The authors examined the impact of cumulative neighborhood risk of psychosocial stress on allostatic load (AL) among adolescents as a mechanism through which life stress, including neighborhood conditions, may affect health and health inequities. They conducted multilevel analyses, weighted for sampling and propensity score-matched, among adolescents aged 12–20 years in the National Health and Nutrition Examination Survey (1999–2006). Individuals (first level, n = 11,886) were nested within families/households (second level, n = 6,696) and then census tracts (third level, n = 2,191) for examination of the contextual effect of cumulative neighborhood risk environment on AL. Approximately 35% of adolescents had 2 or more biomarkers of AL. A significant amount of variance in AL was explained at the neighborhood level. The likelihood of having a high AL was approximately 10% higher for adolescents living in medium-cumulative-risk neighborhoods (adjusted odds ratio (OR) = 1.09, 95% confidence interval (CI): 1.08, 1.09), 28% higher for those living in high-risk neighborhoods (adjusted OR = 1.28, 95% CI: 1.27, 1.30), and 69% higher for those living in very-high-risk neighborhoods (adjusted OR = 1.69, 95% CI: 1.68, 1.70) as compared with adolescents living in low-risk areas. Effect modification was observed by both individual- and neighborhood-level sociodemographic factors. These findings offer support for the hypothesis that neighborhood risks may culminate in a range of biologically mediated negative health outcomes detectable in adolescents.

Before the age of 18 years, approximately two-thirds of children are exposed to multiple types of violence.¹ A greater understanding of the effect on children’s health owing to exposure to violence across socioecological contexts is critical, as differential exposure to social environmental conditions likely contributes mechanistically to health disparities.^2,3 Socioeconomically disadvantaged communities have higher exposure to violence, suggesting that the effects of such exposure also may be accentuated.^1,4 Exposure to violence may create persistent biological effects across multiple stress response systems (SRS), resulting in lasting physiological and psychological vulnerability.^5,6 There has been limited information on racial and socioeconomic differences in biological stress and antecedent factors among children,⁷ and few studies have examined within-race or socioeconomic differences in biological stress.

In this ecological study, we examined the associations between state-level income inequality and pregnancy-related mortality among non-Hispanic (NH) black and NH white populations across the US. We estimated total population and race-specific 5-year pregnancy-related mortality ratios in each state based on national death and live birth records from 2011 to 2015. We obtained data on Gini coefficients for income inequality and population-level characteristics from the US Census American Community Survey. Poisson regression with robust standard errors estimated pregnancy-related mortality rate ratios (RR) and 95% confidence intervals (CI) associated with a one unit increase in income inequality overall and separately within black and white populations. Adjusted linear regression models estimated the associations between income inequality and magnitude of the absolute and relative racial inequity in pregnancy-related mortality within states. Across all states, increasing contemporaneous income inequality was associated with a 15% and 5-year lagged inequality with 14% increase in pregnancy-related mortality among black women (aRR = 1.15, 95% CI = 1.05; 1.25 and aRR = 1.14, 95% CI = 1.04; 1.24, respectively) after controlling for states' racial compositions and socio-economic conditions. In addition, both lagged and contemporaneous income inequality were associated with larger absolute and relative racial inequities in pregnancy-related mortality. These findings highlight the role of contextual factors in contributing to pregnancy-related mortality among black women and the persistent racial inequity in maternal death in the US.

We examined the association between telomere length and prenatal tobacco exposure (PTE) in 104 children aged 4 to 14 years. Salivary telomere length (STL) was determined from salivary DNA using quantitative polymerase chain reaction. Of the children, 18% had maternal reported PTE. Mean STL was significantly lower among children with PTE (6.4 vs 7.5, P < .05). Findings extend the literature demonstrating the negative long-term effects of PTE to include a cellular marker of aging linked to multiple negative health outcomes.