Toxicity of iron nanoparticles towards primary cultures of human bronchial epithelial cells.

Air pollution is a public health issue and the toxicity of ambient particulate matter (PM) is well-recognized. Although it does not mostly contribute to the total mass of PM, increasing evidence indicates that the ultrafine fraction has generally a greater toxicity than the others do. A better knowledge of the underlying mechanisms involved in the pathological disorders related to nanoparticles (NPs) remains essential. Hence, the goal of this study was to determine better whether the exposure to a relatively low dose of well-characterized iron-rich NPs (Fe-NPs) might alter some critical toxicological endpoints in a relevant primary culture model of human bronchial epithelial cells (HBECs). We sought to use Fe-NPs representative of those frequently found in the industrial smokes of metallurgical industries. After having noticed the effective internalization of Fe-NPs, oxidative, inflammatory, DNA repair, and apoptotic endpoints were investigated within HBECs, mainly through transcriptional screening. Taken together, these results revealed that, despite it only produced relatively low levels of reactive oxygen species without any significant oxidative damage, low-dose Fe-NPs quickly significantly deregulated the transcription of some target genes closely involved in the proinflammatory response. Although this inflammatory process seemed to stay under control over time in case of this acute scenario of exposure, the future study of its evolution after a scenario of repeated exposure could be very interesting to evaluate the toxicity of Fe-NPs better.