Exposure to concentrated ambient particles does not affect vascular function in patients with coronary heart disease.
BACKGROUND
Exposure to fine particulate air pollution is associated with increased cardiovascular morbidity and mortality. We previously demonstrated that exposure to dilute diesel exhaust causes vascular dysfunction in humans.


OBJECTIVE
We conducted a study to determine whether exposure to ambient particulate matter causes vascular dysfunction.


METHODS
Twelve male patients with stable coronary heart disease and 12 age-matched volunteers were exposed to concentrated ambient fine and ultrafine particles (CAPs) or filtered air for 2 hr using a randomized, double-blind cross-over study design. We measured peripheral vascular vasomotor and fibrinolytic function, and inflammatory variables-including circulating leukocytes, serum C-reactive protein, and exhaled breath 8-isoprostane and nitrotyrosine-6-8 hr after both exposures.


RESULTS
Particulate concentrations (mean +/- SE) in the exposure chamber (190+/-37 microg/m(3)) were higher than ambient levels (31+/-8 microg/m(3)) and levels in filtered air (0.5+/-0.4 microg/m(3); p<0.001). Chemical analysis of CAPs identified low levels of elemental carbon. Exhaled breath 8-isoprostane concentrations increased after exposure to CAPs (16.9+/-8.5 vs. 4.9+/-1.2 pg/mL, p<0.05), but markers of systemic inflammation were largely unchanged. Although there was a dose-dependent increase in blood flow and plasma tissue plasminogen activator release (p<0.001 for all), CAPs exposure had no effect on vascular function in either group.


CONCLUSIONS
Despite achieving marked increases in particulate matter, exposure to CAPs--low in combustion-derived particles--did not affect vasomotor or fibrinolytic function in either middle-aged healthy volunteers or patients with coronary heart disease. These findings contrast with previous exposures to dilute diesel exhaust and highlight the importance of particle composition in determining the vascular effects of particulate matter in humans.
Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom. nick.mills@ed.ac.uk
Nicholas L
NL
Mills
Simon D
SD
Robinson
Paul H B
PH
Fokkens
Daan L A C
DL
Leseman
Mark R
MR
Miller
David
D
Anderson
Evelyn J
EJ
Freney
Mathew R
MR
Heal
Robert J
RJ
Donovan
Anders
A
Blomberg
Thomas
T
Sandström
William
W
MacNee
Nicholas A
NA
Boon
Ken
K
Donaldson
David E
DE
Newby
Flemming R
FR
Cassee
D002097:C-Reactive Protein / Q000378:metabolism; D002319:Cardiovascular System / Q000187:drug effects* / Q000503:physiopathology; D003327:Coronary Disease / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D018592:Cross-Over Studies; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D004311:Double-Blind Method; D005342:Fibrinolysis / Q000187:drug effects; D006801:Humans; D019570:Inhalation Exposure; D008297:Male; D008875:Middle Aged; D052638:Particulate Matter / Q000008:administration & dosage* / Q000737:chemistry; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism; D014666:Vasomotor System / Q000187:drug effects / Q000503:physiopathology
D052638:Particulate Matter; C075750:8-epi-prostaglandin F2alpha; C002744:3-nitrotyrosine; D014443:Tyrosine; D002097:C-Reactive Protein; D015237:Dinoprost