Liver Disease-triggering Chemicals are Making Babies Sick Before They’re Even Born

By Study Finds

Babies are being exposed to liver disease-triggering chemicals — before they are even born, a new study warns.

The toxic particles – found in plastic food containers, toiletries, toys, and other consumer and industrial products – are fueling rising cases among young children.

“These findings can inform more efficient early-life prevention and intervention strategies to address the current non-alcoholic fatty liver disease epidemic,” says first author Dr. Vishal Midya from the Icahn School of Medicine at Mount Sinai in a media release.

Non-alcoholic fatty liver disease cases have skyrocketed over the last four decades, currently affecting a quarter of the global population.

NAFLD is the ​​most common form of liver disease in children. It may trigger cirrhosis or liver cancer later in life, with some patients requiring a transplant.

“We are all daily exposed to these chemicals through the food we eat, the water we drink, and the use of consumer products,” adds senior author Dr. Damaskini Valvi. “This is a serious public health problem. These findings show that early life exposure to many endocrine-disrupting chemicals is a risk factor for pediatric non-alcoholic fatty liver disease and draw attention for additional investigation needed to elucidate how environmental chemical exposures may interact with genetic and lifestyle factors in the pathogenesis of liver disease.”

Where are these chemicals hiding?

The study finds newborns with higher levels of the chemicals in their system were more prone to liver damage. The molecules harm health by influencing hormonal shifts during pregnancy. These chemical additives are part of the manufacturing process, extending an item’s shelf life. Previous studies have found them in countless items, including bottled water, perfume, toys, vinyl flooring, and shampoo.

The findings in JAMA Network Open come from blood and urine samples. The Mount Sinai team used a biomarker called cytokeratin-18 that has a link to the disease.

Non-alcoholic fatty liver disease affects up to one in 10 youngsters, rising to a third of those with obesity. Hormone-disrupting chemicals are a wide class of environmental pollutants that include several pesticides, plastics, flame retardants, and toxic metals.

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Examples include PFAS (perfluoroalkyl substances), also known as “forever chemicals.” They are a common ingredient in nonstick cookware and food packaging. Others harmful chemicals include PBDEs (polybrominated diphenyl ethers), used as flame retardants in furniture and infant products.

Experimental studies have shown that exposure to these chemicals can lead to liver injury and NAFLD. However, the potential effects of pre-natal exposures haven’t been studied in humans – until now. Researchers measured 45 chemicals in the blood or urine of 1,108 pregnant women from 2003 to 2010.

The chemicals included PFAS, organochlorine and organophosphate pesticides, plasticizers such as phenols and phthalates, PBDEs, and parabens. When the children reached the ages of six to 11, the researchers measured their levels of enzymes and cytokeratin-18. They found elevated levels in children with higher exposure to environmental chemicals during pregnancy.

“By understanding the environmental factors that accelerate fatty liver disease, we can reduce people’s risk by giving them actionable information to make informed choices that reduce the risk or impact of the disease,” says Prof. Robert Wright, co-director of the Institute for Exposomic Research at Icahn. “Exposomics is the wave of the future because once you’ve sequenced the human genome, which has been done, there isn’t much more you can do in genomics alone.”

“The missing piece of the puzzle for us to understand different diseases is to measure their environmental causes, and exposomics is a way to accelerate our knowledge of how the environment is affecting our health,” the researcher concludes.

South West News Service writer Mark Waghorn contributed to this report.