This commentary presents a scientific basis for managing as one chemical class the thousands of chemicals known as PFAS (per-and polyfluoroalkyl substances). The class includes perfluoroalkyl acids, perfluoroalkylether acids, and their precursors; fluoropolymers and perfluoropolyethers; and other PFAS. The basis for the class approach is presented in relation to their physicochemical, environmental, and toxicological properties. Specifically, the high persistence, accumulation potential, and/or hazards (known and potential) of PFAS studied to date warrant treating all PFAS as a single class. Examples are provided of how some PFAS are being regulated and how some businesses are avoiding all PFAS in their products and purchasing decisions. We conclude with options for how governments and industry can apply the class-based approach, emphasizing the importance of eliminating non-essential uses of PFAS, and further developing safer alternatives and methods to remove existing PFAS from the environment.
The time-dependent stock of PBDEs contained in in-use products (excluding building materials and large vehicles) was estimated for the U.S. and Canada from 1970 to 2020 based on product consumption patterns, PBDE contents, and product lifespan. The stocks of penta- and octaBDE peaked in in-use products at 17,000 (95% confidence interval: 6000-70,000) and 4,000 (1,000-50,000) tonnes in 2004, respectively, and for decaBDE at 140,000 (40,000-300,000) tonnes in 2008. Products dominating PBDE usage were polyurethane foam used in furniture (65% of pentaBDE), casings of electrical and electronic equipment or EEE (80% of octaBDE), and EEE and automotive seating (35% of decaBDE for each category). The largest flow of PBDEs in products, excluding automotive sector, to the waste phase occurred between 2005 and 2008 at ∼10,000 tonnes per year. Total consumption of penta-, octa-, and decaBDE from 1970 to 2020 in products considered was estimated at ∼46,000, ∼25,000, and ∼380,000 tonnes, respectively. Per capita usage was estimated at 10-250, 10-150, and 200-2000 g·capita(-1)·y(-1) for penta-, octa-, and decaBDE, respectively, over the time span. Considering only the first use (no reuse and/or storage) of PBDE-containing products, approximately 60% of the stock of PBDEs in 2014 or ∼70,000 tonnes, of which 95% is decaBDE, will remain in the use phase in 2020. Total emissions to air of all PBDEs from the in-use product stock was estimated at 70-700 tonnes between 1970 and 2020, with annual emissions of 0.4-4 tonnes·y(-1) for each of penta- and octaBDE and 0.35-3.5 tonnes·y(-1) for decaBDE in 2014.
Major gaps in current efforts limit policy responses
Chemical pollution can have profound and far-reaching effects on biodiversity and ecosystem health (Bernhardt et al., 2017;Groh et al., 2022;Rillig et al., 2019; Secretariats of the BRS and MC, 2021a, 2021b). Among the five major drivers of biodiversity loss, the greatest pressure is currently exerted by habitat destruction, whereas contributions from other drivers have been estimated to be 3-4 times lower
Background: To date, the toxicity of organophosphate esters has primarily been studied regarding their use as pesticides and their effects on the neurotransmitter acetylcholinesterase (AChE). Currently, flame retardants and plasticizers are the two largest market segments for organophosphate esters and they are found in a wide variety of products, including electronics, building materials, vehicles, furniture, car seats, plastics, and textiles. As a result, organophosphate esters and their metabolites are routinely found in human urine, blood, placental tissue, and breast milk across the globe. It has been asserted that their neurological effects are minimal given that they do not act on AChE in precisely the same way as organophosphate ester pesticides. Objectives: This commentary describes research on the non-AChE neurodevelopmental toxicity of organophosphate esters used as flame retardants and plasticizers (OPEs). Studies in humans, mammalian, nonmammalian, and in vitro models are presented, and relevant neurodevelopmental pathways, including adverse outcome pathways, are described. By highlighting this scientific evidence, we hope to elevate the level of concern for widespread human exposure to these OPEs and to provide recommendations for how to better protect public health. Discussion: Collectively, the findings presented demonstrate that OPEs can alter neurodevelopmental processes by interfering with noncholinergic pathways at environmentally relevant doses. Application of a pathways framework indicates several specific mechanisms of action, including perturbation of glutamate and gamma-aminobutyric acid and disruption of the endocrine system. The effects may have implications for the development of cognitive and social skills in children. Our conclusion is that concern is warranted for the developmental neurotoxicity of OPE exposure. We thus describe important considerations for reducing harm and to provide recommendations for government and industry decision makers. https://doi.org/10.1289/EHP9285
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