Summary of Study ST001930
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
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST001930 |
| Study Title | Integrated molecular response of exposure to traffic-related pollutants in the US trucking industry |
| Study Type | Untargeted Metabolomics |
| Study 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 |
| douglas.walker@mssm.edu | |
| Phone | 1-212-241-4392 |
| Submit Date | 2021-09-30 |
| Num Groups | 1 |
| Total Subjects | 95 |
| Num Males | 94 |
| Num Females | 1 |
| 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 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | mzXML, raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2021-10-29 |
| Release Version | 1 |
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Project:
| 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 |
