Airway InflammationNCT00814281
Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?
A study testing Montelukast in people with Airway Inflammation, run by Marywood University at 1 site in United States.
Trial 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… Read more about this study
- Who is it for?
- Ages 18 to 30 years, men onlyHealthy volunteers can take part
- Conditions the study is for
- Airway Inflammation
- What is being tested?
- Montelukast
- Type of treatment
- Pill or oral medicine
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 24 participants
- Where
- 1 siteUnited States
- Study dates
- May 2007to May 2009
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 30 years
- Men only
- Healthy volunteers accepted
- Adult
Who may be able to join
- Healthy male subjects
- between 18 and 30 years of age
- participant in endurance sport
Who cannot join
- history of blood clotting
- history of coagulation problems
- History of spontaneous pneumothorax
Trial locations and contacts
1 site in 1 country.
About this study
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.
Read the 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.
- Conditions
- Airway Inflammation
- Being tested
- placebo, Montelukast
- Keywords
- particulate air pollution, leukotriene, asthma, montelukast, vascular endothelial dysfunction, nitric oxide(NO)endothelin (ET) system
- Medical subject headings
- Asthma
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
placeboOther
Also called Sugar Pill
Placebo
MontelukastDrug
Also called Singulair
10 mg ingested orally 1 hour prior to exercise testing
| Study group | Role | What they receive |
|---|---|---|
| 1 | Placebo comparator | Subject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo. Receives: Other: placebo |
| 2 | Placebo comparator | Subject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo. Receives: Other: placebo |
| 3 | Experimental | Subject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally. Receives: Drug: Montelukast |
| 4 | Experimental | Subject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally. Receives: Drug: Montelukast |
What is being measured
The primary outcome is the main question the study is designed to answer.
Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction.
Measured: February 2009
Secondary outcomes (1)
Montelukast protects against pollution induced vascular dysfunction.
Measured: February 2009
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted24 Dec 2008 (estimated)
- Study startMay 2007
- Primary completionMar 2009
- Study completionMay 2009
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Airway InflammationStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind
- Who is masked
- Participant, Care provider, Investigator
- Enrolment
- 24 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Marywood University
- Sponsor type
- University, hospital or other
- Investigators
- Kenneth W Rundell, PhD, Principal investigator, Marywood University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00814281
- Sponsor's protocol ID
- MU2007-005
- Status last verified
- May 2009
- First submitted
- 22 Dec 2008
- Last updated
- 21 May 2009
- Results posted
- No
- Data monitoring committee
- No
Study at a glance
From the registry record, last updated by the sponsor on 21 May 2009. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Airborne Ultrafine and Fine Particulate Matter: A Cause for Endothelial Dysfunction in Man?
- ClinicalTrials.gov ID
- NCT00814281
- Acronym / sponsor ID
- MU2007-005
- Conditions
- Airway Inflammation
- Keywords
- particulate air pollution, leukotriene, asthma, montelukast, vascular endothelial dysfunction, nitric oxide(NO)endothelin (ET) system
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 24 participants (estimated)
- Lead sponsor
- Marywood UniversityUniversity, hospital or other
- Study start
- May 2007
- Primary completion
- Mar 2009 (actual)
- Study completion
- May 2009 (actual)
- First posted
- 24 Dec 2008 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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 design
- Primary purpose
- Basic science
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Triple blind (participant, care provider, investigator)
- Number of arms
- 4
| Arm | Type | Receives |
|---|---|---|
| 1 | Placebo comparator | Other: placeboSubject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo. |
| 2 | Placebo comparator | Other: placeboSubject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting a placebo. |
| 3 | Experimental | Drug: MontelukastSubject will exercise in high levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally. |
| 4 | Experimental | Drug: MontelukastSubject will exercise in low levels of ultrafine and fine particulate air pollution 1 hour after ingesting Montelukast 10 mg orally. |
Who may qualify
- Ages
- 18 to 30 years
- Sex
- Male only
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (3 listed)
- Healthy male subjects
- between 18 and 30 years of age
- participant in endurance sport
Key exclusion criteria (3 listed)
- history of blood clotting
- history of coagulation problems
- History of spontaneous pneumothorax
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| placeboAlso: Sugar PillPlacebo | Other | 1, 2 |
| MontelukastAlso: Singulair10 mg ingested orally 1 hour prior to exercise testing | Drug | 3, 4 |
Primary outcome
Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction.
Time frame: February 2009
1 secondary outcome
Montelukast protects against pollution induced vascular dysfunction.
Time frame: February 2009
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 21 May 2009.
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RecruitingPhase 4
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Kenneth W Rundell, PhD principal investigator
Marywood University
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Montelukast in people with Airway Inflammation, run by Marywood University at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 3 inclusion and 3 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 21 May 2009. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Exposure to airborne ultrafine and fine particulate matter causes vascular dysfunction. (time frame: February 2009). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 21 May 2009.