Ozone-induced neurotoxicity: In vitro and in vivo evidence

Together with cities in higher-income nations, it is anticipated that the real global ozone is rising in densely populated areas of Asia and Africa. This review aims to discuss the possible neurotoxic pollutants and ozone-induced neurotoxicity: in vitro and in vivo, along with possible biomarkers to assess ozone-related oxidative stress. As a methodical and scientific strategy for hazard identification and risk characterization of human chemical exposures, toxicological risk assessment is increasingly being implemented. While traditional methods are followed by in vitro toxicology, cell culture techniques are being investigated in modern toxicology. In both human and rodent models, aging makes the olfactory circuitry vulnerable to spreading immunological responses from the periphery to the brain because it lacks the blood-brain barrier. The ozone toxicity is elusive as it shows ventral and dorsal root injury cases even in the milder dose. Its potential toxicity should be disclosed to understand further the clear mechanism insights of how it acts in cellular aspects. Human epidemiological research has confirmed the conclusions that prenatal and postnatal exposure to high levels of air pollution are linked to behavioral alterations in offspring. O3 also enhances blood circulation. It has antibacterial action, which may have an impact on the gut microbiota. It also activates immunological, anti-inflammatory, proteasome, and growth factor signaling Prolonged O3 exposure causes oxidative damage to plasma proteins and lipids and damages the structural and functional integrity of the mitochondria. Finally, various studies need to be conducted to identify the potential biomarkers associated with ozone and the brain.