Residual oil fly ash

Lambert, A.L., et al., Enhanced allergic sensitization by residual oil fly ash particles is mediated by soluble metal constituents, Toxicol. Appl. Pharmacol. 165, 1, 84, 2000. 

Lindroos PN, Coin PG, Badgett A, et al. 1997. Alveolar macrophages stimulated with titanium dioxide, chrysotile asbestos, and residual oil fly ash upregulate the PDGF receptor-alpha on lung fibroblasts through an IL-1 beta-dependent mechanism. Am J Respir Cell Mol Biol 16 283-292. 

Doremus RH (1985) Rates of Phase Transformations. New York Academic Press Dreher KL, Jaskot RH, Lehmann JR, Richards JH, McGee JK, Ghio AJ, Costa DL (1997) Soluble transition metals mediate residual oil fly ash induced acute lung injury. J Toxicol Environ Health 50 285-305... 

Dreher K, Jaskot R, Kodavanti U, Lehmann J, Winsett D, Costa D (1996) Soluble transition metals mediate the acute pulmonary injury and airways hyperreactivity by residual oil fly ash particles. Chest 109 541-554... 

Katsouyanni K, Touloumi G, Samoli E et al (2001) Confounding and effect modification in the short-term effects of ambient particles on total mortality results from 29 European cities within the APHEA2 project. Epidemiology 12 521-531 Kodavanti UP, Jaskot RH, Costa DL et al (1997) Pulmonary proinflammatory gene induction following acute exposure to residual oil fly ash roles of particle-associated metals. Inhal Toxicol 9 679-701... 

Residual oil fly ash (ROFA) is an emission-source air pollutant which is generated from the burning of low sulphur residual oil. ROFA is composed of metals, sulphates, acids, and unknown materials, which are complexed to an insoluble, inert particulate core (Pritchard etal. 1996, Dreher etal. 1997). ROFA is an industrial air pollutant, the tracheal instillation of which produced airways hyperresponsiveness and acute lung injury, consisting of... 

Through activation of both capsaicin-pH sensitive irritant receptors, particulate matter as residual oil fly ash immediately (< 30 s) increased intracellular calcium levels ([Ca ],)in a human bronchial epithelial cell line (BEAS-2B) and, within 2 h exposure, key inflammatory cytokine transcripts (i.e., IL-6, IL-8, TNF-a) and subsequent release of IL-6 and IL-8 cytokine protein after 4 h exposure (Vero-NESi et al. 1999). 

Human alveolar epitheUal cells exposed to residual oil fly ash release inflanunatory cytokines including IL-6, IL-8, and tumour necrosis factor (Carter et al. 1997). The IL-6 response was inhibited by the metal chelator deferoxamine and the free radical scavenger N-acetyl-L-cysteine, suggesting that the activation of NFxB may be mediated through reactive oxygen intermediates generated by transition metals found in residual oil fly ash (Quay et al. 1998). 

Fly ashes from coal combustion have been used in various animal studies, with only modest effects (183). However, coal fly ash contrasts with fly ashes from oil combustion, from which the metals can be considerably more bioavailable (water- or acid-soluble). Early studies of residual oil fly ash have shown enhancement of pulmonary infections in mice and cytotoxicity to alveolar macrophages (180). The degree of acute inflammation (as measured by PMNs, lactic... 

Carter J, Ghio AJ, Samet JM, Devlin RB. Residual oil fly ash induces increases in mRNAs and proteins for IL-6, IL-8, and TNF in human airway epithelial cells. Am J Physiol 1997 146 180-188. 

Samet JM, Reed W, Ghio AJ, Devlin RB, Carter J, Dailey LM, Bromberg PA, Madden MC. Induction of prostaglandin H synthase 2 in cultured airway epithelial cells exposed to residual oil fly ash. Toxicol Appl Pharmocol 1996 141 159-168. 

Quay J, Reed W, Devlin RB. Residual oil fly ash upregulates IL-6 gene expression by processes involving NF-kB. Am J Cell Respir Mol Biol 1998 19 98-106. Schroeder WH, Dobson D, Kane DM, Johnson ND. Toxic trace elements associated with airborne particulate matter a review. Environ Sci Technol 1987 9 838-845. Mathias-Maser S, Jaenicke R. Examination of atmospheric bioaerosol particles with radii > 0.2 J.m. J Aerosol Sci 1994 25 1605-1613. 

Dye JA, Adler KB, Richards JH, Dreher KL. Epithelial injury induced by exposure to residual oil fly-ash particles role of reactive oxygen species Am J Respir Cell Mol Biol 1997 17 625-633. 

Watkinson WP, Campen MJ, Costa DL. Cardiac arrhythmia induction after exposure to residual oil fly ash particles in a rodent model of pulmonary hypertension. Toxicol Sci 1998 41 209-216. 

Figure 2 Mortality to streptococcal infection after intratracheal instillation of dusts increases with chelatable and total iron concentrations. Differences in mortality at 15 days were demonstrated for baghouse dust collected over Bochum, Germany (solid diamond), and a residual oil fly ash (open diamond) compared with those for saline (open circle) and Mount St. Helens dust (solid circle). (From Ref. 41.)...

Figure 5 Total IgE in the serum of rats exposed to residual oil fly ash 3 days before sensitization with dust mite (ROF/SAL), 3 days before challenge (SAL/ROF), and 3 days before each immunization procedure (ROF/ROF). indicates significant differences p < 0.05) from controls (SAL/SAL). IgE was quantified by ELISA n 5.

---