ABSTRACT The increasing inevitable exposure to nanoparticles, along with other ubiquitous environmental pollutants, raises concern over their human health toxicity. Further, the elevated ROS level on exposure to nanoparticles depends on its physicochemical characteristics and interaction with biological elements. Moreover, immunotoxicity (immune cells act as a first line defence) induced by exposure to aluminium oxide nanoparticles (Al 2 O 3 ‐NPs) and titanium dioxide nanoparticles (TiO 2 ‐NPs) and their additive effect with 16 polycyclic aromatic hydrocarbons (PAHs) (High Priority Pollutants designated by EPA) has not been studied. This present study involved the dynamic light scattering (DLS) technique to analyze the size and zeta potential of both the nanoparticles in different media. The THP‐1 macrophage cell culture was established to study different oxidative stress (superoxide, total ROS, mitochondrial ROS, and lipid peroxidation) and cell stress (ER stress, mitochondrial dysfunction, and intracellular calcium) events. Alongside, kinase signalling studies were performed. Further, the adverse effects during inflammatory risk factor (LPS) and PAHs co‐exposure were studied to assess the effects on vulnerable groups. The current result demonstrates a dose‐dependent increase in cytotoxicity, oxidative distress, and the involvement of various kinase signalling pathways in macrophages. Notably, pre‐treatment with p38 MAPKi, NFκBi, NAC, and MitoTEMPO ameliorated the cytotoxicity induced by both nanoparticles, highlighting the significant role of oxidative stress during nanoparticle toxicity. In summary, the current study presents a considerable role of oxidative stress and related signalling pathways in Al 2 O 3 ‐ and TiO 2 ‐NPs toxicity pathways in THP‐1 macrophage‐like cells.
Maadurshni et al. (Sun,) studied this question.