exposures with blood pressure were found only in models with adjustment for time-varying age but not adjustment for both time-varying age and calendar time. For example, [Formula: see text] higher annual average [Formula: see text] concentrations were associated with 2.7 (95% CI: 1.5, 4.0) and [Formula: see text] (95% CI: [Formula: see text] 1.0) mmHg in systolic blood pressure with and without additional adjustment for time, respectively. Associations with incident hypertension were similarly weakened by additional adjustment for time. Sensitivity analyses indicated that air pollution did not likely cause the temporal trends in blood pressure.In contrast to experimental evidence, we found no associations between long- or short-term exposures to air pollution and blood pressure after accounting for both time-varying age and calendar time. This research suggests that careful consideration of both age and time is needed in longitudinal studies with trending exposures. https://doi.org/10.1289/EHP2966.

BackgroundGene expression may be an important biological mediator in associations between social factors and health. However, previous studies were limited by small sample sizes and use of differing cell types with heterogeneous expression patterns. We use a large population-based cohort with gene expression measured solely in monocytes to investigate associations between seven social factors and expression of genes previously found to be sensitive to social factors.MethodsWe employ three methodological approaches: 1) omnibus test for the entire gene set (Global ANCOVA), 2) assessment of each association individually (linear regression), and 3) machine learning method that performs variable selection with correlated predictors (elastic net).ResultsIn global analyses, significant associations with the a priori defined socially sensitive gene set were detected for major or lifetime discrimination and chronic burden (p = 0.019 and p = 0.047, respectively). Marginally significant associations were detected for loneliness and adult socioeconomic status (p = 0.066, p = 0.093, respectively). No associations were significant in linear regression analyses after accounting for multiple testing. However, a small percentage of gene expressions (up to 11%) were associated with at least one social factor using elastic net.ConclusionThe Global ANCOVA and elastic net findings suggest that a small percentage of genes may be "socially sensitive," (i.e. demonstrate differential expression by social factor), yet single gene approaches such as linear regression may be ill powered to capture this relationship. Future research should further investigate the biological mechanisms through which social factors act to influence gene expression and how systemic changes in gene expression affect overall health.

Although epidemiologic studies of telomere length have become increasingly common, few population-based, multi-ethnic studies include data on telomere shortening, which may be a better predictor of morbidity and mortality than a single measure of telomere length. This study used stored blood samples from 1,169 participants in the Multi-Ethnic Study of Atherosclerosis (MESA) to examine age, sex, race/ethnicity, marital status, income, and education as predictors of change in telomere length over a 10-year period in linear mixed effects models. Mean age at baseline was 61 years, and the sample was 54% female, 27% white, 30% African-American, and 43% Hispanic. At baseline, 58% of the sample was married; 32% had household income below $25,000 per year, 35% had income between $25,000 and $49,999 per year, and 34% had income above $50,000 per year; 41% had a high school education or less, 30% had some college, and 29% had a college degree or more. Relative telomere length (T/S ratio) was measured by the quantitative polymerase chain reaction method. In general, ten-year telomere attrition was greater for groups that had longer telomere length at baseline, including younger people, whites, and women. After adjusting for baseline telomere length, race/ethnic differences in telomere attrition were attenuated, and age and sex differences were reversed, such that older people and men showed greater telomere shortening. There were no significant differences in telomere attrition by marital status, income, or education. There is not yet a consensus in the field regarding whether to adjust for baseline telomere length in models examining predictors of telomere attrition. To ensure comparability across studies, researchers should report results both with and without adjustment for baseline telomere length.

ObjectiveTo examine the associations of individual and food environmental factors with fruit and vegetable (F&V) intake in a city in a low-to-middle-income country (LMIC).DesignCross-sectional.SettingRepresentative sample of the Brazilian Primary Care service known as the Health Academy Program (HAP) in Belo Horizonte, a Brazilian city.SubjectsUsing a conceptual model as a guide, individual and food environment data were obtained through: (i) face-to-face interviews with participants aged 20 years or older; and (ii) F&V food store audits. A broad set of individual, household, and community and consumer nutrition environment variables was investigated. Multilevel linear regression was used to quantify area-level variations in F&V intake and to estimate associations with the factors.ResultsEighteen HAP centres were selected and 2944 participants and 336 food stores were included. F&V intake varied between contexts, being higher in areas with better socio-economic conditions and food store quality, such as specialised F&V markets. Individual-level factors, including age, income, food insecurity, stage of change, self-efficacy and decisional balance, were significantly associated with F&V intake. After controlling for individual-level characteristics, greater F&V intake was also associated with higher quality of food stores.ConclusionsIn one of the first studies to comprehensively assess the food environment in an LMIC, individual-level factors accounted for the largest variation in F&V intake; however, the food environment was also important, because area-level variables explained 10·5 % of the F&V intake variation. The consumer nutrition environment was more predictive of healthy eating than was the community nutrition environment. The findings suggest new possibilities for interventions.

The US Great Recession resulted in an alarming number of home foreclosures that weakened the social and physical environment of thousands of neighborhoods. Few studies have evaluated whether these neighborhood changes were related to changes in individual behaviors. We examined the relationship between changes in neighborhood-level home foreclosure within a quarter-mile (0.4-km) buffer of the residence and changes in cigarette smoking and alcohol use among 3,807 adults enrolled in the Multi-Ethnic Study of Atherosclerosis during 2005-2012, using econometric individual-level fixed-effects models. Increases in neighborhood-level foreclosure were associated with small decreases in the number of cigarettes smoked per day (mean difference = -0.08, 95% confidence interval: -0.11, -0.04) and small increases in the number of alcoholic beverages consumed per week (mean difference = 0.11, 95% confidence interval: 0.05, 0.17). Neighborhood-level foreclosure may not uniformly influence high-risk behaviors. The impact of home foreclosure on adult drinking should be further explored, given its potentially negative implications for health.

BackgroundRacial residential segregation has been linked to adverse health outcomes, but associations may operate through multiple pathways. Prior studies have not examined associations of neighbourhood-level racial segregation with an index of cardiometabolic risk (CMR) and whether associations differ by race/ethnicity.MethodsWe used data from the Multi-Ethnic Study of Atherosclerosis to estimate cross-sectional and longitudinal associations of baseline neighbourhood-level racial residential segregation with a composite measure of CMR. Participants included 5015 non-Hispanic black, non-Hispanic white and Hispanic participants aged 45–84 years old over 12 years of follow-up (2000–2012). We used linear mixed effects models to estimate race-stratified associations of own-group segregation with CMR at baseline and with the rate of annual change in CMR. Models were adjusted for sociodemographics, medication use and individual-level and neighbourhood-level socioeconomic status (SES).ResultsIn models adjusted for sociodemographics and medication use, high baseline segregation was associated with higher baseline CMR among blacks and Hispanics but lower baseline CMR among whites. Individual and neighbourhood-level SES fully explained observed associations between segregation and CMR for whites and Hispanics. However, associations of segregation with CMR among blacks remained (high vs low segregation: mean difference 0.17 SD units, 95% CI 0.02 to 0.32; medium vs low segregation: mean difference 0.18 SD units, 95% CI 0.03 to 0.33). Baseline segregation was not associated with change in CMR index scores over time.ConclusionAssociations of own-group racial residential segregation with CMR varied by race/ethnicity. After accounting for SES, living in a more segregated neighbourhood was associated with greater risk among black participants only.

Troubling Trends in Health Disparities A National Center for Health Statistics report shows that U.S. life expectancy has decreased for 2 years. Age-adjusted mortality (1999–2016) shows that progre...

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.

Neighborhood problems constitute sources of chronic stress that may increase the risk of poor self-rated health. The associations of census tract level income and perceived neighborhood problems with self-rated health were examined in Florianópolis, Santa Catarina State, Brazil (1,720 adults). Odds ratios (OR) and their 95% confidence intervals (95%CI) of poor self-rated health were estimated through multilevel models. Residents in census tracts in the lower and intermediate tertiles of income reported poorer health than those in the highest tertile. OR of reporting poorer health was 2.44 (95%CI: 2.35- 2.54) in the higher tertile of social disorder (adjusting for mental health). The chances of reporting the poorer health with neighborhood problems ranged from 1.07 (95%CI: 1.03-1.11) to 2.02 (95%CI: 1.95-2.10) for the higher tertile of social disorder (physical health) and physical problem (health-related variables). Perceived neighborhood problems were independently associated with poor health. The perception of a neighborhood among its residents should be considered by health policymakers.

Summary Objective Prior studies have shown a bidirectional association between depression and type 2 diabetes mellitus (T2DM); however, the prospective associations of anger and anxiety with T2DM have not been established. We hypothesized that trait anger and anxiety would predict incident T2DM, independently of depressive symptoms. Research design and methods In the Multi-ethnic Study of Atherosclerosis (MESA), we prospectively examined the association of trait anger and trait anxiety (assessed via the Spielberger Trait Anger and Anxiety Scales, respectively) with incident T2DM over 11.4 years in 5598 White, Black, Hispanic, and Chinese participants (53.2% women, mean age 61.6 years) at baseline without prevalent T2DM or cardiovascular disease. We used Cox proportional hazards models to calculate the hazard ratios (HR) of incident T2DM by previously defined anger category (low, moderate, high), and anxiety quartile, as there were no previously defined categories. Results High total trait anger was associated with incident T2DM (HR 1.50; 95% CI 1.08–2.07) relative to low total trait anger. The association was attenuated following adjustment for waist circumference (HR 1.32; 95% CI 0.94–1.86). Higher anger reaction was also associated with incident T2DM (HR = 1.07; 95% CI 1.03–1.11) that remained significant after adjusting for potential confounders/explanatory factors. In contrast, trait anxiety did not predict incident T2DM. Conclusions High total trait anger and anger reaction are potential modifiable risk factors for T2DM. Further research is needed to explore the mechanisms of the anger–diabetes relationship and to develop preventive interventions.

Using Jackson Heart Study data, we examined associations of multiple measures of perceived discrimination with health behaviours among African-Americans (AA).The cross-sectional associations of everyday, lifetime and burden of discrimination with odds of smoking and mean differences in physical activity, dietary fat and sleep were examined among 4925 participants aged 35-84 years after adjustment for age and socioeconomic status (SES).Men reported slightly higher levels of everyday and lifetime discrimination than women and similar levels of burden of discrimination as women. After adjustment for age and SES, everyday discrimination was associated with more smoking and a greater percentage of dietary fat in men and women (OR for smoking: 1.13, 95% CI 1.00 to 1.28 and 1.19, 95% CI 1.05 to 1.34; mean difference in dietary fat: 0.37, p0.05 and 0.43, p0.01, in men and women, respectively). Everyday and lifetime discrimination were associated with fewer hours of sleep in men and women (mean difference for everyday discrimination: -0.08, p0.05 and -0.18, p0.001, respectively; and mean difference for lifetime discrimination: -0.08, p0.05 and -0.24, p0.001, respectively). Burden of discrimination was associated with more smoking and fewer hours of sleep in women only.Higher levels of perceived discrimination were associated with select health behaviours among men and women. Health behaviours offer a potential mechanism through which perceived discrimination affects health in AA.

We examined cross-sectional and longitudinal associations between neighborhood socioeconomic status, social cohesion and safety and features of the diurnal cortisol curve including: area under the curve (AUC), wake-to-bed slope, wake-up, cortisol awakening response (CAR, wake-up to 30 minutes post-awakening), early decline (30 minutes to 2 hours post-awakening) and late decline (2 hours post-awakening to bed time). In cross-sectional analyses, higher neighborhood poverty was associated with a flatter early decline and a flatter wake-to-bed slope. Higher social cohesion and safety were associated with higher wake-up cortisol, steeper early decline and steeper wake-to-bed slope. Over 5 years, wake-up cortisol increased, CAR, early decline, late decline and wake-to-bed slope became flatter and AUC became larger. Higher poverty was associated with less pronounced increases in wake-up and AUC, while higher social cohesion was associated with greater increases in wake-up and AUC. Adverse neighborhood environments were cross-sectionally associated with flatter cortisol profiles, but associations with changes in cortisol were weak and not in the expected direction.

Perceived discrimination is positively related to cardiovascular disease (CVD) risk factors; its relationship with incident CVD is unknown. Using data from the Multi-Ethnic Study of Atherosclerosis, a population-based multiethnic cohort study of 6,508 adults aged 45-84 years who were initially free of clinical CVD, we examined lifetime discrimination (experiences of unfair treatment in 6 life domains) and everyday discrimination (frequency of day-to-day occurrences of perceived unfair treatment) in relation to incident CVD. During a median 10.1 years of follow-up (2000-2011), 604 incident events occurred. Persons reporting lifetime discrimination in ≥2 domains (versus none) had increased CVD risk, after adjustment for race/ethnicity and sociodemographic factors, behaviors, and traditional CVD risk factors (hazard ratio (HR) = 1.36, 95% confidence interval (CI): 1.09, 1.70) and after control for chronic stress and depressive symptoms (HR = 1.28, 95% CI: 1.01, 1.60). Reported discrimination in 1 domain was unrelated to CVD (HR = 1.05, 95% CI: 0.86, 1.30). There were no differences by race/ethnicity, age, or sex. In contrast, everyday discrimination interacted with sex (P = 0.03). Stratified models showed increased risk only among men (for each 1-standard deviation increase in score, adjusted HR = 1.14, 95% CI: 1.03, 1.27); controlling for chronic stress and depressive symptoms slightly reduced this association (HR = 1.11, 95% CI: 0.99, 1.25). This study suggests that perceived discrimination is adversely related to CVD risk in middle-aged and older adults.

Type 2 diabetes mellitus (DM) affects 11% of US adults, and the prevalence is double in people 65 years of age or older (1). It has been suggested that more than 90% of adult-onset DM is attributable to modifiable factors, such as lifestyle behaviors and diet (2). Increasing evidence suggests that environmental exposures also contribute to the development of diabetes (3, 4). Recently, air pollution has been proposed as a risk factor for the development of type 2 DM (5). In a mouse model of diet-induced obesity, 6-month inhalation exposures to high concentrations of particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) induced insulin resistance and systemic inflammation and increased visceral adiposity (6). In the same mouse model, exposure to PM2.5 for 10 months induced insulin resistance, impaired glucose tolerance, lower circulating levels of adipokines (adiponectin and leptin), and mitochondrial alteration (7). Numerous studies have also shown associations of PM2.5 with systemic inflammatory responses and cardiac autonomic dysfunction (8–10), which might lead to diminished insulin action (11, 12). However, human epidemiologic studies on the relationship between air pollution and DM have yielded inconsistent results (13), with some finding an association (14–16), others finding associations only in subpopulations (17–21), and still others finding no association (22). Such inconsistencies might be attributed to sociodemographic and geographic differences. More evidence in prospectively followed cohorts is required to determine whether air pollution exposures are causally related to the development of type 2 DM. We investigated the associations of prevalent and incident DM with individual-level estimates of exposure to PM2.5 and nitrogen oxides and residential proximity to major roadways, a proxy of exposure to traffic-related pollution, in the Multi-Ethnic Study of Atherosclerosis (MESA). We also examined effect modification by sex, given that some studies reported a significant association between air pollution and DM only among women (19, 21, 22).

Background: Air pollution is linked to low lung function and to respiratory events, yet little is known of associations with lung structure. Objectives: We examined associations of particulate matter (PM2.5, PM10) and nitrogen oxides (NOx) with percent emphysema-like lung on computed tomography (CT). Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) recruited participants (45–84 years of age) in six U.S. states. Percent emphysema was defined as lung regions < –910 Hounsfield Units on cardiac CT scans acquired following a highly standardized protocol. Spirometry was also conducted on a subset. Individual-level 1- and 20-year average air pollution exposures were estimated using spatiotemporal models that included cohort-specific measurements. Multivariable regression was conducted to adjust for traditional risk factors and study location. Results: Among 6,515 participants, we found evidence of an association between percent emphysema and long-term pollution concentrations in an analysis leveraging between-city exposure contrasts. Higher concentrations of PM2.5 (5 μg/m3) and NOx (25 ppb) over the previous year were associated with 0.6 (95% CI: 0.1, 1.2%) and 0.5 (95% CI: 0.1, 0.9%) higher average percent emphysema, respectively. However, after adjustment for study site the associations were –0.6% (95% CI: –1.5, 0.3%) for PM2.5 and –0.5% (95% CI: –1.1, 0.02%) for NOx. Lower lung function measures (FEV1 and FVC) were associated with higher PM2.5 and NOx levels in 3,791 participants before and after adjustment for study site, though most associations were not statistically significant. Conclusions: Associations between ambient air pollution and percentage of emphysema-like lung were inconclusive in this cross-sectional study, thus longitudinal analyses may better clarify these associations with percent emphysema. Citation: Adar SD, Kaufman JD, Diez-Roux AV, Hoffman EA, D’Souza J, Stukovsky KH, Rich SS, Rotter JI, Guo X, Raffel LJ, Sampson PD, Oron AP, Raghunathan T, Barr RG. 2015. Air pollution and percent emphysema identified by computed tomography in the Multi-Ethnic Study of Atherosclerosis. Environ Health Perspect 123:144–151; http://dx.doi.org/10.1289/ehp.1307951