The Cardiovascular Effects of Nitrogen Dioxide Exposure

Status

Completed

Phases

Study type

Interventional

Source

ClinicalTrials.gov

Registry ID

NCT00774514

Enrollment

Registered

2008-10-17

Start date

2008-10-31

Completion date

2008-12-31

Last updated

2009-04-09

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Endothelial Dysfunction

Keywords

Air Pollution, Nitrogen Dioxide, NO2, Endothelial dysfunction

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.

Interventions

PROCEDUREForearm 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)

Study design

Allocation

RANDOMIZED

Intervention model

CROSSOVER

Primary purpose

BASIC_SCIENCE

Masking

TRIPLE (Subject, Investigator, Outcomes Assessor)

Eligibility

Sex/Gender

MALE

Healthy volunteers

Yes

Inclusion criteria

* Healthy male volunteers

Exclusion criteria

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

Design outcomes

Primary

Measure	Time frame
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

Measure	Time frame
Plasma t-PA concentrations after infusion of bradykinin	During forearm study
Exhaled nitric oxide	4-6 hours after exposure

Countries

Sweden

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026