Bioaccumulation of Perfluorinated Alkyl Acids: Observations and Models

摘要

In this review, we consider the two prevailing hypotheses for the mechanisms that control the bioaccumulation of perfluorinated alkyl adds (PFAAs). The first assumes that partitioning to membrane phospholipids, which have a higher affinity for charged species than neutral storage lipids, can erplain the high bioaccumulation potential of these compounds. The second assumes that interactions with proteins-including serum albumin, liver fatty add binding proteins (L-FABP), and organic anion transporters-determine the distribution, accumulation and half-lives of PFAAs. We consider three unique phenomena to evaluate the two models: (1) observed patterns of tissue distribution in the laboratory and field, (2) the relationship between perfluorinated chain length and bioaccumulation, and (3) species- and gender-specific variation in elimination half-lives. Through investigation of these three characteristics of PFAA bioaccumulation, we show me strengths and weaknesses of the two modeling approaches. We conclude mat the models need not be mutually exclusive, but mat protein interactions are needed to explain some important features of PFAA bloacumulation. Although open questions remain, further research should include perfluorinated alkyi substances (PFASs) beyond the long-chain PFAAs, as these substances are being phased out and replaced by a wide variety of PFASs with largely unknown properties and bioaccumulation behavior.