Enhanced Pulmonary Response to the Inhalation of Freshly Fractured Silica as Compared with Aged Dust Exposure

Castranova, Vincent; Pailes, William H.; Dalai, Nar S.; Miles, P. R.; Bowman, Linda; Vallyathan, Val; Pack, Donna; Weber, Karen C.; Hubbs, Ann F.; Schwegler‐Berry, Diane; Xiang, Jean; Dey, Richard D.; Blackford, Jack; Y.C., Jane; Barger, Mark; Shoemaker, Dale A.; Pretty, Jack R.; Ramsey, Dawn; McLaurin, Jeff; Khan, Amir; Baron, Paul A.; Childress, C. P.; Stettler, L. E.; Teass, Alex

doi:10.1080/1047322x.1996.10389993

Cited by 45 publications

(36 citation statements)

References 9 publications

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“…The production of *NO, measured as (Figure 2). Similar upregulation of 'NO production is also observed after inhalation of silica (9). These results (not presented here) indicate that freshly fractured silica is a more potent stimulant of *NO-dependent CL than aged dust.…”

Section: Resultssupporting

confidence: 69%

Enhancement of Nitric Oxide Production by Pulmonary Cells following Silica Exposure

Castranova¹,

Huffman²,

Judy³

et al. 1998

Environmental Health Perspectives

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In vivo exposure of rat lungs to crystalline silica either by intratracheal instillation or by inhalation results in an increase in mRNA levels for inducible nitric oxide synthase (iNOS) in bronchoalveolar lavage cells (BALC), elevated nitric oxide ('NO) production by BALC, and an increase in 'NOdependent chemiluminescence (CL) from alveolar macrophages (AM). Induction of iNOS message occurs in both AM and polymorphonuclear leukocytes (PMN) harvested from silicaexposed lungs but is not significantly elevated in lavaged lung tissue. In vitro exposure of AM to silica does not stimulate 'NO production or enhance iNOS message. However, treatment of naive AM with conditioned media from BALC harvested from silica-exposed rats does increase iNOS message and 'NO production by these AM. The potency of this conditioned medium is dependent on interaction between AM and PMN. In the rat model, a relationship exists between the ability of various dusts to cause PMN recruitment or protein leakage into the alveolar space and the induction of iNOS message in BALC, i.e., silica > coal mine dust > carbonyl iron > titanium dioxide. Similarly, a comparison of BALC from a healthy volunteer, a silica-exposed coal miner with a normal chest radiograph, and a silica-exposed coal miner with an abnormal chest radiograph shows a correlation between pathology and both the level of iNOS message in BALC and the magnitude of 'NO-dependent CL from AM. These data suggest that 'NO may play a role in silicosis and that human pulmonary phagocytes exhibit enhanced 'NO production in response to an inflammatory insult.

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Section: Resultssupporting

confidence: 69%

Enhancement of Nitric Oxide Production by Pulmonary Cells following Silica Exposure

Castranova¹,

Huffman²,

Judy³

et al. 1998

Environmental Health Perspectives

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“…There appears to be a direct relationship between the ability of silica particles to generate hydroxyl radicals and the potential to cause lipid peroxidation and cytotoxicity in vitro (17,91). A similar relationship has been demonstrated in vivo as well (18,86). Surface iron plays an important role in augmenting silica-induced hydroxyl radical production and cytotoxicity both in vitro and in vivo (17,92).…”

Section: Mechanisms Of Silica and Coal Pathogenicitymentioning

confidence: 62%

“…This greater potency of fresh silica dust has been demonstrated after both in vitro and inhalation exposures of rat alveolar macrophages (86,99). Similarly, extremely high levels of chemiluminescence have been reported from a rock driller who was exposed to fresh silica and was diagnosed with acute siicosis (97).…”

Section: Activation Ofoxidant Species Production By Alveolar Macrophagesmentioning

confidence: 99%

“…In studies of silica exposure of rats, the recruitment of PMNs from the pulmonary capillaries to the alveolar airspaces is a hallmark of the initiation and progression of silica-induced lung disease (83,85,86,103). As with cytotoxic responses, the degree of pulmonary inflammation is related to the ability of the silica particles to generate radicals, i.e., freshly fractured silica exhibits more surface radicals and causes more PMN recruitment than aged silica (18,86). PMN recruitment has also been demonstrated as a hallmark of acute silicosis in humans (97).…”

Section: Stimulation Ofinflammatory Cytokine Releasementioning

confidence: 99%

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Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

309

176

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Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; o) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

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“…For example, it has been suggested that the presence of highly reactive radicals on the surfaces of fractured silica that may be present in certain workplaces make the fractured silica highly cytotoxic (Castranova et al, 1996;Clouter et al, 2001). Dobias et al (2006) suggested that quartz dust is genotoxic and is an important contributor to the genotoxicity of complex mixtures of fibrogenic respirable airborne particles in ambient air in certain workplaces.…”

Section: Introductionmentioning

confidence: 99%

Variation of airborne quartz in air of Beijing during the Asia-Pacific Economic Cooperation Economic Leaders' Meeting

Zhang

et al. 2016

Journal of Environmental Sciences

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Enhanced Pulmonary Response to the Inhalation of Freshly Fractured Silica as Compared with Aged Dust Exposure

Cited by 45 publications

References 9 publications

Enhancement of Nitric Oxide Production by Pulmonary Cells following Silica Exposure

Enhancement of Nitric Oxide Production by Pulmonary Cells following Silica Exposure

Silicosis and coal workers' pneumoconiosis.

Variation of airborne quartz in air of Beijing during the Asia-Pacific Economic Cooperation Economic Leaders' Meeting

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