Inhalation of nanoplastics in the mouse model: Tissue bio-distribution and effects on the olfactory system
G. M. Prosperi, Natalia Marchetti, Alessandro D’Elia, Roberto Massari, M Giusto, Adriana Pietrodangelo, Thomas R. Rossi, A Nucara, Ferdinando Scavizzi, Georgios Strimpakos, Sara Marinelli, Silvia Mandillo, Francesca R. D’Amato, Stefano Farioli‐Vecchioli
Abstract
The impact of plastic fragments on human health is currently under investigation, with nanoplastics (NPs) being particularly concerning due to their small size. This allows them to be inhaled, pass through blood barriers, and reach various organs. In this study, we evaluated the effects of airborne NPs on the mouse olfactory system, which is a primary target of NPs inhalation. Adult mice were exposed to an aerosol solution containing synthetic polystyrene nanoplastics (PS-NPs) labelled with a red fluorophore for 5 h a day over 7 days. Biodistribution analysis revealed that PS-NPs accumulated in tissues, such as brain, lung, adipose tissue, and testicles, but were cleared after one month. This study is the first to investigate the effects of inhaled PS-NPs on the olfactory bulb (OB) and subventricular neurogenesis in adult mice. We observed long-term impairments in olfactory discrimination, decreased neuronal functionality, and pro-inflammatory activation in microglia in OB following PS-NPs exposure. Surprisingly, we noted a compensatory increase in olfactory neurogenesis, although insufficient to counteract the olfaction impairment induced by the PS-NPs. These results provide novel insights into the potential neurotoxic effects of inhaled PS-NPs and emphasize the importance of assessing occupational and environmental exposure to these pollutants. • Inhaled NPs accumulate in different organs of mice. • Long-term olfactory sensitivity impairment is found in mice after NPs inhalation. • Inhalation of NPs decreases neuronal activation in olfactory bulb of mice. • Inhalation of NPs induces transient inflammation in olfactory bulb of mice. • Subventricular neurogenesis is triggered by NPs, likely as compensatory mechanism.