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Superparamagnetic iron oxide nanoparticles (SPIONs) have gained increasing interest in nanomedicine, but most of those that have entered the clinical trials have been withdrawn due to toxicity concerns. Therefore, there is an urgent need to design low-risk and biocompatible SPION formulations. In this work, we present an original safe-by-design nanoplatform made of silica nanoparticles loaded with SPIONs and decorated with polydopamine (SPIONs@SiO2-PDA) and the study of its biocompatibility performance by an ad hoc thorough in vitro to in vivo nanotoxicological methodology. The results indicate that the SPIONs@SiO 2 -PDA have excellent colloidal stability in serum-supplemented culture media, even after long-term (24 h) exposure, showing no cytotoxic or genotoxic effects in vitro and ex vivo. Physiological responses, evaluated in vivo using Caenorhabditis elegans as the animal model, showed no impact on fertility and embryonic viability, induction of an oxidative stress response, and a mild impact on animal locomotion. These tests indicate that the synergistic combination of the silica matrix and PDA coating we developed effectively protects the SPIONs, providing enhanced colloidal stability and excellent biocompatibility.

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The prevalence of allergic diseases is constantly increasing since few decades.Anthropogenic ultrafine particles (UFPs) and allergenic aerosols is highly involved in this increase; however, the underlying cellular mechanisms are not yet understood.Studies observing these effects focused mainly on singular in vivo or in vitro exposures of single particle sources, while there is only limited evidence on their subsequent or combined effects. Our study aimed at evaluating the effect of subsequent exposures to allergy-related anthropogenic and biogenic aerosols on cellular mechanism exposed at air-liquid interface (ALI) conditions. Bronchial epithelial BEAS-2B cells were exposed to UFP-rich combustion aerosols for 2 h with or without allergen pre-exposure to birch pollen extract (BPE) or house dust mite extract (HDME). The physicochemical properties of the generated particles were characterized by stateof-the-art analytical instrumentation. We evaluated the cellular response in terms of cytotoxicity, oxidative stress, genotoxicity, and in-depth gene expression profiling.We observed that single exposures with UFP, BPE, and HDME cause genotoxicity.Exposure to UFP induced pro-inflammatory canonical pathways, shifting to a more xenobiotic-related response with longer preincubation time. With additional allergen exposure, the modulation of pro-inflammatory and xenobiotic signaling was more pronounced and appeared faster. Moreover, aryl hydrocarbon receptor (AhR) signaling activation showed to be an important feature of UFP toxicity, which was especially pronounced upon pre-exposure. In summary, we were able to demonstrate the importance of subsequent exposure studies to understand realistic exposure situations and to identify possible adjuvant allergic effects and the underlying molecular mechanisms.

Traffic emissions contribute to ambient air pollution, posing a threat to human health. The installation of stricter exhaust emission standards and particle filters led to a significant decrease of particulate matter emissions by cars. However, little is known about how atmospheric transformation changes the toxicity of exhaust emissions from modern cars. We evaluated the physico-chemical properties and toxicological effects of fresh and photochemically aged aerosols from a gasoline EURO 6 car equipped with a particulate filter. A549 alveolar and BEAS-2B bronchial epithelial cells were exposed for 4h to aerosols at the air-liquid interface. The toxicity was determined by measuring cell viability, cytotoxicity, oxidative stress, primary and oxidative DNA damage. Particle number concentration (PN) in fresh aerosol was negligible while photochemical aging with an equivalent photochemical age of 5 days led to PN of 6.6´106 cm-3 with a mean size of 35 nm. Secondary aerosol particles predominantly consisted of organic matter, nitrate, and ammonium, which were formed by the oxidative gas-to-particle conversion of volatile organic compounds (VOCs), particularly aromatic hydrocarbons, and NOx in the exhaust. Significant levels of oxygenated VOCs were also detected. Fresh aerosol caused no cytotoxicity in lung cells, but led to slight DNA damage whereas aged aerosol caused toxicity to both cell models, oxidative stress and oxidative DNA damage mainly due to the gas phase. Our results indicate a significant toxification of the emissions by photochemical aging. This calls for considering atmospheric processes in future exhaust emission standards for the transport sector toward health effect-driven emission regulations.