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BackgroundExposure to some - but not all - quartz particles is associated to silicosis, lung cancer and autoimmune diseases. What imparts pathogenicity to any single quartz source is however still unclear. Crystallinity and various surface features are implied in toxicity. Quartz dusts used so far in particle toxicology have been obtained by grinding rocks containing natural quartz, a process which affects crystallinity and yields dusts with variable surface states. To clarify the role of crystallinity in quartz pathogenicity we have grown intact quartz crystals in respirable size.MethodsQuartz crystals were grown and compared with a fractured specimen obtained by grinding the largest synthetic crystals and a mineral quartz (positive control). The key physico-chemical features relevant to particle toxicity - particle size distribution, micromorphology, crystallinity, surface charge, cell-free oxidative potential - were evaluated. Membranolysis was assessed on biological and artificial membranes. Endpoints of cellular stress were evaluated on RAW 264.7 murine macrophages by High Content Analysis after ascertaining cellular uptake by bio-TEM imaging of quartz-exposed cells.ResultsQuartz crystals were grown in the submicron (n-Qz-syn) or micron (μ-Qz-syn) range by modulating the synthetic procedure. Independently from size as-grown quartz crystals with regular intact faces did not elicit cellular toxicity and lysosomal stress on RAW 264.7 macrophages, and were non-membranolytic on liposome and red blood cells. When fractured, synthetic quartz (μ-Qz-syn-f) attained particle morphology and size close to the mineral quartz dust (Qz-f, positive control) and similarly induced cellular toxicity and membranolysis. Fracturing imparted a higher heterogeneity of silanol acidic sites and radical species at the quartz surface.ConclusionsOur data support the hypothesis that the biological activity of quartz dust is not due to crystallinity but to crystal fragmentation, when conchoidal fractures are formed. Besides radical generation, fracturing upsets the expected long-range order of non-radical surface moieties - silanols, silanolates, siloxanes - which disrupt membranes and induce cellular toxicity, both outcomes associated to the inflammatory response to quartz.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-016-0136-6) contains supplementary material, which is available to authorized users.

Calcite crystals were nucleated and grown from supersaturated aqueous solutions in the presence of variable concentrations of lithium. The diagram of supersaturation vs [Li+]/[Ca2+] concentration ratio (“morphodrome”) shows a continuous habit variation, from the dominant {011̄1} rhombohedron (at low [Li+]/[Ca2+] ratio) to the dominant {0001} form (at high [Li+]/[Ca2+] ratio). The morphological change is interpreted in terms of two-dimensional layers having the structure of the monoclinic Li2CO3 crystal which are epitaxially adsorbed on the restructured {0001} form of calcite. Hence, even if {0001} is a K form (in the sense of Hartman-Perdok), the corresponding surface behaves like a F form, growing layer by layer from low to high supersaturation values.