Ozone effect on the inflammatory and proteomic profile of human macrophages and airway epithelial cells

Ozone (O₃) is one of the most harmful urban pollutants, but its biological mechanisms have not been fully elucidated yet. Human bronchial epithelial cells (HBEpC) and human macrophage cells (differentiated human monocytic cell line) were exposed to O₃ at the concentration of 240 μg/m³ (120 ppb), corresponding to the European Union alert threshold. Cell viability, reactive oxygen species (ROS) production, and pro-inflammatory cytokines release (IL-8 and TNF-α) were evaluated. Results indicated that O₃ exposure increases ROS production in both cell types and enhances cytokines release in macrophages. O₃ stimulated IL-8 and TNF-α in HBEpC when the cells were pretreated with Lipopolysaccharide, used to mimic a pre-existing inflammatory condition. Proteomics analysis revealed that, in HBEpC, O₃ caused the up-regulation of aldo-keto reductase family 1 member B10, a recognized critical protein in lung carcinogenesis. In conclusion, our results show that 120 ppb O₃ can lead to potential damage to human health suggesting the need for a revision of the actual alert levels.