The quartz hazard: effects of surface and matrix on inflammogenic activity.
Modification of the quartz surface during the history of the particle is a powerful idea in understanding the variability of the quartz hazard. Interactions between quartz and other minerals are likely to occur in sediments, during industrial processing, or in matrix-bound quartz. We discuss new evidence regarding the basis of changes in the quartz surface that relate to changes in its ability to cause inflammation. Different samples of quartz were subjected to various biological assays. Endpoints included instillation of quartz into the tracheobronchial tree and measurement of PMN numbers in bronchoalveolar lavage (BAL) and in lung tissue, levels of the chemokine MIP-2 in BAL, and nuclear translocation of the transcription factor NF-kappaB in BAL cells. In vitro biological assays included cytotoxicity to epithelial cells, hemolytic activity, and radical activity of the particle surface as measured by electron spin resonance. Treatment of quartz with aluminium lactate impaired its ability to cause PMN recruitment, chemokine release, and NF-kappaB nuclear translocation in BAL. Workplace quartzes had no proinflammatory activity, which correlated with their ability to cause hemolysis but not their electron spin resonance (ESR) activity. Quartz in a matrix with coalmine dust or fly-ash showed different effects. In fly-ash, the toxicity was masked, but coalmine dusts were more toxic to epithelial cells than pure quartz in vitro; however, after instillation, the long-term inflammation was not related to the in vitro activity. Amelioration of quartz surface activity can occur in workplace samples of quartz and quartz samples whose surface is protected, to the extent that they have very little inflammogenic activity and display an inability to activate key subcellular pathways that lead to inflammation. Quartz from a workplace whose surface has been affected, or in a matrix such as coalmine dust or fly-ash, can have its toxicity modulated. These effects are due to minerals and organic compounds that can both decrease (e.g., aluminium salts) or enhance (e.g., coalmine dust matrix) biological activity and thus may contribute to toxicity in a complex way that is not easily predicted. Iron is a good example. There are reports that it can enhance quartz toxicity, or it may have little role to play in its toxicity, as shown here for almost pure quartz particles. A broad program of further research is needed before we have a sound understanding of the mechanisms of quartz toxicity.
Donaldson
K
K
Biomedicine Research Group, Napier University, Edinburgh, Scotland. k.donaldson@napier.ac.uk
Stone
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Duffin
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Clouter
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A
Schins
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Borm
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D000395:Air Pollutants, Occupational / Q000737:chemistry / Q000633:toxicity*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D002244:Carbon / Q000737:chemistry / Q000633:toxicity; D060729:Coal Ash; D004391:Dust; D006801:Humans; D007249:Inflammation / Q000378:metabolism*; D052638:Particulate Matter; D011791:Quartz / Q000737:chemistry / Q000633:toxicity*; D012822:Silicon Dioxide / Q000737:chemistry / Q000633:toxicity; D013499:Surface Properties
D000395:Air Pollutants, Occupational; D060729:Coal Ash; D004391:Dust; D052638:Particulate Matter; D011791:Quartz; D002244:Carbon; D012822:Silicon Dioxide