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.

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Study IDST001930
Study TitleIntegrated molecular response of exposure to traffic-related pollutants in the US trucking industry
Study TypeUntargeted Metabolomics
Study SummaryExposure 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
DepartmentEnvironmental Medicine and Public Health
LaboratoryHigh Resolution Exposomics
Last NameWalker
First NameDouglas
AddressAtran Building RM AB3-39, 1428 Madison Ave, New York, NY, 10029, USA
Emaildouglas.walker@mssm.edu
Phone1-212-241-4392
Submit Date2021-09-30
Num Groups1
Total Subjects95
Num Males94
Num Females1
PublicationsDI 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 AvailableYes
Raw Data File Type(s)mzXML, raw(Thermo)
Analysis Type DetailLC-MS
Release Date2021-10-29
Release Version1
Douglas Walker Douglas Walker
https://dx.doi.org/10.21228/M84Q3H
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

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

Subject:

Subject ID:SU002008
Subject Type:Human
Subject Species:Homo sapiens
Taxonomy ID:9606
Gender:Male and female
Species Group:Mammals

Factors:

Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Class
SA178554q15bQC
SA178555q16aQC
SA178556q11aQC
SA178557q5aQC
SA178558q6aQC
SA178559q14bQC
SA178560q15aQC
SA178561q4bQC
SA178562q16bQC
SA178563q18aQC
SA178564q3aQC
SA178565q17bQC
SA178566q3bQC
SA178567q17aQC
SA178568q4aQC
SA178569q6bQC
SA178570q7aQC
SA178571q11bQC
SA178572q12aQC
SA178573q9bQC
SA178574q10aQC
SA178575q10bQC
SA178576nist1aQC
SA178577q9aQC
SA178578q8bQC
SA178579q13bQC
SA178580q14aQC
SA178581q7bQC
SA178582q8aQC
SA178583q12bQC
SA178584q13aQC
SA178585q2bQC
SA178586q5bQC
SA178587q19aQC
SA178588q1bQC
SA178589q18bQC
SA178590q19bQC
SA178591nist1bQC
SA178592q2aQC
SA178593q1aQC
SA178594S-001175855Study
SA178595S-001175864Study
SA178596S-001175846Study
SA178597S-001175954Study
SA178598S-001175828Study
SA178599S-001175837Study
SA178600S-001175873Study
SA178601S-001175827Study
SA178602S-001175872Study
SA178603S-001175881Study
SA178604S-001175952bStudy
SA178605S-001175998bStudy
SA178606S-001175863Study
SA178607S-001175854Study
SA178608S-001175939Study
SA178609S-001175963Study
SA178610S-001175836Study
SA178611S-001175845Study
SA178612S-001175882Study
SA178613S-001175883Study
SA178614S-001175857Study
SA178615S-001175866Study
SA178616S-001175875Study
SA178617S-001175884Study
SA178618S-001175848Study
SA178619S-001175839Study
SA178620S-001175821Study
SA178621S-001175999Study
SA178622S-001175990Study
SA178623S-001175830Study
SA178624S-001175941Study
SA178625S-001175820Study
SA178626S-001175865Study
SA178627S-001175874Study
SA178628S-001175890Study
SA178629S-001175940Study
SA178630S-001175972Study
SA178631S-001175981Study
SA178632S-001175829Study
SA178633S-001175838Study
SA178634S-001175847Study
SA178635S-001175856Study
SA178636S-001175819Study
SA178637S-001175989bStudy
SA178638S-001175760Study
SA178639S-001175769Study
SA178640S-001175816Study
SA178641S-001175705Study
SA178642S-001175751Study
SA178643S-001175742Study
SA178644S-001175715Study
SA178645S-001175953bStudy
SA178646S-001175724Study
SA178647S-001175733Study
SA178648S-001175714Study
SA178649S-001175723Study
SA178650S-001175815Study
SA178651S-001175704Study
SA178652S-001175713Study
SA178653S-001175722Study
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Collection:

Collection ID:CO002001
Collection Summary:A total of four blood samples was collected from each participant over the course of the workweek. The first blood sample was collected from each participant prior to the day’s work shift on their first day back after at least two days off, followed by a second blood sample at the end of the first work shift. Pre- and post-shift samples were collected again on the last day of the same workweek. Following each blood draw, blood tubes were stored at 4°C until processing. EDTA plasma samples for metabolomic analysis were centrifuged, aliquoted, and stored in the vapor phase of liquid nitrogen freezers at < -130°C.
Sample Type:Blood (plasma)

Treatment:

Treatment ID:TR002020
Treatment Summary:This study included workers employed in the US trucking industry as drivers, dockworkers and office workers. Within this study population, exposure to common traffic-related pollutants was evaluated. No intervention was used.

Sample Preparation:

Sampleprep ID:SP002014
Sampleprep Summary:Untargeted HRM profiling was completed using verified protocols. (Accardi et al. 2016a; Go et al. 2015) Plasma aliquots were removed from storage and thawed on ice. A 65 μL aliquot of plasma was then added to 130 μL of acetonitrile containing a mixture of stable isotopic standards that included [13C6]-D- glucose, [15N]-indole, [2-15N]-L-lysine dihydrochloride, [13C5]-L-glutamic acid, [13C7]-benzoic acid, [3,4-13C2]- cholesterol, [15N]-L-tyrosine, [trimethyl-13C3]-caffeine, [15N2]-uracil, [3,3-13C2]-cystine, [1,2-13C2]-palmitic acid, [15N,13C5]-L-methionine, [15N]-choline chloride, and 2’- deoxyguanosine-15N2,13C10-5’-monophosphate, vortexed, and allowed to equilibrate for 30 minutes. (Soltow et al. 2013)
Processing Storage Conditions:On ice
Extraction Method:2:1 addition of acetonitrile
Sample Spiking:[13C6]-D-glucose, [15N,13C5]-L-methionine, [13C5]-L-glutamic acid, [15N]-L-tyrosine, [3,3-13C2]-cystine, [trimethyl-13C3]-caffeine, [U-13C5, U-15N2]-L-glutamine, [15N]-indole

Combined analysis:

Analysis ID AN003138
Analysis type MS
Chromatography type Reversed phase
Chromatography system Thermo Dionex Ultimate 3000
Column Targa 100 mm x 2.1mm x 2.6 μm, Higgins Analytical Inc
MS Type ESI
MS instrument type Orbitrap
MS instrument name Thermo Q Exactive Orbitrap
Ion Mode POSITIVE
Units Peak area

Chromatography:

Chromatography ID:CH002320
Chromatography Summary:Triplicate 10 μL aliquots were analyzed by reverse-phase C18 liquid chromatography (Targa 100 mm x 2.1mm x 2.6 μm, Higgins Analytical Inc) with detection by a Thermo Scientific Q-Exactive high-resolution mass spectrometer. Analyte separation was accomplished using water, acetonitrile and 2% [v/v] formic acid in water (solution A) mobile phases operating under the following gradient: initial 2 min period of 80% A, 5% water, 15% acetonitrile, followed by linear increase to 0% A, 5% water, 95% acetonitrile at 6 min and then held for an additional 4 min. Mobile phase flow rate was held at 0.35 mL/min for 6 min, and then increased to 0.5 mL/min.
Instrument Name:Thermo Dionex Ultimate 3000
Column Name:Targa 100 mm x 2.1mm x 2.6 μm, Higgins Analytical Inc
Column Temperature:60
Flow Gradient:initial 2 min period of 80% A, 5% water, 15% acetonitrile, followed by linear increase to 0% A, 5% water, 95% acetonitrile at 6 min and then held for an additional 4 min
Flow Rate:Held at 0.35 mL/min for 6 min, and then increased to 0.5 mL/min
Solvent A:water/acetonitrile; 2% formic acid
Chromatography Type:Reversed phase

MS:

MS ID:MS002918
Analysis ID:AN003138
Instrument Name:Thermo Q Exactive Orbitrap
Instrument Type:Orbitrap
MS Type:ESI
MS Comments:The high-resolution mass spectrometer was equipped with an electrospray ionization source operated in positive ion mode with spray voltage of 4.5 kV, probe, capillary temperature 275°C, sheath gas flow 45 (arbitrary units), auxiliary gas flow 5 (arbitrary units) and S-lens RF level of 69. Resolution was set at 70,000 (FWHM) and mass-to-charge (m/z) scan range 85-1275. Spectra were collected in full scan only without MSMS. Samples were analyzed in batches of 20, in addition to a quality control (QC) pooled reference sample included at the beginning and end of each batch of samples to evaluate batch effects and reproducibility of the detected metabolite features. Upon injection of all study and quality control samples, mass spectral features with replicate coefficient of variation (CV) ≤ 100% were extracted and aligned using apLCMS (Yu et al. 2013) with modifications by xMSanalyzer (Uppal et al. 2013) and batch effect correction by ComBat (Johnson et al. 2007).
Ion Mode:POSITIVE
Capillary Voltage:275
Ionization:Positive
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