Inhalation toxicity of carbon black depends on surface coating with polycyclic aromatic hydrocarbons

The aim of this study was to assess differences in the toxic potential of surface modified carbon black particles. To this end a 14-day inhalation study was conducted in rats using nose-only exposure to compare the effects of pristine Printex®90 with surface modified carbon black, i.e. acetylene soot particles and Printex®90 coated with benzo[a]pyrene. This set of particles was also tested in different in vitro and ex vivo systems. On day one after the end of the 14-day inhalation period, acetylene soot alone caused an increase in relative lung wet weights. Furthermore, acetylene soot caused the most frequent histological alterations like interstitial inflammatory cell infiltration and bronchiolo-alveolar hyperplasia. Cytotoxicity tests with human pulmonary cell lines and precision cut lung slices (PCLS) were limited due to solubility of compounds. However, measurement of the transepithelial electrical resistance (TEER) in Calu-3 cells as well as the analysis of reactive oxygen species (ROS) in A549 and 16HBE14o- cells were able to differentiate between the carbon black modifications. Murine ex vivo airway preparations also proved to be a valuable model as acetylene soot was found to be the most toxic carbon black modification for epithelial cells, and the mechanism of action was linked to CYP1A1 induction. In summary, the results of this study suggest that the acute inhalation toxicity of carbon black is low, but increased if the surface is coated with polycyclic aromatic hydrocarbons. In vitro models with proven CYP1A1 inducibility seem to be useful tools to predict the in vivo effects of carbon black, coated with polycyclic aromatic hydrocarbons, on pulmonary epithelia