A Model of Racial Residential History and Its Association with Self-Rated Health and Mortality Among Black and White Adults in the United States.
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ABSTRACT:
SUBMITTER: Ruel E
PROVIDER: S-EPMC2729931 | biostudies-other | 2009 Jul
REPOSITORIES: biostudies-other
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Project description:How do Mexicans of distinct racial backgrounds fit into the recognized patterns of racial health disparities? We conduct regression analyses using data from the 2000-2017 National Health Interview Survey to determine if Mexicans who self-identify as White or Black have a relative advantage or disadvantage in self-rated health in relation to Non-Hispanic (NH) Whites and Blacks in the U.S. Our results indicate that both Black Mexicans and White Mexicans have a significant disadvantage in relation to NH-Whites while White Mexicans have a slight advantage in relation to both NH-Blacks and Black Mexicans. Overall, our results suggest that studying health outcomes among Hispanics without considering race may mask inequalities not observed in the aggregate.
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Project description:The clinical presentation and outcome of sarcoidosis varies by race. However, the race difference in mortality outcome remains largely unknown.We studied mortality related to sarcoidosis from 1999 through 2010 by examining data on multiple causes of death from the National Center for Health Statistics. We compared the comorbid conditions between sarcoidosis-related deaths with deaths caused by car accidents (previously healthy control subjects) and rheumatoid arthritis (chronic disease control subjects) in both African Americans and Caucasians.From 1999 through 2010, sarcoidosis was reported as an immediate cause of death in 10,348 people in the United States with a combined overall mean age-adjusted mortality rate of 2.8 per 1 million person-years. Of these, 6,285 were African American and 3,984 Caucasian. The age-adjusted mortality rate for African Americans was 12 times higher than for Caucasians. African Americans died at an earlier age than Caucasians. African Americans living in the District of Columbia and North Carolina and Caucasians living in Vermont had higher mortality rates. Although the total sarcoidosis age-adjusted mortality rate had not changed over the 12 year period studied, this rate increased for Caucasians (R = 0.747, P = .005) but not for African Americans. Compared with the control groups, pulmonary hypertension was significantly more common in individuals with sarcoidosis.This nationwide population-based study exposes a significant difference in ethnicity and sex among people dying of sarcoidosis in the United States. Pulmonary hypertension investigation should be considered in all patients with sarcoidosis, especially African Americans.
| S-EPMC4314818 | biostudies-other
Project description:ObjectivesTo understand which causes of death are higher in black than white community-dwelling older adults and determine whether differences in baseline risk factors explain racial differences in mortality.DesignLongitudinal cohort study (Health, Aging, and Body Composition Study).SettingPittsburgh, Pennsylvania; and Memphis, Tennessee.ParticipantsBlack and white men and women aged 70 to 79 during recruitment (N=3,075; 48% men, 42% black) followed for a median of 13 years.MeasurementsA committee of physicians adjudicated cause of death, which was categorized as cardiovascular disease (CVD), stroke, cancer, dementia, pulmonary, infection, kidney, or other causes. Using competing risks regression, we examined whether known risk factors at baseline (demographic characteristics, smoking, body mass index, chronic diseases, physical function, cognition) could explain racial differences in cause-specific mortality risk.ResultsDuring follow-up, 1,991 (65%) participants died. Black participants died at higher rates from cancer (hazard ratio (HR)=1.36, 95% confidence interval (CI)=1.14-1.63), kidney disease (HR=2.09, 95% CI=1.16-3.74), stroke (HR=1.31, 95% CI=0.98-1.76); and CVD (HR=1.16, 95% CI=0.98-1.37). Poorer physical and cognitive performance at baseline among black participants explained most of the racial difference in risks of dying from kidney disease, stroke, and CVD but not cancer. When examining types of cancer deaths, black participants died at higher rates from multiple myeloma, pancreatic cancer, and prostate cancer, which baseline risk factors did not explain either.ConclusionFactors contributing to poorer physical and cognitive performance in similarly aged black men and women could be targets to reduce excess mortality from CVD, stroke, and kidney disease. More work is needed to identify factors contributing to cancer mortality disparities.
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Project description:BackgroundBlack populations in the United States are being disproportionately affected by the COVID-19 pandemic, but the increased mortality burden after accounting for health and other demographic characteristics is not well understood. We examined characteristics of individuals who died from COVID-19 in Michigan by race stratified by their age, sex and comorbidity prevalence to illustrate and understand this disparity in mortality risk.MethodsWe evaluate COVID-19 mortality in Michigan by demographic and health characteristics, using individual-level linked death certificate and surveillance data collected by the Michigan Department of Health and Human Services from March 16 to October 26, 2020. We identified differences in demographics and comorbidity prevalence across race among individuals who died from COVID-19 and calculated mortality rates by age, sex, race, and number of comorbidities.FindingsAmong the 6,065 COVID-19 related deaths in Michigan, Black individuals are experiencing 3·6 times the mortality rate of White individuals (p<0.001), with a mortality rate for Black individuals under 65 years without comorbidities that is 12·6 times that of their White counterparts (p<0.001). After accounting for age, race, sex, and number of comorbidities, we find that Black individuals in all strata are at higher risk of COVID-19 mortality than their White counterparts.InterpretationOur findings demonstrate that Black populations are disproportionately burdened by COVID-19 mortality, even after accounting for demographic and underlying health characteristics. We highlight how disparities across race, which result from systemic racism, are compounded in crises.FundingASP, AP and APG were funded by NSF Expeditions grant 1918784, NIH grant 1R01AI151176-01, NSF Rapid Response Research for COVID-19 grant RAPID-2027755, and the Notsew Orm Sands Foundation. MCF was supported by NIH grant K01AI141576.
| S-EPMC7933264 | biostudies-literature
Project description:Close kin provide many important functions as adults age, affecting health, financial well-being, and happiness. Those without kin report higher rates of loneliness and experience elevated risks of chronic illness and nursing facility placement. Historical racial differences and recent shifts in core demographic rates suggest that white and black older adults in the United States may have unequal availability of close kin and that this gap in availability will widen in the coming decades. Whereas prior work explores the changing composition and size of the childless population or those without spouses, here we consider the kinless population of older adults with no living close family members and how this burden is changing for different race and sex groups. Using demographic microsimulation and the United States Census Bureau's recent national projections of core demographic rates by race, we examine two definitions of kinlessness: those without a partner or living children, and those without a partner, children, siblings, or parents. Our results suggest dramatic growth in the size of the kinless population as well as increasing racial disparities in percentages kinless. These conclusions are driven by declines in marriage and are robust to different assumptions about the future trajectory of divorce rates or growth in nonmarital partnerships. Our findings draw attention to the potential expansion of older adult loneliness, which is increasingly considered a threat to population health, and the unequal burden kinlessness may place on black Americans.
| S-EPMC5651770 | biostudies-literature
Project description:Against the backdrop of late 20th century declines in heart disease mortality in the United States, race-specific rates diverged because of slower declines among blacks compared with whites. To characterize the temporal dynamics of emerging black-white racial disparities in heart disease mortality, we decomposed race-sex-specific trends in an age-period-cohort (APC) analysis of US mortality data for all diseases of the heart among adults aged ≥35 years from 1973 to 2010. The black-white gap was largest among adults aged 35-59 years (rate ratios ranged from 1.2 to 2.7 for men and from 2.3 to 4.0 for women) and widened with successive birth cohorts, particularly for men. APC model estimates suggested strong independent trends across generations ("cohort effects") but only modest period changes. Among men, cohort-specific black-white racial differences emerged in the 1920-1960 birth cohorts. The apparent strength of the cohort trends raises questions about life-course inequalities in the social and health environments experienced by blacks and whites which could have affected their biomedical and behavioral risk factors for heart disease. The APC results suggest that the genesis of racial disparities is neither static nor restricted to a single time scale such as age or period, and they support the importance of equity in life-course exposures for reducing racial disparities in heart disease.
| S-EPMC4528952 | biostudies-literature
Project description:PurposeRacism, whether defined at individual, interpersonal, or structural levels, is associated with poor health among Blacks. This association may arise because exposure to racism causes poor health, but geographic mobility patterns pose an alternative explanation-namely, Black individuals with better health and resources can move away from racist environments.MethodsWe examine the evidence for selection effects using nationally representative, longitudinal data (1990-2009) from the Panel Study on Income Dynamics (n = 33,852). We conceptualized state-level racial animus as an ecologic measure of racism and operationalized it as the percent of racially-charged Google search terms in each state.ResultsAmong those who move out of state, Blacks reporting good self-rated health (SRH) are more likely to move to a state with less racial animus than Blacks reporting poor SRH (P = .01), providing evidence for at least some selection into environments with less racial animus. However, among Blacks who moved states, over 80% moved to a state within the same quartile of racial animus, and fewer than 5% resided in states with the lowest level of racial animus.ConclusionsGeographic mobility patterns are therefore likely to explain only a small part of the relationship between racial animus and SRH. These results require replication with alternative measures of racist attitudes and health outcomes.
| S-EPMC5610069 | biostudies-literature
Project description:BackgroundDisparities in insulin resistance between Black and White adults in the United States are well documented, yet relatively little is known about the psychosocial or biological antecedents of these inequities. The current study examined childhood adversity and contemporaneous psychosocial stressors in adulthood as possible mediators of the racial disparity in insulin resistance. Inflammatory and hypothalamic-pituitary adrenal (HPA) axis mechanisms implicated in associations between lifespan stress exposure and insulin resistance were also considered.MethodsData were derived from the biomarker component of the Midlife in the United States Study (N = 1170, 20% Black, 56% female, Mean age = 54.7 years, SD = 11.6). A homeostatic model assessment of insulin resistance (HOMA-IR) was calculated from fasting glucose and insulin concentrations. Twelve risk factors relating to household dysfunction, socioeconomic disadvantage, and maltreatment were sum scored to index childhood adversity. Measures of adult stress included socioeconomic adversity, major stressful events, everyday discrimination, and lifetime discrimination.ResultsLevels of insulin resistance were higher among Black than White adults. Childhood adversity was positively associated with HOMA-IR, and attenuated 18% of the race difference. Measures of adult stress mediated 33% of the association between childhood adversity and HOMA-IR, and accounted for an additional 47% of the race difference. Higher inflammation and lower nocturnal cortisol both played an important role in mediating the association between stress exposure and HOMA-IR.ConclusionsFindings are consistent with prior research showing that childhood adversity and adult stress are salient predictors of glucose metabolism, and extend this work by showing that lifespan stress exposures attenuate a significant portion of the Black-White disparity in HOMA-IR. Results also suggest stress effects on insulin resistance through inflammatory and HPA-axis pathways.
| S-EPMC6635018 | biostudies-literature
Project description:Background Life expectancy has been higher for Hispanic versus non-Hispanic White (NHW) individuals; however, data are limited on cardiovascular disease (CVD) mortality. Method and Results Using the Centers for Disease Control and Prevention's Wide-Ranging Online Data for Epidemiologic Research death certificate database (1999-2018), we compared age-adjusted mortality rates for total CVD and its subtypes (ischemic heart disease, stroke, heart failure, hypertensive heart disease, other CVD), and average annual percentage changes among Hispanic and NHW adults. The age-adjusted mortality rate per 100 000 was lower for Hispanic than NHW adults for total CVD (186.4 versus 254.6; P<0.001) and its subtypes. Between 1999 and 2018, mortality decline was higher in Hispanic than NHW adults for total CVD (average annual percentage change [AAPC], -2.90 versus -2.41) and ischemic heart disease (AAPC: -4.44 versus -3.82) (P<0.001). In contrast, stroke mortality decline was slower in Hispanic versus NHW adults (AAPC: -2.05 versus -2.60; P<0.05). Stroke mortality increased in Hispanic but stalled in NHW adults since 2011 (AAPC: 0.79 versus -0.09). For ischemic heart disease (AAPC: -0.80 versus -1.85) and stroke (AAPC: -1.32 versus -1.43) mortality decline decelerated more for Hispanic than NHW adults aged <45 years (P<0.05). For heart failure, Hispanic adults aged <45 (3.55 versus 2.16) and 45 to 64 (1.88 versus 1.54) showed greater rise in age-adjusted mortality rate than NHW individuals (P<0.05). Age-adjusted heart failure mortality rate also accelerated in Hispanic versus NHW men (1.00 versus 0.67; P<0.001). Conclusions Disaggregating data by CVD subtype and demographics unmasked heterogeneities in CVD mortality between Hispanic and NHW adults. NHW adults had greater CVD mortality rates and slower decline than Hispanic adults, whereas marked demographic differences in mortality signaled concerning trends among the Hispanic versus NHW population.
| S-EPMC9075497 | biostudies-literature
Project description:Black Veterans have higher a incidence of localized and metastatic prostate cancer compared to White Veterans yet are underrepresented in reports of frequencies of somatic and germline alterations. This retrospective analysis of somatic and putative germline alterations was conducted in a large cohort of Veterans with prostate cancer (N = 835 Black, 1613 White) who underwent next generation sequencing through the VA Precision Oncology Program, which facilitates molecular testing for Veterans with metastatic cancer. No differences were observed in gene alterations for FDA approved targetable therapies (13.5% in Black Veterans vs. 15.5% in White Veterans, P = .21), nor in any potentially actionable alterations (25.5% vs. 28.7%, P =.1). Black Veterans had higher rates of BRAF (5.5% vs. 2.6%, P < .001) alterations, White Veterans TMPRSS2 fusions (27.2% vs. 11.7%, P < .0001). Putative germline alteration rates were higher in White Veterans (12.0% vs. 6.1%, P < .0001). Racial disparities in outcome are unlikely attributable to acquired somatic alterations in actionable pathways.
| S-EPMC10243786 | biostudies-literature