Socioeconomic Disadvantage, Neighborhood Belonging, and Inflammation Among Adolescents.

OBJECTIVE: Childhood socioeconomic disadvantage is associated with a host of adverse health outcomes across the lifespan. However, there is increasing interest in identifying factors that may promote resilience to disadvantage's effects on health. One promising candidate in this regard is a sense of neighborhood belonging, which could offset health risks by providing a sense of connection to others, as well as a sense of belonging to a community larger than oneself. METHODS: In a sample of 245 adolescents (age: M = 15.98 years, SD = 0.54; sex: 64.1% female; race: 41.6% White, 37.6% Black/African American, 9.8% Other; ethnicity: 68.6% non-Hispanic), we examined neighborhood belonging as a moderator of the relationship between socioeconomic disadvantage (measured on a 0-5-point scale, M = 1.21; SD = 1.36) and low-grade inflammation (measured via a composite of circulating inflammatory biomarkers including IL-6, IL-8, IL-10, TNF-a, CRP, and suPAR). Covariates included age, sex, race/ethnicity, and pubertal status. RESULTS: Neighborhood belonging buffered the relationship between socioeconomic disadvantage and low-grade inflammation, a key mechanistic pathway to multiple chronic diseases. Specifically, there was a positive relationship between socioeconomic disadvantage and low-grade inflammation among individuals with low neighborhood belonging, but not among individuals with high neighborhood belonging. CONCLUSIONS: These findings suggest that neighborhood belonging is one type of social connection factor that can mitigate the relationship between socioeconomic disadvantage and low-grade inflammation in youth.

Ambient PM2.5 and specific sources increase inflammatory cytokine responses to stimulators and reduce sensitivity to inhibitors.

Ambient exposure to fine particulate matter (PM2.5) is associated with increased morbidity and mortality from multiple diseases. Recent observations suggest the hypothesis that trained immunity contributes to these risks, by demonstrating that ambient PM2.5 sensitizes innate immune cells to mount larger inflammatory response to subsequent bacterial stimuli. However, little is known about how general and durable this sensitization phenomenon is, and whether specific sources of PM2.5 are responsible. Here we consider these issues in a longitudinal study of children. The sample consisted of 277 children (mean age 13.92 years; 63.8% female; 38.4% Black; 32.2% Latinx) who completed baseline visits and were re-assessed two years later. Fasting whole blood was ex vivo incubated with 4 stimulating agents reflecting microbial and sterile triggers of inflammation, and with 2 inhibitory agents, followed by assays for IL-1ß, IL-6, IL-8, and TNF-α. Blood also was assayed for 6 circulating biomarkers of low-grade inflammation: C-reactive protein, interleukin-6, -8, and -10, tumor necrosis factor-α, and soluble urokinase-type plasminogen activator receptor. Using machine learning, levels of 15 p.m.2.5 constituents were estimated for a 50 m grid around children's homes. Models were adjusted for age, sex, race, pubertal status, and household income. In cross-sectional analyses, higher neighborhood PM2.5 was associated with larger cytokine responses to the four stimulating agents. These associations were strongest for constituents released by motor vehicles and soil/crustal dust. In longitudinal analyses, residential PM2.5 was associated with declining sensitivity to inhibitory agents; this pattern was strongest for constituents from fuel/biomass combustion and motor vehicles. By contrast, PM2.5 constituents were not associated with the circulating biomarkers of low-grade inflammation. Overall, these findings suggest the possibility of a trained immunity scenario, where PM2.5 heightens inflammatory cytokine responses to multiple stimulators, and dampens sensitivity to inhibitors which counter-regulate these responses.

Responsive parental support buffers the link between chronic stress and cardiometabolic risk among adolescents.

Youth exposed to chronic stress exhibit increased cardiometabolic risk which parental social support may attenuate. Notably, theories emphasize that support should be delivered responsively for it to exert buffering effects, but this has not been thoroughly tested empirically. This study examined whether timing of support is an important but unrecognized element of responsiveness during adolescence in buffering the link between chronic stress and cardiometabolic risk. Participants were 242 adolescents aged 15 years (63 % female, 38 % Black). Adolescents completed assessments of chronic stress (Life Stress Interview), and trained personnel collected anthropometric measures and blood samples to assess cardiometabolic risk (reflected in low-grade inflammation and metabolic syndrome). Adolescents also completed an eight-day diary assessment to report daily stressor exposure and parental support. Using the diary data, responsiveness of parental support was operationalized as the within-individual difference in parental support received on stressor (vs. non-stressor) days, such that increased parental support on stressor days reflected more timely support. Results suggest that responsive parental support buffered the link between chronic stress and cardiovascular risk. Specifically, chronic stress was associated with greater risk only when parental support was not temporally aligned with stress exposure, but this association was not observed among adolescents who received timely parental support. These findings shed light on why parental support may not always exert buffering effects during adolescence, highlighting the importance of taking a developmental approach to understanding protective effects.