A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

A peer-reviewed open access journal published by the National Institute of Environmental Health Sciences

Per- and polyfluoroalkyl substances (PFAS) are transferred from mother to infants through breastfeeding, a time when children may be particularly vulnerable to PFAS-mediated adverse health effects. Infants can also be exposed to PFAS from infant formula consumption. Our recent literature-based scoping of breast milk levels reported that four PFAS often exceeded the United States Agency for Toxic Substances and Disease Registry (ATSDR) children's drinking water screening levels in both the general population and highly impacted communities in the U.S. and Canada. This work presents a comparison of global breast milk and infant formula PFAS measurements with the only reported health-based drinking water screening values specific to children. We focused on four PFAS for which ATSDR has developed children's drinking water screening values: PFOA (perfluorooctanoic acid), PFOS (perfluorooctanesulfonic acid), PFHxS (perfluorohexanesulfonic acid), and PFNA (perfluorononanoic acid). Published literature on PFAS levels in breast milk and infant formula were identified via PubMed searches. Data were compared to children's drinking water screening values. Breast milk concentrations of PFOA and PFOS often exceed children's drinking water screening values, regardless of geographic location. The limited information on infant formula suggests its use does not necessarily result in lower PFAS exposures, especially for formulas reconstituted with drinking water containing PFAS. Unfortunately, individuals generally cannot know whether their infant's exposures exceed children's drinking water screening values. Thus, it is essential that pregnant and lactating women and others, especially those having lived in PFAS-contaminated communities, have data required to make informed decisions on infant nutrition. An international monitoring effort and access to affordable testing are needed for breast milk, drinking water and infant formula to fully understand infant PFAS exposures. Currently, our understanding of demonstrable methods for reducing exposures to emerging PFAS is limited, making this research and the communications surrounding it even more important.

Background: Despite experimental evidence, most epidemiologic studies to date have not supported an association between exposure to persistent organic pollutants (POP) and breast cancer incidence in humans. This may be attributable to difficulties in estimating blood/tissue POP concentration at critical time periods of carcinogenesis. Objectives: In this work we aimed to develop a tool to estimate lifetime POP blood/tissue exposure and levels during any hypothesized time window of susceptibility in breast cancer development. Methods: We developed a physiologically based pharmacokinetic (PBPK) model that can account for any given physiologic lifetime history. Using data on pregnancies, height, weight, and age, the model estimates the values of physiologic parameters (e.g., organ volume, composition, and blood flow) throughout a woman’s entire life. We assessed the lifetime toxicokinetic profile (LTP) for various exposure scenarios and physiologic factors (i.e., breast-feeding, growth, pregnancy, lactation, and weight changes). Results: Simulations for three POPs [hexachlorobenzene, polychlorinated biphenyl (PCB)-153, PCB-180] using different lifetime physiologic profiles showed that the same blood concentration at 55 years of age can be reached despite totally different LTP. Aside from exposure levels, lactation periods and weight profile history were shown to be the factors that had the greatest impact on the LTP. Conclusions: This new lifetime PBPK model, which showed the limitations of using a single sample value obtained around the time of diagnosis for lifetime exposure assessment, will enable researchers conducting environmental epidemiology studies to reduce uncertainty linked to past POP exposure estimation and to consider exposure during time windows that are hypothesized to be mechanistically critical in carcinogenesis.