This study focuses on the intracellular transformation of amphibole particles, and complements the extensive literature describing asbestos bodies (ABs), i.e., extracellular Fe-covered РІР‚СљfibersРІР‚Сњ found in lung tissue, and their role in triggering related malignancies. amphibole asbestos and/or asbestiform zeolites. Our systematic approach can be more effective in reducing and partially controlling the involved variables (e.g., chemical composition and surface physicochemical state) than the frequently used comparison between crystal-chemically and physically dissimilar minerals like chrysotile vs. Here, we tested the interaction of the three selected minerals with the AEC line A549 (ATCCР’В® CCLР’В185РІвЂћСћ), to study the alterations induced by the AECs. AEC injury is a key trigger, which promotes the development of asbestosis and lung cancer 1, 21, 22, 23, 24. For these reasons, our study focuses on the in-vitro uptake by alveolar epithelial cells (AECs) and the transformation of amosite (the asbestiform variety of the mineral grunerite) and non-asbestiform amphiboles (anthophyllite and grunerite). Moreover, the related malignancies can also be caused by non-regulated asbestiform minerals 13, with an unclear role of nano-sized EMPs, non-regulated fibers, cleavage fragments and split mineral particles internalized by human lung cells 14, 15, 16, 17, 18, 19, 20. To support the medical community in tracking the fate of elongate mineral particles (EMPs) in cells (EMP is a term that includes asbestos minerals 7), we have approached the problem from the opposite end: instead of focusing on the amphibole-related transformation of cells, we studied how amphibole particles internalized by human lung cells are transformed at the near-atomic- to nano-scale.Р”Р„sbestos is an all-inclusive, confusing, non-scientific, industrial term 8, 9, 10, 11, 12. Moreover, the disease-triggering mechanism of these minerals is still puzzling 4, although new findings have recently advanced the understanding of asbestos-related mesothelioma, lung cancer, and fibrosis 1, 5, 6.

Asbestos-related tumors are difficult to diagnose and have long latency periods, and it is not clear whether there is a minimum threshold exposure for carcinogenesis 3. The carcinogenic potency of amphibole asbestos was proven both epidemiologically and toxicologically 2. Internalized particles and ABs follow two distinct formation mechanisms reaching different physicochemical end-states.Р”В®xposure to amphibole asbestos is in many cases associated with asbestosis, pleural abnormalities, bronchogenic carcinomas and mesotheliomas 1.

We show that: (i) an Fe-rich layer is formed on the internalized particles, (ii) particle grain boundaries are transformed abiotically by the internal chemical environment of AECs and/or by a biologically induced mineralization mechanism, (iii) the Fe-rich material produced on the particle surface does not contain large amounts of P, in stark contrast to extracellular ABs, and (iv) the iron in the Fe-rich layer is derived from the particle itself. Here we document the near-atomic- to nano-scale transformations induced by, and taking place within, AECs of three distinct amphiboles (anthophyllite, grunerite, РІР‚СљamositeРІР‚Сњ) with different Fe-content and morphologic features. These internalized particles may directly interact with the cell nucleus and the organelles, exerting a synergistic action with asbestos bodies (AB) from a different location. The literature focuses primarily on the role and formation of asbestos bodies in lung tissues, but there is a distinct lack of studies on amphibole particles that have been internalized by alveolar epithelial cells (AECs). The disease-triggering mechanisms still challenge our diagnostic capabilities and are still far from being fully understood. Amphibole asbestos is related to lung fibrosis and several types of lung tumors.

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