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Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?

This study has been completed.
Sponsor:
ClinicalTrials.gov Identifier:
NCT00814281
First Posted: December 24, 2008
Last Update Posted: May 21, 2009
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by:
Marywood University
  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
Intervention Model: Parallel Assignment
Masking: Triple (Participant, Care Provider, Investigator)
Primary Purpose: Basic Science
Official Title: Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?

Resource links provided by NLM:


Further study details as provided by Marywood University:

Primary Outcome Measures:
  • Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction. [ Time Frame: February 2009 ]

Secondary Outcome Measures:
  • Montelukast protects against pollution induced vascular dysfunction. [ Time Frame: February 2009 ]

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

Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years to 30 Years   (Adult)
Sexes Eligible for Study:   Male
Accepts Healthy Volunteers:   Yes
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
  Contacts and Locations
Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00814281


Locations
United States, Pennsylvania
Marywood University
Scranton, Pennsylvania, United States, 18509
Sponsors and Collaborators
Marywood University
Investigators
Principal Investigator: Kenneth W Rundell, PhD Marywood University
  More Information

Responsible Party: Kenneth W. Rundell Ph.D., Marywood University
ClinicalTrials.gov Identifier: NCT00814281     History of Changes
Other Study ID Numbers: MU2007-005
First Submitted: December 22, 2008
First Posted: December 24, 2008
Last Update Posted: May 21, 2009
Last Verified: May 2009

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
Anti-Asthmatic Agents
Respiratory System Agents
Leukotriene Antagonists
Hormone Antagonists
Hormones, Hormone Substitutes, and Hormone Antagonists
Physiological Effects of Drugs
Cytochrome P-450 CYP1A2 Inducers
Cytochrome P-450 Enzyme Inducers
Molecular Mechanisms of Pharmacological Action


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