ToxSci Advance Access published online on July 13, 2006
Toxicological Sciences, doi:10.1093/toxsci/kfl062
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1 Center for Health and the Environment, University of California, Davis, CA
* To whom correspondence should be addressed. Although primary particle emissions of ash from coal-fired power plants are well controlled, coal fly ash (CFA) can still remain a significant fraction of the overall particle exposure for some plant workers and highly impacted communities. The effect of CFA on pulmonary and systemic inflammation and injury was measured in male Sprague-Dawley rats exposed to filtered air or to CFA for 4 hours/day for 3 days. The average concentration of CFA (PM2.5) was 1400 µg/m3, of which 600 µg/m3 was PM1. Animals were examined 18 and 36 hours post exposure. Chemical analysis of CFA detected silicon, calcium, aluminum, and iron, as major components. Total number of neutrophils in bronchoalveolar lavage fluid (BALF) following exposure to CFA was significantly increased along with significantly elevated blood neutrophils. Exposure to CFA caused slight increases in MIP-2, and marked increases in transferrin in BALF. IL-1 The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, United States Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflect the views and the policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.
Received April 17, 2006
Accepted July 6, 2006
Respiratory Toxicology
Acute Pulmonary and Systemic Effects of Inhaled Coal Fly Ash in Rats: Comparison to Ambient Environmental Particles
Kevin R. Smith 1,
John M. Veranth 2,
Urmila P. Kodavanti 3,
Ann E. Aust 4,
and
Kent E. Pinkerton 1 *
2 Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, UT
3 NHEERL, USEPA, Research Triangle Park, NC
4 Department of Chemistry and Biochemistry, Utah State University, Logan, UT
Kent E. Pinkerton, E-mail: kepinkerton{at}ucdavis.edu
Abstract 
and total antioxidant potential in lung tissues were also increased in rats exposed to CFA. Histological examination of lung tissue demonstrated focal alveolar septal thickening and increased cellularity in select alveoli immediately beyond terminal bronchioles. These responses are consistent with the ability of CFA to induce mild neutrophilic inflammation in the lung and blood following short-term exposure at levels that could be occupationally relevant. However, when comparing the effects of CFA with those of concentrated ambient particles, CFA does not appear to have greater potency to cause pulmonary alterations. This study furthers our understanding of possible mechanisms by which specific sources of particulate air pollution affect human health.
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