Layered double hydroxides as effective adsorbents for the removal of lead from contaminated water

Dinamani Muthaiah¹

Section:Research Paper, Product Type: Isroset-Journal
Vol.6 , Issue.1 , pp.10-15, Feb-2019

CrossRef-DOI:   https://doi.org/10.26438/ijsrcs/v6i1.1015

Online published on Feb 28, 2019

Copyright © Dinamani Muthaiah . This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
 

View this paper at   Google Scholar | DPI Digital Library

XML View     PDF Download

How to Cite this Paper

474 Views    232 Downloads    100 Downloads

Abstract :
Layered double hydroxides have fascinated materials chemists due to their wide variety of applications in various fields. The unique property of layered double hydroxides is their interlayer spacing that entertains the intercalation and deintercalation of a variety of anionic species. A wide variety of organic anions have been intercalated into the interlayer galleries of layered double hydroxides and used for desirable applications. This article focuses on the utilization of ethylene diamine tetra acetic acid intercalated layered double hydroxides for the removal of toxic Lead ions from contaminated water.

Key-Words / Index Term :
Layered double hydroxides,Ion exchange, Sorbents, Lead contamination

References :
[1]. D.G. Evans and R.C.T. Slade, “Structural aspects of Layered double hydroxides” Springer-Verlag Berlin, printed in German, 2006
[2]. Vicente Rives, “Layered Double Hydroxides: Present and Future” By Nova Science Publishers Ind. New Yark. 2001.
[3]. P. Steven, Newman and William Jones “Synthesis, characterization and applications of layered double hydroxides containing organic guests” New J. Chem., 22, 105-115, 1998.
[4]. .V.R.L. Constantino and T. J. Pinnavia, “ Basic properties of Mg-Al-LDHs intercalated by Carbonate, hydroxide, Chloride and sulfate anions” Inorg. Chem., 34, 883-892, 1995.
[5]. P. N. Gabby, “Lead: in Mineral Commodity Summaries. Reston, VA: U.S. Geological Survey; 2006.
[6]. P. N. Gabby, “Lead.” Environmental Defense “Alternatives to Lead-Acid Starter Batteries,” Pollution Prevention Fact Sheet.” 2003.
[7]. “Centers for Disease control (CDC). Preventing Lead Poisoning in Young children: A statement by the Centers for Disease Control.” Atlanta, GA: 1991.
[8]. D. E. Jacobs, R.P. Clickner, J.Y. Zhou, et al. “The prevalence of lead-based paint hazards in U.S.housing.” Environ Health Perspect.; 110:A599–A606. [PubMed: 12361941], 2002.
[9]. M.R. Farfel, J.J. Chisolm “An evaluation of experimental practices for abatement of residential lead-based paint” report on a pilot project. Environ Res.; 55:199–212. [PubMed: 1868818], 1991.
[10]. Centers for Disease Control and Prevention CDC). Managing Elevated Blood Lead Levels Among Young Children: Recommendations From the Advisory Committee on Childhood Lead Poisoning Prevention. Atlanta: 2001.
[11]. Lanphear BP, Matte TD, Rogers J, et al. The contribution of lead-contaminated house dust and residential soil to children`s blood lead levels. A pooled analysis of epidemiologic studies. Environ Res.; 79:51–68. [PubMed: 9756680], 1998.
[12]. E. Charney, J. Sayre, M. Coulter, “Increased lead absorption in inner city children: where does the lead come from?” Pediatrics.; 6:226–231. [PubMed: 7354967] 1980.
[13]. Agency for Toxic Substances and Disease Registry (ATSDR. Public Health Service. Atlanta: U.S. Department of Health and Human Services;. Toxicological Profile for Lead, 1999.
[14]. Agency for Toxic Substances and Disease Registry (ATSDR). Case Studies in Environmental Medicine - Lead Toxicity. Atlanta: Public Health Service, U.S. Department of Health and Human Services; 1992.
[15]. S.J.S Flora, G.J.S Flora, G. Saxena,. “Environmental occurrence, health effects and management of lead poisoning.” In: S.B. Cascas,. Sordo, J., editors. Lead: Chemistry, Analytical Aspects, Environmental Impacts and Health Effects. Netherlands: Elsevier Publication; p. 158-228, 2006.
[16]. J.L. Pirkle, D.J. Brady, E.W. R.A. Gunter, D.C. Kramer, Paschal, K.M. Flegal, T.D. Matte. “The decline in blood lead levels in the United States: The National Health and Nutrition Examination Surveys” (NHANES). J Am Med Assoc.; 272:284–291, 1994.
[17]. J.L. Pirkle, R.B. Kaufmann, D.J. Brody, T. Hickman, E.W. Gunter, D.C. Paschal, “Exposure of the U.S. population to lead” 1991–1994. Environ Health Perspect.; 106(11):745–750. [PubMed:9799191], 1998.
[18]. United States Environmental Protection Agency (U.S. EPA). Lead Compounds. Technology Transfer Network- Air Toxics Website. 2002.
[19]. B. Kaul, R.S. Sandhu, C. Depratt, F. Reyes. Follow-up screening of lead-poisoned children near an auto battery recycling plant, Haina, Dominican Republic. Environ Health Perspect.; 107(11):917–920. [PubMed: 10544160], 1999.
[20]. C.N. Ong, W.O. Phoon, H.Y. Law, C.Y. Tye, H.H. Lim. “Concentrations of lead in maternal blood, cord blood, and breast milk.” Arch Dis Child. 60:756–759. [PubMed: 4037861], 1985.
[21]. I. Corpas, I. Gaspar, S. Martinez, J. Codesal, S. Candelas, M.T. Antonio. “Testicular alterations in rats due to gestational and early lactational administration of lead.” Report Toxicol.; 9:307–313, 1995.
[22]. K.W. Andrews, D.A. Savitz I. Hertz-Picciotto. “Prenatal lead exposure in relation to gestational age and birth weight: a review of epidemiologic studies”. Am J Ind Med. 26:13–32. [PubMed:8074121], 1994.
[23]. Joint effect of gestational age and maternal lead exposure on psychomotor development of the child at six years. Neurotoxicol.; 13:249–254.Tchounwou et al. Page 27, 1992.
[24]. P. Litvak, V. Slavkovich, X. Liu, D. Popovac, E. Preteni, S. Capuni-Paracka, S. Hadzialjevic, V. Lekic, N. Lolacono, J. Kline, J. Graziano, “Hyperproduction of erythropoietin in nonanemic leadexposed children. Environ Health Perspect.” 1998; 106(6):361–364. [PubMed: 9618353].
[25]. R, Amodio-Cocchieri, A. Arnese, E. Prospero, A. Roncioni, L. Barulfo, R. Ulluci, V. Romano. “Lead in human blood form children living in Campania,” Italy. J Toxicol Environ Health.; 47:311–320. [PubMed: 8600285], 1996.
[26]. I. Hertz-Picciotto. “The evidence that lead increases the risk for spontaneous abortion.” Am J Ind Med. 38:300–309. [PubMed: 10940968], 2000.
[27]. P. Apostoli, P. Kiss, P. Stefano, J.P. Bonde, M. Vanhoorne. “Male reproduction toxicity of lead in animals and humans.” Occup Environ Med. 55:364–374. [PubMed: 9764095], 1998.
[28]. S.J.S. Flora, G. Saxena, P. Gautam, P. Kaur, K.D. Gill. “Lead induced oxidative stress and alterations in biogenic amines in different rat brain regions and their response to combined administration of DMSA and MiADMSA.” Chem Biol Interac. 170:209–220, 2007.
[29]. M. Hermes-Lima, B. Pereira, E.J. Bechara. “Are free radicals involved in lead poisoning?” Xenobiotica.; 8:1085–1090. [PubMed: 1776279], 1991.
[30]. Y.S. Jiun, L.T. Hsien. “Lipid peroxidation in workers exposed to lead.” Arch Environ Health. 49:256–259. [PubMed: 8031181], 1994.
[31]. E.J. Bechara, M.H. Medeiros, H.P. Monteiro, M. Hermes-Lima, B. Pereira, M. Demasi. “A free radical hypothesis of lead poisoning and inborn porphyrias associated with 5-aminolevulinic acid overload.” Quim Nova. 16:385–392. 1993.
[32]. C.G,Yedjou, M. Steverson, P.B. Paul Tchounwou, “Lead nitrate-induced oxidative stress in human liver carcinoma (HepG2) cells.” Metal Ions Biol Med. 9:293–297, 2006.
[33]. C.G. Yedjou, J. Milner, C. Howard, P.B. Tchounwou. “Basic apoptotic mechanisms of lead toxicity in human leukemia (HL-60) cells.” Intl J Environ Res Public Health. 7(5):2008–2017, 2010.
[34]. G. Goldstein. “Evidence that lead acts as a calcium substitute in second messenger metabolism.” Neurotoxicol.; 14:97–102, 1993.
[35]. T. Simons. “Lead-calcium interactions in cellular lead toxicity.” Neurotoxicol. 14:77–86. 1993.
[36]. H.P.M. Vijverberg, M. Oortgiesen, T. Leinders, RGDM van Kleef. “Metal interactions with voltageand receptor-activated ion channels.” Environ Health Perspect. 102(3):153–158, 1994.
[37]. F.A. Schanne, G.J. Long, J.F. Rosen. “Lead induced rise in intracellular free calcium is mediated through activation of protein kinase C in osteoblastic bone cells.” Biochim Biophys Acta. 1360(3):247–254. [PubMed: 9197467]. 1997.
[38]. M.P. Waalkes, B.A. Hiwan, J.M. Ward, D.E. Devor, R.A. Goyer. “Renal tubular tumors and a typical hepper plasics in B6C3F, mice exposed to lead acetate during gestation and lactation occur with minimal chronic nephropathy.” Cancer Res. 55:5265–5271. [PubMed: 7585586], 1995.
[39]. 39. R.A. Goyer. “Lead toxicity: current concerns”. Environ Health Prospect. 100:177–187. 1993.
[40]. International Agency for Research on Cancer (IARC). In IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol. Volumes 1–42. Lyons, France: IARC;. Overall Evaluation of Carcinogenicity: An updating of Monographs; p. 230-232. 1987.
[41]. S. Jadoon, A. Malik “DNA Damage by Heavy Metals in Animals and Human Beings: An Overview.” .Biochem Pharmacol 6: 1000235, 2017.
[42]. Roy, Nirmal & G. Rossman, Toby. “Mutagen and comutagenesis by lead compounds.” Mutation research. 298. 97-103, 1993.
[43]. A. H. Mahvi. “Application of agricultural fibers in pollution removal from aqueous solution.” Int. J. Environmental Science & Technology, 5(2), 275-285, 2008
[44]. P. King, P. Srinivas, Y. P. Kumar, , & V. S. R. K. Prasad, “Sorption of copper(II) ion from aqueous solution by Tecton grandis l.f.(teak leaves powder).” J. Hazard. Mater., 136(3), 560-566. 2006.
[45]. M. R. Perez, I Pavlovic, C. Barriga,., J. Cornejo, M. C. Hermosin, , and M. A. Ulibarri, “Uptake of Cu2+, Cd2+ and Pb2+ on Zn-Al layered double hydroxide intercalated with EDTA”, Applied Clay Sci. 32, 345-251, 2006.
[46]. C. Li, G. Wang,., D.G. Evans, X. .Duan, “Incorporation of rare earths ions in Mg–Al layered double hydroxides: intercalation with an [Eu(EDTA)]-chelate”, J. Solid State Chem. 177, 4569– 4575 2004.