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ToxSci Advance Access originally published online on July 13, 2006
Toxicological Sciences 2006 93(2):390-399; doi:10.1093/toxsci/kfl062
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Acute Pulmonary and Systemic Effects of Inhaled Coal Fly Ash in Rats: Comparison to Ambient Environmental Particles

Kevin R. Smith*, John M. Veranth{dagger}, Urmila P. Kodavanti{ddagger}, Ann E. Aust§ and Kent E. Pinkerton*,1

* Center for Health and the Environment, University of California, Davis, California 95616; {dagger} Department of Pharmacology and Toxicology, University of Utah, Salt Lake City, Utah 84112; {ddagger} NHEERL, USEPA, Research Triangle Park, North Carolina 27711; and § Department of Chemistry and Biochemistry, Utah State University, Logan, Utah 84322-0300

Received April 17, 2006; accepted July 6, 2006

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 CFA for 4 h/day for 3 days. The average concentration of CFA particulate matter less than 2.5 µm (PM2.5) was 1400 µg/m3, of which 600 µg/m3 was PM1. Animals were examined 18 and 36 h postexposure. 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 macrophage inflammatory protein-2, and marked increases in transferrin in BALF. Interleukin-1ß 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.

Key Words: coal fly ash; BALF; IL-1ß; TNF-{alpha}; MIP-2; PM2.5; inhalation; pulmonary toxicology; concentrated ambient particles; iron; inflammation.


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