Pathogenesis and Genetics of Environmental Asthma Ozone Study

This study has been completed.
Sponsor:
Information provided by (Responsible Party):
Michael Foster, National Institute of Environmental Health Sciences (NIEHS)
ClinicalTrials.gov Identifier:
NCT00574158
First received: December 14, 2007
Last updated: September 25, 2014
Last verified: September 2014

December 14, 2007
September 25, 2014
July 2005
November 2011   (final data collection date for primary outcome measure)
Pathogenesis and genetics of environmental asthma ozone study [ Time Frame: acute and at 18 to 24 hour followup. ] [ Designated as safety issue: No ]
Phenotype physiologic responses to ambient level of ozone exposure.
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Complete list of historical versions of study NCT00574158 on ClinicalTrials.gov Archive Site
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Pathogenesis and Genetics of Environmental Asthma Ozone Study
Project 2: Genetic Regulation of Ozone Induced Inflammation in Humans.

The goals of the research are designed to accomplish genetic association studies of candidate genes in healthy normal individuals exposed to 0.2 ppm for 2.25 hours with intermittent exercise in order to search for associations between defined genotypes/haplotypes and 3 specific in vivo respiratory endpoints: a) change in FEV1 immediately after ozone exposure; b) change nonspecific bronchial reactivity as reflected in the change in methacholine PC20 FEV1 24 hours after ozone exposure ; and c) change in lung epithelial integrity as reflected in the Clearance Halftime of technetium 24 hours after ozone exposure. These studies have been carried forward to take place in 4 phases:

i) healthy individuals have been exposed to O3 using our standard exposure protocol; and we will increase the numbers of individuals available for study.

ii) perform genetic association studies for the endpoints of spirometry (FEV1, FVC, FEV1/FVC), PC20 FEV1 for methacholine, and epithelial integrity (Clearance Halftime) for 3 candidate O3 response genes taken from literature searches and/or previously characterized to demonstrate associations. These physiologic endpoints have been examined in terms of both a continuum of response, and discrete "responder" and "non-responder" endpoints.

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Observational
Observational Model: Cohort
Time Perspective: Prospective
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Retention:   Samples With DNA
Description:

plasma, and ebc collected.

Probability Sample

Healthy adults, 18-35 y of age, both genders.

  • Asthma
  • Inflammation
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
170
June 2012
November 2011   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Subjects with normal lung function values, and of normal body habitus (i.e., < BMI of 30);
  • Do not have a history of lung disease, and not taking any medications for lung disease or other clinical disorders, and no prior or current smoking history.

Exclusion Criteria:

  • Non-willingness to sign a consent form for participation.
Both
18 Years to 35 Years
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00574158
12496-CP-004, ES012496
No
Michael Foster, National Institute of Environmental Health Sciences (NIEHS)
National Institute of Environmental Health Sciences (NIEHS)
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Principal Investigator: W Michael Foster, PhD Duke University
National Institute of Environmental Health Sciences (NIEHS)
September 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP