Abstract:
RATIONALE:Exposure to combustion-derived air pollution is associated with an early (1-2 h) and sustained (24 h) rise in cardiovascular morbidity and mortality. We have previously demonstrated that inhalation of diesel exhaust causes an immediate (within 2 h) impairment of vascular and endothelial function in humans. OBJECTIVES:To investigate the vascular and systemic effects of diesel exhaust in humans 24 hours after inhalation. METHODS:Fifteen healthy men were exposed to diesel exhaust (particulate concentration, 300 microg/m(3)) or filtered air for 1 hour in a double-blind, randomized, crossover study. Twenty-four hours after exposure, bilateral forearm blood flow, and inflammatory and fibrinolytic markers were measured before and during unilateral intrabrachial bradykinin (100-1,000 pmol/min), acetylcholine (5-20 microg/min), sodium nitroprusside (2-8 microg/min), and verapamil (10-100 microg/min) infusions. MEASUREMENTS AND MAIN RESULTS:Resting forearm blood flow, blood pressure, and basal fibrinolytic markers were similar 24 hours after either exposure. Diesel exhaust increased plasma cytokine concentrations (tumor necrosis factor-alpha and interleukin-6, p < 0.05 for both) but appeared to reduce acetylcholine (p = 0.01), and bradykinin (p = 0.08) induced forearm vasodilatation. In contrast, there were no differences in either endothelium-independent (sodium nitroprusside and verapamil) vasodilatation or bradykinin-induced acute plasma tissue plasminogen activator release. CONCLUSIONS:Twenty-four hours after diesel exposure, there is a selective and persistent impairment of endothelium-dependent vasodilatation that occurs in the presence of mild systemic inflammation. These findings suggest that combustion-derived air pollution may have important systemic and adverse vascular effects for at least 24 hours after exposure.
journal_name
Am J Respir Crit Care Medauthors
Törnqvist H,Mills NL,Gonzalez M,Miller MR,Robinson SD,Megson IL,Macnee W,Donaldson K,Söderberg S,Newby DE,Sandström T,Blomberg Adoi
10.1164/rccm.200606-872OCsubject
Has Abstractpub_date
2007-08-15 00:00:00pages
395-400issue
4eissn
1073-449Xissn
1535-4970pii
200606-872OCjournal_volume
176pub_type
杂志文章,随机对照试验abstract::Damage to the airway epithelium is one prominent feature of chronic asthma. Corticosteroids induce apoptosis in inflammatory cells, which in part explains their ability to suppress airway inflammation. However, corticosteroid therapy does not necessarily reverse epithelial damage. We hypothesized that corticosteroids ...
journal_title:American journal of respiratory and critical care medicine
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