The Cardiovascular Effects of Nitrogen Dioxide Exposure - Full Text View

Sponsor:	University of Edinburgh
Collaborator:	Umeå University
Information provided by:	University of Edinburgh
ClinicalTrials.gov Identifier:	NCT00774514

Purpose

Exposure to air pollution has been linked to increased cardiorespiratory morbidity and mortality. The exact component of air pollution that mediates this effect is unknown, but the link is strongest for fine combustion derived particulate matter derived from traffic sources. It has been demonstrated that inhalation of diesel exhaust impairs vascular vasomotor tone and endogenous fibrinolysis. Recent studies using an inline retrofit particle trap to reduce the particulate component of exhaust have shown that filtering particles leads to a reversal of the endothelial dysfunction seen after diesel exhaust exposure, and have even suggested an augmentation of vascular function. This raises the question of the cardiovascular effects of the gaseous pollutants, the most abundant of which is nitrogen dioxide. In this study we plan to investigate the cardiovascular effects of nitrogen dioxide exposure.

Condition	Intervention
Endothelial Dysfunction	Procedure: Forearm Vascular Study

Study Type:	Interventional
Study Design:	Basic Science, Randomized, Double Blind (Subject, Investigator, Outcomes Assessor), Crossover Assignment
Official Title:	The Cardiovascular Effects of Nitrogen Dioxide Exposure

Resource links provided by NLM:

MedlinePlus related topics: Air Pollution

U.S. FDA Resources

Further study details as provided by University of Edinburgh:

Primary Outcome Measures:

Forearm blood flow measured by venous occlusion plethysmography in response to intraarterial vasodilators (acetylcholine, sodium nitroprusside, bradykinin and verapamil) [ Time Frame: 4-6 hours after exposure ] [ Designated as safety issue: No ]

Secondary Outcome Measures:

Plasma t-PA concentrations after infusion of bradykinin [ Time Frame: During forearm study ] [ Designated as safety issue: No ]
Exhaled nitric oxide [ Time Frame: 4-6 hours after exposure ] [ Designated as safety issue: No ]

Estimated Enrollment:	12
Study Start Date:	October 2008
Study Completion Date:	December 2008
Primary Completion Date:	December 2008 (Final data collection date for primary outcome measure)

Arms	Assigned Interventions
Air exposure: Experimental 1 hour exposure to filtered air during intermittent exercise	Procedure: Forearm Vascular Study Forearm venous occlusion plethysmography to measure forearm blood flow during intrabrachial infusion of vasodilators Acetylcholine (5-20 mg/min), sodium nitroprusside (2-8 µg/min), bradykinin (100-1000 pmol/min) and verapamil (10-100 µg/min)
NO2 exposure: Experimental 1 hour exposure to nitrogen dioxide at 4ppm during intermittent exercise	Procedure: Forearm Vascular Study Forearm venous occlusion plethysmography to measure forearm blood flow during intrabrachial infusion of vasodilators Acetylcholine (5-20 mg/min), sodium nitroprusside (2-8 µg/min), bradykinin (100-1000 pmol/min) and verapamil (10-100 µg/min)

Eligibility

Genders Eligible for Study:	Male
Accepts Healthy Volunteers:	Yes

Criteria

Inclusion Criteria:

Healthy male volunteers

Exclusion Criteria:

Current smokers
Significant occupational exposure to air pollution
Regular medication use
Intercurrent illness

Contacts and Locations

Please refer to this study by its ClinicalTrials.gov identifier: NCT00774514

Locations

Sweden
Umeå University
Umeå, Sweden

Sponsors and Collaborators

University of Edinburgh

Umeå University

Investigators

Principal Investigator:	Thomas Sandström, MD PhD	Umeå University
Principal Investigator:	Anders Blomberg, MD PhD	Umeå University

More Information

No publications provided

Responsible Party:	Umeå University ( Dr Anders Blomberg )
Study ID Numbers:	Dnr 08-113M
Study First Received:	October 16, 2008
Last Updated:	April 8, 2009
ClinicalTrials.gov Identifier:	NCT00774514 History of Changes
Health Authority:	Sweden: Regional Ethical Review Board

Keywords provided by University of Edinburgh:

Air Pollution
Nitrogen Dioxide
NO2
Endothelial dysfunction

ClinicalTrials.gov processed this record on November 20, 2009