Summary of project PR001219

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001219. The data can be accessed directly via it's Project DOI: 10.21228/M84Q3H This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR001219
Project DOI:doi: 10.21228/M84Q3H
Project Title:Integrated molecular response of exposure to traffic-related pollutants in the US trucking industry
Project Summary:Exposure to traffic-related pollutants, including diesel exhaust, is associated with increased risk of cardiopulmonary disease and mortality; however, the precise biochemical pathways underlying these effects are not known. To investigate biological response mechanisms underlying exposure to traffic related pollutants, we used an integrated molecular response approach that included high-resolution metabolomic profiling and peripheral blood gene expression to identify biological responses to diesel exhaust exposure. Plasma samples were collected from 73 non-smoking males employed in the US trucking industry between February 2009 and October 2010 and analyzed using untargeted high-resolution metabolomics to characterize association with shift- and week-averaged levels of elemental carbon (EC), organic carbon (OC) and particulate matter with diameter ≤ 2.5 μm (PM2.5). Annotated metabolites associated with exposure were then tested for relationships with the peripheral blood transcriptome using multivariate selection and network correlation. Week-averaged EC and OC levels, which were averaged across multiple shifts during the workweek, resulted in the greatest exposure-associated metabolic alterations compared to shift-averaged exposure levels. Metabolic changes associated with EC exposure suggest increased lipid peroxidation products, biomarkers of oxidative stress, thrombotic signaling lipids, and metabolites associated with endothelial dysfunction from altered nitric oxide metabolism, while OC exposures were associated with antioxidants, oxidative stress biomarkers and critical intermediates in nitric oxide production. Correlation with whole blood RNA gene expression provided additional evidence of changes in processes related to endothelial function, immune response, inflammation, and oxidative stress. We did not detect metabolic associations with PM2.5. This study provides an integrated molecular assessment of human exposure to traffic-related air pollutants that includes diesel exhaust. Metabolite and gene expression changes associated with exposure to EC and OC are consistent with increased risk of cardiovascular diseases and the adverse health effects of traffic-related air pollution.
Institute:Icahn School of Medicine at Mount Sinai
Department:Environmental Medicine and Public Health
Laboratory:High Resolution Exposomics
Last Name:Walker
First Name:Douglas
Address:Atran Building RM AB3-39, 1428 Madison Ave, New York, NY, 10029, USA
Email:douglas.walker@mssm.edu
Phone:1-212-241-4392
Funding Source:This work was supported by funds received from the National Institute of Health, award numbers ES019776, ES025632, ES030859, ES013726, CA090792, ES016284, P30 ES000002 and OD018006.
Publications:DI Walker, JE Hart, CJ Patel, R Rudel, J Chu, E Garshick, KD Pennel, F Laden, DP Jones. Integrated molecular response of exposure to traffic-related pollutants in the US trucking industry. Environment International. In review

Summary of all studies in project PR001219

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)		 Release
Date		VersionSamplesDownload
(* : Contains raw data)
ST001930 Integrated molecular response of exposure to traffic-related pollutants in the US trucking industry Homo sapiens Icahn School of Medicine at Mount Sinai MS* 2021-10-29 1 420 Uploaded data (535.8G)*
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