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Document Number: 

49) 11-1-66 

Docket Number: 

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A STATEMENT BY THE CENTERS FOR DISEASE CONTROL - JANUARY 1985 

U.S. DEPARTMENT OF HEALTH AN D HUMAN SERVICES/PUBLIC HEALTH SERVICE/CENTERS FOR DISEASE CONTROL 
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CENTERS FOR DISEASE CONTROL 

CHILDHOOD LEAD POISONING PREVENTION AD HOC ADVISORY COMMITTEE 

May 17,1984 - September 28,1984 •Im 

CHAIRPERSON 

Rosen, John F., M.D. 

Head, Division of Pediatric Metabolism 

Albert Einstein College of Medicine 

Montefiore Medical Center 

Bronx, New York 10467 

EXECUT1 VE SECR ETA R Y 

Houk, Vernon N., M.D. 

Director 

Center for Environmental Health 

Centers for Disease Control 

Atlanta, Georgia 30333 

Braud, Sara M., M.D. 

Health Deputy Assistant Secretary 

Office of Health Services and 

Environmental Quality 

Louisiana Department of Health and 

Human Resources 

P.O. Box 60630 

New Orleans, Louisiana 70160 

Beljan, John R., M.D. 

Provost and Vice President for 

Academic Affairs 

Dean, School of Medicine 

Hahnemann University 

Broad and Vine Streets 

Philadelphia, Pennsylvania 19102 

Cole, Jerome F., Sc.D. 

President 

International Lead Zinc Research 

Organization 

292 Madison Avenue 

New York, New York 10017 

Davidson, Cliff I., Ph.D. 

Associate Professor of Civil 

Engineering 

Department of Civil Engineering 

Carnegie-Mellon University 

Pittsburgh, Pennsylvania 15213 

Davis, Devera Lee, Ph.D. 

Executive Director 

Board of Toxicology and 

Environmental Health Hazards 

National Academy of Sciences 

2101 Constitution Avenue, N.W. 

Washington, D.C. 20418 

Field, Patricia H., Ph.D. 

Director, Toxicology Laboratory 

State Laboratory of Hygiene 

465 Henry Hall 

Madison, Wisconsin 53706 

Gebbie, Kristine M., R.N. 

Administrator, Health Division 

Department of Human Resources 

1400 S.W. 5th Avenue 

Portland, Oregon 97201 

Jackson, Rudolph Ellsworth, M.D. 

Acting Chairman 

Department of Pediatrics 

Morehouse School of Medicine 

720 West view Drive, S.W. 

Atlanta, Georgia 30310 

MacLean, Robert A., M.D. 

Deputy Commissioner 

Professional Health Services 

Texas Slate Department of Health 

1100 West 49th Street 

Austin, Texas 78756 

Piomelli, Sergio, M.D. 

Director of Pediatric HematologyOncology -

College of Physicians and Surgeons 

of Columbia University 

3959 Broadway 

New York, New York 10012 

Reigarl, J. Routt, M.D. 

Associate Professor 

Department of Pediatrics 

Medical University of South 

Carolina 

171 Ashley Street 

Charleston, South Carolina 29425 

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Children 

A STATEMENT BY THE 

CENTERS FOR DISEASE CONTROL 

JANUARY 1985 

Reprinted July 1985 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

PUBLIC HEALTH SERVICE 

CENTERS FOR DISEASE CONTROL 

CENTER FOR ENVIRONMENTAL HEALTH 

CHRONIC DISEASES DIVISION 

ATLANTA, GEORGIA 30333 
P.5 

Use of trade names is for identification only and does not constitute endorsement by the Public 

Health Service or by the U.S. Department of Health and Human Services. 

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Preface 

This second revision ofthe Centers for Disease Control's (CDC's) statement. Preventing Lead 

Poisoning in Young Children, is more comprehensive than the two previous versions. With help 

from members of CDC's Ad Hoc Advisory Committee on Childhood Lead Poisoning Prevention 

and other expert consultants, we have considered new research findings on lead toxicity, redefined 

lead poisoning al a lower blood lead level, and updated our recommendations on lead-based paint 

abatement. In addition, a recent article on a new treatment scheme for lead poisoning (symptomatic and asymptomatic) is included. 

The precise threshold for the harmful effects of lead on the central nervous system is not 

known. In the meantime, we have used our best judgment as to what levels oflead are toxic and 

what practical interventions will lower blood lead levels. As public health officials, our duly is to 

protect children as best we can—given the limitations of science and the need lo make decisions 

without perfect data. This is ihe Department of Healih and Human Services' major policy statemeni 

on the issue. 

The progressive removal of lead from leaded gasoline is lowering average blood lead levels in 

the United Stales, but the problem of ihe major source of high blood lead levels in our 

country—millions of old housing units painted with lead-based paint —is largely unsolved. Until 

belter approaches and more resources are available for removing lead paint hazards in older dwellings where children live, lead poisoning will continue lo be a public health problem. 

The Committee considered a number of controversial issues, and members vigorously debated 

until a majority indicated that they could support the point under consideration. Readers should 

carefully weigh the recommendations in this document, and they should pay particular attention to 

references to work done since the 1978 CDC statemeni on lead. This 1985 statement represents 

agreement of 11 ofthe 12 Advisory Committee members. One member, Dr. Jerome F. Cole of the 

International Lead Zinc Research prganization, did not support the recommendations. Minutes of 

the Advisory Committee meeting on May 17-18, 1984, and Dr. Cole's statement of dissent are 

available upon request. 

ACKNOWLEDGMENTS 

The lime, effort, and meticulous care the Committee devoted to this statement are gratefully acknowledged. This group of dedicated health professionals, along with notable expert consultants, 

labored through ihe results of several years of research in order lo gain consensus on extremely 

complex issues. The various drafts of ihis document had the benefit of thoughtful suggestions from 

Committee members and consultants alike. Their work will help protect the children of this nation 

from this preventable disease for many years to come. 

Vernon N.Houk, M.D. 

Director 

Center for Environmental Health 

1 

in 
P.7 

Contents 

I. INTRODUCTION 1 

Definitions 1 

II. BACKGROUND .' 3 

III. SOURCES OF LEAD EXPOSURE 5 

Lead-Based Paint 5 

Airborne Lead 5 

Soil & Dust 7 

Occupational Sources 7 

Food & Drinking Water 7 

Lead-Glazed Poltery 7 

Other Sources 7 

IV. SCREENING 8 

Goal of Childhood Lead Poisoning :... . 8 

Target Population 8 

Screening Schedule 8 

Screening Methods 9 

Intervention Levels 9 

Measurements of Erythrocyte Protoporphyrin 10 

Measurement of Blood Lead 12 

Screening Schemes 12 

Interpretation of Screening 12 

V. DIAGNOSTIC EVALUATION 14 

Tests 14 

VI. CLINICAL MANAGEMENT 16 

Urgent Risk 16 

High Risk 17 

Moderate Risk 17 

Low Risk 17 

VII. ENVIRONMENTAL EVALUATION AND LEAD HAZARD ABATEMENT 18 

Lead-Based Paint 18 

Airborne Lead 20 

Soil & Dust 20 

Food & Water 20 

Occupational 20 

Lead-Glazed Pottery 21 

VIII. HEALTH EDUCATION 22 

IX. REPORTING LEAD TOXICITY AND ELEVATED BLOOD LEAD LEVELS 22 

X. REFERENCES 23 

APPENDIX — Management of Childhood Lead Poisoning: Special Article 26 

mmmmmmmmma ^ m ^ m 
P.8 

1 

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Contents - continued 

Figure 1. Sources of Lead in a Child's Environment 6 

Table 1. Suggested Priority Groups for Lead Screening : 8 

Table 2.A Zinc Protoporphyrin (ZnPP) by Hemalofluorometer: Risk Classification of 

Asymptomatic Children for Priority Medical Evaluation 11 

Table 2.B Erythrocyte Protoporphyrin (EP) by Extraction: Risk Classification of 

Asymptomatic Children for Priority Medical Evaluation 11 

vi 

^HMH^HHH 
I. Introduction 

P.9 

Lead is ubiquitous in the human environment as a 

result of industrialization. It has no known physiologic 

value. Excessive absorption of lead is one of the most 

prevalent and preventable childhood health problems in 

the United Stales today. Children are particularly susceptible lo its toxic effect. 

Since 1970, ihe detection and management of children 

exposed to lead has changed substantially. Before the 

mid-1960's, a level below 60 micrograms of lead per 

deciliter (^tg/dl) of whole blood was not considered 

dangerous enough to require intervention (Chisolm, 

1967). By 1975, the intervention level had declined 

•50%-to 30 /ig/dl (CDC, 1975). In that year, the Center 

(now Centers) for Disease Control (CDC) published Increased Lead Absorption and Lead Poisoning in Young 

Cliildren: A Statement by the Center for Disease Control. 

Since then, new epidemiologic, clinical, and experimental 

evidence has indicated thai lead is toxic al levels previously thought to be nontoxic. Furthermore, it is now 

generally recognized that lead toxicity is a widespread 

problem — one that is neither unique to inner city children 

nor limited lo one area ofthe country. 

Progress has been made. The Second National Health 

and Nutrition Examination Survey (NHANES II) has established average blood lead levels for ihe U.S. population; lead-coniaminated soil and dust have emerged as 

important contributors lo blood lead levels, as has leaded 

gasoline, through its contribution to soil and dusl lead 

levels. An increasing body of data supports Ihe view that 

lead, even al levels previously thought to be "safe," is 

loxic lo the developing central nervous system; and 

screening programs have shown the extent oflead poisoning in target populations. 

A major advance in primary prevention is the phased 

reduction of lead in gasoline. Il is probably responsible 

for the findings of reduced average blood lead levels in 

children nationwide (Annest et al., 1983) and in two 

major cities (Rabinowitz and Needleman, 1982; Billick et 

al., 1980; Kaul et al., 1983). Lead is no longer allowed in 

paint to be applied to residential dwellings, furniture, and 

toys. 

The sources of lead are many. They include air, waler, 

and food. Despite the 1977 ruling by the Consumer Product Safely Commission (CPSC) that limits the lead conlent of newly applied residential paints, millions of housing units still contain previously applied leaded painls. 

Older houses ihal are dilapidated or thai are being 

renovated are a particular danger lo children. In many 

urban areas, lead is found in soil (Mielke el al., 1983) and 

house dust (Chantey et al., 1983). Consequently, screening programs—a form of secondary prevention—are still 

needed to minimize the chance oflead poisoning developing among susceptible young children. 

Lead poisoning challenges clinicians, public health authorities, and regulatory agencies lo put into action the 

findings from laboratory and field studies thai define the 

risk for this preventable disease. Although screening programs have been limited, they have reduced the number 

of children with severe lead-relaied encephalopathy and 

other forms oflead poisoning. 

The revised recommendations in this 1985 Statement 

reflect current knowledge concerning screening, diagnosis, treatment, followup, and environmental intervention 

for children with elevated blood lead levels. Clearly, the 

goal is to remove lead from the environment of children 

before it enters their bodies. Until this goal is reached, 

screening, diagnosis, treatment, followup, and secondary 

environmental management will continue to be essential 

public health activities. 

DEFINITIONS 

The two lerms defined below—elevated blood lead 

level and lead toxicity—are for use in classifying children 

(whose blood has been tested in screening programs) for 

followup and treatment. The terms should not be interpreted as implying thai a safe level of blood lead has been 

established. Furthermore, they are to be used as guidelines. They may not be precisely applicable in every case. 

Each child needs lo be evaluated on an individual basis. 

The CDC is lowering its definition of an elevated 

blood lead level from 30 to 25 /*g/dl. The definitions 

below are simplified versions of those in Preventing Lead 

Poisoning in Young Children: A Statement by the Center for 

Disease Control: April 1978 (CDC, 1978). 

• elevated blood lead level, which reflects excessive 

absorption of lead, is a confirmed concentration of 

lead in whole blood of 25 /ig/dl or greater; 

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• lead toxicity is an elevated blood lead level with an 

erythrocyte protoporphyrin (EP)* level in whole 

blood of 35 /xg/dl or greater. , 

J 

As defined by blood lead and EP levels, the terms lead 

toxiciiy and lead poisoning are used synonymously in Ihis 

document. "Poisoning" is generally used to describe episodes of acute, obviously symptomatic illness. The term 

"toxicity" is used more commonly in this document, 

since screening programs usually involve asymptomatic 

children. 

According lo this Statement, the severity oflead toxicity is graded by Iwo distinci scales—one for use in screening, the other for use in clinical management. In Ihe scale 

used in screening, children wilh lead toxiciiy are divided 

into classes I, II, III, and IV (section IV). These classes 

indicate the urgency of further diagnostic evaluation (seclion V). After Ihe diagnostic evaluation, ihey are placed 

in one of four risk groups: urgent, high, moderate, and 

low (section VI). 

*EP results are expressed in equivalents of free erythrocyte protoporphyrin (FEP) extraded by the ethyl acetate-acetic acid-HCI method and reported in micrograms per deciliter of whole blood. In this Statement, zinc protoporphyrin (ZnPP) and FEP are referred lo as EP. 

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II. Background 

A nationwide survey, conducted from 1976-1980, 

showed that children from all geographic areas and socioeconomic groups are at risk oflead poisoning (Mahaffey, 

Annest et al., 1982). Data from that survey indicate that 

3.9% of all U.S. children under the age of 5 years had 

blood lead levels of 30 ug/dl or more. Extrapolating this 

to the entire population of children in the United States 

indicates that an estimated 675,000 children 6 months to 

5 years of age had blood lead levels of 30 /ig/dl or more. 

There was, in addition, a marked racial difference in 

those data. Two percent of white children had elevated 

blood lead levels, but 12.2% of black children had elevated levels. Further, among black children living in the 

cores of large cities and in families with annual incomes 

of less than $6,000, the prevalence of levels of 30 /xg/dl 

or more was 18.6%. Among white children in lower 

income families, the prevalence of elevated lead levels 

was eight times that of families with higher incomes. 

In the past decade, our knowledge of lead toxicity has 

greatly increased. Previously, medical attention focused 

on the effects of severe exposure and resultant high body 

burdens associated with clinically recognizable signs and 

symptoms of toxicity (Perlstein and Attala, 1966; Chisolm, 1968; Byers and Lord, 1943). It is now apparent 

that lower levels of exposure may cause serious behavioral and biochemical changes (De la Burde and Choate, 

1972, 1975; NAS, 1976; WHO, 1977). Recent studies 

have documented lead-associated reductions in the biosynthesis of heme (Piomelli et al., 1982), in concentrations of 1,25-dihydroxy vitamin D (Rosen et al., 1980; 

Mahaffey, Rosen et al., 1982), and in the metabolism of 

erythrocyte pyrimidine (Angle and Mclntire, 1978; 

Paglia et al., 1977). Results ofa growing number of studies indicate that chronic exposure to low levels oflead is 

associated with altered neurophysiological performance 

and that the young child is particularly vulnerable to this 

effect (Needleman et al., 1979; Winneke, 1982; Yule et 

al., 1981). Investigations have also shown alterations in 

electroencephalograms (EEG's) (Burchfiel et al., 1980; 

Benignus et al., 1981; Otto et al., 1982) and decreased 

velocity in nerve conduction (Seppalainen and Hernberg, 

1982; Feldman etal., 1977). 

Many factors can affect the absorption, distribution, 

and toxicity of lead. Children are more exposed to lead 

than older groups because their normal hand-to-mouth 

activities introduce many nonfood items into their bodies 

(Lin-Fu, 1973). Once absorbed, lead is distributed 

throughout soft tissue and bone. Blood levels reflect the 

dynamic equilibration between absorption, excretion, 

and deposition in soft- and hard-tissue compartments 

(Rabinowitz et al., 1976). Young children absorb and 

retain more lead on a unit-mass basis than adults. Their 

bodies also handle lead differently. Higher mineral turnover in bone means that more lead is available to sensitive 

systems. The child's nutritional status is also significant 

in determining risks. Deficiencies in iron, calcium, and 

phosphorus are directly correlated with increased blood 

lead levels in humans and experimental animals (Mahaffey, 1981; Mahaffey and Michaelson, 1980). Increased 

dietary fat and decreased dietary intake of calcium 

(Barltrop and Khoo, 1975; Rosen et al., 1980), iron 

(Mahaffey-Six and Goyer, 1972), and possibly other nutrients enhance the absorption oflead from the intestine 

(NAS, 1976; Barltrop and Khoo, 1975). 

Since lead accumulates in the body and is only slowly 

removed, repeated exposures to small amounts over 

many months may produce elevated blood lead levels. 

Lead toxicity is mainly evident in the red blood cells 

and their precursors, the central and peripheral nervous 

systems, and the kidneys. Lead also has adverse effects 

on reproduction in both males and females (Lane, 1949). 

New data (Needleman et al., 1984) suggest that prenatal 

exposure to low levels of lead may be related to minor 

congenital abnormalities. In animals, lead has caused 

tumors of the kidney. The margin of safety for lead is 

very small compared with other chemical agents (Royal 

Commission on Environmental Pollution, 1983). 

The heme biosynthetic pathway is one ofthe biochemical systems most sensitive to lead. An elevated EP level 

is one of the earliest and most reliable signs of impaired 

function due to lead. A problem in determining lead 

levels in blood specimens is that the specimen may be 

contaminated with lead, and thus the levels obtained may 

be falsely high. Therefore, in the initial screening of 

asymptomatic children, the EP level (instead of the lead 

level) is determined. 

The effects of lead toxicity are nonspecific and not 

readily identifiable. Parents, teachers, and clinicians may 

identify the altered behaviors as .attention disorders, 

learning disabilities, or emotional disturbances. Because 
ofthe large number of children susceptible to lead poisoning, these adverse effects are a major cause for concern. 

Symptoms and signs of lead toxicity are fatigue, pallor, 

malaise, loss of appetite, irritability, sleep disturbance, 

sudden behavioral change, and developmental regression. More serious symptoms are clumsiness, muscular 

irregularities (ataxia), weakness, abdominal pain, persistent vomiting, constipation, and changes in consciousness 

due to early encephalopathy. Children who display these 

symptoms urgently need thorough diagnostic evaluations 

and, should the disease be confirmed, prompt treatment. 

In this Statement, screening is distinct from diagnosis. 

"S'cfeWi1Tf'''Wda 

large numbers of presumably asymptomatic children 

to determine if they have been exposed to lead and, if 

so, what the risks of continued exposure are. Diagnosis, on the other hand, means the calegorization of a 

child appearing to have excess exposure to lead according to the severity of burden and toxicity so that appropriate management can be started. No child with 

symptoms suggesting lead toxicity should be put 

through the screening process. He or she should be 

brought directly to medical attention. 

" 
P.13 

III. Sources of Lead Exposure 

. Children may be exposed to lead from a wide variety 

of man-made sources. All U.S. children are exposed to 

lead in the air, in dust, and in the normal diet (Figure 1). 

Airborne lead comes from both mobile and stationary 

sources. Lead in water can come from piping and distribution systems. Lead in food can come from airborne lead 

deposited on crops, from contact with "leaded" dust 

during processing and packaging, and from lead leaching 

from the seams of lead-soldered cans. In addition to exposure from these sources, some children, as a result of 

their typical, normal behavior, can receive high doses of 

lead through accidental or deliberate mouthing or swallowing of nonfood items. Examples include paint chips, 

contaminated soil and dust, and, less commonly, solder, 

curtain weights, bullets, and other items. 

LEAD-BASED PAINT 

Lead-based paint continues to be the major source of 

high-dose lead exposure and symptomatic lead poisoning 

for children in the United States (Chisolm, 1971). Since 

1977, household paint must, by regulation, contain no 

more than 0.06% (600 parts per million (ppm)) lead by 

dry weight. In the past, some interior paints contained 

more than 50% (500,000 ppm) lead. The interior surfaces 

of about 27 million households in this country are contaminated by lead paint produced before the amount of 

lead in residential paint was controlled. Painted exterior 

surfaces are also a source of lead. Unfortunately, leadbased paint that is still available for industrial, military, 

and marine usage occasionally ends up being used in 

homes. 

Usually, overt lead poisoning occurs in children under 

6 years of age who live in deteriorated housing built 

before World War II. Pica, the repealed ingestion of nonfood substances, has frequently been implicated in the 

etiology oflead toxicity in young children. In many cases, 

however, lead-paint ingestion is simply the result ofthe 

normal mouthing behavior of small children who live in 

lead-contaminated homes. Cases of children poisoned by 

lead paint have been reported from all regions of the 

United Slates and from bolh urban and rural settings. Increasingly, ihis poisoning has been reported when families move into a city as "urban homesteaders," and the 

children are inadvertently exposed lo chips, fumes, or 

dust from lead-based paint as houses are rehabilitated. 

Clusters of lead-based paint poisonings have also resulted 

from demographic shifts wilhin cities, when families wilh 

young children have moved into neighborhoods wilh 

deterioraiing older housing. Increased lead absorption 

has been reported in children exposed to chips or dusl 

from lead-based paini produced during the deleading of 

exterior painted steel structures, such as bridges and expressways (Landrigan et al., 1982). 

AIRBORNE LEAD 

Generally, inhalation of airborne lead is a minor exposure pathway for individual children, but lead-containing 

particles—airborne and then deposited—can be responsible for high concentrations of lead in dust that children 

ingest. Studies in New Jersey (Caprio et al., 1974) and 

California (Johnson et al., 1975) have shown that children living within 100 feet of major roadways have higher 

blood lead levels than those living farther away. These 

levels also correlate positively with the average daily traffic volume on roads near homes (Caprio et al., 1974). 

Previous estimates ofthe quantitative relationship between ambient air lead levels and blood lead levels may 

need io be revised because of new experimental and 

survey data. Preliminary results from an isotopic lead experiment (Facchetti and Geiss, 1982) suggest ihat lead 

from leaded gasoline is a much more importanl contaminant than ii was previously thought to be. The preliminary 

estimates from thai study indicate that al least 25% of ihe 

blood lead of residents of Turin, Italy, is derived from 

lead in gasoline. In Turin, the average blood lead level in 

adult males is 25 ug/dl; this corresponds lo about 6 ug/dl 

attributable lo gasoline. 

Daia from NHANES II also indicate that leaded gasoline is a more significant source of lead than previously 

thought. Annest el al. (1983) correlated major reductions 

in the amounts of lead added lo gasoline sold in the 

United Stales with significant reductions in children's 

blood lead levels. They found that between 1976 and 

1980, the overall mean blood lead levels in the U.S. population dropped from 14.6 ug/dl to 9.2 ug/dl. A similar 

relationship between leaded gasoline sales and umbilical 

cord blood lead levels has been shown by Rabinowiiz and 

Needleman (1983). 

Stationary sources can produce concentrated zones of 

exposure, especially where climatic conditions such as 

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P.14 

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Figure 1 

SOURCES OF LEAD IN A CHILD'S ENVIRONMENT 

HOST 

CHILD 

Ingestion 

Other 

Nonfood 

Items** 

'Production of bullets or fishing sinkers 

Soldering and stained-glass work 

Gasoline sniffing 

Pottery glazing 

Burning of batteries, colored newsprint, lead-painted objects, and waste oil 

'Toys and figures containing lead 

Folk remedies 

Cosmetics (especially Oriental cosmetics, e.g.. Surma, a black eyeliner) 

Jewelry (painted with lead to simulate pearl) 

Lead-containing dust transmitted on clothing from workplace 

TT^.r*^TTTT3.:. 
P.15 

aridity, low wind velocity, and frequent thermal inversions minimize dispersal of airborne lead. The worst situations of this kind in ihe United Slates have existed in the 

vicinity of primary lead smelters (Baker, Hayes et al., 

1977). 

SOIL AND DUST 

Soil and dust that contain lead are often an important 

source of lead exposure for children. The particles of airborne lead deposited in soil and dusl usually come from 

automotive, industrial, and similar sources. Flaking lead 

paint adds lo this contamination, particularly in and 

around houses. In soil, lead tends lo remain in ihe lop 

centimeter, but mosi soils are contaminaled to a much 

greater depth when the lopsoil is disturbed and turned 

under. 

Children appear to obtain lead from dust and soil as a 

result of their normal exploratory behavior (Barltrop, 

1966; Sayre et al., 1974; Roels et al., 1976), coupled in 

some instances with pica. Because of those mouthing 

tendencies, young children who live near major sources 

of airborne lead pollution must be considered at risk of 

exposure both by inhalation of airborne lead and by ingestion of deposited lead from soil and dust. 

In general, lead in soil and dust appears to be responsible for blood lead levels in children increasing above 

background levels when the concentration in the soil or 

dust exceeds 500-1,000 ppm. 

OCCUPATIONAL SOURCES 

Lead dusl can cling to the skin, hair, shoes, clothing, 

and vehicles of workers, and lead can be carried from 

workplace to home in ihis way. In a study in Memphis, 

Tennessee, when a parent worked with lead, the amount 

of lead in the children's blood correlated with ihe concentration of lead in dust in iheir homes (Baker, Folland et 

al., 1977). Of 91 children tested, 38 (41.8%) had blood 

lead levels of 30 ug/dl or more, and 10 either had blood 

lead levels of 80 ug/dl or more or EP levels above 190 

ug/dl. 

Strict compliance with Occupational Safely and Health 

Administration (OSHA) standards is quite effective in 

decreasing this type of exposure. However, many occupational exposures to lead are noi covered by the OSHA 

standards. Companies wilh fewer than 10 employees (cottage industries, "hobby" production of pollery and 

slained glasswork, and home manufacturing of bullets 

and fishing sinkers) are excluded from OSHA standards. 

The OSHA standard for lead workers is a blood lead 

level of 40 ug/dl. In a pregnant woman, lead crosses the 

placenia, and lead concentrations in umbilical cord blood 

are nearly equal to those in maternal blood (Barlirop, 

1966). Since the growing brain ofthe fetus is likely lo be 

at least as sensitive lo the neurologic effects oflead as the 

brain ofa young child, umbilical cord blood levels should 

be al least below 25 ug/dl. Therefore, the OSH A standard 

is probably not sufficiently strict to protect the feius. Further study is needed lo define acceptable lead levels 

among women of childbearing age. 

FOOD AND DRINKING WATER 

Lead in food, although rarely responsible for lead 

poisoning in ihe United Stales, is a ubiquitous source of 

background low-dose exposure for children (Beloian, 

1982). Agricultural crops grown near heavily traveled 

roads or near stationary sources oflead can have significant concentrations because of airborne lead deposited 

on them. Lead may also be inadvertently added lo foods 

during processing and handling. Canned foods may have 

particularly high lead contents, because acidic foods can 

leach lead from the solder in the seams of the cans 

(Lamm etal., 1973).' 

Generally, lead in drinking water has been leached 

from pipes and soldered joints by sofi water having an 

acidic pH. Severe lead exposure has been reported among 

children in Glasgow, Scotland, where pure, acidic water 

was allowed to stand overnight in aitic cisterns lined with 

lead (Beattie el al., 1972). The problem was alleviaied by 

changing ihe pH of ihe water in the water treatment 

plant. In the United Stales, lead waler pipes are most 

commonly found in older sections of northeastern cities 

and, occasionally, in rural areas ofthe northeast (Morse 

ei al., 1979). 

LEAD-GLAZED POTTERY 

Although not a widespread source oflead, lead-glazed 

pottery can release large amounts of lead into food and 

drink. It has been responsible for outbreaks of serious 

poisoning (Klein el al., 1970). In several episodes reported to CDC, the pollery had been imported. Homemade 

or craft pottery and porcelain-glazed vessels have been 

found lo release large quantities oflead, particularly ifthe 

glaze is chipped, cracked, or improperly applied (Osterud 

el al., 1973). If the vessels are repeatedly washed, the 

glaze may deteriorate and pottery previously lested as 

safe can become unsafe (D. M. Wallace, personal 

communication). 

OTHERSOURCES 

Lead is found in a variety of items, some of which 

endanger specific populations or ethnic groups. A variety 

of folk remedies contain lead, including azarcon and greta 

used by Mexican groups and pay-loo-ah used by Hmong 

refugees from Laos. Serious poisoning can also result 

from gasoline sniffing; the burning of waste oil, colored 

newsprint, battery casings, or lead-painted wood; and 

target practice in poorly ventilated, indoor firing ranges. 

^^?|si2aSige>s 
IV. Screening 

P.16 

GOAL OF A CHILDHOOD LEAD POISONING 

PREVENTION PROGRAM 

The goal of a childhood lead poisoning screening program is to identify children with significant exposure to 

lead early enough to prevent serious toxicity. Elevated 

blood lead levels must be detected in asymptomatic children, and appropriate medical and environmental interventions must follow. The goal can be reached only 

through — 

1. A screening program that enrolls the maximum 

number of children in high-risk populations. 

2. A referral system that ensures a comprehensive diagnostic evaluation of every child with a positive 

screening test. 

3. A program that assures identification and elimination ofthe source (s) of the child's lead exposure. 

4. A system that monitors the adequacy of the treatment and the followup of each child with a diagnosis 

oflead toxicity. 

Screening is of no value without prompt, thorough, 

and continuing medical and environmental followup for 

those children found to have lead toxicity—that is, as 

stated earlier, an elevated blood lead level (a confirmed 

concentration in whole blood of 25 jug/dl or greater) and 

an EP level in whole blood of 35 ug/dl or greater. Also as 

stated earlier, screening must be distinguished from 

diagnosis: 

Screening refers to the testing of large numbers of 

children considered to be ASYMPTOMATIC in order 

to identify those who need further evaluation. 

Diagnosis, on the other hand, refers to categorizing a 

child's condition according to severity of lead burden 

and toxicity. Then, on the basis of the category, 

management is selected. 

Children whose elevated blood lead levels are detected 

by screening should be brought directly to medical attention, and the diagnostic process should be started without 

delay. Children with symptoms suggestive oflead poisoning require urgent and thorough diagnostic evaluation 

and, if the diagnosis is confirmed, immediate treatment. 

The symptoms oflead poisoning are nonspecific; they are 

described in section V. 

TARGET POPULATION 

Lead is most harmful to children between the ages of 9 

months and 6 years. Ideally, all children in this age group 

should be screened. As more children are screened for 

iron deficiency with EP testing, simultaneous lead screening ofthese same groups becomes feasible. The list of priority groups in Table 1 highlights groups for which 

screening is strongly indicated. Testing children in lowrisk groups for lead toxicity may not be practical unless it 

is done simultaneously with EP tests for iron deficiency. 

Children in the 12- to 36-month-old age group who 

live in or are frequent visitors in deteriorating older buildings (including day-care centers) make up the highest priority group. 

Siblings, housemates, and playmates of children with 

identified lead toxicity probably have similar exposures 

to lead, and they should be promptly screened. Suggested 

rankings for these and other priority groups are in Table 2. 

Table 1 

Suggested Priority Groups for Lead Screening 

Priority 

1. HIGHEST—Children, age 12 lo 36 months, who live in or are frequent visitors in older, dilapidated housing 

Children, age 9 months to 6 years, who are siblings, housemates, 

visitors, and playmates ofchildren with known lead toxicity 

Children, age 9 months to 6 years, living in older, dilapidated 

housing 

Children, age 9 months to 6 years, who live near lead smelters and 

processing plants or whose parents or other household members 

participate in a lead-related occupation or hobby 

Children, age 9 months to 6 years, who live near highways with 

heavy traffic or near hazardous waste sites where lead is a major 

pollutant 

All children 12 lo 36 months of age 

All children 9 months lo 6 years of age 

2. 

3. 

4. 

5. 

SCREENING SCHEDULE 

Screening for lead poisoning should be incorporated 

into a general pediatric health care program, and children 

in the target population should be screened at least once a 

year. The first screening should be done when the child is 

between 9 and 12 months old. Children generally have 

higher blood lead levels between May and October 

(NAS, 1976), so screening efforts should be concentrated 

in those months. Since negative screening tests in children living in a hazardous environment do not rule out 

subsequent exposure, children 12 to 36 months old who 

are at high risk of exposure should be screened every 2 to 

3 months, especially during the summer. Children who 

move into a high-risk area after age 3 years may also need 

to be screened more than once a year. 

r^T'yy-^'"-''^-^-'' •L^'-'^'AttR'*^.***^ 
SCREENING METHODS 

Currently, the most useful screening tests are those 

for. erythrocyte protoporphyrin (EP) and blood lead. 

Venous or capillary blood can be used fonboth tests, but 

papillary specimens are easier to collect and are, therefore, more widely used. Capillary blood may be transported in a capillary tube with an anticoagulant or dried on 

filter paper. Sampling methods used in the field must be 

compatible with laboratory capabilities. 

EP and blood lead tests measure different aspects of 

lead toxicity. As stated earlier, EP tests measure the level 

of EP in whole blood, and a level of 35 ug/dl or more indicates impaired heme synthesis, which may be due to the 

toxic effects oflead; blood lead tests measure lead absorption, and a confirmed concentration of 25 ug/dl or more, 

referred to as an elevated blood lead level, reflects an excessive absorption oflead. Usually, there is a close correlation between results ofthe two tests for specimens from 

the same child, but, occasionally, the result of one test 

may be elevated and the result of the other, not elevated. 

The EP test has three advantages over the blood lead test: 

(1) when blood lead levels are moderately elevated, the 

EP test better identifies children with rising blood lead 

levels (Reigart and Whitlock, 1976); (2) if the specimen 

is contaminated with lead, the contamination does not 

affect the EP test; and (3) the EP test is an accepted 

screening test for iron deficiency. 

INTERVENTION LEVELS 

Children screened for lead poisoning can be grouped 

into two categories: those who require further evaluation 

and those who do not. Choosing the intervention level 

that divides these two groups is based on a compromise 

among the following: 

(1) the desire to identify all children with any degree 

oflead toxicity 

(2) a judgment about the urgency of preventing various detectable effects 

(3) the sensitivity and specificity ofa practical screening test 

(4) society's ability to remove the sources of lead 

exposure 

A. Pathophysiological Considerations 

In recent years, levels of exposure previously considered "safe" have been shown to produce adverse effects. 

In addition, contemporary people (including children) 

living in remote areas with negligible exposure to lead 

have blood lead levels much lower than people living in 

the United States (Piomelli, 1980). Thus, the blood lead 

levels of U.S. children reflect a high degree of environmental contamination by lead. Today, the average blood 

lead level in the U.S. population is about 10 

p.g/dl —approximately three times the average level 

found in some remote populations. These observations 

suggest that the average level in the U.S.A. should be reduced. At present, however, because of practical considerations, the goal of reducing U.S. levels to those of 

remote populations is unattainable. Therefore, the blood 

lead level at which intervening action should be taken 

should be based on (1) criteria that indicate significant 

risk to the individual child and (2) the best combination 

of tests: a test for the blood lead level as an indicator of absorption and a test for EP as an indicator of biochemical 

derangement. 

Since the CDC's 1978 statement on lead poisoning, 

several investigators have demonstrated effects of lowlevel lead exposures in these areas: 

1. children's behavior and intelligence (Needleman et 

al., 1979; Winneke, 1982; Yule et al., 1981) 

2. the central and peripheral nervous systems of adult 

workers (Mantere et al., 1982; Seppalainen and 

Hernberg, 1982) 

3. heme biosynthesis in children (Piomelli et al., 1982) 

4. nucleotide metabolism (Angle and Mclntire, 1978) 

5. vitamin D metabolism in children (Rosen et al., 

1980; Mahaffey, Rosen et al., 1982). 

The precise level at which lead exposure begins to 

cause developmental or neurobehavioral problems in 

children may be impossible to define in the near future. 

In the meantime, decisions on public health measures 

have to be made on the basis of (1) other, more objectively measurable effects and (2) an adequate margin of 

safety. 

The elevation of EP, a toxic effect of lead in humans, 

has been well studied and it can be measured objectively. 

Among the biologic markers oflead toxicity, EP measurements have been the most useful in screening programs 

for lead poisoning. Recent studies have shed new light on 

the effects oflead and of iron deficiency on EP levels. 

Several years ago, Roels et al. (1976), basing their 

argument on EP measurements, stated that a blood lead 

level of 25 ug/dl should be the maximum permissible 

concentration. Cavalieri et al. (1981), who made a study 

around a lead smelter, indicated that even this level may 

be too high. This group found an EP response at blood 

lead levels ranging between 10 and 20 ug/dl, suggesting 

that the EP no-response level is lower than 10 ug/dl. In a 

more recent and comprehensive examination of the 

issue, Piomelli et al. (1982) studied data from over 2,000 

children. Blood lead and EP tests were done on venous 

specimens collected from children throughout New York 

City. Piomelli and his colleagues were trying lo find the 

blood lead level at which the EP level began to increase. 

A variety of statistical techniques were used, and the findings were consistent; when blood lead levels increased 

linearly above the area of 15-18 ug/dl, the EP level increased exponentially. 

Recent studies of EDTA (calcium disodium ethylene 

diamine tetraacetic acid) mobilization testing indicate 

that the amount oflead excreted by children with blood 

lead levels of 30-40 ug/dl may often be comparable to 

that excreted by children with levels of 50-70 ug/dl (Markowitz and Rosen, 1984). This finding suggests that the 
biood lead level may underestimate tne ooay ouraen oi 

lead. 

In summary, the EP data, with data from the other 

studies referred to, indicate that the 1978 blood lead 

guideline of 30 ug/dl has little or no margin of safety and 

should be lowered. 

B. Practical Considerations 

Although the biologic threshold for lead toxicity, as 

manifested by increasing EP levels, is less than 20 ug/dl, 

the criteria for a screening program have lo take into account additional factors: (1) acceptability, sensitivity, and 

specificity of the screening procedure; (2) costeffecliveness; and (3) the feasibility of effective intervention and followup. 

The identification of children with blood leads below 

25 ug/dl would require screening with a blood lead assay 

rather than an EP test, since the latter screening test has a 

very poor sensitivity and specificity below a blood lead 

level of 25 ug/dl. Such a recommendation would require 

most programs lo use venous blood samples or to adopt 

impractically rigorous training and quality control procedures. Capillary blood samples are prone to environmental contamination with lead. In most programs, particularly those in high-risk areas, the use of "routine" capillary 

blood-drawing techniques results in an unacceptably high 

frequency of falsely elevated blood lead levels. On the 

other hand, taking blood samples from the veins of small 

children is less acceptable to parents and technically 

much more difficult. In addition, the cost ofthe screening 

program would increase severalfold. For all these reasons, 

an intervention level set at blood lead values below 25 

ug/dl might ultimately substantially decrease the number 

of children being screened. 

If local screening programs evaluate the distribution of 

moderately and highly elevated blood lead levels within a 

community, the findings may identify sources oflead that 

might go unnoticed if the program focused solely on 

children with high lead levels. 

Even when slightly elevated blood lead levels are 

found, some interventions are possible and effective. 

House dust is an insidious but apparently effective carrier 

of lead to children in contaminated environments. In 

urban areas dust frequently contains large amounts of 

lead, thought to come primarily from airborne sources or 

leaded paint. Charney el al. (1983) have documented the 

effectiveness of controlling house dust; thus, in some situations, low and moderately elevated blood lead levels 

can be reduced simply by controlling house dust. 

Considering these factors, CDC recommends as the intervention level a blood lead level of 25 ug/dl associated 

with an EP level of 35 ug/dl. When the blood lead level is 

25 ug/dl or greater associated with an EP value of 35 

ug/dl or greater, lead toxicity is present; identification of 

such children is the focus of CDC's new recommendations. 

Children may have mildly elevated blood lead levels without concurrent increases in EP concentrations, and it is 

desirable to ideriiiiy wese cniiaftin;-BiM,-ahp.reseni, imy is 

impractical and beyond the criteria set for screening programs. Nonetheless, when resources and capabilities 

permit both blood lead and EP to be measured in the primary screening program, additional children with elevated blood lead levels will be identified. A more practical 

method for identifying such children needs to be 

developed. 

The CDC recommends the following cutoff levels for 

determining a high risk for lead toxicity: for EP screening, 

a level of 35 ug/dl (whole blood should be tested); for followup testing, all children with a blood lead of 25 ug/dl or 

more should be considered at risk for the toxic effects of 

lead. Since the EP level is also elevated in iron deficiency, 

an elevated EP test alone should not be considered to be 

diagnostic oflead toxicity. 

MEASUREMENT OF 

ERYTHROCYTE PROTOPORPHYRIN 

Erythrocyte protoporphyrin (EP) may be measured by 

fluorometry after it has been extracted from the red 

blood cells or by direct fluorescence in intact cells 

(Lamola et al., 1975; Blumberg et al., 1977). In lead 

toxicity and iron deficiency, this metabolite is present in 

the red cells mainly as zinc protoporphyrin (ZnPP), but 

the ethyl acetate-acetic acid extraction procedure converts 

zinc protoporphyrin to erythrocyte protoporphyrin. 

Measuring ZnPP by hematofluorometer and EP after it 

has been extracted from the cells reflects essentially the 

same compound. In erythropoietic protoporphyria, an extremely rare disease, EP is markedly elevated—usually 

above 300 ug/dl. This is the free EP base, but it is detected by the EP extraction method and, to a lesser extent, by 

the hematofluorometer. 

EP is also elevated in sickle cell anemia and other 

hemolytic anemias (Langer et al., 1972). Hyperbilirubinemia (jaundice) will cause falsely elevated EP readings 

with the hematofluorometer, but not with the extraction 

method (Buhrmann et al., 1978). Recent colds, ear infections, and other minor illnesses may also cause slight elevations of EP (Reeves et al., 1984). Nevertheless, lead 

toxicity should always be ruled out as the cause of elevated EP levels. 

A. Use of Hematofluorometers 

Hematofiuorometers measure ZnPP and report values 

in EP equivalents. They are calibrated against the extraction method and theoretically should yield corresponding 

values. In practice, the values obtained with these instruments are usually not 100% ofthe EP present and may be 

considerably less. At least two studies (Kaul et al., 1983; 

Hammond et al., 1984) indicate that, at high levels, 

values obtained with hematofiuorometers are lower than 

those obtained with the extraction method, but that up to 

35 ug/dl the results are similar. Because hematofiuorometers give immediate results and are economical, 

they are eminently suitable for field screening. 

P.18 

10 
For both the hematofluorometer and the extraction 

method, the distinction between a positive and negative 

screening test should be based on a cutoff level of 35 

ug/dl. However, for risk classification, the cutoff points 

for ZnPP measured by hematofluorometer (Table 2.A) 

differ from those for EP measured by the extraction 

method (Table 2.B). If possible, centralized laboratories 

should use extraction methods, and, if the followup 

laboratory has extraction capability, all confirmatory tests 

for EP should be done by extraction, not hematofluorometer. Hematofiuorometers are most likely to give 

accurate results when used to analyze freshly collected 

blood specimens. The differences between methods need 

further study. 

B. Erythrocyte Protoporphyrin and Iron Deficiency 

A benefit of EP screening is that when an elevated EP 

level proves not to be due to lead, it usually reflects iron 

deficiency (Piomelli, 1977). The first signs of iron deficiency are biochemical abnormalities (low serum ferritin, 

low transferrin saturation, and high EP) followed by cellular abnormalities (microcytosis and hypochromia). 

Iron deficiency anemia follows these changes as the 

hemoglobin and hematocrit values fall. 

The EP test proved to be practical in screening for iron 

deficiency in a population of 4,160 children (Yip et al., 

1983). The upper limit of normal for EP in this study was 

35 ug/dl. The predictive value appeared to be satisfactory. 

Iron deficiency is common in many of the groups at 

risk for lead poisoning—especially among inner-city 

children of low socioeconomic status living in old, dilapidated housing. Iron deficiency is common among infants 

ages 9 to 24 months; the highest frequency oflead poisoning extends through 36 months. Iron deficiency and lead 

toxicity may occur in the same child. Furthermore, experimental evidence indicates that iron deficiency increases the proportion oflead absorbed from the intestine 

and aggravates the toxic effects of lead. 

Analysis ofthe NHANES II data has clarified the relationship between elevated EP values, blood lead levels, 

and iron deficiency in a representalive sample ofthe U.S. 

population. Among children in the NHANES II survey 

with elevated EP values, 31% have elevated blood lead 

levels, 18% have iron deficiency (as evidenced by a transferrin saturation of less than or equal to 12%), and 11% 

have evidence of both conditions (R. Yip, personal communication). On the other hand, among children with 

elevated blood lead levels, only about 26% have lead 

toxicity-that is, an elevated EP level (NCHS, 1984). In 

high priority populations (Table 1), in which iron deficiency is more common and lead levels are higher, a 

greater proportion of children with elevated blood lead 

levels would have elevated EP levels. Analyses by both 

Yip and NCHS confirm that a synergistic effect exists between lead toxicity and iron deficiency in children, as experimental studies in animals have suggested. 

Table Z.Am * " 

Zinc Protoporphyrin (ZnPP) by Hematofluorometer 

Risk Classification of Asymptomatic Children 

for Priority Medical Evaluation 

P.19 

Blood Lead # 

Not done 

<24 

25-49 

50-69 

> 70 

<35 

I 

I 

lb 

• • 

• * 

Erythrocyte Protoporphyrin (EP) # 

35-74 

• 

la 

11 

HI 

• • 

75-174 

• 

Ia 

III 

HI 

IV 

>175 

• 

EPP + 

111 

IV 

IV 

# = Units are in fig/dl of whole blood. 

* = Blood lead lest needed to estimate risk. 

EPP + = Erythropoietic protoporphyria. Iron deficiency may cause 

elevated EP levels up lo 300 pg/dl, but this is rare. 

** = In practice, this combination of results is not generally observed; if it is observed, immediately relesi with whole blood. 

NOTE: Diagnostic evaluation is more urgent than the classification indicates for— 

1. Children wilh any symptoms compatible wilh lead toxicity. 

2. Children under 36 months of age. 

3. Children whose blood lead and EP levels place them in ihe 

upper part of a particular class. 

4. Children whose siblings are in a higher class. 

These guidelines refer lo the interpretation of screening results, bul the 

final diagnosis and disposition rest on a more complete medical and 

laboratory examination of the child. 

Table 2.B 

Erythrocyte Protoporphyrin (EP) by Extraction 

Risk Classification of Asymptomatic Children 

for Priority Medical Evaluation 

Blood Lead # 

Not done 

<24 

25-49 

50-69 

>70 

<35 

I 

I 

lb 

*• 

• • 

Erythrocyte Protoporphyrin (EP) # 

35-109 

• 

la 

II 

HI 

*• 

110-249 

* 

Ia 

III . 

III 

IV 

>250 

• 

EPP + 

III 

IV 

IV 

# = Units are in/xg/dl of whole blood. 

* = Blood lead test needed to estimate risk. 

EPP+ = Erythropoietic protoporphyria. Iron deficiency may cause 

elevated EP levels up to 300 pg/dl, but this is rare. 

*' = In practice, this combination of results is not generally observed; if il is observed, immediately retest with venous 

blood. 

NOTE: Diagnostic evaluation is more urgent than the classification indicates for— 

1. Children with any symptoms compatible with lead toxicity. 

2. Children under 36 months of age. 

3. Children whose blood lead and EP levels place them in the 

upper part ofa particular class. 

4. Children whose siblings are in a higher class. 

These guidelines refer to the interpretation of screening results, but the 

final diagnosis and disposition rest on a more complete medical and 

laboratory examination of the child. 

11 
MEASUREMENT OF BLOOD LEAD 

Unlike elevated EP levels (which may be caused by 

iron deficiency or other illnesses), elevated blood lead 

levels are specific for lead absorption. Fluctuations in 

blood lead values over a short period can be due lo physiologic variations or sporadic acute lead exposure. 

Capillary samples are highly sensitive to contamination 

with environmental lead. If such samples are to be taken 

for blood lead assays, the personnel must be rigorously 

trained before any screening program is begun, and duplicate capillary blood specimens should be drawn. A single 

tube of capillary blood should never be used for the diagnosis of elevated blood lead, because an elevated value 

may be caused by contamination. If results of tests for 

blood lead from two tubes differ substantially, the higher 

value can be considered spurious. Even when the results 

are equally elevated, contamination cannot be excluded. 

Therefore, only venous blood samples should be used to 

confirm a diagnosis or to determine or assess treatment. 

There is less likelihood of contamination in a venipuncture, but venous blood may be difficult to collect from 

very young children. Neither the blood lead nor the extraction EP test should be considered a routine procedure 

in the clinical laboratory. To help insure credible test results, laboratories performing these tests should participate in the CDC proficiency testing program or the 

equivalent. 

SCREENING SCHEMES 

Three feasible screening strategies are— 

1. Screening with EP tests, followed by blood lead 

measurements if indicated. This is the most 

common procedure. 

2. Screening with both EP and blood lead tests. 

3. Screening with blood lead tests, followed by EP 

measurements if indicated. 

The CDC recommends EP tests, followed by blood 

lead measurements for all children with an elevated EP 

level. The EP test has these advantages: 

1. Ease of measurement by hematofluorometer or the 

extraction method. 

2. Results that are not affected if specimens are contaminated with environmental lead. 

3. More cost effective than screening with the blood 

lead test. 

4. Ability to detect a child's metabolic response to the 

toxicity oflead. 

5. Possibility of differentiating between children with 

stable blood lead levels and those with declining 

levels. 

6. Possibility of identifying children who have iron 

deficiency. 

In some areas, where the environment is grossly contaminated with lead, a strategy of simultaneous testing 

for EP and blood lead levels is recommended. In these 

cases, venous samples should be used for measuring lead. 

When tt* is the primary screening I'bSlilWO'appruai'nU!" 

are possible: 

1. EP measured on site. A capillary blood specimen is 

collected, and while the child waits at the screening 

site, EP is determined by hematofluorometer. 

Children found to have EP values of 34 ug/dl or 

less are discharged until the next routine screening. 

For those with EP values of 35 ug/dl or more, additional blood samples are taken (preferably by venipuncture) for laboratory analysis of blood lead and 

of EP—by extraction, ifthe method is available. 

2. EP measured off site. A venous blood sample or 

duplicate capillary samples are collected at the 

screening site and sent to the laboratory for measurement of EP, preferably by the extraction 

method. The amount of blood collected should be 

sufficient for confirmatory tests. Unused specimens 

of blood from children whose EP levels are 34 /xg/dl 

or less may be discarded. For those children with 

EP levels of 35 ug/dl or more, the blood lead levels 

and hematocrits or hemoglobin concentrations 

should be determined. 

On site, EP is nearly always measured by hematofluorometer; off site—preferably—it is measured by the extraction method. If the blood specimen is protected from 

temperature extremes and light, it may be stored for a 

week to 10 days before being analyzed by the extraction 

method. Blood collected on filter paper may be stored for 

several weeks before it is analyzed. 

INTERPRETATION OF SCREENING RESULTS 

A single screening test, either for EP or blood lead, 

cannot be used to categorize children for priority in followup. Both EP and blood lead levels must be used to 

determine the potential risk of lead toxicity in the children screened. 

Children can be arbitrarily divided into four classes on 

the basis of EP and blood lead screening results. In view 

of the observed discrepancy between results from the 

hematofluorometer and extraction methods, two tables 

are given: Tables 2.A and 2.B (derived from Kaul et al., 

1983). This classification merely suggests the relative 

risk and the priority for medical evaluation and environmental intervention, and the tables should be used only 

as general guidelines. Children 12 to 36 months old 

should be given priority over older ones, and children 

whose EP and blood lead levels fall into the upper range 

ofa class should be given priority over those whose levels 

fall into the lower range. For example, the urgency for followup is greater for a 1-year-old whose EP level by extraction is 109 ug/dl and whose blood lead level is 49 ug/dl 

than for a 5 1/2-year-old whose EP level, by the extraction method, is 36 ug/dl and whose blood lead level is 26 

ug/dl. Yet both children fall into class II. 

Children in class IV—at urgent risk of lead 

toxicity—should be medically evaluated within 24 hours, 

P.20 

12 
and in no case later !Wah with'i\Y 45J~'rr^u"fTsr"*bhiIdiidri-IIH 

class III are at high risk. Those in class II are at moderate 

risk, and those in class I, at low risk. 

Class I can be subdivided into two additional categories. Class Ia (blood lead, 25 ug/dl or less, and EP, 35 

ug/dl or more) includes children with iron deficiency. 

These children should be retested, with additional assessment of iron status. Class lb (blood lead, 25-40 ug/dl, 

and EP, less than 35 ug/dl) covers children who appear 

to have transient, stable, declining, or increasing blood 

> r>lUkU»|,t!^11 W^-UJUi ij _ 

the children should be carefully foro^elf^fSmFcase's^ 

the btood lead and EP results will differ. When the EP 

value is significantly higher than the value suggested by 

the blood lead level, the child probably has both iron deficiency and excessive lead absorption. 

Screening should focus on asymptomatic children. 

Children with symptoms should be referred for immediate evaluation, regardless oftheir risk classification. 

P.21 

13 

p.^l-jj^li. -•.-.•„•:..», 
V. Diagnostic Evaluation 

T l 

Screening tests are not diagnostic. Therefore, every 

child with a positive screening test should be referred to a 

physician for evaluation, with the degree of urgency indicated by the risk classification. At the first diagnostic 

evaluation, if the screening test was done on capillary 

blood, a venous blood lead level should be determined in 

a laboratory that participates in CDC's blood lead proficiency testing program. Even when tests are done by experienced personnel, blood lead levels may vary 10% to 

15%, depending on the level being tested. Tests for the 

same child may vary as much as ± 5 ug/dl in a 24-hour 

period. Thus, differences of 1 to 5 ug/dl between screening and diagnostic levels in either direction should not 

necessarily be interpreted as indicative of actual changes 

in the child's lead absorption or excretion. 

Additional blood samples may be needed for tests such 

as complete blood counts, serum iron, total iron binding 

capacity, and serum ferritin. The amounts necessary for 

these tests, which usually exceed the amount obtainable 

by capillary sample, can be obtained with a single 

venipuncture. 

Symptoms, if present, constitute an urgent risk, warranting prompt hospitalization (section VI). Symptoms 

must be looked for, and they can be missed (Piomelli et 

al., 1984): 

Acute lead encephalopathy is characterized clinically 

by some or all of these symptoms: coma, seizures, 

bizarre behavior, ataxia, apathy, incoordination, 

vomiting, alteration in the state of consciousness, and 

subtle loss of recently acquired skills. Any one or a 

mixture ofthese symptoms, associated with an elevated blood lead level, constitutes an acute medical 

emergency. Lead encephalopathy is almost always associated with a blood lead level exceeding 100 ug/dl, 

although, occasionally, it has been reported at blood 

lead levels as low as 70 ug/dl. 

Symptomatic lead poisoning without encephalopathy 

is characterized by one or several symptoms: decrease 

in play activity, lethargy, anorexia, sporadic vomiting, 

intermittent abdominal pain, and constipation. It is 

usually associated with a blood lead level above 70 

ug/dl, although, occasionally, cases are associated 

with a level as low as 50 ug/dl. Iftheblood lead level is 

below 50 fig/dl, other causes should be' vigorously sought. 

Since any symptomatic child may develop acute lead 

encephalopathy, treatment and supportive measures 

must be started immediately on an emergency basis. 

Whether or not symptomatic lead poisoning is present, 

the child should have a complete pediatric evaluation. 

Special attention should be given to— 

1. A detailed history, including the presence or absence of clinical symptoms, child's mouthing activities, existence of pica, nutritional status, family history of lead poisoning, possible source of exposure, 

and previous blood lead or EP determinations. 

2. The physical.examination, especially the neurologic 

examination. 

3. Nutritional status and hematologic evaluation for 

iron deficiency. Iron deficiency contributes to an 

elevated EP and can enhance lead absorption and 

toxicity. 

4. Confirmatory diagnostic tests. 

5. Trends in EP and blood lead levels. 

Since trends are important in diagnosis and management, serial measurements of blood lead and EP (and 

other measurements as indicated) are far more valuable 

than data obtained at one time. To be comparable and interpretable, serial EP levels should be analyzed by the 

same method. 

Probably the most reliable method for determining the 

source of exposure is obtaining a careful, complete environmental history (section III), inspecting the home for 

lead hazards, and learning about the child's handto-mouth behavior through careful questioning. Pica, the 

Latin word for "magpie," describes the habitual ingestion 

of nonfood substances. This should not be regarded as 

synonymous with the normal oral behaviors of small children, such as finger and thumb sucking and nail biting, 

An initial plan for management requires that all interacting factors be taken into account. The plan should be 

modified as indicated by long-term trends in lead absorption, exposure, and clinical status. 

TESTS 

In addition to confirmatory and serial EP and blood 

lead determinations, the following tests can be useful (if 

available) in assessing the patient's lead absorption status. 

14 
1. Tests for Iron Deficiency 

Because the EP can reflect iron deficiency as well as 

lead'exposure, the presence of iron deficiency must be established or ruled out if EP levels are to be properly 

interpreted. 

A common misconception is that a child with a 

"normal" hematocrit (33% or more) or hemoglobin concentration (11 g/dl or more) could not be iron deficient. 

This is not true, particularly with respect to iron deficiency sufficient to affect.EP and, worse, to enhance lead absorption and retention. Thus, although a complete blood 

count (CBC) and a reticulocyte count are indicated in the 

evaluation oflead toxicity, they are not sensitive enough 

to rule out iron deficiency. 

Of the red blood cell (RBC) indices, a decreased mean 

corpuscular volume (MCV) is a useful indicator of iron 

deficiency. Normal values depend on age (Dallman, 

1982). 

Serum iron and iron binding capacity are more sensitive than the MCV. In general, an elevated iron binding 

capacity of more than 350 ug/dl is more likely to accurately indicate iron deficiency than a normal or low serum 

iron, since the serum iron is quite sensitive to both dietary iron and diurnal variation. Thus, if a child has eaten 

an iron-rich food within 2-4 hours before the blood for 

the test is drawn, the result may be closer to the normal 

level than is actually the case. Under standardized conditions, an abnormally low ratio of serum iron to iron binding capacity (transferrin saturation) is consistent with 

iron deficiency. In addition to the level of EP itself, the 

serum ferritin level is an accurate indication of overall 

iron status. 

2. Flat Plate of the Abdomen 

Radiologic examination (fiat plate) of the abdomen 

may reveal radiopaque foreign material, but only if the 

material has been ingested during the preceding 24 to 36 

hours. Since lead ingestion is sporadic, this examination 

is significant only if the results are positive; negative results do not rule out lead poisoning. Positive results indicate recent ingestion of large amounts oflead. 

3. X-ray of Long Bones 

X-rays of the long bones, usually the knees, may help 

estimate the duration of exposure. Lines of increased 

density in the metaphyseal plate of the distal femur and 

proximal libia and fibula are "growth arrest lines." They 

are caused by lead, which disrupts the metabolism of the 

bone matrix. As a result, areas of increased mineralization or calcification may be present at the metaphyses of 

the long bones. Though sometimes called "lead lines," 

they are not an x-ray shadow of deposited lead. 

Although definitive data are not available, these lines 

are thought to become visible after at least 4 to 8 weeks 

from the time exposure began; the length of time 

depends on the age of the child and the degree of lead 

exposure. The width and intensity ofthe lines reflect prolonged previous lead absorption but 36 rii'ot indicate current ingestion. They are seldom seen in children under 

24 months of age. Negative x-rays do not rule out lead 

poisoning. 

4. Calcium Disodium EDTA Mobilization (or Provoca-

* tive Test) 

This test is used to identify children who will respond 

to chelation therapy with a brisk lead diuresis. Children 

whose blood lead level exceeds 55 ug/dl should not receive a provocative chelation test. Instead, appropriate 

chelation therapy should be started. The mobilization test 

is particularly useful when the screening test indicates 

that the child has lead toxicity and there is some question 

as to whether chelation therapy is indicated. This test provides an index ofthe mobile or potentially toxic fraction 

ofthe total body lead burden (Saenger et al., 1982). 

Since CDC's 1978 statement, an 8-hour mobilization 

test has been shown to be as reliable as a 24-hour mobilization test (Markowitz and Rosen, 1984). Although an 

8-hour test may be done on an outpatient basis, the patient should not leave the clinic. The careful use of "leadfree" apparatus is mandatory.* 

5. Lumbar Puncture 

CAUTION: 

If a lumbar puncture is needed to rule out meningitis 

or other serious disease, it should be performed cautiously and only after a careful search for signs and 

symptoms of increased intracranial pressure. The fluid 

should be obtained drop by drop, and no more than 1 

milliliter (ml) should be removed. 

The following tests are not useful in diagnosing lead 

toxicity. 

1. Microscopic Examination of Red Cells for Basophilic 

Stippling 

Since basophilic stippling is not universally found in 

chronic clinical lead poisoning and is relatively insensitive 

to lesser degrees of lead toxicity, it is noi considered 

useful in diagnosis. 

2. Tests of Hair and Fingernails for Lead Levels 

The levels oflead in hair or fingernails are not well correlated with blood lead levels; therefore, tests for these 

levels are not considered useful in diagnosis. 

P.23 

'Special lead-free collection apparatus musi be used if valid lest results 

are lo be obtained. The laboratory performing the analysis may supply 

the proper collection apparatus. Preferably, urine should be voided 

directly into polyethylene or polypropylene bottles that have been 

cleaned by the usual procedures, then washed in 1% nitric acid, and 

thoroughly rinsed with deionized, distilled waler. For children who are 

noi toilet trained, plastic pediatric urine collectors, with double compartments, may be used. Urine collected in this manner should be 

transferred directly to the urine collection bottles. Preserving the collected urine wilh hydrochloric acid will stabilize noi only lead bul also Saminolevulinic acid (ALA). 

15 
YL Clinical Management 

P.24 

The system described in section IV is for an initial 

classification, to be modified by results ofthe diagnostic 

evaluation. Thus, after all information is available to the 

clinician, the child's true risk classification is established. 

Clinical management includes eliminating the source of 

the child's lead exposure; providing general pediatric 

care, family education, and, when appropriate, chelation 

therapy; and correcting any nutritional deficiencies. In addition, followup examinations must be performed until 

the risk of further damage is minimal. The single most important factor in pediatric management is to reduce the 

amount oflead ingested. The family must be fully informed 

of the child's condition and of the clinical and environmental actions to follow. 

One recommended approach to the treatment of children with symptomatic and asymptomatic lead poisoning 

is described in detail in the Appendix. The major new feature of this approach is an increased reliance on calcium 

disodium EDTA mobilization testing among children 

with moderate blood lead levels. The test results are used 

to decide whether chelation is indicated. A full course of 

chelation therapy should not be given without either a 

confirmed blood lead level equal to or greater than 56 

ug/dl or a positive mobilization test in children with 

blood lead levels of 25-55 ug/dl. This approach is recommended by four major medical centers in which the staffs 

have had extensive experience in the diagnosis and treatment of children with lead poisoning. 

The cornerstones of clinical management are careful 

clinical and laboratory surveillance of the child and a reduction in lead exposure lo prevent further accumulation 

of lead. This approach allows previously absorbed lead to 

be slowly excreted. Most children with lead toxicity do 

not require chelation therapy, but those who do may 

need more than one course of treatment. 

The followup program for asymptomatic children 

depends upon the degree of risk determined during the 

diagnostic evaluation. 

For the purposes of clinical management and followup, 

the risk categories are ranked from urgent to low. 

Urgent — Blood lead levels of 70 ug/dl or more with 

or without symptoms. 

High — Children whose repeat EP and confirmatory 

venous blood lead levels fall in the class II and III 

ranges of the screening test, but who also have a positive calcium disodium EDTA mobilization lest or 

other confirmatory diagnostic tests or risk factors. 

Children in class III who have not had confirmatory diagnostic tests should be considered high risk until evidence places them in another risk category. 

Moderate — Children whose repeat EP and venous 

blood lead levels fall into the class II range of the 

screening test but whose other confirmatory diagnostic 

tests are negative. 

Low — Children whose repeat EP and venous blood 

lead levels fall into the class 1 range of the screening 

tests. These children are usually not given other diagnostic tests. 

This categorization is arbitrary and can be adapted to a 

particular child. For example, a 20-month old with persistent pica whose environmental lead hazard cannot be 

controlled satisfactorily may be considered high risk, 

even if his or her repeat EP and venous blood lead levels 

fall in ihe range of class II and other diagnostic tests are 

negative. 

URGENT RISK 

Children with blood lead levels of 70 ug/dl or more, 

regardless of the presence or absence of clinical symptoms, should be treated with the same intensity as children with frank neurologic manifestations. The higher 

the confirmed venous blood lead, the greater the need for 

chelation therapy. Severe and permanent brain damage 

may occur in as many as 80% of children who have acute 

encephalopathy (Perlstein and Attala, 1966). Treatment 

before onset of encephalopathy will improve this grim 

prognosis. 

Lead toxicity is a chronic medical problem. Children 

who require chelation therapy will need long-term medical surveillance and care. The EP levels can fluctuate 

during and immediately after chelation therapy. After an 

apparently successful course of therapy with calcium disodium EDTA (incorporating BAL, British Anti-Lewisite, 

as necessary), the "rebound" phenomenon may be 

observed. 

First, the blood lead level drops during treatment. 

This is not a reason to interrupt therapy. Then, after treatment is stopped, the blood lead level almost invariably 

rises again. This phenomenon reflects a reequilibration of 

16 
stored lead. The decision to repeat chelation therapy is 

based on the blood lead level after the "rebound." 

, Reduction of lead intake is urgent for all children in 

this category, both as part of immediate therapy and as 

part of the followup preventive procedure. Children receiving chelation therapy should not be released from the 

hospital until lead hazards in their homes and environ? 

ment are controlled. Otherwise, suitable alternative housing must be arranged. Thus, the appropriate public 

agency in the community must be notified immediately 

so that environmental investigation and intervention can 

begin. 

After their hospitalization and after lead has been removed from their environments, these children are still 

at high risk. Close followup, with blood lead and EP measurements, is required. At first, these tests should be 

done every 1 to 2 weeks. Ifthe blood lead level rebounds 

to its pretreatment level, a repeat ofthe chelation therapy 

should be considered. If the blood lead level remains 

stable or shows a continual decline after the first few 

weeks, the interval between testing may be incrementally 

increased from 1 to 6 months until the blood lead and EP 

levels return to normal or the child reaches 6 years of age. 

HIGH RISK 

Many children in the high-risk category will have been 

given a calcium disodium EDTA mobilization test to 

determine whether chelation therapy is needed. If it is 

needed, inpatient chelation should be performed. Under 

some conditions, however, children without urgent risk 

factors may be treated as outpatients. Outpatient treatment should be reserved, however, for those centers 

capable of providing closely monitored outpatient care 

and followup supervision, and in those centers it should 

be provided only if the child's source of lead exposure 

has been eliminated (Piomelli et al., 1984). In addition, 

the parents should be cooperative and should demonstrate that they can follow instructions. 

Followup of high-risk children should consist of blood 

lead or EP tests, or both, at least monthly (especially in 

the summer), until the sources oflead in their environments have been removed. If their blood lead or EP 

levels have declined or stabilized, the interval between 

testing may be incrementally increased, except in 

summer, from 1 to 6 months, until the blood lead and EP 

levels return to normal or the child reaches 6 years of age. 

Careful neurological and psychological assessment is advised so that any behavioral or neurological deviation can 

Be Selected early and proper th'eTapy afid school placement begun. 

MODERATE RISK 

Generally, children in this category do not require chelation therapy. Reducing lead intake from all sources and 

careful monitoring ofthe child usually suffices. 

Until the lead hazards are eliminated from their environment, these children should be tested monthly in the 

summer and every 2 months in other seasons. If the 

blood lead and EP levels remain stable or show a continual decline after the first few months, the interval between 

testing may be incrementally increased from 2 to 6 

months until the blood lead and EP levels return to 

normal or the child reaches 6 years of age. 

NOTE: All children in the urgent-, high-, and 

moderate-risk categories may have concomitant nutritional deficiencies. These deficiencies may increase the 

child's risk from lead by increasing absorption, retention, 

and toxicity. All children in these categories should receive a careful nutritional evaluation, including appropriate laboratory tests. In addition to the care given for lead 

toxicity, nutritional therapy should be provided. When increased lead absorption is found, it may be particularly 

important to correct iron deficiency and maintain an adequate calcium intake. 

LOW RISK 

When tested, children in this category do not have significant evidence of lead toxicity. However, they require 

periodic screening until they reach their sixth birthday. 

Children whose elevated EP levels are not caused by lead 

absorption should receive medical attention and care for 

the medical condition responsible for the elevation. 

Children with elevated blood lead levels but no evidence 

of toxicity should be evaluated monthly until lead toxicity 

can be ruled out. This can usually be done within 3 

months. 

In conclusion, the clinical management of children 

with lead poisoning must include appropriate treatment, 

adequate followup, environmental intervention, and 

family education. Chelation therapy is indicated for some 

children with lead toxicity. Using it indiscriminantly is 

unwise, but so is withholding or delaying it when it is indicated. The physician providing clinical management 

must know the current status of the child's environment. 

The optimal frequency of followup depends on many factors, including the child's age and environment and the 

trend in results ofthe child's tests. 

P.25 

17 
VIL Environmental Evaluation and 

Lead Hazard Abatement 

Environmental investigation and intervention should 

begin as soon as lead toxicity is confirmed. Lead hazards 

must be identified and removed from the environments 

of these children. Priorities for action should be determined by the child's risk classification. The higher the 

blood lead level and the lower the child's age, the higher 

the priority for removing the lead hazards. Children who 

require hospitalization and chelation therapy are at the 

highest risk of permanent neurologic damage from continued high-level exposure and another episode of lead 

toxicity. Therefore, children in the urgent- and high-risk 

categories should receive first priority for environmental 

investigation and intervention. It is strongly recommended that abatement oflead hazards in a hospitalized child's 

home be completed during the first few days of the 

child's hospitalization. 

Children in the moderate-risk category are next in priority. For them, identifying lead hazards and reducing 

lead intake are as much a medical necessity as clinical 

management. The effectiveness of environmental intervention is judged by the child's response and not by the 

services performed. Environmental management is not 

successful or complete until the child's EP and blood lead 

levels have declined and stabilized for at least 12 months. 

The identification and removal of one source of lead 

exposure does not necessarily mean that the child's exposure to lead has ended. 

Because lead is a ubiquitous and powerful toxin, with 

no known beneficial function in the human body, the 

goal of prevention is to reduce children's exposure to 

lead to the maximum extent. Lead-based paint is the 

most common, remediable source of lead that causes 

symptomatic lead poisoning. Detailed procedures for 

removing lead paint from the home environment are described, but only general guidelines are given for controlling other sources of lead discussed in section III. Ideal 

prevention goals are given first; when these goals cannot 

be reached immediately, short-term, substitute goals are 

offered. 

LEAD-BASED PAINT 

The ultimate goal is to remove all leaded paint from 

housing in the United States. Reaching that goal will be 

expensive. Short-term goals of partial removal help, but 

they tend to postpone efforts for complete removal. 

All painted interior and exterior surfaces should be tested 

for lead. Portable x-ray fluorescence (XRF) analyzers are 

most convenient for identifying lead-based paint hazards. 

These instruments can measure lead content in paint surfaces within ±0.2 mg/cm2

 of exposed surface. Readings 

of 0.7 mg/cm2 are considered positive. The XRF analyzer 

is a probability sampling device, and reliability depends 

on repeated readings. If an XRF analyzer is not available, 

wet chemical methods of analysis must be used. 

A lead-based paint hazard exists when (a) the XRF 

reading is positive and (b) the surfaces being tested are 

chewable or contain damaged (cracked, chipped, 

loosened, chewed) paint. Lead-based paint on intact 

walls, ceilings, or other surfaces that are not chewable 

does riot constitute an immediate hazard. Inspectors 

should obtain measurements on any interior or exterior 

surface that may constitute a lead hazard. This includes 

walls, doors, window frames, baseboards, guardrails, 

fences, and sidings. Outside inspection should encompass 

garages and other adjacent structures as well as the main 

building. 

Next, the inspector should classify each interior and 

exterior part of the building where lead is found according 

to the degree of hazard. If nonchewable surfaces with 

lead paint are smooth and intact and the supporting structure is sound, they do not present an immediate hazard 

and may be left alone. Property owners and residents, 

however, should be warned that smooth surfaces containing lead can become hazardous if they are not properly 

maintained and are allowed to fall into disrepair. All leadpainted surfaces that are identified as positive by XRF (or 

wet chemical analysis) and that are in unsound condition 

are classified as immediate hazards requiring prompt 

abatement. This includes all wood trim —both interior 

and exterior—with blistering, scaling, peeling, or powdering paint and walls with unsound paint, painted plaster, 

or painted, peeling wallpaper. Floors and ceilings, if painted with lead-based paint and if in an unsound condition, 

are also included. 

New information has revealed the importance of leadbearing dust as another major hazard for young children. 

18 
P.27 

In the past, blistering, scaling, peeling, or powdering 

paint was frequently removed only to a level of 4 or 5 feet 

above-the floor, because, usually, a small child can reach 

no higher. However, dust or paint chips from unsound 

lead paint above this level could fall into the child's play 

area. CDC now recommends that all unsound leaded 

paint be removed from the interiors of dwellings, including areas beyond the reach of children. Likewise, exterior 

leaded paint (on porches, woodwork, and walls) that 

either is in or can fall into the child's play area should be 

removed immediately. Places in and about the home 

where young children spend much of their 

time—namely, near windows, doors, and porches—are 

particularly hazardous. 

In summary, paint in unsound condition or on chewable surfaces is classified as an immediate hazard requiring 

prompt abatement: other lead paint in sound condition 

may not require immediate attention, but it must be 

identified as a potential hazard. 

Next, some common methods for reducing lead-based 

paint hazards are outlined. 

Phase I — Emergency Intervention 

As soon as an elevated blood lead level is confirmed, 

residents should be advised to remove all scaling paint 

from places such as window sills, door frames, doors, and 

porch railings that are within easy reach of the child. A 

stiff brush should be used for this. Residents should also 

be advised to avoid inhaling the dust or contaminating 

other areas. The debris should be vacuumed and bagged 

for safe disposal. Then the area should be thoroughly 

scrubbed, preferably with high-phosphate detergents 

such as Spic and Span (Milar and Mushak, 1982). If a crib 

is next to a surface with scaling paint, the crib should be 

moved away. Similarly, a piece of furniture should be 

moved to prevent the child from reaching areas of scaling 

paint. In the past, it was advised that window sills and 

other wood trim with peeling paint be covered with masking tape or some other adhesive-backed paper. This is no 

longer recommended. Inquisitive young children often 

remove this tape, thereby rendering the technique ineffective. Families should be instructed on ways to keep 

these areas free from loose or flaking paint until more 

definitive steps can be taken to reduce the hazard. Housekeeping techniques such as frequent wet mopping and 

damp dusting are essential in maintaining a reduced level 

of hazard. 

Phase II — Long-Term Hazard Reduction 

Only when an old dwelling with lead-based paint is 

gutted and completely restored can the lead hazards be 

considered "permanently abated." Less extensive, commonly used procedures may be called "long term"; however, how long the hazard will remain under control 

depends on such factors as the thoroughness ofthe procedure, the soundness ofthe underlying structure, and the 

condition of the plumbing. Increased moisture from 

leaky pipes behind walls can quickly cause paint that was 

smooth and intact to blister and scale. 

Abatement entails four steps: 

1. Removing lead paint from wood trim or walls. 

2. Thorough vacuuming to clean up the debris. 

3. Wel scrubbing for maximum elimination of fine 

lead-bearing particles. 

4. Repainting the area with lead-free paint (thai is, 

paint containing less than 0.06% of lead in the final 

dried solid). 

The property owner's responsibility is not met until all 

four steps have been completed. 

Just prior to and during abatement, certain precautions 

are essential. Carpets, rugs, upholstered furniture, bedding, clothing, and eating and cooking utensils must be 

sealed as tightly as possible in plastic to protect them 

from the enormous increase in lead-bearing dust created 

by the removal procedures. Once items such as rugs are 

impregnated with fine, lead-bearing particles, it is almost 

impossible to remove the lead (Milar and Mushak, 

1982). When feasible, this work should be carried out in 

one room at a time, with the room closed off and all furnishings removed. Until steps 1, 2, and 3 ofthe cleanup 

process are completed, all young children and pregnant 

women should live elsewhere both day and night. If this 

is not possible, they, as well as the child with the index 

case, should have serial blood lead tests before, during, 

and after the abatement work. Those doing the work 

should comply with OSHA standards; they should use respirators and wear coveralls, which must not be taken to 

the workers' homes for laundering. 

Walls 

Removing lead paint from walls, particularly lead paint 

applied to plaster, is usually difficult. In most cases, a barrier, such as wallboard, hardboard, fiberglass, plywood 

paneling or a similar durable, fire-resistant material, can 

be placed over the lead paint on the walls. These materials 

must be firmly nailed, cemented, or glued in place to prevent the child from removing them. The barriers should 

be verminproof and, in certain areas ofthe dwelling (that 

is, next to furnaces and stoves and in common hallways), 

fire retardant. Wallpaper painted with lead paint should 

be stripped off to the maximum extent possible. 

Woodwork 

Lead-based paint in unsound condition on both interior and exterior wood trim (for example, window units, 

door units, stair risers, bannisters, and railings) presents 

considerable danger for children. Paint can be removed 

from wood surfaces by heat (from gas torches and heat 

guns), sanding, scraping, and with liquid paint removers. 

All of these methods are hazardous. Most solvents in 

liquid paint removers evaporate rapidly and are flammable and toxic. These removers must be used with the 

utmost caution and only in well-ventilated areas with 

proper protective clothing and equipment. When the underlying wood has rotted, no attempt should be made to 

remove the paint. Instead, the wood.should be replaced, 

including,1 when necessary, entire window units and 

doors or door frames. Exterior rotted wood should also 

19 
be replaced. When torches, heal guns, and sanding 

devices are used lo remove paini, air lead levels increase 

enormously in the work area. Ofthese, sanding is by far 

the worst offender. It also produces the greatest deposition oflead in dusl, wilh rates as high as lOmgof lead/sq 

ft/hour (Inskip and Attenbury, 1983). Therefore, fine 

sanding down to the bare wood surface is not recommended. Scraping ihe surface after a heat gun has been 

used will probably produce fewer fine particles than 

sanding. 

The above information emphasizes the urgency of 

proper cleanup after lead-based paint has been removed. 

After the dusl has settled, the entire area, including 

walls, floors, and ceiling, should be vacuumed, preferably 

with an industrial vacuum cleaner. All surfaces should be 

wet-scrubbed with phosphate-containing detergents. Immediately thereafter, all surfaces from which paint has 

been removed should be repainted with lead-free paint. 

For safe disposal the debris should be placed in a toxic 

waste dump approved by ihe Environmental Protection 

Agency, not in an ordinary landfill or storm or sanitary 

sewer system. For best results, the wel cleaning procedures should be repealed (Milar and Mushak, 1982). 

Workers who remove the paint should be responsible for 

ihe cleanup, inasmuch as many of the affected families 

have neither the equipment nor the resources lo carry 

out an adequate cleanup. 

Supplemental Addresses 

Children often spend substantial amounts of time with 

relatives or babysitters who live at a different address. If 

lead-based paint in unsound condition is found at these 

addresses, it should be removed in the manner described. 

Similarly, day-care centers and other facilities may be 

located in old buildings with lead-based paint. These, loo, 

should be checked and handled accordingly. 

Followup 

The effectiveness of the initial abatement can be determined only through coordinated medical and environmental followup. When the initial abatement has been 

inadequate, a high recurrence rale of blood lead levels 

above 50 ug/dl has been found (Chisolm, 1983). Ideally, 

a communitywide code-enforcement program should be 

developed io remove all lead-based paint in housing. But, 

until then, the appropriate governmental unit in which 

the child lives is responsible for identifying and abating 

lead hazards for children with lead toxicity. Removing 

lead hazards in housing is ihe major factor in the success 

ofa lead poisoning prevention program. 

AIRBORNE LEAD 

Blood lead levels are decreasing as the use of leaded 

gasoline decreases (Annest et al., 1983). In terms of 

reducing background blood lead levels, removing lead 

from gasoline as rapidly as feasible is probably the most 

important public health measure. 

Emissions from industrial sources should be reduced 

sufficiently to achieve the current ambient air lead standard. New factories, as part of their licensing specifications, should be required to have minimal lead emissions 

The public should be informed about the hazards associated with burning old batlery casings, colored newsprint, waste oil, and lead-painted wood. 

SOIL AND DUST 

The optimal goal is to prevent lead from being transferred from any source to soil and dust. For the goal to be 

reached, air lead levels must be reduced to near zero. For 

those areas where concentrations of lead in soil and dust 

are high, large-scale excavation of soil or relocation of 

populations is the ideal means of reducing the exposure 

of children to lead. 

When the lead content of household dust is high, wetmopping and other cleanup measures help reduce children's blood lead levels (Charney el al., 1983). These 

measures provide a reasonable, short-term and mid-term 

solution to the problem of contaminated house dust. 

In severely contaminated residential areas, unless an 

effective barrier can be established between the children 

and the soil, surface soil must be removed and replaced 

with soil having a low lead content. 

FOOD AND WATER 

The lead content of air and soil, important contributors 

to the contamination of food and water, should be reduced. Food cans should be made so that lead does not 

leach from soldered seams. Lead is also added inadvertently to foods during processing and handling (Wolnik 

et al., 1983). Although the percentage of canned foods 

packaged in cans with lead-soldered side seams has declined substantially, some are still packaged this way. 

These foods should not be stored in the opened cans because, after the cans have been opened, even more lead 

migrates from the side seam into the food. 

When feasible, lead plumbing and lead water mains 

should be replaced. Water from taps in the home should 

be assessed for lead content. If a hazard is found, consumers should be educated to run water for several minutes 

before drinking it and not to drink water from the "hot" 

side ofthe lap. Acidic water supplies should bealkalinized 

to help prevent leaching. 

OCCUPATIONAL 

Ideally, engineering features should prevent workers 

from being exposed to lead dust and vapors. When workers are exposed, compliance with Occupational Safety 

and Health Administration (OSHA) regulations appears 

to be effective in protecting them and in preventing them 

from transporting lead home to children. Under the 

OSHA lead standard, factories that use lead must provide 

workers with facilities for showering and changing 

20 
P.29 

clothes and shoes before going home from work. This 

standard now applies only to industries covered by OSHA 

regulations. For the protection of children, it should be 

extended to all industries that use lead. The prevention 

of lead exposure to the fetus needs special emphasis. 

Women^of childbearing age should be excluded from 

working at jobs where significant lead exposure occurs. 

LEAD-GLAZED POTTERY 

All glazed pottery used for foodstuff should be free of 

leachable lead. Hobbyists and consumers should be 

educated to the risks associated with pottery glazes. 

Consumers should not use pottery for cooking or for storing food or beverages unless the pottery has recently 

been determined to be free of leachable lead. 

21 

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VIII. Health Education 

The community and especially parents of preschool 

children who live in older, deteriorating neighborhoods 

should be informed at every available opportunity ofthe 

need to have children screened periodically for lead 

poisoning. Basic preventive measures should be emphasized. These include frequent wet mopping and vacuuming of accessible paint flakes and dust to reduce potential 

lead hazards in the child's environment. The danger of ingesting paint chips, dust, and soil should be stressed. 

Older siblings of children at high risk should also be informed about the sources and risks oflead poisoning because they often take care of younger children. 

If a child is screened and the lead level is not elevated, 

the risk remains, and until the sixth birthday, rescreening 

is required, particularly during the summer. Until hazardfree housing is available for all and other high-risk 

sources of lead are removed, periodic screening will 

reduce the risk oflead poisoning. 

Education should start when the child is screened, and 

physicians, nurses, environmentalists, and aides should 

reinforce it at every opportunity. When a child is found to 

have lead toxicity, education of the family is essential for 

successful followup ofthe child. The family must be fully 

informed about the condition and the clinical and environmental actions to follow. Health professionals must 

emphasize the importance of the family's understanding 

the child's condition, its cause, and the possible result of 

lead toxicity. In addition, they should stress the importance of the child's having a balanced diet that includes 

enough calcium and iron. 

IX. Reporting Lead Toxicity and 

Elevated. Blood Lead Levels 

Primary care physicians and persons in charge of 

screening programs should report both presumptive and 

confirmed cases oflead toxicity to the appropriate health 

agency, and laboratories performing blood lead or EP 

tests should report any abnormal results to the appropriate health agency. 

22 

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P.31 

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Kovar MG. Chronological trend in blood lead levels 

between 1976 and 1980. N Engl J Med 1983; 

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Baker EL Jr, Folland DS, Taylor TA, et al. Lead poisoning in children of lead workers: home contamination 

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Baker EL Jr, Hayes CG, Landrigan PJ, et al. A nationwide 

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Barltrop D. The prevalence of pica. Am J Dis Child 

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Barltrop D, Khoo HE. The influence of nutritional factors 

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Beattie AD, Moore MR, Devenay WT, et al. Environmental lead pollution in an urban soft water area. Br 

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Beloian A. Use ofa food consumption model to estimate 

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Vegas, Nev., USA, Oct. 19-22, 1981. Environ Monit 

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Benignus BA, Otto DA, Muller KE, Seiple KJ. Effects of 

age and body lead burden on CNS function in young 

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Neurophysiol 1981;52:240-8. 

Billick IH, Shier DR, Curran AS. Relation of pediatric 

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23 
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24 

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25 

•y^"-^**"*-'^^-^:.*?.'^ •Bsaea^a^-a^^a ^ 
Appendix 

P.34 

Reprinted with permission by the 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

PUBUC HEALTH SERVICE 

from the Journal of Pediatrics, Volume 105, October 1984, Number 4. pp. 523—532 

SPECIAL ARTICLE 

Management of childhood lead poisoning 

Sergio Piomelli, M.D., John F. Rosen, M.D., J. Julian Chisolm, Jr., M.D., 

and John W. Graef, M.D. New York, New York, Baltimore, Maryland, 

and Boston, Massachusetts 

CHELATION TREATMENT for childhood lead poisoning 

may be life-saving and decreases the body burden of lead 

far more rapidly than normal excretory processes can.1 

Furthermore, chelating agents markedly enhance removal 

of that fraction of body lead that is readily mobile and 

considered to be the most toxic.1"* However, lead poisoning 

is a wholly preventable disorder caused by the wide 

dissemination of lead into the environment.'-' Medical 

treatment with chelating agents must not be considered a' 

substitute for dedicated preventive efforts to eradicate 

controllable sources of lead (e.g., substandard housing that 

contains lead-bearing paints, combustion of leaded gasoline). Although repeated courses of chelation therapy may 

be necessary for medical reasons, the source(s) of environmental lead must be identified and removed for preventive 

reasons. 

This review is based on our experience in four different 

lead poisoning treatment clinics and reflects our consensus 

on current management criteria. 

PHARMACOLOGIC CONSIDERATIONS 

Lead poisoning is treated with drugs capable of binding 

(chelating) lead and of enhancing its excretion. These 

From the Division of Pediatric Hemalology/Oncology, Department of Pediatrics. Columbia University, College of Physicians 

and Surgeons: the Department of Pediatrics and Clinical 

Research Center, Albert Einstein College of Medicine. Monleftore Medical Center; the Department of Pediatrics. John Hopkins University School of Medicine and the John F. Kennedy 

Institute, and the Baltimore City Hospitals: and the Division of 

Clinical Pharmacology and Toxicology. Department of Pediatrics, Children's Hospital Medical Center. 

Supported by Cram ES02343 from the National Institutes of 

Health, and by a grant from the Francis Florio Fund ofthe New 

York Community Trust IS.P.); by Projects 917 and MCJ-240458. 

Maternal and Child Health. Department of Health and Human 

Services [J. J.C); and by Grants ES0I06O-O9 and RR-53 from the 

National Institutes of Health, and by Project MCJ-360488-OI. 

Maternal and Child Health. DHHS (J.F.R.). 

Reprint requests: Sergio Piomelli. M.D.. Columbia University. 

College of Physicians and Surgeons, Division of Pediatric Hemalology/Oncology. 630 West 168th St.. New York. NY 10032. 

drugs deplete the soft tissues of lead and may thus reduce 

its acute toxicity. They are also used, in asymptomatic 

children, to reduce a potentially dangerous body burden of 

lead. All drugs are used to enhance the slow process of 

natural lead excretion. All drugs have potential side effects 

and should be used carefully. A brief description of the 

essential pharmacologic aspects of the various drugs follows. Detailed guidelines for specific situations are given in 

the next section. 

BAL 

Mechanism of action. Two molecules of BAL combine 

with one atom of heavy metal to form a stable complex. 

BAL enhances fecal as well as urinary excretion of lead 

and diffuses well into erythrocytes. It can be administered 

in the presence of renal impairment because it is predominantly excreted in bile.1 

BAL 

CaNa,-EDTA 

EP 

G-6-PD 

(British anti-lewisite) Dimercaptopropanol 

Disodium calcium-edetate 

Erythrocyte protoporphyrin 

Glucose-6-phosphate dehydrogenase 

' Route of administration and dosage. BAL is available 

only in oil for intramuscular administration. It must be 

given every 4 hours'. Dosages are discussed below. 

Toxiciiy. Mild febrile reactions may occur, and transient elevation of hepatic transaminase activities may be 

observed. Other minor adverse effects include, in order of 

frequency, nausea and occasional vomiting, headache, 

mild conjunctivitis, lacrimation, rhinorrhea, and salivation. 

Most side effects are transient and rapidly subside as the 

drug is metabolized and excreted. 

Precautions. In patients with G-6-PD deficiency, BAL 

should be used only in life-threatening situations, because 

it may induce hemolysis. Medicinal iron should never be 

administered during BAL therapy, because the combination is very toxic. If iron deficiency coexists, its management should be postponed until BAL therapy is concluded. 

In cases of extreme anemia blood transfusions are preferable. 

26 

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P.35 

CaNa2-EDTA**'6 

,0nly CaNarEDTA (calcium disodium versenate) 

should be used for treatment of lead poisoning. Nar 

EDTA (endrate disodium) should never be used for 

treatment of lead poisoning, because it may induce fatal 

hypocalcemia and tetany. 

Mechanism of action. CaNa2-EDTA increases urinary 

lead excretion 20- to 50-fold. CaNa2-EDTA does not enter 

the cells; thus it removes lead from the extracellular 

compartment. Indirectly, lead is reduced in the soft tissue, 

central nervous system, and red blood cells.' 

Route of administration and dosage. CaNa2-EDTA 

may be given intravenously or intramuscularly. The preferred and most effective route is a continuous intravenous 

infusion; a given dose is most effective if infused over 6 

hours.10 CaNa,-EDTA should be diluted to a concentration 

<0.5% in dextrose and water or 0.9% saline solution. When 

administered intravenously as a single dose, it should be 

similarly diluted and administered by slow infusion over 15 

to 20 minutes. Intramuscular administration of CaNa2-

EDTA is extremely painful and should be given with 

procaine (0.5%) by deep injection. 

CaNa2-EDTA should not be given orally, because it may 

enhance absorption of lead from the gastrointestinal 

tract. 

Dosages vary in different situations and are discussed 

below. In all cases, courses should be limited to 5 days, 

followed by at least 2- to 5-day intervals to allow recovery 

from zinc depletion. 

Toxicity. The kidney is the principal site of toxicity. 

Renal toxicity is dose related, reversible, and rarely occurs 

at doses <1500 mg/m2. The renal toxicity may be reduced 

by assuring adequate diuresis. CaNa2-EDTA should never 

be given in the absence of an adequate urine flow. Before 

administering it intramuscularly in children in good clinical condition, adequate oral intake of fluids must be 

assured. 

Precautions. During chelation with CaNa2-EDTA, 

urine and its sediment, BUN, serum creatinine, and liver 

function tests must be carefully monitored. The appearance of protein and formed elements in urinary sediment, 

and rising BUN and serum creatinine values signify 

impending renal failure, the serious toxicity associated 

with excessive or prolonged administration of EDTA. 

Inasmuch as CaNa2-EDTA may deplete zinc stores and 

cellular injury may be associated with zinc depletion, 

CaNa2-EDTA should be used with great caution. 

CaNa2-EDTA, used alone without concomitant BAL 

therapy, may aggravate symptoms in patients with very 

high blood lead levels. Thus it should be used exclusively in 

conjunction with BAL when the blood lead level is >70 

/ig/dl or clinical symptoms consistent with lead poisoning 

are present. In such cases the first dose of BAL should 

always precede the first dose of CaNa2-EDTA by at least 4 

hours. 

- D-PeniciUamine. D-Penicillamine is not licensed by the 

Food and Drug Administration for the treatment of lead 

poisoning. Its use for this indication is thus to be considered experimental. It is the only commercially available 

oral chelating agent. It can be given over a long period 

(days). Toxic side effects may occur in as many as 20% of 

patients given the drug." 

Mechanism of action. D-Penicillamine enhances urinary 

excretion of lead, although not as effectively as CaNa2-

EDTA. Its specific mechanism of action is not well 

understood. 

Route of administration and dosage. D-Penicillamine is 

administered orally. It is currently available in capsules 

(125 and 250 nig). These capsules may be opened and 

suspended in liquid, if necessary. The usual dose is 30 

mg/kg. Side effects can be minimized by initiating therapy 

with small doses, for example, 25% of the desired final 

dose, increased after 1 week to 50% and again after 1 week 

to the full dose, while monitoring for possible toxicity. 

Toxicity. The main side effects of D-penicillamine are 

reactions resembling those of penicillin sensitivity, including fevers, rashes, leukopenia, thrombocytopenia, and 

eosinophilia. Rarely, more severe and even life-threatening 

reactions (autoimmune hemolytic anemia, Stevens-Johnson syndrome) have been observed. Anorexia, nausea, and 

vomiting are infrequent. Of most concern, however, are 

isolated reports of nephrotoxicity, possibly from hypersensitivity reactions. For these reasons, patients should be 

carefully and frequently monitored for clinically obvious 

side effects, and frequent blood counts, urinalysis, and 

renal function tests should be performed. In particular, 

blood counts and urinalysis should be done twice weekly, at 

least in the first 3 weeks of treatment. If the absolute 

neutrophil count falls to <1500//d it should be immediately rechecked, and treatment should be stopped if it falls to 

<1200//zl. D-Penicillamine should therefore not be given 

on an outpatient basis if there is any question about 

compliance with appointments. 

D-Penicillamine should not be administered in patients 

with known penicillin allergy. 

New agents. Dimercaptosuccinic acid and 2-3-dimercapto-propane-1-sulphonate are both water-soluble derivatives of BAL. Although both appear promising and safe 

and have been used successfully in treatment of other 

heavy-metal poisoning, these drugs are presently in the 

investigative stage for the treatment of lead poisoning."" , 

27 

•^^.^rrJWia?j?-j.~..^'jy'^?T-,;;.^-y^'j ~'£*i2*j~£'£"'*E*Ja£'£~i^ iSgESB-gsaa I 
P.36 

ACUTE LEAD ENCEPHALOPATHY 

' Acute lead encephalopathy is characterized clinically by 

some or all of the following symptoms: coma, seizures, 

bizarre behavior, ataxia, apathy, incoordination, vomiting, 

alteration in the state of consciousness, and subtle loss of 

recently acquired skills. Any one or a matrix of these 

symptoms associated with an elevated blood lead concentration constitutes an acute medical emergency. Lead 

encephalopathy is almost always associated with a blood 

lead concentration >100 /xg/dl, although it has been 

reported at blood lead levels as low as 70 /ig/dl.M 

General supportive management. All oral intake is prohibited initially until the child's condition has significantiy 

improved. Parenteral fluid therapy is begun immediately; 

volume is restricted to basal requirements plus a careful 

assessment of continuing losses. Excessive intravenous 

fluid administration must be avoided. Once urine flow is 

established by administering dextrose in water (10 to 20 

ml/kg body weight), chelation treatment, already begun 

with BAL alone for one dose, is continued with simultaneous administration of CaNa2-EDTA. An adequate flow 

of urine must be established before intravenous chelation 

therapy. Parenteral fluid therapy minimizes vomiting that 

may accompany administration of BAL and ensures 

prompt excretion of CaNa2-EDTA, a drug excreted exclusively by the kidney. For initial control of seizures, 

diazepam or paraldehyde is the preferred drug. Barbiturate and phenytoin are reserved for the long-term management of recurring seizures, only after the acute episode is 

managed and consciousness has been fully recovered. 

Although it is desirable to evacuate any residual lead from 

the bowel, this should not delay the start of chelation 

therapy. Surgical decompression and hypertonic solutions 

to relieve intracranial pressure and cerebral edema are 

contraindicated. 

The diagnosis of acute lead encephalopathy can usually 

be made without lumbar puncture, which is extremely 

risky because of the presence of increased intracranial 

pressure. In fulminant lead encephalopathy, increased 

intracranial pressure may be present in the absence of any 

of the usual preliminary signs (changes in blood pressure, 

pulse or respiration, retinal hemorrhage or edema). If 

examination of the CSF is absolutely essential for the 

differential diagnosis, the very least amount of fluid, not 

exceeding a few drops, should be carefully obtained. 

Chelation therapy. Treatment is begun with a priming 

dose of 75 mg/m2 BAL only, given by deep intramuscular 

injection; BAL is administered at a dose of 450 mg/m2/24 

hours, in divided doses of 75 mg/m2 every 4 hours. Once 

the priming dose is given and an adequate urine flow is 

established, administration of CaNa2-EDTA is begun at a 

28 

dose of 1500 mg/m2/24 hours. CaNa2-EDTA is given by 

continuous intravenous drip in dextrose and water or 0.9% 

saline solution. The concentration of CaNa2-EDTA should 

not exceed 0.5% in the parenteral fluid. (In the treatment 

of acute encephalopathy, restriction of parenteral fluids 

takes precedence, so that CaNa2-EDTA may have to be 

given intramuscularly if fluid overload is to be avoided.) 

Combined BAL-CaNa2-EDTA therapy is given for a total of 5 days. During treatment, renal and hepatic function and serum electrolyte levels should be monitored 

daily. 

A second course of chelation therapy with CaNa2-

EDTA alone or with BAL, depending on the blood lead 

concentration, may be required after a 2-day interval. A 

third course is required only ifthe blood lead concentration 

rebounds to a value >50 /ig/dl within 48 hours after 

treatment. Unless there are compelling clinical reasons, it 

is desirable to wait at least 5 to 7 days before beginning a 

third course of CaNa2-EDTA. 

SYMPTOMATIC LEAD POISONING 

WITHOUT ENCEPHALOPATHY 

Symptomatic lead poisoning without encephalopathy is 

characterized by one or several of the following symptoms: 

decrease in play activity, lethargy, anorexia, sporadic 

vomiting, intermittent abdominal pain, and constipation. 

Symptomatic lead poisoning is usually associated with a 

blood lead concentration >70 /tg/dl, although occasionally 

may be associated with a blood lead concentration as low 

as 50 fig/dl. Ifthe blood lead concentration is <50 ug/dl, 

other diagnostic possibilities should be vigorously sought. 

Because all symptomatic children potentially have acute 

lead encephalopathy, treatment and supportive measures must be instituted immediately on an emergency 

basis.'-4 

General supportive management. All oral intake is prohibited and the guidelines of parenteral fluid therapy are 

followed as noted above for the treatment of lead encephalopathy. Intravenous fluids are given at a rate consistent 

with basal requirements plus ongoing losses. Excessive 

fluid administration must be avoided. 

Chelation therapy. Treatment is begun with a priming 

dose of 50 mg/m2 BAL by deep intramuscular injection; 

BAL is administered at a dose of 300 mg/m2/24 hours in 

divided doses of 50 mg/m2 every 4 hours. Once the priming 

dose is given and an adequate urine flow is established, 

administration of CaNa2-EDTA is begun at a dose of 1000 

mg/m2/24 hours. CaNa2-EDTA is given by continuous 

intravenous drip in dextrose and water or 0.9% saline 

solution. Although continuous infusion of CaNa2-EDTA is 

preferable, it may be replaced by doses of 175 mg/m2 every 

rrr..^\.apiwr-xr^i&v.-ra-ac%atv±:&>-riirt-f.-j--f-. r,rr.-'fr~ft'^*'*gyi,*:*^**'-'%^'"'''^^ HjBjflHHfifiififi B 
P.37 

4 hours, given either intravenously over 15 to 20 minutes 

through a heparin lock or by deep intramuscular injection 

mixed with procaine. The concentration of CaNa2-EDTA 

should not exceed 0.5% in the parenteral fluid. Combined 

BAL-CaNa2-EDTA therapy is given for a total of 5 

days. 

During treatment, renal and hepatic function and serum 

electrolyte levels should be monitored daily. It is advisable 

to measure the blood lead concentration daily. (It will be 

necessary to interrupt the CaNa2-EDTA infusion for 1 

hour before this sample is obtained, to avoid a spuriously 

high value). If the blood lead concentration reaches <50 

/ig/dl, as it may within 3 days of combined BALCaNa;-EDTA therapy, BAL may be safely discontinued 

and CaNa2-EDTA continued for a full 5-day course of 

treatment. If measurements of blood lead cannot be 

obtained in time, it is safe to continue BAL for the full 

5-day course. Except under highly unusual circumstances, 

CaNa2-EDTA should not be administered for more than 5 

consecutive days. 

A second course of chelation therapy may be required 

after a 2- to 4-day interval, to be started with CaNa;-

EDTA alone or with concomitant BAL, depending on the 

blood lead concentration. A third course may be required if 

the blood lead concentration rebounds to a value >50 

Mg/dl within 7 to 10 days after treatment. Unless there are 

compelling clinical reasons, it is highly desirable to allow 5 

to 7 days before beginning a third course of CaNa,-

EDTA. 

ASYMPTOMATIC CHILDREN WITH 

INCREASED BODY BURDEN OF LEAD 

Although children with increased body burden of lead 

are clinically asymptomatic, it is likely that they have 

pervasive metabolic effects involving heme synthesis,200-' 

red cell nucleotide metabolism,24 vitamin D and Cortisol 

metabolism""' and renal function,'-4 and subclinical neurobehavioral effects.2

"

11

 Some of these profound metabolic 

and cellular effects of lead have been observed at blood 

lead concentrations <25 ^g/dl.20'*'•-*<•• J0*' 

Diagnostic assessment. In asymptomatic children it is 

essential to have a firm diagnosis based on an elevated 

blood lead level before treatment is initiated. Measurements of blood lead concentration in capillary samples are 

subject to contamination and should never be the only basis 

for treatment. Treatment should be initiated only after a 

confirmatory measurement of the venous blood lead concentration. Even when there is strong additional evidence 

of lead poisoning, such as paint flakes in the abdomen or 

lead lines in the bones on x-ray examination, it is preferable to wait for a confirmatory measurement of venous 

blood lead. Although measurements of erythrocyte protoporphyrin may be helpful in evaluating overall toxicity, 

blood lead measurement is the criterion on which to base a 

decision as to whether chelation therapy should be considered. (The EP may increase initially during chelation 

therapy.) Therapeutic decisions should also be based on 

the results of the CaNa2-EDTA provocative test. 

Chelation therapy 

Blood lead concentration >70 pg/dl. If the blood lead 

level is *>70 fig/dl, BAL and CaNa2-EDTA should be 

given, in the same doses and with the same guidelines as 

for treatment of symptomatic lead poisoning without 

encephalopathy. 

A second course of chelation therapy with CaNa:-

EDTA alone may be required if the blood lead concentration rebounds to a value >50 jig/dl within 5 to 7 days after 

treatment. Unless there are compelling clinical reasons, it 

is highly desirable to allow at least 5 to 7 days before 

beginning a second course of CaNa2-EDTA. 

Blood lead concentration 56 to 69 pg/dl. If the blood 

lead value is between 56 and 69 /"g/dl, treatment should be 

limited to CaNa;-EDTA only. 

CaNa2-EDTA is given for 5 days at a dose of 1000 

mg/m2/day, preferably by continuous infusion (or in 

divided doses intravenously as above). Alternatively, however, if environmental control of the lead hazards has been 

achieved, this treatment may be given on an outpatient 

basis, at a dose of 1000 mg/m2/day, preferably by intravenous infusion over 1 hour, with adequate hydration (250 

ml/m2). As a least preferable option, CaNa2-EDTA may 

be administered intramuscularly mixed with procaine, at 

the same single daily dose of 1000 mg/nr for 5 consecutive days. This route of administration may represent a 

painful but practical alternative, when circumstances dictate it. 

During treatment, renal and hepatic function and serum 

electrolyte levels should be monitored. A blood lead 

concentration should be obtained at 72 hours of treatment 

(it will be necessary to interrupt the CaNa2-EDTA infusion for 1 hour before this sample is obtained, to avoid a 

spuriously high value) to monitor the effectiveness of 

treatment. 

CaNa2-EDTA treatment should be continued for 5 days. 

Except under highly unusual circumstances, it should not 

be administered for more than 5 consecutive days. 

A second course of chelation therapy, with CaNa2-

EDTA alone, may be required if the blood lead concentration rebounds to a value >50 ug/d\ within 5 to 7 days after 

treatment. Unless there are compelling clinical reasons, it 

is highly desirable to allow a period of 5 to 7 days before 

beginning a second course of CaNa2-EDTA. 

Blood lead concentration 25 to 55 iig/dl. When the 

blood lead value is persistently between 25 and 55 Mg/dl 

and accompanied by EP persistently >35 Mg/dl, the 

decision to proceed with chelation therapy should be based 

29 

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Table. Choice of chelation therapy based on symptoms and blood lead concentration 

Clinical presentation Treatment Comments 

Symptomatic children 

Acute encephalopathy 

Other symptoms 

BAL 450 mg/m"/day Start with BAL 75 mg/m1 IM every 4 hours. 

CaNa2-EDTA 1500 mg/m'/day After 4 hours start continuous infusion of CaNa2-EDTA 1500 

mg/m2/day. 

Therapy with BAL and CaNa2-EDTA should be continued for 

5 days. 

Interrupt therapy for 2 days. 

Treat for 5 additional days, including BAL if blood Pb remains 

high. 

Other cycles may be needed depending on blood Pb rebound. 

BAL 300 mg/m'/day Start with BAL 50 mg/m2 IM every 4 hours. 

CaNa2-EDTA 1000 mg/m"/day After 4 hours start CaNa2-EDTA 1000 mg/m2/day, preferably 

by continuous infusion, or in divided doses IV (through a 

heparin lock). 

Therapy with CaNa2-EDTA should be continued for 5 days. 

BAL may be discontinued after 3 days if blood Pb <50 jig/dl. 

Interrupt therapy for 2 days. 

Treat for 5 additional days, including BAL if blood Pb remains 

high. 

Other cycles may be needed depending on blood Pb rebound. 

Asymptomatic children 

Before treatment, measure venous blood lead. 

Blood Pb >70 /xg/dl 

BAL 300 mg/m'/day 

CaNa2-EDTA 1000 mg/m*/day 

Blood Pb 56 to 69 Mg/dl 

CaNa,-EDTA 1000 mg/m"/day 

Blood Pb 25 to 55 jig/dl 

Perform CaNarEDTA provocation test to assess lead excretion 

Start with BAL 50 mg/m2 IM every 4 hours. 

After 4 hours start CaNa2-EDTA 1000 mg/m'/day, preferably 

by continuous infusion, or in divided doses iv (through a 

heparin lock). 

Treatment with CaNa2-EDTA should be continued for 5 days. 

BAL may be discontinued after 3 days if blood Pb <50 Mg/dl. 

Other cycles may be needed depending on blood Pb rebound. 

CaNa2-EDTA for 5 days, preferably by continuous infusion, or 

in divided doses (through a heparin lock). 

Alternatively, if lead exposure is controlled, CaNa2-EDTA may 

be given as a single daily outpatient dose IM or iv. 

Other cycles may be needed depending on blood Pb rebound. 

IT ratio >0.70 

If ratio 0.60 to 0.69 

Age <3 years of age 

Age >3 years of age 

If ratio <0.60 

ratio (see text). 

CaNa2-EDTA 1000 mg/m2/day Treat for 5 days iv or IM, as above. 

CaNa2-EDTA 1000 mg/m"/day Treat for 3 days iv or IM, as above. 

No treatment Repeat blood Pb and CaNa,-EDTA provocation test 

periodically. 

No treatment Repeat blood Pb and CaNa2-EDTA provocation test 

periodically. 

on positive findings of a carefully performed CaNa2-

EDTA provocation test. (It must again be emphasized that 

chelation therapy should complement, not replace, abatement of controllable lead sources.) 

CaNa,-EDTA PROVOCATION TEST. First, a repeated baseline blood lead level is obtained and the patient is asked to 

empty the bladder. Then CaNa2-EDTA is administered at 

a dose of 500 mg/m2 intravenously in 250 ml/m2 of 5% 

dextrose, infused over 1 hour. (A painful but practical 

alternative is to administer the same dose intramuscularly 

mixed with procaine and to encourage the child to drink as 

much as possible in the first 2 hours). All urine must be 

collected with lead-free equipment over 8 hours. The urine 

volume should be carefully measured, and aliquots should 

be sent to the laboratory for measurement of the concentration of lead. Extreme care should be.exercised to use 

only lead-free equipment. If this is not available in the 

clinic, it may be best that the entire urine volume be sent to 

30 

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" " 0 10.0 20.0 30.0 40.0 50.0 60.0 70.0 

Blood Lead (#g/dl) 

Figure. Lead excretion ratio as a function of blood lead. Data expressed as decimal logarithm of CaNa,-EDTA excretion 

ratio (\i% lead excreted/mg EDTA administered) versus blood lead. There is a significant correlation (r = 0.466, 

P < 0.001). with a slope of 0.014 and an intercept of -0.95. 

Data shown were obtained by different techniques. At Columbia University. 77 children in an outpatient setting 

received CaNa2-EDTA as a 20-minute intravenous infusion at a dose of 50 mg/kg. followed by 250 ml/m2 5% dextrose 

over 1 hour; urine was collected for 7 to 8 hours. At Albert Einstein College of Medicine (Montefiore Hospital), 37 

hospitalized children received CaNaj-EDTA intramuscularly with procaine at a dose of 500 mg/m2; urine was collected 

for 8 hours. At John Hopkins University School of Medicine, 50 hospitalized children received CaNaj-EDTA 

intramuscularly at a dose of 25 mg/kg at 0 and 12 hours; urine was collected for 24 hours. At Children's Hospital Medical 

Center, 46 children in the outpatient clinic received CaNaj-EDTA intramuscularly with procaine at a dose or 50 mg/kg: 

urine was collected for 6 to 7 hours. Despite these differences, slopes and intercept of regression lines were remarkably 

similar: excretion ratio makes the CaNaj-EDTA provocation test independent of both the dose administered and the 

child's age and body weight. Therefore, data could be pooled together in a single regression line. Combined data represent, 

to the best of our knowledge, the largest series of CaNaj-EDTA provocation tests in children. 

a laboratory where the volume can be measured with 

lead-free equipment and aliquots for lead and creatinine 

measurements can be taken without contaminating the 

sample. 

INTERPRETATION OF CaNa2-EDTA PROVOCATION TEST. 

The concentration of lead in the urine (in micrograms per 

milliliter) is multiplied by the volume (in milliliters), to 

obtain the total excretion (in micrograms). The total 

urinary excretion of lead (micrograms) is divided by the 

amount of CaNa2-EDTA given (milligrams) to obtain the 

"lead excretion ratio": 

Lead excreted (jig) 

CaNa2-EDTA given (mg) 

The CaNa2-EDTA provocation test is considered positive 

if the lead excretion ratio exceeds 0.60. 

The recommendations of the authors are based on their 

experience with 210 provocation tests1"

1

-

6)2)J

 (Figure). 

Inspection of the Figure shows that a ratio >0.60 is never 

obtained in 12 children with blood lead level <30 jig/dl, 

and is always obtained in 19 children with blood lead level 

>60 Mg/dl. At blood lead level 30 to 39 ug/dl, the ratio is 

>0.60 in six (11.5%) of 52 children; at blood lead level 40 

to 49 jjg/dl the ratio is >0.60 in 25 (37.9%) of 66 children; 

and at blood level 50 to 59 jxg/dl the ratio is >0.60 in 30 

(49.2%) of 61 children. 

It appears, therefore, that a ratio <0.60 represents an 

appropriate cutoff point to distinguish children with 

"markedly increased" excretion. (It is not possible to 

define a normal excretion range because no data are 

available and it would be unethical to obtain them in 

children with blood lead values <25 Mg/dl. In addition, 

even the lower blood lead levels observed in children from 

industrialized countries are significantly higher than those 

in children from remote areas uncontaminated by lead, 

which most likely represent the truly normal blood lead 

level.34 However, extrapolation from these data predicts, at 

31 

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P.40 

blood lead level 1 <jg/dl,-an excretion ratio of 0.1, six times 

lower than the proposed cutoff of 0.60). 

' GUIDELINES FOR TREATMENT BASED ON CaNa2-EDTA 

PROVOCATION TEST. If the lead excretion ratio is >0.70, a 

5-day course of CaNa2-EDTA 1000 mg/m2 intramuscularly or intravenously should be given, as above. 

If the lead excretion ratio is between 0.60 and 0.69, (1) 

children younger than 3 years should receive treatment for 

3 consecutive days with 1000 mg/m2 CaNa2-EDTA, as 

discussed above; and (2) in children older than 3 years the 

test should be repeated every 2 to 3 months and treatment 

started if the lead excretion ratio increases to >0.70 (in 

which case treatment shall consist of 3 days with 1000 

mg/m2 CaNa2-EDTA, as above). 

In children who have received chelation therapy, repeated cycles are indicated if the blood lead concentration 

rebounds to within 5 /Jg/dl of the original value, 7 to 10 

days after treatment. 

In all children, regardless of age, with elevated blood 

lead and EP values but with an excretion ratio <0.60, 

blood lead and EP should be monitored frequently. If the 

elevation of blood lead values persists, the CaNa2-EDTA 

provocation test should be repeated periodically (every 2 to 

3 months). 

IMMEDIATE TREATMENT FOLLOW-UP 

The goal of chelation therapy is to permanently reduce 

the blood lead level to <25 /ig/dl and that of EP to <35 

iig/dl. To achieve this goal it may be necessary to give 

several courses of treatment. It cannot be overemphasized, 

however, that repeated courses of therapy are counterproductive unless the source of lead has been identified and 

eradicated. Children receiving chelation therapy should 

not be released from the hospital until all lead hazards in 

their homes and elsewhere have been controlled and 

eliminated and, if necessary, suitable alternative housing 

has been arranged. With vigorous public health measures 

complete and safe abatement should be achieved during 

the treatment period.' If a child with elevated blood lead 

concentration cannot be moved to new hpusing, multiple 

repeated courses of CaNa2-EDTA in a clinically asymptomatic child with stable blood lead values may be counterproductive; parents may despair at the ineffectiveness of 

therapy and fail to return to the clinic. It is more important 

in these unfortunate situations to maintain follow-up so 

that a rise in blood lead concentrations is detected promptly. 

At the end of each treatment cycle the blood lead 

concentration usually declines to values <25 /.g/dl. However, within a few days reequilibration takes place and 

results in a rebound; thus the blood lead level must be 

rechecked 7 to 10 days after the end of treatment. 

If the blood lead level rebounds to within 5 i-g/dl of the 

value before the last cycle, additional treatment cycles are 

indicated (unless the concentration after rebound is <25 

jig/dl). A blood lead concentration that rebounds to above 

the pretreatment value is evidence of renewed and excessive intake. 

If the blood lead level remains low, its measurement 

must be repeated, initially biweekly, then at monthly 

intervals, to assure that the decreased level is permanent. 

Iron deficiency states, which may accompany lead 

poisoning, require therapeutic doses of iron in addition to 

the correction of other possible nutritional deficiencies. 

LONG-TERM CLINICAL FOLLOW-UP AND 

MANAGEMENT 

The vast majority of children with lead poisoning now 

referred to pediatricians from screening clinics are asymptomatic. Acute lead encephalopathy is rare. Lead poisoning (with or without clinical symptoms) should be reported to the local health authorities, who usually have 

prime responsibility for environmental investigation and 

abatement of lead hazards in the home or elsewhere. 

Because lead has been widely disseminated into the 

environment, thereby providing multiple opportunities for 

repeated overexposure, lead poisoning should be managed 

as a chronic disorder. A team approach involving public 

health personnel, pediatrician, pediatric nurse practitioner, 

and social worker is likely to be the most effective. 

Commonly this can be accomplished best if children with 

lead poisoning are referred for long-term follow-up to a 

special clinic where all phases of clinical management can 

be coordinated and continuity of care is maintained. 

At the outset, a long-term plan of management is 

developed. Age, the intensity of hand-to-mouth activity, 

pica, diet modification, environmental exposure, and serial 

laboratory data arc taken into account. The objectives are 

to reduce the body burden of lead and to prevent recurrences. All preschool-aged housemates of index cases 

should be examined. All cases should be reported to social 

service for assistance in obtaining safe housing. Extended 

follow-up to at least 6 years of age is usually necessary. 

Identification of lead sourcefs). In all cases, first priority 

is given to identification of important sources of excess 

lead in the child's environment and prompt separation of 

the child therefrom.* A thorough history can facilitate the 

identification and abatement of the most important 

sources of lead. Although this crucial part of therapy 

(abatement) is usually performed by health department 

personnel, not uncommonly information obtained in the 

clinic provides clues to unsuspected sources. The environmental history obtained in the clinic should include a list of 

all dwellings currently or recently visited by the child 

32 

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(primary residence, homes of relatives and baby sitters, 

schools, daycare centers) and evaluation of each building's 

age and state of repair. In the United States a high 

proportion of buildings constructed prior to 1960 have 

lead-bearing paints and putty on both exterior and interior 

areas accessible to the child. Structures in poor repair often 

have lead-containing chips or pulverized fragments in the 

household dust. Play areas, especially urban playgrounds 

near vehicular traffic, dirt playgrounds and dirt yards, 

painted metal fences and walls, and vacant lots formerly 

containing lead-painted structures should be identified as 

potential lead sources. Occupational histories for all adults 

in various dwellings should be ascertained to learn if any 

are working in lead-related industries. Lead trades include, 

but are not limited to, secondary lead smelting (recovery of 

lead from old storage batteries), lead scrap smelting, 

storage battery manufacturing and repair, metal founding, 

ship breaking, automobile assembly and body and radiator 

repair, demolition of painted metal structures (such as 

bridges), and demolition and renovation of old houses and 

other structures. Adults who work in lead industries must 

shower before coming home and must leave all work 

clothes, including shoes, at the work place; these clothes 

must not be cleaned or washed at home. Thus lead-bearing 

dust from the place of employment will not contaminate 

the house. Additional sources may include old lead-painted 

cribs and beds and the burning of lead-painted wood in 

wood-burning stoves. Proximity to lead smelters, ingestion 

of lead-containing dust, and inhalation of lead from the 

combustion of gasoline contribute to the overall body 

burden of lead in children, but the high concentration of 

lead that ultimately results in clinical lead poisoning is 

most frequently associated with ingestion of lead-bearing 

paint. Uncommon causes of poisoning include ingestion 

and retention in the stomach of metallic lead (fishing 

weights, curtain weights, shot, jewelry painted with lead to 

simulate pearl), contamination of acidic foods and beverages from improperly lead-glazed ceramic pitchers, pots, 

and cups and from opened lead-soldered food cans, and the 

home burning of battery casings. Inhalation of fumes 

(sniffing) from small leaded-gasoline containers has 

occurred in older children. Poisoning has also been traced 

to oriental cosmetics (surma, a black eyeliner containing 

up to 85% lead) and to Mexican and Oriental folk 

remedies (azarcon, greta, paylooah). 

Medical management during abatement of lead paint 

hazards. If the source of lead is limited to such items as 

retention of a metallic lead object in the stomach or an 

improperly lead-glazed food or beverage container, the 

child can be promptly separated from the source. Such is 

not the case when lead paint in the home is the principal 

source. Several methods are used to remove old lead-based 

paint from walls and woodwork. Some methods, particularly removal by burning and sanding, greatly increase the 

amount of air and dustborne lead in the home. Very fine 

lead-bearing particulates settle out slowly over many hours 

after burning and sanding is completed, ll is ofthe utmost 

importance to remove all young children and pregnant 

women from a dwelling until the abatement process is 

completed. They should live elsewhere day and night, and 

should not return until removal of all lead-bearing paint 

has been completed and the dwelling has been thoroughly 

vacuumed and scrubbed with high-phosphate-detergent 

solutions. The sources that have been denuded during the 

abatement process should be repainted to seal any residual 

lead behind the surface. Children should be removed from 

the home during abatement whether or not they have 

increased lead absorption. When this procedure is not 

followed, it is not uncommon to observe 30 to 50 pg/dl 

increments in whole blood lead concentration within a 

matter of a few days or weeks. 

Long-range dust control. It must be understood that 

dust control is not a substitute for abatement. In areas 

heavily contaminated with lead, such as deteriorating old 

housing and dwellings adjacent to lead-emitting industrial 

plants or heavy vehicular traffic, it may be helpful to 

institute a regular program in and about the home to 

control lead-bearing dust, which constantly reaccumulates. 

Because hand-to-mouth activity is common in young 

children, parents must institute a specific type of cleaning 

program; vacuuming and wet cleaning are recommended. 

Sweeping with a broom, although it may remove large 

fragments, serves only to stir up smaller particulates. It is 

recommended that all floors and woodwork be scrubbed 

weekly with high-phosphate detergents such as Tide or 

Spic and Span. For all surfaces that the child can touch, 

the weekly scrubbing should be supplemented with daily 

damp dusting with a cloth rinsed in a solution of highphosphate detergent. Although such cleaning programs 

may be helpful, the definitive way to prevent recurrences is 

for affected children and their families to move into 

housing free of lead paint hazards. 

Dietary factors. Although reduction in exposure to 

environmental lead must receive first priority, steps should 

be taken to identify and correct deficient dietary intake, 

particularly of calcium25-" and iron as well as excessive 

dietary fat, each of which may increase the absorption and 

retention of lead. A diet adequate in minerals and limited 

in fat should be assured. For those intolerant of .cow milk, 

lactose-free milk products such as yogurt or some alternative source are necessary to ensure adequate calcium 

intake. The use of low-fat milk and the avoidance of fried 

foods should limit excessive dietary fat. .Acidic foods such 

as fruits, fruit juices, tomatoes, sodas, and cola drinks may 

33 

y , i»y.'iy % »w * T»i^t'^-f*>>'g.g«» -J" ^ »- S*ISVTT. .LV,':*. T?**r *-••••1--, 
leach lead from cans with leaded-soldered seams. Dietary 

lead intake may be reduced if the above items are 

purchased fresh, frozen, or packaged in aluminum, glass, 

cardboard, or plastic containers. 

Neurobehavioral considerations. A major problem is 

presented by the high level of hand-to-mouth activity of 

many preschool-aged children. If hand-to-mouth activity 

or pica (ingestion of nonfood items) is particularly severe, 

a behavioral psychologist can be helpful in developing a 

program to reduce the activity. 

For children given any combination of chelating agents, 

neurologic and psychologic assessment should be obtained 

at the time of initial diagnosis and during the following 

years. This will facilitate appropriate school placement for 

children with learning handicaps, if they are identified 

through thorough psychometric evaluation prior to the 

child's entry into the school system. For the child who has 

had acute lead encephalopathy, long-term anticonvulsant 

therapy with phenytoin (or phenobarbital) is indicated if 

there were seizures or coma during the encephalopathic 

episode. Additional clinical and laboratory evaluation may 

be indicated to detect other sequelae of chronic lead 

poisoning, such as renal impairment. Metabolic disorders 

associated with acute lead poisoning are reversible after 

chelation therapy and substantial reduction of lead exposure. 

Frequency of follow-up. When the results of initial 

venous blood lead and EP values and CaNa2-EDTA 

testing indicate the need for chelation therapy, long-term 

follow-up is indicated. For those children who have not 

received chelation therapy, follow-up at 3-month intervals, 

together with abatement and dust control in the home and 

correction of dietary deficiencies, should be continued until 

the child has maintained normal blood lead and EP values 

for 1 year. 

Those children who initially received a course of chelation therapy require more intensive follow-up. Abatement 

of environmental lead hazards in the home is rarely 

accomplished within a matter of a few days, so that as a 

general rule the first course of chelation therapy is given in 

the hospital. Outpatient chelation therapy while a child is 

still overexposed to lead is counterproductive and likely to 

be associated with enhanced absorption and retention of 

lead. In children who have received a course of chelation 

therapy, blood lead and EP determinations should be 

repeated 5 to 7 days after therapy and then after another 1 

to 4 weeks, depending on the progress. If some improvement is observed, follow-up may be scheduled at 2- to 

4-week intervals for 6 months. Thereafter, blood lead and 

EP tests should be repeated at 3-month intervals until the 

child is 6 years of age. At each visit the environmental and 

housing situations are updated and reevaluated and dust 

control and diet are reviewed. If serial blood lead and EP 

data show continued improvement, it may be assumed that 

new assimilation of new lead is not occurring; rising blood 

lead concentrations, which may be followed by a rising EP 

level, indicate increased ingestion of lead. Often, reinvestigation reveals new sources of environmental lead not 

previously detected. When a child with earlier elevated 

blood lead concentrations approaches school age, psychometric evaluation may be indicated, even though the blood 

lead concentration at the time is <25 pg/dl. 

Summary. Increased body lead burden must be managed 

as a chronic disorder. The final evaluation and disposition 

of each case must take into account the entire prior record. 

It is prudent to observe mentally or developmentally 

handicapped children with persistent pica during school 

years, because recurrences after the age of 6 years are most 

likely to occur in these children. The need to remove 

infants, young children, and pregnant women from a home 

during abatement of lead paint hazards is crucial to 

prevent acute episodes of sharply increased lead toxicity. 

We thank Ms. Barbara Cirella, P.N.P., for performing the 

CaNa-EDTA provocation studies, and Ms. Carol Seaman for 

statistical analysis of the data; Dr. Morri E. Markowitz. and the 

CRC staff at Albert Einstein College of Medicine: Ms. Barbara 

Mahan, and the nursing staff in the Pediatric Lead Clinic at 

Children's Hospital: and Ms. Victoria Sadoff for careful and 

painstaking assistance with preparation of the manuscript. 

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34 

"V*?S"ig..gr'I^.^>"»'"r*ifw<*^-^^^^ *» ?;*'V6^1

^Tff;*frg.;^^r^1,'yfr^ "e^-SF&i$s'--liM>?-&lZu.^*'*.l.?-\ 
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27 

28. 

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J, Schroeder S: Effects of low to moderate lead exposure on 

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Glover B, Padgett R: Blood lead concentrations in a remote 

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34. 

35 

35 
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