Summary of Study ST000417

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 PR000326. The data can be accessed directly via it's Project DOI: 10.21228/M8C31Q 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 IDST000417
Study TitleControlled Human Exposure to Particulate Matter (PM) and Gaseous Co-Pollutants
Study TypeExposome Evaluation
Study SummaryThis study is designed to provide the environmental aspects to support both the acquisition of study samples and the advancement of environmental chemical speciation information and data analyis needed. The aims of the study are as follows:1)Do the metabolomics profiles appear to be impacted by exposure to PM and NO2+PM. 2)are the metabolomic profiles related to the PM and NO2+PM distinct 3)which features (chemical or physical) of the PM and NO2+PM have the most significant impact on the metabolomic profiles.
Institute
RTI International
DepartmentRCMRC
Last NameSumner
First NameSusan
Address3040 E Cornwallis Road, Research Triangle Park, NC, 27519, USA
Emailssumner@rti.org
Phone919-541-7479
Submit Date2016-06-15
Num Groups3
Total Subjects87
Num Males47
Num Females40
Raw Data AvailableYes
Raw Data File Type(s)cdf
Analysis Type DetailGC-MS
Release Date2018-06-05
Release Version1
Susan Sumner Susan Sumner
https://dx.doi.org/10.21228/M8C31Q
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:

Project:

Project ID:PR000326
Project DOI:doi: 10.21228/M8C31Q
Project Title:Controlled Human Exposure to Particulate matter (PM) and Gaseous Co-Pollutants
Project Type:Exposome Evaluation
Project Summary:During the past decade, several epidemiological studies have reported statistically significant positive correlations between daily concentrations of ambient air particles and acutely increased mortality and morbidity. It has been estimated that 50,000 - 60,000 excess deaths in the U.S. each year may be attributable to ambient particles. Several panel studies have reported associations between fine PM and decreased heart rate variability and increased vascular markers of inflammation. In addition, recent controlled human exposure studies have reported that fine particles can increase pulmonary inflammation, decrease heart rate variability, and increase vascular factors of inflammation and blood coagulation. However, these latter studies only assessed the effects of particulate matter. In the real world, people are simultaneously exposed to both gaseous pollutants (e.g. ozone, nitrogen dioxide) and particles. Recognition of this leads the National Research Council to list studies of PM and gaseous co-pollutants as one of the ten highest priorities in PM research. One of these co-pollutants that frequently occur together with PM is nitrogen oxides (NOx), which is produced during combustion processes. NOx consists of nitric oxide (NO) and nitrogen dioxide (NO2). NO dominates near roadsides and peaks in morning rush hours while NO2 levels show less temporal and spatial variability. NO and NO2 concentrations may reach values over 1 ppm and 0.5 ppm respectively during smog situations. NO2 is an oxidant capable of oxidizing and nitrating lipids and proteins and can cause cytotoxic effects on the cell membranes of epithelial cells as well as macrophages. Controlled exposure of healthy humans to 2 ppm NO2 reduced phagocytic capacity in macrophages. At similar concentrations controlled NO2 exposure produced small changes in large airway function and increased airway reactivity to methacholine. The inflammatory effects of NO2 may thus enhance the adverse effects of PM. In this study we hypothesize that NO2 and PM2.5 affect the cardiopulmonary system beyond what either pollutant is capable of inducing by itself. Cardiopulmonay impairment will be assessed by measuring changes in bronchoalveolar lavage (BAL) neutrophils and cytokines, heart rate variability, and plasma factors involved in inflammation and coagulation.
Institute:EPA
Laboratory:National Health and Environmental Effects Research Laboratory
Last Name:Devlin
First Name:Robert
Address:109 Alexander Drive, Research Triangle Park, NC 27709
Email:devlin.robert@epa.gov
Phone:919-966-6255

Subject:

Subject ID:SU000923
Subject Type:Human
Subject Species:Homo sapiens
Taxonomy ID:9606
Weight Or Weight Range:Normal/Overweight/Obese
Gender:Male/Female
Human Race:Black/White
Species Group:Human

Factors:

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

mb_sample_id local_sample_id Group Collection Time Gender
SA051553219_AIR_24HRPOSTAIR 24HRPOST F
SA051554213_AIR_24HRPOSTAIR 24HRPOST F
SA051555218_AIR_24HRPOSTAIR 24HRPOST F
SA051556215_AIR_24HRPOSTAIR 24HRPOST M
SA051557208_AIR_24HRPOSTAIR 24HRPOST M
SA051558224_AIR_24HRPOSTAIR 24HRPOST M
SA051559220_AIR_24HRPOSTAIR 24HRPOST M
SA051560221_AIR_24HRPOSTAIR 24HRPOST M
SA051561213_AIR_POSTAIR Post F
SA051562218_AIR_POSTAIR Post F
SA051563219_AIR_POSTAIR Post F
SA051564215_AIR_POSTAIR Post M
SA051565224_AIR_POSTAIR Post M
SA051566208_AIR_POSTAIR Post M
SA051567221_AIR_POSTAIR Post M
SA051568220_AIR_POSTAIR Post M
SA051569213_AIR_PREAIR Pre F
SA051570218_AIR_PREAIR Pre F
SA051571219_AIR_PREAIR Pre F
SA051572215_AIR_PREAIR Pre M
SA051573224_AIR_PREAIR Pre M
SA051574220_AIR_PREAIR Pre M
SA051575221_AIR_PREAIR Pre M
SA051576208_AIR_PREAIR Pre M
SA051577213_NO2PM_24HRPOSTNO2PM 24HRPOST F
SA051578214_NO2PM_24HRPOSTNO2PM 24HRPOST F
SA051579218_NO2PM_24HRPOSTNO2PM 24HRPOST F
SA051580219_NO2PM_24HRPOSTNO2PM 24HRPOST F
SA051581209_NO2PM_24HRPOSTNO2PM 24HRPOST F
SA051582221_NO2PM_24HRPOSTNO2PM 24HRPOST M
SA051583208_NO2PM_24HRPOSTNO2PM 24HRPOST M
SA051584225_NO2PM_24HRPOSTNO2PM 24HRPOST M
SA051585215_NO2PM_24HRPOSTNO2PM 24HRPOST M
SA051586210_NO2PM_24HRPOSTNO2PM 24HRPOST M
SA051587219_NO2PM_POSTNO2PM Post F
SA051588213_NO2PM_POSTNO2PM Post F
SA051589214_NO2PM_POSTNO2PM Post F
SA051590209_NO2PM_POSTNO2PM Post F
SA051591218_NO2PM_POSTNO2PM Post F
SA051592221_NO2PM_POSTNO2PM Post M
SA051593215_NO2PM_POSTNO2PM Post M
SA051594208_NO2PM_POSTNO2PM Post M
SA051595210_NO2PM_POSTNO2PM Post M
SA051596218_NO2PM_PRENO2PM Pre F
SA051597214_NO2PM_PRENO2PM Pre F
SA051598209_NO2PM_PRENO2PM Pre F
SA051599213_NO2PM_PRENO2PM Pre F
SA051600208_NO2PM_PRENO2PM Pre M
SA051601210_NO2PM_PRENO2PM Pre M
SA051602215_NO2PM_PRENO2PM Pre M
SA051603221_NO2PM_PRENO2PM Pre M
SA051604225_NO2PM_PRENO2PM Pre M
SA051605220_PM_24HRPOSTPM 24HRPOST F
SA051606219_PM_24HRPOSTPM 24HRPOST F
SA051607215_PM_24HRPOSTPM 24HRPOST F
SA051608210_PM_24HRPOSTPM 24HRPOST F
SA05160911_PM_24HRPOSTPM 24HRPOST M
SA051610218_PM_24HRPOSTPM 24HRPOST M
SA051611221_PM_24HRPOSTPM 24HRPOST M
SA051612227_PM_24HRPOSTPM 24HRPOST M
SA051613213_PM_24HRPOSTPM 24HRPOST M
SA051614213_PM_POSTPM Post F
SA051615218_PM_POSTPM Post F
SA051616219_PM_POSTPM Post F
SA051617227_PM_POSTPM Post F
SA051618214_PM_POSTPM Post F
SA051619220_PM_POSTPM Post M
SA051620221_PM_POSTPM Post M
SA051621215_PM_POSTPM Post M
SA051622210_PM_POSTPM Post M
SA05162311_PM_POSTPM Post M
SA051624219_PM_PREPM Pre F
SA051625214_PM_PREPM Pre F
SA051626218_PM_PREPM Pre F
SA051627227_PM_PREPM Pre F
SA051628213_PM_PREPM Pre F
SA051629210_PM_PREPM Pre M
SA05163011_PM_PREPM Pre M
SA051631221_PM_PREPM Pre M
SA051632220_PM_PREPM Pre M
SA051633215_PM_PREPM Pre M
Showing results 1 to 81 of 81

Collection:

Collection ID:CO000917
Collection Summary:Plasma collected Pre-exposure, immediately Post-exposure or 24 hour Post Exposure
Sample Type:Blood

Treatment:

Treatment ID:TR000937
Treatment Summary:Healthy adults were exposed to clean air and subsequently to air into which PM concentrated from the ambient, outdoor environment or PM in combination with NO2 had been introduced.

Sample Preparation:

Sampleprep ID:SP000930
Sampleprep Summary:Aliquots of 30µL plasma were mixed with 1mL 3:3:2 ACN:IPA:H2O by vortex mixer then centrifuged. Supernatant recovered. Archived 450µL of supernatant. Continued prep of remaining 450µL supernatant. Evaporated to dryness w/speed vac. Formation of methoximes by adding 10µL of 40mg/mL MeOx in pyridine to each sample. Placed onto Thermomixer for 90 min at 30⁰C. Then FAME retention index markers and MSTFA added to each sample for derivatization step. Samples returned to Thermomixer for 45 min at 70⁰C.

Combined analysis:

Analysis ID AN001448
Analysis type MS
Chromatography type GC
Chromatography system Leco Pegasus 4D GC
Column Restek Rtx-5Sil (30m x 0.25mm,0.25um)
MS Type EI
MS instrument type GC x GC-TOF
MS instrument name Leco Pegasus 4D GCxGC TOF
Ion Mode POSITIVE
Units Intensity

Chromatography:

Chromatography ID:CH001017
Instrument Name:Leco Pegasus 4D GC
Column Name:Restek Rtx-5Sil (30m x 0.25mm,0.25um)
Column Pressure:12.8psi
Flow Gradient:constant flow
Flow Rate:1ml/min
Injection Temperature:250C
Retention Index:FAME markers C8-C30
Chromatography Type:GC

MS:

MS ID:MS001338
Analysis ID:AN001448
Instrument Name:Leco Pegasus 4D GCxGC TOF
Instrument Type:GC x GC-TOF
MS Type:EI
Ion Mode:POSITIVE
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