Forever Chemicals in Children May Cast a Health Shadow Lasting Decades

A sweeping review published in Pediatric Research argues that the pediatric consequences of exposure to per- and polyfluoroalkyl substances, the synthetic compounds widely known as forever chemicals, may extend far beyond childhood and shape disease risk for an entire lifetime. The review, authored by environmental health researcher Philippe Grandjean of the University of Southern Denmark and the University of Rhode Island, synthesizes decades of epidemiological and toxicological evidence on a class of industrial chemicals that has been in commercial use for roughly 75 years. Its central message is sobering: because these compounds persist in the human body for years and are transferred from mother to child both before birth and through breastfeeding, the earliest stages of human development are precisely when exposure peaks, and precisely when developing organs are most vulnerable to lasting damage.

The chemistry behind the concern is deceptively simple. PFAS molecules are built on a carbon backbone in which hydrogen atoms have been replaced by fluorine, and the carbon-fluorine bond is one of the strongest in chemistry. That bond confers extraordinary thermal, chemical, and biological inertness, which is exactly what made PFAS so attractive to industry: they repel oil, water, and grease, making them ideal for surface protectants, food packaging coatings, and aqueous film-forming firefighting foams. But the same indestructibility means the compounds do not break down in the environment or in the body. The two most historically prominent members of the family, perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), were largely phased out after health concerns emerged in the early 2000s, yet their legacy persists in blood, food, and drinking water worldwide.

How long these chemicals actually linger in the human body has been quantified through serial blood analyses of retired 3M production workers. Those measurements yield biological half-lives of roughly three years for PFOA, about five years for PFOS, and nearly nine years for perfluorohexane sulfonic acid (PFHxS), with perfluorononanoic acid (PFNA) at slightly under two and a half years. Because exposure is rarely eliminated completely, apparent half-lives stretch even longer as the body continues to accumulate new doses. For a newborn, the arithmetic is far worse than for an adult. PFAS cross the placenta efficiently, so a pregnant woman shares her accumulated body burden with her fetus, and the compounds are then excreted in human milk, meaning an infant’s serum concentrations can greatly exceed the mother’s.

The review catalogs a strikingly broad range of adverse outcomes linked to prenatal and early-life exposure. The most extensively documented are preterm birth, low birth weight, and delayed fetal growth, findings echoed by multiple agency assessments. A recent ecological study from a PFAS-contaminated region of Italy found that women who gave birth there faced at least a 50 percent higher risk of preeclampsia and gestational diabetes, along with increased numbers of infants born small for gestational age. In later childhood, elevated prenatal exposure has been associated with increased body weight and body mass index, a connection reinforced by recent meta-analyses. Evidence also suggests possible links to congenital heart defects, supported by experimental demonstrations that PFOS disrupts heart development in mouse models, and to altered sex hormone concentrations in both boys and girls during and after puberty, including earlier peripheral puberty development in girls below nine years of age.

Endocrine disruption emerges as a unifying mechanism across many of these outcomes. The thyroid gland appears to be a particular target, with associations between elevated PFOA and PFOS exposure and thyroid disruption recognized since the court-mandated C8 investigations, and confirmed even at background exposure levels. Recent studies focused on pregnant women and newborns suggest thyroid toxicity may begin prenatally and remain detectable into adolescence. The stakes are high because thyroxine delivery is tightly coupled to early neurological development; even a marginal reduction in maternal thyroid hormone output is a concern, given that fetal brain development is exquisitely vulnerable to such deficiencies. PFAS have been detected in human cerebrospinal fluid and at low concentrations in brain tissue, and studies point to possible cognitive deficits, hyperactivity, and internalizing behaviors, although results on autism and ADHD remain variable across study designs.

Perhaps the most consequential findings concern the immune system. The National Toxicology Program classified both PFOS and PFOA as presumed human immunotoxicants in 2016, and subsequent evidence implicates PFHxS and PFNA as well. The critical data come from prospective studies of vaccinated children: in a landmark cohort of 587 seven-year-olds, a doubling of serum PFOS and PFOA concentrations was associated with an overall decrease of 50 percent or more in vaccine-specific antibody concentrations, meaning some children failed to reach clinically protective levels even after three or four vaccinations. Norwegian children with elevated PFOA, PFNA, and PFHxS showed significantly increased frequencies of common colds and gastroenteritis, and elevated prenatal exposure has been linked to increased hospitalizations for pneumonia in young children. Because the immune system also surveils and eliminates cancer cells, immunotoxicity may feed into carcinogenesis, and PFAS carry several additional key characteristics of carcinogens.

On cancer, the regulatory picture has hardened considerably. The International Agency for Research on Cancer classified PFOA as a possible human carcinogen in 2016 but upgraded it to Group 1, a known human carcinogen, in 2023, while placing PFOS in Group 2B. The U.S. Environmental Protection Agency now considers both PFOA and PFOS carcinogenic to humans. Substantial evidence links PFOA to kidney and testicular cancer, and associations have been reported for prostate, bladder, and breast cancer, with a large National Cancer Institute study finding clear associations specifically for hormone receptor-positive breast tumors. A recent study also suggested that prenatal PFOS and PFOA exposure might increase the risk of retinoblastoma in children, and PFAS exposure has been tied to increased numbers of metastatic lymph nodes in colorectal cancer patients.

Woven through the review is an indictment of industrial secrecy that delayed this scientific reckoning by half a century. 3M researchers documented the presence of PFOS and PFOA in fish as early as the 1970s, and internal documents show company scientists were aware of PFOA health risks as early as the 1960s. A 1978 monkey study demonstrated lethal toxicity and immune system lesions at high doses, yet no follow-up studies were reported. A 1993 internal document acknowledged preliminary evidence that PFOS transfers into the milk of lactating goats and was likely to do so in lactating human females, but the results were not published. DuPont and 3M recorded PFAS in the blood of pregnant workers and newborns by 1980, and unusual malformations were observed at childbirths among exposed female workers, yet women were returned to PFOA-exposed work areas the following year. A published worker study by 3M authors omitted extensive draft results without p values, and the review’s author has characterized the discrepancy as possible scientific dishonesty; the article remains unretracted and has been cited more than 300 times.

Regulatory responses have lagged but are now accelerating dramatically. The EPA’s drinking water advisory for PFOA and PFOS fell from 400 parts per trillion in 2009 to 70 ppt in 2016, and interim advisories issued in June 2022, based on childhood immunotoxicity, imply chronic reference doses corresponding to just 0.004 ppt for PFOA and 0.02 ppt for PFOS, with enforceable limits proposed at 4 ppt and maximum contaminant level goals of zero. Over less than two decades, recommended exposure limits have dropped by more than a thousandfold, a strengthening the review describes as highly unusual. The European Union has announced a proposal to eliminate PFAS uses by 2030, describing the compounds as persisting in the environment longer than any other man-made substance.

The review closes with a forward-looking warning grounded in emerging biology. Experimental studies demonstrate that PFAS exposure can induce epigenetic changes inherited by future, unexposed generations, and although such transgenerational effects have not yet been confirmed for PFAS in humans, a recent study suggests polychlorinated biphenyls, another class of persistent organic pollutants considered obesogens like PFAS, may cause epigenetically mediated obesity across generations. Because most human evidence on PFAS is recent, the full toxicological picture, particularly for delayed outcomes of developmental exposure, remains incomplete, and today’s evidence may well underestimate the true extent of toxicity. The National Academies recommends clinical testing and follow-up for people with likely elevated exposure, a need that has largely gone unmet due to cost. Meanwhile, essentially everyone carries a PFAS body burden that will persist for years, and children will continue to be exposed at the most vulnerable moments of their lives. The review’s author argues that prudent public health decisions must be made now, despite incomplete evidence, because waiting for certainty is precisely the mistake that allowed seventy-five years of hidden harm.

Subject of Research: Pediatric and long-term health effects of prenatal and early-life exposure to persistent PFAS chemicals

Article Title: Pediatric effects of forever chemicals may last for a long time

Article References: Grandjean, P. (2026). Pediatric effects of forever chemicals may last for a long time. Pediatric Research. https://doi.org/10.1038/s41390-026-05366-w

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05366-w

Keywords: PFAS, forever chemicals, pediatric health, prenatal exposure, immunotoxicity, endocrine disruption, breastfeeding, PFOA, PFOS, cancer risk, industrial secrecy, environmental regulation