Introduction Carbon black (CB) is used as an easily accessible proxy for ultrafine particles (UFP) from diesel combustion, an important contributor to air pollution. CB are well-defined particles <100 nm in size (nanoparticles (NP)) and consist almost exclusively of carbon. Damage can be caused either by mechanical disturbance or chemically through molecules attached on the CB surface. Therefore, not only particle size, but also its capacity to bind molecules determine the toxicity of UFP and NP. Studies in mice show inconclusive data on CB toxicity, whereas cell lines intended to mimic bronchi, lung, and immune cells often report cyto- and genotoxic effects of CB after 2-24h.

Methods In the interest of generating data of high translational value for UFP risk assessment, we nebulized dissolved CB at the air-liquid interface on differentiated human primary mucosal models of the upper airways at commonly investigated time points (2h and 24h). We analyzed cytotoxicity (MTT and LDH-test), genotoxicity (Comet assay) and epithelial barrier integrity (TEER).

Results The tissue models differentiated to the mucociliary phenotype. Two hours after CB exposure, neither acute cytotoxic or genotoxic effects, nor barrier disruption was observed (4-6 donors). 24h after CB exposure, no significant changes had occurred either. However, maximum values and variance in cytotoxicity were higher, and the mean barrier integrity was reduced in exposed models.

Conclusion Taken together, our data from several replicates of highly differentiated human airway models indicate a mild barrier disturbance induced by CB at 24h. Future research will address long-term effects and repeated exposures of CB using our tissue models to obtain further insights in risk assessment of UFP/NP.

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