As a group I carcinogen, environmental exposures to formaldehyde (FA) have been associated with various types of malignancies. However, exact mechanisms of FA-triggered carcinogenesis are still not clear. Lactylation is recently identified as a post-translational modification driven by overproduced lactic acid (LA) that regulates protein activities in different cellular processes. Our previous studies clearly demonstrated that environmentally relevant levels of FA could elevate LA in tumor cells. Poly (ADP-ribose) polymerase 1 (PARP1) is a major player in DNA repair and tumor cell survival, which has been shown to be activated by lactylation. In order to examine if PARP1 lactylation is promoted by FA environmental exposure, subcutaneous tumor models were established using BALB/c nude mice, which were exposed to 2.0 mg/m