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The occurrence of thermal runaway (TR) events continues to rise as the need for lithium-ion batteries (LIB) for energy storage increases. However, the inhalation risks associated with LIB TR events remain widely unknown. The objective of this study was to evaluate the impact of LIB TR particulate emission exposures on primary small airway epithelial cells (SAEC). TR was triggered by subjecting lithium-ion cells to thermal abuse at different states of charge (SOC). Two different battery cathode chemistry compositions, namely, nickel manganese cobalt (NMC) or lithium iron phosphate (LFP) were evaluated. Aerosol monitoring and sampling instrumentation were employed followed by physicochemical particle characterization and inhalation dosimetry modeling. SAEC were treated with TR particulate emission extracts for 24 h and 7 days at doses representing a cumulative 1- and 5-year inhalation exposure. Following treatment, cellular viability, reactive oxygen species (ROS) production, and protein expression of DNA damage and epithelial mesenchymal transition (EMT) markers were assessed. TR particulate emissions consisted of ultrafine particles containing a variety of heavy metals. Cellular senescence was induced by NMC-derived TR extracts, but not LFP-derived TR extracts. SAEC treated with the 5-year dose of NMC-derived TR extract, induced significant ROS production. In cells treated with NMC-derived TR extract, regulators of DNA repair and cell cycle arrest were perturbed. Oxidative stress subsequently induced EMT, as SAEC treated with NMC-derived TR particulate emissions reduced E-cadherin expression and upregulated Fascin and Vimentin expression. This study reveals the respiratory implications of TR particulate emissions and the role of battery chemistry.
Meister et al. (Sat,) studied this question.