Summary of Study ST001004
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 PR000679. The data can be accessed directly via it's Project DOI: 10.21228/M8X10M 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 | ST001004 |
Study Title | Denver Asthma Panel Study-CHEAR Ancillary Study |
Study Type | Untargeted high-resolution mass spectrometry profiling |
Study Summary | Urban environments remain a poorly understood toxic environment for children with asthma, where improved exposure characterization and estimation of exposurehealth outcome relationships are clearly needed. The goal of this project is to investigate the interactions between relevant environmental exposures and asthma severity in a year-long longitudinal study of urban children with asthma. Environmental and clinical samples are being collected at 3 seasonal visits. Using these samples, we will measure the effects of multiple relevant exposures (environmental tobacco smoke (ETS), polycyclic aromatic hydrocarbons (PAHs), phthalates, and volatile organic compounds (VOCs)) on biological responses (metabolomics, oxidative stress, inflammatory markers, and endocannabinoids) and asthma outcomes. Our overall hypothesis is that relevant environmental exposures and their interactions drive disease severity in urban children with asthma. We will test this hypothesis by investigating the following aims: Aim 1: To investigate how environmental exposures (ETS, PAHs, phthalates, and VOCs) and their interactions contribute to asthma severity in urban children. Aim 2: To determine if environmental exposures in children with asthma are associated with changes in in biological responses (metabolomics, oxidative stress, inflammatory markers, and endocannabinoids). Aim 3: To determine which biological responses mediate the relationships between environmental exposures and asthma severity. Aim 4: To compare environmental exposures and biological responses in asthmatic and non-asthmatic children |
Institute | Emory University |
Department | School of Medicine |
Laboratory | Clincal Biomarkers Laboratory |
Last Name | Uppal |
First Name | Karan |
Address | 615 Michael St. Ste 225, Atlanta, GA, 30322, USA |
kuppal2@emory.edu | |
Phone | (404) 727 5027 |
Submit Date | 2018-06-21 |
Total Subjects | 66 |
Study Comments | Both CHEAR and Clinical Biomarker Laboratory pooled plasma samples were used for quality control. Study specific sample pools were not created |
Raw Data Available | Yes |
Raw Data File Type(s) | raw(Thermo) |
Chear Study | Yes |
Analysis Type Detail | LC-MS |
Release Date | 2021-08-31 |
Release Version | 1 |
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Project:
Project ID: | PR000679 |
Project DOI: | doi: 10.21228/M8X10M |
Project Title: | Denver Asthma Panel Study-CHEAR Ancillary Study |
Project Type: | NIH/NIEHS 1U2CES026560-01 |
Project Summary: | Urban environments remain a poorly understood toxic environment for children with asthma, where improved exposure characterization and estimation of exposurehealth outcome relationships are clearly needed. The goal of this project is to investigate the interactions between relevant environmental exposures and asthma severity in a year-long longitudinal study of urban children with asthma. Environmental and clinical samples are being collected at 3 seasonal visits. Using these samples, we will measure the effects of multiple relevant exposures (environmental tobacco smoke (ETS), polycyclic aromatic hydrocarbons (PAHs), phthalates, and volatile organic compounds (VOCs)) on biological responses (metabolomics, oxidative stress, inflammatory markers, and endocannabinoids) and asthma outcomes. Our overall hypothesis is that relevant environmental exposures and their interactions drive disease severity in urban children with asthma. We will test this hypothesis by investigating the following aims: Aim 1: To investigate how environmental exposures (ETS, PAHs, phthalates, and VOCs) and their interactions contribute to asthma severity in urban children. Aim 2: To determine if environmental exposures in children with asthma are associated with changes in in biological responses (metabolomics, oxidative stress, inflammatory markers, and endocannabinoids). Aim 3: To determine which biological responses mediate the relationships between environmental exposures and asthma severity. Aim 4: To compare environmental exposures and biological responses in asthmatic and non-asthmatic children |
Institute: | Emory University |
Department: | School of Medicine |
Laboratory: | Clinical Biomarkers Laboratory |
Last Name: | Uppal |
First Name: | Karan |
Address: | 615 Michael St. Ste 225, Atlanta, GA, 30322, USA |
Email: | kuppal2@emory.edu |
Phone: | (404) 727 5027 |
Funding Source: | NIEHS ES026560 |
Contributors: | Andrew Lui (University of Colorado Denver), Tasha Fingerlin ( University of Colorado Denver), Jonathon Thornburg (University of Colorado Denver), and Dean P. Jones (Emory University) |