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(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"

Nicholas L. Mills, MRCP; Simon D. Robinson, MRCP; Nicholas A. Boon, MD; David E. Newby, DM, PhD

Centre for Cardiovascular Science, Edinburgh University, Edinburgh, United Kingdom

Håkan Törnqvist, MD; Manuel Gonzalez, MD; Anders Blomberg, MD, PhD; Thomas Sandstrom, MD, PhD

Department of Respiratory Medicine and Allergy, Umeå University, Umeå, Sweden

Kareen Darnley, RN

Wellcome Trust Clinical Research Facility, Edinburgh, United Kingdom

William MacNee, MD; Ken Donaldson, PhD

ELEGI Colt Laboratory, Centre for Inflammation Research, Edinburgh University, Edinburgh, United Kingdom

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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 . . . [Full Text of this Article]