Neurotoxicity can be linked to the ability of particles to accumulate in the mitochondria, leading to mitochondrial dysfunction [32], the induction of oxidative stress [26,33], direct physical damage [28,34], altered neurotransmitter levels [26,30], or disruption of the gut microbiome [33,34,35], inducing pro-apoptotic protein expression (BAX, caspase 3, caspase 8, caspase 9, DR5, and cytochrome c) and pro-inflammatory cytokines (IL-8, NF-κB and TNF-α) [36]. This evidence concerns the gene CASP3 and toxic encephalopathy.