Dataset Information

An (Eco)Toxicity Life Cycle Impact Assessment Framework for Per- And Polyfluoroalkyl Substances.

ABSTRACT: A framework for characterizing per- and polyfluoroalkyl substances (PFASs) in life cycle impact assessment (LCIA) is proposed. Thousands of PFASs are used worldwide, with special properties imparted by the fluorinated alkyl chain. Our framework makes it possible to characterize a large part of the family of PFASs by introducing transformation fractions that translate emissions of primary emitted PFASs into the highly persistent terminal degradation products: the perfluoroalkyl acids (PFAAs). Using a PFAA-adapted characterization model, human toxicity as well as marine and freshwater aquatic ecotoxicity characterization factors are calculated for three PFAAs, namely perfluorooctanoic acid (PFOA) perfluorohexanoic acid (PFHxA) and perfluorobutanesulfonic acid (PFBS). The model is evaluated to adequately capture long-term fate, where PFAAs are predicted to accumulate in open oceans. The characterization factors of the three PFAAs are ranked among the top 5% for marine ecotoxicity, when compared to 3104 chemicals in the existing USEtox results databases. Uncertainty analysis indicates potential for equally high ranks for human health impacts. Data availability constitutes an important limitation creating uncertainties. Even so, a life cycle assessment (LCA) case study illustrates practical application of our proposed framework, demonstrating that even low emissions of PFASs can have large effects on LCA results.

SUBMITTER: Holmquist H

PROVIDER: S-EPMC7304862 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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An (Eco)Toxicity Life Cycle Impact Assessment Framework for Per- And Polyfluoroalkyl Substances.

Holmquist Hanna H Fantke Peter P Cousins Ian T IT Owsianiak Mikołaj M Liagkouridis Ioannis I Peters Gregory M GM

Environmental science & technology 20200504 10

A framework for characterizing per- and polyfluoroalkyl substances (PFASs) in life cycle impact assessment (LCIA) is proposed. Thousands of PFASs are used worldwide, with special properties imparted by the fluorinated alkyl chain. Our framework makes it possible to characterize a large part of the family of PFASs by introducing transformation fractions that translate emissions of primary emitted PFASs into the highly persistent terminal degradation products: the perfluoroalkyl acids (PFAAs). Usi ...[more]

PMID: 32364377

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Project description:Per- and polyfluoroalkyl substances (PFAS) are some of the most prominent organic contaminants in human blood that have the potential to disrupt biological processes and pathways in the liver. Although the toxicological implications from human exposure to perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are well established, data on other, lesser-understood PFAS are limited. A challenge for regulatory authorities is to determine acceptable levels of human exposure to large, diverse classes of environmental contaminants. New approach methodologies (NAMs) that apply bioinformatics tools to interpret biological data are being increasingly considered to inform risk assessment when traditional toxicology methodologies are not amenable. The aim of the current investigation was to identify the biological responses relevant to PFAS mode of action as the concentration (benchmark dose) that these effects take place in order to utililze this information to inform/facilitate read-across for risk assessment of data-poor PFAS. A TempO-Seq platform (BioSpyder) measured gene expression changes in human liver microtissues (i.e., spheroids) after 1-day and 10-day exposures to increasing concentrations of PFAS. A bioinformatics framework was applied to 23 PFAS sub-classed into carboxylates (PFCAs), sulfonates (PFSAs), or PFAS precursors that were analyzed for the total altered transcripts, the concentration where effects take place, and identifying target genes of interest. Both PFCAs and PFSAs exhibited a trend toward increased transcriptional changes with carbon chain-length. Specifically, longer-chain compounds (7 to 10 carbons) were more likely to surpass liver-toxic transcriptomic thresholds established from previous studies than shorter chain PFAS. Longer-chain PFAS were also more potent, inducing transcriptional effects at lower concentrations. However, PFOS was the most potent PFAS and of all precursors, only PFOSA (a PFOS precursor) induced a response. The combined high-throughput transcriptomic and bioinformatics analyses revealed the capability of NAMs to assess the effects of PFAS in liver microtissues; such data improves our understanding of PFAS-related effects in humans and facilitates the use of read-across in human health risk assessment for other data-poor chemicals.

Project description:Per- and polyfluoroalkyl substances (PFASs) represent a highly ubiquitous group of synthetic chemicals used in products ranging from water and oil repellents and lubricants to firefighting foam. These substances can enter and accumulate in multiple tissue matrices in up to 100% of people assessed. Though animal models strongly identify these compounds as male reproductive toxicants, with exposed rodents experiencing declines in sperm count, alterations in hormones, and DNA damage in spermatids, among other adverse outcomes, human studies report conflicting conclusions as to the reproductive toxicity of these chemicals. Using an innovative, human stem-cell-based model of spermatogenesis, we assessed the effects of the PFASs perfluorooctanesulfonic acid (PFOS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and a mixture of PFOS, PFOA, and PFNA for their impacts on human spermatogenesis in vitro under conditions relevant to the general and occupationally exposed populations. Here, we show that PFOS, PFOA, PFNA, and a mixture of PFOS, PFOA, and PFNA do not decrease in vitro germ cell viability, consistent with reports from human studies. These compounds do not affect mitochondrial membrane potential or increase reactive oxygen species generation, and they do not decrease cell viability of spermatogonia, primary spermatocytes, secondary spermatocytes, or spermatids in vitro under the conditions examined. However, exposure to PFOS, PFOA, and PFNA reduces expression of markers for spermatogonia and primary spermatocytes. While not having direct effects on germ cell viability, these effects suggest the potential for long-term impacts on male fertility through the exhaustion of the spermatogonial stem cell pool and abnormalities in primary spermatocytes. ABBREVIATIONS:CDC: Centers for Disease Control; DMSO: dimethyl sulfoxide; GHR: growth hormone receptor; hESCs: human embryonic stem cells; PFASs: per- and polyfluoroalkyl substances; PFCs: perfluorinated compounds; PFNA: perfluorononanoic acid; PFOS: perfluorooctanesulfonic acid; PFOA: perfluorooctanoic acid; PLZF: promyelocytic leukemia zinc finger; ROS: reactive oxygen species; HILI: RNA-mediated gene silencing 2; SSC: spermatogonial stem cell.

Dataset Information

An (Eco)Toxicity Life Cycle Impact Assessment Framework for Per- And Polyfluoroalkyl Substances.

Publications

An (Eco)Toxicity Life Cycle Impact Assessment Framework for Per- And Polyfluoroalkyl Substances.

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