Summary of Study ST001039

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.

Perform statistical analysis  |  Show all samples  |  Show named metabolites  |  Download named metabolite data  |  Perform analysis on untargeted data  
Download mwTab file (text)   |  Download mwTab file(JSON)   |  Download data files
Study IDST001039
Study TitleDenver Asthma Panel Study-CHEAR Ancillary Study (part II)
Study SummaryUrban 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
DepartmentSchool of Medicine
LaboratoryClincal Biomarkers Laboratory
Last NameUppal
First NameKaran
Address615 Michael St. Ste 225, Atlanta, GA, 30322, USA
Emailkuppal2@emory.edu
Phone(404) 727 5027
Submit Date2018-07-12
Total Subjects169
Study CommentsBoth CHEAR pooled urine samples and Clinical Biomarker Laboratory pooled plasma samples were used
Chear StudyYes
Analysis Type DetailLC-MS
Release Date2021-08-31
Release Version1
Karan Uppal Karan Uppal
https://dx.doi.org/10.21228/M8X10M
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

Select appropriate tab below to view additional metadata details:


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)
  logo