This study investigates the translocation of inhaled ultrafine manganese oxide (MnO) particles to the central nervous system (CNS) in rats. Researchers exposed rats to MnO particles (30 nm) via intranasal instillation and whole-body inhalation, assessing their accumulation in the olfactory bulb and other brain regions. Results showed significant increases in Mn levels in the olfactory bulb, striatum, frontal cortex, and cerebellum after 12 days of exposure. Lung Mn levels also increased, but no signs of lung inflammation were observed. Gene and protein analyses revealed elevated tumor necrosis factor-α (TNF-α) expression in the olfactory bulb and other brain regions, indicating inflammatory changes. When one nostril was occluded, Mn accumulated only in the opposite olfactory bulb, supporting the olfactory translocation pathway. The solubility of MnO particles was low (<1.5% per day), suggesting that translocation occurs primarily as solid particles. The study concludes that the olfactory neuronal pathway is efficient for translocating inhaled MnO particles to the CNS, leading to inflammatory changes. Despite differences between human and rodent olfactory systems, this pathway is likely relevant in humans. The findings highlight the importance of particle size and solubility in olfactory translocation processes. The study also suggests that Mn oxide UFPs may contribute to neurotoxicity, as seen in occupational exposures, such as welding, where high Mn levels in fumes have been linked to Parkinson-like symptoms. The study underscores the need for further research on the mechanisms of Mn translocation and its potential health impacts.This study investigates the translocation of inhaled ultrafine manganese oxide (MnO) particles to the central nervous system (CNS) in rats. Researchers exposed rats to MnO particles (30 nm) via intranasal instillation and whole-body inhalation, assessing their accumulation in the olfactory bulb and other brain regions. Results showed significant increases in Mn levels in the olfactory bulb, striatum, frontal cortex, and cerebellum after 12 days of exposure. Lung Mn levels also increased, but no signs of lung inflammation were observed. Gene and protein analyses revealed elevated tumor necrosis factor-α (TNF-α) expression in the olfactory bulb and other brain regions, indicating inflammatory changes. When one nostril was occluded, Mn accumulated only in the opposite olfactory bulb, supporting the olfactory translocation pathway. The solubility of MnO particles was low (<1.5% per day), suggesting that translocation occurs primarily as solid particles. The study concludes that the olfactory neuronal pathway is efficient for translocating inhaled MnO particles to the CNS, leading to inflammatory changes. Despite differences between human and rodent olfactory systems, this pathway is likely relevant in humans. The findings highlight the importance of particle size and solubility in olfactory translocation processes. The study also suggests that Mn oxide UFPs may contribute to neurotoxicity, as seen in occupational exposures, such as welding, where high Mn levels in fumes have been linked to Parkinson-like symptoms. The study underscores the need for further research on the mechanisms of Mn translocation and its potential health impacts.