doi: 10.1161/CIRCULATIONAHA.105.621789
(Circulation. 2006;113:e872.)
© 2006 American Heart Association, Inc.
Correspondence |
Response to Letter Regarding Article "Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis"
Centre for Cardiovascular Science, Edinburgh University, Edinburgh, United Kingdom
Department of Respiratory Medicine and Allergy, Umeå University, Umeå, Sweden
Wellcome Trust Clinical Research Facility, Edinburgh, United Kingdom
ELEGI Colt Laboratory, Centre for Inflammation Research, Edinburgh University, Edinburgh, United Kingdom
We thank Dr Brook and colleagues for their interest in our study,1 in which we describe an acute impairment of vascular and endogenous fibrinolytic function after exposure to dilute diesel exhaust. Brook et al propose that vascular dysfunction may cause vasoconstriction and increase blood pressure to explain the cardiovascular risk associated with air pollution exposure. This is an interesting and potentially important hypothesis. They comment that, in our study, there appeared to be small differences (6 to 8 mm Hg) in both diastolic and systolic pressure 2 hours after diesel exhaust exposure. However, although these differences could potentially be clinically important, they were not statistically significant.
There have been previous reports of increases in diastolic pressure after a 2-hour exposure to ambient particles in supine volunteers.2 In our study,1 volunteers exercised intermittently during the exposure, and arterial pressure was measured in resting conditions after the exposure. This protocol design may have obscured any potential hypertensive effects, and we do not believe the study had sufficient power to detect meaningful differences in blood pressure. However, although vasoconstriction could have occurred in other vascular beds, we did not observe any effect on resting forearm blood flow. Conditions associated with endothelial dysfunction, such as hypercholesterolemia,3 often do not cause hypertension or alterations in basal vascular tone, and our findings are consistent with the absence of hypertensive or peripheral vasoconstrictive effects. This does not preclude the induction of other mechanisms, such as alterations in autonomic nervous system activity that may be operating in addition to vascular dysfunction.
We agree with Dr Brook and colleagues and suggest that there is a need for further appropriately designed and powered studies to determine whether exposure to diesel exhaust increases arterial pressure. These studies will need to consider the role of the autonomic nervous system, as well as constitutive nitric oxide, as important potential modulators of arterial pressure.
 |
Acknowledgments |
|---|
Disclosures
None.
|
References |
|---|
 Top References |
|---|
- Mills NL, Tornqvist H, Robinson SD, Gonzalez M, Darnley K, MacNee W, Boon NA, Donaldson K, Blomberg A, Sandstrom T, Newby DE. Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation. 2005; 112: 3930–3936.
[Abstract/Free Full Text] - Urch B, Silverman F, Corey P, Brook JR, Lukic KZ, Rajagopalan S, Brook RD. Acute blood pressure responses in healthy adults during controlled air pollution exposures. Environ Health Perspect. 2005; 113: 1052–1055.[Medline]
[Order article via Infotrieve]
- Casino PR, Kilcoyne CM, Quyyumi AA, Hoeg JM, Panza JA. The role of nitric oxide in endothelium-dependent vasodilation of hypercholesterolemic patients. Circulation. 1993; 88: 2541–2547.
[Abstract/Free Full Text]
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||