Association between prenatal exposure to air pollution and inflammatory markers in children

Abstract

TPS 911: Air pollution, epigenetics, biomarkers, Exhibition Hall, Ground floor, August 26, 2019, 3:00 PM - 4:30 PM Background/Aim: Early-life exposure to ambient air pollution has been associated with adverse health effects in children but little is known about its potential effects on cytokine levels. We evaluated the association of pregnancy exposure to particulate matter with child inflammatory biomarkers in 500 mother-child pairs from the RHEA pregnancy cohort in Crete, Greece. Methods: Mean concentrations of particulate matter with an aerodynamic diameter of less than 2.5 µm (PM2.5) and less than 10 µm (PM10) during pregnancy were estimated at maternal home addresses with temporally adjusted land-use regression models. Levels of several inflammatory biomarkers were determined in child serum at 4 years of age via immunoassay. Exposure-outcome associations were assessed using log-binomial or Poisson regression with robust variances, in cases of non-convergence. Potential effect modification from maternal and offspring characteristics was examined by introducing interaction terms in multivariate models. Results: A 5 µg/m3 increase in concentration of PM2.5 and PM10 during pregnancy was associated with an increased risk of high levels (in the 5th quantile) of child interleukin-6 (IL-6) levels at 4 years (RR=2.68, 95%CI: 1.38, 5.20 and 1.28, 95%CI: 1.04, 1.57, respectively). Effects of prenatal exposure to both PM2.5 and PM10 remained significant only for non-smoking mothers in stratified analysis by maternal smoking status (p-interaction: 0.037 and 0.071, respectively). Child overweight/obesity (p-interaction: 0.013 and 0.001) and asthma status (p-interaction: 0.007 and 0.001) more than doubled the effects of maternal exposure to PM2.5 and PM10 on IL-6 at 4 years. Similar effects were found with other inflammatory biomarkers under study. Conclusions: Our results indicate alterations in systemic inflammatory markers in 4-y-old children in relation to prenatal exposure to traffic-related air pollution. Further work is needed to examine the underlying mechanisms and interactions between cytokines in the inflammatory response following air pollution exposure.