Lithium is used heavily and increasingly in rechargeable batteries for mobile devices electric vehicles and elsewhere. It is used in various formulations in these batteries including lithium nickel manganese cobalt oxide (LiNMC) particles. Currently these batteries are rarely recycled. As a result they can end up as waste either in outside of landfills which may lead to exposure and toxic effects to people and wildlife. However our understanding of the toxicity of LiNMC particles is limited. Based on previous literature investigating the mechanisms of toxicity of the constituent metals as well as lithium cobalt oxide (LCO) nanoparticles we hypothesized that LiNMCs would cause toxicity via mitochondrial impairment and oxidative stress. We further hypothesized that LiNMC toxicity would be exacerbated by knockdown of the human mitochondrial disease genes frataxin and NDUFS2. Finally we predicted that LiNMC exposure would cause developmental neurotoxicity. We tested these predictions in the model organism Caenorhabditis elegans and found that LiNMCs did not significantly impact the redox state steady-state ATP levels mitochondrial:nuclear DNA ratio or oxygen consumption in worms exposed developmentally to amounts of LiNMC that caused mild growth inhibition. Furthermore while knockdown of frataxin and NDUFS2 altered a number of parameters knockdown of these genes did not increase or decrease the effects of LiNMCs. However we did find that LiNMC exposure caused degeneration of dopaminergic cholinergic glutamatergic and GABAergic neurons but not serotonergic neurons or glial cells. Interestingly it appears that the developmental neurotoxicity was driven either by a particle-specific effect or a component other than lithium because lithium chloride at the same concentration had no effect.
