Metal and Sulfate Composition of Residual Oil Fly Ash Determines Airway Hyperreactivity and Lung Injury in Rats

Gavett, Stephen H.; Madison, Sharon L.; Dreher, Kevin L.; Winsett, Darrell W.; McGee, John K.; Costa, Daniel L.

doi:10.1006/enrs.1997.3732

Cited by 145 publications

(69 citation statements)

References 35 publications

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“…# p < 0.05 versus allergic mice exposed at challenge phase to control filter extract and to Zerbst PM 2.5 . oil fly ash (ROFA) samples with different sulfate and metal compositions, the sample with higher zinc caused significantly greater lung inflammation and airway hyperresponsiveness in rats than the sample with higher sulfate, nickel, and vanadium (Gavett et al 1997). Accordingly, the relationships of zinc, nickel, and vanadium content with pulmonary effects observed in normal, nonallergic rats (Gavett et al 1997) are consistent with those observed in this study.…”

Section: Discussionsupporting

confidence: 87%

“…oil fly ash (ROFA) samples with different sulfate and metal compositions, the sample with higher zinc caused significantly greater lung inflammation and airway hyperresponsiveness in rats than the sample with higher sulfate, nickel, and vanadium (Gavett et al 1997). Accordingly, the relationships of zinc, nickel, and vanadium content with pulmonary effects observed in normal, nonallergic rats (Gavett et al 1997) are consistent with those observed in this study. In a Brown-Norway rat model of house dust mite allergy, administration of ROFA or its soluble metal constituents before sensitization increased serum house dust mitespecific IgE levels, immediate allergic responses, and numbers of BAL eosinophils (Lambert et al 1999(Lambert et al , 2000.…”

Section: Discussionsupporting

confidence: 87%

“…The BAL fluid was centrifuged, supernatants were saved for biochemical and cytokine analyses, total cells were counted, and cell differentials were calculated (500 cells/sample). BAL supernatant levels of total protein, albumin, LDH, and NAG are routine measures of lung injury (Henderson et al 1985) and were carried out as previously described (Gavett et al 1997).…”

Section: Metal Composition Of Ambient Pm 25 Influences Severity Of Amentioning

confidence: 99%

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Metal composition of ambient PM2.5 influences severity of allergic airways disease in mice.

Gavett

Haykal-Coates

Copeland

et al. 2003

Environ Health Perspect

159

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Children living in Hettstedt in eastern Germany have been reported to have a higher prevalence of sensitization to common aeroallergens than another cohort living in the neighboring city of Zerbst; these differences correlated with the presence of industrial air pollution. Samples of fine particulate matter (< 2.5 micro m aerodynamic diameter; PM(2.5)) collected in Hettstedt in 1999 had several-fold higher levels of zinc, magnesium, lead, copper, and cadmium than samples from Zerbst. To determine if the results from epidemiologic studies could be repeated in an animal model, we administered PM(2.5) from Hettstedt and Zerbst to ovalbumin-allergic mice. In Balb/c mice, PM(2.5) from Hettstedt, but not PM(2.5) from Zerbst or control filter extract, caused a significant increase in immediate responses to ovalbumin challenge when aspirated 2 hr before challenge, but not when aspirated immediately before sensitization 2 weeks earlier. Antigen-specific IgE was increased by Hettstedt PM(2.5) whether administered before sensitization or challenge. Airway responsiveness to methacholine aerosol and lung inflammatory cell numbers were significantly increased only in allergic mice exposed to Hettstedt PM(2.5) before challenge. Both Hettstedt and Zerbst PM(2.5) significantly increased lung injury parameters and proinflammatory cytokines. These results are consistent with epidemiologic findings and show that metal composition of ambient PM(2.5) influences the severity of allergic respiratory disease.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionsupporting

confidence: 87%

Section: Metal Composition Of Ambient Pm 25 Influences Severity Of Amentioning

confidence: 99%

See 1 more Smart Citation

Metal composition of ambient PM2.5 influences severity of allergic airways disease in mice.

Gavett

Haykal-Coates

Copeland

et al. 2003

Environ Health Perspect

159

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“…The metal composition of the ash appears critical to the development of airway hyperreactivity, as assessed by acetylcholine challenge (9). In addition, there are effects of ROFA on sensitization to allergens in animal models of pulmonary allergy, with significant elevations in eosinophils, IL-10, antigen specific immunoglobulin E, and associated immediate bronchoconstriction responses to antigen challenge (36)(37)(38)(39). This effect can be reproduced by the metal leachate of ROFA as well as individual metallic constituents of ROFA (35) and can be abrogated by DMTU pretreatment (40).…”

Section: Physiologic Biochemical Cellular and Molecular Effects Ofmentioning

confidence: 99%

Biologic effects of oil fly ash.

Ghio

Silbajoris

Carson

et al. 2002

Environ Health Perspect

176

104

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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.

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“…This complexity has hampered investigations into the culpable factor(s) of PM toxicity and suggests that PM may target a variety of pathways. Consequently, most experimental research has focused on the individual chemical components identi®ed on certain industrial PM such as transition metals (Hatch et al, 1985;Gilmour et al, 1996;Pritchard et al, 1996;Dreher et al, 1997;Carter et al, 1997;Gavett et al, 1997;Kadiiska et al, 1997;Dreher et al, 1998), biologicals (e.g. endotoxins, pollen) (Becker et al, 1996), and acidic components (Chen et al, 1992;Brauer et al, 1995;Lippmann and Thurston, 1996;Kimmel et al, 1997;Zelikoff et al, 1997;Gwynn et al, 2000).…”

Section: Particulate Matter (Pm)mentioning

confidence: 99%

Neurogenic Inflammation and Particulate Matter (PM) Air Pollutants

Veronesi

Oortgiesen

2001

NeuroToxicology

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Exposure to a class of airborne pollutants known as particulate matter (PM) is an environmental health risk of global proportions. PM is thought to initiate and/or exacerbate respiratory disorders, such as asthma and airway hyperresponsiveness and is epidemiologically associated with causing death in the elderly and those with pre-existing respiratory or cardiopulmonary disease. Plausible mechanisms of action to explain PM in¯ammation and its susceptible sub-population component are lacking. This review describes a series of published studies which indicate that PM initiates airway in¯ammation through sensory neural pathways, speci®cally by activation of capsaicin-sensitive vanilloid (e.g. VR1) irritant receptors. These acid-sensitive receptors are located on the sensory C nerve ®bers that innervate the airways as well as on various immune and non-immune airway target cells. The activation of these receptors results in the release of neuropeptides from the sensory terminals that innervate the airways. Their interactions with airway target cells, result in signs of in¯ammation (e.g. bronchoconstriction, vasodilation, histamine release, mucous secretion etc.). Our data have linked the activation of the VR1 receptors to the surface charge carried on the colloidal particulates which constitute PM pollution. Related studies have examined how genetic and non-genetic factors modify the sensitivity of these irritant receptors and enhance the in¯ammatory responsiveness to PM. In summary, this review proposes a mechanism by which neurogenic elements initiate and sustain PM-mediated airway in¯ammation. Although neurogenic in¯uences have been appreciated in normal airway homeostasis, they have not, until now, been associated with PM toxicity. The sensitivity of the sensory nervous system to irritants and its interactions with pulmonary target tissues, should encourage neuroscientists to explore the relevance of neurogenic in¯uences to toxic disorders involving other peripheral target systems. Crown

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Metal and Sulfate Composition of Residual Oil Fly Ash Determines Airway Hyperreactivity and Lung Injury in Rats

Cited by 145 publications

References 35 publications

Metal composition of ambient PM2.5 influences severity of allergic airways disease in mice.

Metal composition of ambient PM2.5 influences severity of allergic airways disease in mice.

Biologic effects of oil fly ash.

Neurogenic Inflammation and Particulate Matter (PM) Air Pollutants

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