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Bisphenol A (BPA) replacement chemicals are used in products like food packaging, plastic piping, and sportswear. While they can be toxic, their neurotoxicity is less understood. This study treated differentiated human SH-SY5Y cells with Bisphenol S (BPS) and Bisphenol F (BPF) to explore mechanisms of toxicity. BPS reduced cell viability (50 µM at 48 h) more than BPF (200 µM at 48 h), with dose- and time-dependent effects. Both chemicals induced caspase 3/7 activity at 250 µM after 48 h, though no changes were observed in reactive oxygen species or mitochondrial ATPase activity, suggesting mitochondrial function was unaffected. RNA-seq analysis at 0.1 nM revealed distinct transcriptional networks affected by each bisphenol. BPS altered IL15R → NF-kB/NFATC and CD8 → NF-kB signaling, while BPF affected TLR9 and TNF → NF-kB targets. Pathway analysis showed that genes involved in neuroinflammation, protein folding, microglial function, and motor neuron regulation were disrupted. Despite low acute toxicity, both BPS and BPF altered gene expression at low, environmentally relevant concentrations. These transcriptomic changes may contribute to long-term neurological effects.