Racial Disparities in Neighborhood Arrest Rates during the COVID-19 Pandemic.

Structural racism in police contact is an important driver of health inequities among the U.S. urban population. Hyper-policing and police violence in marginalized communities have risen to the top of the national policy agenda, particularly since protests in 2020. How did pandemic conditions impact policing? We assess neighborhood racial disparities in arrests after COVID-19 stay-at-home orders in Boston, Charleston, Pittsburgh, and San Francisco census tracts (January 2019-August 2020). Using interrupted time series models with census tract fixed effects, we report arrest rates across tract racial and ethnic compositions. In the weeks following stay-at-home orders, overall arrest rates were 39% lower (95% CI: 37-41%) on average compared to rates the year prior. Although arrest rates steadily increased thereafter, most tracts did not reach pre-pandemic arrest levels. However, despite declines in nearly all census tracts, the magnitude of racial inequities in arrests remained unchanged. During the initial weeks of the pandemic, arrest rates declined significantly in areas with higher Black populations, but average rates in Black neighborhoods remained higher than pre-pandemic arrest rates in White neighborhoods. These findings support urban policy reforms that reconsider police capacity and presence, particularly as a mechanism for enforcing public health ordinances and reducing racial disparities.

Validation of a prostate cancer polygenic risk score.

BACKGROUND: Genome-wide association studies have identified over 100 single-nucleotide polymorphisms (SNPs) associated with prostate cancer (PrCa), and polygenic risk scores (PRS) based on their combined genotypes have been developed for risk stratification. We aimed to assess the contribution of PRS to PrCa risk in a large multisite study. METHODS: The sample included 1972 PrCa cases and 1919 unaffected controls. Next-generation sequencing was used to assess pathogenic variants in 14 PrCa-susceptibility genes and 72 validated PrCa-associated SNPs. We constructed a population-standardized PRS and tested its association with PrCa using logistic regression adjusted for age and family history of PrCa. RESULTS: The mean age of PrCa cases at diagnosis and age of controls at testing/last clinic visit was 59.5 ± 7.2 and 57.2 ± 13.0 years, respectively. Among 1740 cases with pathology data, 57.4% had Gleason score ≤ 6, while 42.6% had Gleason score ≥ 8. In addition, 39.6% cases and 20.1% controls had a family history of PrCa. The PRS was significantly higher in cases than controls (mean ± SD: 1.42 ± 1.11 vs 1.02 ± 0.76; P < .0001). Compared with men in the 1st quartile of age-adjusted PRS, those in the 2nd, 3rd, and 4th quartile were 1.58 (95% confidence interval [CI]: 1.31-1.90), 2.36 (95% CI: 1.96-2.84), and 3.98 (95% CI: 3.29-4.82) times as likely to have PrCa (all P < .0001). Adjustment for family history yielded similar results. PRS predictive performance was consistent with prior literature (area under the receiver operating curve = 0.64; 95% CI: 0.62-0.66). CONCLUSIONS: These data suggest that a 72-SNP PRS is predictive of PrCa, supporting its potential use in clinical risk assessment.

A clinical guide to hereditary cancer panel testing: evaluation of gene-specific cancer associations and sensitivity of genetic testing criteria in a cohort of 165,000 high-risk patients.

PURPOSE: Despite the rapid uptake of multigene panel testing (MGPT) for hereditary cancer predisposition, there is limited guidance surrounding indications for testing and genes to include. METHODS: To inform the clinical approach to hereditary cancer MGPT, we comprehensively evaluated 32 cancer predisposition genes by assessing phenotype-specific pathogenic variant (PV) frequencies, cancer risk associations, and performance of genetic testing criteria in a cohort of 165,000 patients referred for MGPT. RESULTS: We identified extensive genetic heterogeneity surrounding predisposition to cancer types commonly referred for germline testing (breast, ovarian, colorectal, uterine/endometrial, pancreatic, and melanoma). PV frequencies were highest among patients with ovarian cancer (13.8%) and lowest among patients with melanoma (8.1%). Fewer than half of PVs identified in patients meeting testing criteria for only BRCA1/2 or only Lynch syndrome occurred in the respective genes (33.1% and 46.2%). In addition, 5.8% of patients with PVs in BRCA1/2 and 26.9% of patients with PVs in Lynch syndrome genes did not meet respective testing criteria. CONCLUSION: Opportunities to improve upon identification of patients at risk for hereditary cancer predisposition include revising BRCA1/2 and Lynch syndrome testing criteria to include additional clinically actionable genes with overlapping phenotypes and relaxing testing criteria for associated cancers.

Racism and Health: Evidence and Needed Research.

In recent decades, there has been remarkable growth in scientific research examining the multiple ways in which racism can adversely affect health. This interest has been driven in part by the striking persistence of racial/ethnic inequities in health and the empirical evidence that indicates that socioeconomic factors alone do not account for racial/ethnic inequities in health. Racism is considered a fundamental cause of adverse health outcomes for racial/ethnic minorities and racial/ethnic inequities in health. This article provides an overview of the evidence linking the primary domains of racism-structural racism, cultural racism, and individual-level discrimination-to mental and physical health outcomes. For each mechanism, we describe key findings and identify priorities for future research. We also discuss evidence for interventions to reduce racism and describe research needed to advance knowledge in this area.

False-positive results released by direct-to-consumer genetic tests highlight the importance of clinical confirmation testing for appropriate patient care.

PURPOSE: There is increasing demand from the public for direct-to-consumer (DTC) genetic tests, and the US Food and Drug Administration limits the type of health-related claims DTC tests can market. Some DTC companies provide raw genotyping data to customers if requested, and these raw data may include variants occurring in genes recommended by the American College of Medical Genetics and Genomics to be reported as incidental/secondary findings. The purpose of this study was to review the outcome of requests for clinical confirmation of DTC results that were received by our laboratory and to analyze variant classification concordance. METHODS: We identified 49 patient samples received for further testing that had previously identified genetic variants reported in DTC raw data. For each case identified, information pertaining to the outcome of clinical confirmation testing as well as classification of the DTC variant was collected and analyzed. RESULTS: Our analyses indicated that 40% of variants in a variety of genes reported in DTC raw data were false positives. In addition, some variants designated with the "increased risk" classification in DTC raw data or by a third-party interpretation service were classified as benign at Ambry Genetics as well as several other clinical laboratories, and are noted to be common variants in publicly available population frequency databases. CONCLUSION: Our results demonstrate the importance of confirming DTC raw data variants in a clinical laboratory that is well versed in both complex variant detection and classification.

Frequency of mutations in a large series of clinically ascertained ovarian cancer cases tested on multi-gene panels compared to reference controls.

OBJECTIVES: Given the lack of adequate screening modalities, knowledge of ovarian cancer risks for carriers of pathogenic alterations in predisposition genes is important for decisions about risk-reduction by salpingo-oophorectomy. We sought to determine which genes assayed on multi-gene panels are associated with ovarian cancer, the magnitude of the associations, and for which clinically meaningful associations could be ruled out. METHODS: 7768 adult ovarian cancer cases of European ancestry referred to a single clinical testing laboratory underwent multi-gene panel testing for detection of pathogenic alterations in known or suspected ovarian cancer susceptibility genes. A targeted capture approach was employed to assay each of 19 genes for the presence of pathogenic or likely pathogenic alterations. Mutation frequencies in ovarian cancer cases were compared to mutation frequencies in individuals from the Exome Aggregation Consortium (ExAC). Analyses stratified by family and personal history of other cancers and age at diagnosis were also performed. RESULTS: Significant associations (p<0.001) were identified between alterations in 11 genes and ovarian cancer, with eight of these displaying ≥5-fold increased risk (BRCA1, BRCA2, BRIP1, MSH2, MSH6, RAD51C, RAD51D). Relative risks of ovarian cancer greater than two-fold were also observed for ATM, but could reliably be ruled out for RAD50 and CHEK2. CONCLUSIONS: These results will inform clinical management of women found to carry pathogenic alterations in genes tested on multi-gene panels. The knowledge that some genes are not associated with OC can reduce concerns of women found to carry pathogenic alterations in those genes.

Racial and Ethnic Disparities in Oncotype DX Test Receipt in a Statewide Population-Based Study.

Background: Racial disparities have been reported in breast cancer care, yet little is known about disparities in access to gene expression profiling (GEP) tests. Given the impact of GEP test results, such as those of Oncotype DX (ODx), on treatment decision-making for hormone receptor-positive (HR+) breast cancer, it is particularly important to assess disparities in its use. Methods: We conducted a retrospective population-based study of 8,784 patients diagnosed with breast cancer in Connecticut during 2011 through 2013. We assessed the association between race, ethnicity, and ODx receipt among women with HR+ breast cancer for whom NCCN does and does not recommend ODx testing, using bivariate and multivariate logistic analyses. Results: We identified 5,294 women who met study inclusion criteria: 83.8% were white, 6.3% black, and 7.4% Hispanic. Overall, 50.9% (n=4,131) of women in the guideline-recommended group received ODx testing compared with 18.5% (n=1,163) in the nonrecommended group. More white women received the ODx test compared with black and Hispanic women in the recommended and nonrecommended groups (51.4% vs 44.6% and 47.7%; and 21.2% vs 9.0% and 9.7%, respectively). After adjusting for tumor and clinical characteristics, we observed significantly lower ODx use among black (odds ratio [OR], 0.64; 95% CI, 0.47-0.88) and Hispanic women (OR, 0.59; 95% CI, 0.45-0.77) compared with white women in the recommended group and in the guideline-discordant group (blacks: OR, 0.39; 95% CI, 0.20-0.78, and Hispanics: OR, 0.44; 95% CI, 0.23-0.85). Conclusions: In this population-based study, we identified racial disparities in ODx testing. Disparities in access to innovative cancer care technologies may further exacerbate existing disparities in breast cancer outcomes.

Diagnostic Exome Sequencing Identifies a Novel Gene, EMILIN1, Associated with Autosomal-Dominant Hereditary Connective Tissue Disease.

Heritable connective tissue diseases are a highly heterogeneous family of over 200 disorders that affect the extracellular matrix. While the genetic basis of several disorders is established, the etiology has not been discovered for a large portion of patients, likely due to rare yet undiscovered disease genes. By performing trio-exome sequencing of a 55-year-old male proband presenting with multiple symptoms indicative of a connective disorder, we identified a heterozygous missense alteration in exon 1 of the Elastin Microfibril Interfacer 1 (EMILIN1) gene, c.64G>A (p.A22T). The proband presented with ascending and descending aortic aneurysms, bilateral lower leg and foot sensorimotor peripheral neuropathy, arthropathy, and increased skin elasticity. Sanger sequencing confirmed that the EMILIN1 alteration, which maps around the signal peptide cleavage site, segregated with disease in the affected proband, mother, and son. The impaired secretion of EMILIN-1 in cells transfected with the mutant p.A22T coincided with abnormal protein accumulation within the endoplasmic reticulum. In skin biopsy of the proband, we detected less EMILIN-1 with disorganized and abnormal coarse fibrils, aggregated deposits underneath the epidermis basal lamina, and dermal cells apoptosis. These findings collectively suggest that EMILIN1 may represent a new disease gene associated with an autosomal-dominant connective tissue disorder.

BRAT1 mutations present with a spectrum of clinical severity.

Mutations in BRAT1, encoding BRCA1-associated ATM activator 1, are associated with a severe phenotype known as rigidity and multifocal seizure syndrome, lethal neonatal (RMFSL; OMIM # 614498), characterized by intractable seizures, hypertonia, autonomic instability, and early death. We expand the phenotypic spectrum of BRAT1 related disorders by reporting on four individuals with various BRAT1 mutations resulting in clinical severity that is either mild or moderate compared to the severe phenotype seen in RMFSL. Representing mild severity are three individuals (Patients 1-3), who are girls (including two sisters, Patients 1-2) between 4 and 10 years old, with subtle dysmorphisms, intellectual disability, ataxia or dyspraxia, and cerebellar atrophy on brain MRI; additionally, Patient 3 has well-controlled epilepsy and microcephaly. Representing moderate severity is a 15-month-old boy (Patient 4) with severe global developmental delay, refractory epilepsy, microcephaly, spasticity, hyperkinetic movements, dysautonomia, and chronic lung disease. In contrast to RMFSL, his seizure onset occurred later at 4 months of age, and he is still alive. All four of the individuals have compound heterozygous BRAT1 mutations discovered via whole exome sequencing: c.638dupA (p.Val214Glyfs*189); c.803+1G>C (splice site mutation) in Patients 1-2; c.638dupA (p.Val214Glyfs*189); c.419T>C (p.Leu140Pro) in Patient 3; and c.171delG (p.Glu57Aspfs*7); c.419T>C (p.Leu140Pro) in Patient 4. Only the c.638dupA (p.Val214Glyfs*189) mutation has been previously reported in association with RMFSL. These patients illustrate that, compared with RMFSL, BRAT1 mutations can result in both moderately severe presentations evident by later-onset epilepsy and survival past infancy, as well as milder presentations that include intellectual disability, ataxia/dyspraxia, and cerebellar atrophy. © 2016 Wiley Periodicals, Inc.

Enhanced utility of family-centered diagnostic exome sequencing with inheritance model-based analysis: results from 500 unselected families with undiagnosed genetic conditions.

PURPOSE: Diagnostic exome sequencing was immediately successful in diagnosing patients in whom traditional technologies were uninformative. Herein, we provide the results from the first 500 probands referred to a clinical laboratory for diagnostic exome sequencing. METHODS: Family-based exome sequencing included whole-exome sequencing followed by family inheritance-based model filtering, comprehensive medical review, familial cosegregation analysis, and analysis of novel genes. RESULTS: A positive or likely positive result in a characterized gene was identified in 30% of patients (152/500). A novel gene finding was identified in 7.5% of patients (31/416). The highest diagnostic rates were observed among patients with ataxia, multiple congenital anomalies, and epilepsy (44, 36, and 35%, respectively). Twenty-three percent of positive findings were within genes characterized within the past 2 years. The diagnostic rate was significantly higher among families undergoing a trio (37%) as compared with a singleton (21%) whole-exome testing strategy. CONCLUSION: Overall, we present results from the largest clinical cohort of diagnostic exome sequencing cases to date. These data demonstrate the utility of family-based exome sequencing and analysis to obtain the highest reported detection rate in an unselected clinical cohort, illustrating the utility of diagnostic exome sequencing as a transformative technology for the molecular diagnosis of genetic disease.

How Connecticut health directors deal with public health budget cuts at the local level.

OBJECTIVES: We investigated the perspectives of local health jurisdiction (LHJ) directors on coping mechanisms used to respond to budget reductions and constraints on their decision-making. METHODS: We conducted in-depth interviews with 17 LHJ directors. Interviews were audio recorded, transcribed, and analyzed using the constant comparative method. RESULTS: LHJ directors use a range of coping mechanisms, including identifying alternative revenue sources, adjusting services, amending staffing arrangements, appealing to local political leaders, and forming strategic partnerships. LHJs also face constraints on their decision-making because of state and local statutory requirements, political priorities, pressures from other LHJs, and LHJ structure. CONCLUSIONS: LHJs respond creatively to budget cuts to maintain important public health services. Some LHJ adjustments to administrative resources may obscure the long-term costs of public health budget cuts in such areas as staff morale and turnover. Not all coping strategies are available to each LHJ because of the contextual constraints of its locality, pointing to important policy questions on identifying optimum jurisdiction size and improving efficiency.

The impact of county-level fees & fines as exploitative revenue generation on US birth outcomes 2011-2015.

Fees and fines collected through courts and law enforcement can comprise a considerable proportion of revenue for local governments. Law enforcement, as agents of revenue generation, change policing behavior to increase revenue, at times targeting Black and brown neighborhoods to bolster municipal budgets. This structural racism in revenue generation has not yet been assessed as an exposure for adverse health. Using the 2012 Census of Governments, and 2011-2015 vital statistics from the National Center of Health Statistics, we examine the relationship between countyaverage fees and fines as a percent of total own-source revenue and county-level characteristics, and risk of preterm birth and low birthweight across the United States. Mothers residing in counties with the greatest reliance on fees and fines had 1.08 (95% CI: 1.03-1.12) times the odds of preterm birth and 1.07 (95% CI: 1.02-1.11) times the odds of low birthweight than mothers residing in counties with the least reliance on fees and fines, controlling for individual- and county-level covariates. The addition of countylevel racial composition, and the Index of Concentration at the Extremes (ICE), reduced these associations yet remained statistically significant. Future studies should continue to examine how racist, exploitative revenue generation through police and court activities influences the health of residents.

Improving The Measurement Of Structural Racism To Achieve Antiracist Health Policy.

Antiracist health policy research requires methodological innovation that creates equity-centered and antiracist solutions to health inequities by centering the complexities and insidiousness of structural racism. The development of effective health policy and health equity interventions requires sound empirical characterization of the nature of structural racism and its impact on public health. However, there is a disconnect between the conceptualization and measurement of structural racism in the public health literature. Given that structural racism is a system of interconnected institutions that operates with a set of racialized rules that maintain White supremacy, how can anyone accurately measure its insidiousness? This article highlights methodological approaches that will move the field forward in its ability to validly measure structural racism for the purposes of achieving health equity. We identify three key areas that require scholarly attention to advance antiracist health policy research: historical context, geographical context, and theory-based novel quantitative and qualitative methods that capture the multifaceted and systemic properties of structural racism as well as other systems of oppression.

Racial/Ethnic Differences in Burnout: a Systematic Review.

BACKGROUND: Awareness of burnout and its implications within the medical field has been growing. However, an understanding of the prevalence and consequences of burnout among underrepresented minority (URM), specifically underrepresented minority in medicine (UiM) populations, is not readily available. OBJECTIVE: To examine literature investigating burnout among UiM compared to non-UiM, with particular attention to which measures of burnout are currently being used for which racial/ethnic groups. METHODS: The authors identified peer-reviewed articles, published in English through systematic examination using PubMed, PsycINFO, Countway Discovery Medicine, and Web of Science databases. Studies meeting the inclusion criteria were summarized and study quality was assessed. RESULTS: Sixteen studies assessing racial/ethnic differences in burnout were eligible for inclusion. Nearly all studies were cross-sectional (n = 15) in design and conducted among populations in North America (n = 15). Most studies examined burnout among medical students or physicians and used the Maslach Burnout Inventory. Differences in burnout among UiM and non-UiM are inconclusive, although several studies have nuanced findings. CONCLUSION: Increased focus on burnout measurement, conceptualization, and mitigation among UiM populations may be useful in improving recruitment, retention, and thriving.

Gestational exposure to fatal police violence and pregnancy loss in US core based statistical areas, 2013-2015.

BACKGROUND: Fatal police violence in the United States disproportionately affects Black, Native American, and Hispanic people, and for these groups it is a racially oppressive population-level stressor that we hypothesize increases the risk of pregnancy loss. Focusing on core based statical areas (CBSAs) surrounding small and large urban centers, we accordingly tested whether gestational exposure to fatal police violence decreased the number of live births, which is reflective of a rise in lost pregnancies. METHODS: Our observational study linked microdata for all births (N = 7,709,300) in 520 CBSAs with at least one incident of fatal police violence in 2013-2015 to Fatal Encounters, a database that prospectively identified 2594 police-related fatalities using online media reports and public records. We estimated the association between month-to-month fatal police violence and conceptions resulting in live births using distributed lag quasi-Poisson models with CBSA-level fixed effects, adjusted for seasonality and stratified by maternal race/ethnicity. FINDINGS: For each additional police-related fatality that occurred in the first through sixth months of gestation, we observed a 0.14% decrease (95% confidence interval: 0.05%, 0.23%) in the total number of live births within CBSAs, and a 0.29% decrease in births to Black women (95% CI: 0.11%, 0.48%). The association was null for births to White women. INTERPRETATION: Our findings suggest fatal police violence may have population-level consequences for pregnancy loss and adds to the evidence regarding the importance of preventing these fatalities.

Racial and Ethnic Differences in Multigene Hereditary Cancer Panel Test Results for Women With Breast Cancer.

To evaluate the racial and ethnic differences in prevalence of germline pathogenic variants (PVs) and the effect of race and ethnicity on breast cancer (BC) risk among carriers, results of multigene testing of 77 900 women with BC (non-Hispanic White [NHW] = 57 003; Ashkenazi-Jewish = 4798; Black = 6722; Hispanic = 5194; and Asian = 4183) were analyzed, and the frequency of PVs in each gene were compared between BC patients (cases) and race- and ethnicity-matched gnomAD reference controls. Compared with NHWs, BRCA1 PVs were enriched in Ashkenazi-Jews and Hispanics, whereas CHEK2 PVs were statistically significantly lower in Blacks, Hispanics, and Asians (all 2-sided P < .05). In case-control studies, BARD1 PVs were associated with high risks (odds ratio > 4.00) of BC in Blacks, Hispanics, and Asians; ATM PVs were associated with increased risk of BC among all races and ethnicities except Asians, whereas CHEK2 and BRIP1 PVs were associated with increased risk of BC among NHWs and Hispanics only. These findings suggest a need for personalized management of BC risk in PV carriers based on race and ethnicity.

Race or racial segregation? Modification of the PM2.5 and cardiovascular mortality association.

BACKGROUND: Many studies have identified an inequitable distribution of exposure to PM2.5 (particulate matter less than 2.5 microns) by race. We investigated the association of PM2.5 and cardiovascular mortality considering both the decedents' race and neighborhood racial composition as potential modifiers. METHODS: We obtained geocoded cardiovascular mortality records of all black and white decedents from urban block-groups in Massachusetts between 2001 and 2011 (n = 130,863). We examined the association between PM2.5 and cardiovascular mortality, and assessed effect modification by three types of racial modifiers: decedents' race, census block-group percent black and white, and two novel measures of racial segregation. The Racial Residential Segregation (RRS) quantifies the concentration of non-Hispanic blacks and whites in each block-group. The Index of Racial Dissimilarity measures dissimilarity in non-Hispanic black and white racial distribution between the smaller census block-group and larger tract. RESULTS: We found a 2.35%(95%CI: 0.92%;3.79%) increase in mortality for each 10µg/m3 increase in two-day average exposure to PM2.5. The effect was modified by the block-group racial composition, with higher risks in block-groups with the highest percentage of black residents (interaction p-value = 0.04), and in block-groups with the lowest RRS (i.e. higher black to white resident ratio, interaction p-value = 0.072). Racial dissimilarity did not modify the associations. CONCLUSION: Current levels of PM2.5 are associated with increased cardiovascular deaths in Massachusetts, with different risks between areas with different racial composition and segregation. This suggests that pollution reductions in neighborhoods with the highest percentage of non-Hispanic blacks would be most beneficial in reducing cardiovascular mortality and disparities.

Splicing profile by capture RNA-seq identifies pathogenic germline variants in tumor suppressor genes.

Germline variants in tumor suppressor genes (TSGs) can result in RNA mis-splicing and predisposition to cancer. However, identification of variants that impact splicing remains a challenge, contributing to a substantial proportion of patients with suspected hereditary cancer syndromes remaining without a molecular diagnosis. To address this, we used capture RNA-sequencing (RNA-seq) to generate a splicing profile of 18 TSGs (APC, ATM, BRCA1, BRCA2, BRIP1, CDH1, CHEK2, MLH1, MSH2, MSH6, MUTYH, NF1, PALB2, PMS2, PTEN, RAD51C, RAD51D, and TP53) in 345 whole-blood samples from healthy donors. We subsequently demonstrated that this approach can detect mis-splicing by comparing splicing profiles from the control dataset to profiles generated from whole blood of individuals previously identified with pathogenic germline splicing variants in these genes. To assess the utility of our TSG splicing profile to prospectively identify pathogenic splicing variants, we performed concurrent capture DNA and RNA-seq in a cohort of 1000 patients with suspected hereditary cancer syndromes. This approach improved the diagnostic yield in this cohort, resulting in a 9.1% relative increase in the detection of pathogenic variants, demonstrating the utility of performing simultaneous DNA and RNA genetic testing in a clinical context.

Understanding how discrimination can affect health.

BACKGROUND: To provide an overview of the empirical research linking self-reports of racial discrimination to health status and health service utilization. METHODS: A review of literature reviews and meta-analyses published from January 2013 to 2019 was conducted using PubMed, PsycINFO, Sociological Abstracts, and Web of Science. Articles were considered for inclusion using the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) framework. RESULTS: Twenty-nine studies met the criteria for review. Both domestic and international studies find that experiences of discrimination reported by adults are adversely related to mental health and indicators of physical health, including preclinical indicators of disease, health behaviors, utilization of care, and adherence to medical regimens. Emerging evidence also suggests that discrimination can affect the health of children and adolescents and that at least some of its adverse effects may be ameliorated by the presence of psychosocial resources. CONCLUSIONS: Increasing evidence indicates that racial discrimination is an emerging risk factor for disease and a contributor to racial disparities in health. Attention is needed to strengthen research gaps and to advance our understanding of the optimal interventions that can reduce the negative effects of discrimination.