The Cardiovascular Effects of Nitrogen Dioxide Exposure

NCT00774514 | Completed

• 1 other identifier: Dnr 08-113M
• Study Type: interventional
• Target: 12
• Locations: 1 country
• Sites: 1

Brief Summary

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.

Conditions

Endothelial Dysfunction

Keywords

Air Pollution; Nitrogen Dioxide; NO2; Endothelial dysfunction

Outcome Measures

Primary Outcomes (1)

• Forearm blood flow measured by venous occlusion plethysmography in response to intraarterial vasodilators (acetylcholine, sodium nitroprusside, bradykinin and verapamil)

  4-6 hours after exposure

Secondary Outcomes (2)

• Plasma t-PA concentrations after infusion of bradykinin

  During forearm study

• Exhaled nitric oxide

  4-6 hours after exposure

Study Arms (2)

Air exposure

EXPERIMENTAL

1 hour exposure to filtered air during intermittent exercise

Procedure: Forearm Vascular Study

NO2 exposure

EXPERIMENTAL

1 hour exposure to nitrogen dioxide at 4ppm during intermittent exercise

Procedure: Forearm Vascular Study

Interventions

Forearm Vascular Study PROCEDURE

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)

Also known as: ACh, SNP, BK

Air exposure; NO2 exposure

Eligibility Criteria

• Sex: male
• Healthy Volunteers: Yes
• Age Groups: Child (0-17), Adult (18-64), Older Adult (65+)

You may qualify if:

• Healthy male volunteers

You may not qualify if:

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

Sponsors & Collaborators

• University of Edinburgh: lead
• Umeå University: collaborator

Study Sites (1)

Umeå University

Umeå, Sweden

Location

Study Officials

• Thomas Sandström, MD PhD

  Umeå University

  PRINCIPAL INVESTIGATOR

• Anders Blomberg, MD PhD

  Umeå University

  PRINCIPAL INVESTIGATOR

Study Design

• Study Type: interventional
• Phase: not applicable
• Allocation: RANDOMIZED
• Masking: TRIPLE
• Who Masked: PARTICIPANT, INVESTIGATOR, OUTCOMES ASSESSOR
• Purpose: BASIC SCIENCE
• Intervention Model: CROSSOVER
• Sponsor Type: OTHER

Study Record Dates

• First Submitted: October 16, 2008
• First Posted: October 17, 2008
• Study Start: October 1, 2008
• Primary Completion: December 1, 2008
• Study Completion: December 1, 2008
• Last Updated: April 9, 2009

Record last verified: 2009-04

Locations

SE (1)