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Some studies link certain PFAS chemicals with gestational hypertension or changes in blood-pressure patterns during pregnancy, but findings are mixed and do not prove that PFAS causes hypertension in an individual. No validated PFAS-specific profile or blood test can predict who will develop it. The practical step is usual prenatal care, including close blood-pressure monitoring, as the Agency for Toxic Substances and Disease Registry (ATSDR) advises.
What studies have found
Per- and polyfluoroalkyl substances (PFAS) are a large group of chemicals. Studies have examined whether exposure is associated with hypertensive disorders of pregnancy (HDP), including gestational hypertension and preeclampsia. The results are not consistent, and the studies described here are observational: they can identify associations but cannot establish that PFAS caused an outcome.
Project Viva: an association with gestational hypertension
A Project Viva study followed 1,558 pregnant participants recruited from 1999 to 2002. Researchers measured eight PFAS in plasma collected at a median of 9.7 weeks of pregnancy. In this cohort, 7% developed gestational hypertension and 4% developed preeclampsia. For each doubling of PFOA, PFOS, and PFHxS, the study reported higher odds of gestational hypertension, but not higher odds of preeclampsia. Some trimester-specific models also found modest increases in mean diastolic blood pressure associated with doubling of PFOA and PFOS. These are study-level associations, not an estimate of an individual’s chance of developing hypertension. Preston et al., Environmental International, 2022.
The paper cites “up to 10% of pregnancies in the United States” as a background estimate for hypertensive disorders. That is not the rate observed in the Project Viva cohort; its participants had the separate 7% gestational hypertension and 4% preeclampsia figures reported above.
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A separate cohort found no association
An analysis of 513 participants in the Atlanta African American Maternal-Child Cohort, enrolled from 2014 through 2020, measured serum PFAS at 8–14 weeks of pregnancy. It found no association between early-pregnancy PFAS levels and HDP. The authors noted that comparatively low PFAS levels in this population might be relevant to the result. One null study does not rule out associations in other populations or studies. Atlanta cohort study.
Blood-pressure patterns are not the same as a diagnosis
A second Project Viva analysis examined blood-pressure trajectories rather than whether participants developed a hypertensive disorder. PFOS was associated with greater trajectory magnitude and faster systolic trajectory velocity in some models; some measures showed stronger associations among participants with at least one prior live birth. The overall PFAS mixture was not significantly associated with either trajectory magnitude or velocity. These findings do not demonstrate that PFOS causes gestational hypertension or preeclampsia. Project Viva blood-pressure trajectory analysis.
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ATSDR’s summary of the human evidence also describes epidemiological associations between PFOA or PFOS and pregnancy-induced hypertension and preeclampsia, while noting that research continues and human findings can be inconsistent. ATSDR: PFAS and pregnancy.
Who may be at greater risk?
There is no established PFAS-specific risk profile or clinical score that can identify who will develop hypertension during pregnancy. Exposure history can help describe possible exposure, but it cannot predict an individual outcome.
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Exposure context
ATSDR says exposure-related risk depends on factors such as dose, frequency, route, and duration. Individual sensitivity and disease burden, as well as broader determinants such as access to safe water and quality healthcare, may also matter. A suspected or documented source is useful context to discuss with a clinician; it is not proof that PFAS will cause a pregnancy complication. ATSDR clinical overview for PFAS.
Established pregnancy-health factors
The Atlanta cohort paper lists advanced maternal age, obesity, pre-existing diabetes or hypertension, family history of hypertensive disorders, and socioeconomic disadvantage such as lower educational attainment as established HDP risk factors. These are general clinical risk factors; the study does not establish that they increase or decrease the effect of PFAS. Your prenatal clinician can consider your health history and pregnancy circumstances directly. Atlanta cohort study.
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What to do about blood-pressure monitoring
ATSDR’s clinician guidance, updated August 18, 2026, states: “Usual prenatal care, including monitoring a patient’s blood pressure closely, is appropriate.” A possible PFAS exposure alone is not a reason to change prenatal screening without guidance from your clinician. Tell your prenatal care team about a known or plausible exposure and ask what monitoring is appropriate for you. ATSDR clinician guidance.
If your clinician recommends home monitoring, follow their instructions on when to measure, how to record results, and what readings or symptoms should prompt a call. A home monitor measures blood pressure; it does not measure PFAS and does not replace prenatal visits.
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What a PFAS blood test can—and cannot—tell you
ATSDR says a blood test can measure concentrations of certain PFAS at a point in time. It cannot, by itself:
- Identify where or how exposure occurred.
- Represent every PFAS a person may have encountered.
- Establish that an illness was caused by PFAS.
- Predict future health outcomes, including whether someone will develop pregnancy hypertension.
Comparisons between laboratories can also be difficult. When considering testing, ATSDR advises weighing a person’s exposure history, whether water or other exposure routes can be tested, and whether the result could help guide exposure reduction or health promotion. A PFAS blood test is not a screening test for preeclampsia or gestational hypertension. ATSDR clinician guidance.
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