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Vinyl chloride is primarily metabolized in the liver to multiple metabolites. Chloroethylene oxide and chloroacetaldehyde are the reactive intermediate metabolites and their formation of DNA and protein adducts is closely related to the carcinogenic property of vinyl chloride. Meanwhile, 2‐chloroethanol, in addition to vinyl chloride, is involved in the enhanced susceptibility to liver injury by dysregulating glucose metabolism and inducing mitochondrial damage.

Exposure to sub‐parts per million levels of vinyl chloride can increase the risk of developing liver injury