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Owing to increased applications, it is important to study the biological effects of Cr<jats:sub>2<\/jats:sub>O<jats:sub>3<\/jats:sub> NPs on human health. The lung is one of the main exposure routes to nanomaterials; therefore, the present study was designed to determine the genotoxic and apoptotic effect of Cr<jats:sub>2<\/jats:sub>O<jats:sub>3<\/jats:sub> NPs in human lung epithelial cells (A549). The study also elucidated the molecular mechanism of its toxicity. Cr<jats:sub>2<\/jats:sub>O<jats:sub>3<\/jats:sub> NPs led to DNA damage, which was deduced by comet assay and cytokinesis block micronucleus assay. The damage could be mediated by the increased levels of reactive oxygen species. Further, the oxygen species led to a decrease in mitochondrial membrane potential and an increase in the ratio of BAX\/Bcl\u20102 leading to mitochondria\u2010mediated apoptosis induced by Cr<jats:sub>2<\/jats:sub>O<jats:sub>3<\/jats:sub> NPs, which ultimately leads to cell death. Hence, there is a need of regulations to be imposed in NP usage. The study provided insight into the caspase\u2010dependent mechanistic pathway of apoptosis. 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