Abstract Body: Introduction: Chronic neighborhood stressors contribute to disparate CVD outcomes, with neighborhood socioeconomic deprivation (NSD) linked to inflammation. Separately, relationships have been seen with CVD and specific monocyte phenotypes. However, the connection between neighborhood exposures and monocyte subsets is less clear. Thus, we examined NSD with monocyte phenotypes, hypothesizing that chronic NSD cross-sectionally associates with monocyte subsets.
Methods: This study utilized data from the Multi-Ethnic Study of Atherosclerosis (MESA), a population-based prospective cohort of adults aged 45-84 years (N=6814). NSD was scored from principal factor analyses using U.S. Census data (2000), with higher values indicating higher deprivation. Monocyte phenotypes were measured from cryopreserved peripheral blood mononuclear cells by flow cytometry at MESA Exam 1 (2000-02). Subsets were characterized as classical monocytes (CMs, CD14++CD16-), intermediate monocytes (IMs, CD14+CD16+), and non-classical monocytes (NCMs, CD14+CD16++). Linear regression models were used to examine associations between NSD and monocyte phenotypes, adjusting for individual-level covariates.
Results: Of the MESA cohort, participants with monocyte phenotypes (n=1527) were included in analyses (age 62.9±10.5 years, 50.5% male, 37.4% White, 28.6% Black, 20.6% Hispanic). Higher NSD was associated with lower CMs but higher IMs and NCMs (Table). When gender-stratified, relationships remained significant for CMs but not for IMs. In men, higher NSD was associated with higher NCMs but not when adjusted for covariates.
Conclusion: Neighborhood deprivation as a marker of chronic stress was associated with shifts in monocyte subsets in a partially sex-dependent manner, with differential relationships with CMs, IMs, and NCMs. With IMs and NCMs associated with accelerated CVD, these findings may help illuminate the role of monocytes in how neighborhood exposures lead to CVD. Future analyses will examine interactions with race/ethnicity and inflammatory biomarkers.