Basic pathogenetic mechanisms in silicosis: current understanding

Rimal, Binaya; Greenberg, Alissa K.; Rom, William N.

doi:10.1097/01.mcp.0000152998.11335.24

Cited by 281 publications

(221 citation statements)

References 41 publications

(34 reference statements)

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“…The effects of these samples were compared to those of Dörentrup quartz DQ12, which has a genotoxic potential and may contribute to the carcinogenicity of silica in humans. Respirable quartz powder has been classified as a Group 1 carcinogen [IARC, 1997] and has been investigated in numerous studies [Donaldson and Borm, 1998;Fubini, 1998;Rimal et al, 2005;Wang et al, 2007]. Furthermore, benzo[a]pyrene (B[a]P), a PAH known to be a human carcinogen, was chosen as a second positive control in the genotoxicity assays.…”

Section: Introductionmentioning

confidence: 99%

Genotoxic effects of three selected black toner powders and their dimethyl sulfoxide extracts in cultured human epithelial A549 lung cells in vitro

Gminski

Decker

Heinz

et al. 2010

Environ and Mol Mutagen

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Until now, the adverse effects of toner powders on humans have been considered to be minimal. However, several recent reports have suggested possible significant adverse health effects from toner dust inhalation. The aim of this study was to evaluate the genotoxic potential of black toner powders in vitro. For the study of DNA damage, A549 cells were exposed to toner-powder suspensions and to their DMSO extracts, and then subjected to the comet assay and to the in-vitro cytokinesis block micronucleus test (CB-MNvit). Cytotoxic effects of the toner samples were assessed by the erythrosin B assay. Furthermore, size, shape, and composition of the toner powders were investigated. None of the three toner powders or their DMSO extracts reduced cell viability; however, they did induce DNA damage and formed micronuclei at concentrations from 80 to 400 lg cm 22 , although to a varying extent. All toner powders contain considerable amounts of the pigments carbon black and magnetite (Fe 3 O 4 ) as well as small amounts of polycyclic aromatic hydrocarbons (PAHs). The overall results of our invitro study suggest that the investigated toner-powder samples are not cytotoxic but genotoxic. From the results of the physical and chemical characterization, we conclude that metals and metalloids as components of magnetite, or PAHs as components of the carbon-bearing material, are responsible for the genotoxic effects. Further research is necessary to determine the relevance of these in-vitro observations for private and occupational toner powder exposure.

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Section: Introductionmentioning

confidence: 99%

Genotoxic effects of three selected black toner powders and their dimethyl sulfoxide extracts in cultured human epithelial A549 lung cells in vitro

Gminski

Decker

Heinz

et al. 2010

Environ and Mol Mutagen

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“…Histology of asbestosis demonstrates pulmonary fibrosis with honeycombing, fibroblast foci in the interstitium and respiratory bronchioles and asbestos bodies (Rimal et al, 2005) (Figure 2A). Asbestos bodies are asbestos fibers coated with iron and protein and the presence of asbestos bodies strongly testifies to the etiology of the pulmonary fibrosis (Mongan et al, 2000;Rimal et al, 2005) (Figure 2B).…”

Section: Asbestosismentioning

confidence: 99%

“…The nodules may measure 4 to 10 mms and enlarge further with continued exposure (Flynn and Susi, 2003). A silicotic nodule has concentric fibrotic hyalinized laminar layers of collagen, fibroblasts, and lymphocytes (Rimal et al, 2005) and dust (Flynn and Susi, 2003). The dust may be in macrophages in the center of the nodule and be refractile in polarized light (Arakawa et al, 2005).…”

Section: Silicosismentioning

confidence: 99%

“…Asbestos bodies are asbestos fibers coated with iron and protein and the presence of asbestos bodies strongly testifies to the etiology of the pulmonary fibrosis (Mongan et al, 2000;Rimal et al, 2005) (Figure 2B). Most patients with asbestosis present many years after exposure with slowly progressive cough and dyspnoea (Mongan et al, 2000;Attfield and Wood, 2004), and on auscultation there are inspiratory crackles.…”

Section: Asbestosismentioning

confidence: 99%

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Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

et al. 2007

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Pulmonary fibrosis is a general term that refers to a collection of connective tissue around alveolar structures. There are over 200 disorders where the lungs may be involved in a fibrotic response. To determine the cause of pulmonary fibrosis requires an in depth understanding of the pathogenesis of pulmonary fibrosis and breadth of knowledge of the causative agents and associated disorders that may lead to pulmonary fibrosis. A comprehensive evaluation of the patient is absolutely essential, starting with detailed history that includes an occupational and environmental history because fibrogenic exposures can occur in many settings. Equally important is a history of ingestion of pharmaceutical or nonpharmaceutical substances. A physical examination and judicious investigations are always a part of any comprehensive clinical assessment but they are not commonly helpful in elucidating the cause of most pulmonary fibrotic disorders. Although, a chest film is invariably done, a logical and strongly recommended next step is a high-resolution computed tomography (HRCT). HRCT provides a better assessment of the radiological pattern, may suggest a diagnosis as well as direct the site, and type of lung biopsy. If the history and investigations do not lead to a diagnosis then a lung biopsy is required. Prevention or removal of the inciting agent is critical to the treatment of these disorders and in some instances corticosteroids may be of help.

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“…The lung illustrates the injurious nature of a prolonged and futile immune response where the chronic presence of mineral particles leads to an ineffectual phagocytic attack by alveolar macrophages. This ultimately leads to severe pathologic changes involving inflammatory cytokines [24]. Analogous futile inflammatory responses in the brain may be toward aggregated amyloid peptide and other insoluble proteinaceous inclusions [25].…”

Section: Inflammation and The Aged Brainmentioning

confidence: 99%

Melatonin, Oxidative Stress, and the Aging Brain

Bondy

Sharman

2010

Aging and Age-Related Disorders

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The changes associated with brain aging are discussed with emphasis on altered oxidative and inflammatory events and on mitochondrial dysfunction. Many of these changes are exacerbated in a variety of age-related neurologic diseases. This commonality has led to the idea that similar therapeutic approaches may be used in the treatment of several apparently unrelated neurodegenerative disorders. When aspects of these diseases are modeled in experimental animals and cell lines, the application of melatonin has been reported to be advantageous. The means by which melatonin can be protective probably is mediated by way of activation of melatonin receptors, of which several subtypes can be identified. This can initiate a sequence of intracellular signaling events and by activation of transcription factors lead to altered gene expression. The culmination of this cascade can lead to increased levels of antioxidant enzymes and depressed levels of inflammation. Melatonin may be useful both in the retardation of nonpathologic brain aging and in the amelioration of chronic brain disease associated with aging. The inexpensive nature and ready availability of melatonin together with its very low toxicity reinforce the need to place the beneficial properties of this agent on a firmer basis.

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Basic pathogenetic mechanisms in silicosis: current understanding

Cited by 281 publications

References 41 publications

Genotoxic effects of three selected black toner powders and their dimethyl sulfoxide extracts in cultured human epithelial A549 lung cells in vitro

Genotoxic effects of three selected black toner powders and their dimethyl sulfoxide extracts in cultured human epithelial A549 lung cells in vitro

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

Melatonin, Oxidative Stress, and the Aging Brain

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