Hormone-disrupting chemical mixtures linked to excess childhood weight 

Early-life exposure to PFAS, pesticides and other chemicals may increase obesity risk into adolescence

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Key findings

  • Multiple hormone-disrupting chemicals were linked to obesity from childhood through adolescence.
  • Prenatal exposure to metals, organochlorine pesticides, and PFAS was linked to higher obesity.
  • Childhood exposure to phenols and certain phthalates was linked to more body fat in adolescence.

Children exposed during pregnancy and early life to combinations of chemicals that disrupt hormones and metabolism may face a greater risk of excess weight that persists into adolescence, a new study suggests.

Published this month [September 2026] in Environment International, the study followed 1,301 mother-child pairs from six European birth cohorts. Researchers measured prenatal and childhood exposure to 45 endocrine-disrupting chemicals (EDCs) across nine chemical classes. These included per- and polyfluoroalkyl substances (PFAS), phthalates, pesticides, polychlorinated biphenyls (PCBs), flame retardants, metals, parabens, and phenols, including bisphenol A (BPA) and triclosan.

Researchers found that greater exposure to certain combinations of EDCs was associated with higher BMI. They also found links to more body fat and higher odds of overweight. About 28% of the children had overweight or obesity at age 8, rising to about 30% by age 15.

The findings add to growing evidence linking chemical exposures during critical stages of development to obesity risk. Obesity in children is defined as having a body mass index (BMI), an estimate of total body fat, at or above the 95th percentile for age and sex.

Unlike most earlier studies, which examined chemicals one at a time, this research assessed mixtures that more closely reflect real life. People typically encounter many chemicals at once through food, drinking water, plastics, and personal care products.

Prenatal exposure to metals, synthetic, chlorine-containing pesticides, and PFAS was linked to higher obesity rates, while childhood phenols and some phthalates were associated with more adolescent excessive body fat (adiposity). PFAS — also known as “forever chemicals” — are highly persistent chemicals used in nonstick cookware, food packaging, stain-resistant fabrics, and firefighting foams, among other common items.

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Which chemical exposures were linked to higher BMI and body fat?

Researchers found:

  • Children with higher prenatal organochlorine pesticide exposure had higher BMI and 48% higher odds of overweight in childhood and 45% higher odds in adolescence. Researchers saw the link in boys but not girls. Hexachlorobenzene (HCB), a persistent chemical once widely used as a fungicide, contributed most strongly to the association. 
  • Children with higher prenatal PFAS exposure had more body fat in childhood and adolescence.
  • Children with higher prenatal metal exposure had higher BMI and 47% higher odds of overweight in childhood. Those with higher childhood metal exposure had 72% higher odds of overweight in adolescence and more body fat.
  • Children with greater exposure to phenols and certain phthalates used in polyvinyl chloride (PVC), a plastic used in pipes, flooring, and packaging, had higher adolescent BMI. Those with more exposure to organochlorine pesticides, PCBs and parabens had lower BMI.
  • Higher prenatal PCB exposure was linked to 20% lower odds of overweight in childhood and 33% lower odds in adolescence, though researchers said reverse causation may partly explain the pattern. Body fat can reduce the amount of these chemicals circulating in the blood. PCBs are long-lasting industrial chemicals once used in electrical equipment and other products.
  • Children with relatively high prenatal exposure to cadmium and manganese had the largest increases in BMI by adolescence, suggesting chemicals may also act together.

“These findings have important public health implications, as they underscore the need to prevent exposure to harmful chemical mixtures—particularly during pregnancy and early childhood—as a way to curb the growing obesity epidemic,” the researchers wrote.

Joseph Braun, professor of epidemiology at Brown University’s School of Public Health, called the results “significant.”

 “[They] show that prenatal exposure to EDCs may have effects that extend to late adolescence, a time when body fatness stabilizes,” he said. “More importantly, this study accounted for the potential impact of mixtures of EDCs, rather than just one chemical at a time. Given that we live in this ‘chemical soup,’ it is important to understand the total effect of these EDCs.”

Why early-life exposure to endocrine-disrupting chemicals matters

Early life is a critical period for tissue and organ development, making babies and children especially vulnerable. Organochlorine pesticides, for instance, may increase body fat by disrupting hormones. They may also promote fat storage, interfere with metabolism, and trigger inflammation in fat tissue.

More than one-third of U.S. children and adolescents ages 2 to 19 have overweight or obesity, according to the latest federal data. In 37 European countries, more than one in four children ages 7 to 9 have overweight or obesity, WHO data shows.

Children with obesity face an increased risk of chronic diseases in adulthood, including type 2 diabetes, cardiovascular disease, and cancer.

Meanwhile, exposure to EDCs is widespread. Some EDCs, including pesticides, PCBs, and PFAS, persist and accumulate in body tissues. Others, including phenols and phthalates, break down quickly in the body but repeated exposure leads to more risk.

How did researchers measure chemical exposures and obesity risk?

Researchers used data from the European Human Early Life Exposure (HELIX) project, which includes birth cohorts in the U.K., France, Spain, Lithuania, Norway and Greece.

They measured prenatal chemical exposure using maternal blood or urine during pregnancy or cord blood at birth. They used blood or urine to measure childhood exposure. At follow-ups between ages 6 and 18, trained staff measured height, weight, waist circumference and body fat.

They also accounted for factors that could affect both chemical exposure and weight, including maternal age and BMI, smoking during pregnancy, fish consumption, and childhood exposure to tobacco smoke.

Researchers measured 36 blood proteins to look for biological pathways linking prenatal chemical exposure to adolescent BMI.

They found that inflammatory and metabolic proteins accounted for about 30% of the link between prenatal metal exposure and higher adolescent BMI, they found. These may affect insulin signaling, which helps control blood sugar, energy balance, and fat storage.

“Early-life exposure to EDC mixtures may reprogram metabolic and inflammatory pathways, predisposing children to obesity that persists into adolescence,” the researchers wrote.

While the analysis does not prove that inflammation caused the later weight changes, the finding aligns with earlier HELIX and other research. The study suggests immune changes may also play a much smaller role.

Protecting children’s health from endocrine disruptor harms 

Some study participants dropped out before later follow-ups, reducing the available data. Of the original group, 607 had complete adolescent body measurements. Statistical adjustments for those losses did not substantially change the results.

Some chemicals were not detected in many samples, and the researchers had particular difficulty measuring short-lived chemicals. A single urine measurement may not reflect a child’s usual exposure, they noted. Measurements also could not identify whether exposure occurred through food, air or skin contact.

Future research should include larger, more diverse populations and better measurement of short-lived chemicals, the researchers noted. It should also include other types of biological data to better understand how chemical exposures might contribute to obesity.

“Strengthening chemical regulation and promoting safer alternatives in consumer products and food packaging may represent actionable strategies to mitigate early-life environmental contributors to obesity and related chronic diseases,” they wrote.

Reference

Güil-Oumrait N, Midya V, India-Aldana S, et al. Prenatal and childhood exposure to mixtures of endocrine-disrupting chemicals in association with measures of adiposity in childhood and adolescence. Environ Int. 2026;215:110495. doi:10.1016/j.envint.2026.110495