Table 1.
Clinical and epidemiological studies exploring the rule of PFAS in cardiovascular disease and cardiovascular risk factors.
| Author, year and reference | Study Design | Population | n. of subjects | PFAS plasma concentration (ng/mL) | Observation period | Main results |
|---|---|---|---|---|---|---|
| Shankar et al., 2012 (16) | Cohort | US adults ≥ 40 years old from “National Health and Nutrition Examination Survey” (NHANES) | 1216 | Values in the 4th quartile PFOA: ≥ 5.6 for women and ≥ 6.1 for men |
4 years | Higher PFOA levels positively associated with cardiovascular disease and peripheral arterial disease |
| Huang et al., 2018 (2) | Cohort longitudinal | US participants from the NHANES 1999–2014 | 10859 | range in quartile (Qn) Q1:<12.11, Q2: 12.11–20.61, Q3: 20.61–33.6, Q4: > 33.63. Analysed compounds: PFOA, PFOS, PFHxS, EPAH, MPAH, PFDA, PFBS, PFHP, PFNA, PFSA, PFUA, and PFDO |
approximately 15 years | Total PFAS were positively associated with cardiovascular disease. Serum levels of MPAH and PFDO were positively associated with congestive heart failure; PFNA, PFDA, and PFUA were positively associated with coronary heart disease; PFUA and PFDO were positively associated with angina pectoris; and PFNA was positively associated with heart attack. |
| Mastrantonio et al., 2018 (17) | Ecological mortality study | Populations from Veneto municipalities with PFAS contaminated and uncontaminated drinking water | 41841 deaths | PFOS: ≥30, PFOA: ≥ 500, PFUnA: ≥ 500 | 33 years | Higher mortality levels for some causes of death (diabetes, cerebrovascular diseases, myocardial infarction Alzheimer’s disease Parkinson’s diseases) associated with PFAS exposure. |
| Simpson et al., 2013 (10) | Cohort longitudinal | Participants from —the community-based 2005–2006 C8 Health Project (11) and the cohort of workers in polymer production plant (DuPont Washington Works) (18) | 32254 | Mean – SD - median PFOA:
non worker: 70.9 -151.2 - 24.2, workers 324.6 - 920.6 - 112.7, combined cohort: 86.6 - 278.9 - 26.1 |
Over 50 years | Modest evidence of an association between PFOA and stroke incidence. |
| Hutcheson et al., 2020 (19) | Cohort | US adults ≧̸20 years old from “The C8 Health Project” (11) | 3921 with diabetes 44,285 without diabetes |
Median (IQR), natural logarithm PFHxS: D 2.8 (1.8-4.3), ND 3.0 (1.9-4.8), PFOA: D 28.7(12.9-73.6), ND 27.6 (13.4-70.4), PFOS: D 21.4(13.8-31.9), ND 20.1(13.5-29.0) PFNA: D 1.3(1.0-1.8), ND 1.4(1.0-1.08) |
Approximately 20 years | Serum levels of PFHs and PFOS were inversely associated with stroke in adult with diabetes. PFAS compounds do not increase risk of stroke among persons with or without diabetes. |
| Lind et al., 2018 (20) | Cohort | Adults ≧̸70 years old from the “Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study”. | 602 | Median and interquartile range PFHpA:0.05 (0.03-0.09), PFHxS: 2.08 (1.6-3.42), PFOS: 13.23 (9.95-17.77), PFOA: 3.3 (2.52-4.39), PFNA: 0.70 (0.52-0.97), PFDA: 0.31 (0.24-0.40), PFOSA: 0.11 (0.07-0.17), PFUnDA: 0.28 (0.22-0.37) |
Follow-up 10-year | PFASs were related to the increase in carotid intima-media thickness. PFNA, PFDA, and PFUA, were all related to intima-media thickness in women, while the relationship was negative in men. The plasma concentration of PFUA was significantly related to carotid plaque in women, but not in men. |
| Lin et al., 2013 (21) | Cohort | Subject 12–30 years old from the “Young Taiwanese Cohort Study” | 664 | Median (range) PFOA:3.49 (0.75–52.2), PFOS: 8.65 (0.11–85.90), PFNA: 0.38 (0.38–25.4), PFUA: 6.59 (1.50–105.7) |
Approximately 8 years | Higher serum concentrations of PFOS were associated with an increase of carotid intima–media thickness. |
| Mobacke et al., 2018 (22) | Cohort | Subjects ≧̸70 years old from the PIVUS study | 801 | Mean ± SD PFHpA: 0.7 ± 0.7, PFHxS: 3.41 ± 3.64, PFOS: 14.9 ± 8.88, PFOA: 3.59 ± 1.69, PFNA: 0.8 ± 0.43, PFDA: 0.34 ± 0.15, PFOSA: 0.14 ± 0.14, PFUnDA: 0.31 ± 0.14. |
Follow-up 10-years | PFASs were not significantly related to left ventricular mass. PFNA, PFDA and PFUnDA were related to relative wall thickness in a negative fashion. PFNA was also positively related to left ventricular end-diastolic volume. |
| Mattsson et al., 2015 (23) | Cohort longitudinal | Male Sweden farmers, born during the period 1930–1949 | 253 with and 253 without a cardio vascular disease | Medians (interquartile range) in person with (CHD) and without cardio vascular disease (non CHD) PFOS: CHD 22.8 (10.0), non CHD 22.0 (10.1), PFOA: CHD 4.2 (1.8), non CHD 4.0 (2.0), PFNA: CHD 0.5 (0.3), non CHD 0.5 (0.4), PFDA: 0.2 (0.1), non CHD 0.2 (0.1), PFHpA: CHD 0.06 (0.05), non CHD 0.04 (0.04), PFHxS: CHD1.6 (0.7), non CHD 1.6 (0.7), PFUnDA: CHD 0.2 (0.1), non CHD 0.2 (0.1), PFDoDA: CHD 0.02 (0.02), non CHD 0.02 (0.02) |
Approximately 14 years | No statistically significant associations between PFASs levels and risk for developing coronary heart disease. A significant association between higher Levels of PFHpA and coronary heart disease. |
EPAH, 2-(N-ethyl-perfluorooctane sulfona- mido) acetate; MPAH, 2-(N-methyl-perfluorooctane sulfonamido) acetate; PFAS, Polyfluoro- and perfluoro–alkyl substances; PFBA, perfluorobutyric acid; PFBS, perfluorobutane sulfonate; PFDA, perfluorodecanoic acid; PFDO, perfluorododecanoic acid; PFHP/PFHpA, perfluoroheptanoic acid; PFHS, perfluorohexane sulfonate; PFHxA, perfluorohexanoic acid; PFHxS, perfluorohexane sulfonic acid; PFNA, perfluorononanoic acid; PFOA, perfluorooctanoic acid; PFOS, perfluorooctane sulfonic acid; PFPeA, perfluoropentanoic acid; PFSA, perfluorooctane sulfonamide; PFUnA/PFUA/PFUnDA, perfluoroundecanoic acid.