Air Pollution and Mortality at the Intersection of Race and Social Class.

BACKGROUND: Black Americans are exposed to higher annual levels of air pollution containing fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm [PM2.5]) than White Americans and may be more susceptible to its health effects. Low-income Americans may also be more susceptible to PM2.5 pollution than high-income Americans. Because information is lacking on exposure-response curves for PM2.5 exposure and mortality among marginalized subpopulations categorized according to both race and socioeconomic position, the Environmental Protection Agency lacks important evidence to inform its regulatory rulemaking for PM2.5 standards. METHODS: We analyzed 623 million person-years of Medicare data from 73 million persons 65 years of age or older from 2000 through 2016 to estimate associations between annual PM2.5 exposure and mortality in subpopulations defined simultaneously by racial identity (Black vs. White) and income level (Medicaid eligible vs. ineligible). RESULTS: Lower PM2.5 exposure was associated with lower mortality in the full population, but marginalized subpopulations appeared to benefit more as PM2.5 levels decreased. For example, the hazard ratio associated with decreasing PM2.5 from 12 µg per cubic meter to 8 µg per cubic meter for the White higher-income subpopulation was 0.963 (95% confidence interval [CI], 0.955 to 0.970), whereas equivalent hazard ratios for marginalized subpopulations were lower: 0.931 (95% CI, 0.909 to 0.953) for the Black higher-income subpopulation, 0.940 (95% CI, 0.931 to 0.948) for the White low-income subpopulation, and 0.939 (95% CI, 0.921 to 0.957) for the Black low-income subpopulation. CONCLUSIONS: Higher-income Black persons, low-income White persons, and low-income Black persons may benefit more from lower PM2.5 levels than higher-income White persons. These findings underscore the importance of considering racial identity and income together when assessing health inequities. (Funded by the National Institutes of Health and the Alfred P. Sloan Foundation.).

Can the gap in Aboriginal outcomes be explained by DOHaD.

In Australia, there are two distinct populations, each with vastly disparate health outcomes: Aboriginal and Torres Strait Islander People and non-Aboriginal Australians. Aboriginal Australians have significantly higher rates of health and socioeconomic disadvantage, and Aboriginal babies are also more likely to be born low birth weight or growth restricted. The Developmental Origins of Health and Disease (DOHaD) hypothesis advocates that a sub-optimal intrauterine environment, often manifested as diminished foetal growth, during critical periods of foetal development has the potential to alter the risk of non-communicable disease in the offspring. A better understanding of the role of the intrauterine environment and subsequent developmental programming, in response to both transgenerational and immediate stimuli, in Aboriginal Australians remains a relatively unexplored field and may provide insights into the prevailing health disparities between Aboriginal and non-Aboriginal children. This narrative review explores the role of DOHaD in explaining the ongoing disadvantage experienced by Aboriginal People in today's society through a detailed discussion of the literature on the association between foetal growth, as a proxy for the quality of the intrauterine environment, and outcomes in the offspring including perinatal health, early life development and childhood education. The literature largely supports this hypothesis and this review therefore has potential implications for policy makers not only in Australia but also in other countries that have minority and Indigenous populations who suffer disproportionate disadvantage such as the United States, Canada and New Zealand.

Trends in Susceptibility to Smoking by Race and Ethnicity.

OBJECTIVES: Examine racial/ethnic differences in smoking susceptibility among US youth nonsmokers over time and age. METHODS: We used nationally representative samples of youths who never tried cigarettes (N = 143 917; age, 9-21, mean, 14.01 years) from National Youth Tobacco Survey, 1999 to 2014. We used time-varying effect modeling to examine nonlinear trends in smoking susceptibility adjusted for demographics, living with smokers, and exposure to tobacco advertising. RESULTS: Compared with non-Hispanic whites (NHWs), Hispanics were more susceptible to smoking from 1999 to 2014 (highest adjusted odds ratio [aOR], 1.67 in 2012). Non-Hispanic blacks were less susceptible to smoking than NHWs from 2000 to 2009 (lowest aOR, 0.80 in 2003-2005). Non-Hispanic Asian Americans were less susceptible to smoking from 2000 to 2009 (aOR, 0.83), after which they did not differ from NHWs. Other non-Hispanics were more susceptible to smoking than NHWs from 2012 to 2014 (highest aOR, 1.40 in 2014). Compared with NHWs, non-Hispanic blacks and other non-Hispanics were more susceptible to smoking at ages 11 to 13 (highest aOR, 1.22 at age 11.5 ) and 12 to 14 (highest aOR, 1.27 at age 12 ), respectively. Hispanics were more susceptible to smoking throughout adolescence peaking at age 12 (aOR, 1.60) and age 16.5 (aOR, 1.46). Non-Hispanic Asian Americans were less susceptible to smoking at ages 11 to 15 (lowest aOR, 0.76 at ages 11-13 ). CONCLUSIONS: Racial/ethnic disparities in smoking susceptibility persisted over time among US youth nonsmokers, especially at ages 11 to 13 . Interventions to combat smoking susceptibility are needed.

Racial differences between blacks and whites with systemic sclerosis.

PURPOSE OF REVIEW: Racial disparities appear to exist in the susceptibility and severity of systemic sclerosis (SSc, scleroderma) and are responsible for a greater health burden in blacks as compared with whites. Disparities in socioeconomic status and access to healthcare do not sufficiently explain the observed differences in prevalence and mortality. It is important to determine whether there might be a biologic basis for the racial disparities observed in SSc. RECENT FINDINGS: We present data to suggest that the increased susceptibility and severity of SSc in blacks may result in part from an imbalance of profibrotic and antifibrotic factors. Racial differences in the expression of transforming growth factor-ß1 (TGF-ß1) and caveolin-1, as well as differences in the expression of hepatocyte growth factor and PPAR-γ, have been demonstrated in blacks with SSc, as well as in normal black individuals. A genetic predisposition to fibrosis may account for much of the racial disparities between black and white patients with SSc. SUMMARY: A better understanding of the biologic basis for the racial disparities observed in SSc may lead to improved therapies, along with the recognition that different therapies may need to be adapted for different groups of patients.

Racial and sex differences in chronic obstructive pulmonary disease susceptibility, diagnosis, and treatment.

PURPOSE OF REVIEW: Chronic obstructive pulmonary disease (COPD) is an increasing cause of morbidity and mortality worldwide. Although COPD has historically been considered a disease of white male smokers, it now clearly impacts both sexes and all races, with mortality rising fastest in women and African-Americans. Given the scarcity of data about non-African-American minorities, this review will focus on the disparities in COPD susceptibility, diagnosis, and treatment between men and women and between African-Americans and whites. RECENT FINDINGS: Although the changing epidemiology of COPD in part reflects the changing epidemiology of cigarette smoking, there are data suggesting that women and African-Americans may be particularly susceptible to tobacco smoke and that the diagnosis, treatment, and natural history of the disease are influenced by race and sex. SUMMARY: The possibility that sex or race or both, may influence COPD susceptibility and progression is of critical importance, and may mean that the potential future impact of the disease has been underestimated. Unfortunately, our understanding of these differences and the efficacy of standard COPD treatments in women and minorities remains limited by the low enrollment in clinical trials.

Prevalence of rubella susceptibility among pregnant mothers in a community-based antenatal clinic in Malaysia: a cross-sectional study.

INTRODUCTION: routine rubella antibody screening is not done for antenatal mothers in community health clinics in Malaysia. However, congenital rubella syndrome has persisted with its associated health burden. OBJECTIVES: to determine the prevalence of rubella susceptibility among pregnant mothers and its associated risk factors. METHODOLOGY: a cross-sectional study was carried out in the Petaling district, Selangor, Malaysia, where 500 pregnant mothers were recruited, and face-to-face interviews were conducted. Rubella IgG tests were performed. RESULTS: the prevalence of rubella susceptibility among pregnant mothers was 11.4%. Using logistic regression, a history of not having received rubella vaccination or having unknown rubella vaccination status was found to be a significant predictor for mothers to be rubella susceptible (odds ratio = 2.691; 95% confidence interval = 1.539-4.207). CONCLUSIONS: routine rubella IgG screening tests need to be offered to all antenatal mothers in view of the high prevalence found.

An assessment of renal failure in an SLE cohort with special reference to ethnicity, over a 25-year period.

OBJECTIVES: Although the prognosis for patients with renal lupus has improved, a small number still progress to renal failure. Studies from the USA have found it difficult to distinguish whether the higher rate of renal failure in African-Americans is due to genetic or socio-economic factors. Our aim was to identify ethnic and other factors in a UK lupus cohort that contribute to renal failure. METHODS: The University College London (UCL) Hospitals lupus cohort of 401 patients (Whites 64%, Blacks 19%), followed since 1978, has 127 patients with renal disease, of whom 21 have gone into renal failure. We determined the characteristics and possible causes of renal failure in this group. Black patients were disproportionately represented in the renal failure group (62% vs 19% for Whites). RESULTS: Those in the renal failure group had persistently low C3 compared with the renal disease cohort. A high proportion of patients in the renal failure group were felt to be non-adherent to treatment. CONCLUSIONS: Given that health-care for patients in the UK is free at the point of delivery, we postulate that in our cohort genetic factors rather than socio-economic status are likely to be more significant in causing renal failure. However, there may be cultural and other reasons for this, which requires further study.