Faroud Lopez Roi, Huayta Javier, Williams Gordon D Z, Seay Sarah A, Lalwani Pooja D, Bacot Sasha N, Vengosh Avner, Meyer Joel N
Nicholas School of the Environment, Duke University Durham NC USA
Env Sci Adv. 2025 Sep 25. doi: 10.1039/d5va00103j.
Lithium is increasingly used in rechargeable batteries for mobile devices, electric vehicles, and energy storage, among other applications. One of the common formulations of lithium batteries is lithium nickel manganese cobalt oxide (LiNMC) particles. Increasing utilization of LiNMC batteries would require adequate disposal and/or recycling, and yet the potential disposal of lithium batteries as waste either in or outside of landfills might lead to toxic effects to people and wildlife. However, understanding of the potential 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 mitochondrial impairment and oxidative stress. We further hypothesized that LiNMC toxicity would be exacerbated by knockdown of and , orthologs of human mitochondrial disease genes frataxin and NDUFS2. Finally, we predicted that LiNMC exposure would cause developmental neurotoxicity. We tested these predictions by carrying out LiNMC exposures, and found these 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. We discuss possible reasons for the difference between our results and previous publications, including particle size. Furthermore, while knockdown of and altered several parameters, knockdown of these genes did not increase or decrease the effects of LiNMCs. However, we did find that exposure to LiNMC 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 exposure to lithium chloride at the same concentration had no effect.
锂越来越多地用于移动设备、电动汽车和储能等的可充电电池中。锂电池的常见配方之一是锂镍锰钴氧化物（LiNMC）颗粒。LiNMC电池使用量的增加将需要适当的处置和/或回收利用，然而，锂电池作为废物在垃圾填埋场内外的潜在处置可能会对人类和野生动物产生毒性影响。然而，对LiNMC颗粒潜在毒性的了解有限。基于先前研究组成金属毒性机制以及钴酸锂（LCO）纳米颗粒的文献，我们假设LiNMC会导致毒性、线粒体损伤和氧化应激。我们进一步假设，人类线粒体疾病基因frataxin和NDUFS2的直系同源基因被敲低后，LiNMC的毒性会加剧。最后，我们预测LiNMC暴露会导致发育性神经毒性。我们通过进行LiNMC暴露来测试这些预测，发现在发育过程中暴露于导致轻度生长抑制量的LiNMC的蠕虫中，这些暴露并未显著影响氧化还原状态、稳态ATP水平、线粒体与核DNA比率或氧气消耗。我们讨论了我们的结果与先前出版物之间差异的可能原因，包括颗粒大小。此外，虽然对 和 的敲低改变了几个参数，但敲低这些基因并没有增加或减少LiNMC的影响。然而，我们确实发现暴露于LiNMC会导致多巴胺能、胆碱能、谷氨酸能和GABA能神经元退化，但不会导致5-羟色胺能神经元或神经胶质细胞退化。有趣的是，发育性神经毒性似乎是由颗粒特异性效应或锂以外的其他成分驱动的，因为暴露于相同浓度的氯化锂没有影响。
