Environmental Pollution: A Tangible Risk for NAFLD Pathogenesis

Abstract

The liver is crucial for human life, and the health of this organ often mirrors the health of the individual. The liver can be the target of several diseases, the most prevalent of which, as a consequence of development and changes in human lifestyles, is the nonalcoholic fatty liver disease (NAFLD). NAFLD is a multifactorial disease that embraces many histo-pathologic conditions and is highly linked to metabolic derangements. Technological progress and industrialization have also had the consequence of releasing pollutants in the environment, for instance pesticides or solvents, as well as by-products of discharge, such as the particulate matter. In the last decade, a growing body of evidence has emerged, shedding light on the potential impact of environmental pollutants on liver health and, in particular, on NAFLD occurrence. These contaminants have a great steatogenic potential and need to be considered as tangible NAFLD risk factors. There is an urgent need for a deeper comprehension of their molecular mechanisms of action, as well as for new lines of intervention to reduce their worldwide diffusion. This review wishes to sensitize the community to the effects of several environmental pollutants on liver health.

Fetal exposure to arsenic results in hyperglycemia, hypercholesterolemia, and nonalcoholic fatty liver disease in adult mice

“…More importantly, the studies by Smith's group provided some of the first evidence in humans of the detrimental health effects from IU arsenic exposure resulting in an increased incidence of myocardial infarction in adults [10]. Similarly, arsenic exposure has been linked to NAFLD, obesity and diabetes, even though the exact the molecular mechanisms are not fully understood [40]. Although these associations have been shown before, to our knowledge, no reports of fetal arsenic exposure exist showing an association to NAFLD.…”

The Effects of Dark Chocolate Consumption on Lipid Profile, Fasting Blood Sugar, Liver Enzymes, Inflammation, and Antioxidant Status in Patients with Non-Alcoholic Fatty Liver Disease: A Randomized, Placebo-Controlled, Pilot study

“…Nonetheless, the actual underlying molecular and cellular mechanisms of liver injury in NAFLD are still unknown [1] . However, the NAFLD patho-physiology was firstly described by the 'two-hit hypothesis', and subsequently [8] , there is currently an accepted concept for NAFLD pathogenesis that is called "multiple hit" hypothesis.…”

“…However, the NAFLD patho-physiology was firstly described by the 'two-hit hypothesis', and subsequently [8] , there is currently an accepted concept for NAFLD pathogenesis that is called "multiple hit" hypothesis. According to this hypothesis, multiple mechanisms, including insulin resistance, oxidative stress, inflammation, and genetic factors interact to initiate the NAFLD development [9] and also these are etiological factors associated with metabolic derangements [1] . Moreover, it has become evident that development of NAFLD is due to multiple interrelated factors including visceral obesity, dyslipidemia, diabetes, and hypertension, all of them are key risk factors related to NAFLD.…”

“…The liver tissue can be the target of several diseases, all able to change the hepatic functions. One of the most common causes of primary and chronic hepatic disorders worldwide is the non-alcoholic fatty liver disease (NAFLD) [1] which is an important health problem in various age groups [2] .…”

Relationship between Methyl Tertiary Butyl Ether Exposure and Non-Alcoholic Fatty Liver Disease: A Cross-Sectional Study among Petrol Station Attendants in Southern China

“…NAFLD is the most typical chronic liver disease worldwide [21,22,23,24,25,26]. The spectrum of NAFLD ranges from simple hepatic steatosis to steatohepatitis, which may develop into cirrhosis and ultimately into liver carcinoma [22,23,24,25].…”