HypertensionResearch article
Perfluoroalkyl/Polyfluoroalkyl Substances, Hemostatic/Inflammatory Biomarkers, and Incident Hypertension
- Linear mixed-effects models
- quantile-g-computation
- causal mediation analyses
Authors' conclusion
These findings suggest, but do not establish, that PFAS may be linked to inflammation and impaired fibrinolysis in midlife women.
Study context
- Population
- Midlife women in the Study of Women's Health Across the Nation, 1999 to 2000 to 2015 to 2016
- Participants
- 1,387 women
- Comparison
- Association of 7 perfluoroalkyl/polyfluoroalkyl substances (PFAS) with high-sensitivity C-reactive protein (hs-CRP), fibrinogen, factor VII activity, PAI-1 and tissue plasminogen activator antigen, and mediation of the PFAS-hypertension association
Main finding
As reported in the abstract
hs-CRP per doubling of PFAS
branched perfluorooctane sulfonic acid isomers
3.59% (95% CI: 0.01%-7.30%)
2-(N-methyl-perfluorooctane sulfonamido) acetic acid
5.32% (95% CI: 1.67%-9.10%)
Further findings
PAI-1 per doubling of PFAS
- linear perfluorooctane sulfonic acid isomer
- 2.41% (95% CI: −0.86% to 5.78%)
- 2-(N-methyl-perfluorooctane sulfonamido) acetic acid
- 3.04% (95% CI: 0.24%-5.93%)
- range across individual PFAS
- none remained statistically significant after false discovery rate correction
PFAS mixture effects
- hs-CRP
- 6.15% (95% CI: −0.83% to 13.58%)
- PAI-1
- 6.05% (95% CI: 0.29%-12.14%)
Other markers; mediation of PFAS-hypertension association
- No associations were found with other markers
- biomarkers did not mediate the PFAS-hypertension association
Original publication
Perfluoroalkyl/Polyfluoroalkyl Substances, Hemostatic/Inflammatory Biomarkers, and Incident Hypertension. JACC Adv. Published 28 July 2026. doi:10.1016/j.jacadv.2026.103071
Summarised from the published abstract; every number is checked against it