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Available data indicate that vinyl chloride is absorbed rapidly and virtually completely absorbed following inhalation and oral exposure. Dermal absorption of gaseous vinyl chloride is not significant. After a 2 -2.5 h exposure of rhesus monkeys to 800 and 7000 ppm vinyl chloride, dermal absorption was estimated to be 0.031% and 0.023% of total bioavailable vinyl chloride, respectively.

In rats, absorbed vinyl chloride is distributed primarily to the liver and skin.

Metabolism is believed to proceed via different pathways, the extent of which is dependent on vinyl chloride concentrations. At low concentrations, vinyl chloride is oxidized sequentially to 2-chloroethanol, 2-chloroacetaldehyde and 2 -chloroacetic acid by alcohol dehydrogenase, while at higher concentrations it is metabolized by liver cytochrome P-450 IIE1 to the reactive oxirane, 2 -chloroethylene oxide and its rearrangement product 2-chloroacetaldehyde. Chloroethylene oxide and chloroacetaldehyde react with nucleic acid bases, forming DNA adducts, which are thought to play a role in carcinogenicity of vinyl chloride.

The elimination of vinyl chloride follows first-order kinetics. At low exposure levels, the majority is excreted into the urine, while at higher exposure levels, the proportion of exhaled unmetabolized vinyl chloride increases.