CC BY 4.0Ehret-Kasemo, TottaTottaEhret-KasemoOppmann, MaximilianMaximilianOppmannDembski, SofiaSofiaDembskiSteinke, Maria R.Maria R.SteinkeLajtha, ElenaElenaLajthaMoratin, HelenaHelenaMoratinStöth, Manuel BerndManuel BerndStöthScherzad, AgmalAgmalScherzadDelaval, Mathilde N.Mathilde N.DelavalZimmermann, RalfRalfZimmermannBucchianico, Sebastiano diSebastiano diBucchianicoHackenberg, StephanStephanHackenbergMeyer, Till JasperTill JasperMeyer2025-10-132025-10-132025https://publica.fraunhofer.de/handle/publica/497292https://doi.org/10.24406/publica-573710.1016/j.etap.2025.10482910.24406/publica-57372-s2.0-10501743577041016621Airborne pollutants harm human health, but the mechanisms involved remain unclear. Impaired epithelial barrier function is, as in respiratory diseases, one possible pathomechanism. To investigate this, carbon black (CB) as a model for ultrafine particles (UFP), was applied to respiratory mucosa models of primary fibroblasts and epithelial cells cultured at the air-liquid interface (ALI). Models were assessed for the mucociliary phenotype. Cytotoxicity, DNA damage, and barrier integrity were evaluated by the lactate dehydrogenase (LDH) and comet assays, and by transepithelial electrical resistance (TEER) measurements. Cilia movement and ultrastructure, secretory cells, and intact cell-cell contacts were confirmed. Subtle changes were observed: the LDH release had increased 2 h post exposure and barrier disturbance 24 h post exposure was detected, both without mucosal damage or genotoxic effects. Donor-specific differences were present. Barrier disruption without cell detachment or death suggests model feasibility for long-term studies of, e.g., tissue regeneration or fibrosis following UFP exposure.enfalseair-liquid interfacebarrierCarbon blackprimary cell modelrespiratory mucosatoxicologyultrafine particlesjournal article