Vinyl Chloride/Diet Interaction: Implications for Steatohepatitis


VC is a clinically relevant chemical toxicant and an important occupational/environmental pollutant. It is released by industries or formed by the breakdown of other chlorinated chemicals in landfills, and elsewhere, and enters the air and drinking water supplies. Owing to its widespread distribution and its known potential human harm, VC is ranked #4 on the ATSDR Hazardous Substance Priority List. High levels of vinyl chloride exposure frequently cause steatohepatitis in chemical workers. The metabolism of VC is very similar to that of ethanol, which also causes fatty liver disease/steatohepatitis. VC is metabolized by CYP2E1 to form the highly reactive genotoxic epoxide, chloroethylene oxide, which is then converted to chloroacetaldehyde. Increased dietary levels of the ω-6 unsaturated fat, linoleic acid, markedly enhance alcohol-induced liver injury and increase levels of toxic OXLAMs. The potential interactions of lower (clinically relevant) doses of organochlorides and different types of dietary fats have not been explored in this context.


A normal liver takes a hit from obesity to become a fatty liver, which takes a hit from environmental pollution to turn into steatohepatitis. Proposed Model of Steatohepatitis Normal Liver 1st Hit Obesity Fatty Liver 2nd Hit Environmental pollution Steatohepatitis

Exposure to vinyl chloride and other organochlorides interact additively/synergistically with increased dietary fat consumption to cause steatohepatitis through mechanisms common to ASH and NASH.

About Researcher

Principal Investigator

Juliane Beier

Juliane Beier, PhD

Assistant Professor

E-mail Dr. Beier


Pharmacology & Toxicology, University of Louisville

Related Project

Enhancement of NAFLD Risk by Vinyl Chloride: Interaction of Gut-Liver-Adipose Axi