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John M. Veranth,¹ Tyler A. Moss,¹ Judith C. Chow,² Raed Labban,³ William K. Nichols,¹ John C. Walton,⁴ John G. Watson,² and Garold S. Yost¹

¹Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah, USA; ²Atmospheric Sciences Division, Desert Research Institute, Reno, Nevada, USA; ³Department of Chemical Engineering, University of Utah, Salt Lake City, Utah, USA; ⁴Department of Civil and Environmental Engineering, University of Texas at El Paso, El Paso, Texas, USA

Abstract
We treated human lung epithelial cells, type BEAS-2B, with 10-80 µg/cm² of dust from soils and road surfaces in the western United States that contained particulate matter (PM) < 2.5 µm aerodynamic diameter. Cell viability and cytokine secretion responses were measured at 24 hr. Each dust sample is a complex mixture containing particles from different minerals mixed with biogenic and anthropogenic materials. We determined the particle chemical composition using methods based on the U.S. Environmental Protection Agency Speciation Trends Network (STN) and the National Park Service Interagency Monitoring of Protected Visual Environments (IMPROVE) network. The functionally defined carbon fractions reported by the ambient monitoring networks have not been widely used for toxicology studies. The soil-derived PM_2.5 from different sites showed a wide range of potency for inducing the release of the proinflammatory cytokines interleukin-6 (IL-6) and IL-8 in vitro. Univariate regression and multivariate redundancy analysis were used to test for correlation of viability and cytokine release with the concentrations of 40 elements, 7 ions, and 8 carbon fractions. The particles showed positive correlation between IL-6 release and the elemental and pyrolyzable carbon fractions, and the strongest correlation involving crustal elements was between IL-6 release and the aluminum:silicon ratio. The observed correlations between low-volatility organic components of soil- and road-derived dusts and the cytokine release by BEAS-2B cells are relevant for investigation of mechanisms linking specific air pollution particle types with the initiating events leading to airway inflammation in sensitive populations. Key words: air pollutants, BEAS-2B, carbonaceous aerosol, cell line, environmental analysis, fugitive dust, interleukin-6, interleukin-8, lung epithelial cells, Speciation Trends Network, thermal/optical reflectance. Environ Health Perspect 114: 341-349 (2006) . doi:10.1289/ehp.8360 available via http://dx.doi.org/ [Online 29 September 2005]

Address correspondence to J.M. Veranth, Department of Pharmacology and Toxicology, University of Utah, 30 South 2000 East, Room 112 Skaggs Hall, Salt Lake City, UT 84112-5820 USA. Telephone: (801) 581-3789. Fax: (801) 585-3945. E-mail: John.Veranth@utah.edu

We thank R. Devlin and L. Dailey for providing training in U.S. Environmental Protection Agency (EPA) laboratory cell culture procedures ; N. Kimball, D. Lanza, E. Kaser, M. Veranth, and S. Kohl for technical assistance ; and L. Garcia, E. Duran, E. Laija, B. Musick, R. Putman, and various land owners and managers for assistance with field sampling.

This work was supported by National Institute of Environmental Health Sciences grant K25 ES011281 (J.M.V.) , Southwest Center for Environmental Research and Policy grant EH-03-03 (J.C.W. and students) , the U.S. EPA Science to Achieve Results (STAR) program (G.S.Y.) , and the Strategic Environmental Research and Development Program grant CP-1190 (J.C.C., J.G.W.) .

The authors declare they have no competing financial interests.

Received 25 May 2005 ; accepted 29 September 2005.