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Nicholas L. Mills,¹ Simon D. Robinson,¹ Paul H. B. Fokkens,² Daan L. A. C. Leseman,² Mark R. Miller,¹ David Anderson,³ Evelyn J. Freney,⁴ Mathew R. Heal,⁴ Robert J. Donovan,⁴ Anders Blomberg,⁵ Thomas Sandström,⁵ William MacNee,³ Nicholas A. Boon,¹ Ken Donaldson,³ David E. Newby,¹ and Flemming R. Cassee²

¹Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom; ²National Institute for Public Health and the Environment (RIVM), Bilthoven, Netherlands; ³ELEGI Colt Laboratory, Centre for Inflammation Research, University of Edinburgh, Edinburgh, United Kingdom; ⁴School of Chemistry, University of Edinburgh, Edinburgh, United Kingdom; ⁵Department of Respiratory Medicine and Allergy, Umeå University, Umeå, Sweden

Abstract
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.

Objectives: 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 µg/m³) were higher than ambient levels (31 ± 8 µg/m³) and levels in filtered air (0.5 ± 0.4 µg/m³ ; 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.

Key words: air pollution, blood flow, endothelium, fibrinolysis, inflammation. Environ Health Perspect 116:709–715 (2008) . doi:10.1289/ehp.11016 available via http://dx.doi.org/ [Online 22 February 2008]

Address correspondence to N. L. Mills, Centre for Cardiovascular Science, Chancellor's Building, The University of Edinburgh, Edinburgh, EH16 4SU UK. Telephone: 44 131 242 1850. Fax: 44 131 242 6379. E-mail: nick.mills@ed.ac.uk

This study was supported by the British Heart Foundation Project (03/017/15071) and Programme Grants (PG/05/003) and by the British Cardiovascular Society Research Fellowship (N.L.M.) .

We thank J. Boere for logistical support and assistance with this study, and C. Sioutas for technical advice on the concentrator technologies. We are grateful to P. Dawson, K. Darnley, and all the staff at the Wellcome Trust Clinical Research Facility for their assistance.

The authors declare they have no competing financial interests.

Received 24 October 2007 ; accepted 22 February 2008.