Yes. At present, with the rapid development of the economy and industrialisation, many chemicals are released into the environment, which can cause harm to human health and result in lipid metabolism disorder due to long-term exposure.
In the last one 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 great steatogenic potential, and they must 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.
What comprises air pollution?
The particulate matter is often encompassed in the term “air pollution”, i.e., any solid or liquid particle suspended in the air. A particulate matter is an assortment of a wide range of contaminants. It consists of smoke, vapours, smut, besides other derivatives of combustion, and it also includes sand, sea salt, spores and pollen. However, the leading role among the particulate constituents is played by the particles derived from exhausts, by-products of vapourised materials, and oxidised gases in the atmosphere such as sulphates and nitrates.
Can air pollution affect Non-Alcoholic Fatty Liver Disease?
Studies state that so far it has been known that PM2.5 results from fuel combustion (motor vehicles, power generation, industrial facilities), residential fireplaces and wood stoves. PM2.5 are usually selected as indicators of air pollution since those particles cause morbidity. In fact, the exposure of PM2.5 alone could cause inflammation via tumour necrosis and hamper factor-alpha, endothelial function and autonomic nervous system injuries.
According to the Journal of Hepatology, exposure elevates the risk of oxidative stress-driven nonalcoholic fatty liver disease by triggering an increase of dyslipidemia. Specifically, fine particulate matter exposure may trigger non-alcoholic steatohepatitis (NASH) like phenotype, impair hepatic glucose metabolism and promote hepatic fibrogenesis.
Further studies should investigate the effects of long-lasting exposures to cigarette smoking and to ambient air PM2.5 on specific pathways of hepatic metabolism, and the obesity-related NAFLD, favouring the development of NASH (a disease characterised by a worse prognosis due to its progression towards fibrosis, liver cirrhosis and hepatocarcinoma).
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