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Ralph J. Delfino,¹ Constantinos Sioutas,² and Shaista Malik³

¹Epidemiology Division, Department of Medicine, University of California, Irvine, Irvine, California, USA; ²Department of Civil and Environmental Engineering, University of Southern California, Los Angeles, California, USA; ³Cardiology Division, Department of Medicine, University of California, Irvine, Irvine, California, USA

Abstract
Numerous epidemiologic time-series studies have shown generally consistent associations of cardiovascular hospital admissions and mortality with outdoor air pollution, particularly mass concentrations of particulate matter (PM) ≤ 2.5 or ≤ 10 µm in diameter (PM_2.5, PM₁₀) . Panel studies with repeated measures have supported the time-series results showing associations between PM and risk of cardiac ischemia and arrhythmias, increased blood pressure, decreased heart rate variability, and increased circulating markers of inflammation and thrombosis. The causal components driving the PM associations remain to be identified. Epidemiologic data using pollutant gases and particle characteristics such as particle number concentration and elemental carbon have provided indirect evidence that products of fossil fuel combustion are important. Ultrafine particles < 0.1 µm (UFPs) dominate particle number concentrations and surface area and are therefore capable of carrying large concentrations of adsorbed or condensed toxic air pollutants. It is likely that redox-active components in UFPs from fossil fuel combustion reach cardiovascular target sites. High UFP exposures may lead to systemic inflammation through oxidative stress responses to reactive oxygen species and thereby promote the progression of atherosclerosis and precipitate acute cardiovascular responses ranging from increased blood pressure to myocardial infarction. The next steps in epidemiologic research are to identify more clearly the putative PM casual components and size fractions linked to their sources. To advance this, we discuss in a companion article (Sioutas C, Delfino RJ, Singh M. 2005. Environ Health Perspect 113:947-955) the need for and methods of UFP exposure assessment. Key words: cardiovascular diseases, cytokines, diesel, epidemiology, oxidative stress, particle size, toxic air pollutants. Environ Health Perspect 113:934-946 (2005) . doi:10.1289/ehp.7938 available via http://dx.doi.org/ [Online 16 March 2005]

Address correspondence to R.J. Delfino, Epidemiology Division, Department of Medicine, University of California, Irvine, 224 Irvine Hall, Irvine, CA 92697-7550 USA. Telephone: (949) 824-7401. Fax: (949) 824-4773. E-mail: rdelfino@uci.edu

This work was supported by grant ES-12243 from the National Institute of Environmental Health Sciences (NIEHS) , National Institutes of Health (NIH) ; the contents of this article are solely the responsibility of the author and do not necessarily represent the official views of the NIEHS, NIH. This work was also supported by the Southern California Particle Center and Supersite funded by the U.S. Environmental Protection Agency (U.S. EPA ; STAR award R82735201) .

This manuscript has not been subjected to the U.S. EPA peer and policy review and therefore does not necessarily reflect the views of the agencies. No official endorsement should be inferred.

The authors declare they have no competing financial interests.

Received 14 January 2005 ; accepted 16 March 2005.