The PFAS-Tox Database: A systematic evidence map of health studies on 29 per- and polyfluoroalkyl substances

Pelch, Katherine E.; Reade, Anna; Kwiatkowski, Carol F.; Merced‐Nieves, Francheska M.; Cavalier, Haleigh; Schultz, Kim; Wolffe, Taylor; Varshavsky, Julia

doi:10.1016/j.envint.2022.107408

Cited by 39 publications

(25 citation statements)

References 33 publications

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“…A protocol for conducting this systematic evidence map was initially published on Zenodo (Pelch et al 2019c), then peer reviewed and published in Environment International (Pelch et al 2019d). An update to the protocol and a summary of the changes (see below) was made available on the project webpage on the Open Science Framework (OSF), available at https://osf.io/f9upx/, which is also where additional guidance and supplemental files are housed (Pelch et al 2021). PFAS were prioritized…”

Section: Methodsmentioning

confidence: 99%

“…The interactive display and supporting contextual documentation was published to Tableau Public and PFASToxDatabase.org where it is freely and publicly available. The entire data set and all supplementary materials are also available at the project website on Open Science Framework (https://osf.io/f9upx/) as detailed in the Data Availability section (Pelch et al 2021).…”

Section: Tablementioning

confidence: 99%

“…Selected data can be downloaded directly from PFASToxDatabase.org following the onscreen instructions or the additional instructions that are detailed in the "How To Use the PFAS-Tox Database" file. The entire data set and all supplementary data are also available at the project website on Open Science Framework at https://osf.io/f9upx/ (Pelch et al 2021).…”

Section: Data Availabilitymentioning

confidence: 99%

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The PFAS-Tox Database: A systematic evidence map of health studies on per- and polyfluoroalkyl substances

Varshavsky

Reade

Kwiatkowski

et al. 2022

ISEE Conference Abstracts

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Background: PFAS (per-and polyfluoroalkyl substances) are a large class of synthetic chemicals widely used in consumer products and industrial processes. The scientific literature on PFAS has increased dramatically in the last decade. Many stakeholders, including regulators, scientists, non-governmental organizations, and concerned individuals could benefit from an efficient way to access the health and toxicological literature related to PFAS. Objective: To create a systematic evidence map of the available peer-reviewed health or toxicological research for 29 PFAS. Methods: A protocol for conducting this systematic evidence map was initially published on Zenodo (Pelch et al. 2019c), then peer reviewed and published in Environment International (Pelch et al. 2019d). PubMed database was searched through January 25, 2021. Studies were screened for inclusion and exclusion according to the Populations, Exposures, Comparators, and Outcomes (PECO) statement. Inclusion criteria were intentionally broad and included any human, animal, and/or in vitro study that investigated exposure to one of the 29 PFAS of interest and a human health or toxicological effect. Selected study details were extracted from included studies as described in the protocol. Study appraisal was not conducted. The included studies and extracted meta-data are freely available in the online, interactive systematic evidence map at https://pfastoxdatabase.org. Results: Over 15,000 studies were retrieved from the PubMed literature searches. After manual screening, 1,067 studies were identified and included as investigating the health or toxicological effect of one or more PFAS of interest. There were 505 human, 385 animal, and 220 in vitro studies. Summary tables of the extracted data and overall observations are included in this report. Conclusions: The PFAS-Tox Database is a useful tool for searching, filtering, and identifying peer reviewed research on the health and toxicological effects of the included PFAS. In this summary of the evidence map we provide examples of data gaps and clusters revealed by the database, with the goal of helping direct future

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Section: Methodsmentioning

confidence: 99%

Section: Tablementioning

confidence: 99%

Section: Data Availabilitymentioning

confidence: 99%

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The PFAS-Tox Database: A systematic evidence map of health studies on per- and polyfluoroalkyl substances

Varshavsky

Reade

Kwiatkowski

et al. 2022

ISEE Conference Abstracts

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“…PFAS are recognized by their hydrophobic carbon backbone, which is fully or partially saturated with fluorine atoms, and by possessing a hydrophilic functional group. PFAS, because of the C-F bonds, are very stable [ 2 ] and highly persistent in the environment, which can have a huge impact on humans and living organisms [ 5 , 6 ]. Continuous usage of PFAS leads to their accumulation in the environment and simultaneously increases the likelihood of harmful effects [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

How the Structure of Per- and Polyfluoroalkyl Substances (PFAS) Influences Their Binding Potency to the Peroxisome Proliferator-Activated and Thyroid Hormone Receptors—An In Silico Screening Study

Kowalska¹,

Sosnowska²,

Buławska³

et al. 2023

Molecules

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In this study, we investigated PFAS (per- and polyfluoroalkyl substances) binding potencies to nuclear hormone receptors (NHRs): peroxisome proliferator-activated receptors (PPARs) α, β, and γ and thyroid hormone receptors (TRs) α and β. We have simulated the docking scores of 43 perfluoroalkyl compounds and based on these data developed QSAR (Quantitative Structure-Activity Relationship) models for predicting the binding probability to five receptors. In the next step, we implemented the developed QSAR models for the screening approach of a large group of compounds (4464) from the NORMAN Database. The in silico analyses indicated that the probability of PFAS binding to the receptors depends on the chain length, the number of fluorine atoms, and the number of branches in the molecule. According to the findings, the considered PFAS group bind to the PPARα, β, and γ only with low or moderate probability, while in the case of TR α and β it is similar except that those chemicals with longer chains show a moderately high probability of binding.

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“…The Agency for Toxic Substances and Disease Registry (ATSDR) has recently summarized the literature concerning human exposures and health effects in both humans and laboratory animals for 12 PFAS of varying carbon chain length and structure (ATSDR, 2021). A database of PFAS health studies called the PFAS‐Tox Database has been created that covers 29 PFAS, currently not including PFOA and PFOS due to the enormity of the literature on these legacy PFAS (Pelch et al, 2022). This database currently includes over 15,000 studies.…”

Section: Introductionmentioning

confidence: 99%

A putative adverse outcome network for neonatal mortality and lower birth weight in rodents: Applicability to per‐ and polyfluoroalkyl substances and relevance to human health

Rogers

Heintz

Thompson

et al. 2023

Birth Defects Research

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Background Some per‐ and poly‐fluoroalkyl substances (PFAS) cause neonatal mortality and lower birth weight in rodents. We constructed an Adverse Outcome Pathway (AOP) network for neonatal mortality and lower birth weight in rodents, comprising three putative AOPs. We then assessed strengths of the evidence for the AOPs and applicability to PFAS. Finally, we considered the relevance of this AOP network to human health. Methods Literature searches targeted PFAS, peroxisome proliferator‐activated receptor (PPAR) agonists, other nuclear receptors, relevant tissues, and developmental targets. We used reviews of established biology and described results of studies with prenatal PFAS exposure that assessed birth weight and neonatal survival. Molecular initiating events (MIEs) and key events (KEs) were proposed and strengths of KE relationships (KERs), applicability to PFAS, and human relevance were assessed. Results Neonatal mortality has been observed in rodents following gestational exposure to most longer chain PFAS studied, often coincident with lower birth weight. In AOP 1, PPARα activation and PPARγ activation or downregulation are MIEs; placental insufficiency, fetal nutrient restriction, neonatal hepatic glycogen deficit, and hypoglycemia are KEs leading to neonatal mortality and lower birth weight. In AOP 2, constitutive androstane receptor (CAR) and pregnane X receptor (PXR) activation upregulates Phase II metabolism, lowering maternal circulating thyroid hormones. In AOP 3, disrupted pulmonary surfactant function and PPARγ downregulation cause neonatal airway collapse and mortality from respiratory failure. Conclusions It is likely that different components of this AOP network will apply to different PFAS, largely determined by which nuclear receptors they activate. The MIEs and KEs in this AOP network can occur in humans, but differences in PPAR structure and function, and the timeline of liver and lung development, suggest that humans may be less susceptible to this AOP network. This putative AOP network elucidates knowledge gaps and research needed to better understand the developmental toxicity of PFAS.

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The PFAS-Tox Database: A systematic evidence map of health studies on 29 per- and polyfluoroalkyl substances

Cited by 39 publications

References 33 publications

The PFAS-Tox Database: A systematic evidence map of health studies on per- and polyfluoroalkyl substances

The PFAS-Tox Database: A systematic evidence map of health studies on per- and polyfluoroalkyl substances

How the Structure of Per- and Polyfluoroalkyl Substances (PFAS) Influences Their Binding Potency to the Peroxisome Proliferator-Activated and Thyroid Hormone Receptors—An In Silico Screening Study

A putative adverse outcome network for neonatal mortality and lower birth weight in rodents: Applicability to per‐ and polyfluoroalkyl substances and relevance to human health

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