Growing international exploitation of rare earth oxides (REOs) for commercial and biological use has introduced the possibility of adverse health effects, as exemplified by occupational exposures leading to pneumoconiosis or gadolinium-containing MRI contrast agents causing nephrogenic systemic fibrosis. In order to prevent similar problems arising from the expanded use of REO nanoparticles, we obtained a mechanistic understanding of material hazard through cellular and animal studies, which demonstrated that rare earth ion shedding in an acidifying lysosomal environment leads to biotic phosphate complexation and nanoparticle transformation into urchin-shaped structures. Stripping of phosphates from the lipid bilayer of lysosomes damages these organelles, and sets into motion a progressive march of events in which NLRP3 inflammasome activation, IL-1� release and pro-fibrogenic growth factor production results in pulmonary fibrosis. However, pre-treatment of REO nanoparticles with phosphate in a neutral pH environment prevents biological transformation and pro-fibrogenic effects. This can be used as a safer design principle that making rare earth nanoparticles for biological use. This work was published on ACS NANO (10.1021/nn406166n), selected as ACS Editors' Choice and reported by EHS news.

Surface interactions with compartmentalized cellular phosphates explain rare earth oxide nanoparticle hazard and provide opportunities for safer design

248th National Meeting (2014)

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