Banrida Wahlang1,2, Jian Jin3, Juliane I Beier4,5, Josiah E Hardesty1, Erica F Daly3, Regina D Schnegelberger6, K Cameron Falkner1, Russell A Prough7, Irina A Kirpich1,8,9, Matthew C Cave10,11,12,13,14,15,16,17,18. 1. Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY, 40202, USA. 2. University of Louisville Superfund Research Center, University of Louisville, Louisville, KY, 40202, USA. 3. Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY, 40202, USA. 4. Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Pittsburgh, Pittsburgh, PA, 15213, USA. 5. Pittsburgh Liver Research Center, University of Pittsburgh, Pittsburgh, PA, 15213, USA. 6. Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, 15213, USA. 7. Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, KY, 40202, USA. 8. Hepatobiology & Toxicology COBRE Center, University of Louisville School of Medicine, Louisville, KY, 40202, USA. 9. University of Louisville Alcohol Research Center, University of Louisville, Louisville, KY, 40202, USA. 10. Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 11. University of Louisville Superfund Research Center, University of Louisville, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 12. Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 13. Department of Biochemistry and Molecular Genetics, University of Louisville School of Medicine, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 14. Hepatobiology & Toxicology COBRE Center, University of Louisville School of Medicine, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 15. University of Louisville Alcohol Research Center, University of Louisville, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 16. The Robley Rex Veterans Affairs Medical Center, Louisville, KY, 40206, USA. matt.cave@louisville.edu. 17. The Jewish Hospital Liver Transplant Program, Louisville, KY, 40202, USA. matt.cave@louisville.edu. 18. Kosair Charities Clinical & Translational Research Building, 505 South Hancock Street, Louisville, KY, 40202, USA. matt.cave@louisville.edu.
Abstract
PURPOSE: Fatty liver disease (FLD) affects over 25% of the global population and may lead to liver-related mortality due to cirrhosis and liver cancer. FLD caused by occupational and environmental chemical exposures is termed "toxicant-associated steatohepatitis" (TASH). The current review addresses the scientific progress made in the mechanistic understanding of TASH since its initial description in 2010. RECENT FINDINGS: Recently discovered modes of actions for volatile organic compounds and persistent organic pollutants include the following: (i) the endocrine-, metabolism-, and signaling-disrupting chemical hypotheses; (ii) chemical-nutrient interactions and the "two-hit" hypothesis. These key hypotheses were then reviewed in the context of the steatosis adverse outcome pathway (AOP) proposed by the US Environmental Protection Agency. The conceptual understanding of the contribution of environmental exposures to FLD has progressed significantly. However, because this is a new research area, more studies including mechanistic human data are required to address current knowledge gaps.
PURPOSE:Fatty liver disease (FLD) affects over 25% of the global population and may lead to liver-related mortality due to cirrhosis and liver cancer. FLD caused by occupational and environmental chemical exposures is termed "toxicant-associated steatohepatitis" (TASH). The current review addresses the scientific progress made in the mechanistic understanding of TASH since its initial description in 2010. RECENT FINDINGS: Recently discovered modes of actions for volatile organic compounds and persistent organic pollutants include the following: (i) the endocrine-, metabolism-, and signaling-disrupting chemical hypotheses; (ii) chemical-nutrient interactions and the "two-hit" hypothesis. These key hypotheses were then reviewed in the context of the steatosis adverse outcome pathway (AOP) proposed by the US Environmental Protection Agency. The conceptual understanding of the contribution of environmental exposures to FLD has progressed significantly. However, because this is a new research area, more studies including mechanistic human data are required to address current knowledge gaps.
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