Ignite Creation Date:
2025-12-24 @ 1:59 PM
Ignite Modification Date:
2026-01-21 @ 5:19 AM
Study NCT ID:
NCT02284295
Status:
COMPLETED
Last Update Posted:
2015-04-14
First Post:
2014-11-03
Is NOT Gene Therapy:
True
Has Adverse Events:
False
Brief Title:
Molecular, Cytological Features and Genetic Susceptibility of COPD Attributable to Different Environmental Exposures 2
Sponsor:
Organization:
Raw JSON
{'hasResults': False, 'derivedSection': {'miscInfoModule': {'versionHolder': '2025-12-24'}, 'conditionBrowseModule': {'meshes': [{'id': 'D029424', 'term': 'Pulmonary Disease, Chronic Obstructive'}], 'ancestors': [{'id': 'D008173', 'term': 'Lung Diseases, Obstructive'}, {'id': 'D008171', 'term': 'Lung Diseases'}, {'id': 'D012140', 'term': 'Respiratory Tract Diseases'}, {'id': 'D002908', 'term': 'Chronic Disease'}, {'id': 'D020969', 'term': 'Disease Attributes'}, {'id': 'D010335', 'term': 'Pathologic Processes'}, {'id': 'D013568', 'term': 'Pathological Conditions, Signs and Symptoms'}]}}, 'protocolSection': {'designModule': {'bioSpec': {'retention': 'SAMPLES_WITH_DNA', 'description': 'whole blood, serum,bronchoalveolar lavage fluid'}, 'studyType': 'OBSERVATIONAL', 'designInfo': {'timePerspective': 'CROSS_SECTIONAL', 'observationalModel': 'CASE_CONTROL'}, 'enrollmentInfo': {'type': 'ACTUAL', 'count': 352}, 'patientRegistry': False}, 'statusModule': {'overallStatus': 'COMPLETED', 'startDateStruct': {'date': '2014-11'}, 'expandedAccessInfo': {'hasExpandedAccess': False}, 'statusVerifiedDate': '2015-04', 'completionDateStruct': {'date': '2014-11', 'type': 'ACTUAL'}, 'lastUpdateSubmitDate': '2015-04-13', 'studyFirstSubmitDate': '2014-11-03', 'studyFirstSubmitQcDate': '2014-11-05', 'lastUpdatePostDateStruct': {'date': '2015-04-14', 'type': 'ESTIMATED'}, 'studyFirstPostDateStruct': {'date': '2014-11-06', 'type': 'ESTIMATED'}, 'primaryCompletionDateStruct': {'date': '2014-11', 'type': 'ACTUAL'}}, 'outcomesModule': {'primaryOutcomes': [{'measure': 'Difference in serum interleukin 1 beta (IL-1β) level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in serum tumor necrosis factor alpha (TNFα) level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in spontaneous thrombocyte aggregation between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in collagen induced thrombocyte aggregation between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in epinephrine induced thrombocyte aggregation between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in adenosine diphosphate induced thrombocyte aggregation between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in fibrinogen level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in fibrinogen degradation products level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in D-dimer level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in serum endothelin1 level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Difference in serum nitric oxide level between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Differences in cytological analysis of bronchoalveolar lavage fluid results between COPD patients exposed to dust, chemicals and tobacco smoke', 'timeFrame': '1 day (a single measurement)', 'description': 'Comparison of groups'}, {'measure': 'Association of SNPs rs1800470 TGF β1 gene, rs1828591 HHIP gene, rs4129267 IL-6R gene, rs1051730 CHRNA3 gene with COPD in subjects exposed to dust and in those exposed to chemicals. (Odds ratio and 95% confidence interval)', 'timeFrame': '1 day (a single measurement)', 'description': 'Odds ratio and 95% confidence interval will be calculated for each occupational group. Controls - healthy people.'}], 'secondaryOutcomes': [{'measure': 'Relationship between genotype and phenotype characteristics, such as an inflammation activity, assessed by hsCRP and TNF α serum concentration, in different occupational COPD groups.', 'timeFrame': '1 day (a single measurement)', 'description': 'For SNPs that will occur associated with occupational COPD differences in hsCRP and TNFα serum concentration between subjects with different genotypes will be established separately for exposed to dust COPD group and for exposed to chemicals COPD group.'}]}, 'oversightModule': {'oversightHasDmc': False}, 'conditionsModule': {'keywords': ['chronic obstructive pulmonary disease', 'silica dust', 'aromatic hydrocarbons', 'genetic', 'occupational'], 'conditions': ['Chronic Obstructive Pulmonary Disease']}, 'descriptionModule': {'briefSummary': 'The objective of this study is to investigate molecular, cytological and genetic features of occupational chronic obstructive pulmonary disease (COPD) in conditions of different occupational exposures. In order to achieve this goal serum pro-inflammatory cytokines and standard inflammation markers level, hemostasis, cytological analysis of bronchoalveolar lavage fluid and association of single nucleotide polymorphisms (SNPs) rs1800470 transforming growing factor β1 (TGF β1) gene, rs1828591 hedgehog interacting protein (HHIP) gene, rs4129267 interleukin 6 receptor (IL-6R) gene, rs1051730 nicotinic acetylcholine receptor 3 (CHRNA3) gene with COPD in subjects exposed to silica dust and in those exposed to polycyclic aromatic hydrocarbons exhaust will be investigated. The relationship between genotype and phenotype characteristics, such as an inflammation activity, assessed by C-reactive protein (hsCRP) and tumor necrosis factor alpha (TNF α) serum concentration, in different occupational COPD groups will be studied. The hypothesis is that the mechanisms underlying disease development and progression are different due to environmental risk factor that reflex in differs in disease attributes - molecular biomarkers, cytology results and genetic susceptibility between COPD due to dust, COPD due to chemicals and COPD in smokers therefore COPD can be subdivided into ecological phenotypes according to environmental risk factor.', 'detailedDescription': 'Study rationale: The main risk factors of COPD are tobacco smoking, biomass smoking and occupational factors. Tobacco smoking is well-known risk factor so tobacco induced COPD is completely established. Nevertheless the meaning of occupational factors which are less famous are equally important. Based on comprehensive literature review ATS endorsed the notion that strong evidence implicates occupational factors as cause of COPD. Occupational COPD takes 19.2 % of all COPD patients and 31.1 % of never smokers as resulted NHANESIII study. A considerable number of work-related factors have evidence for a causal association with COPD including (and of course not limited) silica and silicates and aromatic hydrocarbons. Individuals in a variety of occupations and industries such as coal miners, painters, coke workers, tunnel workers, metallurgists, welding workers, transportation workers, builders, farmers are exposed to factors cited above. Despite this the clinical and pathophysiological features of COPD caused by occupational factors are still unclear.\n\nOccupational factors leading airflow limitation are various entities - vapors, dusts, gases and fumes with different physical, chemical, biological and other features, so the mechanisms underlying disease development and progression may be different attributable to risk factor.\n\nAn environmental risk factors exposure as well as tobacco smoking results in COPD only in part of the subjects which indicates the significant genome and gene environmental interactions role. COPD develops in predisposed subjects undergoing risk factors exposure. Therefore the risk of COPD is individual and depends on both genetic and environments. There are few data concerning the effects of genetic on COPD risk in this specific subgroup - people who are exposed to occupational risk factors related to the certain environmental factor.\n\nStatistical analysis: Statistical analysis will be carried out by Statistica 9.0 software. Significance level will be considered p = 0.05. The qualitative variables will be expressed as counts and percentages. The quantitative continuous variables will be expressed as means and standard error of means (M ± m) for variables that meet the criteria of normality and minimum and maximum, median for those that do not meet the criteria of normality. Kruskal-Wallis test will be used for comparing multiply independent samples and Mann-Whitney U test for comparing two independent samples if variable under consideration will continuous and that it will be measured on an ordinal scale. For comparisons of proportions, the Chi-square will be used.\n\nFor associations assessment we will use logistic regression method. The odds ratios (OR) and 95% confidence intervals (CI) will be calculated for each professional group. Multiple regression model will be used to explore the relationships between demographic characteristics, cytokine concentrations, hemostasis and airflow limitation in professional groups.'}, 'eligibilityModule': {'sex': 'MALE', 'stdAges': ['ADULT', 'OLDER_ADULT'], 'maximumAge': '75 Years', 'minimumAge': '40 Years', 'samplingMethod': 'PROBABILITY_SAMPLE', 'studyPopulation': 'Residents of a certain town (Novosibirsk, Russian Federation)', 'healthyVolunteers': False, 'eligibilityCriteria': 'Inclusion Criteria:\n\n* Post- bronchodilator forced Expiratory Volume in 1 second (FEV1)/Forced Vital Capacity (FVC) ratio less than 0.7\n* Stable phase of COPD\n* History of exposure to respirable silica dust, nonsmokers with no of passive exposure of tobacco smoke or history of exposure to aromatic hydrocarbons, nonsmokers with no of passive exposure of tobacco smoke or current tobacco smokers without history of occupational exposure\n* COPD risk factor exposure (occupational or tobacco smoke) duration not less than 12 months\n* Male\n* Caucasian\n* Age of 40 - 75 years old\n\nExclusion Criteria:\n\n* history of biomass smoke exposure\n* age less than 40 and above 75 years old\n* current COPD exacerbation\n* concomitant asthma\n* tuberculosis and other pulmonary diseases\n* allergic and autoimmune disorders\n* active infections\n* immunodeficiency, including HIV infection\n* parasitological diseases\n* malignancies\n* lack of informed consent.'}, 'identificationModule': {'nctId': 'NCT02284295', 'briefTitle': 'Molecular, Cytological Features and Genetic Susceptibility of COPD Attributable to Different Environmental Exposures 2', 'organization': {'class': 'OTHER', 'fullName': 'Novosibirsk City Hospital #2'}, 'officialTitle': 'Molecular, Cytological Features and Genetic Susceptibility of Occupational Chronic Obstructive Pulmonary Disease Attributable to Different Environmental Exposures 2.', 'orgStudyIdInfo': {'id': '01201463369/2'}, 'secondaryIdInfos': [{'id': '01201463369', 'type': 'OTHER', 'domain': 'Education and Science Ministry of Russian Federation'}]}, 'armsInterventionsModule': {'armGroups': [{'label': 'occupational COPD', 'description': 'Consists of 2 subgroups\n\n1. COPD patients with history of exposure to respirable silica dust\n2. COPD patients with history of exposure to aromatic hydrocarbons', 'interventionNames': ['Other: exposure to respirable silica dust', 'Other: exposure to aromatic hydrocarbons']}, {'label': 'smokers with COPD and healthy control', 'description': '1. patients with COPD, history of tobacco smoke and no history of occupational exposure\n2. healthy subjects'}], 'interventions': [{'name': 'exposure to respirable silica dust', 'type': 'OTHER', 'description': 'History of exposure to respirable silica dust due to job', 'armGroupLabels': ['occupational COPD']}, {'name': 'exposure to aromatic hydrocarbons', 'type': 'OTHER', 'description': 'history of exposure to aromatic hydrocarbons due to job', 'armGroupLabels': ['occupational COPD']}]}, 'contactsLocationsModule': {'locations': [{'zip': '630084', 'city': 'Novosibirsk', 'country': 'Russia', 'facility': 'Novosibirsk City Hospital #2', 'geoPoint': {'lat': 55.02259, 'lon': 82.93175}}], 'overallOfficials': [{'name': 'Liubov Shpagina, PhD', 'role': 'PRINCIPAL_INVESTIGATOR', 'affiliation': 'Novosibirsk City Hospital #2, Novosibirsk State Medical University'}]}, 'sponsorCollaboratorsModule': {'leadSponsor': {'name': 'Novosibirsk City Hospital #2', 'class': 'OTHER'}, 'collaborators': [{'name': 'Siberian Branch of the Russian Academy of Medical Sciences', 'class': 'OTHER'}], 'responsibleParty': {'type': 'PRINCIPAL_INVESTIGATOR', 'investigatorTitle': 'Prof., Dr', 'investigatorFullName': 'Liubov A Shpagina', 'investigatorAffiliation': 'Novosibirsk City Hospital #2'}}}}