lead poisoning: from screening to primary prevention · hood lead poisoning has vastly expanded...

Lead Poisoning: From Screening to Primary Prevention

176 PEDIATRICS Vol. 92 No. 1 July 1993

Committee on Environmental Health

Knowledge of the extent and seriousness of child-hood lead poisoning has vastly expanded since thelast statement regarding lead poisoning by the Amer-ican Academy of Pediatrics in 1987.’ Blood lead 1ev-els once thought to be safe have been shown to beassociated with IQ deficits, behavior disorders,slowed growth, and impaired hearing.2 In fact, leadpoisoning is, according to the Department of Healthand Human Services, “the most important environ-mental health problem for young children.”3 Therapid development of the scientific database requiresrecognition by physicians of the significance of ef-fects at lower levels and a change in clinical practice.

During the last 30 years the Centers for DiseaseControl and Prevention (CDC) has revised down-ward the definition of the blood level at which leadpoisoning occurs from 60 pg/dL whole blood in theearly 1960s, to 30 pg/dL in 1975, and 25 jig/dL in1985. The 1991 CDC statement “Preventing Lead Poi-soning in Young Children” recommended loweringthe community intervention level to 10 pg/dL andsetting several action levels (Table 1).2 In 1987 theAmerican Academy of Pediatrics stated that lead 1ev-els greater than 25 pg/dL were unacceptable for chil-dren.1 The Academy now recognizes that impair-ment of cognitive function begins to occur at levelsgreater than 10 pg/dL, even though clinical symp-toms are not seen. In the late 1970s, the average bloodlead level for US children was 16 pg/dL.4 The meanblood lead level for US children has declined since1976 due to the phaseout of lead in gasoline5 and thereduction of lead in food, and it is now between 4and 6 pg/dL.6 However, severe lead poisoning still

occurs, and there are stifi many children at high riskof exposure.

Childhood lead poisoning is preventable. In Janu-ary 1991, the US Public Health Service issued a stra-tegic plan to eradicate childhood lead poisoningwhich included a cost-benefit analysis.7 This repre-sents a major change from primarily finding andtreating exposed children toward an emphasis onpreventing lead exposure. Identification and treat-ment of the child poisoned with lead continues to beessential, but of greater importance is identification of

the source and prevention of subsequent exposures forthat child and other children in the future.

Until children are in lead-free environments, bloodlead screening is essential to prevent serious disease

The recommendations in this statement do not indicate an exclusive courseof treatment or procedure to be followed. Variations, taking into account

individual circumstances, may be appropriate.PEDIATRKS (ISSN 0031 4005). Copyright © 1993 by the American Acad-emy of Pediatrics.

and disability in the population. Pediatricians willcontinue to play a key role in the identification, treat-

ment, and eradication of lead poisoning.

BACKGROUND

Lead poisoning has been recognized since antiq-uity. In the second century BC, Dioscorides, a Greekphysician, said that “lead makes the mind giveway.”8 Childhood lead poisoning from lead-basedpaint was first described in Brisbane, Australia, inl897.� The cause of this endemic ifiness was identi-fled as painted porch railings,1#{176} and in 1920 the cityof Brisbane passed the first act to prevent poisoning

from lead-based paint. In the United States, plum-bism from lead-based paint was described in the firstdecade of the 20th century.11 It was believed initiallythat if a child recovered from the acute ifiness, therewere no sequelae. Byers and Lord’2 refuted this in1943 in their report of 20 children who had recoveredfrom acute lead intoxication; 19 had obvious behav-ior disorders or mental retardation. During the early1970s several studies were conducted to pursue thisquestion further; some showed lead-related cogni-tive deficits but these studies were controversial.’3Better designed and more sophisticated studies havebeen carried out since that time, and there is a gen-eral consensus of opinion about the relationship be-tween lead and cognitive function.’3

EPIDEMIOLOGY

Lead poisoning is not a disease of poor or minoritychildren alone. In 1984, the last year for which na-tional estimates are available, 17% of American chil-dren had blood lead levels greater than 15 pg/dL.’4There were 12 million children who lived in lead-painted homes, and 6 million children living inhomes built before 1940 when paint with the highestconcentrations of lead was used. For white children,7% in higher socioeconomic status areas and 25% inpoorer communities had blood lead levels greaterthan 15 pg/dL. For black children in poor commu-nities, this prevalence was 55%. Studies are under-way to obtain national estimates of lead levels inchildren. Although children at highest risk certainlydeserve the most attention, exposure throughout allstrata of society presents a problem for all pediatricpractices. Certainly any child living in a house con-taming lead-based paint may be at risk. Such housingand other sources of lead are found throughout theUnited States and not, as commonly believed, just incities in the Northeast. Age of housing, not geo-graphic location, is the best predictor for presence oflead-based paint.’5

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mEncephalopathy .�

Nephropathy .�.

Frank Anemia .�

Colic

Hemoglobin Synthe.is$-. �

Vitamin D MetaboIism$.... �

Nerve Conduction Velocityf-... �

Erythrocyte Protoporphyrin4�Vitamin D Metabolism(I)$J

Developmental Toxicity

IQIH.a#ing $

Transplacental Transfer

4 Increased function $ Decreased function

Figure. Lowest observed effect levels of inorganic lead in chil-

dren. The levels in this diagram do not necessarily indicate thelowest levels at which lead exerts an effect. These are the levels atwhich studies have adequately demonstrated an effect. Source:Agency for Toxic Substances and Disease Registry, 1990.

TABLE 1. The Centers for Disease Control and Prevention (CDC) Recommends Follow-up Using the Following Schedule*

AMERICAN ACADEMY OF PEDIATRICS 177

Class and Blood Lead Level (pg/dL)

I IA II IH IV V

<10 10-14 � . 15-19 20-44+ 45-.69�t 7O�t

Risk: lowAge 6-36mo

If initial screen

at 12 mo, thenretest at 24mo, if possi-

ble

Retest every 3-4mo until 2consecutivetests <10 or 3are <15; thenretest in I y.History, edu-cation, andtest for iron

Refer for case

managementRefer for medi-

cal evaluationand follow-up, identifyand eliminateenvironmental

lead sources

Refer for urgent

medical andenvironmentalfollow-up(within 48 h)

Admit for im-mediate the-lation therapy

Age 37-72 Nonedeficiency�

None Same as above Same as above Same as above Same as abovemo

Risk: high

Age 6-36mo

Retest every 6mo until 2consecutive

tests <10 or 3are <15; thenscreen annu-

ally if possi-

ble

Same as forlow-riskgroup 6-36

mo

Same as above Same as above Same as above Same as above

Age 37-72

moScreen annually

if possibleScreen annually

if possibleSame as above Same as above Same as above Same as above

S Adapted from CDC.2

t Based on confirmed venous blood lead level.:$:Children in this range with symptoms of blood lead poisoning should be considered medical emergencies and admitted immediately

for chelation therapy.§ The CDC recommends these interventions begin at 15 pg/dL for lead poisoning prevention programs.

TOXICITY

Lead is absorbed by ingestion or inhalation. Therelationship between exposure and blood lead levelsis a dynamic process in which blood lead representsa product of recent exposures, excretion, and equili-bration with other tissues. Children deficient in iron,protein, calcium, and/or zinc absorb lead morereadily.’6 Most retained lead is stored in the bones.

At high blood levels (more than 70 pg/dL), leadmay cause encephalopathy and death. Survivors ofencephalopathy may have lifelong severe disabifi-ties, such as seizures and mental retardation.’7 Leadtoxicity affects almost every organ system, most fin-portantly, the central and peripheral nervous sys-tems, kidneys, and blood.’8 Levels at which thetoxic effects of lead are reported to occur are shownin Figure. Lead interferes with enzymes that cata-lyze the formation of heme. It also inhibits both pre-natal and postnatal growth.’� Lead impairs hear-ing acuity.24� Lead is a carcinogen in laboratoryanimals, and there is some evidence for carcinoge-nicity in workers exposed to lead but not in chil-dren.26

Although the impairment of cognition in youngchildren at levels above 10 pg/dL has been reported,no threshold has been identified. At lower blood leadvalues, the impact on an individual child may beundetectable. In contrast, there may be a significantimpact on a population of children with such bloodlevels. A number of studies have found an associa-tion between lead levels and intellectual functioningof children.’3’27� In one study this resulted in anincrease in the number of children with severe defi-

cits (IQs less than 80) from 4% to 16%. In this sample5% of children were expected to have IQs more than125; of the children with high levels oflead, none hadan IQ more than I25.27�� ‘fl� � c�f literature hasbeen examined by meta-analysis. The relationship


178 LEAD POISONING: SCREENING AND PREVENTION

between lead levels and IQ deficits was found to beremarkably consistent.2�3’ A number of studies havefound that for every 10 pg/dL increase in blood leadlevels, there was a lowering of mean IQ in childrenby four to seven points.32’�’39’4�5

Effects of lead on cognition are found after ad-justment for factors such as parental intelligence,socioeconomic status, education, and iron deficien-cy.’3’�’47 Although many of the earlier studies oflead exposure at lower dose did not deal adequatelywith such factors, studies published since 1979 havetaken these into account. Some demonstrated theeffect of lead nonetheless; this was true in the studyby Hansen et al conducted with a group of Danishchildren among whom there was little variabifityin factors such as ethnicity, culture, and medicalcare.3739’4’

The effects of lead exposure in infants from birthonward have also been studied. Bellinger and col-leagues followed a cohort of children born at BostonHospital for Women. Most of these subjects came

from middle-class white families. Covariate-adjustedBayley developmental quotient scores to age 3 weresignificantly lower in children having cord bloodlead levels greater than 10 jig/dL (mean, 14 pg/dL).� The blood lead level at age 2 years exerted aneffect when the children reached the age of 57months. An increase in the 24-month lead level of 10pg/dL in the 0 to 25 pg/dL range was associatedwith a 5.8-point decrease in the Weschler InteffigenceScale For Children-Revised. At 57 months, the effectof prenatal exposure on development was no longerapparent.47 Several studies in other populations haveconfirmed the association between prenatal lead 1ev-els and scores on the Bayley infant developmentscale.”�#{176} Two other studies confirmed the possibleimportance of the 24-month lead level on cognitionin school age children.51’-�2 Exposures during the firsttwo years of life incur a risk of sustained develop-mental delays and impaired cognition.

Recent evidence suggests that the effects of earlylead exposure can persist.53 Subjects in a group wereclassified by dentine lead levels in the first and see-ond grade and followed up into adulthood. Thisstudy showed that those with high tooth lead levelsas children were seven times more likely not to grad-uate from high school and six times more likely tohave reading scores at least two grades below ex-pected, after adjustment for a number of factors in-cluding socioeconomic status and parental IQ.53 Thechildren also had higher absenteeism in the final yearof school, lower class rank, poorer vocabulary andgrammatical reasoning scores, longer reaction times,and poorer hand-eye coordination.

SOURCES

Lead paint is the major source of lead poisoningfor children. As lead paint deteriorates or is removed,house dust and soil become contaminated, and leadenters the body through normal hand-to-mouth ac-tivity.54 Children may also ingest paint chips. Before1955 much white house paint was 50% lead and 50%linseed oil. In 1955, manufacturers adopted a volun-tary house paint lead-content standard of 1%, but

house paint with higher levels of lead continued tobe manufactured.55 The amount of lead allowable inpaint was lowered by law in two steps, to 1% in 1971and then to 0.06% in 1977. Occasionally lead paintmanufactured for nonresidential purposes continuesto be used to paint houses. It is estimated that 5million tons of lead have been applied to houses in

the United States. Of the homes built before 1960,70% are estimated to have lead paint. Most danger-ous are the 3.8 million homes with decaying or de-teriorating lead paint in which 2 million childrenyounger than 6 years of age live.’8

Uncontaminated soil contains lead concentrationsless than 50 ppm, but soil lead levels in many urbanareas exceed 200 ppm. Areas near lead mines, lead-using industries, and smelters may have hi&h levelsof contamination in soil (up to 60 000 ppm).� In theUnited States, the use of leaded gasoline has releasedan estimated 30 miffion tons of lead into the air. Leadin house dust is an important source of exposure andcomes from paint, soil, and other sources.

Acidic water oflow mineral content can leach largeamounts of lead from lead pipes or solder.’4 This isparticularly apt to occur when water has been stand-ing in pipes for extended periods, and hot water maybe of particular concern. An estimated 16% of house-

hold water supplies have lead concentrations greater

than the proposed standard of 20 pg/dL.57 Lead sol-der and fittings can also be found in older drinkingwater coolers and coffee urns. Brass fixtures may alsobe contaminated with lead.’8 Lead-contaminated wa-

ter has been linked to lead poisoning in childrengiven reconstituted infant formula.ss

Lead may also contaminate food. Soil lead is takenup by root vegetables and atmospheric lead may fall

onto leafy vegetables.’8 Lead may also be added tofood during processing. Cans with soldered seamscan add lead to foods. In the United States, solderedcans have largely been replaced by seamless alumi-num containers but some foreign and large commer-cial-sized cans still have lead-soldered seams.18Other modes of food contamination include someceramic tableware (especially imported), certain“natural” calcium supplements, and bright red andyellow paints on bread bags.’8

Other lead sources are ethnic folk remedies (az-arcon and greta used by Hispanics and pay-loo-ahused by Southeast Asians),’8 eye cosmetics (kohlused by Moslems and surma by Hindus), hobbies(eg, stained glass, artist paints, shooting ranges), andaccidental ingestion of small lead objects (eg, fishingweights, curtain weights). Parents who are employed

in a lead-using industry may bring lead dust homeon dothing or expose children by allowing them to

visit work sites.’8 Identification of the source of leadrequires a careful history and usually investigation ofthe household.

PREVENTING CHILDHOOD LEAD POISONING

There are two major ways to prevent lead poison-

ing in children: removal of environmental lead andlead screening.



Remove Lead From Children’s Environment

Removal of environmental lead is the most effec-tive preventive measure. For past contaminationproblems, source reduction involves removal of leador modification of the environment to prevent chil-dren’s contact with lead. Screening of children forlead poisoning is useful in identifying areas in mostneed of environmental cleanup and in preventingother cases of lead exposure.

Screen Children for Lead

Lead poisoning can be prevented with routinescreening followed by appropriate educational andcase management programs. In 1988, the Agency forToxic Substances and Disease Registry estimated that250 000 children had blood lead levels of 25 pg/dL ormore; of those, only 12 000 were identified by leadscreening programs.’8 Past screening efforts have

been inadequate. For example, in California, from

1987 through 1990, less than 100 children with bloodlead � 25 were identified annually. In late 1991 leadscreening of low-income children was implemented;and in the first 8 months of 1992, 707 cases wereidentified.59 Even though average levels have de-dined nationwide, lead exposures of a magnitude tocause blood lead levels of concern are common, evenamong children of middle-income families, far morecommon than rates of phenylketonuria, hypothy-roidism, or galactosemia.

Most lead poisoning is clinically inapparent. Evena carefully taken history can miss many of the com-monly encountered sources of lead. A clinical historycannot achieve the sensitivity of a blood lead test. Ina recent survey in a suburban area generally believedto have no lead poisoning problem, 20% of childrenwere found to have blood lead levels of 10 pg/dL orabove.�#{176}

The toxicity of lead is a function of both dose andduration of exposure. It is the role of the pediatricianto give realistic reassurance that early detection andsource control can minimize intellectual and behav-ioral consequences for the individual child. Parentscan also become alarmed if pediatricians dismisstheir concerns. For the emotional well-being of thefamily appropriate measures to identify and reduceexposure should be instituted promptly.

Since the 1970s the blood erythrocyte protopor-phyrin (EP) has been used for screening. Due to lowsensitivity at lower blood lead concentrations, theCDC in 1991 recommended a change from EP screen-ing to a venous blood lead sample.2’6’ A finger-sticksample can be tested and is preferable from thestandpoint of ease and practicality. However, a fin-ger-stick sample is contaminated easily by environ-mental lead, thereby increasing the false-positiverate. Hence, a finger-stick value exceeding 15 pg/dLshould be confirmed with a venous blood lead sam-ple. Reliability of the finger-stick sample depends onthe blood collection technique, and problems shouldbe obvious from the false positive rate. Wherevenous blood lead samples are readily available, theycan be used for initial screening. The laboratory testfor determining lead levels requires a high degree of

proficiency, best acquired by participation in profi-ciency testing programs, such as that run by theCDC.

Urgency and extent of follow-up depend on therisk classification and confirmed venous blood leadlevel. The first step is to perform a confirmatoryvenous blood lead level. This should be done imme-

diately if the screening result is more than 70 pg/dL;within 48 hours, if between 45 and 69 pg/dL; withinI week, if 20 to 44 pg/dL; and within 1 month, if 15to 19 pg/dL (Table 2). Individual follow-up of chil-dren begins with lead levels at 15 pg/dL and medicalevaluation at 20 pg/dL.

MANAGEMENT AND TREATMENT OF BLOODLEAD LEVELS OF 10 MG/DL AND ABOVE

General Principles

Table 1 shows the treatment and follow-up as rec-ommended by the CDC.2 The most important aspectof treatment is removal of the source of exposure.

Patient Education

Education of parents about nutritional sources ofcalcium, iron, zinc, and ascorbate is important for allchildren, but especially for children with blood leadlevels of 10 pg/dL and above. Parents’ attentionshould be directed to the following steps to avoidlead exposure in their children: (1) removing lead-based paint, renovating, and remodeling in the homeshould be done by trained and experienced individ-uals with the family out of the home and propercleanup before the family returns; (2) controffingdust and paint chip debris; (3) preventing the chil-dren from eating dirt or other foreign substances: (4)changing work clothes and cleaning up before goinghome from a lead-related job; (5) avoiding the use oflead around the home for hobbies and other pur-poses; (6) hand washing; and (7) using cold tap waterfor drinking and especially for mixing infant for-mula. Detailed information is available from localpublic health agencies and in the CDC Statement‘Preventing Lead Poisoning in Children.”2

Nutritional Treatment

Children deficient in iron, calcium, zinc, and ascor-bate more readily absorb and/or retain lead fromtheir diets.62 Dietary fat may promote lead absorp-tion.� Treatment of iron deficiency is important forall children but especially for children with bloodlead levels of 10 pg/dL and above.

TABLE 2. Suggested Timetable for Confirming CapillaryBlood Lead Results With a Venous Blood Lead Measurements

Blood Lead

Level (pg/dL)Time Within Which

Blood Lead LevelShould be Obtained

<10 Not applicable

10-14 Not applicable15-19 Within I mo

20-44 Within I wk45-69 Within 48 h

�70

* From the Centers for Disea

Immediately

se Control and Prevention.2



Environmental Intervention

For persistent blood lead levels of 15 pg/dL orabove or a confirmed venous lead level of 20 pg/dL,referrals should be made so that the child’s environ-ment is investigated and cleaned up. The local publichealth agency should be contacted and care shouldbe coordinated. Public health agencies should keepthe physician informed of results of the investigation.

MEDICAL EVALUATION AND MANAGEMENT OFCONFIRMED BLOOD LEAD LEVELS 20 MGIDL

AND ABOVE

History

Clinicians should inquire further about the natureof housing, condition of paint, pica behavior, use offolk remedies or imported ceramics, hobbies, andparental occupation.

Iron Status

Children with elevated blood lead levels should beevaluated for iron deficiency. Iron deficiency can oc-cur in the absence of anemia. A serum ferritin levelless than 12 pg/dL or an abnormally low ratio ofserum iron to iron binding capacity is the most spe-cific indicator of iron deficiency.TM

Other Diagnostic Procedures

Many traditional tests for lead poisoning are un-necessary. Abdominal radiographs are helpful onlyin cases of acute ingestion or unusual persistence ofhigh blood lead values. Lead lines on bone radio-graphs and basophilic stippling of red blood cellsmay be associated with chronic high level exposure,but can be negative even in the presence of seriouslead exposures. Because testing of hair and finger-nails is subject to external environmental contamina-tion, it is an uncertain estimate of body burden and isnot recommended.

Follow-up Testing

Serial lead level measurements provide the bestinformation about lead exposure. The CDC guide-lines (Table 1) provide recommendations for period-icity of follow-up testing in children with elevatedblood lead levels.

Testing Other Children

Children in the same household of a child with ablood lead level exceeding 20 pg/dL should also betested, if exposure is believed to have occurred in thehome. If other locations such as child-care centers,schools, playgrounds, or baby-sitters’ homes areidentified as being lead contaminated, children inthose environments should be tested as well.

Chelation Therapy

Chelation is not recommended at less than 25 pg/dL. Blood lead reduction has been demonstrated inresponse to chelation, but there are no data on im-provement or prevention of cognitive delay. It is nota substitute for removing a child from exposure. ifthe physician is not experienced in the treatment oflead poisoning, it is wise to seek consultation or re-

ferral when chelation therapy is being consideredand in areas where there are dedicated “lead pro-grams.”

Four chelating agents are available: CaNaEDTA,British Anti-Lewisite (BAL), i-penicillamine, andsuccimer.2 Chelation therapy speeds urinary excre-tion of lead.� Most of the attendant risks of chelationare associated with excretion of essential metals (par-ticularly calcium, magnesium, and zinc) along withthe lead.

t-Penidllamine has side effects similar to otherpenidillins. BAL and succimer are mercaptans; BALand CaNaEDTA are nephrotoxic.

The current practice has been to chelate childrenwith a blood lead level of 45 �g/dL or above and tomonitor and consider chelation for blood lead levelsof 25 jig/dL and above.� At blood lead values lessthan 70 jig/dL, when chelation is warranted, threedrugs, CaNaEDTA, r-penicillamine, and succimer,are used for children. o-Penicfflamine is not labeledfor use in lead poisoning, and the label for succimerspecifies use for levels greater than 45 pg/dL.2 Forblood lead levels of 70 pg/dL and above, treatmentwith two drugs, CaNaEDTA and BAL in combina-tion, is generally recommended.� When the childhas signs of encephalopathy, treatment should beprovided in an intensive care setting. Chelatingagents can greatly enhance the absorption of leadfrom the gastrointestinal tract.6’ Drug therapy maybe dangerous unless the child is removed from leadexposure.2 In the initial stages of treatment, this mayrequire hospitalization when measures to discon-tinue lead exposure and to assure full complianceand follow-up have not been implemented. For thisreason, the oral drugs succimer and i-penidllamineare given most appropriately in inpatient settings,until efforts have been made to reduce the child’sexposure to lead.

CONCLUSIONS

Childhood lead exposure continues to be a publichealth problem. Lead exposure is not a disease of thepoor or minorities only or a result of poor child-rearing practices. The “lead problem” has been re-duced but has not been solved. Despite past legisla-tion to remove lead from gasoline and paint, leadexposure persists. The problem is not well enoughunderstood to permit easy solutions. A coordinatedeffort by public health, environmental protection,housing, and pediatric care providers will be expen-sive. Only with such an effort can this preventabledisease be eradicated. Until lead poisoning has beeneliminated, screening programs will be necessaryThe following recommendations address the needfor more acceptable screening methods and more ag-gressive follow-up and cleanup programs.

AM’ RECOMMENDATIONS TO PEDIATRICIANS

1. Anticipatory Guidance. Pediatric providers need toprovide anticipatory guidance and education toparents. This includes information on:. Promotion of safe environmental and occupa-

tional practices so that parents can prevent theexposure of their children to lead; this would


* From the Centers for Disease Control and Prevention.2


include contact via hobbies and contaminatedwork clothing.

. The risk of normal childhood hand-to-mouthactivity and other likely sources of lead expo-sure (paint, house dust, soil, drinking water,etc).

. Provision of instruction in general measures(hygiene, nutrition) for preventing exposure.

I The high risk of children with developmentaldisabifities, who often engage in pica behaviorand can least afford to lose whatever cognitiveor behavioral strengths they have.

2. Blood Lead Screening. Pediatric care providersshould increase their efforts to screen children forlead exposure. Blood lead screening should be apart of routine health supervision for children andcan be addressed best by increasing children’s ac-cess to health care. Because lead is ubiquitous inthe US environment, this screening should occurat about 9 through 12 months of age and, if pos-sible, again at about 24 months of age. The CDChas raised the possibifity that there may be low-risk communities that don’t require screening, butno explicit guidance has been developed for de-termining a community’s risk. As more data arecollected it may become evident that there arelocales where selective screening of children ismore appropriate than routine screening. Cur-rently there is not adequate laboratory capacitynationwide to screen each child, but the require-ment to phase-in screening should generate thoseresources.

3. Clinical Indications for Lead Testing. A history ofpossible lead exposure should be assessed athealth supervision visits between the ages of 6months and 6 years using a number of specificquestions (Table 3). The risk questions identifychildren at high risk who should be screened morefrequently for blood lead levels (Table 1). Leadpoisoning should be considered in the evaluationof the following disorders, either because the leadmay cause these disorders or because the condi-tions may be associated with increased lead inges-tion: developmental delay, learning disabifities,behavior disorder, autism, convulsions, iron defi-

ciency anemia, intestinal parasitic infections,

TABLE 3. Assessing the Risk of High-Dose Exposure toLead: Sample Questionnaire*

Does your child-1. Live in or regularly visit a house with peeling or

chipping paint built before 1960? This could indudea day-care centei� preschool, the home of a babysitteror a relative, etc.

2. Live in or regularly visit a house built before 1%0

with recent, ongoing, or planned renovation or re-

modeling?

3. Have a brother or sister, housemate, or playmate be-lag followed up or treated for lead poisoning (that is,

blood level �15 mg/dL)?4. Live with an adult whose job or hobby involves ex-

posure to lead?5. Live near an active lead smelter, battery recycling

plant, or other industry likely to release lead?

speech and hearing deficits, encephalopathy, re-current vomiting, and recurrent abdominal pain.

RECOMMENDATIONS TO GOVERNMENT

1. Follow-up by Public Health and Housing Agencies.Lead testing of children is futile in the absence ofpublic health programs to ensure environmentalinvestigation and follow-up for individual cases.The government should establish and fund suchprograms. Lead screening programs in high-risk

areas should be integrated with other publichealth activities.

2. Environmental Cleanup. The Academy supports ef-forts of environmental and housing agencies toremove lead from housing and other areas wherechildren may be exposed. Training and certifica-tion of inspectors and abatement workers and ap-proved training programs are needed to avoid cre-ating lead hazards. Some state health departmentscan provide lists of certified contractors and otherexperts. In addition, there is a need for the devel-opment of less expensive, safe technologies forabatement, in order to make primary preventionefforts more cost-effective.

3. Reduction of New Sources of Lead into the Environ-

ment. The Academy supports legislation seekingto reduce the entry of lead into the overall envi-ronment.

4. Identification of Areas Where Lead Risks Exist. Moredata about the rates of elevated levels of bloodlead in specific communities are needed. TheAcademy encourages government to conduct fo-cused surveys in small areas to determine wherelead screening is and is not needed or where erad-ication efforts have been successful. A better un-derstanding of the distribution of lead poisoningwould allow more efficient screening efforts.

5. Research to Develop a Better Lead Test. There is apressing need for a more efficient and less inva-sive test for lead levels or lead toxicity. The idealmeasure could be used routinely on outpatients,

be inexpensive, rapid, sensitive, resistant to con-tamination, and reliable.

6. Lead Poisoning as a Reportable Disease to the Centersf or Disease Control and Prevention. The Academysupports making lead poisoning reportable bylaboratories on a nationwide basis.

7. Sponsorship of Clinical Studies. The Academy rec-ommends more research in the area of determin-ing effectiveness of various strategies to preventand treat lead poisoning, comparison of methodsfor abating lead in households, and controlledclinical trials of chelating agents with long-termfollow-up.

8. Periodic Update of the Screening Recommendations.The Centers for Disease Control and Preventionneeds to conduct studies of the efficacy of leadscreening and monitor the scientific literature toassure that lead screening is carried out in themost public health-protective, least intrusive, andmost cost-effective manner possible. In particular,the risk questions and frequency of follow-up rec-ommendations need to be studied and evaluated.Recommendations about screening also need to be



reevaluated in the light of research publishedsince the time of the 1991 guidelines.

9. Adequate Funding of Screening Tests. The US De-partment of Health and Human Services needs toreconsider its decision to continue using the out-dated erythrocyte protoporphyrin test for Medic-aid-funded children and instead pay for bloodlead tests. The Early Periodic Screening, Diagnosisand Treatment (EPSDT) Program needs to coverthe blood lead test as a separate billable item on anationwide basis.

Co�timi� ON ENVIRONMENTAL HEALTH, 1992 TO 1993J. Routt Reigart, MD, ChairpersonRuth A. Etzel, MDLynn R. Goldman, MD, MPHJim C. Hendrick, MDHoward C. Mofenson, MDPeter R. Simon, MD

LIAISON REPRESENTATIVES

Henry Falk, MD, Centers for Disease Control and

PreventionRobert W. Miller, MD, National Cancer InstituteWalter Rogan, MD, National Institute of

Environmental Health Sciences

CONSULTANTS

Richard J. Jackson, MDHerbert L. Needleman, MD

REFERENCES

1. American Academy of Pediatrics, Committees on Environmental Haz-

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2. Centers for Disease Control. Preventing Lead Poisoning in Young Children.

Atlanta, GA: US Dept of Health Human Services; 1991

3. Suffivan L Speech by Secretary of US Dept of Health and Human

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4. Mahaffey KR, Annest JL, Roberts J, Murphy RS. National estimates ofblood lead levels: United States, 1976-1980: association with selecteddemographic and socioeconomic factors. N EnglJMed. 1982307:573-579

5. Annest JL, PirkleJL, Makuc D, et aL Chronological trend in blood leadlevels between 1976 and 1980. N Engi J Med. 1983:308:1373-1377

6. US Department of Health and Human Services. Public Health Service.

A Public Health Service Progress Report on Health. People 2000: Envi-ronmental Health. Washington, DC: US Department of Health and Hu-man Services; 1992

7. US Department of Health and Human Services. Strategic Plan to Elimi-

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8. Major RH. A History of Medicine. Springfield, IL: Charles C. Thomas,

Publisher; 1954

9. Turner AJ. Lead poisoning among Queensland children. Aust Med Ga-

zette. 1897;16:475-479

10. Gibson JL. A plea for painted railings painted walls of rooms as thesource oflead poisoning among Queensland children. Aust Med Gazette.

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