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1.
A State-of-the-Science Review of Arsenic's Effects on Glucose Homeostasis in Experimental Models.
Castriota, F, Rieswijk, L, Dahlberg, S, La Merrill, MA, Steinmaus, C, Smith, MT, Wang, JC
Environmental health perspectives. 2020;(1):16001
Abstract
BACKGROUND The prevalence of type 2 diabetes (T2D) has more than doubled since 1980. Poor nutrition, sedentary lifestyle, and obesity are among the primary risk factors. While an estimated 70% of cases are attributed to excess adiposity, there is an increased interest in understanding the contribution of environmental agents to diabetes causation and severity. Arsenic is one of these environmental chemicals, with multiple epidemiology studies supporting its association with T2D. Despite extensive research, the molecular mechanism by which arsenic exerts its diabetogenic effects remains unclear. OBJECTIVES We conducted a literature search focused on arsenite exposure in vivo and in vitro, using relevant end points to elucidate potential mechanisms of oral arsenic exposure and diabetes development. METHODS We explored experimental results for potential mechanisms and elucidated the distinct effects that occur at high vs. low exposure. We also performed network analyses relying on publicly available data, which supported our key findings. RESULTS While several mechanisms may be involved, our findings support that arsenite has effects on whole-body glucose homeostasis, insulin-stimulated glucose uptake, glucose-stimulated insulin secretion, hepatic glucose metabolism, and both adipose and pancreatic β-cell dysfunction. DISCUSSION This review applies state-of-the-science approaches to identify the current knowledge gaps in our understanding of arsenite on diabetes development. https://doi.org/10.1289/EHP4517.
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2.
GPER as a Receptor for Endocrine-Disrupting Chemicals (EDCs).
Périan, S, Vanacker, JM
Frontiers in endocrinology. 2020;:545
Abstract
Endocrine-disrupting chemicals (EDCs) are exogenous chemicals that interfere with endogenous hormonal systems at various levels, resulting in adverse health effects. EDCs belong to diverse chemical families and can accumulate in the environment, diet and body fluids, with different levels of persistence. Their action can be mediated by several receptors, including members of the nuclear receptor family, such as estrogen and androgen receptors. The G protein-coupled estrogen receptor (GPER), a seven-transmembrane domain receptor, has also attracted attention as a potential target of EDCs. This review summarizes our current knowledge concerning GPER as a mediator of EDCs' effects.
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3.
Genomics of Detoxification: How Genomics can be Used for Targeting Potential Intervention and Prevention Strategies Including Nutrition for Environmentally Acquired Illness.
Hausman-Cohen, SR, Hausman-Cohen, LJ, Williams, GE, Bilich, CE
Journal of the American College of Nutrition. 2020;(2):94-102
Abstract
Due to their genomic variants, some individuals are more highly affected by toxicants than others. Toxicant metabolizing and activating variants have been linked with a wide variety of health issues including an increased risk of miscarriages, birth defects, Alzheimer's, benzene toxicity, mercury toxicity and cancer. The study of genomics allows a clinician to identify pathways that are less effective and then gives the clinician the opportunity to counsel their patients about diet, supplements and lifestyle modifications that can improve the function of these pathways or compensate to some extent for their deficits. This article will review a few of these critical pathways relating to phase I and phase 2 detox such as GSTP1, GPX1, GSTT1 deletions, PON1 and some of the CYP 450 system as examples of how an individual's genomic vulnerabilities to toxicants can be addressed by upregulating or downregulating specific pathways via genomically targeted use of foods, supplements and lifestyle changes.
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4.
Mitigation of environmentally-related hazardous pollutants from water matrices using nanostructured materials - A review.
Bilal, M, Rasheed, T, Mehmood, S, Tang, H, Ferreira, LFR, Bharagava, RN, Iqbal, HMN
Chemosphere. 2020;:126770
Abstract
An unprecedented rise in population growth and rapid worldwide industrial development are associated with the increasing discharge of a range of toxic and baleful compounds. These toxic pollutants including dyes, endocrine-disrupters, heavy metals, personal care products, and pharmaceuticals are destructing nature's balance and intensifying environmental toxicity at a disquieting rate. Therefore, finding better, novel and more environmentally sound approaches for wastewater remediation are of great importance. Nanoscale materials have opened up some new horizons in various fields of science and technology. Among a range of treatment technologies, nanostructured materials have recently received incredible interest as an emerging platform for wastewater remediation owing to their exceptional surface-area-to-volume ratio, unique electrical and chemical properties, quantum size effects, high scalability, and tunable surface functionalities. An array of nanomaterials including noble metal-based nanostructures, transition metal oxide nanomaterials, carbon-based nanomaterials, carbon nanotubes, and graphene/graphene oxide nanomaterials to their novel nanocomposites and nanoconjugates have been attempted as the promising catalysts to overcome environmental dilemmas. In this review, we summarized recent advances in nanostructured materials that are particularly engineered for the remediation of environmental contaminants. The toxicity of various classes of relevant tailored nanomaterials towards human health and the ecosystem along with perspectives is also presented. In our opinion, an overview of the up-to-date advancements on this emerging topic may provide new ideas and thoughts for engineering low-cost and highly-efficient nanostructured materials for the abatement of recalcitrant pollutants for a sustainable environment.
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5.
Environmental and ecological factors of stomach cancer incidence and mortality: a systematic review study on ecological studies.
Khazaei, S, Mohammadbeigi, A, Jenabi, E, Asgarian, A, Heidari, H, Saghafipour, A, Arsang-Jang, S, Ansari, H
Reviews on environmental health. 2020;(4):443-452
Abstract
OBJECTIVES Stomach cancer (SC) is one of the most common and deadly types of cancer. It is the third leading cause of cancer deaths worldwide. The effect of environmental and ecological factors in SC have been assessed in some studies. Thus, we aimed to synthesize the environmental and ecological factors of SC incidence and mortality. CONTENT In this systematic review study, the scientific databases, including Web of Science, Scopus and PubMed, were searched from inception to November 2019 for all primary articles written in English by using relevant Medical Subject Heading (Mesh) terms. Two independent authors conducted the screening process to decide on the eligibility and inclusion of the articles in the study. The third author acted as an arbiter to resolve any disagreements. SUMMARY AND OUTLOOK A total of 157 potentially relevant articles were identified from the initial search 38 of which met the eligibility criteria; finally, 34 articles were included in the systematic review. The results revealed that soil arsenic exposure, coal and other opencast mining installations, living near incinerators and installations for the recovery or disposal of hazardous waste, installations for the production of cement, lime, plaster, and magnesium oxide, proximity to a metal industry sources, dietary iron, ingested asbestos, farming, arsenic in soil, altitude, organochlorines and environmental exposure to cadmium and lead have positive associations with SC incidence or death. Most of the ecological and environmental factors such as living near the mineral industries, the disposal of hazardous waste, metal industry sources and environmental exposure to cadmium and lead are positively related to SC mortality and incidence. However, solar UV-B, heat index and dietary zinc can be taken into account as protective factors against SC mortality and incidence.
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6.
[Research on the relationship between environmental chemical pollutant exposure and epigenetics].
Rui, QY, Li, X, Zhang, HB, Guo, XM, Zheng, N, Zhao, L, Guo, LQ, Li, PH, Yue, JJ
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases. 2020;(3):237-240
Abstract
Environmental chemical pollutants are increasing, which brings various harms to human health. Epigenetics may be an important medium between exposure to environmental chemical contaminants and adverse health effects. Many environmental chemical pollutant exposures can regulate gene expression and promote disease occurrence and development through epigenetic mechanisms. This review outlines the mechanisms of epigenetics and the latest research advances in exposure and epigenetics of several environmental chemical substances (heavy metal arsenic, bisphenol A, dioctyl phthalate and benzene). To further understand and study the relationship between environmental chemical pollutant exposures and epigenetics in order to elucidate the mechanisms of disease occurrence and development.
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7.
Principles of fluoride toxicity and the cellular response: a review.
Johnston, NR, Strobel, SA
Archives of toxicology. 2020;(4):1051-1069
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Abstract
Fluoride is ubiquitously present throughout the world. It is released from minerals, magmatic gas, and industrial processing, and travels in the atmosphere and water. Exposure to low concentrations of fluoride increases overall oral health. Consequently, many countries add fluoride to their public water supply at 0.7-1.5 ppm. Exposure to high concentrations of fluoride, such as in a laboratory setting often exceeding 100 ppm, results in a wide array of toxicity phenotypes. This includes oxidative stress, organelle damage, and apoptosis in single cells, and skeletal and soft tissue damage in multicellular organisms. The mechanism of fluoride toxicity can be broadly attributed to four mechanisms: inhibition of proteins, organelle disruption, altered pH, and electrolyte imbalance. Recently, there has been renewed concern in the public sector as to whether fluoride is safe at the current exposure levels. In this review, we will focus on the impact of fluoride at the chemical, cellular, and multisystem level, as well as how organisms defend against fluoride. We also address public concerns about fluoride toxicity, including whether fluoride has a significant effect on neurodegeneration, diabetes, and the endocrine system.
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A combined experimental and computational study on the oxidative degradation of bromophenols by Fe(VI) and the formation of self-coupling products.
Dar, AA, Chen, J, Shad, A, Pan, X, Yao, J, Bin-Jumah, M, Allam, AA, Huo, Z, Zhu, F, Wang, Z
Environmental pollution (Barking, Essex : 1987). 2020;:113678
Abstract
In this study, the degradation of eight bromophenols (BPs), including monobromophenols (2-BP, 3-BP, and 4-BP), dibromophenols (2,4-DBP, 2,6-DBP, and 3,5-DBP), a tribromophenol (2,4,6-TBP) and a pentabromophenol (PBP), by a Fe(VI) reaction process at a pH of 8.0 was systematically studied. It was concluded that their degradation rates increased with increasing Fe(VI) concentrations in solution. The removal of 2,4,6-TBP, 2-BP, and 2,6-DBP was faster than that of the other five BPs, which could be attributed to the position of the substituting Br atom. Moreover, the direct oxidation and coupling reactions greatly influenced the reactivity of the bromophenols with Fe(VI). The electron paramagnetic resonance (EPR) analysis confirmed the presence of hydroxyl radicals in present system. The oxidation reaction products of PBP and 2-BP were recognized by an electrospray time-of-flight mass spectrometer; hydroxylation, hydroxyl substitution, the cleavage of the C-C bond, direct oxidation and polymerization via an end linking mechanism were noticeably found in the reaction process, resulting in the formation of polymerization products and causing hydroxylation to occur. Theoretical calculations further determined the possible oxidation sites of 2-BP and PBP. This study may provide comprehensive and important information on the remediation of BPs by Fe(VI).
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ROS-induced NLRP3 inflammasome priming and activation mediate PCB 118- induced pyroptosis in endothelial cells.
Long, Y, Liu, X, Tan, XZ, Jiang, CX, Chen, SW, Liang, GN, He, XM, Wu, J, Chen, T, Xu, Y
Ecotoxicology and environmental safety. 2020;:109937
Abstract
Growing epidemiological evidence has shown that exposure to polychlorinated biphenyls (PCBs) is harmful to the cardiovascular system. However, how PCB 118-induced oxidative stress mediates endothelial dysfunction is not fully understood. Here, we explored whether and how PCB 118 exposure-induced oxidative stress leads to NLRP3 inflammasome-dependent pyroptosis in endothelial cells. As expected, PCB 118 was cytotoxic to HUVECs and induced caspase-1 activation and cell membrane disruption, which are characteristics of pyroptosis. Moreover, PCB 118-induced pyroptosis may have been due to the activation of the NLRP3 infammasomes. PCB 118 also induced excessive reactive oxygen species (ROS) in HUVECs. The ROS scavenger (±)-α-tocopherol and the NFκB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs. Additionally, PCB 118-induced oxidative stress and pyroptosis were dependent on Aryl hydrocarbon receptor (AhR) activation and subsequent cytochrome P450 1A1 upregulation, which we confirmed by using the AhR selective antagonist CH 223191. These data suggest that PCB 118 exposure induces NLRP3 inflammasome activation and subsequently leads to pyroptosis in endothelial cells in vitro and in vivo. AhR-mediated ROS production play a central role in PCB 118-induced pyroptosis by priming NFκB-dependent NLRP3 expression and promoting inflammasome activation.
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10.
Systematic Review of the Literature of Factors Affecting the Exposure and the Levels of Lead in Human Breast Milk.
Cherkani-Hassani, A, Ghanname, I, Benitez-Rexach, AM, Mouane, N
Reviews of environmental contamination and toxicology. 2020;:97-129
Abstract
Human milk may sometimes contain chemical contaminants, which could have adverse effects on neonates or nursing infants. Lead (Pb) is of considerable interest due to its toxicity and occurrence. Furthermore, it has been suggested that human milk is a significant potential source of lead exposure to nursing infants. A systematic literature search in PubMed, Science Direct, and Google Scholar databases was performed to identify relevant studies, published in English until 2017, that investigated and explored common factors affecting the level of lead in human milk among lactating women around the world. Forty-nine papers were rated and explored the effect of one or several factors on the level of lead in human milk from 28 countries and carried out over a wide time frame from 1983 to 2017 and through Europe, Asia, America, and Africa, reviewing more than 5,000 subjects. Place of residence, maternal age, stage of lactation, smoking habits, maternal dietary intakes, and parity were the mostly assessed factors among the studies and considered as the main factors affecting Pb levels in BM. Other factors were not studied well enough and considered minor because few surveys evaluated their impacts. However, the literature findings are very controversial.