Childhood Lead Poisoning

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1 Chidhood Lead Poisoning

2 Chidhood Lead Poisoning

3 WHO Library Cataoguing-in-Pubication Data Chidhood ead poisoning. 1.Lead poisoning - etioogy. 2.Lead poisoning - prevention and contro. 3.Chid. 4.Infant. 5.Environmenta exposure. 6.Pubic heath practice. I.Word Heath Organization. ISBN (NLM cassification: QV 292) Word Heath Organization 2010 A rights reserved. Pubications of the Word Heath Organization can be obtained from WHO Press, Word Heath Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerand (te.: ; fax: ; e-mai: Requests for permission to reproduce or transate WHO pubications whether for sae or for noncommercia distribution shoud be addressed to WHO Press, at the above address (fax: ; e-mai: who.int). The designations empoyed and the presentation of the materia in this pubication do not impy the expression of any opinion whatsoever on the part of the Word Heath Organization concerning the ega status of any country, territory, city or area or of its authorities, or concerning the deimitation of its frontiers or boundaries. Dotted ines on maps represent approximate border ines for which there may not yet be fu agreement. The mention of specific companies or of certain manufacturers products does not impy that they are endorsed or recommended by the Word Heath Organization in preference to others of a simiar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initia capita etters. A reasonabe precautions have been taken by the Word Heath Organization to verify the information contained in this pubication. However, the pubished materia is being distributed without warranty of any kind, either expressed or impied. The responsibiity for the interpretation and use of the materia ies with the reader. In no event sha the Word Heath Organization be iabe for damages arising from its use. This pubication contains the coective views of an internationa group of experts and does not necessariy represent the decisions or the poicies of the Word Heath Organization. Printed by the WHO Document Production Services, Geneva, Switzerand.

4 Contents Contributors 5 Abbreviations 7 Preface 8 Foreword 9 Summary 11 Introduction: ead poisoning a persistent probem 13 The nature, sources and routes of exposure to ead 15 Lead toxicity and its effects on heath 20 Diagnosing ead poisoning 49 References 55 Annex. Additiona information 69

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6 Chidhood Lead Poisoning Contributors Working group members Yona Amitai, Mother Chid & Adoescent Heath, Ministry of Heath, Jerusaem, Israe Hamed Bakir, WHO Regiona Centre for Environmenta Heath Activities, Amman, Jordan Nida Besbei, WHO European Centre for Environment and Heath, Bonn, Germany Stephan Boese-O Reiy, University for Heath Sciences, Medica Informatics and Technoogy, Tiro, Austria Mariano Cebrian, Centro de Investigación y de Estudios Avanzados de IPN, Mexico City, Mexico Yaohua Dai, Department of Chid Heath Care, Capita Institute of Pediatrics, Beijing, China Pau Dargan, Medica Toxicoogy Unit, Guy s and St Thomas Poisons Unit, London, Engand Eaine Easson, Risk Management Section, Heath Canada, Ottawa, Ontario, Canada Nathan Graber, Division of Environmenta Heath, New York City Department of Heath and Menta Hygiene, New York, NY, United States of America Chems-Eddouha Khassouani, Laboratory of Toxicoogy and Pharmacoogy, Centre Anti-Poison, Rabat, Morocco Norman Heay, Heath Canada, Burnaby, British Coumbia, Canada Zbigniew Koacinski, Cinica Toxicoogy Department, Nofer Institute of Occupationa Medicine, Lodz, Poand Amaia Laborde, Department of Toxicoogy and Poison Contro Center, Universidad de a Repúbica, Montevideo, Uruguay Phiip Landrigan, Mt Sinai Schoo of Medicine, New York, NY, United States of America Bruce Lanphear, Cincinnati Chidren s Hospita Medica Center, Cincinnati, OH, United States of America 5

7 Word Heath Organization Angea Mathee, South African Medica Research Counci, Johannesburg, South Africa Monique Mathieu, Centre Antipoison de Lie, Centre Hospitaier Régiona Universitaire, Lie Cedex, France Geradine McWeeny, WHO Country Office, Begrade, Serbia WHO Secretariat Ruth A. Etze, Department of Pubic Heath and Environment, Word Heath Organization, Geneva, Switzerand Jenny Pronczuk, Department of Pubic Heath and Environment, Word Heath Organization, Geneva, Switzerand Reviewers David Beinger, Harvard Schoo of Pubic Heath, Boston, MA, United States of America Marie-Noe Bruné, Department of Pubic Heath and Environment, Word Heath Organization, Geneva, Switzerand Liian Corra, Asociation Argentina de Médicos por e Medio Ambiente, Buenos Aires, Argentina Pascha Häfiger, Department of Pubic Heath and Environment, Word Heath Organization, Geneva, Switzerand Katheen M. McCarty, Yae University Schoo of Medicine, New Haven, Connecticut USA Mary Kimotho M Mukindia, United Nations Environment Programme, Nairobi, Kenya Dorit Nitzan, WHO Country Office, Begrade, Serbia Judy Stober, Department of Pubic Heath and Environment, Word Heath Organization, Geneva, Switzerand Joanna Tempowski, Department of Pubic Heath and Environment, Word Heath Organization, Geneva, Switzerand 6

8 Chidhood Lead Poisoning Abbreviations Organizations and other entities ASTM CDC CPSC EPA HUD JECFA OAS OECD UNEP American Society for Testing and Materias United States Centers for Disease Contro and Prevention United States Consumer Product Safety Commission United States Environmenta Protection Agency United States Department of Housing and Urban Deveopment United Nations Food and Agricuture Organization and Word Heath Organization Joint Expert Committee on Food Additives Organization of American States Organisation for Economic Co-operation and Deveopment United Nations Environment Programme USPSTF United States Preventive Services Task Force WHO Word Heath Organization Technica terms BLL DALYs EBLL IQ PM 10 bood ead eve disabiity-adjusted ife years eevated bood ead eve inteigence quotient particuate matter ess than 10 µm in diameter 7

9 Word Heath Organization Preface Athough many countries have initiated programmes to ower the eve of ead in the environment, human exposure to ead remains of concern to heath care providers and pubic heath officias wordwide. For over 35 years the Word Heath Organization and the Internationa Programme on Chemica Safety have been concerned about the adverse effects on heath of ead in the environment. The evauation of human heath risks arising from foodborne ead has been carried out by the Word Heath Organization on four occasions since In addition, heath-based guidance vaues for ead in water, air and the workpace have been deveoped by various task groups convened by the Word Heath Organization. Environmenta Heath Criteria 3: Lead, pubished in 1977, examined the effects of ead on human heath, and Environmenta Heath Criteria 85: Lead Environmenta Aspects was pubished in During the past 10 years, a arge body of knowedge on the effects of ead on neurobehavioura deveopment of chidren at ow eves of exposure has accumuated. This booket focuses on what is known about chidhood ead poisoning, an entirey preventabe disease. 8

10 Chidhood Lead Poisoning Foreword Dear Coeagues, It is with great peasure I present to you this booket on Chidhood Lead Poisoning. Lead poisoning has been a scourge to human heath for miennia. Chidhood ead poisoning has been a recognized cinica entity since the first decade of the 20th century. Lead has had devastating consequences for the heath of the word s chidren. At high eves of acute exposure, ead attacks the brain and centra nervous system to cause coma, convusions and even death. Chidren who survive acute ead poisoning are typicay eft with grossy obvious menta retardation and behavioura disruption. At ower eves of exposure that cause no obvious symptoms and that previousy were considered safe, ead is now known to produce a spectrum of injury that causes oss of cognition, shortening of attention span, ateration of behaviour, dysexia, attention deficit disorder, hypertension, rena impairment, immunotoxicity and toxicity to the reproductive organs. For the most part, these effects are permanent. They are irreversibe and untreatabe by modern medicine. When ead exposure is widespread as happened in the 20th century when eaded petro and ead-based paints were extensivey disseminated in the environment the heath and webeing of entire societies are compromised. And when this happened, the economic costs in terms of medica care and diminished opportunity amounted wordwide to hundreds of biions of doars a year. Prevention is the best way to dea with ead poisoning. This booket synthesizes the wisdom of hundreds of peer-reviewed pubications and scores of Word Heath Organization documents. It is intended to be accessibe and practica for heath workers in a counties. I commend it to you. Maria Neira, Director Pubic Heath and Environment Word Heath Organization 9

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12 Chidhood Lead Poisoning Summary This booket describes chidhood ead poisoning, one of the most common and best understood chidhood diseases of toxic environmenta origin. Acute and chronic ead poisoning remain probems of enormous importance for chid heath and deveopment wordwide. Lead has no essentia roe in the human body, and ead poisoning accounts for about 0.6% of the goba burden of disease. Lead poisoning is entirey preventabe. The major sources of chidren s exposure to ead are: ead added to petro ead from an active industry, such as mining (especiay in sois) ead-based paints and pigments ead soder in food cans ceramic gazes drinking-water systems with ead soder and ead pipes ead in products, such as herba and traditiona medicines, fok remedies, cosmetics and toys ead reeased by incineration of ead-containing waste ead in eectronic waste (e-waste) ead in the food chain, via contaminated soi ead contamination as a egacy of historica contamination from former industria sites. Intense, high-dose exposure to ead causes acute symptomatic poisoning, characterized by coic, anaemia, and depression of the centra nervous system that may resut in coma, convusions and death. Acute, symptomatic ead poisoning sti occurs today and is most commony detected among chidren in ow-income countries and marginaized popuations or in chidren iving in ead-pouted sites. Bood ead eves that were considered previousy to be safe are now understood to compromise heath and injure mutipe organs, even in the absence of overt symptoms. The most critica consequence of ow eve ead toxicity in utero and during chidhood is damage to the deveoping 11

13 Word Heath Organization brain and nervous system. The immune, reproductive and cardiovascuar systems are aso adversey affected by reativey ow eves of exposure to ead that is, ess than 10 µg/d. The consequences of brain injury from exposure to ead in eary ife are oss of inteigence, shortening of attention span and disruption of behaviour. Because the human brain has itte capacity for repair, these effects are untreatabe and irreversibe. They cause diminution in brain function and reduction in achievement that ast throughout ife. Recent research indicates that ead is associated with neurobehavioura damage at bood eves of 5 µg/d and even ower. There appears to be no threshod eve beow which ead causes no injury to the deveoping human brain. The Joint FAO/WHO Expert Committee on Food Additives reevauated ead in June, 2010 and withdrew the provisiona toerabe weeky intake guideine vaue on the grounds that it was inadequate to protect against IQ oss. The neurobehavioura toxicity caused by ead paces great economic burdens on famiies and societies. When exposure to ead is widespread, ow eve toxicity can damage heath, reduce inteigence, damage economies, and incapacitate the future eadership and security of entire countries. An economic anaysis conducted in the United States found the current costs of chidhood ead poisoning to be US$ 43 biion per year. A recent cost benefit anaysis undertaken in the United States found that for every US$ 1 spent to reduce ead hazards, there is a benefit of US$ This cost benefit ratio is better than that for vaccines, which have ong been described as the singe most cost-beneficia medica or pubic heath intervention. The goa of this booket is to inform and educate heath professionas paediatricians, other cinicians, nurses, and pubic heath officias at a eves about the importance of chidhood exposure to ead and ead poisoning and its serious consequences. This booket emphasizes that the contexts, sources and routes of exposure to ead differ for chidren in different communities, countries and regions around the word, athough the bioogy of chidhood ead poisoning is the same gobay. 12

14 Chidhood Lead Poisoning Introduction: ead poisoning a persistent probem Lead poisoning is one of the most common and best-recognized chidhood diseases of toxic environmenta origin. Chidren around the word today are at risk of exposure to ead from mutipe sources. Lead poisoning accounts for about 0.6% of the goba burden of disease (WHO, 2009). Patterns and sources of exposure to ead, prevaence rates of ead poisoning and the severity of outcomes vary greaty from country to country and from pace to pace within countries. Countries aso vary greaty in their degree of recognition of the probem and in the strength and effectiveness of their ead poisoning prevention programmes. Some countries have robust programmes for monitoring eves of ead in bood and the environment, as we as strong programmes for primary and secondary prevention of chidhood ead poisoning. These countries have imposed bans on certain uses of ead, have set environmenta standards and have depoyed screening programmes. Some countries have ead hot spots, such as battery recycing pants, smeters, refineries, mines, hazardous waste sites and sites where waste is burned in the open. Some countries recognize that they have a chidhood ead-poisoning probem in reation to certain exposure sources, but have not yet impemented assessment and exposure prevention programmes. And in countries where the potentia probem of ead poisoning has not yet been recognized, there are no screening or surveiance programmes and, as a resut, pubic heath authorities have itte or no knowedge of the existence of a chidhood ead-poisoning probem. Because of this heterogeneous situation, the true picture of goba and regiona ead poisoning in chidren is not yet fuy defined. The contribution of ead poisoning to the goba burden of disease and its effect on the goba economy and human deveopment are probaby sti underestimated. Numerous internationa conferences and decarations have recognized the importance of chidhood ead poisoning and the need to intervene to prevent it (see Annex for exampes). The 1989 Convention of the Rights of the Chid and the 1992 Agenda 21 adopted by the United Nations Conference on Environment and Deveopment both addressed the need to protect chidren from toxic chemicas. The 1997 Decaration of the Environment Leaders of the Eight on Chidren s Environmenta Heath 13

15 Word Heath Organization acknowedged the importance of ead poisoning as a major environmenta hazard and caed for action to reduce chidren s bood ead eves and to fufi the Organisation for Economic Co-operation and Deveopment Decaration on Lead Risk Reduction. The 2002 Bangkok Statement on Chidren s Heath and the Environment caed for the remova of ead from gasoine (Suk, 2002). In 2005, the Heath and Environment Ministers of the Americas agreed in the Decaration of Mar de Pata to strengthen sub-regiona and nationa actions to achieve a compete eimination of ead in gasoine and its reduction from other sources (OAS, 2005). The 2006 Decaration of Brescia on Prevention of the Neurotoxicity of Metas recommended: the immediate eimination of tetra-ethy ead from the gasoine suppies of a nations; the review of a uses of ead, incuding recycing, in a nations; and urgent reduction of current exposure standards (Landrigan et a., 2007). The 2009 Busan Pedge for Action on Chidren s Heath and Environment further affirmed the commitment of the goba community to end chidhood ead poisoning. This booket has its origins in the meeting of the Informa Working Group on Lead Exposure in Chidren convened by the Word Heath Organization (WHO) and hosted by the German Network for Chidren s Heath and the Environment at the Ludwig Maximiians University of Munich, Munich, Germany, on 30 November and 1 December Scientists, cinicians, and pubic heath professionas from ow-, middeand high-income countries presented scientific evidence at this meeting on their experiences in researching the toxicity of ead. 14

16 Chidhood Lead Poisoning The nature, sources and routes of exposure to ead What is ead? Lead is a heavy meta with a buish-grey coour. It has a ow meting point, is easiy mouded and shaped, and can be combined with other metas to form aoys (see Box 1 for more facts about ead). For these reasons, ead has been used by humans for miennia and is widespread today in products as diverse as: pipes; storage batteries; pigments and paints; gazes; viny products; weights, shot and ammunition; cabe covers; and radiation shieding. Box 1. Facts about ead Eementa ead. The chemica symbo for ead is Pb (from the Latin name for ead, pumbum). Lead has an atomic number of 82 and an atomic weight of It is a buish-grey meta that tarnishes easiy in air to a dark grey. The density of ead is g/cm 3. It has a ow meting point of C or F. Naturay occurring ores. Lead ores comprise 0.002% (15g/t) of the earth s crust. They incude gaena (ead sufide), angesite (ead sufate), cerussite (ead carbonate), mimetite (ead choroarsenate) and pyromorphite (ead chorophosphate). Inorganic ead. This is the form of ead found in od paint, soi, dust and various consumer products. The coour varies, depending on the chemica form, and the most common forms are white ead (a ead carbonate compound), yeow ead (ead chromate, ead monoxide) or red ead (ead tetraoxide). Lead acetate has a sweetish taste. Organic ead. Tetra-ethy ead is the form of ead used in eaded gasoine. Organic forms of ead are extremey dangerous, as they are absorbed through the skin and are highy toxic to the brain and centra nervous system, much more so than inorganic ead. The combustion of organic ead when it is added to petro as a fue additive resuts in the reease of ead into the atmosphere. A forms of ead are toxic! Tetra-ethy ead was used extensivey from the 1930s to the 1970s as a petro additive to improve engine performance (Rosner & Markowitz, 1985; Landrigan, 2002). Tetra-ethy ead has been eiminated from the petro suppies of the majority of countries, but is sti used in about 9 countries (UNEP, 2010). 15

17 Word Heath Organization Lead used by industry comes from mined ores (primary) or from recyced scrap meta or batteries (secondary). Today, most of the ead in goba commerce is secondary and is obtained from recycing ead-acid batteries. Most (97%) of the word s batteries are reported to be recyced, mosty in ow-income countries and mosty in informa, argey uncontroed settings. Goba consumption of ead is increasing today, because of increasing demand for energy-efficient vehices. The argest current use of ead is in storage batteries for cars and other vehices. This use now exceeds the use of ead in petro (Internationa Lead and Zinc Study Group, 2009). There are many ead-reated cottage (home-based) industries, incuding repairs of eectrica appiances using ead soder, sma famiy painting businesses and backyard car repairs). Sometimes these harmfu activities are the ony means of iveihood for poor famiies and communities. Prior to human expoitation peope were not exposed to ead Lead constitutes 0.002% of the Earth s crust, and in nature it exists mainy as ead suphide. Lead has become widey distributed in the biosphere ony in the past few thousand years, amost entirey as the resut of human activity (Nationa Research Counci, 1972). Once ead is introduced into the environment, it persists. This trend of increasing environmenta ead eves is iustrated by geochemica data that show the accumuation of ead in the Greenand ice cap over the past three miennia (Murozomi, Chow & Patterson, 1969). By far, the greatest increase occurred in the 20th century, due mosty to the burning of tetra-ethy ead in automotive engines and the subsequent distribution of ead in the atmosphere. In a simiar fashion, measurements of the amount of airborne ead deposited in Scottish and Canadian peat bogs showed that background pre-industria deposition amounted to ony about 0.01 mg ead m -2 a -1. In the 1990s, however, this rate of deposition had increased to 8 mg ead m -2 a -1, even after ead was eiminated from gasoine in many of the surrounding areas (Kyander, Weiss & Kober, 2009). Investigations of human skeeta remains indicate that the body ead burden of today s popuations is times greater than that of their 16

18 Chidhood Lead Poisoning pre-industria counterparts. The pre-industria bood ead eve in peope is estimated to have been about µg/d. In remote regions of the southern and northern hemispheres in the ate 1980s, bood ead eves were reported to be 0.78 µg/d and 3.20 µg/d, respectivey (Fega & Smith, 1992). By far the argest contributor to goba environmenta ead contamination has been the use of ead in petro (OECD, 1999; Landrigan, 2002). Word ead consumption rose steadiy between 1965 and 1990, when it reached about 5.6 miion tonnes. Between 1980 and 1990, the consumption of ead in high- and midde-income countries increased ony sighty, whereas for the same years in ow-income countries it increased from tonnes to tonnes per year. Goba ead contamination resuting from human activities and attributabe to the greaty increased circuation of ead in soi, water and air remains significant. With continued efforts to remove ead from petro, paint and pigments, soder and other we-known sources, bood ead eves wordwide are expected to continue their decine. However, hot spots from smeting, mining, and meta recycing operations some of them ongoing and others the egacy of the past remain significant probems. And despite a century of accumuated evidence about its danger to the heath of chidren, ead continues too often to be added to paints, pigments, toys, traditiona medications, cosmetics and other consumer products, especiay as manufacturing shifts to ow-income countries that ack environmenta and product content contros and poicies. Environmenta sources of ead Lead absorption pathways An exposure pathway must, by definition, have five components: (a) a source of contamination (such as deteriorating ead-based paint on the was, doors and windows of a home; used car batteries; open burning of waste); (b) an environmenta medium and transport mechanism (such as ead contaminated dust on the foor of a home, ead smoke from open burning, or ead exhaust from eaded gasoine); (c) a point of exposure (such as chidren s hands, the foor, or chidren s toys); (d) a route of exposure (such as eating the dust through hand-to-mouth behaviour); and (e) an exposed popuation (such as chidren in the home environment or pregnant women in pouted environments or workpaces). When a 17

19 Word Heath Organization five components are present, the exposure pathway is termed a compete exposure pathway. Ingestion is the most common route of exposure to ead for chidren. Once ead has been swaowed, it enters a chid s body by absorption from the gastrointestina tract. Chidren s innate curiosity and their age-appropriate hand-to-mouth behaviour resut in their bringing ead-containing or eadcoated objects, such as contaminated soi or dust, to their mouth, and thus greaty increase their risk of exposure. This route of exposure is magnified in chidren who engage in pica. The amount of soi and house dust that a typica 1 6-year-od chid ingests is said to be 100 mg/24 h, but a more conservative estimate of 200 mg/24 h with an upper percentie of 400 mg/24 h has aso been suggested. Chidren in the United States who engage in pica may ingest as much as 10 g/24 h (EPA, 2002). These vaues are important when setting standards for remediation that wi not resut in eevated bood ead eves. Inhaation of airborne ead may not typicay be a major source of exposure for chidren, in contrast to occupationay exposed aduts, because the partice size of airborne ead in community environments is usuay too arge to be inhaed. Inhaation can occur, however, when chidren are exposed to ead in particuate matter ess than 10 µm in diameter (PM 10 ) from car exhausts (in countries that sti use eaded gasoine) and smoke from the open burning of waste. Attention shoud aso be paid to the possibiity of inhaation exposure from other unusua circumstances in chidren s environments, such as heat-gun stripping of painted surfaces, weding and torch cutting of ead painted stee or stee aoys containing ead, or burning ead contaminated materias (such as od car batteries) in and near chidren s homes. In these situations, very fine partices of airborne ead are generated and can be inhaed by chidren. Severe cases of paediatric ead poisoning have been documented (Amitai et a., 1987, 1991). 18

20 The most common sources of ead in chidren s environments today Chidhood Lead Poisoning Wordwide, the foowing sources and products account for most cases of chidhood exposure to ead and ead poisoning: ead added to gasoine ead from an active industry, such as mining (especiay in sois) ead-based paints and pigments, ead soder in food cans ceramic gazes drinking-water systems with ead soder and ead pipes ead in products, such as herba and traditiona medicines, fok remedies, cosmetics and toys ead reeased by incineration of ead-containing waste ead in eectronic waste (e-waste) ead in the food chain, via contaminated soi ead contamination as a egacy of historica contamination from former industria sites. Fig. 1 describes some of the routes by which ead moves from its primary source to reach the bodies of chidren. Fig. 1. Sources of chidren s exposure to ead 19

21 Word Heath Organization The reative importance of these various potentia sources of exposure to ead varies both within and between countries and regions. In the United States, for exampe, ead-based paint is an important source of exposure, whie in Mexico, ead-gazed ceramics used for food storage and preparation are much more important (Rojas-López et a., 1994). In the ow-income word the informa recovery of ead from car batteries and the open burning of waste are very important sources of environmenta ead contamination. Socioeconomic factors are important predictors of exposure to ead. Poor famiies are more ikey to ive near industria pants that hande ead, such as battery recycers or smeters. Aso, they are more ikey to dwe on pouted ands, to work in pouting industries, or to ive in oder housing with ead-based paint. Finay, poor chidren are more ikey to have iron or cacium deficient diets, and as a resut they may absorb ead more efficienty. Cuture and ethnicity are strongy reated to such risk factors for exposure to ead as the use of traditiona cosmetics, herba medicine products and pica during pregnancy. These exposures are, however, not imited to their countries of origin, as goba migration and goba markets increase and as the popuarity of compementary and aternative medicine grows in midde- and high-income societies. Lead toxicity and its effects on heath The toxic nature of ead has been known since at east 2000 BC. Lead poisoning was common in Roman times, due to the use of ead in water pipes, earthenware containers and wine storage vesses, and the use of a eaded syrup, caed sapa, to sweeten wine (Eisinger, 1982). Lead poisoning associated with occupationa exposure was first reported in 370 BC. In 1767, the American statesman and phiosopher Benjamin Frankin obtained a ist of patients in La Charité Hospita in Paris who had been admitted because of symptoms which, athough not recognized as such, were evidenty those of ead poisoning. A the patients were engaged in occupations that exposed them to ead (Frankin, 1786). In 1839, the French physician, Tanquera des Panches described the symptoms of acute ead poisoning on the basis of 1213 admissions to La Charité Hospita between 1830 and His study was so thorough that itte has subsequenty been added to the cinica picture of the symptoms and signs of acute ead poisoning in aduts (Tanquere des Panches, 1839). Lead poisoning became 20

22 Chidhood Lead Poisoning common among industria workers in the 19th and eary 20th centuries, when workers were exposed to ead whie engaged in trades invoving smeting, painting, pumbing, printing and many other industria activities (Thackrah, 1832). In 1882, foowing the deaths of severa empoyees in the ead industry in the United Kingdom, a pariamentary enquiry was initiated into working conditions in ead factories. This resuted in passage of the 1883 Factory and Workshop Act, which required ead factories in the United Kingdom to conform to certain minimum standards, such as the provision of ventiation and protective cothing. Lead toxicity in chidren Lead poisoning was first recognized as a paediatric disease in Austraia over 100 years ago. A series of 10 cases in Queensand was reported in 1892; 12 years ater, after extensive investigation, the source was found to be peeing, ead-based, residentia paint on the verandas of the chidren s homes (Gibson, 1904). Chidren are now understood to be at particuary high risk of ead toxicity. From conception onward, chidren have a greater risk of exposure and greater susceptibiity to the toxic effects of ead than do aduts. There exist windows of vunerabiity to ead in eary ife during embryonic, feta and eary postnata ife that have no counterparts in adut ife (American Academy of Pediatrics Committee on Environmenta Heath, 2003). Chidren are at increased risk of exposure to ead because they: are exposed to ead throughout pregnancy. eat more food, drink more water and breathe more air per unit of body weight (American Academy of Pediatrics Committee on Environmenta Heath, 2003); have an innate curiosity to expore their words and engage in deveopmentay appropriate hand-to-mouth behaviour and sometimes aso in pica, an abnorma extreme form of hand-to-mouth behaviour; spend more time in a singe environment, such as the home; are more ikey to have nutritiona deficiencies that ead to increased absorption of ead (Mahaffey, 1995); 21

23 Word Heath Organization have more years of future ife and thus a onger time to deveop deayed consequences of eary exposures, potentiay even incuding dementia that may arise as a deayed consequence of eary exposure to ead (American Academy of Pediatrics Committee on Environmenta Heath, 2003); and ack contro over the circumstances of their environment. From conception onward that is, throughout pregnancy ead that has accumuated in a woman s bones is removed from her bones and passes freey from mother to chid; materna and feta bood ead eves are virtuay identica. Once in the feta circuation, ead readiy enters the deveoping brain through the immature bood brain barrier. Chidren s bioogica susceptibiity to ead is greater than that of aduts because of the foowing. 22 The deveoping human brain undergoes rapid growth, deveopment and differentiation, and ead can interfere with these extraordinariy compex and deicate processes. The sequeae of brain damage caused by chronic, ow-eve exposure to ead are irreversibe and untreatabe (Needeman et a., 1990; Beinger, Sties & Needeman, 1992; Rogan et a., 2001).This great vunerabiity extends from prenata ife into infancy and eary chidhood. Exposure to ead eary in ife can re-programme genes, which can ead to atered gene expression and an associated increased risk of disease ater in ife (Basha et a., 2005; Wu et a., 2008; Pisner et a., 2009). Eary exposure to ead can aso reduce an individua s capacity to successfuy weather other neuroogica insuts ater in ife (Schneider & DeCamp, 2007). Gastrointestina absorption of ead is enhanced in chidhood up to 50% of ingested ead is absorbed by chidren, as compared with 10% in aduts. Reativey ow eves of exposure to ead that may not have any immunotoxic effects on a mature organism can, if experienced during the critica period of immune system deveopment, resut in immune dysfunction ater in ife. The adverse effect may be atent and may not emerge unti the immune system is stressed at a point in time we removed from the exposure. There is a threefod to twevefod

24 Chidhood Lead Poisoning difference in reported in vivo owest-observed-adverse-effect eves between perinata and adut exposure periods for various ead-induced immunotoxic effects (Dietert & Piepenbrink, 2006). Heath effects of ead poisoning in chidren Lead is associated with a wide range of toxicity in chidren across a very broad band of exposures, down to the owest bood ead concentrations yet studied, both in animas and peope. These toxic effects extend from acute, cinicay obvious, symptomatic poisoning at high eves of exposure down to subcinica (but sti very damaging) effects at ower eves. Lead poisoning can affect virtuay every organ system in the body. The principa organs affected are the centra and periphera nervous system and the cardiovascuar, gastrointestina, rena, endocrine, immune and haematoogica systems. Acute cinica toxicity Intense, acute, high-dose exposure to ead can cause symptomatic poisoning in chidren. It is characterized by coic, constipation, fatigue, anaemia and neuroogica features that can vary from poor concentration to stupor. In the most severe cases, a potentiay fata acute encephaopathy with ataxia, coma and convusions can occur. In many instances, chidren who survive acute ead poisoning go on to have permanent and cinicay apparent deficits in their neurodeveopmenta function (Byers & Lord, 1943). Overt cinica signs and symptoms of ead poisoning are sti common today in many ow-income countries and in chidren iving around active ead-pouted sites or egacy hot spots. In contrast, these signs and symptoms are ess common in countries and paces where screening for ead and environmenta monitoring are routiney performed. However, heath professionas and pubic heath agencies everywhere shoud be aware of the signs and symptoms of acute ead poisoning, to ensure prompt diagnosis of individua cases and recognition of custers of cases that may be reated to a new or previousy unrecognized ead source in an exposed community. Subcinica toxicity The term subcinica toxicity denotes the concept that reativey ow-dose exposure to ead at bood ead eves previousy thought to be safe can cause 23

25 Word Heath Organization harmfu effects not evident in a standard cinica examination. Athough they are not cinicay obvious, the subcinica toxic effects of ead can be very damaging. The premise underying the concept of subcinica toxicity is that there is a dose-reated continuum of toxic effects in which cinicay apparent effects have their asymptomatic (but sti very rea) counterparts (Landrigan, 1989) (Fig. 2). Figure egend: Fig. 2. Paediatric effects of ead at various bood ead eves Source: Adapted from Beinger & Beinger (2006). Reproduced with the permission of the American Society for Cinica Investigation. Haematoogica toxicity Anaemia is the cassic cinica manifestation of ead toxicity in erythrocytes. The severity and prevaence of ead-induced anaemia correate directy with the bood ead concentration. Younger and iron deficient chidren are at higher risk of ead-induced cinica anaemia. The anaemia induced by ead is caused primariy by impairment of heme biosynthesis, but an 24

26 Chidhood Lead Poisoning increased rate of erythrocyte destruction may aso occur (Schwartz et a., 1990). Neuroogica toxicity In the periphera nervous system, the motor axons are the principa target of ead toxicity. Lead-induced pathoogica changes in these fibres incude segmenta demyeination and axona degeneration. Extensor musce pasy with wrist and anke drop has been recognized since the time of Hippocrates as the cassic cinica sign of the periphera neuroogica toxicity of ead; however, this generay ony occurs with chronic ead poisoning and is rare in acute exposure to ead. In the centra nervous system, ead causes asymptomatic impairment of neurobehavioura function in chidren at doses insufficient to produce cinica encephaopathy. Eary cross-sectiona studies of the association between ead and inteigence quotient (IQ) were conducted in the 1970s (Landrigan et a., 1975b; Needeman et a., 1979). These studies showed that cinicay asymptomatic chidren with eevated body ead burdens had a four- to five-point deficit in mean verba IQ scores compared with chidren from the same communities with ower ead burdens. (It is notabe that the ower ead burdens of the referent groups incuded in these studies were quite eevated by today s standards, sometimes in excess of 30 µg/ d.) This finding was sti strongy evident after correcting for a wide range of socioeconomic, behavioura and bioogica factors. Simiar resuts were reported in other eary studies. Today, on the basis of mutipe studies in severa countries, it is estimated that about a quarter to a haf of an IQ point is ost for each 1 µg/d increase in the bood ead eve during the preschoo years for chidren who have bood ead eves in the range of µg/d (Schwartz, 1994; Pocock, Smith & Baghurst, 1994). In young chidren, whoe bood ead eves as ow as 1 3 µg/d are associated with subcinica neurobehavioura toxicity (Canfied et a., 2003). The argest of these studies examining this issue based on an anaysis of data from more than 4800 chidren 6 16 years of age who participated in the Third Nationa Heath and Nutrition Examination Survey in the United States found an inverse reationship between bood ead and math and reading scores in chidren at bood ead concentrations ower than 5 µg/d. The reationship was sti evident after adjustment for an extensive series of potentia confounding factors. Indeed, the dose response reationship between bood ead eves and oss of IQ was stronger at bood ead eves 25

27 Word Heath Organization ower than 10 µg/d than at higher eves (Lanphear et a., 2000). An internationa pooed anaysis of data from seven cohorts has confirmed these findings (Lanphear et a., 2005) (see Fig. 3). An increase in bood ead eve from ess than 1 µg/d to 10 µg/d was associated with a six IQ point decrement, which is consideraby greater than the decrement associated with an increase in bood ead eve from 10 µg/d to 20 µg/d. The findings of this pooed anaysis that there are adverse effects beow 10 µg/d and that the effects are steepest at the owest eves of exposure have been confirmed by numerous investigators (Emory et a., 1999, 2003; Beinger & Needeman, 2003; Wasserman et a., 2003; Chiodo, Jacobson & Jacobson, 2004; Despres et a., 2005; Fraser, Mucke & Despres, 2006; Hu et a., 2006; Kordas et a., 2006; Schnaas et a., 2006; Teez-Rojo et a., 2006; Chiodo et a., 2007; Surkan et a., 2007). Fig. 3. Reationship between concurrent bood ead eve and chidren s IQ Source: Lanphear et a. (2005). Reproduced with permission from Environmenta Heath Perspectives. When a popuation s exposure to ead is sufficienty widespread to cause a decrease in its mean IQ, there resuts a substantia increase in the number of chidren with diminished inteigence and menta retardation. At the same time, there is a substantia reduction in the number of chidren with truy superior inteigence (see Fig. 4). The consequences are: (a) a substantia increase in the number of chidren who do poory in schoo, who may require specia education and other remedia programmes, and who may not contribute fuy to society when they become aduts; 26

28 Chidhood Lead Poisoning (b) a reduction in a country s future eadership; and (c) a widening gap in socioeconomic attainment between countries with high and ow eves of popuation exposed to ead (Needeman et a., 1979). Fig. 4. Losses associated with a five-point drop in IQ in 100 miion peope Source: Coborn, Dumanoski & Myers (1996). Prenata exposure to ead and exposure to ead in human mik From conception onward, ead that has been stored in the mother s skeeton in years past is reeased into the circuation under the metaboic stress of pregnancy. Throughout pregnancy, ead readiy crosses from the materna to the infant circuation, and the bood ead concentration of the infant becomes virtuay identica to that of the mother (Markowitz, 2000). Once in the infant, ead can penetrate the immature bood brain barrier to enter the deveoping brain (Lidsky & Schneider, 2003). The deveoping human brain is particuary susceptibe to ead, even at very ow eves of exposure. The source of ead in an infant s bood seems to be a mixture of about two thirds dietary and one third skeeta ead, as shown by studies that expoited the differences in ead isotopes stored in the bones of women migrating from Europe to Austraia (Guson et a., 2003). Athough ead appears in human mik, the concentration is coser to that of pasma ead and much ower than that found in whoe bood, so itte is transferred to the infant. 27

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