What Is the New PFAS and IBD Study About?

A new analysis published in Clinical Gastroenterology and Hepatology adds evidence that early-life exposure to per- and polyfluoroalkyl substances (PFAS), the so-called "forever chemicals" found in nonstick cookware, water-resistant fabrics, and other consumer products, is associated with childhood intestinal inflammation, a biomarker relevant to inflammatory bowel disease (IBD) risk, including Crohn's disease and ulcerative colitis.¹

The study, led by Vishal Midya, PhD, and colleagues at the Icahn School of Medicine at Mount Sinai, is among the first to link PFAS exposure detected in cord blood and newborn dried blood spots to elevated fecal calprotectin, a widely used clinical marker of gut inflammation, in children as young as age 1.¹

What Birth Cohorts Were Used in the PFAS and IBD Study?

Researchers drew on data from 3 separate birth cohorts: 2 in New York, the MECONIUM and MELODY studies, and 1 in Mexico City, the PROGRESS study, together capturing dried blood spots, cord blood, and maternal serum samples from mother-offspring pairs, including families with and without a maternal history of inflammatory bowel disease.¹

The findings add to a growing body of research examining environmental risk factors for pediatric IBD and add support to existing clinical guidance around reducing household PFAS exposure, such as avoiding nonstick cookware, for people at elevated genetic or familial risk of IBD.²

What Did Researchers Find About PFAS and Fecal Calprotectin?

Using untargeted PFAS analyses and longitudinal fecal calprotectin measurements, a standard biomarker of intestinal inflammation, the researchers found:¹

• Increased PFAS mixture levels in both dried blood spots and cord blood were associated with increased fecal calprotectin between ages 1 and 6.
• Elevated maternal serum PFAS during pregnancy was similarly associated with increased calprotectin in late childhood.
• PFAS were detectable across all 3 sample types, indicating exposure begins before birth.
• Mothers with IBD had increased levels of specific PFAS metabolites than mothers without IBD, and those same metabolites were the strongest contributors to their children's elevated calprotectin.

What Are the Key Statistics Behind the PFAS-Calprotectin Link?

The analysis included 84 dyads from the MECONIUM cohort, 9 from MELODY, and 14 from PROGRESS; dried blood spot and cord blood analyses drew on 84 and 93 mother-offspring dyads, respectively, with 55 dyads overlapping across both sample types. Within that population, the strength of the PFAS-calprotectin association varied by sample type and timing.

For each decile increase in the PFAS mixture, log-transformed fecal calprotectin at age 6 increased by an adjusted β of 0.44 (95% Confidence Interval [CI], 0.18–0.70) in dried blood spot analyses and 0.69 (95% CI, 0.53–0.85) in cord blood analyses. Maternal serum PFAS during pregnancy was associated with a smaller but still significant increase in late-childhood calprotectin (β, 0.19; 95% CI, 0.05–0.33).

The metabolites most associated with maternal IBD status were perfluoro-1-octane sulfonamide acetic acid in dried blood spots and 3-perfluorohexyl-2-hydroxypropyl acrylate in cord blood, the same 2 compounds that were the top contributors to offspring fecal calprotectin.

A Pediatric Gastroenterologist and Enrolled Mother Weighs In

To discuss what these findings mean in practice, HCPLive spoke with Elizabeth A. Spencer, MD, Associate Professor of Pediatrics in the Division of Pediatric Gastroenterology at the Icahn School of Medicine at Mount Sinai and Mount Sinai Kravis Children's Hospital.

Spencer was not an investigator on the study but participated as one of the enrolled mothers in the underlying cohort research and also runs Mount Sinai's IBD prevention clinic, which counsels people with a family history of IBD on modifiable risk factors, including PFAS exposure.

Q&A: "Forever Chemicals" Are in Cord Blood — And Tied to Gut Inflammation in Kids

HCPLive: Can you start by walking us through the background on this study — how it connects to what you already know about IBD risk?

Spencer: This work builds on Inga Peter's paired mother-baby studies, along with a related environmental study well known at Mount Sinai. We know there's a bigger force behind the development of IBD than genetics alone. That comes out of some of my own work looking at high-risk family members — even in a family of 10, where everyone is technically at risk because they have a sibling with IBD, the person most likely to actually develop it is the one who lives right next to the person who already has it. So it can't be genetics alone; there has to be some environmental exposure, or mixture of exposures, involved.

That's the backdrop for Inga Peter's studies, which paired moms and babies — moms with IBD and moms without IBD — and followed them over time, collecting stool samples, cord blood, and placentas at birth, out to age 11 in the oldest children. The goal is to see what we can detect at the earliest stages of life, with the idea that we might eventually be able to intervene through social or policy changes.

The PFAS piece specifically comes out of guidance we already give patients. The nonstick coating on pans has long been linked to ulcerative colitis risk, thought to be tied to PFAS exposure,² but we didn't know exactly how that exposure translates into increased IBD risk. This study tried to tease that out — whether babies are already born with PFAS on board, whether levels change over time, and whether that's tied to markers of intestinal inflammation.

HCPLive: What did the researchers actually find, and how was the study designed?

Spencer: They looked at cord blood — which is meant to be the baby's blood but is usually a bit mixed with the mother's — as well as newborn blood-spot cards, and maternal serum from a cohort of mothers in Mexico. Across all of these, they measured PFAS levels and asked whether PFAS exposure tracked with calprotectin, a marker of intestinal inflammation, as the children grew from birth up to age 11.

The design let them look closely at timing. They confirmed you can detect PFAS in cord blood right at birth, which hadn't really been established before, and that those early PFAS levels were tied to higher calprotectin down the road — same pattern in the blood-spot data.

It's worth noting these early-life cohorts with such long follow-up are hard to find, so having consistent findings across three different birth cohorts — including populations exposed to older "legacy" PFAS in Mexico and to newer-generation PFAS in the U.S. — really strengthened the case. Historically, researchers have often looked at just one or two PFAS compounds, but that's not how people are actually exposed. This study looked at broader PFAS mixtures, which better reflects real-world exposure, and the association held consistently across different populations and different PFAS profiles.

HCPLive: Were you surprised by how consistent the associations were across the 3 cohorts?

Spencer: Not really — that's the outcome we hypothesized going in. But it was still useful to see the internal consistency: cord blood and blood-spot measurements, taken close together in time, showed similar patterns, which makes sense given how close those two are chronologically. The maternal serum findings were also interesting — mothers with IBD had higher PFAS levels, and that was associated with their babies also having higher PFAS. It echoes the sibling pattern I mentioned earlier: the closer your environment is linked to someone else's, the more likely you are to share similar PFAS exposure.

HCPLive: What should clinicians take away from this, and what questions are still open?

Spencer: One important caveat: none of these children — now up to age 11 — have actually been diagnosed with IBD. That's good news, but it also means we can't yet say the elevated calprotectin translates into anything clinically meaningful on its own. A calprotectin level that's modestly higher than a peer's doesn't mean much if neither child has IBD. Whether this predicts eventual disease, and whether there's a meaningful cutoff, is a question for future follow-up.

The other key point is that PFAS shouldn't be thought of as a standalone cause. It's more likely one part of a broader environmental mixture that raises intestinal inflammation and, over time, contributes to IBD risk. This is an association, not a proven causal pathway, and it shouldn't cause parents to panic. In our IBD prevention clinic — where we see people ages 5 to 25 with a relative who has IBD — we do advise removing nonstick pans, and I think that's a meaningful step patients can feel good about. But realistically, individual household changes like that only produce small reductions in PFAS levels. Meaningful reduction would require broader, U.S.-wide regulatory change, which is largely out of an individual parent's hands. I'd want parents to hear that this is a signal we need more research and more policy attention on — not something for them to feel guilty about.

There's also a broader question of whether this could eventually help identify IBD risk in people without a family history, since most people who develop IBD don't have one. If we could use existing newborn blood-spot cards to flag high PFAS exposure and combine that with other markers down the line, that could open the door to earlier risk counseling for a wider population.

HCPLive: Is there anything else you'd like to highlight?

Spencer: There's emerging work on how to actually reduce PFAS levels in the body — plasma donation has gotten some attention, and it's mentioned in this paper. There's also interest in bile acid sequestrants, a class of cholesterol medications that can also firm up stool and appears to help remove PFAS. That's a promising area of ongoing research: figuring out how to actively reduce PFAS exposure, beyond policy change and beyond the small steps people can take at home. Our group is actually looking at bile acid sequestrants specifically, more than plasma donation, as a possible intervention in our IBD prevention clinic to reduce future risk. So there's more research coming out of our group on that front.

Editor’s Note: Spencer reports no relevant disclosures.

References

1. Midya V, Maroli AS, Picker M, et al. Per- and Polyfluoroalkyl Substances in Early Life Are Associated With Childhood Intestinal Inflammation: Analyses of Three Birth Cohorts. Clin Gastroenterol Hepatol. Published online July 10, 2026. doi:10.1016/j.cgh.2026.07.001

2. Agrawal M, Midya V, Maroli A, et al. Per- and Poly-Fluoroalkyl Substances Exposure Is Associated With Later Occurrence of Inflammatory Bowel Disease. Clin Gastroenterol Hepatol. Published online December 26, 2023. doi:10.1016/j.cgh.2023.12.020