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

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.

Vinyl Chloride and High-Fat Diet as a Model of Environment and Obesity Interaction

“…This model of toxicant-induced liver injury can be used for other volatile organic compounds and also to study other interactions that may impact the liver and other organ systems 8,22,23 . Moreover, this model has been, and can be further, used to investigate intervention therapies and indepth mechanistic studies of the mode of action for this prevalent toxicant 24 .…”

“…Although the exposure threshold has been lowered, the effect of this concentration of VC on human health is unclear 7 . Additionally, the effect of VC exposure on existing comorbidities, such as liver disease, is largely unknown 8 . This knowledge gap is especially important today due to the increasing global prevalence of nonalcoholic fatty liver disease (NALFD) 4,6,7,9,10,11,12 .…”

Joint Effects of Ethnic Enclave Residence and Air Pollution Exposure on Risk of Gestational Diabetes Mellitus Among Asian/Pacific Islander Women in the United States

“…As part of the normative immune response, cells exposed to an insulting agent release pro-in ammatory cytokines and become in amed in order to isolate damage and protect healthy cells and tissue; as the insult is eliminated, anti-in ammatory cytokines are released and in ammation is contained, thus mitigating development of disease. (36) In contrast, air pollution exposure signals an in ammatory response (27,32,(37)(38)(39)(40), and among those with a compromised immune system, an excessive in ammatory response to air pollution may increase risk for metabolic disease. (41,42) Considering joint social and environmental exposures among API communities in the U.S. will provide new insights into health outcomes among these understudied populations.…”

Ytterbium Doped TiO2 Nanofibers on Activated Carbon Fibers Enhances Adsorption and Photocatalytic Activities for Toluene Removal

“…Volatile organic compounds (VOCs) which are believed as major indoor air pollutants do great harm to human health . Gaseous toluene, a kind of refractory VOCs, will damage skin, nervous system, eye and cerebrum even under low concentrations .…”