Matthew Ryan Smith1, Douglas I Walker, Karan Uppal, Mark J Utell, Philip K Hopke, Timothy M Mallon, Pamela L Krahl, Patricia Rohrbeck, Young-Mi Go, Dean P Jones. 1. Clinical Biomarkers Laboratory, Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia (Dr Smith, Dr Walker, Dr Uppal, Dr Go, Dr Jones); Department of Environmental Medicine, University of Rochester Medical Center, Rochester, New York (Dr Utell); Division of Pulmonary Medicine, Department of Medicine, University of Rochester Medical Center, Rochester, NY (Dr Utell); Department of Public Health Sciences, Division of Pulmonary Medicine, University of Rochester Medical Center, Rochester, New York (Dr Hopke); Department of Preventive Medicine & Biostatistics, F. Edward Hebert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland (Dr Mallon, Dr Krahl); Armed Forces Health Surveillance Center, Silver Springs, Maryland (Dr Rohrbeck).
Abstract
OBJECTIVE: A study was conducted to identifymetabolic-related effects of benzo[a]pyrene (BaP) on human lung epithelial cells and validate these findings using human sera. METHODS: Human lung epithelial cells were treated with BaP, and extracts were analyzed with a global metabolome-wide association study (MWAS) to test for pathways and metabolites altered relative to vehicle controls. RESULTS: MWAS results showed that BaP metabolites were among the top metabolites differing between BaP-treated cells and controls. Pathway enrichment analysis further confirmed that fatty acid, lipid, and mitochondrial pathways were altered by BaP. Human sera analysis showed that lipids varied with BaP concentration. BaP associations with amino acid metabolism were found in both models. CONCLUSIONS: These findings show that BaP has broad metabolic effects, and suggest that air pollution exacerbates disease processes by altered mitochondrial and amino acid metabolism.
OBJECTIVE: A study was conducted to identifymetabolic-related effects of benzo[a]pyrene (BaP) on human lung epithelial cells and validate these findings using human sera. METHODS:Human lung epithelial cells were treated with BaP, and extracts were analyzed with a global metabolome-wide association study (MWAS) to test for pathways and metabolites altered relative to vehicle controls. RESULTS: MWAS results showed that BaP metabolites were among the top metabolites differing between BaP-treated cells and controls. Pathway enrichment analysis further confirmed that fatty acid, lipid, and mitochondrial pathways were altered by BaP. Human sera analysis showed that lipids varied with BaP concentration. BaP associations with amino acid metabolism were found in both models. CONCLUSIONS: These findings show that BaP has broad metabolic effects, and suggest that air pollution exacerbates disease processes by altered mitochondrial and amino acid metabolism.
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