Racial and Ethnic Residential Segregation and Monocyte DNA Methylation Age Acceleration.

Importance: Neighborhood segregation and poverty may be important drivers of health inequities. Epigenomic factors, including DNA methylation clocks that may mark underlying biological aging, have been implicated in the link between social factors and health. Objective: To examine the associations of neighborhood segregation and poverty with 4 DNA methylation clocks trained to capture either chronological age or physiological dysregulation. Design, Setting, and Participants: This cohort study uses data from the Multi-Ethnic Study of Atherosclerosis (MESA), a longitudinal study that started in 2000 to 2002, with follow-up in 2002 to 2004, 2004 to 2005, 2005 to 2007, and 2010 to 2012. In 2000 to 2002, adults who identified as White or Black race or Hispanic or Chinese ethnicity in 6 US sites (Baltimore, Maryland; Chicago, Illinois; Forsyth County, North Carolina; Los Angeles County, California; Northern Manhattan, New York; and St. Paul, Minnesota) were sampled for recruitment. A random subsample of 4 sites (Maryland, North Carolina, New York, and Minnesota) were selected for inclusion in the MESA epigenomics ancillary study at examination 5 (2010-2012). Participants who identified as White or Black race or Hispanic ethnicity, were aged 45 to 84 years, and did not have clinical cardiovascular disease were included in this analysis. Data were analyzed from May 2021 to October 2023. Exposure: Information on 2000 census tract poverty and Getis-Ord G statistic segregation of Hispanic residents, non-Hispanic Black residents, or non-Hispanic White residents were linked to participant addresses at examination 1 (2000-2002). Main Outcomes and Measures: At examination 5, DNA methylation was measured in purified monocytes. DNA methylation age acceleration was calculated using 4 clocks trained on either chronological age or physiological dysregulation. Linear regressions were used to test associations. Results: A total of 1102 participants (mean [SD] age, 69.7 [9.4] years; 562 [51%] women) were included, with 348 Hispanic participants, 222 non-Hispanic Black participants, and 533 non-Hispanic White participants. For non-Hispanic Black participants, living in tracts with greater segregation of Black residents was associated with GrimAge DNA methylation age acceleration, a clock designed to capture physiological dysregulation. A 1-SD increase in segregation was associated with 0.42 (95% CI, 0.20-0.64) years age acceleration (P < .001); this association was not observed with other clocks. This association was particularly pronounced for participants living in high poverty tracts (interaction term, 0.24; 95% CI, 0.07-0.42; P = .006). In the overall sample, census tract poverty level was associated with GrimAge DNA methylation age acceleration (ß = 0.45; 95% CI, 0.20-0.71; adjusted P = .005). Conclusions and Relevance: These findings suggest that epigenomic mechanisms may play a role in the associations of segregated and poor neighborhoods with chronic conditions.

The Mediating Role of Systemic Inflammation and Moderating Role of Race/Ethnicity in Racialized Disparities in Incident Dementia: A Decomposition Analysis.

Background: Exposure to systemic racism is linked to increased dementia burden. To assess systemic inflammation as a potential pathway linking exposure to racism and dementia disparities, we investigated the mediating role of C-reactive protein (CRP), a systemic inflammation marker, and the moderating role of race/ethnicity on racialized disparities in incident dementia. Methods: In the US Health and Retirement Study (n=5,143), serum CRP was measured at baseline (2006, 2008 waves). Incident dementia was classified by cognitive tests over a six-year follow-up. Self-reported racialized categories were a proxy for exposure to the racialization process. We decomposed racialized disparities in dementia incidence (non-Hispanic Black and/or Hispanic vs. non-Hispanic White) into 1) the mediated effect of CRP, 2) the moderated portion attributable to the interaction between racialized group membership and CRP, and 3) the controlled direct effect (other pathways through which racism operates). Results: The 6-year cumulative incidence of dementia was 15.5%. Among minoritized participants (i.e., non-Hispanic Black and/or Hispanic), high CRP levels (> 75th percentile or 4.57µg/mL) was associated with 1.27 (95%CI: 1.01,1.59) times greater risk of incident dementia than low CRP (≤4.57µg/mL). Decomposition analysis comparing minoritized versus non-Hispanic White participants showed that the mediating effect of CRP accounted for 2% (95% CI: 0%, 6%) of the racial disparity, while the interaction effect between minoritized group status and high CRP accounted for 12% (95% CI: 2%, 22%) of the disparity. Findings were robust to potential violations of causal mediation assumptions. Conclusions: Systemic inflammation mediates racialized disparities in incident dementia.

Evaluating Race in Air Pollution and Health Research: Race, PM2.5 Air Pollution Exposure, and Mortality as a Case Study.

PURPOSE OF REVIEW: Racial inequities in air pollution exposure have been documented. There is also interest in documenting the modifying role of race in the link between air pollution and health. However, the empirical literature in this area has yielded mixed results with potentially unclear policy implications. We critically evaluate recent empirical papers on the interactive association between race and air pollution exposure on adult mortality in the USA as a case study of the race, pollution, and health literature. Specifically, we evaluate these studies for the conceptualization and discussion of race and the use of race variables that may contribute to the ambiguous results and policy implications both in this specific literature and in the broader literature. RECENT FINDINGS: We evaluate ten empirical studies from 2016 to 2022 on the modifying role of race in the association between short- and long-term PM2.5 exposure and specific types of adult mortality (all cause, non-accidental, and heart or cardiovascular diseases) in the USA. In addition to comparing and contrasting the empirical results, we focus our review on the conceptualization, measurement, modeling, and discussion of race and the race variables. Overall, the results indicate no consistent role of race in the association between PM2.5 exposure and mortality. Moreover, conceptualization and discussion of race was often brief and incomplete, even when the empirical results were unexpected or counterintuitive. To build on recent discussions in the epidemiology and environmental epidemiology literature more specifically, we provide a detailed discussion of the meaning of race, the race variables, and the cultural and structural racism that some argue are proxied by race variables. We use theoretical scholarship from the humanities and social sciences along with empirical work from the environmental literature to provide recommendations for future research that can provide an evidence base to inform both social and environmental policy.

Racial Segregation and Cognitive Function Among Older Adults in the United States: Findings From the Reasons for Geographic and Racial Differences in Stroke Study.

OBJECTIVES: Residential segregation is one of the fundamental features of health disparities in the United States. Yet little research has examined how living in segregated metropolitan areas is related to cognitive function and cognitive decline with age. We examined the association between segregation at the metropolitan statistical area (MSA) level and trajectories of age-related cognitive function. METHOD: Using data from Black and White older adults in the REasons for Geographic and Racial Differences in Stroke study (n = 18,913), we employed linear growth curve models to examine how living in racially segregated MSAs at baseline, measured by the degree of non-Hispanic Black (NHB) isolation and NHB dissimilarity, was associated with trajectories of age-related cognitive function and how the associations varied by race and education. RESULTS: Living in MSAs with greater levels of isolation was associated with lower cognitive function (b = -0.093, p < .05) but was not associated with rates of change in cognitive decline with age. No effects of living in isolated MSAs were found for those with at least a high school education, but older adults with less than a high school education had lower cognitive function in MSAs with greater isolation (b = -0.274, p < .05). The degree of dissimilarity was not associated with cognitive function. The association between segregation and cognitive function did not vary by race. DISCUSSION: Metropolitan segregation was associated with lower cognitive function among older adults, especially for those with lower education living in racially isolated MSAs. This suggests complex associations between individual socioeconomic status, place, and cognitive health.

Linking History to Contemporary State-Sanctioned Slow Violence through Cultural and Structural Racism.

Environmental scientists started documenting the racial inequities of environmental exposures (e.g., proximity to waste facilities or to industrial pollution) in the 1970s and 1980s. Since then, research has documented inequities in exposures to nearly every studied environmental hazard, showing that American society delivers racial violence toward non-White families. Through cultural racism, a resilient social hierarchy is set where the lives of some groups of people are considered more valuable than others; then, through structural racism, institutions unequally mete and dole environmental benefits and burdens to these groups. We argue that the "slow violence" of environmental racism is linked to other forms of racial violence that have been enacted throughout history. We discuss the meaning of cultural racism as it pertains to the hierarchy of groups of people whose lives are valued unequally and its link to structural racism. To remedy this environmental racial violence, we propose shifts in the empirical research on environmental inequities that are built upon, either implicitly or explicitly, the interconnected concepts of cultural and structural racism that link historical to contemporary forms of racial violence.

Structural Racism: The Rules and Relations of Inequity.

Why do racial inequalities endure despite numerous attempts to expand civil rights in certain sectors? A major reason for this endurance is due to lack of attention to structural racism. Although structural and institutional racism are often conflated, they are not the same. Herein, we provide an analogy of a "bucky ball" (Buckminsterfullerene) to distinguish the two concepts. Structural racism is a system of interconnected institutions that operates with a set of racialized rules that maintain White supremacy. These connections and rules allow racism to reinvent itself into new forms and persist, despite civil rights interventions directed at specific institutions. To illustrate these ideas, we provide examples from the fields of environmental justice, criminal justice, and medicine. Racial inequities in power and health will persist until we redirect our gaze away from specific institutions (and specific individuals), and instead focus on the resilient connections among institutions and their racialized rules.

Understanding the Link between Neighborhoods and Kidney Disease.

Neighborhoods are where we live, learn, work, pray, and play. Growing evidence indicates that neighborhoods are an important determinant of health. The built features of our neighborhoods, such as the ways in which the streets are designed and connected and the availability of green spaces and transit stops, as well as the social features, such as the trust among neighbors and the perceptions of safety, may influence health through multiple pathways, such as access to important resources, psychosocial stress, and health behaviors. In particular, the extant literature consistently documents an association between neighborhood features and renal-associated conditions, such as cardiovascular disease, hypertension, diabetes, and obesity. There is also some evidence suggesting an association between neighborhood poverty and ESKD. The link between neighborhood and earlier stages of CKD, however, has been less clear, with most studies documenting no association. It may be that the neighborhood measures used in previous studies do not capture features of the neighborhood important for earlier stages of disease development and progression. It may also be that our current biomarkers (e.g., eGFR) and urine protein are not able to pick up very early forms of renal damage because of the kidney's overall high reserve capacity. This paper critically reviews the state of the literature on neighborhood and renal disease, with recommendations for neighborhood measures in future research. Neighborhoods are designed, built, and informed by policy, and thus, they are amenable to intervention, making them a potentially powerful way to improve renal health and reduce health inequalities at the population level.

Neighborhood socioeconomic status and risk of hospitalization in patients with chronic kidney disease: A chronic renal insufficiency cohort study.

Patients with chronic kidney disease (CKD) experience significantly greater morbidity than the general population. The hospitalization rate for patients with CKD is significantly higher than the general population. The extent to which neighborhood-level socioeconomic status (SES) is associated with hospitalization has been less explored, both in the general population and among those with CKD.We evaluated the relationship between neighborhood SES and hospitalizations for adults with CKD participating in the Chronic Renal Insufficiency Cohort Study. Neighborhood SES quartiles were created utilizing a validated neighborhood-level SES summary measure expressed as z-scores for 6 census-derived variables. The relationship between neighborhood SES and hospitalizations was examined using Poisson regression models after adjusting for demographic characteristics, individual SES, lifestyle, and clinical factors while taking into account clustering within clinical centers and census block groups.Among 3291 participants with neighborhood SES data, mean age was 58 years, 55% were male, 41% non-Hispanic white, 49% had diabetes, and mean estimated glomerular filtration rate (eGFR) was 44 ml/min/1.73 m. In the fully adjusted model, compared to individuals in the highest SES neighborhood quartile, individuals in the lowest SES neighborhood quartile had higher risk for all-cause hospitalization (rate ratio [RR], 1.28, 95% CI, 1.09-1.51) and non-cardiovascular hospitalization (RR 1.30, 95% CI, 1.10-1.55). The association with cardiovascular hospitalization was in the same direction but not statistically significant (RR 1.21, 95% CI, 0.97-1.52).Neighborhood SES is associated with risk for hospitalization in individuals with CKD even after adjusting for individual SES, lifestyle, and clinical factors.

Life course trauma and muscle weakness in older adults by gender and race/ethnicity: Results from the U.S. health and Retirement Study.

Muscle weakness, as measured by handgrip strength, is a primary determinant of physical functioning and disability. There is a high burden of muscle weakness in the United States with close to 50 percent of older Americans meeting criteria for clinical muscle weakness. While previous racial/ethnic disparities have been documented among older adults, the extent to which lifecourse trauma shapes muscle strength trajectories is unknown. Using U.S. Health and Retirement Study (N = 20,472, Mean Age = 63.8 years) data on grip strength (2006-2014, up to 3 assessments) and retrospectively reported traumatic events, we fit gender-stratified growth curve models to investigate whether traumatic events experienced across the lifecourse or at distinct sensitive periods (childhood, early/emerging adulthood or mid-life) predicted later-life trajectories of grip strength. There was no association between cumulative trauma and trajectories of grip strength and the main effects for the life stage models were largely null. However, among White women, our results suggest that traumatic events experienced during childhood (ß = -0.012; 95% CI = -0.024, 0.0004) compared to middle adulthood are associated with faster declines in grip strength in later life. Traumatic events reported during childhood was related to a slower decline in grip strength over time among Hispanic women compared to that for White women (ß = 0.086, 95% CI = 0.044, 0.128). Among Black men, the association between traumatic events during early/emerging adulthood and age-related declines in grip strength was stronger for Black men than for White men (interaction ß = -0.070; 95% CI = -0.138, 0.001). Traumatic events experienced during distinct life stages may influence later life declines in grip strength and exacerbate racial inequalities in later life. This study addresses an important gap by investigating the life course social determinants of later life muscle strength, which is a key driver of physical functioning and mobility.

Understanding the intersection of race and place: the case of tuberculosis in Michigan.

BACKGROUND: Race and place intersect to produce location-based variation in disease distributions. We analyzed the geographic distribution of tuberculosis (TB) incidence in Michigan, USA to better understand the complex interplay between race and place, comparing patterns in Detroit, Wayne County and the state of Michigan as a whole. METHODS: Using cross-sectional TB surveillance data from the Michigan Department of Health and Human Services, multivariable statistical models were developed to analyze the residence patterns of TB incidence from 2007 through 2012. Two-way interactions among the residence location and race of cases were assessed. RESULTS: Overall, Detroit residents experienced 58% greater TB incidence than residents of Wayne County or the state of Michigan. Racial inequalities were less pronounced in Detroit compared to both Wayne County and the state of Michigan. Blacks in Detroit had 2.01 times greater TB incidence than Whites, while this inequality was 3.62 times more in Wayne County and 8.72 greater in the state of Michigan. CONCLUSION: Our results highlight how race and place interact to influence patterns of TB disease, and the ways in which this interaction is context dependent. TB elimination in the U.S. will require strategies that address the local social environment, as much as the physical environment.

Interpreting Subjective and Objective Measures of Job Resources: The Importance of Sociodemographic Context.

Salutary retirement policy depends on a clear understanding of factors in the workplace that contribute to work ability at older ages. Research in occupational health typically uses either self-reported or objective ratings of the work environment to assess workplace determinants of health and work ability. This study assessed whether individual characteristics and work-related demands were differentially associated with (1) self-reported ratings of job resources from older workers in the Health and Retirement Study, and (2) corresponding objective ratings of job resources from the Occupational Information Network (O*NET). Results from regression and relative weights analyses showed that self-reported ratings were associated with self-reported job demands and personal resources, whereas corresponding O*NET ratings were associated with differences in gender, race, or socioeconomic standing. As a result, subjective ratings may not capture important aspects of aging workers' sociodemographic background that influence work ability, occupational sorting, opportunities for advancement, and ultimately the job resources available to them. Future studies should consider including both subjective and objective measures to capture individual and societal level processes that drive the relationship between work, health, and aging.

Neighborhood Social Context and Kidney Function Over Time: The Multi-Ethnic Study of Atherosclerosis.

RATIONALE & OBJECTIVE: Although socioeconomic status has been associated with chronic kidney disease (CKD), little is known about its relationship to residential neighborhood context. STUDY DESIGN: Secondary analysis of the Multi-Ethnic Study of Atherosclerosis (MESA), a prospective cohort study designed to investigate the development and progression of subclinical cardiovascular disease. SETTING & PARTICIPANTS: 6,814 men and women who were between 45 and 84 years of age and free of cardiovascular disease were recruited between 2000 and 2002 from Baltimore, MD; Chicago, IL; Forsyth County, NC; Los Angeles, CA; New York, NY; and St. Paul, MN. EXPOSURES: A composite neighborhood problem score (calculated based on 7 participant-reported domains at study entry: adequacy of food sources, availability of parks/playground, noise, sidewalks, traffic, trash and litter, and violence) and a social cohesion score (calculated based on 5 participant-reported attributes of people in their neighborhood: close knit; get along; willing to help neighbors; trustworthy; and share values). OUTCOMES: Estimated glomerular filtration rate (eGFR; calculated using the CKD-EPI [CKD Epidemiology Collaboration] creatinine-cystatin C equation) and an indicator of eGFR decline > 30% since study entry using follow-up eGFR quantified at 4 examinations: 2000 to 2002, 2004 to 2005, 2005 to 2007, and 2010 to 2011. ANALYTICAL APPROACH: Associations between each neighborhood measure (in separate models) and eGFR decline > 30% from baseline and annualized eGFR change were estimated using Cox proportional hazards and linear mixed regression models, respectively, adjusting for potential confounders. RESULTS: While neighborhood social context differs by race/ethnicity, neither neighborhood problems nor social cohesion was independently associated with eGFR decline after adjustment for confounders. LIMITATIONS: Incomplete capture of the early stages of eGFR decline, reliance on observational data, limited variation in neighborhood measures, and the potential for residual confounding. CONCLUSIONS: Although we showed no independent association between neighborhood context and eGFR decline, it is associated with many CKD risk factors and further work is needed to clarify whether it has an independent role in CKD.

Neighbourhood racial/ethnic residential segregation and cardiometabolic risk: the multiethnic study of atherosclerosis.

BACKGROUND: Racial 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. METHODS: We 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). RESULTS: In 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. CONCLUSION: Associations 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.

The weight of racism: Vigilance and racial inequalities in weight-related measures.

In the United States, racial/ethnic inequalities in obesity are well-documented, particularly among women. Using the Chicago Community Adult Health Study, a probability-based sample in 2001-2003 (N = 3105), we examined the roles of discrimination and vigilance in racial inequalities in two weight-related measures, body mass index (BMI) and waist circumference (WC), viewed through a cultural racism lens. Cultural racism creates a social environment in which Black Americans bear the stigma burden of their racial group while White Americans are allowed to view themselves as individuals. We propose that in this context, interpersonal discrimination holds a different meaning for Blacks and Whites, while vigilance captures the coping style for Blacks who carry the stigma burden of the racial group. By placing discrimination and vigilance within the context of cultural racism, we operationalize existing survey measures and utilize statistical models to clarify the ambiguous associations between discrimination and weight-related inequalities in the extant literature. Multivariate models were estimated for BMI and WC separately and were stratified by gender. Black women had higher mean BMI and WC than any other group, as well as highest levels of vigilance. White women did not show an association between vigilance and WC but did show a strong positive association between discrimination and WC. Conversely, Black women displayed an association between vigilance and WC, but not between discrimination and WC. These results demonstrate that vigilance and discrimination may hold different meanings for obesity by ethnoracial group that are concealed when all women are examined together and viewed without considering a cultural racism lens.

Child and Adult Socioeconomic Status and the Cortisol Response to Acute Stress: Evidence From the Multi-Ethnic Study of Atherosclerosis.

OBJECTIVE: A long-hypothesized pathway through which low socioeconomic status (SES) harms health is through dysregulation of the physiologic stress response systems. No previous studies have tested this hypothesis by investigating cortisol reactivity and recovery to acute stress in relation to SES at different times in the life course in adults. Alteration of the cortisol response to an acute stressor could signal dysregulation of the hypothalamic-pituitary-adrenal axis and has been associated with chronic illness. METHODS: We used data on 997 adults 54 years or older from a multiethnic, multisite United States study to examine associations between life course SES and cortisol response to a laboratory stress challenge. Informed by life course theory, we hypothesized that lower child and adult SES would be associated with lower reactivity (i.e., smaller increase in cortisol) and a slower recovery rate (i.e., slower rate of decline in cortisol after the challenge). RESULTS: In demographics-adjusted multilevel piecewise linear regression models, low child and adult SES were associated with a 19% (95% CI = 4%-50%) and 27% (7%-55%) slower recovery rate compared with high child and adult SES, respectively. Compared with participants with stable high SES, those with stable low SES had a 48% (16%-70%) slower recovery rate. Differences in reactivity by SES were small. CONCLUSIONS: Our results support the hypothesis that low SES throughout life affects the hypothalamic-pituitary-adrenal axis and in turn the ability to recover from exposure to acute stressors. This mechanism can help explain how socioeconomic disparities contribute to disparities in chronic disease.

Structural racism in the workplace: Does perception matter for health inequalities?

Structural racism has been linked to racial health inequalities and may operate through an unequal labor market that results in inequalities in psychosocial workplace environments (PWE). Experiences of the PWE may be a critical but understudied source of racial health disparities as most adults spend a large portion of their lives in the workplace, and work-related stress affects health outcomes. Further, it is not clear if the objective characteristics of the workplace are important for health inequalities or if these inequalities are driven by the perception of the workplace. Using data from the 2008 to 2012 waves of the Health and Retirement Study (HRS), a probability-based sample of US adults 50 years of age and older and the Department of Labor's Occupational Information Network (O*NET), we examine the role of both standardized, objective (O*NET) and survey-based, subjective (as in HRS) measures of PWEs on health and Black-White health inequalities. We find that Blacks experience more stressful PWEs and have poorer health as measured by self-rated health, episodic memory function, and mean arterial pressure. Mediation analyses suggest that these objective O*NET ratings, but not the subjective perceptions, partially explain the relationship between race and health. We discuss these results within the extant literature on workplace and health and health inequalities. Furthermore, we discuss the use of standardized objective measures of the PWE to capture racial inequalities in workplace environment.

Maternal Social Disadvantage and Newborn Telomere Length in Archived Dried Blood Spots from the Michigan Neonatal Biobank.

Telomeres are the protective caps at the ends of eukaryotic chromosomes. Short telomere length is associated with morbidity and mortality among adults and may mark the biological impact of social experiences. Using archived dried blood spots from the Michigan Neonatal Biobank, this study examined markers of maternal social disadvantage (educational attainment, receipt of public assistance, marital status, and race/ethnicity) from linked birth certificates as predictors of telomere length at birth in a sample of 192 singleton neonates born to non-Hispanic black, non-Hispanic white, and Latina mothers aged 20-35 years. Consistent with two recent studies in newborns, but counter to the idea that maternal social disadvantage is associated with shorter offspring telomere length, we found that infants born to black mothers had longer telomeres than those born to white mothers (b = 0.12, SE = 0.06, p = .05). However, black/white differences in newborn telomere length varied by receipt of public assistance. Among newborns whose mothers received WIC and/or Medicaid, there were no significant black/white differences in telomere length (b = 0.09, SE = 0.08, p = .25). In contrast, among those whose mothers did not receive public assistance-just 6 out of 69 infants born to black mothers versus 41 out of 69 infants born to white mothers-we found that babies born to black mothers had longer telomere length than babies born to white mothers (b = 0.37, SE = 0.16, p = .03). The interaction between black race/ethnicity and receipt of public assistance did not reach the conventional threshold for statistical significance (b = -0.22, SE = 0.15, p = .13), suggesting that this finding may be due to chance. No other markers of maternal social disadvantage were related to infant telomere length. Although replication of these results in a larger sample with more infants born to black mothers with relatively high socioeconomic status is needed, this study offers preliminary support for the hypothesis that race/ethnic differences in newborn telomere length depend on social context.

Measurement and modeling of race and health in Brazil: continuing the discussion.

Recent reviews have discussed the conceptualization of race in health studies in Brazil. This review further documents and discusses specific measurement and modeling issues with regard to race and how this can impact result interpretation. Three scientific databases were used to search the literature on race and three health outcomes. The search yielded 38 empirical studies on birth outcomes, self-rated health, and weight. Results suggest that, while there are racial patterns in the overall literature, conceptual and methodological challenges can be addressed to clarify the ways in which racial group membership is linked to health.