Advanced Materials for Wastewater Treatment E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Serie: Advance Materials Series
- Sprache: Englisch
This comprehensive book deals with the use of novel materials such as plant-derived agents and advanced nanocomposites for the removal of heavy metals, nitrates, and synthetic dyes. Water is an essential component for living organisms on planet earth and its pollution is one of the critical global environmental issues today. The influx of significant quantities of organic and inorganic waste, sediments, surfactants, synthetic dyes, sewage, and heavy metals into all types of water bodies has been increasing substantially over the past century due to rapid industrialization, population growth, agricultural activities, and other geological and environmental changes. These pollutants are very dangerous and are posing serious threat to us all. Advanced Materials for Wastewater Treatment brings together innovative methodologies and research strategies to remove toxic effluents from wastewaters. With contributions from leading scientists from all around the world, the book provides a comprehensive coverage of the current literature, up-to-date overviews of all aspects of toxic chemical remediation including the role of nanomaterials. Together they showcase in a very lucid manner an array of technologies that complement the traditional as well as advanced treatment practices of textile effluents. In particular, the book provides: * Up-to-date overviews of all aspects of toxic chemical remediation * The role of plants and abundantly available agro-wastes in the remediation of wastewater * The removal of nitrates from wastewater using nanocomposites
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Veröffentlichungsjahr: 2017
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Contents
Cover
Title page
Copyright page
Preface
Chapter 1: Arsenic: Toxic Effects and Remediation
1.1 Introduction
1.2 Arsenic Concentration in Water
1.3 Exposure of Arsenic in Human Body
1.4 Metabolism and Excretion of Arsenious Compounds
1.5 Arsenic Toxicity and Mechanism
1.6 Detoxification of Arsenic
1.7 Arsenic Remediation Technologies
1.8 Adsorption and Recent Advancement
1.9 Conclusion
Acknowledgment
Abbreviations
References
Chapter 2: Recent Trends in Textile Effluent Treatments: A Review
2.1 Introduction
2.2 Industrial Dyes, Dying Practices, and Associated Problems
2.3 Wastewater Remediation
2.4 Physical Methods
2.5 Chemical Methods
2.6 Bioremediation
2.7 Products Recognition and Mechanisms of Dye Degradation
2.8 Conclusion
2.9 Future Outlook
References
Chapter 3: Polyaniline as an Inceptive Dye Adsorbent from Effluent
3.1 Introduction
3.2 Pollution Due to Dyes
3.3 Methods Used for the Dye Removal
3.4 Adsorption Kinetics
3.5 Polyaniline: An Emerging Adsorbent
3.6 Conclusion
References
Chapter 4: Immobilized Microbial Biosorbents for Wastewater Remediation
4.1 Introduction
4.2 Immobilized Microbial Biosorbent
4.3 Biosorption Mechanism
4.4 Conclusion
References
Chapter 5: Remediation of Cr (VI) Using Clay Minerals, Biomasses and Industrial Wastes as Adsorbents
5.1 Introduction
5.2 Isotherm Models
5.3 Thermodynamics of Adsorption
5.4 Kinetics of Adsorption
5.5 Solution pH
5.6 Clay Minerals
5.7 Biomasses
5.8 Industrial Wastes
5.9 Conclusion
References
Chapter 6: Microbial Diversity as a Tool for Wastewater Treatment
6.1 Overview of Wastewater; Sources, Pollutants, and Characteristics
6.2 Role of Dominant Wastewater Treatment Communities in Biodegradation
6.3 Methods for the Treatment of Wastewater
6.4 Conclusion
References
Chapter 7: Role of Plant Species in Bioremediation of Heavy Metals from Polluted Areas and Wastewaters
7.1 Introduction
7.2 Heavy Metals (HM) Worldwide
7.3 Allochthonous and Autochthonous Plants
7.4 Phytoremediation of Heavy Metals (HM)
7.5 Methodology
7.6 Analysis of Research on Heavy Metals (HM) and Native and Endemic Plant Species
7.7 Results
7.8 Conclusion
References
Chapter 8: Bioremediation: A Green, Sustainable and Eco-Friendly Technique for the Remediation of Pollutants
8.1 Introduction
8.2 Immobilization
8.3 Enzyme Immobilization Strategies
8.4 Adsorption
8.5 Entrapment
8.6 Encapsulation
8.7 Covalent Binding
8.8 Self-Immobilization
8.9 Properties of Immobilized Enzymes
8.10 Enzymes Sources
8.11 Conditions for Lipid Degradation
8.12 Environmental Applications of Ligninolytic Enzymes
8.13 Conclusions
References
Chapter 9: Role of Plant-Based Biochar in Pollutant Removal: An Overview
9.1 Introduction
9.2 Preparation Methods of Biochar
9.3 Physico-chemical Characterization of Plant-Based Biochar
9.4 Biochar for Heavy Metal Removal
9.5 Biochar for Dye Removal
9.6 Biochar for Fluoride Removal
9.7 Biochar for Persistent Organic Pollutant Removal
9.8 Biochar for Other Pollutant Removal
9.9 Biochar for Soil Treatment/Improvement
9.10 Conclusion
Acknowledgments
References
Chapter 10: A Review on Ferrate(VI) and Photocatalysis as Oxidation Processes for the Removal of Organic Pollutants in Water and Wastewater
10.1 Introduction
10.2 Ferrate(VI)
10.3 Photocatalysis
10.4 Combination of Photocatalysis (UV/TiO
2
) and Ferrate(VI)
10.5 Conclusions
References
Chapter 11: Agro-Industrial Wastes Composites as Novel Adsorbents
11.1 Introduction
11.2 Material and Methods
11.3 Results and Discussion
11.4 Conclusion
References
Chapter 12: A Review on the Removal of Nitrate from Water by Adsorption on Organic–Inorganic Hybrid Biocomposites
12.1 Introduction
12.2 Adsorbents for the Removal of Nitrate from Water
12.3 Models for Adsorption Process
12.4 Column Study
12.5 Conclusion
Nomenclatures
References
Chapter 13: Nitrate Removal and Nitrogen Sequestration from Polluted Waters Using Zero-Valent Iron Nanoparticles Synthesized under Ultrasonic Irradiation
13.1 Introduction
13.2 Materials and Methods
13.3 Results and Discussion
13.4 Conclusion
Acknowledgments
References
Index
End User License Agreement
Guide
Cover
Copyright
Contents
Begin Reading
List of Illustrations
Chapter 1
Figure 1.1
Effects of arsenic.
Figure 1.2
Arsenic methylation pathway in the human body (a): Arsenate reductase or purine nucleoside phosphorylase (PNP), (b): Arsenite methyl transferase (As3MT), (c): Glutathione S-transferase omega 1 or 2 (GSTO1, GSTO2), and (d): Arsenite methyl transferase (As3MT), MMA(V): Monomethylarsenic acid, MMA(III): Monomethylarsonous acid, DMA(V): Dimethylarsenic acid.
Figure 1.3
Toxicity trends of arsenic.
Figure 1.4
Representation of sulfhydryl-arsenic bonding.
Figure 1.5
Detoxification of arsenite oxy anions by lipoic acid.
Figure 1.6
Excreted arsenite chelate complex.
Chapter 2
Figure 2.1
Flow chart showing the process carried in textile industry.
Figure 2.2
A description of the individual operations that are performed on cotton textile and the main pollutants that result from each operation.
Figure 2.3
The chemical composition of man-made dyes mostly used in the textile industry.
Figure 2.4
The mechanisms of light induced degradation of dyes (a) photocatalysis, (b) dye sensitization followed by dye degradation, (c) dye sensitization followed by reduction of a second molecule, and (d) degradation by coupled semiconductors under visible light [10].
Figure 2.5
Mechanism for reduction of azo dye.
Chapter 3
Figure 3.1
Effect of pH on adsorption of tartrazine dye onto polyaniline-coated sawdust (PANI/SD) [154] and PANI/Al
2
O
3
composite [194].
Figure 3.2
Adsorption capacity of different adsorbents for methylene blue dye: polyaniline nickel ferrite nanocomposite (PNFN) [184], Polyaniline-coated sawdust of wood (PCSD1) [185], Polyaniline nanotube base (PNB) [186], Polyaniline-coated sawdust of walnut (PCSD2) [193].
Figure 3.3
Variation in adsorption of congo red dye by HCl and PTSA-doped polyaniline (HCl/PTSA-doped PANI) [210], Polyaniline/chitosan composite (Pn/Ch Composite) [167], polyaniline [211] polyaniline momtmorrillonite composite (PANi-MMT composite) [212].
Figure 3.4
Adsorption capacity of PANI-coated sawdust for different dyes: Eosin Y (EY) [158], methylene blue (MB) [193], methyl orange (MO) [187], reactive orange 16 (RO16) [189], reactive orange 4 (RO4) [215], acid violet 49 (AV49) [139], direct green 6 (DG6) [189].
Chapter 4
Figure 4.1
Copper and cadmium sorption on the modified and pristine biomass at different controlled pHs during the adsorption process. (Reprinted from [15] with permission, Copyright © 2005 American Chemical Society.)
Figure 4.2
Diagram of U(VI) biosorption mechanisms onto the
Pseudomonas putida
@ chitosan bead (PICB). (Reprinted from [62] with permission from Elsevier.)
Figure 4.3
Schematic representation of several mechanisms of heavy metal translocation, sequestration, and uptake in living (Left), as well as, nonliving (Right, brown shaded) microalgae; including Me
n+
-Metal ion, L-liquid(Me
n+
+ L represents metal ion in liquid); Metal-ion transporters (such as NRAMP, CTR, ZIP, and FTR); Phytochelatinbio-synthesis pathway, PC complexes, and enzymes involved in the PC synthesis (GCS-glutamyl–cysteinyl synthase, GS-Glutathione synthase, PCS-phytochelatin synthase); AA-Amino Acids; OA-Organic Acids; LMWPC-MeC-Low Molecular Weight Phytochelatin Metal Ion Complexes; HMWPC-MeC-High Molecular Weight Phytochelatin MetalIon Complexes; MTP-Metallothionein Protein; SA-surface adsorption; P-Precipitation; IE-Ion Exchange; CC-Complexation and Chelation and PD-Passive diffusion. (Reprinted from [17] with permission from Elsevier.)
Figure 4.4
Probable mechanism for sorption and desorption of uranium(VI) with
Penicillium chrysogenum
on activated silica.
Chapter 5
Figure 5.1
Eh-pH diagram of chromium [5].
Figure 5.2
Speciation diagram of Cr (VI) [7].
Figure 5.3
(a) Development of positive charges on the surface of adsorbent at pH < 7.0 and electrostatic attraction of negatively charged Cr (VI) species. (b) Competition between CrO
4
2–
species and OH
–
ions at pH > 7.0. (c) Development of surface positive charges at pH < pH
ZPC
of the adsorbent causing electrostatic attraction of Cr (VI) species for the surface of adsorbent. (d) Development of negative surface charges at pH > pH
ZPC
causing electrostatic repulsion of Cr (VI) species from the surface of adsorbent.
Figure 5.4
Adsorption of Cr (VI) onto natural clay minerals.
Figure 5.5
Road map showing increasing order of adsorption capcpities of clay minerals, modified clay minerals, biomass and industrial wastes for remediation of Cr (VI).
Chapter 6
Figure 6.1
(a) prokaryotic cells and (b) Eukaryotic (E.M.Armstrong, 2001).
Figure 6.2
Binary fission and cell separation.
Figure 6.3
Structure of simple amino-acid (glycine).
Figure 6.4
Schematic diagram of deamination of sulfur amino-acid (cysteine).
Figure 6.5
Dissimmilaterity nitrate.
Figure 6.6
Flowsheet diagram of A/O process.
Figure 6.7
Flowsheet diagram of Phostrip process.
Figure 6.8
Trickling filter for wastewater treatment
Figure 6.9
Activated sludge process flowsheet.
Chapter 9
Figure 9.1
Schematic overview of plant-based biochar applications.
Chapter 10
Figure 10.1
Road map of the chapter.
Figure 10.2
Spectra of ferrate(VI) in Milli-Q water.
Figure 10.3
Speciation of ferrate(VI) [31].
Chapter 11
Figure 11.1
(a) Structure of Congo Red; (b) biomasses screening for Congo Red dye adsorption (sugarcane baggase, peanut hull, cotton stick, and rice bran).
Figure 11.2
CR dye adsorption on composites (bagasse with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and baggase native rice biomass; A: Effect of pH; B: Effect of adsorbent dose.
Figure 11.3
CR dye adsorption on composites (bagasse with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and baggase native rice biomass; A: Effect of contact time; B: Effect of CR initial concentration; and C: Effect of temperature.
Figure 11.4
(A–F) Pseudo-first-order plots (log) for CR dye adsorption on composites (baggase with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and native bagasse biomass.
Figure 11.5
(A–F) Pseudo-second-order plots for CR dye adsorption on composites (baggase with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and native bagasse biomass.
Figure 11.6
(A-F) Intraparticle diffusion model plots for CR adsorption on composites (bagasse with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and native bagasse biomass.
Figure 11.7
(A–F) Langmuir isotherm model curves (Ce/qe (g/L) versus Ce (mg/L)) CR adsorption on composites (bagasse with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and native bagasse biomass.
Figure 11.8
(A–F) Freundlich isotherm model curves CR adsorption on composites (bagasse with polyaniline, starch, pyrrole, chitoson/aniline and chitoson/pyrrole) and native bagasse biomass.
Figure 11.9
ln Kc versus 1/T (Arrhenius plot) for thermodynamic study.
Chapter 12
Figure 12.1
Preparation of ChAl composite.
Chapter 13
Figure 13.1
XRD patterns of the samples prepared under liquid-phase reduction (nZVI
LPR
) and under a combination of liquid-phase reduction-ultrasonic irradiation (nZVI
UI
).
Figure 13.2
TEM images and SAED patterns of the prepared samples without (a and c) and with (b and d) ultrasonic irradiation.
Figure 13.3
Nitrogen Adsorption-desorption isotherms of the nZV
I and
nZVI
LPR
samples.
Figure 13.4
S/N ratios of the reaction time effect on the nitrate removal (a) and the S/N ratios belonging to different types of nanomaterials used including nZVI
LPR
and nZVI
UI
(b). The circles represent the optimal levels of the factors.
Figure 13.5
S/N ratios of effects of the reaction time (min) (a) and the types of nanomaterials (including nZVI
LPR
and nZVI
UI
) (b) on the nitrite production as a possible end-product of the nitrate removal by nano zero-valent iron particles.
Figure 13.6
Raman Spectrum of the nitrate solution after 120 min of treatment with nZVI
UI
.
Figure 13.7
Nitrate removal by the sample prepared under ultrasonic irradiation (nZVI
UI
) (a). (b) indicates the percentage of the nitrogen converted to the final products. The lines and represent the conversion (%) of the initial nitrate to ammonium ion and to nitrite, respectively, measured in the reaction solution. The line represents the conversion (%) of the initial nitrate to nitrogen which was calculated based on the shares of other end-products of the reaction.
Figure 13.8
XRD (a) and EDX (b) patterns of the synthesized struvite.
Figure 13.9
SEM images of the struvite prepared in this study.
List of Tables
Chapter 1
Table 1.1
Techniques utilized for arsenic removal.
Table 1.2
Adsorbents utilized for arsenic removal.
Chapter 2
Table 2.1
Advantages and disadvantages of dye treatment technologies.
Chapter 3
Table 3.1
Different effluent treatment techniques and their advantages and disadvantages [71].
Table 3.2
Different adsorbents used for the dye removal from industrial effluent.
Table 3.3
Effect of initial dye concentration on the adsorption using different adsorbents.
Table 3.4
Effect of pH on the adsorption of dyes on different adsorbents.
Table 3.5
Percentage adsorption of different dyes with the varying adsorbent dosage.
Table 3.6
Work done by different researchers on polyaniline as adsorbent.
Chapter 4
Table 4.1
The maximum adsorption capacity and experimental condition used for the removal of heavy metals various algae-based biosorbent.
Table 4.2
The maximum adsorption capacity and experimental condition used for the removal of heavy metals various bacteria-based biosorbent.
Table 4.3
The maximum adsorption capacity and experimental condition used for the removal of heavy metals various fungi-based biosorbent.
Chapter 5
Table 5.1
Maximum adsorption capacity, optimum adsorption conditions like pH, temperature, initial Cr(VI) concentration, adsorbent dose, fitted isotherm, kinetic model, thermodynamic parameters and mechanism of adsorption of clay minerals.
Table 5.2
Maximum adsorption capacity, optimum adsorption conditions like pH, temperature, initial Cr(VI) concentration, adsorbent dose, fitted isotherm, kinetic model, thermodynamic parameters and mechanism of adsorption of biomass.
Table 5.3
Maximum adsorption capacity, optimum adsorption conditions like pH, temperature, initial Cr(VI) concentration, adsorbent dose, fitted isotherm, kinetic model, thermodynamic parameters and mechanism of adsorption of industrial wastes.
Chapter 7
Table 7.1
Number of metal hyperaccumulator plants.
Table 7.2
Endemic and native vegetation species studied in terms of heavy metals.
Chapter 8
Table 8.1
Reported strategies of enzyme immobilization and effect of immobilization on enzymes.
Table 8.2
Advantages and drawbacks of the four basic immobilization methods.
Table 8.3
Bacterial strains, isolated from different sources, indicating lipolytic activities for lipids.
Table 8.4
Optimized conditions for some lipolytic bacterial strains.
Table 8.5
Reported dyes decolorization efficiency of free and immobilized enzymatic systems.
Table 8.6
Industrial wastes and microbial degradation.
Table 8.7
Application of enzymes in different industrial sectors.
Chapter 9
Table 9.1
Plant material used for biochar production.
Table 9.2
Physicochemical characteristics of plant-derived biochar.
Chapter 10
Table 10.1
Redox potentials for oxidants/disinfectants used in water and wastewater treatment [26–29].
Table 10.2
Efficiency and operational conditions of electrochemical production of ferrate(VI).
Table 10.3
Spectrophotometric methods for ferrate(VI) determination in water [29, 40, 45].
Table 10.4
Apparent second-order rate constants (
k
app
) of the oxidation of PPCPs and EDCs by Fe(VI) at room temperature.
Table 10.5
Stoichiometry of oxidation of organic molecules by Fe(VI) at room temperature.
Table 10.6
Removal of PPCPs and EDCs spiked in real wastewater by Fe(VI).
Table 10.7
Hailsham North Wastewater Treatment Plant of Southern Water Ltd of UK – Pilot scale – performance at 0.03 mg of online and electrochemically produced Fe(VI)/L [36].
Table 10.8
Performance of commercial and electrochemically produced (using NaOH and KOH) Fe(VI) – samples taken from Wastewater Treatment Plant Degremont, in Culiacan city, in Mexico [37].
Table 10.9
Performance (in removal of DOC) of Fe(VI) in comparison with ferric sulfate [24].
Table 10.10
Performance of Fe(VI) in comparison with aluminum and ferric sulfate [94].
Table 10.11
Estimated cost of different water treatment processes [115].
Table 10.12
Comparison of
κ
value in m
2
/m
3
for different types of reactors [116].
Table 10.13
Comparison of reactor specifications of CAR, TLR, and MTR[114].
Table 10.14
Common semiconductors used in photocatalysis [122].
Table 10.15
Extracts used as natural dyes for dye-sensitization [159].
Table 10.16
Photo catalytic degradation of Phenol with different modified photocatalysts [167].
Table 10.17
Pollutants are enabled to Fe(VI)-enhanced photo catalytic oxidation.
Chapter 11
Table 11.1
Adsorption capacities of various composites for the adsorption of dyes and present investigation (polyaniline, starch, polypyrrole, chitoson/aniline and chitoson/pyrrole composites).
Table 11.2
Adsorption capacities of various composites for the adsorption of metal ions and present investigation (polyaniline, starch, polypyrrole, chitoson/aniline and chitoson/pyrrole composites).
Table 11.3
Adsorption capacities of various composites for the adsorption of ions and organic compounds.
Table 11.4
Thermodynamics parameters of congo red dye adsorption on native and composites adsorbents.
Chapter 12
Table 12.1
Nitrate removal.
Table 12.2
Summary of adsorbents for nitrate removal.
Chapter 13
Table 13.1
Recent applications of different methods for the removal of nitrate from polluted waters.
Table 13.2
L8 orthogonal array of experiments.
Table 13.3
Signal to noise ratio, factor effect and ranking for each factor.
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Advanced Materials for Wastewater Treatment
Edited by
Shahid-ul-Islam
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Library of Congress Cataloging-in-Publication Data ISBN 978-1-119-40776-8
Preface
Water is an essential component for living organisms on planet earth and its pollution is one of the critical global environmental issues today. The influx of significant quantities of organic and inorganic waste, sediments, surfactants, synthetic dyes, sewage, and heavy metals into all types of water bodies has been increasing substantially over the past century due to rapid industrialization, population growth, agricultural activities, and other geological and environmental changes. These pollutants are very dangerous and are posing serious threat to us all.
Currently, a number of methods including ion exchange, membrane filtration, advanced oxidation, biological degradation, photocatalytic degradation, electro-coagulation, and adsorption are in operation for removing or minimizing these wastes. This book on Advanced Materials for Wastewater Treatment brings together innovative methodologies and research strategies that remove toxic effluents from wastewaters through fourteen important chapters written by leading scientists working in this field. I have no doubt that readers of this book will benefit from its comprehensive coverage of the current literature, up-to-date overviews of all aspects of toxic chemical remediation, including the role of nanocomposites. Together they showcase in a very lucid manner an array of technologies that complement the traditional as well as advanced treatment practices of textile effluents. I would also like to thank all the authors who contributed chapters to this book and provided their valuable ideas and knowledge. I am also very thankful to the publishers and, in particular, Martin Scrivener, for their generous cooperation at every stage of the book’s compilation and production.
Shahid-ul-Islam Indian Institute of Technology Delhi (IITD), Hauz Khas, New Delhi, India August 2017
Chapter 1Arsenic: Toxic Effects and Remediation
Sharf Ilahi Siddiqui and Saif Ali Chaudhry*
Environmental Chemistry Research Laboratory, Department of Chemistry, Jamia Millia Islamia, New Delhi, India
*Corresponding author: [email protected]
Abstract
Arsenic is associated with cancerous and non-cancerous human diseases. Arsenic from drinking water is the most common source of human exposure and it has becomes major calamity for the world. Pentavalent arsenic, As(V), can be reduced to trivalent arsenic, As(III), in the blood, which is transferred to the liver and metabolized. Arsenic produces various toxic intermediates during the metabolism, and is generally excreted from lever via urine. But on the high exposure, it retains in body and binds to soft or hard tissue. Arsenic replaces the phosphate group, which is involved in various biological pathways, inhibits glucose transporters, alters expression of genes, and can stimulate oxidative stress. This chapter enlighten the toxicity of arsenic toward living cell. Previous literatures evaluated the toxicity profiles of inorganic arsenate, arsenite and methylated metabolites, pentavalent monomethylarsonic acid (MMAV), and dimethylarsinic acid (DMAV). This chapter discusses the recently identified toxic trivalent forms of methylated metabolites. Several detoxifying nutritional supplements are also highlighted. The remediation of arsenic from drinking water is also depicted.
Keywords: Arsenic exposure, metabolism and excretion, toxicity, de-toxification, adsorption
1.1 Introduction
Industrial wastewater released in freshwater without proper treatment causes the contamination in freshwater which responds to various aquatic problems. Pesticides, fertilizers, suspended solids, color stuffs, and toxic metals, etc., are well-known water pollutants that change the quality of freshwater [1]. Natural activities are also involved in the water contamination. Heavy metals, particularly arsenic in water, is creating more serious environmental problems for various continents, particularly Asia. Millions of people from Asian countries are living in the zone of arsenic poisoning [2].
The regular exposure to arsenic containing water is associated with toxicity and harzardous effects toward human health. It is a major calamity for various countries viz Bangladesh, India, Nepal, China, Taiwan, Thailand, Mexico, Japan, and Argentina [3]. In Bangladesh alone, millions of people have died due to arsenic poisoning and are living under the same threat. Over all, more than 140 million people from 70 countries are living in these conditions. [4].
Poisoning and toxicity of arsenic is the resulting effect of regular and high exposure of arsenic contaminated water. When arsenic becomes concentrated in human body, it accumulates in the tissues, binds to sulfhydryl sites, changes their functioning, and causes various damages. These damages have been discussed in literature [5].
To overcome these major environmental problems, concerning agencies from various countries are spending large amounts of money to control the arsenic discharge in freshwater and are collecting data of arsenic concentration in their aquatic environment. This step provides the proper way of controlling the high concentration of arsenic in water and to save the water from arsenic contamination. Various environmental agencies gave the maximum limit of arsenic 0.01 mg/L in water for safe drinking [3].
1.2 Arsenic Concentration in Water
Human activities such as mining, smelting, fossil fuel combustion, pesticides, and fertilizers are the major cause of high arsenic concentration in water [6]. Tailing is a waste that comes from mining which responds to 200 mg/L concentration of arsenic in water, whereas the pesticides and fertilizers formulated with arsenic responds to 612 × 108 g/year and 2380 × 108 g/year of arsenic discharge in water through soil erosion and leaching, respectively [7, 8]. Moreover, more than 200 arsenic containing minerals, particularly sulfide minerals contribute to direct or indirect releasing of arsenic in water [9]. Therefore, nearby areas of mining and mineralizing are under arsenic threat, where the concentration of arsenic rises up to 100–5000 mg/L in water [10]. Generally, natural water acquires arsenic in the range 1 and 2 mg/L, although it may be high up to 12 mg/L in areas containing natural sources [10]. Therefore, the concentration of arsenic in water becomes much higher than the maximum limit of arsenic in water fixed by WHO. More than 100 million of people are drinking arsenious water with a concentration of more than 0.01 mg/L.
High concentration of arsenic beyond WHO guidelines maximum permissible value (0.01 mg/L) has been reported from number of countries such as Indo-Bangladesh region (0.8 mg/L), Argentina (0.2 mg/L), Mexico (0.4 mg/L), and Taiwan (0.05–2.0 mg/L) [11]. –3, 0, +3, and +5 are the major oxidation states of arsenic. Last two oxidation states of arsenic named arsenite (As(III)) and arsenate (As(V)) are generally isolated from the water, which are stable in reducing and oxidizing environments, respectively [12].
Previous reports show that As(III) strongly binds to sulfhydryl sites of proteins and is considered to be the most toxic. As(V) also causes the large poisoning in body. As(III) and As(V) are the arsenic species found in water in the form of either oxy ions or organic and inorganic molecules [13]. Inorganic forms of arsenic are 100 times more toxic than organic forms. Inorganic and organic forms of arsenic in water are the result of pH and redox potential of water [14].
Reports from various regions suggest that the high level exposure of arsenic is associated with various adverse health effects such as cancer, diabetes, hypertension, neurological arteriosclerosis, and cardiovascular diseases [15, 16] (Figure 1.1). Arsenic induces the alteration in the cell calcium signalling, oxidative stress, impairment of cell mitochondrial function, and cell cycle progression where these effects ultimately lead to cancer [17].
Figure 1.1 Effects of arsenic.
1.3 Exposure of Arsenic in Human Body
Arsenic can enter into the human body via ingestion, inhalation, and skin absorption [18]. The ingestion of arsenic through drinking water is considered as a major source of arsenic concentration into body and their toxicity [19]. Aresnic has normal behavior toward body and is easily absorbed by the blood stream from gastrointestinal tract or lungs on ingestion into the body [20]. As(V) molecules are less reactive with membranes of the gastrointestinal tract than As(III), hence, As(V) completely absorbed by blood stream from gastrointestinal tract. In blood stream (erythrocytes), arsenic bounds to the globin, and circulates in various parts of human body viz bones, muscles, lungs, kidneys, across the placenta, and keratinrich tissues such as skin nails and hair [21].
1.4 Metabolism and Excretion of Arsenious Compounds
The liver is the major part of the body where arsenic metabolism occurs. Primarily, metabolism of arsenic is to be considered as normal way of arsenic detoxification but recent studies suggest that intermediates of metabolism induce the toxicity [22]. Briefly, in the arsenic metabolism, ingested As(III) or As(V) molecules convert into the methylated metabolite and inorganic arsenicals [23]. Arsenic metabolism is an enzyme-induced biochemical reaction, where As(V) first reduced to As(III) by glutathione enzyme then methylation of arsenic takes place, and S-adenosylmethionine (SAM) works as methyl donor and glutathione sulfhydryl works as a vital co-factor [24].
The monomethylarsenic acid (MMA) and dimethylarsenic acid (DMA) are the resulting products of methylation of As(III) formed through the enzymatic transfer of the methyl group from SAM to methyl arsenate and dimethyl arsenate [20] (Figure 1.2). MMA is more toxic intermediate than DMA [25]. MMA and DMA are more toxic than other inorganic or organic arsenic molecules [26] (Figure 1.3). Dimethylmonothioarsenic acid (DMMTAV), Dimethyldithioarsenic acid (DMDTAV), arsenosugars, and arsenobetaines are other reported intermediate metabolites of arsenic [26]. The distribution and metabolism of DMMTAV and DMDTAV are similar to DMAIII and DMAV, respectively [27]. DMMTAV is reported as more toxic than DMDTAV [28]. Arsenosugars and arsenobetaines are the products of inorganic arsenic consumed by marine organism [29].
Figure 1.2 Arsenic methylation pathway in the human body (a): Arsenate reductase or purine nucleoside phosphorylase (PNP), (b): Arsenite methyl transferase (As3MT), (c): Glutathione S-transferase omega 1 or 2 (GSTO1, GSTO2), and (d): Arsenite methyl transferase (As3MT), MMA(V): Monomethylarsenic acid, MMA(III): Monomethylarsonous acid, DMA(V): Dimethylarsenic acid.
Figure 1.3 Toxicity trends of arsenic.
Generally, the ingested arsenic molecules excrete from liver through urine either as as-ingested form or as methylated intermediate [30]. Skin arsenic excretes in lower rate than other organs. Blood arsenic excretes most rapidly from the human body, where 50–90% of arsenic excretes within 2–4 days, while remainder excretes slowly [20]. The excess level of arsenic in the blood stream is associated with the retention of arsenic in tissues and its toxicity [13].
1.5 Arsenic Toxicity and Mechanism
Arsenic induces various types of target-based toxicity such as arsenic-induced cardiovascular dysfunction, diabetes mellitus, neurotoxicity, nephrotoxicity, hepatotoxicity, and carcinogenicity [31]. The mechanism of arsenic toxicity is discussed below.
1.5.1 Oxidative Stress
Arsenic causes various adverse health effects by inducing high oxidative stress which affect the antioxidant enzymes found in the body. Arsenic stimulates the production of reactive oxygen species (ROS) and induces the toxicity [32]. The abnormal electron transfer through respiratory organ to mitochondrion of cell is responsible for generating the ROS in mitochondrion followed by the production of hydrogen peroxide (H2O2), superoxide anion (O2−), and hydroxyl radicals (OH−) [33].
The electrons passed through the respiratory organ to mitochondrion of cell trigger the molecular oxygen (O2) to form superoxide anion (O2−) and then dismutate to H2O2. H2O2 is the result of production of methylated metabolites such as dimethylarsinic radicals [(CH3)2As•] and dimethylarsinic peroxyl [(CH3)2AsOO•], during the oxidation of As(III) to As(V) [34]. Therefore, the free radicals generation during inorganic arsenic metabolism is responsible for oxidative stress.
The oxidative stress directly depend on the ingestion level of arsenic in the body, the excess level of arsenic in the cell, consumed oxygen by the cell, resulting the increased ROS production and oxidative stress [32]. Excess level of ROS is responsible for the oxidative damages in cellular and metabolism system which causes the physiological abnormalities and deleterious chronic disorders. Hemeoxygenase-1 (HO-1) is also responsible for the ROS generation which produces the free iron. The resulting free iron takes part in the Fenton reaction and forms the hydroxyl free radical (•OH) [35]. This free radical may attack DNA and impart the adverse effect to health [36].
Recently, Zhao et al. [37] investigated the effect of arsenic exposure on the nervous system of Gallus Gallus in response to oxidative stress and heat shock proteins (Hsps). Histological changes in the antioxidant enzyme activity, and the expressions of Hsps on arsenic exposure were observed. The malondialdehyde (MDA) content was increased on increasing arsenic dose while the activities of Glutathione peroxidase (GSH-Px) and catalase (CAT) were decreased. Moreover, the change in the expression of Hsps and Hsp60 and Hsp70 were also observed. Therefore, they suggested that subchronic exposure to arsenic-induced neurotoxicity in chickens was due to the disturbance in oxidative stress.
The human endothelial cell apoptosis, inflammation, oxidative stress, and nitric oxide (NO) production were also affected by the excessive amount of arsenic (5 µM of As2O3) [38]. Result showed that arsenic induced the significant enhancement in endothelial cell apoptosis and inflammation as indicated by the increase of mRNA and protein expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and pentraxin 3. Moreover, the exposure of arsenic also increased the intracellular ROS. The change in the activity of NADPH oxidase (NOX) and up-regulated mRNA expression of NOX subunits p22phox were also investigated. Oxidative stress and impaired NO production are involved in their pro-inflammatory and pro-apoptotic effects. Similarly, arsenic-induced oxidative stress was also observed in human embryonic kidney (HEK) cells and HaCaT cells [39]. ROS can alter the expression of atherosclerosis-related genes and stimulate the various cell signals by the oxidation of sulfhydryl groups and by changing the intracellular redox status [40–43].
1.5.2 Binding to Sulfhydryl Group
Arsenic shows the high binding affinity for vicinal thiol sites of enzyme, which inhibits their catalytic activities and induce the toxicity (Figure 1.4). The complexes between arsenic and vicinal thiol are generally stable [44]. Generally, arsenic decreases the cellular-reduced glutathione (GSH) level through the reduction of As(V) to As(III), where GSH functions as an electron donor or through arsenic-induced free radical oxidize GSH. Arsenic also decreases the cellular GSH level through binding to their sulfhydryl sites. In comparison to As(V), As(III) easily and strongly bind to sulfhydryl sites of reduced glutathione (GSH) [45]. Monomethylarsonous acid, MMA(III) also affect the functioning of GSH and thioredoxin reductase on thiol binding [46].
Figure 1.4 Representation of sulfhydryl-arsenic bonding.
The arsenic exposure also reduces the generation of ATP in Kreb’s cycle due to their high binding affinity for vicinal thiols sites of enzymes such as GSH resulting the cell damage and death [46]. Moreover, arsenic may bind to the thiol sites of pyruvate dehydrogenase and ketoglutarate dehydrogenase enzyme. The presence of arsenic also disturbs the cellular redox condition which leads to cytotoxicity, synthetic peptides based on the Zn finger region, and the estrogen binding region of the human estrogen receptor-α which contributes to carcinogenicity, tubulin, poly(ADP-ribose) polymerase (PARP-1), thioredoxin reductase, estrogen receptor-alpha, arsenic(+3)methyltransferase, and Keap-1 which leads to the several genetic effects and human breast cancer cell line MCF-7 [47–50].
1.5.3 Replacement of Phosphate Group
Structure and the properties of As(V) resembles to the phosphate anion thus the presence of As(V) disturb the various biochemical reactions viz glycolysis, glycogenesis, gluconeogenesis and glycogenolysis, and pentose phosphate pathway (PPP), which involves the glucose-6-phosphate and 6-phosphogluconate as essential mediator [51]. In vitro, As(V) replaces the phosphate group of glucose-6-phosphate and 6-phosphogluconate during the biochemical reactions and form glucose-6-arsenate and 6-arsenogluconate. Simply, arsenic competes with the phosphate binding sites [52]. The phosphate group involved in the sodium pump and anion exchange transport system of human erythrocytes is also replaced by arsenate [53]. Studies reported that the production of adenosine-tri-phosphate (ATP) during the glycolysis is stopped due to the production of adenosine-tri-arsenate on the replacement of phosphate by As(V) [20]. Generally, 1,3-diphospho-D-glycerate is formed during the glycolysis process by enzymatical addition of phosphate anion to D-gylceraldehyde-3-phosphate. However, in the presence of As(V), one of the phosphate group of 1,3-diphospho-D-glycerate is replaced by the As(V) and form the unstable anhydride named 1-arsenato-3-phospho-D-glycerate, which later easily hydrolyze into As(V) and 3-phosphoglycerate due to the longer As-O bond length [51]. The replacement of phosphate group by As(V) is known to be as arsenolyis.
Decrease in the ATP generation on As(V) exposure was also observed from human and rabbit erythrocytes [54, 55]. Similarly, in mitochondrion of cell, during the oxidative phosphorylation, adenosine-5′-diphosphate (ADP-phosphate) is replaced by ADP-arsenate in the presence of succinate [52, 54]. Moreover, the production of nicotinamide adenine dinucleotide phosphate (NADPH) and glucose-6-phosphate dehydrogenase (G6PDH), an enzyme of pentose phosphate pathway (PPP), are also reduced on exposure to arsenic [20].
1.5.4 Alternation in the Gene Expression
It has been investigated that arsenic can induce the alteration in gene expression [55]. The ingestion of 5 mol/L of As(III) in rat pancreatic cells decreased the mRNA expression. 6 mol/L of As(III) exposed in mouse adipocytes cell altered the gene expression of peroxisome proliferative-activated receptor (PPAR), and high level exposure of As(III) in human adipocyte cells, decreased the expression of AKT genes [56–58]. AKT gene expression is also altered on the ingestion of As(III) into 3T3-L1 adipocytes cell [59]. It also has been reported that As(III) can inhibit the activation of AKT gene. Similarly, exposure of 0.1 and 5mol/L As(III) in human GM847 fibroblast cells caused the alteration of expression of c-fos and c-jun genes, respectively [60].
Moreover, increased expression was also observed in phosphoenol pyruvate carboxykinase (PEPCK) gene on the As(III) ingestion in chick embryos [61, 62]. The immunomodulatory effect of arsenic on cytokine and HSP gene expression in Labeo rohita fingerlings were also investigated [63]. Furthermore, down regulates in the gene expression at the postsynaptic density in mouse cerebellum on arsenic exposure were also observed [64]. Arsenic ingestion is also associated with decreased gene expression and increased DNA methylation in peripheral blood cells in women [65]. Moreover, the low dose of inorganic arsenic, 50 µg/L arsenic trioxide for 90 days, changed the antioxidant genes expression and also triggered the oxidative stress in Zebrafish brain [66].
1.5.5 Arsenic Impairs Glucose Catabolism
It has been reported that arsenic may disturb the glucose metabolism pathway and insulin signalling [67]. Numerous enzyme complexes such as succinyl Co-A synthase, ketoglutarate dehydrogenase, and pyruvate dehydrogenase (PDH) are involved in the glucose metabolism [68]. As(III) may inhibit their function on binding [22].
Generally, PDH enzyme complex viz dihydrolipoyl transacetylase, dihydrolipoyl dehydrogenase, pyruvate decarboxylase, thiamine pyrophosphate, lipoic acid, CoASH, FAD, and NAD+ are most sensitive to As(III) [69]. PDH inhibition in the presence of As(III) was reported on the result of binding between As(III) and lipoic acid moiety [70]. However, MMAIII were reported as stronger inhibitor of PDH than As(III) [69]. Moreover, phenylarsine oxide (PAO), an organic arsenic species, inhibits the basal or insulin stimulated glucose uptake by canine kidney cells, adipocytes and intact skeletal muscle [71–73].
1.6 Detoxification of Arsenic
To control the arsenic effect, detoxification of arsenic through the nutrients and chelation therapy has become meaningful.
1.6.1 Antioxidants Agents
The generation of ROS, on arsenic exposure, reduces the cellular antioxidant which increases the oxidative stress in human body. To prevent the ROS generation or decrease the oxidative stress, numerous endogenous antioxidants such as superoxide dismutase (SOD), glutathione reductase (GR), catalase, glutathione peroxidase (GPx), and reduced glutathione (GSH) are naturally generated in the human body which trigger the antioxidant system [74]. However, the high exposure of arsenic decreases the generation of these antioxidants thus external antioxidants such as vitamin C and E, quercetin, N-acetylcysteine (NAC), lipoic acid, and thiol-based antioxidant are injected in body to scavenge the ROS [75].
Vitamins A, C, and E work as antioxidant and decrease the oxidative stress on resulting arsenic exposure through scavenging of ROS [76]. It has been reported that vitamin C may trap the arsenic and alleviate the arsenic-induced oxidative stress. It may scavenge the ROS by electron transfer to prevent the lipid pre-oxidation. Furthermore, it binds to free radicals to protect the membrane from oxidative damages [77]. Similarly, vitamin E also has ability to trap the free radicals, to protect the membrane from arsenic toxicity and oxidative damages [78]. It has been reported that administration of vitamin C and E could effectively reduce the fragmentation of DNA in the presence of arsenic [79]. Moreover, vitamin A, B, B12, and folic acid may also reduce the arsenic toxicity to reduce the oxidative damages [80].
Quercetin is a bioflavonoid, has also been reported as antioxidant, which protect the cell from oxidative damage through trapping the ROS. Quercetin inhibit the cytotoxicity due to low-density lipoprotein [81].
The N-acetylcysteine (NAC) also shows protective effect against arsenic toxicity. It may also trap arsenic on chelation and recovered the hepatic malondialdehyde level [82]. It may reduce the arsenic-induced hepatic, however, showed renal toxicity on co-administration with zinc [83]. Lipoic acid has also the free radical scavenging properties, which leads to reduction in arsenic toxicity and oxidative damage [84] (Figure 1.5).
Figure 1.5 Detoxification of arsenite oxy anions by lipoic acid.
These are the some reported antioxidants that are externally injected in the body and showed efficient result against the arsenic toxicity due to their free radical scavenging and chelation properties. Most of the antioxidants may be obtained from naturals sources. Antioxidants agents obtained from naturals sources can be better antioxidants than synthetic agents due to easily available, low cost, eco-friendly nature, and no further toxicity. Plant and plant extracts have strong antioxidant activity [85]. Hippophae rhamnoides [86], Moringa oleifera [87], Spirulina [88], Centella asiatica [89], Curcumin [90], Mentha piperita [91], and Aloe vera barbadensis [92] have strong antioxidant properties to protect the cell from arsenic-induced oxidative stress.
1.6.2 Chelating Agents
The complexation between the metal ions and multi-dentate ligand is known as chelation, and the multi-dentate ligand referred to as chelating agent. Chelating agents are organic compounds that are able to donate their electron to metal ions and form the chelate complex. Similarly, to trap and detoxify the arsenic, chelation therapy is being used to generate the chemically inert arsenic-ligand complex [93]. This chemically inert arsenic-ligand complex is further excreted from body without any interaction within body (Figure 1.6).
Figure 1.6 Excreted arsenite chelate complex.
Meso-2,3-dimercaptosuccinic acid (DMSA) and 2,3-dimercapto-1-propanesulphonic acid (DMPS) are the most commonly used chelating agents which could detoxify the arsenic through complex formation [94, 95]. Moreover, numerous derivatives of DMSA viz mono isoamyl DMSA (MiADMSA), mono n-amyl DMSA (MnDMSA), mono n-butyl DMSA (MnBDMSA), mono i-butyl DMSA (MiBDMSA), dimethyl DMSA (DMDMSA), diethyl DMSA (DEDMSA), diisoamyl DMSA, and diisopropyl DMSA (DiPDMSA) have also been reported that could also be effective chelating agents to reduce the arsenic concentration from different parts of body [96]. However, there are large drawbacks of chelating agents such as non-specificity, low therapeutic index, and failure to permeate the plasma membrane. Despite of this, metal redeployment and binding of chelating agents to other sites can also induce the side effects and toxicity [97]. Moreover, the use of antioxidants and chelating agents is not mass effective and limited to the particular body systems, therefore, making arsenic free water for human consumption is the only solution.
1.7 Arsenic Remediation Technologies
The concentration of arsenic in water can be maintained at WHO recommended maximum limits through various treatment processes such as oxidation-coagulation [98], electro-coagulation and co-precipitation [99, 100], oxidation-precipitation [101], reverse osmosis [102], electro dialysis [103], and ion exchange technology [104] (Table 1.1). However, these technologies are hardly handling and are very costly. Besides, adsorption technology is inexpensive; does not involve sophisticated instrumentation and do not require long procedure. The process is simple, safe to handle, and effectively work at low and high arsenic concentration in water [105, 106]. Therefore, adsorption of arsenic can be the better option for cleaning the arsenic contaminated water at different scales ranging from household module to community plants.
Table 1.1 Techniques utilized for arsenic removal.
Removal techniques
Advantages
Disadvantages
Cost
pH Dependency
Precipitation
Simple, low-cost
Slow process and Produce large sludge
Lower
Independent
Less effective
Less effective
[144, 145]
Coagulation
Low costs, simple chemicals used, No monitoring of breakthrough is required
Required Pre-oxidation step, produced toxic sludge and hard to operate
Comparatively low
Dependent
Less effective
>90%
[146, 147]
Ion exchange
Eco-friendly, used for industrial and municipal water, provides high flow rate, removes dissolved inorganics effectively
High-cost medium, high-tech operation and maintenance, need high operation skill, sludge disposal problem
High
Dependent
Very less effective
>90%.
[148, 149]
Membrane filtration
No chemicals required and does not influence water taste and color
Temperature limitation, effective for minor stream sizes, and fouling of the membranes
High
Independent
Less effective
>80%
[150, 151]
Reverse osmosis
Very effective at removing inorganic constituents, little maintenance, and no addition of chemicals
Pre-oxidation of As(III) to As(V) required and high tech operation and maintenance
Very high
Independent
>60%
>90%
[152, 153]
Electro dialysis
Easy to handling
Interference by oxidizing agent’s
High
Independent
25–60%
>70%
[154]
1.8 Adsorption and Recent Advancement
Being surface phenomena, adsorption process is based on interaction between the solute (adsorbate) and solid surface (adsorbent). Low particle diameter, high surface area, high active sites, and magnetic character of adsorbent are responsible for the higher removal capacity for arsenic [107]. Numerous adsorbents with above characteristics have been utilized. Sometimes, pre-oxidation step is preferred to remove As(III), which makes the process costly [108]. Moreover, these steps enhance the chance of formation of un-healthy by-products [109]. Numerous adsorbents having oxidative properties have been utilized for simultaneous oxidation of As(III) to As(V) and adsorption of As(V) [110].
Recently, metal-based adsorbents, metal oxides and nanocomposites are utilized for arsenic cleanup from pollutant sites, followed by easily oxidation of As(III) to As(V) [111].
Nanosized metal oxides and nanocomposites cleanup water under the various water quality constraints such as pH and competing ions [112]. In addition, generation and regeneration of adsorbent make the process significant in respect to cost and removal capacity. Activated carbon (AC) is one of the most utilized highly amorphous and porous adsorbent, however, the generation and regeneration of AC activated carbon is very difficult [113].
These drawbacks of AC generate the large sludge in cleaning sites and made the process costly. This drawback of AC could be avoided in the era of magnetic adsorbent. Metals like iron, titanium, and cobalt-based adsorbent respond to magnet. Moreover, nanosized magnetic adsorbent respond to low gradient magnet [114]. The impregnation or doping of magnetic NPs into AC or organic framework imparts their magnetic characteristics to the AC or organic framework, which makes adsorbent suitable for magnetic separation from water [115]. Recently, various magnetic organic–inorganic hybrid adsorbents have been successfully utilized in the field of water cleaning. This recent development in adsorbents provide a variety of eco-friendly and cost effective adsorbents, having remarkable potential for arsenic remediation from water and wastewater [13]. Various adsorbents utilized for arsenic remediation has been depicted in Table 1.2.
Table 1.2 Adsorbents utilized for arsenic removal.
Adsorbent
As(III)
As(V)
IHB
51.9
59.6
Fe (III)-BSX
54.35
-
IOCSp
4.2
4.6
CCB
–
96.46
GO-ZrO(OH)
2
nanocomposite
–
84.89
α
-Fe
2
O
3
95.0
47.0
γ
-Fe
2
O
3
NPs
74.83
105.25
AAC-Fe
3
O
4
46.06
16.56
Fe-Cu BO
122.3
82.7
Fe-Ce MO
86.29
55.51
MIO-GO
54.18
27.76
GO-MnFe
2
O
4
MNH
97.0
136.0
MnFe
2
O
4
146.0
207.0
Fe
3
O
4
-RGO-MnO
2
Ns
14.0
12.0
Fe-MnO
x
/RGO
47.0
49.0
β
-FeOOH-GONs
77.50
45.70
Diatom-FeO
x
composite
10.0
12.5
HCO NPs
170.0
107.0
1.9 Conclusion
This chapter shows that arsenic can cause a major calamity as well as be a threat for water dependent bodies. Arsenic shows toxicity and carcinogenicity towards human body on bonding with binding sites available on various working enzyme. This chapter is associated with the brief biochemical metabolic pathway mechanism of arsenic ingestion and risk of toxicity. Further, this study attracted the attention of scientists to search ways of detoxifying the arsenic. Although, various therapeutic and nutritional strategies have been incorporated to discard the arsenic toxicity. This study reveals that the adsorptive remediation of arsenic from water is better option instead of detoxification of arsenic. In general, improved adsorption capacity of adsorbents probably is due to higher number of active binding sites on their surface, therefore more number of adsorbents with new functional groups are required to search out. This chapter will help the young scientist to quick understand the toxicity, detoxification, and remediation of arsenic from water.
Acknowledgment
The authors appreciate the Jamia Millia Islamia, New Delhi, India, for equipping the Environmental Chemistry Research Laboratory where this research work was carried out.
Abbreviations
AAC-Fe3O4 (ascorbic acid-coated Fe3O4)
CCB (chitosan-coated biosorbent)
Fe (III)-BSX (Fe (III)-treated biomass of Staphylococcus xylosus)
Fe-MnOx/G (dispersed graphene matrix)
α-Fe2O3 (ultrafine iron oxide)
β-FeOOH/GONs (akaganeite [β-FeOOH] decorated graphene oxide nano composite)
γ-Fe2O3 (saturated magnetic γ-Fe2O3 NPs)
GO (graphene oxide)
GO-MnFe2O4 MNH (graphene oxide-MnFe2O4 magnetic nanohybrid)
ICBO (Fe-Cu binary oxide)
ICF (iron chitosan flakes)
IOCSp (iron oxide-coated sponge)
IHB (inonotus hispidus biomass),
MIO-GO (magnetic iron oxide-loaded graphene oxide)
NPs (nanoparticles)
Ns (nanocomposite)
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