Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?
Overview[ - collapse ][ - ]
| Purpose | The purpose of this study is to examine biological pathways of altered blood vessel function resulting from breathing airborne particulate. Blood artery function in healthy men will be measured after particulate exposure either on placebo or on an asthma medication that stops production of an inflammatory biological agent. Lung and blood profiles will be obtained before and after exposure to exhaust fumes. We believe that the inflammatory agent produced by the lungs from breathing these particles causes abnormal artery function. |
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| Condition | Airway Inflammation |
| Intervention | Other: placebo Drug: Montelukast |
| Phase | N/A |
| Sponsor | Marywood University |
| Responsible Party | Marywood University |
| ClinicalTrials.gov Identifier | NCT00814281 |
| First Received | December 22, 2008 |
| Last Updated | May 20, 2009 |
| Last verified | May 2009 |
Tracking Information[ + expand ][ + ]
| First Received Date | December 22, 2008 |
|---|---|
| Last Updated Date | May 20, 2009 |
| Start Date | May 2007 |
| Estimated Primary Completion Date | May 2009 |
| Current Primary Outcome Measures | Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction. [Time Frame: February 2009] [Designated as safety issue: No] |
| Current Secondary Outcome Measures | Montelukast protects against pollution induced vascular dysfunction. [Time Frame: February 2009] [Designated as safety issue: No] |
Descriptive Information[ + expand ][ + ]
| Brief Title | Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man? |
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| Official Title | Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man? |
| Brief Summary | The purpose of this study is to examine biological pathways of altered blood vessel function resulting from breathing airborne particulate. Blood artery function in healthy men will be measured after particulate exposure either on placebo or on an asthma medication that stops production of an inflammatory biological agent. Lung and blood profiles will be obtained before and after exposure to exhaust fumes. We believe that the inflammatory agent produced by the lungs from breathing these particles causes abnormal artery function. |
| Detailed Description | Hourly ice resurfacing by gas and propane fueled machines creates high levels of ultrafine and fine particulate matter (PM1) in indoor ice rinks. PM1 exposure may disrupt the normal nitric oxide (NO)/endothelin (ET)-1 vasodilation system and promote atherosclerosis, and/or increase the risk of an acute cardiac event. Our specific aims are 1) to determine whether impaired endothelial-mediated vasodilation and forearm muscle tissue reoxygenation rate and blood volume change (to reactive hyperemia following artery occlusion) is associated with combustion-derived PM1 exposure, and 2) To characterize a PM1 induced mechanism of endothelial dysfunction which occurs via a leukotriene (LT)-associated, airway generated tumor necrosis factor-alpha (TNF-a) mediated pathway. Healthy low PM1 exposed males will be evaluated for endothelial dysfunction before and after artery occlusion using high resolution ultrasound and near-infrared spectroscopy (NIRS), before and after moderate exercise in blinded high and low [PM1]. Endothelial dysfunction among chronically PM¬1 exposed ice rink athletes will be determined to evaluate the feasibility of using this population as a model in future studies. TNF-a, IL-8, LTB4, LTC4, LTD4, LTE4, ET-1, NO, and differential cell counts will be measured in sputum and serum. [PM1] will be monitored and exposure levels will be typical of indoor ice rinks. LT involvement will be assessed in vivo by double-blind pharmacological manipulation during PM1 exposure during light exercise. Results will demonstrate whether endothelial-mediated vasodilation and muscle hemodynamics are influenced by PM1 exposure, and will elucidate an LT initiated TNF-a mediated pathway in ET-1 upregulation. Our results should provide information for understanding the effects of PM1 exposure on the atherosclerotic process and cardiovascular risk, and give insight to novel treatment and diagnostic modalities. |
| Study Type | Interventional |
| Study Phase | N/A |
| Study Design | Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Caregiver, Investigator), Primary Purpose: Basic Science |
| Condition | Airway Inflammation |
| Intervention | Other: placebo Placebo Other Names: Sugar PillDrug: Montelukast 10 mg ingested orally 1 hour prior to exercise testing Other Names: Singulair |
| Study Arm (s) |
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Recruitment Information[ + expand ][ + ]
| Recruitment Status | Completed |
|---|---|
| Estimated Enrollment | 24 |
| Estimated Completion Date | May 2009 |
| Estimated Primary Completion Date | March 2009 |
| Eligibility Criteria | Inclusion Criteria: - Healthy male subjects - between 18 and 30 years of age - participant in endurance sport Exclusion Criteria: - history of blood clotting - history of coagulation problems - History of spontaneous pneumothorax |
| Gender | Male |
| Ages | 18 Years |
| Accepts Healthy Volunteers | Accepts Healthy Volunteers |
| Contacts | Not Provided |
| Location Countries | United States |
Administrative Information[ + expand ][ + ]
| NCT Number | NCT00814281 |
|---|---|
| Other Study ID Numbers | MU2007-005 |
| Has Data Monitoring Committee | No |
| Information Provided By | Marywood University |
| Study Sponsor | Marywood University |
| Collaborators | Not Provided |
| Investigators | Principal Investigator: Kenneth W Rundell, PhD Marywood University |
| Verification Date | May 2009 |
Locations[ + expand ][ + ]
| Marywood University | Scranton, Pennsylvania, United States, 18509 |
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