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Chem. Res. Toxicol. 2000, 13, 382-389
Mobilization of Iron from Coal Fly Ash Was Dependent upon the Particle Size and Source of Coal: Analysis of Rates and Mechanisms John M. Veranth,*,† Kevin R. Smith,‡ Autumn A. Hu,† JoAnn S. Lighty,† and Ann E. Aust‡ Department of Chemical and Fuels Engineering, University of Utah, Salt Lake City, Utah 84112-1114, and Department of Chemistry and Biochemistry, Utah State University, Logan, Utah 84322-0300 Received November 10, 1999
The observed iron mobilization rate from size-fractionated coal fly ash is consistent with the model predictions for a limiting case of mass transfer where the dominant resistance is diffusion through a layer of depleted solid between the surface of spherical particles and a shrinking core of unreacted material. The rate of mobilization of iron from coal fly ash under physiologically relevant conditions in vitro was previously shown to depend on the size of the ash particles and on the source of the coal, and these in vitro measurements have been shown to correlate with indirect measurements of excess iron in cultured cells. Existing iron mobilization data were compared to mathematical models for mass transfer and chemical reaction in solid-liquid heterogeneous systems. Liquid-phase diffusion resistance can be ruled out as the rate-limiting mechanism for iron mobilization as the model predictions for this case are clearly inconsistent with the measurements. Other plausible hypotheses, such as a rate limited by a heterogeneous surface reaction, cannot be conclusively ruled out by the available data. These mathematical analysis methods are applicable to the design of future experiments to determine the rate-limiting mechanism for the mobilization of iron and of other transition metals from both ambient air samples and surrogates for major sources of particulate air pollution.
Introduction Particulate air pollution has been associated with an increase in respiratory-related mortality and morbidity (1). This evidence motivated reconsideration of the United States ambient air quality standards for PM101 and PM2.5, even though the regulatory criteria document reported that a toxicological mechanism had not been identified (2, 3). Many hypotheses have been proposed for toxicological mechanisms by which inhaled particles can cause adverse health effects (4, 5). Particulate air pollution has been shown to be a source of bioavailable transition metals (6-8), and excess levels of transition metals in cells have been shown to act as catalysts in the formation of reactive oxygen species, such as the damaging hydroxyl radical (HO•) (9-13). Transition metals from particles have also been associated with the induction of inflammatory cytokines (9, 14). * To whom correspondence should be addressed: Department of Chemical and Fuels Engineering, 1495 E. 100 South, Room 207, University of Utah, Salt Lake City, UT 84112-1114. Phone: (801) 5813789. Fax: (801) 585-5607. E-mail:
[email protected]. † University of Utah. ‡ Utah State University. 1 Abbreviations: PM , particulate air pollution with a mean 10 aerodynamic diameter of
