Environmental Research 99 (2005) 40–47 Redox activity of airborne particulate matter at different sites in the Los Angeles Basin Arthur K. Cho a,b , Constantinos Sioutas a,c , Antonio H. Miguel a , Yoshito Kumagai a,d , Debra A. Schmitz a,b , Manisha Singh a,c , Arantza Eiguren-Fernandez a , John R. Froines a,e,Ã a Southern California Particle Center and Supersite, Institute of the Environment, University of California Los Angeles, Los Angeles, CA 90095, USA b Department of Molecular and Medical Pharmacology, School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA c Department of Civil and Environmental Engineering, University of Southern California, Los Angeles, CA 90089, USA d Department of Environmental Medicine, Institute of Community Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan e Center for Environmental & Occupational Health, School of Public Health, University of California Los Angeles, Los Angeles, CA 90095-172, USA Received 25 June 2004; received in revised form 19 November 2004; accepted 11 January 2005 Available online 28 April 2005 Abstract Epidemiologic studies have shown associations between ambient particulate matter (PM) and adverse health outcomes including increased mortality, emergency room visits, and time lost from school and work. The mechanisms of PM-related health effects are still incompletely understood, but a hypothesis under investigation is that many of the adverse health effects may derive from oxidative stress, initiated by the formation of reactive oxygen species (ROS) within affected cells. While the adverse effects from PM have historically been associated with the airborne concentration of PM and more recently fine-particle PM, we considered it relevant to develop an assay to quantitatively measure the ability of PM to catalyze ROS generation as the initial step in the induction of oxidative stress. This ability of PM could then be related to different sources, chemical composition, and physical and spatial/temporal characteristics in the ambient environment. The measurement of ROS-forming ability in relation to sources and other factors will have potential relevance to control of redox-active PM. If oxidative stress represents a relevant mechanism of toxicity from PM, the measurement of redox activity represents a first step in the elucidation of the subsequent downstream processes. We have developed an assay for PM redox activity, utilizing the reduction of oxygen by dithiothreitol which serves as an electron source. We have found that PM will catalyze the reduction of oxygen and have examined the distribution and chemical characteristics of the redox activity of PM fractions collected in different sites in the Los Angeles Basin. Samples of concentrated coarse, fine, and ultrafine PM, obtained with aerosol concentrators, were studied with regard to their chemical properties and redox activity. Redox activity was highest in the ultrafine fraction, in agreement with results indicating ultrafines were the most potent toward inducing that heme oxygenase expression and depleting intracellular glutathione, which has relevance to induction of oxidative stress. Comparison of the redox activity with chemical composition showed a reasonable correlation of redox activity with elemental carbon (r 2 ¼ 0:79), organic carbon (r 2 ¼ 0:53), and with benzo[ghi]perylene (r 2 ¼ 0:82), consistent with species typically found in mobile emission sources. r 2005 Elsevier Inc. All rights reserved. Keywords: PM; Redox cycling; Dithiothreitol; ROS; DTT; Ultrafine particles; Aerosol concentrators 1. Introduction There is extensive epidemiological evidence associat- ingairborneparticulatematter(PM)withadversehealth effects in humans (Pope et al., 2002, 2004; Johnson, 2004; Donaldson et al., 2001). The mechanisms of ARTICLE IN PRESS www.elsevier.com/locate/envres 0013-9351/$-see front matter r 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.envres.2005.01.003 Ã Corresponding author. Center for Environmental & Occupational Health, School of Public Health, University of California Los Angeles, Los Angeles, CA 90095-172, USA. Fax: +13102069903. E-mail address: jfroines@ucla.edu (J.R. Froines).