Laura E Armstrong1, Grace L Guo2,3,4. 1. Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, USA. 2. Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ, USA. guo@eohsi.rutgers.edu. 3. Environmental and Occupational Health Science Institute, Rutgers University, Piscataway, NJ, USA. guo@eohsi.rutgers.edu. 4. Department of Veterans Affairs, New Jersey Health Care System, East Orange, NJ, USA. guo@eohsi.rutgers.edu.
Abstract
PURPOSE OF REVIEW: Environmental contaminants are considered one of the major factors in the development and progression of NAFLD, the most common liver disease in the USA. RECENT FINDINGS: The evolving knowledge of mechanisms of hepatic steatosis and steatohepatitis has recently been reviewed and characterized as ALD, NAFLD, and TAFLD. The most recent mechanistic studies on PFAS and PCBs have revealed a greater role for toxicants in the initiation of not only TAFLD but also NAFLD and the more progressive inflammatory stage of NAFLD, non-alcoholic steatohepatitis. In addition to insecticides, recent studies support a significant contribution of fungicides and herbicides to NAFLD. The mechanisms of PFAS, PCBs, and fungicides in contributing to the increased prevalence of NAFLD remain unclear. Addressing whether chronic, low-dose exposures could result in liver pathology and whether real-world exposure to mixtures of environmental contaminants pose a significant risk factor for NAFLD is paramount to understand the impact of NAFLD on populations today.
PURPOSE OF REVIEW: Environmental contaminants are considered one of the major factors in the development and progression of NAFLD, the most common liver disease in the USA. RECENT FINDINGS: The evolving knowledge of mechanisms of hepatic steatosis and steatohepatitis has recently been reviewed and characterized as ALD, NAFLD, and TAFLD. The most recent mechanistic studies on PFAS and PCBs have revealed a greater role for toxicants in the initiation of not only TAFLD but also NAFLD and the more progressive inflammatory stage of NAFLD, non-alcoholic steatohepatitis. In addition to insecticides, recent studies support a significant contribution of fungicides and herbicides to NAFLD. The mechanisms of PFAS, PCBs, and fungicides in contributing to the increased prevalence of NAFLD remain unclear. Addressing whether chronic, low-dose exposures could result in liver pathology and whether real-world exposure to mixtures of environmental contaminants pose a significant risk factor for NAFLD is paramount to understand the impact of NAFLD on populations today.
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