Cytotoxicity and inflammatory effects in human bronchial epithelial cells induced by polycyclic aromatic hydrocarbons mixture

Abstract

Polycyclic aromatic hydrocarbons (PAHs) are the most common contaminants in the air pollutants. Inhalation exposure to PAHs could increase the risk of respiratory disease, cardiovascular disease and even cancer. However, the biotoxicity of multi‐component PAHs from atmospheric pollutants has been poorly studies. The main topic of this study was to investigate the PAHs mixture, which derived from atmospheric pollutants, induced toxic effects and inflammatory effects on human bronchial epithelial cells in vitro. The results showed that PAHs mixture could decrease the cell viability, increase the apoptosis rate, and induce cell cycle arrest at S‐phase. Furthermore, the expression of inflammatory factors IL‐1β and IL‐6 were increased and NF‐κB signaling pathway was activated in PAHs mixture‐treated cells. The findings of this study indicate that PAHs mixture‐induced cytotoxicity and inflammation may be related to intracellular ROS generation and to the activated NF‐κB signaling pathway.

Chlorinated Anthracenes Induced Pulmonary Immunotoxicity in 3D Coculture Spheroids Simulating the Lung Microenvironment

“…Previous studies have also revealed that PAHs can independently activate the NF-κB pathway, leading to cellular toxicity and inflammation. 46,47 Additionally, our previous studies have indicated that Cl-PAHs induce immune toxicity by disrupting amino acid metabolism without activating AhR. 12 These findings underscore the complexity of the toxic effects of PAHs/Cl-Ants, suggesting the involvement of multiple pathways and mechanisms beyond AhR activation.…”

MicroRNAs as Potential Biomarkers of Environmental Exposure to Polycyclic Aromatic Hydrocarbons and Their Link with Inflammation and Lung Cancer

“…The respiratory tract is constantly in contact with various pollutants, so PAHs tend to concentrate in bronchial epithelial cells [18]. Due to their lipophilic nature, they can easily penetrate the epithelial barrier and accumulate in adipocytes, which leads to chronic activation of the aryl hydrocarbon receptor (AhR) [19], triggering an inflammatory response.…”