Abstract

OPS 20: Chemicals, biomarkers, omics, Room 110, Floor 1, August 27, 2019, 4:30 PM - 5:30 PM Background/Aim: Prenatal fine particulate matter (PM2.5) exposure is linked with adverse pregnancy outcomes and developmental problems in children; PM2.5-induced changes to maternal immune activity may underlie these relationships. We examined maternal prenatal PM2.5 exposure in relation to inflammatory signals using a targeted proteomics approach. Methods: Analyses include 373 pregnant women enrolled in a prospective study in the northeastern United States between 2011 and 2015. We estimated daily residential PM2.5 exposure using high-resolution satellite data combined with ground monitoring measures and spatiotemporal predictors. We analyzed 92 inflammatory proteins in mid-pregnancy serum using a novel multiplex proximity extension assay. To explore the influence of exposure timing, we examined PM2.5 averaged across the previous 3 months, 1 month, or week of blood draw. We regressed PM2.5 on each inflammatory marker in separate models adjusting for week of gestation, maternal age, and season. For associations with a Bonferroni-adjusted p-value <0.05, we next used multivariable logistic regression to examine continuous PM2.5 exposure in relation to high (highest 20%) versus low (lowest 80%) inflammatory marker levels. Results: Mothers were primarily minorities (60% black or Hispanic). After Bonferroni correction, monocyte-chemotactic protein-3 (MCP-3), interleukin-8 (IL-8), and oncostatin M (OSM) were (p<0.001) positively associated with PM2.5 for one or more exposure interval. The odds of having high MCP-3 levels increased per unit (µg/m3) increase in PM2.5 when averaged across the previous 3 months (OR=1.48, 95% CI=1.22, 1.80), 1 month (OR=1.30, 95%CI=1.12, 1.51), or week (OR=1.18, 95% CI=1.06, 1.31). Parallel findings were true for OSM (1 month: OR=1.24, 95% CI=1.08, 1.44; 1 week: OR=1.22, 95% CI=1.10, 1.35) and IL-8 (1 month: OR=1.27, 95% CI=1.10, 1.46; 1 week: OR=1.23, 95% CI=1.11, 1.37) for more recent exposure only. Conclusions: These data link increased prenatal PM2.5 with markers of enhanced inflammation. Future analysis in this longitudinal cohort will examine whether identified markers (MCP3, OSM and IL8) mediate associations between PM2.5 and maternal-child health outcomes.

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