Is drinking water with low PFAS a significant source of human exposure? Evidence summary

Low-level contamination of drinking water with per- and polyfluoroalkyl substances (PFAS) is widespread, yet the extent to which such concentrations contribute to human PFAS body burdens remains incompletely characterized.

To synthesise evidence on the contribution of low-level PFAS in drinking water (defined as <100 ng/L for any individual PFAS) to PFAS concentrations in human blood.

We systematically searched Embase, MEDLINE, and Scopus using predefined logic grids. Inclusion criteria were original human studies reporting both drinking water PFAS and blood/serum/plasma PFAS concentrations with a focus on low-level water exposures. Ten studies (n = 4576 participants; 4590 blood samples; 1297 water samples) met criteria. Data were extracted on populations, sampling frames, PFAS species and concentrations, and key findings.

Across studies from Sweden, China, USA, Germany, and Spain, "low-range" drinking water concentrations were associated with measurable increases in blood PFAS, with the most consistent and pronounced relationships observed for PFHxS. In children and high-consuming adults, water intake (≥7-8 cups/day or 1.8 Litres/day) and duration of residence on a supply amplified association. Evidence for contribution was most consistent at ~10-100 ng/L; below ~10 ng/L, associations were less consistent, though some data suggest PFHxS may influence serum levels even within this lower range. PFOA and PFOS showed weaker water-serum relationships at very low concentrations, compatible with greater contributions from legacy, non-water exposures. Heterogeneity in exposure assessment, timing, covariate control, and analytic reporting limited cross-study comparability.

Even when drinking water PFAS concentrations are low, certain compounds-particularly PFHxS-can materially contribute to circulating PFAS, especially among children and high-water-consumption subgroups. These findings support compound-specific risk assessment, re-examination of default relative source contribution (RSC) assumptions for sensitive groups, and targeted monitoring that pairs household-level water measurements with biomonitoring. Standardized methods and longitudinal designs are needed to refine low-range concentration-response relationships and cumulative exposure estimates.

By summarising 10 epidemiologic studies that investigated the contribution of low-level PFAS in drinking water to PFAS concentrations in human blood using rigorous methodology, our review provides compelling evidence for a link between exposure to drinking water concentrations in the "low" range and measurable increases in blood PFAS. Additionally, it suggests even when drinking water PFAS concentrations are low, certain compounds-particularly PFHxS-can materially contribute to circulating PFAS, especially among children and high water consumption subgroups. Given the nature of this evidence, there is a need for compound-specific risk assessment, re-examination of default relative source contribution assumptions for sensitive groups, and targeted monitoring that pairs household-level water measurements with biomonitoring.