Combustion Derived Air Pollution and Vascular Function

Not Applicable

Completed

• Conditions: Endothelial Dysfunction

• Registration Number: NCT00775099
• Lead Sponsor: University of Edinburgh

Brief Summary

Air pollution is a major cause of cardiovascular morbidity and mortality. The components of air pollution responsible and the mechanisms through which they might mediate these harmful effects remain only partially understood. The link between cardiovascular disease and air pollution is strongest for fine particulate matter. Fine particulate matter (PM) is produced from the combustion of fossil fuels with the most significant threat thought to be posed by small particles less than 10µm (PM 10) which can be inhaled into the lungs. We propose to identify the precise component of diesel exhaust that mediates the adverse cardiovascular effects using a carbon particle generator, and a particle concentrator. The aim of this study proposal is to assess the vascular effects of different types and components of air pollution in healthy subjects. We intend to test the hypotheses that:

1. Combustion derived nanoparticulate causes an acute impairment of endothelial vasomotor and fibrinolytic function in healthy volunteers.

2. Exposure to combustion derived air pollution is associated with increased thrombus formation.

Detailed Description

Not available

Study Timeline

• Study Start: 2005-09
• Primary Completion: 2006-03
• Study Completion: 2006-03
• Status Verified: 2008-10
• Study First Submitted: 2008-10-16
• Study First Submitted QC: 2008-10-16
• Last Update Submitted: 2008-10-16
• Study First Posted: 2008-10-17
• Last Update Posted: 2008-10-17

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 16

Inclusion Criteria

• Healthy volunteers

Exclusion Criteria

• Current smokers
• Significant occupational exposure to air pollution
• History of lung disease
• Women of child-bearing potential
• Malignant arrhythmias
• Renal or hepatic failure
• Significant co-morbidity
• Systolic blood pressure >190 or <100 mmHg
• Previous history of blood dyscrasia
• Unable to tolerate the supine position
• Lack of informed consent
• Blood donation within last 3 months

Study & Design

• Study Type: INTERVENTIONAL
• Study Design: CROSSOVER

Primary Outcome Measures

Name	Time	Method
Forearm blood flow measured by forearm venous occlusion plethysmography in response to infused vasodilators	6-8 hours after exposure

Secondary Outcome Measures

Name	Time	Method
Ex-vivo thrombus formation assessed using the Badimon chamber	6 hours after exposure
Arterial stiffness measured by radial artery tonometry	Before and after exposure
Heart rate and heart rate variability measured with 3 lead Holter electrographic monitors	During and for 24 hours after exposure
Blood pressure	During and after exposure and during forearm study
Plasma t-PA and PAI concentrations following infusion of bradykinin	During forearm study
Plasma inflammatory markers IL-6, TNF-alpha, IL-1 and hsCRP	Before and after exposure
Platelet monocyte binding as measured by flow cytometry	After the exposure

Trial Locations

Locations (1)

University of Edinburgh; 🇬🇧 Edinburgh, United Kingdom