Pathogenesis and Genetics of Environmental Asthma Ozone Study

NCT00574158 | Completed

• 2 other identifiers: 12496-CP-004ES012496
• Study Type: observational
• Target: 170
• Locations: 1 country
• Sites: 1

Brief Summary

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.

Conditions

Asthma; Inflammation

Keywords

ozone; inflammatory airway disease; polymorphisms

Outcome Measures

Primary Outcomes (1)

• Pathogenesis and genetics of environmental asthma ozone study

  Phenotype physiologic responses to ambient level of ozone exposure.

  acute and at 18 to 24 hour followup.

Eligibility Criteria

• Age: 18 Years - 35 Years
• Sex: all
• Healthy Volunteers: Yes
• Age Groups: Adult (18-64)
• Sampling Method: Probability Sample

Study Population

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

You may qualify if:

• 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.

You may not qualify if:

• Non-willingness to sign a consent form for participation.

Sponsors & Collaborators

• National Institute of Environmental Health Sciences (NIEHS): lead

Study Sites (1)

W Michael Foster, PhD

Durham, North Carolina, 27710, United States

Location

Related Publications (1)

• Hussain S, Johnson CG, Sciurba J, Meng X, Stober VP, Liu C, Cyphert-Daly JM, Bulek K, Qian W, Solis A, Sakamachi Y, Trempus CS, Aloor JJ, Gowdy KM, Foster WM, Hollingsworth JW, Tighe RM, Li X, Fessler MB, Garantziotis S. TLR5 participates in the TLR4 receptor complex and promotes MyD88-dependent signaling in environmental lung injury. Elife. 2020 Jan 28;9:e50458. doi: 10.7554/eLife.50458.

  PMID: 31989925 DERIVED

Biospecimen

Retention: SAMPLES WITH DNA

plasma, and ebc collected.

MeSH Terms

Conditions

Asthma; Inflammation

Condition Hierarchy (Ancestors)

Bronchial Diseases; Respiratory Tract Diseases; Lung Diseases, Obstructive; Lung Diseases; Respiratory Hypersensitivity; Hypersensitivity, Immediate; Hypersensitivity; Immune System Diseases; Pathologic Processes; Pathological Conditions, Signs and Symptoms

Study Officials

• W Michael Foster, PhD

  Duke University

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: observational
• Observational Model: COHORT
• Time Perspective: PROSPECTIVE
• Sponsor Type: NIH
• Responsible Party: PRINCIPAL INVESTIGATOR
• PI Title: Professor

Study Record Dates

• First Submitted: December 14, 2007
• First Posted: December 17, 2007
• Study Start: July 1, 2005
• Primary Completion: November 1, 2011
• Study Completion: June 1, 2012
• Last Updated: September 29, 2014

Record last verified: 2014-09

Locations

US (1)