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BackgroundIn Latin America, where climate change and rapid urbanization converge, non-optimal ambient temperatures contribute to excess mortality. However, little is known about area-level characteristics that confer vulnerability to temperature-related mortality.ObjectivesExplore city-level socioeconomic and demographic characteristics associated with temperature-related mortality in Latin American cities.MethodsThe dependent variables quantify city-specific associations between temperature and mortality: heat- and cold-related excess death fractions (EDF, or percentages of total deaths attributed to cold/hot temperatures), and the relative mortality risk (RR) associated with 1 °C difference in temperature in 325 cities during 2002-2015. Random effects meta-regressions were used to investigate whether EDFs and RRs associated with heat and cold varied by city-level characteristics, including population size, population density, built-up area, age-standardized mortality rate, poverty, living conditions, educational attainment, income inequality, and residential segregation by education level.ResultsWe find limited effect modification of cold-related mortality by city-level demographic and socioeconomic characteristics and several unexpected associations for heat-related mortality. For example, cities in the highest compared to the lowest tertile of income inequality have all-age cold-related excess mortality that is, on average, 3.45 percentage points higher (95% CI: 0.33, 6.56). Higher poverty and higher segregation were also associated with higher cold EDF among those 65 and older. Large, densely populated cities, and cities with high levels of poverty and income inequality experience smaller heat EDFs compared to smaller and less densely populated cities, and cities with little poverty and income inequality.DiscussionEvidence of effect modification of cold-related mortality in Latin American cities was limited, and unexpected patterns of modification of heat-related mortality were observed. Socioeconomic deprivation may impact cold-related mortality, particularly among the elderly. The findings of higher levels of poverty and income inequality associated with lower heat-related mortality deserve further investigation given the increasing importance of urban adaptation to climate change.

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

Urban scaling is a framework that describes how city-level characteristics scale with variations in city size. This scoping review mapped the existing evidence on the urban scaling of health outcomes to identify gaps and inform future research. Using a structured search strategy, we identified and reviewed a total of 102 studies, a majority set in high-income countries using diverse city definitions. We found several historical studies that examined the dynamic relationships between city size and mortality occurring during the nineteenth and early twentieth centuries. In more recent years, we documented heterogeneity in the relation between city size and health. Measles and influenza are influenced by city size in conjunction with other factors like geographic proximity, while STIs, HIV, and dengue tend to occur more frequently in larger cities. NCDs showed a heterogeneous pattern that depends on the specific outcome and context. Homicides and other crimes are more common in larger cities, suicides are more common in smaller cities, and traffic-related injuries show a less clear pattern that differs by context and type of injury. Future research should aim to understand the consequences of urban growth on health outcomes in low- and middle-income countries, capitalize on longitudinal designs, systematically adjust for covariates, and examine the implications of using different city definitions.

Background Residential segregation, a geospatial manifestation of structural racism, is a fundamental driver of racial and ethnic health inequities, and longitudinal studies examining segregation's influence on cardiovascular health are limited. This study investigates the impact of segregation on hypertension in a multiracial and multiethnic cohort and explores whether neighborhood environment modifies this association. Methods and Results Leveraging data from a diverse cohort of adults recruited from 6 sites in the United States with 2 decades of follow-up, we used race- and ethnicity-stratified Cox models to examine the association between time-varying segregation with incident hypertension in 1937 adults free of hypertension at baseline. Participants were categorized as residing in segregated and nonsegregated neighborhoods using a spatial-weighted measure. We used a robust covariance matrix estimator to account for clustering within neighborhoods and assessed effect measure modification by neighborhood social or physical environment. Over an average follow-up of 7.35 years, 65.5% non-Hispanic Black, 48.1% Chinese, and 53.7% Hispanic participants developed hypertension. Net of confounders, Black and Hispanic residents in segregated neighborhoods were more likely to develop hypertension relative to residents in nonsegregated neighborhoods (Black residents: hazard ratio [HR], 1.33; 95% CI, 1.09-1.62; Hispanic residents: HR, 1.33; 95% CI, 1.04-1.70). Results were similar but not significant among Chinese residents (HR, 1.20; 95% CI, 0.83-1.73). Among Black residents, neighborhood social environment significantly modified this association such that better social environment was associated with less pronounced impact of segregation on hypertension. Conclusions This study underscores the importance of continued investigations of groups affected by the health consequences of racial residential segregation while taking contextual neighborhood factors, such as social environment, into account.

BackgroundExposure 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.MethodsSocial 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.ResultsLoneliness (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.ConclusionsThis study highlights gene expression as a biological mechanism through which social factors may affect inflammation.

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.

Longitudinal associations between neighborhood characteristics and body mass index (BMI; weight (kg)/height (m)2) were assessed from 2000 to 2011 among 5,919 participants in the Multi-Ethnic Study of Atherosclerosis. The perceived availability of healthy food and walking environment were assessed via surveys, and 1-mile (1.6-km) densities of supermarkets, fruit-and-vegetable stores, and recreational facilities were obtained through a commercial database. Econometric fixed-effects models were used to estimate the association between within-person changes in neighborhood characteristics and within-person change in BMI. In fully adjusted models, a 1-standard-deviation increase in the healthy food environment index was associated with a 0.16-kg/m2 decrease in BMI (95% confidence interval (CI): -0.27, -0.06) among participants with obesity at baseline. A 1-standard-deviation increase in the physical activity environment index was associated with 0.13-kg/m2 (95% CI: -0.24, -0.02) and 0.14-kg/m2 (95% CI: -0.27, -0.01) decreases in BMI for participants who were overweight and obese at baseline, respectively. Paradoxically, increases in the physical activity index were associated with BMI increases in persons who were normal-weight at baseline. This study provides preliminary longitudinal evidence that favorable changes in neighborhood physical environments are related to BMI reductions in obese persons, who comprise a substantial proportion of the US population.

Investments in neighborhood built environments could increase physical activity and overall health. Disproportionate distribution of these changes in advantaged neighborhoods could inflate health disparities. Little information exists on where changes are occurring. This paper aims to 1) identify changes in the built environment in neighborhoods and 2) investigate associations between high levels of change and sociodemographic characteristics. Using Geographic Information Systems, neighborhood land-use, local destinations (for walking, social engagement, and physical activity), and sociodemographics were characterized in 2000 and 2010 for seven U.S. cities. Linear and change on change models estimated associations of built environment changes with baseline (2000) and change (2010-2000) in sociodemographics. Spatial patterns were assessed using Global Moran's I to measure overall clustering of change and Local Moran's I to identify statistically significant clusters of high increases surrounded by high increases (HH). Sociodemographic characteristics were compared between HH cluster and other tracts using Analysis of Variance (ANOVA). We observed small land-use changes but increases in the destination types. Greater increases in destinations were associated with higher percentage non-Hispanic whites, percentage households with no vehicle, and median household income. Associations were present for both baseline sociodemographics and changes over time. Greater increases in destinations were associated with lower baseline percentage over 65 but higher increases in percentage over 65 between 2000 and 2010. Global Moran's indicated changes were spatially clustered. HH cluster tracts started with a higher percentage non-Hispanic whites and higher percentage of households without vehicles. Between 2000 and 2010, HH cluster tracts experienced increases in percent non-Hispanic white, greater increases in median household income, and larger decreases in percent of households without a vehicle. Changes in the built environment are occurring in neighborhoods across a diverse set of U.S. metropolitan areas, but are patterned such that they may lead to increased health disparities over time.

We used data from 3227 older adults in the Multi-Ethnic Study of Atherosclerosis (2004-2012) to explore cross-sectional and longitudinal associations between walkability and cardiometabolic risk factors. In cross-sectional analyses, linear regression was used to estimate associations of Street Smart Walk Score® with glucose, triglycerides, HDL and LDL cholesterol, systolic and diastolic blood pressure, and waist circumference, while logistic regression was used to estimate associations with odds of metabolic syndrome. Econometric fixed effects models were used to estimate longitudinal associations of changes in walkability with changes in each risk factor among participants who moved residential locations between 2004 and 2012 (n=583). Most cross-sectional and longitudinal associations were small and statistically non-significant. We found limited evidence that higher walkability was cross-sectionally associated with lower blood pressure but that increases in walkability were associated with increases in triglycerides and blood pressure over time. Further research over longer time periods is needed to understand the potential for built environment interventions to improve cardiometabolic health.