Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?
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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.
| Condition | Intervention |
|---|---|
|
Airway Inflammation |
Other: placebo Drug: Montelukast |
| Study Type: | Interventional |
| Study Design: | Allocation: Randomized Endpoint Classification: Efficacy Study Intervention Model: Parallel Assignment Masking: Double Blind (Subject, Caregiver, Investigator) Primary Purpose: Basic Science |
| Official Title: | Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man? |
- Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction. [ Time Frame: February 2009 ] [ Designated as safety issue: No ]
- Montelukast protects against pollution induced vascular dysfunction. [ Time Frame: February 2009 ] [ Designated as safety issue: No ]
| Estimated Enrollment: | 24 |
| Study Start Date: | May 2007 |
| Study Completion Date: | May 2009 |
| Primary Completion Date: | March 2009 (Final data collection date for primary outcome measure) |
| Arms | Assigned Interventions |
|---|---|
|
Placebo Comparator: 1
Subject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo.
|
Other: placebo
Placebo
Other Name: Sugar Pill
|
|
Placebo Comparator: 2
Subject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo.
|
Other: placebo
Placebo
Other Name: Sugar Pill
|
|
Experimental: 3
Subject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally.
|
Drug: Montelukast
10 mg ingested orally 1 hour prior to exercise testing
Other Name: Singulair
|
|
Experimental: 4
Subject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally.
|
Drug: Montelukast
10 mg ingested orally 1 hour prior to exercise testing
Other Name: Singulair
|
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.
Eligibility| Ages Eligible for Study: | 18 Years to 30 Years |
| Genders Eligible for Study: | Male |
| Accepts Healthy Volunteers: | Yes |
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
Contacts and Locations| United States, Pennsylvania | |
| Marywood University | |
| Scranton, Pennsylvania, United States, 18509 | |
| Principal Investigator: | Kenneth W Rundell, PhD | Marywood University |
More Information
No publications provided
| Responsible Party: | Kenneth W. Rundell Ph.D., Marywood University |
| ClinicalTrials.gov Identifier: | NCT00814281 History of Changes |
| Other Study ID Numbers: | MU2007-005 |
| Study First Received: | December 22, 2008 |
| Last Updated: | May 20, 2009 |
| Health Authority: | United States: Institutional Review Board |
Keywords provided by Marywood University:
|
particulate air pollution leukotriene asthma |
montelukast vascular endothelial dysfunction nitric oxide(NO)endothelin (ET) system |
Additional relevant MeSH terms:
|
Inflammation Pathologic Processes Montelukast Leukotriene Antagonists Hormone Antagonists Hormones, Hormone Substitutes, and Hormone Antagonists |
Physiological Effects of Drugs Pharmacologic Actions Anti-Asthmatic Agents Respiratory System Agents Therapeutic Uses |
ClinicalTrials.gov processed this record on June 17, 2013