Abstract Humans are constantly exposed to harmful airborne substances, including emerging pollutants such as ultrafine particles (UFPs) and micro-and nanoplastics (MNPs). Through inhaled air, particles enter the nasal cavity and contact the olfactory mucosa (OM), specialized tissue lining the roof of the cavity. This tissue represents a potential entry route of particles into the brain through the olfactory pathway. Here we use a unique primary cell model of the human OM to investigate the cellular and molecular mechanisms involved in exposure to emerging airborne pollutants. Cells cultured at air-liquid interface (ALI) were exposed to UFPs and MNPs at various concentrations and timepoints, after which toxicity, barrier permeability assays and omics approaches were used to understand particle effects at the human OM. The data demonstrates size- and composition specific effects of particles in OM cells and reveals new exposure targets that can be used to mitigate adverse effects of airborne emerging pollutants at the nose-brain interface.
Behzadpour et al. (Thu,) studied this question.