Prenatal exposure to several types of per- and polyfluoroalkyl substances was associated with blood pressure changes in children from early childhood into adolescence, according to a longitudinal study.
The study followed 1,094 racially and ethnically diverse mother–child pairs in the Boston Birth Cohort from birth to age 18 years. Researchers found that certain per- and polyfluoroalkyl substances (PFAS) compounds—particularly PFDeA, PFNA, and PFUnA—were associated with increased systolic blood pressure (SBP) percentiles, especially during adolescence. In contrast, other compounds such as Me-PFOSA-AcOH, PFHpS, PFOA, and PFOS were inversely associated with diastolic blood pressure (DBP) percentiles, particularly in early childhood.
Blood Pressure Trajectories and Life Stage Sensitivity
Children’s blood pressure was assessed during routine healthcare visits from ages 3 to 18, generating over 13,000 measurements. Notably, the effect of PFAS on blood pressure varied by developmental stage. DBP-lowering associations were strongest between ages 3 and 5 and generally attenuated or reversed in adolescence. For example, each doubling of Me-PFOSA-AcOH was associated with a 1.14 percentile decrease in DBP in early childhood, decreasing to 0.38 by adolescence.
Systolic BP effects became more pronounced in adolescence. For instance, PFDeA exposure was not significantly associated with SBP percentile at ages 3 to 5 but was linked to a 2.55-point increase in SBP percentile by ages 13 to 18. This delayed emergence suggests latent hypertensive effects of some PFAS that may not manifest until later stages of development.
PFAS Mixture Effects
In addition to analyzing individual compounds, the study used a PFAS mixture burden score. This score reflected cumulative exposure to all PFAS and revealed stronger associations with DBP in early childhood and with SBP and elevated BP in adolescence. For example, a higher mixture burden was associated with a 1.70-point decline in DBP percentile at ages 3 to 5, but a 2.43-point increase by ages 13 to 18. This reversal supports the theory that the combined toxicological burden of PFAS may have opposing short- and long-term effects.
Blood Pressure Divergence by Exposure Level
BP trajectory modeling showed a significant divergence in DBP trajectories by PFHpS tertile beginning at age 13, particularly among male children. Those in the highest tertile had lower DBP early on, but steeper increases during adolescence, consistent with dose-dependent divergence of BP trends.
Biological Mechanisms
The study proposed several mechanisms for these effects, including:
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Oxidative stress and mitochondrial dysfunction triggered by PFAS-induced disruptions in placental and fetal lipid metabolism;
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Reduced nephron endowment and altered renin-angiotensin signaling;
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Endocrine disruption, affecting sex and thyroid hormones;
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Epigenetic modifications, particularly in boys.
Sex and Race/Ethnicity Differences
Associations between PFAS and elevated BP were stronger in male children. For example, each doubling of PFDeA was linked to a 1.51-point increase in SBP percentile in boys, but no significant change in girls. Additionally, PFHpS exposure in boys was associated with a 9% to 17% increased risk of elevated BP during school-age years and adolescence.
Racial subgroup analysis revealed that non-Hispanic Black children experienced stronger effects, with each doubling of PFDeA, PFHpS, and PFUnA linked to 6% to 8% increased risk of elevated BP. The authors suggested that socioeconomic, environmental, and structural factors might underlie this disparity.
Conclusion
The study identified associations between prenatal PFAS exposures and later blood pressure outcomes in children, with stronger associations observed during adolescence, in male children, and in non-Hispanic Black children. These findings suggest that prenatal PFAS exposures may have latent, sex-specific, and race-specific effects on blood pressure during critical developmental periods.
