Population projections for U.S. counties by age, sex, and race controlled to shared socioeconomic pathway.
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ABSTRACT:
SUBMITTER: Hauer ME
PROVIDER: S-EPMC6362894 | biostudies-literature | 2019 Feb
REPOSITORIES: biostudies-literature
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Project description:Background:Higher socioeconomic status (SES) indicators such as educational attainment and income reduce the risk of chronic lung diseases (CLDs) such as Chronic Obstructive Pulmonary Disease (COPD), emphysema, chronic bronchitis, and asthma. Marginalization-related Diminished Returns (MDRs) refer to smaller health benefits of high SES for marginalized populations such as racial and ethnic minorities compared to the socially privileged groups such as non-Hispanic Whites. It is still unknown, however, if MDRs also apply to the effects of education and income on CLDs. Purpose:Using a nationally representative sample, the current study explored racial and ethnic variation in the associations between educational attainment and income and CLDs among American adults. Methods:In this study, we analyzed data (n = 25,659) from a nationally representative survey of American adults in 2013 and 2014. Wave one of the Population Assessment of Tobacco and Health (PATH)-Adult study was used. The independent variables were educational attainment (less than high school = 1, high school graduate = 2, and college graduate =3) and income (living out of poverty =1, living in poverty = 0). The dependent variable was any CLDs (i.e., COPD, emphysema, chronic bronchitis, and asthma). Age, gender, employment, and region were the covariates. Race and ethnicity were the moderators. Logistic regressions were fitted to analyze the data. Results:Individuals with higher educational attainment and those with higher income (who lived out of poverty) had lower odds of CLDs. Race and ethnicity showed statistically significant interactions with educational attainment and income, suggesting that the protective effects of high education and income on reducing odds of CLDs were smaller for Blacks and Hispanics than for non-Hispanic Whites. Conclusions:Education and income better reduce the risk of CLDs among Whites than Hispanics and Blacks. That means we should expect disproportionately higher than expected risk of CLDs in Hispanics and Blacks with high SES. Future research should test if high levels of environmental risk factors contribute to the high risk of CLDs in high income and highly educated Black and Hispanic Americans. Policy makers should not reduce health inequalities to SES gaps because disparities sustain across SES levels, with high SES Blacks and Hispanics remaining at risk of health problems.
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Project description:IntroductionIdeal cardiovascular health is present in <50% of children and <1% of adults, yet its prevalence from adolescence through adulthood has not been fully evaluated. This study characterizes the association of age with ideal cardiovascular health and compares these associations across sex, race/ethnicity, and SES subgroups.MethodsThis study, conducted in 2020, analyzed adolescents and adults aged 12-79 years from the cross-sectional National Health and Nutrition Examination Survey 2005-2016 (N=38,706). Polynomial models were used to model the association of age with ideal cardiovascular health, defined using the American Heart Association's Life's Simple 7 criteria (scales 0-14, with higher values indicating better cardiovascular health).ResultsMean cardiovascular health was lower with increasing age, starting in early adolescence and dropping to a nadir by age 60 years before stabilizing. At age 20 years, only 45% of adults had ideal cardiovascular health (≥5 ideal cardiovascular health metrics), and >50% of adults had poor cardiovascular health (≤2 ideal cardiovascular health metrics) at age 53 years. Women had higher mean cardiovascular health than men in early life but lower mean cardiovascular health from age 60 years onward. Mean cardiovascular health scores were highest for non-Hispanic White and higher-income adults and lowest for non-Hispanic Black and low-income adults across all ages. Mean cardiovascular health scores fell from intermediate to poor levels approximately 30 years earlier for non-Hispanic Black than for non-Hispanic White adults and approximately 35 years earlier for low-income adults than in higher-income adults.ConclusionsCardiovascular health scores are lower with increasing age from early adolescence through adulthood. Race/ethnicity and income disparities in cardiovascular health are observed at young ages and are more profound at older ages.
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Project description:Recently, we developed an improved comet assay protocol for evaluating single-strand break repair capacity (SSB-RC) in unstimulated cryopreserved human peripheral blood mononuclear cells (PBMCs). This methodology facilitates control of interexperimental variability [A.R. Trzeciak, J. Barnes, M.K. Evans, A modified alkaline comet assay for measuring DNA repair capacity in human populations. Radiat. Res. 169 (2008) 110-121]. The fast component of SSB repair (F-SSB-RC) was assessed using a novel parameter, the initial rate of DNA repair, and the widely used half-time of DNA repair. The slow component of SSB repair (S-SSB-RC) was estimated using the residual DNA damage after 60 min. We have examined repair of gamma-radiation-induced DNA damage in PBMCs from four age-matched groups of male and female whites and African-Americans between ages 30 and 64. There is an increase in F-SSB-RC with age in white females (P<0.01) and nonsignificant decrease in F-SSB-RC in African-American females (P=0.061). F-SSB-RC is lower in white females than in white males (P<0.01). There is a decrease in F-SSB-RC with age in African-American females as compared to white females (P<0.002) and African-American males (nonsignificant, P=0.059). Age, sex, and race had a similar effect on intercellular variability of DNA damage in gamma-irradiated and repairing PBMCs. Our findings suggest that age, sex, and race influence SSB-RC as measured by the alkaline comet assay. SSB-RC may be a useful clinical biomarker.
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Project description:BackgroundPopulation-based survival studies of adult acute myeloid leukemia (AML) have not simultaneously evaluated age at diagnosis, race and ethnicity, sex, calendar period or AML subtypes/subgroups among chemotherapy-treated patients.MethodsFor 28,473 chemotherapy-treated AML patients diagnosed at ages ≥20 years in population-based cancer registry areas of the Surveillance, Epidemiology, and End Results Program (2001-2018, followed through 2019), we evaluated 1-month through 5-year relative survival (RS) and 95% confidence intervals (95% CI) using the actuarial method in the SEER∗Stat Survival Session and overall survival (OS) using multivariable Cox regression to estimate proportional hazard ratios (HR) and 95% CI.FindingsRS decreased with increasing age (20-39, 40-59, 60-74, 75-84, ≥85 years) at AML diagnosis. RS declined substantially within the first month and, except for acute promyelocytic leukemia, decreasing patterns continued thereafter for core binding factor AML, AML with antecedent condition/therapy, and all other AML. For all ages, acute promyelocytic leukemia RS stabilized after the first year. For total AML the hazard of death was significantly increased for non-Hispanic (NH)-Black (HR = 1.18, 95% CI = 1.12-1.24) and NH-Pacific Islander patients (HR = 1.31, 95% CI = 1.11-1.55) compared with NH-White patients. In contrast, NH-Asian and Hispanic patients had similar OS to NH-White patients across all ages and most AML subgroups. Males had significantly inferior survival to females with some exceptions. Compared to 2001-2006, in 2013-2018 OS improved for all age and AML subgroups.InterpretationChemotherapy-treated U.S. adults with AML have notable differences in survival by age, race and ethnicity, sex, calendar-year period, and AML subgroup. Despite survival gains over time, our findings highlight the need for improving early outcomes across all AML subgroups, older ages, and Black and Pacific Islander patients and long-term outcomes among most treated groups.FundingIntramural Research Program of the U.S. National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics, and the U.S. Food and Drug Administration, Center for Drug Evaluation and Research, Office of Surveillance and Epidemiology.
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