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Abstract
Formaldehyde is a highly reactive compound produced extensively worldwide. People are exposed to formaldehyde in both industrial and occupational settings, and environmentally via off-gassing of vehicle exhaust, cigarette smoke, and home production materials. Formaldehyde has been implicated extensively in human carcinogenicity studies, and thus is classified as a class I human DNA carcinogen. Formaldehyde has been shown to have severe detrimental effects on cellular processes, likely due to induction of its predominant DNA lesion, DNA-protein crosslinks. This covalent linkage of proteins to DNA has been demonstrated to occur with a plethora of proteins, implicated in a wide variety of cellular process. Consequently, studies have identified several DNA repair pathways that play a role in mitigating cytotoxicity and genotoxicity after formaldehyde exposure. In this study, we choose to further define and reconcile discrepancies in the literature by using a high-throughput systems approach to discern the conserved pathways necessary for survival following chronic formaldehyde exposure, across cell type and species.