I spent years filing the forever-chemicals story under problems we noticed and fixed. PFOA got phased out of the Teflon line. PFOS left the Scotchgard formula. Case closed, or so I told myself. Then a Canadian team went looking for the compounds that replaced them, plus the precursor chemicals almost nobody measures, and turned up a dozen-plus of them already sitting in women’s blood, right beside the “banned” ones that never actually left. I have not been able to file the story back.
The setup is close to a shell game. PFAS biomonitoring, as the new CARTaGENE cohort analysis of premenopausal women puts it, “has typically focused on legacy PFAS,” while data on the newer alternative and precursor compounds stay “scarce,” even though they are “critical for assessing exposure and human health risk.” Translated: we have been diligently counting the chemicals we already agreed are bad, and mostly not looking for the ones industry swapped in to replace them. Pull the finished acid off the market, leave its precursors unmeasured, and the exposure never shows up on the ledger.
When you do look, the retired chemicals are everywhere. In a companion analysis from the same Canadian biomonitoring effort, the MIREC-ENDO study of adult women, PFOS showed up in 100 percent of samples. PFOA in nearly 98 percent. PFHxS, another legacy compound, in 100 percent of the women. These are the chemicals we supposedly retired, sitting in essentially everyone, a decade after the phase-outs.
The legacy acids I expected. What I did not expect were the precursors riding along beside them. A compound called PFOSA turned up in 99 percent of the women. N-EtFOSE in almost all of them. Short-chain acids like PFPeA in nearly 80 percent and PFBA in 72 percent. All told, 17 of the 40 PFAS the study screened were detectable in more than half the women.
So why measure a precursor at all, a molecule that is not itself one of the notorious acids? Because a precursor is a legacy PFAS waiting to happen. Your liver does not leave these compounds alone. Its enzymes work N-EtFOSE down into PFOSA, and PFOSA down into PFOS and PFOA, the exact terminal chemicals everyone agreed to stop making. That stopped me for a second: a body carrying precursors is quietly manufacturing the banned stuff from the inside. Count only the finished acids and you undercount the real load, because some of it is still upstream, mid-conversion.
And the flashy “safer” replacements industry likes to name by brand? They register, but far less. GenX turned up in about 47 percent of the women, while ADONA and the F-53B family sat near 16 percent. Lower, yes. But “lower” here mostly means newer. These compounds are recent enough that they have not had decades to accumulate, which is a different thing from safe.
There is a wrinkle here that sounds like good news and is not. Premenopausal women carry lower PFAS than men their age, for a blunt mechanical reason: their bodies have exits men mostly lack. Every period sheds a little. Every pregnancy sends a share across the placenta. Every month of breastfeeding pumps more out in milk. In the MIREC-ENDO women, those with three or more children carried roughly half the PFOA and PFHxS of women with one, and the longest breastfeeders showed the same 2-fold drop. Their bodies genuinely cleared it. I just wish clearing it landed somewhere other than a fetus and an infant, because a 2023 JNCI analysis tied higher maternal PFAS to childhood acute lymphoblastic leukemia, and the exit route and the delivery route are the same pipe.
What all of this does to long-term health is genuinely unsettled, and I will not pretend the arrows point one way. A Multiethnic Cohort study linked serum PFAS to renal cell carcinoma. A conference abstract flagged a possible ovarian-cancer signal. A prediagnostic study of endometrial cancer found no convincing link at all. Lab toxicology in zebrafish suggests some of the alternative compounds are not the clean substitutes they were sold as. Mixed evidence on a chemical class that is in 100 percent of women is not the same as reassurance. It is a class we keep finding in everyone, with a scattered but documented trail of harm, and a replacement generation we have barely started to measure.
This is where the accountability sits. Regulators and manufacturers point to the phase-outs as a job finished. The blood says otherwise: the banned compounds persist at full detection, the precursors that regenerate them are nearly universal, and the branded “alternatives” are mostly just too new to have piled up yet. We are running the same experiment a second time and calling it a solution. It took government biomonitoring, Health Canada funded, to even ask the question, because measuring the replacements is precisely the work industry has no incentive to do. Nobody was systematically checking women’s blood for these compounds until studies like this one forced it.
I am not going to wait for the guideline that reclassifies this year’s “safer” fluorochemical as next decade’s lawsuit. In my own kitchen the nonstick pans are already gone, and I filter my water for PFAS specifically. If I were pregnant or nursing, I would treat lowering my exposure as something to do now, not after the registry catches up. The chemistry outran the regulators once. I would rather not be the data point that proves it did it again.
Sources
- Environmental Health – CARTaGENE cohort: legacy, alternative, and precursor PFAS in premenopausal women (2026)
- Environmental Health – MIREC-ENDO: legacy, alternative, and precursor PFAS in adult Canadian women (2024)
- JNCI – Maternal serum PFAS and childhood acute lymphoblastic leukemia (2023)
- Environment International – Serum PFAS and renal cell carcinoma, Multiethnic Cohort (2023)
- ISEE Conference Abstracts – Serum PFAS and ovarian cancer risk, conference abstract (2024)
- Environmental Health Perspectives – Prediagnostic serum PFAS and endometrial cancer, US cohort (2025)
- Environmental Pollution – Immunotoxicity of legacy and alternative PFAS in zebrafish larvae (2024)