Airway exposure to lithium nickel manganese cobalt oxide particles induces alterations in lung microenvironment and potential kidney and liver damage in mice.

Abstract

With the increasing use of lithium-ion batteries, the exposure and health effects of lithium nickel manganate cobalt (NMC), a popular cathode material for the battery, have attracted widespread attention. However, the main absorption routes and target organs of NMC are unknown. This study aims to systematically investigate the main absorption routes and target organs of NMC. Male adult C57BL/6 J mice were subjected to acute exposure to NMC particles (Ni: Mn: Co = 5: 3: 2, mass median geometric diameter 9.15 μm) by intragastric administration, transdermal drug delivery, and oropharyngeal aspiration (OPA). The OPA group showed a significant increase in NMC metal levels in organs and blood compared to the other exposure routes. After OPA treatment (0.5 or 2 mg, once per day, 3 days), significantly increased metal levels were found in the lung, liver and kidney, but there was no dose-response effect. In the lung, obvious inflammation, and significant elevation of white blood cells, neutrophils and eosinophils in bronchoalveolar lavage fluid were observed, all of which showed a dose-response effect. Reduced urine output and renal tubular cell loss, as well as dysregulated metabolic and immune functions as indicated by the hepatic transcriptome, were observed in NMC-exposed mice. Respiratory exposure is the main exposure route of NMC. Short-term respiratory exposure to NMC results in potential damage to the kidney and liver in addition to severe inflammation in the lung.