In vitro cytotoxicity of chrysotile asbestos to human pulmonary alveolar macrophages is decreased by organosilane coating and surfactant

Dg, Morrison; Tl, McLemore; Ec, Lawrence; Dg, Feuerbacher; Ml, Mace; Dl, Busbee; Ac, Griffin; Mv, Marshall

doi:10.1007/bf00122697

Cited by 9 publications

(5 citation statements)

References 38 publications

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“…In 1986, Morrison et al investigated the protective potential of a hydrophobic organosilane layer to reduce cytotoxicity of chrysotile asbestos. However, using human pulmonary AM as in vitro model, organosilane-mediated decrease in mortality was only observed in the presence of dipalmitoyl lecithin.…”

Section: Discussionmentioning

confidence: 99%

Organosilane-Based Coating of Quartz Species from the Traditional Ceramics Industry: Evidence of Hazard Reduction Using In Vitro and In Vivo Tests

Ziemann

Escrig

Bonvicini

et al. 2017

Annals of Work Exposures and Health

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The exposure to respirable crystalline silica (RCS), e.g. quartz, in industrial settings can induce silicosis and may cause tumours in chronic periods. Consequently, RCS in the form of quartz and cristobalite has been classified as human lung carcinogen category 1 by the International Agency for Research on Cancer in 1997, acknowledging differences in hazardous potential depending on source as well as chemical, thermal, and mechanical history. The physico-chemical determinants of quartz toxicity are well understood and are linked to density and abundance of surface silanol groups/radicals. Hence, poly-2-vinylpyridine-N-oxide and aluminium lactate, which effectively block highly reactive silanol groups at the quartz surface, have formerly been introduced as therapeutic approaches in the occupational field. In the traditional ceramics industry, quartz-containing raw materials are indispensable for the manufacturing process, and workers are potentially at risk of developing quartz-related lung diseases. Therefore, in the present study, two organosilanes, i.e. Dynasylan® PTMO and Dynasylan® SIVO 160, were tested as preventive, covalent quartz-coating agents to render ceramics production safer without loss in product quality. Coating effectiveness and coating stability (up to 1 week) in artificial alveolar and lysosomal fluids were first analysed in vitro, using the industrially relevant quartz Q1 as RCS model, quartz DQ12 as a positive control, primary rat alveolar macrophages as cellular model system (75 µg cm−2; 4 h of incubation ± aluminium lactate to verify quartz-related effects), and lactate dehydrogenase release and DNA strand break induction (alkaline comet assay) as biological endpoints. In vitro results with coated quartz were confirmed in a 90-day intratracheal instillation study in rats with inflammatory parameters as most relevant readouts. The results of the present study indicate that in particular Dynasylan® SIVO 160 (0.2% w/w of quartz) was able to effectively and stably block toxicity of biologically active quartz species without interfering with technical process quality of certain ceramic products. In conclusion, covalent organosilane coatings of quartz might represent a promising strategy to increase workers’ safety in the traditional ceramics industry.

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Section: Discussionmentioning

confidence: 99%

Organosilane-Based Coating of Quartz Species from the Traditional Ceramics Industry: Evidence of Hazard Reduction Using In Vitro and In Vivo Tests

Ziemann

Escrig

Bonvicini

et al. 2017

Annals of Work Exposures and Health

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“…A trypsin-sensitive receptor on alveolar macrophage membranes may cooperate with extracellular calcium to promote particle-cell binding (182), but such ions penetrating the plasma membrane led to cell death (183). The surface charges of amphibole and serpentine asbestos may in vivo be altered by surfactant, although in vitro dipalmitoyl lecithin had little effect on the mortality ofalveolar macrophages from chrysotile (184). Release of lysosomal enzymes from macrophages varied with fiber type, amphiboles and TiO2 in the rutile phase being ineffective but chrysotile, like silica, proving active (185).…”

Section: Mechanisms Of Fibrogenesismentioning

confidence: 97%

Minerals, fibrosis, and the lung.

Heppleston

1991

Environ Health Perspect

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Determinants of pulmonary fibrosis induced by inhaled mineral dusts include quantity retained, particle size, and surface area, together with their physical form and the reactive surface groups presented to alveolar cells. The outstanding problem is to ascertain how these factors exert their deleterious effects. Both compact and fibrous minerals inflict membrane damage, for which chemical mechanisms still leave uncertainty. A major weakness of cytotoxicity studies, even when lipid peroxidation and reactive oxygen species are considered, lies in tacitly assuming that membrane damage suffices to account for fibrogenesis, whereas the parallel occurrence of such manifestations does not necessarily imply causation. The two-phase procedure established that particles, both compact and fibrous, induce release of a macrophage factor that provokes fibroblasts into collagen synthesis. The amino acid composition of the macrophage fibrogenic factor was characterized and its intracellular action explained. Fibrous particles introduce complexities respecting type, durability, and dimensions. Asbestotic fibrosis is believed to depend on long fibers, but scrutiny of the evidence from experimental and human sources reveals that a role for short fibers needs to be entertained. Using the two-phase system, short fibers proved fibrogenic. Other mechanisms, agonistic and antagonistic, may participate. Growth factors may affect the fibroblast population and collagen production, with cytokines such as interleukin-1 and tumor necrosis factor exerting control. Immune involvement is best regarded as an epiphenomenon. Downregulation of fibrogenesis may follow collagenase release from macrophages and fibroblasts, while augmented type II cell secretion of lipid can interfere with the macrophage-particle reaction.

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