Prenatal exposure to chemicals may cause liver disease in kids

Prenatal exposure to several chemicals found in consumer and industrial products may be linked to the growing incidence of liver disease in children, according to a study by researchers including Vishal Midya (L), the primary author. Photo courtesy of Mount Sinai Institute for Exposomic Research
Prenatal exposure to several chemicals found in consumer and industrial products may be linked to the growing incidence of liver disease in children, according to a study by researchers including Vishal Midya (L), the primary author. Photo courtesy of Mount Sinai Institute for Exposomic Research

July 6 (UPI) -- Prenatal exposure to several chemicals found in consumer and industrial products may be linked to the growing incidence of liver disease in children, a new study suggests.

In their study published online Wednesday in JAMA Network Open, researchers said individuals are exposed daily through the food, water and consumer products to certain chemicals they described as "endocrine-disrupting."


Transmission of these chemicals can occur through the placenta, making the issue especially worrisome during embryonic development.

Transmission also is possible to babies through breast milk, but the precise time when liver injury or disease may develop is unclear, according to the researchers.

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They characterize the problematic chemicals as a wide class of environmental pollutants that include several pesticides, plastics, flame retardants and toxic metals.

Specific examples include perfluoroalkyl substances, also known as "forever chemicals," that are used in non-stick cookware and food packaging, as well as and polybrominated diphenyl ethers used as flame retardants in furniture and infant products.


This is the first comprehensive study on the association of prenatal exposure and mixtures of these chemicals to non-alcoholic fatty liver disease, the researchers said.

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They described the illness as a rapidly growing problem in children that may lead to severe chronic liver disease and liver cancer in adulthood. It affects 6% to 10% of the general pediatric population and roughly 34% of children who are obese, the researchers said.

"These chemicals are usually in every human, with different levels of concentration," Vishal Midya, the study's primary author and a postdoctoral researcher in the Department of Environmental Medicine and Public Health at the Icahn School of Medicine at Mount Sinai in New York City, told UPI in a phone interview.

"We do have these chemicals in our system, in our body, but [they] become very toxic in the early stages [of pregnancy] when you're exposed in the womb," Midya said, adding that more research is needed to determine whether in utero exposure to environmental toxins may cause more than liver disease.

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Dr. Aparna Bole, chair of the American Academy of Pediatrics Council on Environmental Health and Climate Change, told UPI the study "provides an example of the well-known fact that critical windows of development in utero, childhood and adolescence confer particular vulnerability to environmental exposures."


"The regulatory framework for chemical safety should take into specific consideration the potential cumulative and longitudinal health effects of exposure in children," said Bole, associate professor in the Department of Pediatrics at Case Western Reserve University School of Medicine in Cleveland.

"Unfortunately, this is not currently the case," she added.

"Studies such as these are helpful in better understanding the contribution of in utero environmental exposures to the development of pediatric non-alcoholic fatty liver disease," Bole said.

"And [they] bolster the case more broadly for a more proactive, rather than reactive, regulatory approach to chemical safety that specifically takes into consideration the unique effects of exposures in pregnancy, childhood and adolescence."

Midya also is a member of the medical school's Mount Sinai Institute for Exposomic Research, which studies the effects of environmental exposures on health.

People in the field describe the measurement of environmental causes for disease as the wave of the future now that the human genome has been sequenced.

According to Midya, the study's findings could lead to more efficient early-life prevention and intervention strategies to address the growing problem of non-alcoholic fatty liver disease in children.

And understanding the environmental factors that accelerate the illness could reduce people's risk by giving them actionable information to make informed choices.


For example, Midya suggests that pregnant women find ways to limit exposure to the problematic chemicals, such as avoiding non-stick cookware, plastic food packaging and furniture that uses flame-retardant chemicals, canned food and beverages, pesticides and some cosmetics.

They also should steer clear of polluted water that may contain lead and more, he suggested.

Endocrine-disrupting chemicals interfere with people's hormone and metabolic systems, the researchers said. Previous studies have shown that exposure to these chemicals can lead to liver injury and non-alcoholic fatty liver disease, but until now the potential effects of prenatal "mixture exposures" to these chemicals have not been studied in humans.

In their study, researchers measured 45 chemicals, including endocrine-disrupting chemicals such as PFAS, organochlorine and organophosphate pesticides, plasticizers (phenols and phthalates), PBDEs and parabens, in the blood or urine of 1,108 pregnant women from 2003 to 2010.

Midya said the term "mixture exposures" means that the scientists looked at all 45 chemicals simultaneously, though they could be broken down to specific ones.

When the offspring of the women participating were 6 to 11 years old, scientists measured the levels of enzymes and cytokeratin-18 that indicate risk for liver disease in the children's blood.

And they found elevated levels of those biomarkers in children who had been more highly exposed to environmental chemicals during pregnancy.


The study participants were enrolled in the Human Early-Life Exposome project, known as HELIX, a collaborative network of six ongoing population-based birth cohort studies in France, Greece, Lithuania, Norway, Spain and Britain.

Midya said there is no comparable data of this size and scope in the United States.

"Most chemicals are like slow poisons, and you have to wait for a long, long time" to gauge potential health effects, he said. "HELIX is attractive because it's already a long-term project, so you can see what's happening slowly, fanning out in front of your eyes."

Researchers acknowledged the study's limitations because they were unable to conduct a liver biopsy, which is considered the gold standard to establish a causal link with non-alcoholic fatty liver disease. That is because of the risk and ethical limitations, given the children's age.

Further research is planned. Midya said the scientists want to collect mothers' data post-pregnancy and children's data over a longer period of time, checking chemical accumulations in the body.

"Not everything gets out of the system easily," he said.

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