Non-alcoholic fatty liver disease in children can occur due to chemicals

According to a study published in the JAMA Network Open, prenatal exposure to chemicals that disrupt the endocrine system may be a cause of higher incidence of non-alcoholic fatty liver disease in children.

According to a study published in JAMA Network OpenPrenatal exposure to endocrine disrupting chemicals may be a cause of higher incidence of non-alcoholic fatty liver disease in children.

Prenatal exposure to endocrine disrupting chemicals (EDCs) may increase the risk of liver damage in children; however, human evidence to date is sparse and previous studies have not considered the potential effects of the EDC blend. In addition, the association between prenatal EDC exposure and hepatocellular apoptosis in children has not been previously studied.

Dr. Vishal Midya, of the Department of Environmental Medicine and Public Health at the Icahn School of Medicine on Mount Sinai, and colleagues reported that NAFLD “is increasingly diagnosed in childhood,” occurring in 6% -10% of cases in the general pediatric population. and in approximately 36% of children with obesity.

To determine whether prenatal exposure to endocrine disrupting chemicals may increase the risk of liver damage and hepatocellular apoptosis in a child, Midya and colleagues analyzed data collected from 1,108 mother-infant couples from prospective birth cohort studies based on the populations of France, Greece. , Lithuania, Norway, Spain and the United Kingdom.

Urine or blood samples were collected from mothers during pregnancy or from umbilical cord blood collected at birth, and serum samples from their children were collected between 6 and 11 years of age. Researchers assessed the risk of liver damage due to serum levels of alanine aminotransferase, aspartate transferase and gamma-glutamyltransferase and hepatocellular apoptosis with cytokeratin 18 (CK-18) levels.

“We applied a new analytical framework using two state-of-the-art statistical methods for exposure mix analysis with different underlying assumptions that allowed us to evaluate the robustness of the results, regardless of the statistical approach,” Midya wrote and colleges.

Researchers assessed exposure to 45 endocrine disrupting chemicals, including 10 phthalates, nine metals, five polychlorinated biphenyls, five perfluoroalkyls, four parabens, four organophosphate pesticides, three organochlorine pesticides, three phenols and two diphenyl bromines.

According to the study results, children were more likely to get liver damage from exposure to organic chlorine pesticides (OR = 1.44; 95% credible range, 1.21-1.71), polybrominated diphenyl ethers (OR = 1, 57; 95% CI, 1 , 34-1.84), perfluoroalkyl substances (OR = 1.73; 95% Cl, 1.45-2.09) and metals (OR = 2.21; 95% Cl, 1.65-3.02). In contrast, the researchers observed that children had a reduced likelihood of liver damage due to exposure to high molecular weight phthalates (OR = 0.74; 95% CI, 0.6-0.91) and phenols (OR = 0.66 95% CI, 0.54-0.78).

In addition, the researchers reported that the increase in CK-18 levels was associated with an increase in polybrominated diphenyl ether (b = 6.46 IU / L; 95% CI, 3.09-9.92) and of polychlorinated biphenyl (b = 5 , 84 IU / L; 95% CI, 1.69-10.08) exposure.

“We found that prenatal exposure to ubiquitous endocrine disrupting chemicals, and in particular organochlorine pesticides, polybrominated diphenyl ethers, perfluoroalkyls and metals, was associated with increased liver damage and / or hepatocellular apoptosis in children,” Midya and colleagues wrote. “Our results may be targeted at more effective prevention and intervention strategies in early childhood to address the current NAFLD epidemic.”


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