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Interaction of volatile organic compounds and underlying liver disease: a new paradigm for risk

  • Anna L. Lang and Juliane I. Beier EMAIL logo
Published/Copyright: June 20, 2018

Abstract

Occupational and environmental exposures to industrial chemicals are known to cause hepatotoxicity and liver injury, in humans and in animal models. Historically, research has focused on severe acute liver injury (e.g. fulminant liver failure) or endstage diseases (e.g. cirrhosis and HCC). However, it has become recently recognized that toxicants can cause more subtle changes to the liver. For example, toxicant-associated steatohepatitis, characterized by hepatic steatosis, and inflammation, was recently recognized in an occupational cohort exposed to vinyl chloride. At high occupational levels, toxicants are sufficient to cause liver damage and disease even in healthy subjects with no comorbidities for liver injury. However, it is still largely unknown how exposure to toxicants initiate and possibly more importantly exacerbate liver disease, when combined with other factors, such as underlying non-alcoholic fatty liver disease caused by poor diet and/or obesity. With better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of toxicant-induced liver disease, rational targeted therapy can be developed to better predict risk, as well as to treat or prevent this disease. The purpose of this review is to summarize established and proposed mechanisms of volatile organic compound-induced liver injury and to highlight key signaling events known or hypothesized to mediate these effects.

Award Identifier / Grant number: K01 DK096042

Award Identifier / Grant number: R03 DK107912

Award Identifier / Grant number: P42 ES023716

Award Identifier / Grant number: P20GM113226

Award Identifier / Grant number: P20GM103492

Award Identifier / Grant number: P50AA024337

Funding statement: Supported by awards from the National Institutes of Health [National Institute of Diabetes and Digestive and Kidney Diseases, Funder id: 10.13039/100000062 (K01 DK096042, R03 DK107912), T32ES011564, and National Institute of Environmental Health Sciences, Funder id: 10.13039/100000066 (P42 ES023716)]. Research was also supported by two Institutional Development Awards (IDeA) from the National Institute of General Medical Sciences of the National Institutes of Health under grant numbers P20GM113226 and P20GM103492 as well as the National Institute on Alcohol Abuse and Alcoholism of the National Institutes of Health under Award Number P50AA024337 (Funder id: 10.13039/100000027). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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Received: 2017-12-22
Accepted: 2018-06-14
Published Online: 2018-06-20
Published in Print: 2018-10-25

©2018 Walter de Gruyter GmbH, Berlin/Boston

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