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

BACKGROUND: 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. OBJECTIVE: 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. METHODS: 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. RESULTS: 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. SIGNIFICANCE: 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. IMPACT STATEMENT: 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.