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

This study has been completed.
Sponsor:
Information provided by:
Marywood University
ClinicalTrials.gov Identifier:
NCT00814281
First received: December 22, 2008
Last updated: May 20, 2009
Last verified: May 2009

December 22, 2008
May 20, 2009
May 2007
March 2009   (final data collection date for primary outcome measure)
Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction. [ Time Frame: February 2009 ] [ Designated as safety issue: No ]
Same as current
Complete list of historical versions of study NCT00814281 on ClinicalTrials.gov Archive Site
Montelukast protects against pollution induced vascular dysfunction. [ Time Frame: February 2009 ] [ Designated as safety issue: No ]
Same as current
Not Provided
Not Provided
 
Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?
Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?

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.

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.

Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator)
Primary Purpose: Basic Science
Airway Inflammation
  • Other: placebo
    Placebo
    Other Name: Sugar Pill
  • Drug: Montelukast
    10 mg ingested orally 1 hour prior to exercise testing
    Other Name: Singulair
  • Placebo Comparator: 1
    Subject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo.
    Intervention: Other: placebo
  • Placebo Comparator: 2
    Subject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo.
    Intervention: Other: placebo
  • Experimental: 3
    Subject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally.
    Intervention: Drug: Montelukast
  • Experimental: 4
    Subject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally.
    Intervention: Drug: Montelukast
Not Provided

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
24
May 2009
March 2009   (final data collection date for primary outcome measure)

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
Male
18 Years to 30 Years
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00814281
MU2007-005
No
Kenneth W. Rundell Ph.D., Marywood University
Marywood University
Not Provided
Principal Investigator: Kenneth W Rundell, PhD Marywood University
Marywood University
May 2009

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP