Letter by Brook et al Regarding Article “Diesel Exhaust Inhalation Causes Vascular Dysfunction and Impaired Endogenous Fibrinolysis”
To the Editor:
We read with interest the results of the article by Mills et al1 demonstrating an acute impairment in microvascular endothelial function after the controlled inhalation of diesel exhaust particles by healthy men. As discussed, their observations complement our findings regarding exposure to both concentrated2 and ambient levels3 of particulate matter. The sum of evidence thus suggests that the acute triggering of systemic vascular dysfunction is likely a central mechanism linking air pollution to increased short-term cardiovascular risk.
However, we believe that an important observation in the study by Mills et al1 was not adequately addressed. When blood pressure was measured in the 15 subjects 2 hours after exposure, they observed a very pronounced, although marginally statistically nonsignificant, elevation of 8 mm Hg (P=0.13) for systolic and 6 mm Hg (P=0.08) for diastolic pressure. No discussion of this trend toward a clinically meaningful pro-hypertensive response was provided.
In 23 healthy adults, we previously demonstrated that diastolic blood pressure rapidly increased by 6 mm Hg after the inhalation of concentrated ambient particles mixed with ozone.4 Zanobetti et al5 also found blood pressure to be increased in direct relation to ambient levels of particulate matter in 62 Boston area residents with heart disease. The lack of statistical significance of the blood pressure elevation in the article by Mills et al1 is most probably explained simply by an inadequate sample size. If more subjects had been tested, it is likely that a significant pressor response would have been found in their study as well. We believe it is crucial to highlight this important vascular response to pollution. The findings of Mills et al1 actually serve to bolster the evidence that an acute increase in blood pressure,4,5 probably mediated by vasoconstriction2 in resistance arterioles within susceptible individuals, is a factor contributing to the increased risk for myocardial infarction/ischemia and stroke after air pollution exposure. The results also suggest that basal arteriole tone and not just agonist-stimulated vasodilatation is altered in a manner favoring vasoconstriction. Their study1 was likely similarly underpowered and not specifically designed to observe air pollution-mediated alterations in resting arterial tone. More detailed studies should be performed to corroborate this hypothesis.
Mills NL, Tornqvist H, Robinson SD, Gonzalez M, Darnley K, MacNee W, Boon NA, Donaldson K, Blomerg A, Sandstrom T, Newby DE. Diesel exhaust inhalation causes vascular dysfunction and impaired endogenous fibrinolysis. Circulation. 2005; 112: 3930–3936.
Brook RD, Brook JR, Urch B, Vinvent R, Rajagopalan S, Silverman F. Inhalation of fine particulate air pollution and ozone causes arterial vasoconstriction in healthy adults. Circulation. 2002; 105: 1534–1536.
O’Neill MS, Veves A, Zanobetti A, Sarnar JA, Gold DR, Economides PA, Horton ES, Schwartz J. Diabetes enhances vulnerability to particulate air pollution-associated impairment in vascular reactivity and endothelial function. Circulation. 2005; 111: 2913–2920.
Zanobetti A, Canner MJ, Stone PH, Schwartz J, Sher D, Eagan-Bengston E, Gates KA, Hartley LH, Suh H, Gold DR. Ambient pollution and blood pressure in cardiac rehabilitation patients. Circulation. 2004; 110: 2184–2189.