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      Fluoride contamination, consequences and removal techniques in water: a review

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          Abstract

          Fluoride contamination has created a drinking water crisis globally.

          Abstract

          Fluoride contamination has created a drinking water crisis globally. At low concentrations, its presence is essential; however, it becomes toxic to human beings upon consumption of more than 1.5 mg L −1 in mainly contaminated drinking water due to geochemical reactions and geological or anthropogenic factors. To better understand the toxicity of fluoride, in this study, we examine the recent research on the possible negative consequences of excess fluoride on diverse species. A high fluoride concentration in drinking water cause skeletal fluorosis and long-term kidney, brain, thyroid, and liver damages. This review also focuses on the different techniques for the defluoridation of water, such as electro-coagulation, adsorption, membrane processes, etc., and compares their adsorption capabilities under various situations, while their changes in the literature are reviewed. Furthermore, we present the advantages and disadvantages of different methods and conclude that each technique has shortcomings, with no single approach fitting all aspects. The condition of water pollution with fluoride and recently created technology to remove fluoride from water is evaluated, although research on fluoride contamination of water resources has been reviewed in the literature. Alternatively, this study also examines fluorosis mitigation strategies in the global and Indian settings and existing physicochemical and biological mitigation approaches. Also, the research and development results in fluoride clean-up are reviewed. Specifically, the following topics will be covered in this review: (1) fluoride contamination status, (2) consequences of fluoride contamination in drinking water on human health, and (3) current defluoridation technology.

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          New trends in removing heavy metals from industrial wastewater

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            Molecular mechanisms of fluoride toxicity.

            Halfway through the twentieth century, fluoride piqued the interest of toxicologists due to its deleterious effects at high concentrations in human populations suffering from fluorosis and in in vivo experimental models. Until the 1990s, the toxicity of fluoride was largely ignored due to its "good reputation" for preventing caries via topical application and in dental toothpastes. However, in the last decade, interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. In recent years, several investigations demonstrated that fluoride can induce oxidative stress and modulate intracellular redox homeostasis, lipid peroxidation and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response, metabolic enzymes, the cell cycle, cell-cell communications and signal transduction. The primary purpose of this review is to examine recent findings from our group and others that focus on the molecular mechanisms of the action of inorganic fluoride in several cellular processes with respect to potential physiological and toxicological implications. This review presents an overview of the current research on the molecular aspects of fluoride exposure with emphasis on biological targets and their possible mechanisms of involvement in fluoride cytotoxicity. The goal of this review is to enhance understanding of the mechanisms by which fluoride affects cells, with an emphasis on tissue-specific events in humans. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
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              Developmental neurotoxicity of industrial chemicals.

              Neurodevelopmental disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common, costly, and can cause lifelong disability. Their causes are mostly unknown. A few industrial chemicals (eg, lead, methylmercury, polychlorinated biphenyls [PCBs], arsenic, and toluene) are recognised causes of neurodevelopmental disorders and subclinical brain dysfunction. Exposure to these chemicals during early fetal development can cause brain injury at doses much lower than those affecting adult brain function. Recognition of these risks has led to evidence-based programmes of prevention, such as elimination of lead additives in petrol. Although these prevention campaigns are highly successful, most were initiated only after substantial delays. Another 200 chemicals are known to cause clinical neurotoxic effects in adults. Despite an absence of systematic testing, many additional chemicals have been shown to be neurotoxic in laboratory models. The toxic effects of such chemicals in the developing human brain are not known and they are not regulated to protect children. The two main impediments to prevention of neurodevelopmental deficits of chemical origin are the great gaps in testing chemicals for developmental neurotoxicity and the high level of proof required for regulation. New, precautionary approaches that recognise the unique vulnerability of the developing brain are needed for testing and control of chemicals.
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                Author and article information

                Contributors
                Journal
                ESANEB
                Environmental Science: Advances
                Environ. Sci.: Adv.
                Royal Society of Chemistry (RSC)
                2754-7000
                November 21 2022
                2022
                : 1
                : 5
                : 620-661
                Affiliations
                [1 ]Department of Civil Engineering, National Institute of Technology Patna, Patna - 800005, Bihar, India
                [2 ]Hyderabad Zonal Centre, CSIR-National Environmental Engineering Research Institute (NEERI), IICT Campus, Tarnaka, Hyderabad, Telangana, 500007, India
                Article
                10.1039/D1VA00039J
                7b3b47aa-5085-4d60-8433-31e03d922bf4
                © 2022

                http://creativecommons.org/licenses/by-nc/3.0/

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