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The growing incidence of nonalcoholic fatty liver disease in children is associated with prenatal exposure to several endocrine-disrupting chemicals (EDCs), according to a new study published in JAMA Network Open.

Nonalcoholic fatty liver disease diagnoses are on the rise in children, affecting 6% to 10% of children in general and 34% of obese children.

One of the most common liver diseases worldwide, it can lead to life-threatening conditions, such as cirrhosis (late-stage scarring in the liver) and liver cancer.

“These findings can inform more efficient early-life prevention and intervention strategies to address the current non-alcoholic fatty liver disease epidemic,” the study’s lead author, Vishal Midya, Ph.D., told Science Daily.

Pregnancy is a sensitive window of development for the fetus, and the evidence is mounting from animal and human studies that the programming of cells that leads to nonalcoholic fatty liver disease may begin in utero.

Early life exposures to EDCs can affect liver development and metabolic programming in the fetus through hormone and epigenetic changes, leading to long-term toxic effects on the liver.

These changes can then interact with other established risk factors for fatty liver disease, such as genetic variations, diet and obesity.

This is the first comprehensive study of the link between prenatal exposure to mixtures of EDCs — instead of to individual chemicals — and nonalcoholic fatty liver disease.

This is significant because EDCs are found in a wide variety of products, including pesticides, plasticizers, toxic metals and many other chemicals used in commercial and industrial applications — which means humans are exposed to combinations of them, not just to one chemical at a time.

EDCs are “substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction.”

In other words, EDCs disrupt the normal function of hormones, which can have a significant impact on the health and reproduction of humans and other species.

Examples of EDCs include perfluoroalkyl substances (PFAS), also known as “forever chemicals”), used in nonstick cookware and food packaging, and polybrominated diphenyl ethers (PBDEs), used as flame retardants in infant products and furniture.

The authors of the study set out to answer this: “Is prenatal exposure to EDCs associated with liver injury and hepatocellular apoptosis in school-aged children?” Hepatocellular apoptosis refers to the death of liver cells.

They studied mother-child pairs from the Human Early-Life Exposome project, a collaborative network of six ongoing, population-based prospective birth cohort studies from six European countries: France, Greece, Lithuania, Norway, Spain and the U.K.

The data for the prospective cohort study was collected from April 1, 2003, to Feb. 26, 2016. Data were analyzed from April 1, 2021, to Jan. 31, 2022.

The study included 1,108 mothers who gave birth to a single child and whose average age when giving birth was 31. Mothers who gave birth to multiple children were excluded.

The researchers used blood or urine samples collected in pregnancy or from cord blood collected at birth to determine the mothers’ levels of each chemical group for the 45 EDCs measured.

The EDCs included three organochlorine pesticides, 5 polychlorinated biphenyls (PCBs), 2 PBDEs, three phenols, four parabens, 10 phthalates, four organophosphate pesticides, five PFAS and nine metals.

The children’s liver health was later assessed when children were aged 6 to 11 (on average, children were 8 years old when they were assessed).

The researchers measured the levels of certain enzymes and caspase–generated cytokeratin 18, which is a novel marker of liver cell death and nonalcoholic liver disease in children.

They found elevated levels of these biomarkers in children who had been more highly exposed to EDCs during pregnancy.

Specifically, prenatal exposures to organochlorine pesticides, PBDEs, PFAS and metals were associated with increased liver injury risk in children, and exposure to PBDEs and PCBs were further associated with increased cytokeratin 18 levels.

Organochlorine pesticides and PBDEs are persistent, lipophilic (fat-loving) chemicals that cross the placental barrier and may disrupt fetal metabolic programming.

Phenols, parabens, phthalates and organophosphate pesticides are nonpersistent chemicals that are metabolized and excreted rapidly from the body, within hours or days.

There is previous evidence in rodents that supports a link between perinatal bisphenol A (BPA) and prenatal diethylhexyl phthalate exposure and liver damage.

However, in this study, no associations with liver injury were found for the nonpersistent chemicals examined, with the exception of negative associations observed for phenols and high-molecular-weight phthalates.

The researchers wrote one limitation of the study was potential measurement error in the assessment of nonpersistent chemicals because they used spot urine samples, which could miss nonpersistent chemicals that are excreted from the body so quickly.

Another limitation of the study was that the researchers did not directly measure liver damage in children via a liver biopsy, considered the gold standard to establish a causal link with nonalcoholic fatty liver disease, because of the risk and ethical limitations due to the children’s age. Therefore they used biomarkers instead.

How to reduce your personal exposure to EDCs

“We are all daily exposed to these chemicals through the food we eat, the water we drink, and the use of consumer products,” Damaskini Valvi, M.D., Ph.D., one of the study’s authors, told Science Daily. “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,” Valvi said.

This study adds to considerable evidence that pregnant women need to avoid exposure to EDCs — but how?

The 10 common ways we are exposed to EDCs include: personal care products; drinking water; canned and packaged foods; conventionally grown produce and concentrated animal feeding operations; meat, poultry and dairy products; high-mercury fish; plastic and nonstick kitchenware; cleaning products; household dust; office products; and cash register receipts.

A few tips to help reduce exposure to EDCs include: eating organic food and low-mercury seafood; using glass, ceramic or cast iron cookware; using plastic-free food storage containers; avoiding products that contain flame retardants; and making or buying non-toxic personal care and cleaning products.

For more in-depth information on avoiding EDCs, Environmental Working Group lists the “Dirty Dozen” EDCs and how to avoid them. Dr. Joseph Mercola wrote about the 10 common ways we are exposed and how to avoid them.

Holding industry accountable

In the short term, the above tips can help people reduce their exposure to EDCs. Longer-term, though, the companies that profit from EDCs need to be held accountable, and must stop generating and releasing these chemicals into our environment, according to the advocacy group Beyond Pesticides.

The overarching message from a series published in The Lancet in July 2020 is that “the growing body of evidence implicating EDCs as human health hazards supports urgent action to reduce exposure to EDCs and this can be best achieved through regulation.”

In December 2021, the European Food Safety Authority proposed reducing the tolerable daily intake of BPA by a factor of 100,000. This huge reduction “could lead to a de facto ban on the cheap and durable material in food-related uses, such as lining metal cans,” reported Science.

It could also mark a shift in how European regulators use research findings to set exposure limits.

Traditionally, exposure limits have been shaped by large studies that link a chemical directly to an increased risk of disease. According to Science, “In this case, however, risk assessors put greater weight on smaller studies showing low levels of BPA can cause subtle changes that could lead to future health problems. This approach, if adopted widely, could justify much lower exposure limits for other chemicals.”

In the U.S., a number of groups last year petitioned the U.S. Food and Drug Administration to consider new limits on BPA.

On June 2, Greenwire reported the FDA agreed to reconsider BPA limits, and will come to a final decision on its safety by Oct. 31.