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Andrew J. Ghio,¹ Robert Silbajoris,¹ Johnny L. Carson,² and James M. Samet¹

¹National Health and Environmental Effects Research Laboratory, Office for Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA; ²Department of Pediatrics and the Center for Environmental Medicine and Lung Biology, University of North Carolina, Chapel Hill, North Carolina, USA

Abstract

Epidemiologic studies have demonstrated increased human morbidity and mortality with elevations in the concentration of ambient air particulate matter (PM) . Fugitive fly ash from the combustion of oil and residual fuel oil significantly contributes to the ambient air particle burden. Residual oil fly ash (ROFA) is remarkable in the capacity to provoke injury in experimental systems. The unique composition of this emission source particle makes it particularly useful as a surrogate for ambient air PM in studies of biologic effects testing the hypothesis that metals mediate the biologic effects of air pollution particles. A majority of the in vitro and animal model investigations support the postulate that transition metals present in ROFA (especially vanadium) participate in Fenton-like chemical reactions to produce reactive oxygen species. This is associated with tyrosine phosphorylation, nuclear factor kappa B and other transcription factor activation, induction of inflammatory mediator expression, and inflammatory lung injury. It is also evident that vanadium accounts for a significant portion of the biologic activity of ROFA. The extrapolation of this body of investigation on ROFA to the field of ambient air PM is difficult, as particles in numerous environments have such small amounts of vanadium. Key words: air pollution, lung diseases, oxidative stress, vanadium. Environ Health Perspect 110(suppl 1) :89-102 (2002) .

http://ehpnet1.niehs.nih.gov/docs/2002/suppl-1/89-94ghio/abstract.html