Exposure to per- and polyfluoroalkyl substances (PFAS) ― a class of widely used synthetic chemicals dubbed "forever chemicals" ― may be a modifiable risk factor for the development of hypertension. PFAS are not only forever chemicals, they are everywhere chemicals as well. Possible sources of PFAS exposure run the gamut from nonstick cookware, food wrappers, and waterproof fabrics to cosmetics and drinking water. They have been detected in the blood of most people and have been linked to a variety of health concerns. On June 13, 2022 a new study examining the association between serum concentrations of PFAS and risks of developing hypertension was published online in Hypertension.
This study included 1058 midlife women initially free of hypertension from the multiracial and multiethnic SWAN (Study of Women’s Health Across the Nation) with annual follow-up visits between 1999 and 2017. During 11,722 person-years of follow-up, 470 of the women developed hypertension, at a rate of 40.1 cases per 1000 person-years. Hypertension was defined as blood pressure ≥140 mm Hg systolic or ≥90 mm Hg diastolic, or receiving antihypertensive treatment.
Women in the highest tertile of baseline serum concentration of perfluorooctane sulfonate (PFOS) had a 42% higher risk of developing hypertension compared to peers in the lowest tertile (adjusted hazard ratio [aHR], 1.42; 95% CI, 1.19 – 1.68; P trend = .01). Similar results were found for perfluorooctanoate (PFOA) and 2-N-ethyl-perfluorooctane sulfonamido acetate (EtFOSAA), with 47% (aHR, 1.47; 95% CI, 1.24 – 1.75; P trend = .01) and 42% (aHR, 1.42; 95% CI, 1.19 – 1.70; P trend = .01) higher risks of incident hypertension, comparing the highest to the lowest tertiles. The risks persisted after adjusting for various factors, including race, study site, education, financial strain, smoking status, alcohol use, total calorie intake, and menopausal status. In the PFAS "mixture" analysis, women in the highest tertile of overall PFAS concentrations were 71% more likely to develop hypertension during follow-up compared with women in the lowest tertile (aHR, 1.71; 95% CI, 1.15 – 2.54; P trend = .008).
These findings suggest that PFAS might be an underappreciated contributing factor to women’s cardiovascular disease risk. However, it is still to be determined whether PFAS are the causative agent or if there is an unmeasured/unadjusted for entity which has resulted in both increased PFAS exposure and hypertension as well as if PFAS are causative, if reduction in PFAS exposure would be result in blood pressure reduction