Academic literature on the topic 'PFAS neurotoxicity'
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Journal articles on the topic "PFAS neurotoxicity"
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Foguth, Rachel, Maria S. Sepúlveda, and Jason Cannon. "Per- and Polyfluoroalkyl Substances (PFAS) Neurotoxicity in Sentinel and Non-Traditional Laboratory Model Systems: Potential Utility in Predicting Adverse Outcomes in Human Health." Toxics 8, no. 2 (June 15, 2020): 42. http://dx.doi.org/10.3390/toxics8020042.
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Per- and polyfluoroalkyl substances (PFAS) are a class of chemicals that were widely used in manufacturing and are now present in the environment throughout the world. It is known that various PFAS are quantifiable in human in blood, but potential adverse health outcomes remain unclear. Sentinel and non-traditional model species are useful to study potential toxicity of PFAS in order to understand the relationship between environmental and human health. Here, we present a critical review of studies on the neurotoxicity of PFAS in sentinel and non-traditional laboratory model systems, including Caenorhabditis elegans (nematode), Dugesia japonica (planarian), Rana pipiens (frogs), Danio rerio and Oryzias melastigma (fish), and Ursus maritimus (polar bears). PFAS have been implicated in developmental neurotoxicity in non-traditional and traditional model systems as well as sentinel species, including effects on neurotransmitter levels, especially acetylcholine and its metabolism. However, further research on the mechanisms of toxicity needs to be conducted to determine if these chemicals are affecting organisms in a similar manner. Overall, findings tend to be similar among the various species, but bioaccumulation may vary, which needs to be taken into account in future studies by quantifying target organ concentrations of PFAS to better compare different species. Furthermore, data on the majority of PFAS is lacking in neurotoxicity testing, and additional studies are needed to corroborate findings thus far.
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Sammi, Shreesh Raj, Rachel M. Foguth, Claudia Sofía Nieves, Chloe De Perre, Peter Wipf, Cynthia T. McMurray, Linda S. Lee, and Jason R. Cannon. "Perfluorooctane Sulfonate (PFOS) Produces Dopaminergic Neuropathology in Caenorhabditis elegans." Toxicological Sciences 172, no. 2 (August 19, 2019): 417–34. http://dx.doi.org/10.1093/toxsci/kfz191.
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AbstractPerfluorooctane sulfonate (PFOS) has been widely utilized in numerous industries. Due to long environmental and biological half-lives, PFOS is a major public health concern. Although the literature suggests that PFOS may induce neurotoxicity, neurotoxic mechanisms, and neuropathology are poorly understood. Thus, the primary goal of this study was to determine if PFOS is selectively neurotoxic and potentially relevant to specific neurological diseases. Nematodes (Caenorhabditis elegans) were exposed to PFOS or related per- and polyfluoroalkyl substances (PFAS) for 72 h and tested for evidence of neuropathology through examination of cholinergic, dopaminergic, gamma-amino butyric acid (GABA)ergic, and serotoninergic neuronal morphologies. Dopaminergic and cholinergic functional analyses were assessed through 1-nonanol and Aldicarb assay. Mechanistic studies assessed total reactive oxygen species, superoxide ions, and mitochondrial content. Finally, therapeutic approaches were utilized to further examine pathogenic mechanisms. Dopaminergic neuropathology occurred at lower exposure levels (25 ppm, approximately 50 µM) than required to produce neuropathology in GABAergic, serotonergic, and cholinergic neurons (100 ppm, approximately 200 µM). Further, PFOS exposure led to dopamine-dependent functional deficits, without altering acetylcholine-dependent paralysis. Mitochondrial content was affected by PFOS at far lower exposure level than required to induce pathology (≥1 ppm, approximately 2 µM). Perfluorooctane sulfonate exposure also enhanced oxidative stress. Further, mutation in mitochondrial superoxide dismutase rendered animals more vulnerable. Neuroprotective approaches such as antioxidants, PFAS-protein dissociation, and targeted (mitochondrial) radical and electron scavenging were neuroprotective, suggesting specific mechanisms of action. In general, other tested PFAS were less neurotoxic. The primary impact is to prompt research into potential adverse outcomes related to PFAS-induced dopaminergic neurotoxicity in humans.
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Balaguer-Trias, Jordina, Deepika Deepika, Marta Schuhmacher, and Vikas Kumar. "Impact of Contaminants on Microbiota: Linking the Gut–Brain Axis with Neurotoxicity." International Journal of Environmental Research and Public Health 19, no. 3 (January 26, 2022): 1368. http://dx.doi.org/10.3390/ijerph19031368.
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Over the last years, research has focused on microbiota to establish a missing link between neuronal health and intestine imbalance. Many studies have considered microbiota as critical regulators of the gut–brain axis. The crosstalk between microbiota and the central nervous system is mainly explained through three different pathways: the neural, endocrine, and immune pathways, intricately interconnected with each other. In day-to-day life, human beings are exposed to a wide variety of contaminants that affect our intestinal microbiota and alter the bidirectional communication between the gut and brain, causing neuronal disorders. The interplay between xenobiotics, microbiota and neurotoxicity is still not fully explored, especially for susceptible populations such as pregnant women, neonates, and developing children. Precisely, early exposure to contaminants can trigger neurodevelopmental toxicity and long-term diseases. There is growing but limited research on the specific mechanisms of the microbiota–gut–brain axis (MGBA), making it challenging to understand the effect of environmental pollutants. In this review, we discuss the biological interplay between microbiota–gut–brain and analyse the role of endocrine-disrupting chemicals: Bisphenol A (BPA), Chlorpyrifos (CPF), Diethylhexyl phthalate (DEHP), and Per- and polyfluoroalkyl substances (PFAS) in MGBA perturbations and subsequent neurotoxicity. The complexity of the MGBA and the changing nature of the gut microbiota pose significant challenges for future research. However, emerging in-silico models able to analyse and interpret meta-omics data are a promising option for understanding the processes in this axis and can help prevent neurotoxicity.
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Gaballah, Shaza, Adam Swank, Jon R. Sobus, Xia Meng Howey, Judith Schmid, Tara Catron, James McCord, Erin Hines, Mark Strynar, and Tamara Tal. "Evaluation of Developmental Toxicity, Developmental Neurotoxicity, and Tissue Dose in Zebrafish Exposed to GenX and Other PFAS." Environmental Health Perspectives 128, no. 4 (April 2020): 047005. http://dx.doi.org/10.1289/ehp5843.
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Wang, Yong, Jiaqi Guo, Sumita Sumita, Changjie Shi, Qijia Zhu, Cong Li, and Weihai Pang. "A Review of Recent Advances in Detection and Treatment Technology for Perfluorinated Compounds." Water 14, no. 23 (December 1, 2022): 3919. http://dx.doi.org/10.3390/w14233919.
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Perfluorinated compounds (PFCs) are a novel type of environmental pollutant with a specific structure. PFCs have become a global concern due to their environmental persistence and biotoxicity properties. In this paper, we review the hazardous effects, detection technologies, and treatment methods of PFCs. We present the current status of PFCs pollution in water, the atmosphere, soil, and organisms. Moreover, we show that PFCs have toxic effects, such as hepatotoxicity, neurotoxicity, immunotoxicity, endocrine disruption, and reproductive and developmental toxicity. Six sample pretreatment techniques and four assays for PFCs are listed in this paper. This review focuses on the analysis of the treatment methods for PFCs, such as physical adsorption, microbial degradation, photochemical oxidation, electrochemical oxidation, acoustic oxidation, Fenton oxidation, and so on. We systematically analyze the treatment effects, removal mechanisms, and future directions of various technologies to provide support and suggestions for PFCs pollution control technologies.
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Starnes, Hannah M., Kylie D. Rock, Thomas W. Jackson, and Scott M. Belcher. "A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior." Frontiers in Toxicology 4 (April 11, 2022). http://dx.doi.org/10.3389/ftox.2022.881584.
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Per- and polyfluoroalkyl substances (PFAS) are a class of structurally diverse synthetic organic chemicals that are chemically stable, resistant to degradation, and persistent in terrestrial and aquatic environments. Widespread use of PFAS in industrial processing and manufacturing over the last 70 years has led to global contamination of built and natural environments. The brain is a lipid rich and highly vascularized organ composed of long-lived neurons and glial cells that are especially vulnerable to the impacts of persistent and lipophilic toxicants. Generally, PFAS partition to protein-rich tissues of the body, primarily the liver and blood, but are also detected in the brains of humans, wildlife, and laboratory animals. Here we review factors impacting the absorption, distribution, and accumulation of PFAS in the brain, and currently available evidence for neurotoxic impacts defined by disruption of neurochemical, neurophysiological, and behavioral endpoints. Emphasis is placed on the neurotoxic potential of exposures during critical periods of development and in sensitive populations, and factors that may exacerbate neurotoxicity of PFAS. While limitations and inconsistencies across studies exist, the available body of evidence suggests that the neurobehavioral impacts of long-chain PFAS exposures during development are more pronounced than impacts resulting from exposure during adulthood. There is a paucity of experimental studies evaluating neurobehavioral and molecular mechanisms of short-chain PFAS, and even greater data gaps in the analysis of neurotoxicity for PFAS outside of the perfluoroalkyl acids. Whereas most experimental studies were focused on acute and subchronic impacts resulting from high dose exposures to a single PFAS congener, more realistic exposures for humans and wildlife are mixtures exposures that are relatively chronic and low dose in nature. Our evaluation of the available human epidemiological, experimental, and wildlife data also indicates heightened accumulation of perfluoroalkyl acids in the brain after environmental exposure, in comparison to the experimental studies. These findings highlight the need for additional experimental analysis of neurodevelopmental impacts of environmentally relevant concentrations and complex mixtures of PFAS.
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Liu, Ferra, and Wei Zhu. "PFOA and PFOS induced neuronal cell apoptosis via the FADD ligand of the death pathway." Journal of Student Research 11, no. 1 (February 28, 2022). http://dx.doi.org/10.47611/jsrhs.v11i1.2483.
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Per and polyfluoroalkyl substances (PFAS chemicals) have been prevalent since the 1940s. Yet, the impacts of these synthetic substances on human health still remain uncertain. Both in vivo and in vitro studies exhibit cytotoxicity targets including: hepatotoxicity, reproductive toxicity, thyroid disruption, neurotoxicity, and many more. In this study, 2 specific PFAS chemicals - Perfluoroooctane sulfonate and Perfluorooctanoic acid - were tested for their effects on HTB-11 neuronal cells. Molecular docking was utilized to determine linkages with death ligands. PFOS and PFOA prompted caspase activity on targeted neuronal cells, indicating that these chemicals significantly induce apoptosis. Evidence of high binding affinities with a death ligand was also present. PFOS and PFOA, in addition, reduced target neuronal cell survival in the MTT assay, with all concentrations significant. Based on this evidence, researchers should study more closely the health effects PFAS chemicals can instigate in human bodies.
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Yu, Guoqi, Fei Luo, Min Nian, Shuman Li, Bin Liu, Liping Feng, and Jun Zhang. "Exposure to Perfluoroalkyl Substances During Pregnancy and Fetal BDNF Level: A Prospective Cohort Study." Frontiers in Endocrinology 12 (June 1, 2021). http://dx.doi.org/10.3389/fendo.2021.653095.
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BackgroundHumans are widely exposed to environmental perfluoroalkyl substances (PFAS), which may affect fetal neurodevelopment. Brain-derived neurotrophic factor (BDNF) is an important factor in neurodevelopment, but its role in PFAS-induced neurotoxicity is unclear. We investigated the association between prenatal PFAS exposure and fetal BDNF level in the umbilical cord blood in a large prospective cohort.MethodsA total of 725 pregnant women who participated in the Shanghai Birth Cohort were included. 10 PFAS were measured by high-performance liquid chromatography/tandem mass spectrometry (HPLC/MS-MS) in the plasma samples of early pregnancy. The BDNF level was determined by ELISA. The concentration of total mercury (Hg) in the umbilical cord blood was tested by cold vapor atomic absorption spectrometry (AAS) and included as a main confounder, along with other covariates. Multiple linear regression was used to explore the associations between PFAS concentrations and BDNF level. Quantile-based g-computation was applied to explore the joint and independent effects of PFAS on BDNF level.ResultsThe mean BDNF level in the total population was 10797 (±4713) pg/ml. Male fetuses had a higher level than female fetuses (P<0.001). A significant positive association was observed between PFHxS and BDNF level after adjusting for potential confounders [β=1285 (95% CI: 453, 2118, P=0.003)]. No association was observed between other PFAS congeners and BDNF level. Results of the mixed exposure model showed that the joint effects of PFAS mixture were not associated with BDNF [β=447 (95% CI: -83, 978, P=0.10)], while the positive association with PFHxS exposure remained significant after controlling for other PFAS [β=592 (95% CI: 226, 958, P=0.002)]. The above associations were more prominent in male [β=773 (95% CI: 25, 1520, P= 0.04)] than female fetuses [β=105 (95% CI: -791, 1002, P= 0.82)] for the mixed effects.ConclusionsPrenatal exposure to PFHxS was associated with an increased BDNF level in the umbilical blood, especially in male fetuses.
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Di Nisio, Andrea, Maria Santa Rocca, Luca De Toni, Iva Sabovic, Diego Guidolin, Stefano Dall’Acqua, Laura Acquasaliente, Vincenzo De Filippis, Mario Plebani, and Carlo Foresta. "Endocrine disruption of vitamin D activity by perfluoro-octanoic acid (PFOA)." Scientific Reports 10, no. 1 (October 8, 2020). http://dx.doi.org/10.1038/s41598-020-74026-8.
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Abstract Perfluoroalkyl substances (PFAS) are a class of compounds used in industry and consumer products. Perfluorooctanoic acid (PFOA) is the predominant form in human samples and has been shown to induce severe health consequences, such as neonatal mortality, neurotoxicity, and immunotoxicity. Toxicological studies indicate that PFAS accumulate in bone tissues and cause altered bone development. Epidemiological studies have reported an inverse relationship between PFAS and bone health, however the associated mechanisms are still unexplored. Here, we present computational, in silico and in vitro evidence supporting the interference of PFOA on vitamin D (VD). First, PFOA competes with calcitriol on the same binding site of the VD receptor, leading to an alteration of the structural flexibility and a 10% reduction by surface plasmon resonance analysis. Second, this interference leads to an altered response of VD-responsive genes in two cellular targets of this hormone, osteoblasts and epithelial cells of the colorectal tract. Third, mineralization in human osteoblasts is reduced upon coincubation of PFOA with VD. Finally, in a small cohort of young healthy men, PTH levels were higher in the exposed group, but VD levels were comparable. Altogether these results provide the first evidence of endocrine disruption by PFOA on VD pathway by competition on its receptor and subsequent inhibition of VD-responsive genes in target cells.
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Bell, Kiersten S., and Katherine L. O’Shaughnessy. "The development and function of the brain barriers – an overlooked consideration for chemical toxicity." Frontiers in Toxicology 4 (October 18, 2022). http://dx.doi.org/10.3389/ftox.2022.1000212.
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It is well known that the adult brain is protected from some infections and toxic molecules by the blood-brain and the blood-cerebrospinal fluid barriers. Contrary to the immense data collected in other fields, it is deeply entrenched in environmental toxicology that xenobiotics easily permeate the developing brain because these barriers are either absent or non-functional in the fetus and newborn. Here we review the cellular and physiological makeup of the brain barrier systems in multiple species, and discuss decades of experiments that show they possess functionality during embryogenesis. We next present case studies of two chemical classes, perfluoroalkyl substances (PFAS) and bisphenols, and discuss their potential to bypass the brain barriers. While there is evidence to suggest these pollutants may enter the developing and/or adult brain parenchyma, many studies suffer from confounding technical variables which complicates data interpretation. In the future, a more formal consideration of brain barrier biology could not only improve understanding of chemical toxicokinetics but could assist in prioritizing environmental xenobiotics for their neurotoxicity risk.
Dissertations / Theses on the topic "PFAS neurotoxicity"
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Lee, Iwa. "Developmental neurotoxicity of persistent and non-persistent pollutants : Behavioral and neurochemical assessments of a perfluorinated compound, pesticides and interaction effects." Doctoral thesis, Uppsala universitet, Institutionen för organismbiologi, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-261742.
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The focus of this thesis was to investigate developmental neurotoxic effects of different persistent and non-persistent environmental pollutants, alone or in binary mixtures, when exposure occurs during a critical period of brain development, in mice. The compounds investigated included a perfluorinated compound, perfluorohexane sulphonate (PFHxS), and four different pesticides, endosulfan, cypermethrin, chlorpyrifos and carbaryl. Both persistent and non-persistent pollutants are detected in the environment and in humans, which shows that exposure to these compounds is occurring in real life. Humans can therefore be exposed to various pollutants during their whole lifetime, starting from the gestational period to adulthood. Furthermore, exposure to environmental pollutants is rarely exclusive to a single compound, but rather occurs through combinations of various pollutants present in the environment. Exposure to environmental pollutants during human brain development have been suggested to be a possible cause for neuropsychiatric disorders, such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). Previous studies have shown that chemicals can induce irreversible disorders in brain function when exposure to these chemicals occurs during a critical defined period of the brain development known as the brain growth spurt (BGS). The BGS is characterized by a rapid growth and development of the immature brain. In humans, and mice, this period also overlaps the lactation period indicating that newborns and toddlers can be exposed via mothers’ milk as well. This thesis has shown that a single oral exposure to PFHxS, endosulfan, cypermethrin, chlorpyrifos or carbaryl can induce developmental neurotoxic effects in mice, when exposure occurs during a critical period of brain development. These effects are manifested as persistent altered adult spontaneous behavior in a novel home environment, modified habituation, altered susceptibility of the cholinergic system and changed levels of neuroproteins in the mouse brain. Furthermore, a single neonatal co-exposure to a binary mixture of carbaryl/chlorpyrifos or PFHxS/endosulfan can interact and exacerbate the adult behavioral effects. These effects were seen at dosages were the single compound did not elicit a response or induced a much weaker behavioral effect. This indicates that risk assessments conducted on single compounds might underestimate interaction effects of mixtures when co-exposed.
Book chapters on the topic "PFAS neurotoxicity"
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Li, Chunna, Xiaohui Liu, Qi Liu, Shuangyue Li, Yachen Li, Hong Hu, and Jing Shao. "Protection of Taurine Against PFOS-Induced Neurotoxicity in PC12 Cells." In Advances in Experimental Medicine and Biology, 907–16. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1079-2_72.
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