Alternatively, Clois30B exposure reduced THP-1 cell viability which coincided with LDH and DAMP (i.e. IL-1α, and ATP) release suggesting that plasma membrane damage is a potential mode of action for ONC-induced macrophage toxicity, which aligns with previous studies [56, 57] and confirms the MIE in the lung fibrosis AOP [37]. Here, IL1A is linked to pulmonary fibrosis.