Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants, where their genotoxic potential raises significant public health concerns. This study evaluated the cytotoxic and genotoxic effects of an environmentally relevant mixture of 11 PAHs measured in indoor air from Zagreb households. Biological responses were assessed in three human-derived models: peripheral blood cells (PBCs), lung epithelial cells (A549), and liver carcinoma cells (HepG2). Short-term exposure scenarios were designed to mimic indoor inhalation over 1, 8, and 16 hours, with treatments lasting 4 or 24 hours. Cytotoxicity was evaluated via acridine orange/ethidium bromide staining in PBCs and the MTT assay in A549 and HepG2 cells, while genotoxicity was assessed using the alkaline comet and cytokinesis-block micronucleus assays. Overall, A549 and HepG2 cells displayed nonsignificant cyto- and genotoxic responses across all concentrations and exposure durations. In contrast, PBCs exhibited statistically significant, time- and concentration-dependent cytotoxicity. Genotoxic analyses revealed a biologically relevant, though statistically non-significant, threefold increase in micronuclei formation at the highest PAHs concentration after 4 hours. A statistically significant increase in nucleoplasmic bridges was observed at the medium (8-hour) concentration after 24 hours, compared with controls. The limited biological responses align with the mixture’s low toxic- (TEF) and genotoxic equivalency factor (GEF)-weighted toxicity derived from literature values, as the most abundant PAHs were low-potency compounds. Accordingly, under the experimental conditions applied, exposure did not result in detectable DNA or chromosomal damage. In silico analysis indicated that the mixture’s toxicity is largely driven by the AHR–CYP–NQO1 axis. • Environmentally relevant indoor PAH mixture showed low overall toxicity. • Primary blood cells showed the strongest cytotoxic and genotoxic responses. • Lymphocytes showed a significant rise in nucleoplasmic bridge formation. • A549 and HepG2 cells exhibited minimal effects across all exposure scenarios. • In silico analysis showed toxicity driven by the AHR–CYP–NQO1 pathway.
Kazensky et al. (Sun,) studied this question.