Harvard John A. Paulson School of Engineering and Applied Sciences, Harvard University, Cambridge, MA, USA, 02138. jennifersun@.g.harvard.edu.
Meta Analytical Inc., Calgary, AB, T3H 2Z5, Canada.
Environ Sci Process Impacts. 2022 Aug 17;24(8):1152-1164. doi: 10.1039/d2em00047d.
Per- and polyfluoroalkyl substances (PFAS) are a large class of highly fluorinated anthropogenic chemicals. Some PFAS bioaccumulate in aquatic food webs, thereby posing risks for seafood consumers. Existing models for persistent organic pollutants (POPs) perform poorly for ionizable PFAS. Here we adapt a well-established food web bioaccumulation model for neutral POPs to predict the bioaccumulation behavior of six perfluoroalkyl acids (PFAAs) and two perfluoroalkyl ether acids (HFPO-DA, 9-Cl-PF3ONS) produced as PFAA replacements. The new model includes sorption to blood plasma proteins and phospholipids, empirically parameterized membrane transport, and renal elimination for PFAAs. Improved performance relative to prior models without these updates is shown by comparing simulations to field and lab measurements. PFAS with eight or more perfluorinated carbons ( ≥ 8, , C8 perfluorosulfonic acid, C10-C11 perfluorocarboxylic acid, 9-Cl-PF3ONS) are often the most abundant in aquatic food webs. The new model reproduces their observed bioaccumulation potential within a factor of two for >80% of fish species, indicating its readiness to support development of fish consumption advisories for these compounds. Results suggest bioaccumulation of ≥ 8 PFAS is primarily driven by phospholipid partitioning, and that renal elimination is negligible for these compounds. However, specific protein binding mechanisms are important for reproducing the observed tissue concentrations of many shorter-chain PFAAs, including protein transporter-mediated renal elimination. Additional data on protein-binding and membrane transport mechanisms for PFAS are needed to better understand the biological behavior of shorter-chain PFAAs and their alternatives.
全氟和多氟烷基物质（PFAS）是一大类高度氟化的人为化学品。一些 PFAS 在水生食物网中生物积累，从而对海鲜消费者构成风险。现有的持久性有机污染物（POPs）模型对可离子化的 PFAS 表现不佳。在这里，我们改编了一个成熟的中性 POPs 食物网生物积累模型，以预测六种全氟烷基酸（PFAAs）和两种全氟烷基醚酸（HFPO-DA、9-Cl-PF3ONS）的生物积累行为，这些酸是作为 PFAAs 的替代品生产的。新模型包括与血浆蛋白和磷脂的吸附、经验参数化的膜转运以及 PFAAs 的肾脏排泄。通过将模拟结果与现场和实验室测量结果进行比较，证明了与没有这些更新的先前模型相比，该模型的性能有所提高。在水生食物网中，通常含有 8 个或更多全氟化碳原子（≥8，包括全氟磺酸 C8、C10-C11 全氟羧酸、9-Cl-PF3ONS）的 PFAS 最为丰富。新模型在 80%以上的鱼类物种中，将其观察到的生物积累潜力再现到两倍以内，表明其已准备好支持为这些化合物制定鱼类消费建议。结果表明，≥8 PFAS 的生物积累主要由磷脂分配驱动，并且这些化合物的肾脏排泄可以忽略不计。然而，对于许多短链 PFAAs，包括蛋白转运体介导的肾脏排泄，特定的蛋白结合机制对于再现观察到的组织浓度是重要的。需要更多关于 PFAS 的蛋白结合和膜转运机制的数据，以更好地理解短链 PFAAs 及其替代品的生物学行为。
