Salivary Metabolomics and Air Pollution Exposure in Toddlers: Black Carbon and PM2.5 are Associated with Pathways Related to Inflammatory Regulation

ROBY GREENWALD, Yu Jung Lin, Bisan Hammid, Nadia Alhadidi, Patrick Chepaitis, Donghai Liang, Georgia State University

     Abstract Number: 567
     Working Group: Health-Related Aerosols

Abstract
The Air Pollution Exposure in Child Care Settings (APECCS) study measures air pollution exposure in healthy children ages 3-4 years and explores biological mechanisms of response using salivary metabolomics. We coordinated exposure assessment activities at child care centers in Atlanta, Georgia, and we measured air pollutant levels indoors and outdoors at the centers, the homes of participating families, and in ambulatory settings using small backpacks accompanying the children in transport environments. Air pollutant measurements included PM2.5, black carbon (BC), nitrogen dioxide (NO2), ozone (O3), particle number concentration (PNC), and elemental speciation of metals present in PM2.5. Health outcome assessment included a metabolome-wide association study (MWAS) of saliva samples collected weekly. Untargeted metabolomics analysis measured the intensity of ~16000 metabolomic features using both C18 and HILIC column for separation. We assessed the association of exposure with feature intensity using linear mixed-effects models and the lme4 package for R. We sequentially ran models for all features in the database using the weekly exposure of each measured pollutant as the dependent variable and the change in feature intensity over the corresponding time period as the predictor while controlling for ambient temperature, sex, and race. We additionally included a random effect for subject. After adjusting resulting p-values for multiple comparisons, we performed pathway analysis using the mummichog network analysis tool for metabolomics. Numerous statistically-significant associations were observed for all pollutant metrics and various metabolomic pathways. Notably, exposure to PM2.5 was strongly associated with multiple pathways related to inflammatory regulation. Exposure to BC was also strongly associated with inflammatory regulation and additionally to pathways identified as indicators of asthma pathogenesis. Analysis of this extensive dataset is ongoing, and it is likely that additional noteworthy observations will be reported at the time of presentation.