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.

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.

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.

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.

Air Pollution, Cardiovascular Outcomes, and Social Disadvantage: The Multi-ethnic Study of Atherosclerosis.

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.

Invited Commentary: Fundamental Causes, Social Context, and Modifiable Risk Factors in the Racial/Ethnic Inequalities in Blood Pressure and Hypertension.

Racial and ethnic inequalities in blood pressure and hypertension have been well documented, but their causes remain unclear, making efforts to reduce these inequalities challenging. In this issue of the Journal, Basu et al. (Am J Epidemiol. 2015;182(4):345-353) address this gap in our knowledge by using an econometric approach to examine the role of 4 conventional risk factors for hypertension. Their results suggest that targeting certain risk factors will reduce racial inequalities in the prevalence of hypertension. However, racial differences in modifiable risk factors are enmeshed within disparate socioenvironmental contexts which are in turn determined by inequalities in the distribution of social, economic, and political resources and constraints. A small but growing body of literature suggests that targeting the intermediate risk factors that link racial group membership to hypertension, rather than the context or the inequalities in the distribution of resources and constraints, will ultimately result in little change in hypertension inequalities, increase these inequalities, or even create inequalities in poor mental health.

Racial/ethnic disparities in hypertension prevalence: reconsidering the role of chronic stress.

OBJECTIVES: We investigated the association between anticipatory stress, also known as racism-related vigilance, and hypertension prevalence in Black, Hispanic, and White adults. METHODS: We used data from the Chicago Community Adult Health Study, a population-representative sample of adults (n = 3105) surveyed in 2001 to 2003, to regress hypertension prevalence on the interaction between race/ethnicity and vigilance in logit models. RESULTS: Blacks reported the highest vigilance levels. For Blacks, each unit increase in vigilance (range = 0-12) was associated with a 4% increase in the odds of hypertension (odds ratio [OR] = 1.04; 95% confidence interval [CI] = 1.00, 1.09). Hispanics showed a similar but nonsignificant association (OR = 1.05; 95% CI = 0.99, 1.12), and Whites showed no association (OR = 0.95; 95% CI = 0.87, 1.03). CONCLUSIONS: Vigilance may represent an important and unique source of chronic stress that contributes to the well-documented higher prevalence of hypertension among Blacks than Whites; it is a possible contributor to hypertension among Hispanics but not Whites.

Fine particulate matter air pollution and blood pressure: the modifying role of psychosocial stress.

BACKGROUND: Consensus is growing on the need to investigate the joint effects of psychosocial stress and environmental hazards on health. Some evidence suggests that psychosocial stress may be an important modifier of the association between air pollution respiratory outcomes, but few have examined cardiovascular outcomes. OBJECTIVES: We examined the modifying effect of psychosocial stress on the association between fine particulate matter air pollution (PM2.5) and blood pressure (BP). METHODS: Our data came from the Detroit Healthy Environments Partnership (HEP) 2002-2003 survey. Of 919 participants, BP was collected at two time points in a subset of 347. Building on previous work reporting associations between PM2.5 and BP in this sample, we regressed systolic (SBP) and diastolic (DBP) BP and pulse pressure (PP), in separate linear models, on the interaction among psychosocial stress, PM2.5, and HEP neighborhood (Southwest, Eastside, Northwest). RESULTS: The association between PM2.5 and SBP was stronger for those who reported high levels of stress, but this interaction was significant only in the Southwest Detroit neighborhood. Southwest Detroit residents who reported low stress showed 2.94 mmHg (95% CI: -0.85, 6.72) increase in SBP for each 10 µg/m(3) increase in 2-day prior PM2.5 exposure. Those who reported high stress showed 9.05 mmHg (95% CI: 3.29, 14.81) increase in SBP for each 10 µg/m(3) increase in PM2.5 exposure. CONCLUSIONS: These results suggest that psychosocial stress may increase vulnerability to the hypertensive effects of PM2.5. This work contributes to an understanding of the ways in which the social and physical environments may jointly contribute to poor health and to health disparities.

The mediating role of systemic inflammation and moderating role of racialization in disparities in incident dementia.

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 the racialization process in incident dementia. METHODS: In the US Health and Retirement Study (n = 6,908), 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 is 12%. Among minoritized participants (i.e., non-Hispanic Black and/or Hispanic), high CRP levels ( ≥ 75th percentile or 4.73µg/mL) are associated with 1.26 (95%CI: 0.98, 1.62) times greater risk of incident dementia than low CRP ( < 4.73µg/mL). Decomposition analysis comparing minoritized versus non-Hispanic white participants shows that the mediating effect of CRP accounts for 3% (95% CI: 0%, 6%) of the racial disparity, while the interaction effect between minoritized group status and high CRP accounts for 14% (95% CI: 1%, 27%) of the disparity. Findings are robust to potential violations of causal mediation assumptions. CONCLUSIONS: Minoritized group membership modifies the relationship between systemic inflammation and incident dementia.

Higher levels of inflammation in blood are linked to greater dementia risk in older adults. Non-Hispanic Black and Hispanic Americans have higher inflammation levels compared to non-Hispanic white Americans. We conducted a study to examine whether high levels of inflammation could explain differences in dementia risk among these racial groups. We found that differences in inflammation levels in non-Hispanic Black or Hispanic adults modestly explain their higher risk of dementia compared to non-Hispanic white adults. These findings suggest that interventions aimed at reducing high levels of inflammation in minoritized US adults could ameliorate racial differences in dementia risk.

DNA Methylation Age Acceleration Mediates the Relationship between Systemic Inflammation and Cognitive Impairment.

Background: Chronic inflammation and DNA methylation are potential mechanisms in dementia etiology. The linkage between inflammation and DNA methylation age acceleration in shaping dementia risk is understudied. We explored the association of inflammatory cytokines with cognitive impairment and whether DNA methylation age acceleration mediates this relationship. Methods: In a subset of the 2016 wave of the Health and Retirement Study (n=3,346, age>50), we employed logistic regression to estimate the associations between each inflammatory cytokine (interleukin-6 (IL-6), C-reactive protein (CRP), and insulin-like growth factor-1 (IGF-1)), and both Langa-Weir classified cognitive impairment non-dementia and dementia, respectively. We calculated DNA methylation age acceleration residuals by regressing GrimAge on chronologic age. We tested if DNA methylation age acceleration mediated the relationship between systemic inflammation and cognitive impairment, adjusting for sociodemographic, behavioral factors, chronic conditions, and cell type proportions. Results: The prevalence of cognitive impairment was 16%. In the fully-adjusted model, participants with a doubling of IL-6 levels had 1.12 (95% CI: 1.02-1.22) times higher odds of cognitive impairment. Similar associations were found for CRP and IGF-1. Participants with a doubling of IL-6 levels had 0.77 (95% CI: 0.64, 0.90) years of GrimAge acceleration. In mediation analyses with each cytokine as predictor separately, 17.7% (95% CI: 7.0%, 50.9%) of the effect of IL-6 on cognitive impairment was mediated through DNA methylation age acceleration. Comparable mediated estimates were found for CRP and IGF-1. Conclusions: Systemic inflammation is associated with cognitive impairment, with suggestive evidence that this relationship is partially mediated through DNA methylation age acceleration.

Do psychosocial stress and social disadvantage modify the association between air pollution and blood pressure?: the multi-ethnic study of atherosclerosis.

Researchers have theorized that social and psychosocial factors increase vulnerability to the deleterious health effects of environmental hazards. We used baseline examination data (2000-2002) from the Multi-Ethnic Study of Atherosclerosis. Participants were 45-84 years of age and free of clinical cardiovascular disease at enrollment (n = 6814). The modifying role of social and psychosocial factors on the association between exposure to air pollution comprising particulate matter less than 2.5 µm in aerodynamic diameter (PM2.5) and blood pressure measures were examined using linear regression models. There was no evidence of synergistic effects of higher PM2.5 and adverse social/psychosocial factors on blood pressure. In contrast, there was weak evidence of stronger associations of PM2.5 with blood pressure in higher socioeconomic status groups. For example, those in the 10th percentile of the income distribution (i.e., low income) showed no association between PM2.5 and diastolic blood pressure (b = -0.41 mmHg; 95% confidence interval: -1.40, 0.61), whereas those in the 90th percentile of the income distribution (i.e., high income) showed a 1.52-mmHg increase in diastolic blood pressure for each 10-µg/m(3) increase in PM2.5 (95% confidence interval: 0.22, 2.83). Our results are not consistent with the hypothesis that there are stronger associations between PM2.5 exposures and blood pressure in persons of lower socioeconomic status or those with greater psychosocial adversity.

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 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.

A novel look at racial health disparities: the interaction between social disadvantage and environmental health.

OBJECTIVES: We explored the notion that social disadvantage increases vulnerability to the health effects of environmental hazards. Specifically, we examined (1) whether race modifies the association between blood lead and blood pressure and (2) whether socioeconomic status (SES) plays a role in this modifying effect. METHODS: Using the National Health and Nutrition Examination Survey (2001-2008) and linear regression, we estimated the association between blood lead and blood pressure. Using interactions among race, SES, and lead, we estimated this association by levels of social disadvantage. RESULTS: Black men and women showed a 2.8 (P < .001) and 4.0 (P < .001) millimeters mercury increase in SBP, respectively, for each doubling of blood lead. White adults showed no association. This lead-SBP association exhibited by Blacks was primarily isolated to Blacks of low SES. For example, poor but not nonpoor Black men showed a 4.8 millimeters mercury (P < .001) increase in SBP for each doubling of blood lead. CONCLUSIONS: Our results suggest that social disadvantage exacerbates the deleterious health effects of lead. Our work provides evidence that social and environmental factors must be addressed together to eliminate health disparities.

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.

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.

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.