Association Between Fine Particulate Air Pollution and Chronic Liver Diseases
TL;DR
No hypothesis clearly characterizes the role of PM in the pathogenesis of the discussed liver diseases, in particular, at the molecular genetic level, and creating a formalized description of the processes mediating the effect of PM on the human body helps to better understand their role.
Abstract
The review highlights current understanding of the role of air pollution with particulate matter (PM) in the pathogenesis of chronic non-infectious liver diseases (CLD). For this purpose, the materials of articles indexed in the PubMed and Russian Science Citation Index (RSCI) databases were used. PM with an aerodynamic diameter of ≤2.5 μm are recognized as the most dangerous. It was found that long-term exposure to fine particulate matter (PM2.5), especially those containing metals, significantly increases the risk and mortality from liver cancer, cirrhosis, and non-alcoholic fatty liver disease. Exposure to PM2.5 can contribute to the development of CLD by causing oxidative stress, systemic inflammation, and dysregulation of lipid metabolism. Damage to the intestinal epithelium and disruption of microbiotic homeostasis causes stress to the endoplasmic reticulum of cells, inducing abnormal expression of specific microRNAs or inflammatory factors. The review discusses modern terminology and hypotheses of the pathogenesis of the most common chronic non-infectious liver diseases. Unfortunately, no hypothesis clearly characterizes the role of PM in the pathogenesis of the discussed liver diseases, in particular, at the molecular genetic level. Creating a formalized description of the processes mediating the effect of PM on the human body helps to better understand their role in the pathogenesis of various diseases, in particular CLD, which can contribute to the improvement of early diagnostic methods, treatment, and preventive measures.