Ignite Creation Date:
2025-12-24 @ 11:58 PM
Ignite Modification Date:
2026-02-23 @ 8:09 PM
Study NCT ID:
NCT00574158
Status:
COMPLETED
Last Update Posted:
2014-09-29
First Post:
2007-12-14
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Pathogenesis and Genetics of Environmental Asthma Ozone Study
Sponsor:
Organization:
Raw JSON
{'hasResults': False, 'derivedSection': {'miscInfoModule': {'versionHolder': '2025-12-24'}, 'conditionBrowseModule': {'meshes': [{'id': 'D001249', 'term': 'Asthma'}, {'id': 'D007249', 'term': 'Inflammation'}], 'ancestors': [{'id': 'D001982', 'term': 'Bronchial Diseases'}, {'id': 'D012140', 'term': 'Respiratory Tract Diseases'}, {'id': 'D008173', 'term': 'Lung Diseases, Obstructive'}, {'id': 'D008171', 'term': 'Lung Diseases'}, {'id': 'D012130', 'term': 'Respiratory Hypersensitivity'}, {'id': 'D006969', 'term': 'Hypersensitivity, Immediate'}, {'id': 'D006967', 'term': 'Hypersensitivity'}, {'id': 'D007154', 'term': 'Immune System Diseases'}, {'id': 'D010335', 'term': 'Pathologic Processes'}, {'id': 'D013568', 'term': 'Pathological Conditions, Signs and Symptoms'}]}}, 'protocolSection': {'designModule': {'bioSpec': {'retention': 'SAMPLES_WITH_DNA', 'description': 'plasma, and ebc collected.'}, 'studyType': 'OBSERVATIONAL', 'designInfo': {'timePerspective': 'PROSPECTIVE', 'observationalModel': 'COHORT'}, 'enrollmentInfo': {'type': 'ACTUAL', 'count': 170}}, 'statusModule': {'overallStatus': 'COMPLETED', 'startDateStruct': {'date': '2005-07'}, 'expandedAccessInfo': {'hasExpandedAccess': False}, 'statusVerifiedDate': '2014-09', 'completionDateStruct': {'date': '2012-06', 'type': 'ACTUAL'}, 'lastUpdateSubmitDate': '2014-09-25', 'studyFirstSubmitDate': '2007-12-14', 'studyFirstSubmitQcDate': '2007-12-14', 'lastUpdatePostDateStruct': {'date': '2014-09-29', 'type': 'ESTIMATED'}, 'studyFirstPostDateStruct': {'date': '2007-12-17', 'type': 'ESTIMATED'}, 'primaryCompletionDateStruct': {'date': '2011-11', 'type': 'ACTUAL'}}, 'outcomesModule': {'primaryOutcomes': [{'measure': 'Pathogenesis and genetics of environmental asthma ozone study', 'timeFrame': 'acute and at 18 to 24 hour followup.', 'description': 'Phenotype physiologic responses to ambient level of ozone exposure.'}]}, 'oversightModule': {'oversightHasDmc': False}, 'conditionsModule': {'keywords': ['ozone', 'inflammatory airway disease', 'polymorphisms'], 'conditions': ['Asthma', 'Inflammation']}, 'referencesModule': {'references': [{'pmid': '31989925', 'type': 'DERIVED', 'citation': '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.'}]}, 'descriptionModule': {'briefSummary': '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:\n\ni) healthy individuals have been exposed to O3 using our standard exposure protocol; and we will increase the numbers of individuals available for study.\n\nii) 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.'}, 'eligibilityModule': {'sex': 'ALL', 'stdAges': ['ADULT'], 'maximumAge': '35 Years', 'minimumAge': '18 Years', 'samplingMethod': 'PROBABILITY_SAMPLE', 'studyPopulation': 'Healthy adults, 18-35 y of age, both genders.', 'healthyVolunteers': True, 'eligibilityCriteria': 'Inclusion Criteria:\n\n* Subjects with normal lung function values, and of normal body habitus (i.e., \\< BMI of 30);\n* 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.\n\nExclusion Criteria:\n\n* Non-willingness to sign a consent form for participation.'}, 'identificationModule': {'nctId': 'NCT00574158', 'briefTitle': 'Pathogenesis and Genetics of Environmental Asthma Ozone Study', 'organization': {'class': 'NIH', 'fullName': 'National Institute of Environmental Health Sciences (NIEHS)'}, 'officialTitle': 'Project 2: Genetic Regulation of Ozone Induced Inflammation in Humans.', 'orgStudyIdInfo': {'id': '12496-CP-004'}, 'secondaryIdInfos': [{'id': 'ES012496'}]}, 'contactsLocationsModule': {'locations': [{'zip': '27710', 'city': 'Durham', 'state': 'North Carolina', 'country': 'United States', 'facility': 'W Michael Foster, PhD', 'geoPoint': {'lat': 35.99403, 'lon': -78.89862}}], 'overallOfficials': [{'name': 'W Michael Foster, PhD', 'role': 'PRINCIPAL_INVESTIGATOR', 'affiliation': 'Duke University'}]}, 'sponsorCollaboratorsModule': {'leadSponsor': {'name': 'National Institute of Environmental Health Sciences (NIEHS)', 'class': 'NIH'}, 'responsibleParty': {'type': 'PRINCIPAL_INVESTIGATOR', 'investigatorTitle': 'Professor', 'investigatorFullName': 'Michael Foster', 'investigatorAffiliation': 'National Institute of Environmental Health Sciences (NIEHS)'}}}}