Due to its excellent physicochemical properties, cerium oxide (CeO₂) has attracted much attention in recent years. CeO₂ nanomaterials (nanoceria) are widely being used, which has resulted in them getting released to the environment, and exposure to humans (mostly via inhalation) is a major concern. In the present study, CeO₂ nanoparticles were synthesized by hydroxide-mediated method and were further characterized by Scanning Electron Microscopy (SEM), Field Emission Scanning Electron Microscopy (FESEM), Energy Dispersive X-ray Spectroscopy (EDX), Fourier Transform Infrared Spectroscopy (FTIR), and X-ray Diffraction Spectroscopy (XRD). Human lung epithelial (Beas-2B) cells were used to assess the cytotoxicity and biocompatibility activity of CeO₂ nanoparticles. 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) and Live/Dead assays were performed to determine the cytotoxicity and biocompatibility of CeO₂ nanoparticles. Generation of reactive oxygen species (ROS) by cerium oxide nanoparticles was assessed by ROS assay. MTT assay and Live/Dead assays showed no significant induction of cell death even at higher concentrations (100 μg per 100 μL) upon exposure to Beas-2B cells. ROS assay revealed that CeO₂ nanoparticles did not induce ROS that contribute to the oxidative stress and inflammation leading to various disease conditions. Thus, CeO₂ nanoparticles could be used in various applications including biosensors, cancer therapy, catalytic converters, sunscreen, and drug delivery.

With the widespread application of carbon nanotubes (CNTs) in diverse commercial processes, scientists are now concerned about the potential health risk of occupational exposures. In this study, CNT-induced pulmonary toxicity was investigated by exposing BALB/c mice to aerosolized single-wall (SW) CNT and multiwall (MW) CNT (5 μg/g of mice) for 7 consecutive days in a nose-only exposure system. Microscopic studies showed that inhaled CNTs were homogeneously distributed in the mouse lung. The total number of bronchoalveolar lavage polymorphonuclear leukocytes recovered from the mice exposed to SWCNT and MWCNT (1.2 × 10⁶ ± 0.52 and 9.87 × 10⁵ ± 1.45; respectively) was significantly greater than control mice (5.46 × 10⁵ ± 0.78). Rapid development of pulmonary fibrosis in mice that inhaled CNT was also confirmed by significant increases in the collagen level. The lactate dehydrogenase levels were increased nearly 2- and 2.4-fold in mice that inhaled SWCNT and MWCNT, respectively, as compared with control mice. In addition, exposure of CNTs to mice showed a significant (p < 0.05) reduction of antioxidants (glutathione, superoxide dismutase, and catalase) and induction of oxidants (myloperoxidase, oxidative stress, and lipid peroxidation) compared with control. Apoptosis-related proteins such as caspase-3 and -8 activities were also significantly increased in mice that inhaled CNT than in control mice. Together, this study shows that inhaled CNTs induce inflammation, fibrosis, alteration of oxidant and antioxidant levels, and induction of apoptosis-related proteins in the lung tissues to trigger cell death.