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A STATEMEN T B Y TH E CENTER S FO R DISEAS E CONTRO L - JANUAR Y 198 5

U.S . DEPARTMEN T O F HEALT H AN D HUMA N SERVICES/PUBLI C HEALT H SERVICE/CENTER S FO R DISEAS E CONTRO L"?"^~"ff l

CENTER S FORDISEAS E CONTROL CHILDHOO D LEA D POISONIN G PREVENTIO N AD HO C ADVISOR Y COMMITTE E Ma y 17,198 4 - Septembe r 28,198 4 •Im CHAIRPERSON Rosen , Joh n F. , M.D
. Head , Divisio n o

f Pediatri c Metabolis m Albert Einstei n Colleg e o

f Medicin e Montefior e Medical Cente r Bronx , Ne w Yor

k 1046 7 EXECUT1 VE

SECR ETA R Y Houk , Verno n N. , M.D
. Directo r Cente r fo r Environmenta l Healt

h Center s fo

r Diseas e Contro l Atlanta , Georgi a3033 3 Braud , SaraM. , M.D
. Health Deput y Assistan t

Secretary Offic e of Health Service s an d Environmenta l Quality Louisian aDepartmen t

o f Healt h an d Huma n Resource s P.O
. Bo x 6063 0 Ne w Orleans , Louisian a7016 0 Beljan , Joh n R. , M.D
. Provos t an dVic e Presiden t

fo r Academi c Affair s Dean , Schoo l of

Medicin e Hahneman n Universit y Broadan dVin e Street s Philadelphia , Pennsylvani a1910 2 Cole , Jerom e F. , Sc.D
. Presiden t Internationa l LeadZin c Researc h Organizatio n 29 2 Madiso n Avenu e Ne w York , Ne w Yor

k 1001 7 Davidson , Clif

f I. , Ph.D
. Associat e Professo r

o f Civi l Engineerin g Departmen t

o f Civi l Engineerin g Carnegie-Mello n Universit y Pittsburgh , Pennsylvani a1521 3 Davis , Dever aLee , Ph.D
. Executiv e Directo r Boar do f Toxicology an d Environmenta l Healt

h Hazard s Nationa l Academ y o f Science s 210 1 Constitutio n Avenue , N.W
. Washington , D.C
. 2041 8 Field , Patrici aH. , Ph.D
. Director , Toxicology Laborator y Stat e Laborator

y o f Hygiene 46 5 Henr y Hal l Madison , Wisconsi n 5370 6 Gebbie , Kristin e M. , R.N
. Administrator , Healt

h Divisio n Departmen t

o f Huma n Resource s 140 0 S.W
. 5t h Avenu e Portland , Orego n 9720 1 Jackson , Rudolp h Ellsworth , M.D
. Actin g Chairman Departmen t

of Pediatric s Morehous e Schoo l o

f Medicin e 72 0 Wes t vie w Drive , S.W
. Atlanta , Georgi a3031 0 MacLean , Rober

t A. , M.D
. Deput y Commissione r Professiona

l Healt h Service s Texa s Slate Departmen t

o f Healt h 110 0 West 49t h Street Austin , Texa s 7875 6 Piomelli , Sergio , M.D
. Directo r o f Pediatri c Hematology

Oncology - Colleg e o f Physician s an dSurgeon s o f Columbi aUniversit

y 395 9 Broadwa

y Ne w York , Ne

w Yor k 1001 2 Reigarl , J
. Routt , M.D
. Associate Professo r Departmen t

o f Pediatric s Medica l Universit

y o f Sout h Carolin a 17 1 Ashley Stree t Charleston , Sout

h Carolin a2942 5 

# m

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# oisorun g i n 

# \bun g Childre n

A STATEMEN T B Y TH E CENTER S FO R DISEAS E CONTRO L JANUAR Y 198 5 Reprinte d Jul y 198 5

U.S . DEPARTMEN T O F HEALT H AN D HUMA N SERVICE S PUBLI C HEALT H SERVIC E CENTER S FO R DISEAS E CONTRO L CENTE R FO R ENVIRONMENTA L HEALT H CHRONI C DISEASE S DIVISIO N ATLANTA , GEORGI A 3033 3P. 5

Us e of trad e name s i s for

identificatio n only an ddoe s no t constitut e endorsemen t

b y th e Publi c Health Servic e o r

by th e U.S
. Departmen t

o f Healt h an dHuma

n Services
.

•*t.-aw*i.'-.-iT-***^rV>^>*'' - •rr-'*;«•.*-•••-'*•*-•• . '-'•."'<' ?P. 6 -"'••Taf r^wfT" ^ 

# Prefac e
Thi s secon drevisio n ofth e Center s fo r Diseas e Control' s (CDC's ) statement . Preventin g Lea d Poisonin g i

n Youn g Children , i s mor e comprehensiv e tha n th e two previou s versions
. Wit h hel p frommember s of

CDC' s A

dHo c Advisory Committe e o n Childhoo dLea

dPoisonin g Preventio n an dothe r expert consultants , w

e hav e considere dne

w researc h findings o

n lea dtoxicity , redefine d lead poisonin g a

l alowe r bloo dlea

dlevel , an dupdate dour

recommendation s o

n lead-base dpaint abatement
. I

n addition , arecen t

articl e on ane w treatmen t schem e fo

r lea dpoisonin g (symptomat

i c an dasymptomatic ) i s included
. Th e precis e threshol dfo r th e harmfu l effect s o

f lea do n th e centra

l nervou s syste mi s no t known
. I n th e meantime , we hav e use dou r bes t judgmen t

a s to wha

t level s oflea d are toxi c an d wha t practical intervention s wil l lowe r bloo dlea

dlevels
. As publi c healt

h officials , our

dul y i s t o protec t childre n a s bes t

we can—give n th e limitation s o f scienc e an

dth e nee dl o mak

e decision s withou t perfec t data
. Thi s i s ih e Departmen t o f Heali h an dHuma

n Services ' majo

r policy statemen i on th e issue
. Th e progressiv e remova l o f lea dfromleade dgasolin e i s lowerin g averag e bloo dlea dlevel s i n th e Unite dStales , bu t

th e proble mo

f ih e majo

r sourc e o

f hig h bloo dlea

dlevel s i

n ou r country—million s o

f oldhousin g unit s painte dwit h lead-base dpain

t —i s largely unsolved
. Unti l belte r approache s an dmor e resource s ar e availabl e fo r removin g lea

dpain t hazard s i n olde r dwell

ing s wher e childre n live , leadpoisonin g wil l continu e l o b e apubli c healt h problem
. Th e Committe e considere danumbe r of controversia l issues , an

dmember s vigorousl y debate d unti l amajorit

y indicate dtha t

the y coul dsupport

th e point unde r consideration
. Reader s shoul d carefull y weigh th e recommendation s in thi s document , an dthe y shoul dpa y particula

r attentio n t o reference s t o wor

k don e sinc e th e 197 8 CD C statemen i on lead
. Thi s 198 5 statemen t represent s agreemen t

o f 1 1 ofth e 1 2 Advisory Committe e members
. On e member , Dr
. Jerom e F
. Col e o f th e Internationa l Lea

dZin c Researc h prganization , di dno t suppor t th e recommendations
. Minute s o f th e Advisory Committe e meetin g o n Ma y 17-18 , 1984 , an dDr
. Cole' s statemen t o f dissen t are availabl e upo n request . ACKNOWLEDGMENTS Th e lime , effort , an dmeticulou s car e th e Committe e devote dto thi s statemen t are gratefully ac knowledged
. Thi s grou p o f dedicate dhealt

h professionals , alon g wit h notabl e expert

consultants , labore dthroug h ih e result s o f severa l year s o

f researc h i

n order l o gai n consensu s o

n extremel y comple x issues
. Th e variou s draft s o f ihi s documen t

ha dth e benefi

t o f thoughtfu l suggestion s fro m Committe e member s an dconsultant s alike
. Thei r wor k wil l help protec t

th e childre n o

f thi s natio n fromthi s preventabl e diseas e fo r man y year s to come . Vernon N.Houk , M.D
. Directo r Cente r fo r Environmenta l Healt

h 

# 1

i nP. 7



# Content s I
. INTRODUCTIO N 1 Definition s 1 II
. BACKGROUN D .' 3 III
. SOURCE S O F LEA D EXPOSUR E 5 Lead-Base dPain t

5 Airborn e Lead5 Soi l & Dus t

7 Occupationa l Source s 7 Foo d& Drinkin g Wate r

7 Lead-Glaze dPolter y 7 Othe r Source s 7 IV
. SCREENIN G 8 Goal of Childhoo dLeadPoisonin g :... . 8 Targe t Populatio n 8 Screenin g Schedul e 8 Screenin g Method s 9 Interventio n Level s 9 Measurement s o

f Erythrocyt e Protoporphyri n 1 0 Measuremen t

of Bloo dLead1 2 Screenin g Scheme s 1 2 Interpretatio n of

Screenin g 1 2 V
. DIAGNOSTI C EVALUATIO N 1 4 Test s 1 4 VI
. CLINICA L MANAGEMEN T 1 6 Urgen t Ris k 1 6 Hig h Ris k 1 7 Moderat e Ris k

1 7 Lo w Ris k 1 7 VII
. ENVIRONMENTA L EVALUATIO N AN D LEA D HAZAR D ABATEMEN T 1 8 Lead-Base dPain t

1 8 Airborn e Lead20 Soil & Dus t

2 0 Foo d& Wate r

20 Occupationa l 2 0 Lead-Glaze dPotter y 2 1 VIII
. HEALT H EDUCATIO N 22 IX
. REPORTIN G LEA D TOXICIT Y AN D ELEVATE D BLOOD LEA D LEVEL S 22 X
. REFERENCE S 2 3 APPENDI X —Managemen t of Childhoo dLeadPoisoning : Specia l Articl e 2 6

mmmmmmmmma 

### ^ m 

### ^ mP. 8 

# 1

t 

# Content s - continue

d Figur e 1
. Source s o

f Lea di n aChild' s Environmen t

6 Tabl e 1
. Suggeste dPriorit y Group s fo

r LeadScreenin g : 8 Tabl e 2. A Zin c Protoporphyri n (ZnPP ) by Hemalofluorometer : Risk Classificatio n o

f Asymptomati c Childre n for Priority Medica

l Evaluatio n 1 1 Tabl e 2. B Erythrocyt e Protoporphyri n (EP ) b y Extraction : Risk

Classificatio n o

f Asymptomati c Childre n for Priority Medica

l Evaluatio n 1 1

v i


# ^HMH^HH H

# I
. Introduction P. 9

Leadi s ubiquitou s i

n th e huma n environmen t a s a resul t o f industrialization
. I

t ha s n o know n physiologi c value
. Excessiv e absorptio n o f lea d i s on e o

f th e mos t prevalen t an dpreventabl e childhoo dhealth problem s i n th e Unite dStale s today
. Childre n ar e particularl y sus ceptibl e l o it s toxi c effect
. Sinc e 1970 , ih e detectio n an dmanagemen t o f childre n expose dt o leadha s change dsubstantially
. Befor e th e mid-1960's , aleve l belo w 6 0 microgram s o f leadpe r decilite r (^tg/dl ) o

f whol e bloo dwa s no t

considere d dangerou s enoug h t o requir e interventio n (Chisolm , 1967)
. B y 1975 , th e interventio n leve l haddecline d •50%-t o 3 0 /ig/d l (CDC , 1975)
. I n tha t year , th e Cente r (no w Centers ) fo

r Diseas e Contro l (CDC ) publishe dIncreased Lead Absorption and

Lead Poisoning in Young Cliildren: A Statement

by the Center

for Disease Control. Sinc e then , ne w epidemiologic , clinical , an dexperimenta l evidenc e ha s indicate dtha i leadi s toxi c a l level s pre viousl y though t

t o b e nontoxic
. Furthermore , i t i s no w generall y recognize dtha t lea dtoxicit y i s awidesprea d proble m—on e that

i s neithe r

uniqu e t o inne r

cit y childre n no r limite dl o on e are aofth e country . Progres s ha s bee n made
. Th e Secon dNationa l Healt h an dNutritio n Examinatio n Surve y (NHANE S II ) ha s es tablishe daverag e bloo dleadlevel s fo r ih e U.S
. popula

tion ; lead-coniaminate d soi l an ddus t hav e emerge da s importan t contributor s l o bloo dlea dlevels , a s ha s leade d gasoline , throug h it s contributio n t o soi l an ddus l lead levels
. A n increasin g bod

y of dat asupport s Ih e view that lead , eve n a

l level s previousl y though t t o b e "safe, " i s loxi c l o th e developin g centra l nervou s system ; an d screenin g program s hav e show n th e exten t oflea d poison

in g i n targe t populations
. A majo r advanc e in primary preventio n i s th e phase d reductio n o

f leadi n gasoline
. Il i s probabl y responsibl e fo r th e finding s of

reduce daverag e bloo dlea dlevel s i n childre n nationwid e (Annes t e t al. , 1983 ) an di

n tw o major citie s (Rabinowit z an dNeedleman , 1982 ; Billic k e t al. , 1980 ; Kaul e t

al. , 1983)
. Leadi s n o longe r allowe di n pain t t o b e applie dt o residentia l dwellings , furniture , an d toys . Th e source s of

lea dar e many . The y includ e air , waler , an dfood
. Despit e th e 197 7 rulin g b y th e Consume r

Pro

duc t Safely Commissio n (CPSC ) tha t limit s th e lea

dcon len t

o f newl y applie dresidential paints , million s o f hous

in g unit s stil l contai n previousl y applie dleade d painls
. Older house s ihal ar

e dilapidate do

r tha i ar e bein g renovate dar

e aparticula

r danger l o children
. I

n man y urban areas , lea

di s foun di n soi l (Mielk

e e l al. , 1983 ) an d hous e dus t

(Chante y e t

al. , 1983)
. Consequently , screen in g programs—afor

mo f secondar y prevention—ar e stil l neede dt o minimiz e th e chanc e oflea d poisonin g devel

opin g amon g susceptibl e youn g children
. Lea dpoisonin g challenge s clinicians , publi c healt h au thorities , andregulator

y agencie s l o put

int o actio n th e finding s fro

mlaborator

y an dfieldstudie s tha i defin e th e ris k fo r thi s preventabl e disease
. Althoug h screenin g pro gram s hav e been limited , the y hav e reduce dth e numbe r o f childre n wit

h sever e lead-relaie d encephalopath y an d othe r form s oflea d poisoning
. Th e revise drecommendation s in thi s 198 5 Statemen t reflec t curren t knowledg e concernin g screening , diagno

sis , treatment , followup , an denvironmenta l interventio n for childre n wit

h elevate dbloo dlea

dlevels
. Clearly , th e goa l i s t o remov e lea

dfro mth e environmen t

o f childre n befor e i t enter s thei r

bodies
. Until thi s goa

l i s reached , screening , diagnosis , treatment , followup , an dsecondary environmenta l managemen t wil l continu e t o b e essentia l publi c healt

h activities
. DEFINITION S Th e tw o lerm s define dbelow—elevate d bloo d lea d leve l an dlea

dtoxicity—ar

e fo r us e i n classifying childre n (whos e bloo dha s been teste di n screenin g programs ) fo

r followu p an dtreatment . Th e term s shoul dno t b e inter

prete da s implyin g tha

i asaf e level o f bloo dlea d ha s bee n established
. Furthermore , the y ar e to b e use da s guide

lines
. The y ma

y no t b e precisely applicabl e i

n every case . Eac h chil dneed s l o b e evaluate do n a n individual basis
. Th e CD C i s lowerin g it s definitio n o f a n elevate d bloo dlea dleve l fro

m3 0 t o 25 /*g/dl
. Th e definition s belo w ar e simplifie dversion s o f thos e i n Preventing Lead Poisoning in Young Children: A Statement by the Center

for Disease Control: April

1978(CDC , 1978)
.

• elevate dbloo dlea dlevel , whic h reflect s excessiv e absorptio n o

f lead , i s aconfirme dconcentratio n o f lea di n whol e bloo do

f 2 5 /ig/d l o r greater ;

•>ava;i < )rTj.^;jTay>«..:Tr:<-ts?.rs i ra.p r r.^.-?:.~->.Tx^-'-!'^J^-KT!~'.,^J^rr:ra-A-s^t^,...P.1 0 '"""•I * L U |"*""| L (,i W " i
• lea dtoxicit y i s a

n elevate dbloo dleadleve l wit h a n erythrocyt e protoporphyri n (EP) * leve l i n whol e bloo dof 3 5 /xg/dl o r

greater . , J A s define db y bloo dlea dan dE P levels , th e term s lead toxiciiy an d leadpoisoning ar e use dsynonymousl y i n Ihi s document
. "Poisoning " i s generall y use dt o describ e epi

sode s of acute , obviousl y symptomati c illness
. Th e ter m "toxicity " i s use dmor e commonl y i n thi s document , sinc e screenin g program s usuall y involv e asymptomati c children
. Accordin g l o thi s Statement , th e severit y oflea d toxici

t y i s grade db

y Iw o distinc i scales—on e fo

r us e i n screen ing , th e othe r

fo r us e i n clinica l management . I

n Ih e scal e use din screening , childre n wil h lea dtoxicii y ar e divide d int o classe s I , II , III , an dI V (sectio n IV)
. Thes e classe s indicat e th e urgenc y o

f further diagnosti c evaluatio n (sec

lio n V)
. Afte

r Ihe diagnosti c evaluation , ihe y ar e placed i n on e o f fou r risk groups : urgent , high , moderate , and low (sectio n VI)
.

*E P result s ar e expresse d i n equivalent s o f fre e erythrocyt e protoporphyri n (FEP ) extrade d by th e ethy l acetate-aceti c acid-HC I metho d an d report e d i n microgram s pe r decilite r o f whol e blood . In thi s Statement , zin c protoporphyri n (ZnPP ) an d FE P ar e referre d l o a s EP .

•TT^^Taa-r^-Try.'. K- • •'..•''-->'•- " >.'?r-^',f?ayi.rT;'? s r-.T.Kr. ••: . • 5rr^-. ' •: T J XM TP. n



# II
. Backgroun

d

A nationwid e survey , conducte dfrom1976-1980 , showe dtha t

childre n fro mal l geographi c area s an dsocio

economi c group s ar e a

t ris k oflea d poisonin g (Mahaffey , Annes t e t al. , 1982)
. Dat afro mtha t surve y indicat e tha t 3.9 % of all U.S
. childre n unde r th e ag e of

5 year s had bloo dlea dlevel s of

3 0 ug/d l o r

more . Extrapolatin g thi s t o th e entir e populatio n o f childre n i n th e Unite dState s indicate s tha t

a n estimate d675,00 0 childre n 6 month s t o 5 year s o f ag e ha dbloo dlea dlevel s of 3 0 /ig/d l or

more . Ther e was , i n addition , amarke dracia l differenc e in thos e data
. Tw o percen t of whit e childre n ha delevate d bloo dlea dlevels , bu t

12.2 % of blac k childre n hadelevat

e dlevels
. Further , amon g blac k childre n livin g in th e core s of larg e citie s an di n familie s wit h annua l income s of les s tha n $6,000 , th e prevalenc e of level s of 3 0 /xg/dl o r mor e wa s 18.6%
. Amon g whit e childre n i n lower incom e families , th e prevalenc e of elevate dleadlevel s wa s eigh t time s tha t

of familie s wit

h highe r incomes
. I n th e pas t

decade , ou r

knowledg e of

leadtoxicit

y ha s greatl y increased
. Previously , medica l attentio n focuse d o n th e effect s of

sever e exposur e an dresultan t hig h body burden s associate dwit

h clinicall y recognizabl e sign s an d symptom s of

toxicity (Perlstei n an dAttala , 1966 ; Chi

solm , 1968 ; Byer s an dLord , 1943)
. It i s no w apparen t tha t lowe r level s of exposur e ma

y caus e seriou s behavior

a l an dbiochemica l change s (D e l aBurd e an dChoate , 1972 , 1975 ; NAS , 1976 ; WHO , 1977)
. Recen t studie s hav e documente dlead-associate dreduction s in th e bio

synthesi s o

f hem e (Piomell i e t

al. , 1982) , i n concentra
tion s of 1,25-dihydrox y vitami n D (Rose n e t al. , 1980 ; Mahaffey , Rose n e t

al. , 1982) , an di n th e metabolis mo f erythrocyt e pyrimidin e (Angl e an dMclntire , 1978 ; Pagli ae t al. , 1977)
. Result s of agrowin g numbe r o f stud

ie s indicat e tha t

chroni c exposur e t o lo w level s oflea d i s associate dwit

h altere dneurophysiologica l performanc e an dtha t th e youn g chil di s particularl y vulnerabl e t o thi s effec t (Needlema n e t

al. , 1979 ; Winneke , 1982 ; Yul e e t al. , 1981)
. Investigation s hav e als o show n alteration s i n electroencephalogram s (EEG's ) (Burchfie l e t al. , 1980 ; Benignu s e t

al. , 1981 ; Ott o e t

al. , 1982 ) an ddecrease d velocity in nerv e conductio n (Seppalaine n an dHernberg , 1982 ; Feldma n etal. , 1977)
. Man y factor s ca

n affect th e absorption , distribution , an dtoxicit

y of lead
. Childre n ar e mor e expose dt o lea d tha n olde r

group s becaus e thei r

norma l hand-to-mout h activitie s introduc e man y nonfoo ditem s int o thei r bodie s (Lin-Fu , 1973)
. Onc e absorbed , lea di s distribute d throughou t

sof t tissu e an dbone
. Bloodlevel s reflec t th e dynami c equilibratio n betwee n absorption , excretion , an ddepositio n i

n soft

- an dhard-tissu e compartment s (Rabinowitz e

t al. , 1976)
. Youn

g childre n absor

b an d retai n mor e lea

do n aunit-mas s basi s than adults
. Thei r bodie s als o handl e lea

d differently
. Higher

mineral turn
ove r i n bon e mean s tha

t mor e lea di s availabl e to sensitiv e systems . Th e child' s nutritiona l statu s i s als o significant i n determinin g risks
. Deficiencie s i n iron , calcium , an d phosphoru s ar

e directl y correlate dwit

h increase dbloo d lea dlevel s i n human s an dexperimenta l animal s (Mahaf

fey , 1981 ; Mahaffe

y an dMichaelson , 1980)
. Increase d dietar y fa t anddecrease ddietar

y intak e o

f calciu m (Barltro p andKhoo , 1975 ; Rose n e t al. , 1980) , iro n (Mahaffey-Si

x an dGoyer , 1972) , andpossibly othe r nu trient s enhanc e th e absorptio n oflea d fro mth e intestin e (NAS , 1976 ; Barltrop an

dKhoo , 1975)
. Sinc e lea daccumulate s in th e bod y an di s only slowly removed , repeate dexposure s to smal l amount s ove r man y month s ma

y produc e elevate dbloo dlea dlevels
. Lea dtoxicit y i s mainly eviden t

i n th e re dbloo dcell s an dthei r precursors , th e central an dperipheral nervou s systems , an

dth e kidneys
. Lea

dals o ha s advers e effect s on reproductio n i

n bot h male s andfemale s (Lane , 1949)
. Ne w data(Needlema

n e t al. , 1984 ) sugges t

tha t prenatal exposur e to lo

w level s o

f lea dma y b e relate dto mino r congenital abnormalities
. I n animals , lea

dha s cause d tumor s o f th e kidney
. Th e margin o f safet y fo r lea di s ver y smal l compare dwit

h othe r chemica l agent s (Roya

l Commissio n on Environmenta l Pollution , 1983)
. Th e hem e biosyntheti c pathwa y i s on e ofth e biochemi

ca l system s mos t

sensitiv e t o lead
. A

n elevate dE

P leve l i s on e o f th e earlies t

andmos t

reliabl e sign s o

f impaire d functio n du e t o lead
. A proble mi n determinin g lea

d level s in bloo dspecimen s i s tha t th e specime n ma

y b e contaminate dwit

h lead , an dthu s th e level s obtaine dma y b e falsel y high
. Therefore , i

n th e initia

l screenin g o

f asymptomati c children , th e E P level (instea do

f th e lea d level ) i s determined
. Th e effects o

f lea dtoxicit y are nonspecifi c an d no t readil y identifiable
. Parents , teachers , an dclinician s ma y identif y th e altere dbehavior s a s .attentio n disorders , learnin g disabilities , o

r emotional disturbances
. Becaus eofth e larg e numbe r o f childre n susceptibl e t o lea dpoison

ing , thes e advers e effect s ar e amajo r caus e for concern . Symptom s an dsign s o f

lea dtoxicit y ar e fatigue , pallor , malaise , los s of

appetite , irritability , slee p disturbance , sudde n behaviora l change , an ddevelopmenta l regres sion
. Mor e seriou s symptom s ar e clumsiness , muscular irregularitie s (ataxia) , weakness , abdomina l pain , persist

en t vomiting , constipation , an dchange s i n consciousnes s du e t o earl y encephalopathy
. Childre n wh o displa y thes e symptom s urgentl y nee dthoroug h diagnosti c evaluation s and , shoul dth e diseas e b e confirmed , promp t treatment . In thi s Statement , screenin g i s distinc t fromdiagnosis
. "S'cfeWi1Tf'''Wda

larg e number s o

f presumabl y asymptomati c childre n t o determin e i

f they hav e bee n expose dto leadand , i f so , wha t th e risk s of

continue dexposur e are . Diagno

sis , o n th e othe r

hand , mean s th e calegorizatio n o f a chil dappearin g t o hav e exces s exposur e t o leadaccord

in g t o th e severit

y o f burde n an dtoxicit

y s o tha t ap propriat e managemen t

ca n b e started
. N o chil dwit h symptom s suggestin g leadtoxicit y shoul d b e put throug h th e screenin g process . H e o r sh e shoul db e brough t directl y t o medica

l attention
. "P.1 3



# III
. Source s o

f Lea dExposur e

. Childre n ma

y b e expose dt o lea dfro mawid e variet y of man-mad e sources . Al

l U.S
. childre n ar e expose dt o lea di n th e air , i

n dust , an di

n th e norma l die t

(Figure 1)
. Airborn e leadcome s fromboth mobile an dstationary sources . Leadi n wate r

ca n com e fro mpipin g an ddistribu

tio n systems . Leadi

n foo dca n com e fromairborn e lead deposite do n crops , fromcontac t wit h "leaded " dus t durin g processin g an dpackaging , an dfromlea dleachin g fromth e seam s o

f lead-soldere dcans . In additio n t o expo sur e fro mthes e sources , som e children , a s aresul t of thei r typical , norma l behavior , ca n receiv e high dose s o

f leadthroug h accidenta l or deliberat e mouthin g or

swal

lowin g of nonfoo ditems
. Example s includ e pain t chips , contaminate dsoi l an ddust , and , les s commonly , solder , curtai n weights , bullets , an dothe r items
. LEAD-BASE D PAIN T Lead-base dpain t

continue s t o b e th e major sourc e o f high-dos e lea dexposur e an dsymptomati c lea dpoisonin g for childre n i n th e Unite dState s (Chisolm , 1971)
. Sinc e 1977 , househol dpain t

must , b y regulation , contai n n o mor e tha n 0.06 % (60 0 part s pe r millio n (ppm) ) lea db

y dr y weight
. I n th e past , som e interio r paint s containe d mor e tha n 50 % (500,00 0 ppm ) lead
. Th e interio r surface s o f abou t 2 7 millio n household s i n thi s countr y ar e con taminate db

y lea dpain t

produce dbefor e th e amoun t o f lea di n residentia l pain t

wa s controlled
. Painte dexterio r surface s ar e als o asourc e o f lead
. Unfortunately , lead

base dpain t

tha t i s stil l availabl e for

industrial , military , an dmarin e usag e occasionall y end s u p bein g use din homes
. Usually , over t

leadpoisonin g occur s i

n childre n unde r 6 year s of

ag e wh o liv e in deteriorate dhousin g buil t befor e Worl dWa

r II
. Pica , th e repeale dingestio n o f non foo dsubstances , ha s frequentl y bee n implicate di n th e etiolog y oflea d toxicity in youn g children
. I n many cases , however , lead-pain t

ingestio n i s simpl y th e resul t ofth e norma l mouthin g behavio r o f smal l childre n wh o liv e i n lead-contaminate dhomes
. Case s of childre n poisone db

y lea dpaint

hav e bee n reporte dfromal l region s o

f th e Unite dSlate s an dfrombol h urba n an drural settings
. In

creasingly , ihi s poisonin g ha s bee n reporte dwhen fami

lie s mov e int o acit

y a s "urba n homesteaders, " an dth e childre n ar e inadvertentl y expose dl o chips , fumes , o r dus t fro mlead-base dpain t

a s house s ar e rehabilitated
. Cluster s o f lead-base dpain

t poisoning s hav e als o resulte d fromdemographi c shift s wilhi n cities , when familie s wil h youn g childre n hav e move dint o neighborhood s wil h deterioraiin g older

housing
. Increase dlea

d absorptio n ha s bee n reporte di

n childre n expose dt o chip s or dus l fromlead-base dpaini produce ddurin g th e deleadin g o f exterio r painte dstee l structures , suc h a s bridge s an dex pressway s (Landriga

n e t al. , 1982)
. AIRBORN E LEAD Generally , inhalatio n o

f airborn e lea di s amino r

expo sur e pathwa

y fo r individual children , bu t

lead-containin g particles—airborn e an dthe n deposited—can b e responsi

bl e fo r hig h concentration s o

f lea din dus t tha t childre n ingest
. Studie s i

n Ne w Jerse y (Capri o e t

al. , 1974 ) an d Californi a(Johnso n e t

al. , 1975 ) hav e show n that chil

dre n livin g withi n 10

0 fee t o f majo r roadway s hav e highe r bloo dlea dlevel s than thos e livin g farthe r away . Thes e level s als o correlat e positivel y wit h th e averag e dail

y traf

fic volum e o

n road s nea

r home s (Capri o e t

al. , 1974)
. Previou s estimate s ofth e quantitativ e relationshi p be

twee n ambient

air lea dlevel s an dbloo dlea

dlevel s ma

y nee di o b e revise dbecaus e o f ne w experimenta l and surve y data
. Preliminar

y result s fro

ma n isotopi c lea

dex perimen t (Facchett

i an dGeiss , 1982 ) sugges t iha t lea d fro mleade dgasolin e i s amuc h more importan l contami

nan t tha n ii wa s previousl y though t

t o be
. Th e preliminar

y estimate s fro

mtha i study indicate tha

t a l leas t 25 % o f ih e bloo dlea do f resident s o

f Turin , Italy , i s derive dfro m lea din gasoline
. I

n Turin , th e averag e bloo dlea dleve l i n adul t male s i s 25 ug/dl ; thi s correspond s l o abou t 6 ug/d l attributabl e l o gasoline
. Dai afro mNHANE S I

I als o indicat e tha

t leade dgaso lin e i s amore significan

t sourc e o f leadtha n previousl y thought
. Annes t

el al
. (1983 ) correlate dmajo r reduction s in th e amount s o

f lea dadde dl o gasolin e sol di n th e Unite dStale s wit

h significan

t reduction s i

n children' s bloo dlea dlevels
. The y foundtha t betwee n 197 6 an d 1980 , th e overal l mea

n bloo dlea

dlevel s i n th e U.S
. popu latio n droppe dfro

m14. 6 ug/d l to 9. 2 ug/dl
. A simila r relationshi p betwee n leade dgasolin e sale s an dumbilica l cordbloo dlea

dlevel s ha s been show n b y Rabinowii z an d Needleman (1983)
. Stationar y source s ca

n produc e concentrate dzone s o f exposure , especially wher e climati c condition s suc h a s



## muimmmyiiLms&\mL\&P.1 4 t W/l- B ' ( <W"fq*'|!"""" ' 1 * " 1 **' 1 T"''' , ».**I.J|t ' ' 5""P«*""

- Figur e 1 SOURCE S O F LEA D I N A CHILD' S ENVIRONMEN T

HOS T CHIL D

Ingestio n

Othe r Nonfoo d Items* *

'Productio n o f bullet s o r fishin g sinker s Solderin g an d stained-glas s wor k Gasolin e sniffin g Pottery glazin g Burnin g o

f batteries , colore d newsprint , lead-painte d objects , an d wast e oi l 'Toy s an d figures containin g lea d Fol k remedie s Cosmetics (especiall y Orienta l cosmetics , e.g. . Surma , a blac k eyeliner ) Jewelr y (painte d wit h lea d t o simulat e pearl ) Lead-containin g dust transmitte d o n clothin g fro m workplac e

TT^.r*^TTTT3.:
.P.1 5

aridity , low win dvelocity , an dfrequen t therma l inver

sion s minimiz e dispersa l of airborn e lead
. Th e wors t situ

ation s of thi s kin di

n ih e Unite dSlate s hav e existe di n th e vicinit y o f primar y lea dsmelter s (Baker , Haye s e t al. , 1977)
. SOI L AN D DUS T Soil an ddus t

that contai n lea dar e often a n importan t sourc e of leadexposur e for

children
. Th e particle s of air

born e lea ddeposite di

n soi l an ddus l usuall y com e fro m automotive , industrial , an dsimilar sources . Flakin g lea

d pain t add s l o thi s contamination , particularl y i n an d aroun dhouses
. I

n soil , lea dtend s l o remai n i n ih e lo p centimeter , bu t

mos i soil s ar e contaminale dto amuc h greate r depth whe n th e lopsoi l i s disturbe dan dturne d under
. Childre n appear

t o obtai n lea dfro mdus t an dsoi l a s a resul t of thei r norma l explorator y behavio r (Barltrop , 1966 ; Sayre e t

al. , 1974 ; Roel s e t

al. , 1976) , couple di

n som e instance s wit

h pica
. Becaus e of

thos e mouthin g tendencies , youn g childre n wh o liv e near major source s o f airborn e lea dpollutio n mus t b e considere da

t ris k o f exposur e both by inhalatio n o f airborn e leadan db

y inges

tio n of deposite dlea dfro msoi l an ddust
. In general , lea din soi l an ddus t appear s t o b e responsi

bl e for bloo dleadlevel s i n childre n increasin g abov e backgroun dlevel s whe n th e concentratio n in th e soi l or dus t exceed s 500-1,00 0 ppm . OCCUPATIONA L SOURCE S Lea ddus l ca n clin g t o th e skin , hair , shoes , clothing , an dvehicle s of

workers , an dleadca

n b e carrie dfro

m workplac e t o hom e i

n ihi s way . I

n astud y i

n Memphis , Tennessee , whe n aparen t worke dwit

h lead , th e amoun t of leadi n th e children' s bloo dcorrelate dwit h ih e concen tratio n of leadi n dus t in ihei r home s (Baker , Follan de t al. , 1977)
. O

f 9 1 childre n tested , 3 8 (41.8% ) ha dbloo d lea dlevel s o

f 3 0 ug/d l o r

more , an d1 0 eithe r

ha dbloo d lea dlevel s of

8 0 ug/d l o r

mor e or E P level s abov e 19

0 ug/dl
. Stric t complianc e wit

h Occupationa l Safel

y an dHealt

h Administratio n (OSHA ) standard s i s quit e effectiv e i n decreasin g thi s typ e o

f exposure . However , many occupa tiona l exposure s t o leadar e no i covere db y th e OSH

A standards
. Companie s wil h fewer than 1 0 employee s (cot

tag e industries , "hobby " productio n o f pollery an d slaine d glasswork , an dhom e manufacturin g o f bullet s an dfishin g sinkers ) ar e exclude dfromOSHA standards
. Th e OSHA standar dfo

r lea dworker s i s abloo dlea d leve l o f 4 0 ug/dl
. I

n apregnan t

woman , lea

dcrosse s th e placenia , an dleadconcentration s i n umbilical cor

dbloo d ar e nearl y equa l to thos e in materna l bloo d(Barlirop , 1966)
. Sinc e th e growin g brai n ofth e fetu s i s likely l o b e a t leas t a s sensitiv e l o th e neurologi c effect s oflea d a s th e brai n of ayoun g child , umbilica

l cor dbloo dlevel s shoul d b e a l leas t below 25 ug/dl
. Therefore , th e OS H A standar d i s probably not

sufficiently stric t

to protec t th e feius
. Fur

the r stud y i s neede dl o defin e acceptabl e lea d level s amon g wome

n o f childbearin g age . FOO D AN D DRINKIN G WATE R Lea di n food , althoug h rarely responsibl e fo r lea d poisonin g i

n ih e Unite dStales , i s aubiquitou s sourc e of backgroun dlow-dos e exposur e fo r childre n (Beloian , 1982)
. Agricultura

l crop s grow

n nea r heavily travele d road s or nea r stationar y source s oflea d ca

n hav e signifi

cant concentration s becaus e o f airborn e lea

ddeposite d on them
. Lea

dma y als o b e inadvertentl y adde dl o food s durin g processin g an

dhandling
. Canne dfood s ma y hav e particularl y hig

h lea dcontents , becaus e acidi c food s ca n leach lea dfro mth e solde r

i n th e seam s o

f th e can s (Lam metal. , 1973). ' Generally , lea

di n drinkin g wate

r ha s bee n leache d fro mpipe s andsoldere djoint s b y sof i wate r havin g a n acidi c pH
. Sever

e lea dexposur e ha s bee n reporte damon g childre n i n Glasgow , Scotland , where pure , acidi c water was allowe

dto stan dovernigh t

i n aiti c cistern s line dwit

h lea d(Beatti e el al. , 1972)
. Th e proble mwa s alleviaie d b

y changin g ih e p

H o f ih e wate

r i n th e wate

r treatmen t plant
. I n th e Unite dStales , lea

d waler pipe s are mos t commonl y foun

di n olde r section s o

f northeaster n citie s and , occasionally , i

n rura l area s ofth e northeas t

(Mors e e i al. , 1979)
. LEAD-GLAZED POTTER Y Althoug h no t

awidesprea

dsourc e oflead , lead-glaze d potter y ca n releas e larg e amount s o f lea dint o foodan d drink
. I t ha s been responsibl e fo

r outbreak s o

f seriou s poisonin g (Klein e l al. , 1970)
. I n several episode s report
e dt o CDC , th e poller

y ha dbeen imported
. Homemad e o r craf t potter y andporcelain-glaze dvessel s hav e bee n foundl o releas e larg e quantitie s oflead , particularl y ifth e glaz e i s chipped , cracked , o r improperl y applie d(Osteru d e l al. , 1973)
. I

f th e vessel s ar

e repeatedl y washed , th e glaz e ma y deteriorat e an

dpotter y previousl y leste d a s saf e ca n become unsaf

e (D
. M
. Wallace , personal communication)
. OTHER SOURCE S Lea di s foun di n avariet y o f items , som e o

f which endange r specifi c population s o r

ethni c groups . A variet

y o f fol k remedie s contai n lead , includin g azarco n andgret a use db y Mexica n group s andpay-loo-a

h use db y Hmon g refugee s fro

mLaos
. Seriou s poisonin g ca n als o resul t fro mgasolin e sniffing ; th e burnin g of wast e oil , colore d newsprint , batter

y casings , o

r lead-painte dwood ; an d targe t practic e i n poorly ventilated , indoo r firing ranges .

^^?|si2aSige> s

# IV
. Screening P.1 6

GOA L O F A CHILDHOO D LEA D POISONIN G PREVENTIO N PROGRA M Th e goa l of achildhoo dleadpoisonin g screenin g pro gra mi s t o identif

y childre n wit

h significan t

exposur e to lea dearl y enoug h t o preven t seriou s toxicity
. Elevate d bloo dlea dlevel s mus t

b e detecte di n asymptomati c chil

dren , an dappropriat e medical an denvironmenta l inter

vention s mus t

follow
. Th e goa

l can b e reache donly throug h — 1
. A screenin g programtha t enroll s th e maximu m numbe r o f childre n i n high-ris k

populations
. 2
. A referral syste mtha t

ensure s acomprehensiv e di

agnosti c evaluatio n of

ever y chil dwit

h apositiv e screenin g test . 3
. A programtha t

assure s identificatio n an delimina

tio n ofth e sourc e (s ) o

f th e child' s lea dexposure . 4
. A syste mtha t

monitor s th e adequac y of th e treat
men t an dth e followup o f

eac h chil dwit

h adiagnosi s oflea dtoxicity
. Screenin g i s of

n o valu e withou t

prompt , thorough , an dcontinuin g medica l an denvironmenta l followu p fo r thos e childre n foun dt o hav e lea dtoxicity—tha t is , a s state dearlier , a

n elevate dbloo dlea dleve l ( aconfirme d concentratio n i n whol e bloo do f 2 5 jug/d l or

greater ) an d a n E P leve l i n whol e bloo do

f 3 5 ug/d l o r

greater . Als o a s state dearlier , screenin g mus t b e distinguishe dfrom diagnosis : Screenin g refer s t o th e testin g o f larg e number s of childre n considere dt o b e ASYMPTOMATI C i n orde r t o identif y thos e wh o nee dfurthe r evaluation
. Diagnosis , on th e othe r

hand , refer s t o categorizin g a child' s conditio n accordin g t o severit y o f leadburde n an dtoxicity
. Then , o n th e basi s o f th e category , managemen t

i s selected
. Childre n whos e elevate dbloo dlea dlevel s ar e detecte d b y screenin g shoul db e brough t directl y t o medical atten
tion , an dth e diagnosti c proces s shoul db e starte dwithou t delay
. Childre n wit

h symptom s suggestiv e oflea d poison

in g requir e urgen t

an dthoroug h diagnosti c evaluatio n and , i f th e diagnosi s i s confirmed , immediat e treatment . Th e symptom s oflea d poisonin g ar e nonspecific ; the y ar e describe din sectio n V
. TARGE T POPULATIO N Lea di s mos t

harmfu l t o childre n betwee n th e age s o f 9 month s an d6 years . Ideally , all childre n i n thi s ag e grou p shoul db e screened
. A s mor e childre n ar e screene d fo r iro n deficienc y wit

h E P testing , simultaneou s lea dscreen in g ofthes e sam e group s become s feasible
. Th e lis t o f pri

orit y group s in Tabl e 1 highlight s group s fo r which screenin g i s strongl y indicated
. Testin g childre n i n low

ris k group s fo r lea dtoxicit y ma y no t b e practica

l unles s i t i s don e simultaneousl y wit h E P test s fo r iro n deficiency
. Childre n i

n th e 12

- t o 36-month-ol d ag e grou p wh o liv e i n or are frequent

visitor s i n deterioratin g olde r

build

ing s (includin g day-care centers ) make u p th e highes t pri

orit y group . Siblings , housemates , an dplaymate s o f childre n wit

h identifie dlea

dtoxicit y probably hav e simila

r exposure s t o lead , andthe y shoul db e promptl y screened
. Suggeste d ranking s fo

r thes e an dothe r

priorit y group s ar e in Tabl e 2
. Tabl e 1 Suggeste dPriorit y Group s fo r LeadScreenin g Priorit y 1 . HIGHEST—Children , ag e 1 2 l o 3 6 months , wh o liv e i n o r ar e fre quen tvisitor s in older , dilapidate d housin g Children , ag e 9 month s t o 6 years , wh o ar e siblings , housemates , visitors , an

d playmate s ofchildre n wit h know n lea d toxicit y Children, ag e 9 month s t o 6 years , livin g i n older , dilapidate d housin g Children , ag e 9 month s t o 6 years , wh o liv e nea r lea d smelter s an d processin g plants o r whos e parents o r othe r househol d member s participat e i n a lead-relate d occupatio n o r hobb y Children, ag e 9 month s t o 6 years , wh o liv e nea r highway s wit h heav y traffic o r nea r hazardou s wast e site s wher e lea d i s a majo r pollutan t Al l childre n 1 2 l o 3 6 month s o f ag e All childre n 9 month s l o 6 year s o f ag e 2
. 3
. 4
. 5 .

SCREENIN G SCHEDUL E Screenin g fo

r lea dpoisonin g shoul db e incorporate d int o agenera

l pediatri c healt

h car e program , an dchildre n i n th e targe t

populatio n shoul db e screene da t leas t onc e a year . Th e first

screenin g shoul db e don e whe n th e chil di s betwee n 9 and1 2 month s old
. Childre n generall y hav e highe r bloo dlea

dlevel s betwee n Ma

y an dOctobe r (NAS , 1976) , s o screenin g effort s shoul db e concentrate d in thos e months
. Sinc e negativ e screenin g test s i n chil

dre n livin g in ahazardou s environmen t d o no t rul e ou t subsequen t

exposure , childre n 1 2 to 3 6 month s oldwh o ar e a t high risk o f exposur e shoul db e screene dever y 2 t o 3 months , especially durin g th e summer . Childre n wh o mov e int o ahigh-ris k

are aafte r age 3 year s ma

y als o nee d t o b e screene dmor e than onc e ayear .

r^T'yy-^'"-''^-^-'' •L^'-'^'AttR'*^.***^SCREENIN G METHOD S

Currently , th e mos t

usefu l screenin g test s ar e thos e for
. erythrocyt e protoporphyri n (EP ) an dbloo dlead
. Venou s o r

capillar y bloo dca

n b e use dfonboth tests , bu t papillar y specimen s ar e easie r

t o collec t

an dare , there

fore , mor e widely used
. Capillar y bloo dma

y b e transport
e din acapillar

y tub e wit

h a n anticoagulan t

o r drie don filter paper . Samplin g method s use din th e fieldmus t b e compatibl e wit

h laborator y capabilities
. E P an dbloo dleadtest s measur e differen t aspect s o

f leadtoxicity
. A s state dearlier , E P test s measur e th e leve l o f E P in whol e blood , an daleve l o f 3 5 ug/d l o

r mor e indi

cate s impaire dhem e synthesis , whic h ma y b e du e t o th e toxi c effect s oflead ; bloo dleadtest s measur e lea dabsorp

tion , an daconfirme dconcentratio n o f 25 ug/d l or

more , referre dt o a s a

n elevate dbloo dleadlevel , reflect s a n ex cessiv e absorptio n oflead
. Usually , ther e i s aclos e corre latio n betwee n result s ofth e tw o test s fo r specimen s fro

m th e sam e child , but , occasionally , th e resul t o f on e tes t ma y b e elevate dan dth e resul t o f th e other , no t

elevated
. Th e E P tes t

ha s thre e advantage s ove r th e bloo dlea

dtest : (1 ) whe n bloo dlea dlevel s ar e moderatel y elevated , th e E P tes t bette r identifie s childre n wit

h risin g bloo dlea

d level s (Reigart

an dWhitlock , 1976) ; (2 ) i f th e specime n i s contaminate dwit

h lead , th e contaminatio n doe s no t affect th e E P test ; an d(3 ) th e E P tes t i s a n accepte d screenin g tes t

fo r iro n deficiency
. INTERVENTIO N LEVEL S Childre n screene dfo

r leadpoisonin g ca

n b e groupe d int o tw o categories : thos e wh o requir e furthe r evaluatio n an dthos e wh o d o not . Choosin g th e interventio n leve l tha t divide s thes e tw o group s i s base do n acompromis e amon g th e following : (1 ) th e desir e t o identif

y al l childre n wit

h any degre e oflea dtoxicity (2 ) ajudgmen t

abou t th e urgenc y of

preventin g vari

ou s detectabl e effect s (3 ) th e sensitivit y an dspecificit y of apractica l screen in g tes t (4 ) society' s abilit

y t o remov e th e source s o f lea d exposur e A
. Pathophysiologica l Consideration s I n recen t years , level s o

f exposur e previousl y consid

ere d"safe " hav e bee n show n t o produc e advers e effects
. I n addition , contemporar y peopl e (includin g children ) livin g i n remot e area s wit

h negligibl e exposur e t o lea d hav e bloo dleadlevel s muc h lowe r tha n peopl e livin g i

n th e Unite dState s (Piomelli , 1980)
. Thus , th e bloo dlea d level s of U.S
. childre n reflec t

ahig h degre e o

f environ

menta l contaminatio n by lead
. Today , th e averag e bloo d lea dleve l i n th e U.S
. populatio n i s abou t 1 0 p.g/d l —approximatel y thre e time s th e averag e leve l foun di n som e remot e populations
. Thes e observation s sugges t tha t th e averag e leve l i

n th e U.S.A
. shoul db e re duced
. A t present , however , becaus e o f practica l consid

erations , th e goa l o f reducin g U.S
. level s t o thos e o f remot e population s i s unattainable
. Therefore , th e bloo d leadleve l a

t whic h intervenin g actio n shoul db e take n shoul db e basedo

n (1 ) criteri atha

t indicat e significant ris k t o th e individua

l chil dand(2 ) th e bes t

combinatio n o f tests : ates t

fo r th e bloo dlea

dleve l a s a

n indicato r

o f ab

sorptio n andates t

fo r E P as a n indicato r

o f biochemical derangement
. Sinc e th e CDC' s 197 8 statemen t o n lea dpoisoning , severa l investigator s hav e demonstrate deffect s o f low

leve l lea d exposure s i

n thes e areas : 1
. children' s behavio r

andintelligenc e (Needleman e t al. , 1979 ; Winneke , 1982 ; Yul e e t al. , 1981 ) 2
. th e centra

l an dperiphera

l nervou s system s o

f adul t worker s (Mantere e

t al. , 1982 ; Seppalaine n an d Hernberg , 1982) 3
. hem e biosynthesi s i

n childre n (Piomell i e t

al. , 1982 ) 4
. nucleotid e metabolis m(Angl e an dMclntire , 1978 ) 5
. vitami n D metabolis mi n childre n (Rosen e

t al. , 1980 ; Mahaffey , Rosen e

t al. , 1982)
. Th e precis e level a

t whic h lea dexposur e begin s t o caus e developmental o

r neurobehaviora l problem s i n childre n ma

y b e impossibl e to defin e i n th e nea r future
. I n th e meantime , decision s on publi c health measure s hav e to b e made o

n th e basi s o

f (1 ) other , mor e objective

l y measurabl e effects and(2 ) a n adequat e margi n o

f safety
. Th e elevatio n o

f EP , atoxi c effect

o f lea d i n humans , ha s bee n wel

l studie dan di

t ca n b e measure d objectively
. Amon g th e biologi c marker s oflea d toxicity , E P measure ment s hav e been th e mos t useful i n screenin g program s fo r lea dpoisoning
. Recent

studie s hav e she dne

w ligh t o n th e effect s oflea d ando

f iro n deficienc y o

n E P levels
. Severa l year s ago , Roel s e

t al
. (1976) , basin g thei r argumen t on E P measurements , state dthat abloo dlea

d leve l o f 2 5 ug/d l shoul db e th e maximu mpermissibl e concentration
. Cavalier

i e t al
. (1981) , wh o mad e astud y aroun dalea

dsmelter , indicate dtha

t eve n thi s level ma

y b e to o high
. Thi s group foun da n E P respons e a

t bloo d leadlevel s rangin g betwee n 1 0 an d2 0 ug/dl , suggestin g tha t th e E P no-respons e leve l i s lowe r than 1 0 ug/dl
. I

n a mor e recen t

an dcomprehensiv e examinatio n o f th e issue , Piomelli e

t al
. (1982 ) studie ddat afro mover 2,00 0 children
. Bloo

dlea dandE P test s wer

e don e o n venou s specimen s collecte dfro

mchildre n throughou t

Ne w Yor k City
. Piomelli andhi s colleague s were tryin g l o findth e bloo dlea dlevel a t whic h th e E P leve l bega

n t o increase
. A variet y o f statistica l technique s were used , an dth e finding s wer e consistent ; whe

n bloo dlea

dlevel s increase d linearl y abov e th e are ao

f 15-1 8 ug/dl , th e E

P level in

crease dexponentially
. Recen t studie s o f EDT A (calciumdisodiu methylen e diamin e tetraaceti c acid ) mobilizatio n testin g indicat e that th e amoun t

oflea d excrete db

y childre n wit

h bloo d lea dlevel s o

f 30-4 0 ug/d l ma

y ofte n b e comparabl e to tha t excrete db

y childre n wit

h level s o f 50-7 0 ug/d l (Mar

kowit z andRosen , 1984)
. Thi s finding suggest s tha t th ebioo d lea

dleve l ma

y underestimat e tn e ooa y ourae n oi lead
. I n summary , th e E

P data , wit

h dat afromth e othe r studie s referre dto , indicat e tha t th e 197 8 bloo dlea

d guidelin e of

3 0 ug/d l ha s littl e o r

n o margi n o

f safet y an d shoul db e lowered
. B
. Practica l Consideration s Althoug h th e biologi c threshol dfo r lea dtoxicity , a s manifeste db

y increasin g E

P levels , i s les s than 20 ug/dl , th e criteri afo

r ascreenin g programhav e l o take int o ac coun t additiona l factors : (1 ) acceptability , sensitivity , an d specificit y o f th e screenin g procedure ; (2 ) cost
effecliveness ; an d(3 ) th e feasibilit y of effectiv e interven

tio n an dfollowup
. Th e identificatio n of

childre n wit

h bloo dlead s belo w 2 5 ug/d l woul drequir e screenin g wit h abloo dlea

dassa y rathe r than a n E P test , sinc e th e latte r

screenin g tes t

ha s a ver y poo r sensitivit y an dspecificit y belo w abloo dlead leve l of 2 5 ug/dl
. Suc h arecommendatio n woul drequir e mos t program s l o us e venou s bloo dsample s or to adop t impracticall y rigorou s trainin g an dquality contro l proce dures
. Capillar

y bloo dsample s ar e pron e t o environmen

ta l contaminatio n wit

h lead
. I n mos t programs , particular

l y thos e in high-ris k

areas , th e us e of

"routine " capillar

y blood-drawin g technique s result s i n a n unacceptabl y hig h frequenc y o

f falsely elevate dbloo dleadlevels
. O n th e othe r hand , takin g bloo dsample s fro mth e vein s of smal l childre n i s les s acceptabl e t o parent s an dtechnicall y muc h mor e difficult
. I

n addition , th e cos t

ofth e screenin g programwoul dincreas e severalfold
. Fo r all thes e reasons , a n interventio n leve l se t

a t bloo dleadvalue s belo w 2 5 ug/d l migh t

ultimatel y substantiall y decreas e th e numbe r of childre n bein g screened
. I f loca l screenin g program s evaluat e th e distributio n o f moderatel y an dhighl y elevate dbloo dleadlevel s withi n a community , th e findings ma y identif y source s oflea d tha t migh t g o unnotice di

f th e programfocuse dsolel y on childre n wit

h hig h leadlevels
. Even whe n slightl y elevate dbloo dleadlevel s ar e found , som e intervention s ar e possibl e an deffective
. Hous e dus t

i s a n insidiou s bu t

apparentl y effectiv e carrie r of lea dt o childre n i

n contaminate denvironments
. I n urban area s dus t

frequentl y contain s larg e amount s o f lead , though t

t o com e primaril y fro

mairborn e source s or leade dpaint
. Charne y e l al
. (1983 ) hav e documente dth e effectivenes s o

f controllin g hous e dust ; thus , i n som e sit

uations , low an dmoderatel y elevate dbloo dlea dlevel s ca n b e reduce dsimpl y b

y controllin g hous e dust
. Considerin g thes e factors , CD C recommend s a s th e in

terventio n leve l abloo dlea dleve l o f 2 5 ug/d l associate d wit h a n E P leve l o f

3 5 ug/dl
. Whe n th e bloo dlea dleve l i s 2 5 ug/d l or

greate r associate dwit

h a n E P valu e o

f 3 5 ug/d l or greater , lead

toxicity is present; identification of such children is the focus of CDC's new recommendations. Childre n ma

y hav e mildl y elevate dbloo dlea dlevel s with

ou t concurren t

increase s i

n E P concentrations , an di

t i s desirabl e t o ideriiii y wes e cniiaftin;-BiM,-ahp.reseni , im y i s impractica l an dbeyondth e criteri ase t

fo r screenin g pro grams . Nonetheless , when resource s andcapabilitie s permi t bot h bloo dlea

dan dE P t o b e measure di

n th e pri

mar y screenin g program , additional childre n wit h elevat

e dbloo dlea

dlevel s wil

l b e identified
. A more practica l metho dfo

r identifyin g suc h childre n need s t o b e developed
. Th e CD C recommend s th e following cutof f level s fo r determinin g ahig

h ris k fo r lea d toxicity : fo

r E P screening , aleve l o f 3 5 ug/d l (whol e bloo dshoul db e tested) ; fo r fol

lowu p testing , al

l childre n wit

h abloo dlea

do f 25 ug/d l or mor e shoul db e considere da t ris k fo r th e toxi c effect s o

f lead
. Sinc e th e E

P level i s als o elevate di

n iro n deficiency , a n elevate dE

P tes t alon e shoul dno t

b e considere dt o b e diagnosti c oflead toxicity
. 

### MEASUREMEN T O F ERYTHROCYT E PROTOPORPHYRI N Erythrocyte protoporphyri n (EP ) ma y b e measure db

y fluorometr

y afte r i t ha s bee n extracte dfro mth e re d bloo dcell s or

b y direc t fluorescenc e i

n intac t cell s (Lamol ae

t al. , 1975 ; Blumberg e t

al. , 1977)
. I

n lea d toxicit y an diro n deficiency , thi s metabolit e i s presen t in th e re dcell s mainly a s zin c protoporphyri n (ZnPP) , bu t th e ethy l acetate-aceti c aci dextractio n procedur e convert s zin c protoporphyri n t o erythrocyt e protoporphyrin
. Measurin g ZnPP b

y hematofluoromete r

an dE P afte r i t ha s been extracte dfro

mth e cell s reflect s essentiall y th e sam e compound
. I

n erythropoieti c protoporphyria , a n ex tremel y rar

e disease , E

P i s markedl y elevated—usuall y abov e 30 0 ug/dl
. Thi s i s th e free E

P base , bu t

i t i s detect

e db y th e E P extractio n metho dand , t o alesser extent , b y th e hematofluorometer
. E P i s als o elevate di

n sickl e cell anemi aan dothe r hemolyti c anemia s (Langer e t al. , 1972)
. Hyperbiliru

binemi a(jaundice ) wil

l caus e falsel

y elevate dE

P reading s wit h th e hematofluorometer , bu t no t wit h th e extractio n metho d(Buhrman

n e t al. , 1978)
. Recen t

colds , ea r infec

tions , andothe r

mino r illnesse s ma

y als o caus e slight

ele

vation s o f E P (Reeve s e

t al. , 1984)
. Nevertheless , lea d toxicit y shoul dalway s b e rule dou t a s th e caus e o

f elevat

e dE P levels
. A
. Us e o f Hematofluorometer s Hematofiuorometer s measur e ZnP P an drepor t value s in E P equivalents
. The y ar e calibrate dagains t th e extrac
tio n metho dan

dtheoreticall y shoul dyiel dcorrespondin g values
. I n practice , th e value s obtaine dwit h thes e instru

ment s ar e usuall y no t 100% ofth e E

P presen t an d ma y b e considerabl y less
. A

t leas t tw o studie s (Kaul e t

al. , 1983 ; Hammon de

t al. , 1984 ) indicat e that , a t high levels , value s obtaine dwit

h hematofiuorometer s are lowe r tha n thos e obtaine dwit

h th e extractio n method , bu t tha t u p to 3 5 ug/d l th e result s ar e similar
. Becaus e hematofiuo

rometer s give immediat e result s an dar e economical , the y ar e eminentl y suitabl e fo

r fieldscreening
. P.1 8

1 0Fo r

bot h th e hematofluoromete r an dth e extractio n method , th e distinctio n betwee n apositiv e an dnegativ e screenin g tes t

shoul db e base do n acutof f leve l o f 3 5 ug/dl
. However , fo

r ris k classification , th e cutof

f point s fo r ZnP P measure db

y hematofluoromete r

(Tabl e 2.A ) diffe r fro mthos e fo

r E P measure db y th e extractio n metho d(Tabl e 2.B)
. I

f possible , centralize dlaboratorie s shoul dus e extractio n methods , and , i f th e followu

p laborator y ha s extractio n capability , al l confirmatory test s fo r E P shoul db e don e b

y extraction , no t

hematofluo

rometer . Hematofiuorometer s ar e mos t likel y t o giv e accurat e result s whe n use dt o analyz e freshly collecte d bloo dspecimens
. Th e difference s betwee n method s nee d furthe r study
. B
. Erythrocyt e Protoporphyri n an dIro n Deficienc y A benefi t of E P screenin g i s tha t

whe n a n elevate dE

P leve l prove s no t

t o b e du e t o lead , i t

usuall y reflect s iro n deficienc y (Piomelli , 1977)
. Th e first sign s of iro n defi

cienc y ar e biochemica l abnormalitie s (lo w seru mferritin , lo w transferri n saturation , an dhig h EP ) followedb y cel

lular abnormalitie s (microcytosi s an dhypochromia)
. Iro n deficienc y anemi afollow s thes e change s a s th e hemoglobi n an dhematocri t value s fall
. Th e E P tes t

prove dt o b e practical i n screenin g fo r iro n deficienc y in apopulatio n o f 4,16 0 childre n (Yi

p e t al. , 1983)
. Th e uppe r

limi t of norma l for

E P in thi s stud y wa s 3 5 ug/dl
. Th e predictiv e valu e appeare dt o b e satisfactory
. Iro n deficienc y i s commo n i n man y of th e group s a

t ris k fo r lea dpoisoning—especiall y amon g inner-city childre n o f

lo w socioeconomi c statu s livin g in old , dilap

idate dhousing
. Iro n deficienc y i s commo n amon g infant s age s 9 t o 24 months ; th e highes t frequenc y oflea d poison

in g extend s throug h 3 6 months
. Iro n deficienc y an dlead toxicity ma

y occu r i n th e sam e child
. Furthermore , ex perimenta l evidenc e indicate s tha t iro n deficienc y in

crease s th e proportio n oflea d absorbe dfromth e intestin e an daggravate s th e toxi c effect s o f lead
. Analysi s ofth e NHANE S I I dat aha s clarifie dth e rela

tionshi p betwee n elevate dE P values , bloo dleadlevels , an diro n deficienc y i n arepresentaliv e sampl e ofth e U.S
. population
. Amon g childre n i n th e NHANE S I I surve y wit h elevate dE P values , 31 % hav e elevate dbloo dlea d levels , 18 % hav e iro n deficienc y (a s evidence dby atrans
ferri n saturatio n o

f les s tha n o r

equa l t o 12%) , an d11 % hav e evidenc e of

both condition s (R
. Yip , persona l com munication)
. O n th e othe r hand , amon g childre n wit h elevate dbloo dlea dlevels , onl y abou t 26 % hav e lea

d toxicity-tha t

is , a n elevate dE P leve l (NCHS , 1984)
. I n hig h priority population s (Tabl e 1) , i n whic h iro n defi

cienc y i s mor e commo n an dlea dlevel s ar e higher , a greate r proportio n of

childre n wit

h elevate dbloo dlead level s woul dhav e elevate dE P levels
. Analyse s by both Yi p an dNCH S confir

mtha t asynergisti c effect

exist s be

twee n leadtoxicity an diro n deficienc y in children , a s ex perimenta l studie s i n animal s hav e suggested
. Tabl e Z.A m * " Zin c Protoporphyri

n (ZnPP ) b

y Hematofluoromete r Ris k Classificatio n o f

Asymptomati c Childre n fo r Priorit y Medica l Evaluatio n P.1 9

Bloo d Lea d # No tdon e <2 4 25-4 9 50-6 9 > 7 0 <3 5

I I l b • • • * Erythrocyt e Protoporphyri n (EP ) #

35-7 4 • l a 1 1 H I • • 75-17 4

• I a II I H I I V >17 5

• EP P + 11 1 I V I V #= Unit s are in fig/d l o f whol e blood . * = Bloo d lea d les tneede d t o estimat e risk . EP P + = Erythropoieti c protoporphyria . Iro n deficienc y ma y caus e elevate d E

P level s u p l o 30 0 pg/dl , bu tthi s i s rare . * * = I

n practice , thi s combinatio n o f result s i s no tgenerall y ob served ; i f

i ti s observed , immediatel y reles i with whol e blood . NOTE : Diagnosti c evaluatio n i s mor e urgen ttha n th e classificatio n indi cate s for — 1 . Childre n wil h an y symptom s compatibl e wil h lea d toxicity . 2 . Childre n unde r 3 6 month s o f age . 3 . Childre n whos e bloo d lea d an d EP level s plac e the m i n ih e uppe r par

to f a particular class . 4 . Childre n whos e sibling s ar e i n a highe r class . Thes e guideline s refe r l o th e interpretatio n o f screenin g results , bu l th e final diagnosi s an d dispositio n res to n a mor e complet e medica l an d laborator y examinatio n o f th e child .

Tabl e 2. B Erythrocyt e Protoporphyri n (EP ) b y Extractio n Ris k Classificatio n of

Asymptomati c Childre n fo r Priorit y Medica l Evaluatio n Bloo d Lea d # No tdon e <2 4 25-4 9 50-6 9 >7 0 <3 5

I I lb * • • • Erythrocyt e Protoporphyri n (EP ) #

35-10 9 • l a I I H I * • 110-24 9

* I a II I . II I I V >25 0

• EP P + II I I V I V #= Unit s ar e in/xg/d l o f whol e blood . * = Bloo d lea d tes tneede d t o estimat e risk . EPP + = Erythropoieti c protoporphyria . Iro n deficienc y ma y caus e

elevate d E

P level s u

p t o 30 0 pg/dl , bu tthi s i s rare . * ' = I

n practice , thi s combinatio n o f result s i s no tgenerall y ob served ; i f

il i s observed , immediatel y retes twith venou s blood . NOTE : Diagnosti c evaluatio n i s mor e urgen ttha n th e classificatio n indi cate s for — 1 . Childre n wit

h any symptom s compatibl e wit h lea d toxicity . 2 . Childre n unde r 3 6 month s o f age . 3 . Childre n whos e bloo d lea d an d E P level s plac e the m i n th e uppe r par tof a particular class . 4 . Childre n whos e sibling s ar e i n a highe r class . Thes e guideline s refe r t o th e interpretatio n o f screenin g results , bu tth e final diagnosi s and dispositio n res to n a mor e complet e medica l an d laborator y examinatio n o f th e child .
1 1MEASUREMEN T O F BLOOD LEA D

Unlik e elevate dE P level s (whic h ma y b e cause dby iro n deficienc y or

othe r illnesses) , elevate dbloo dlea d level s ar e specifi c fo

r lea dabsorption
. Fluctuation s i n bloo dlead value s ove r

ashor t perio dca

n b e du e l o physi

ologi c variation s or

sporadi c acut e lea dexposure . Capillar y sample s ar e highl y sensitiv e t o contaminatio n wit h environmenta l lead
. I

f suc h sample s ar e t o b e take n fo r bloo dlea

d assays , th e personne l mus t b e rigorousl y traine dbefor e an y screenin g progra mi s begun , an ddupli

cat e capillar

y bloo dspecimen s shoul db e drawn
. A singl e tub e of capillar y bloo dshoul dneve r

b e use dfo

r th e diag

nosi s of elevate dbloo dlead , becaus e a n elevate dvalu e ma y b e cause db

y contamination
. I

f result s o f test s fo r bloo dleadfromtw o tube s diffe r substantially , th e highe r valu e ca n b e considere dspurious
. Eve n when th e result s ar e equall y elevated , contaminatio n canno t b e excluded
. Therefore , onl y venou s bloo dsample s shoul db e use dt o confir madiagnosi s o r

t o determin e o r

asses s treatment . Ther e i s les s likelihoo dof contaminatio n i

n avenipunc

ture , bu t venou s bloo dma

y b e difficul t

t o collec t

fro m ver y youn g children
. Neithe r th e bloo dlea

dno r th e ex tractio n E

P tes t shoul db e considere daroutin e procedur e i n th e clinica

l laboratory
. T

o hel p insur e credibl e tes t re sults , laboratorie s performin g thes e test s shoul dpartici

pat e i n th e CD C proficienc y testin g programo r th e equivalent
. SCREENIN G SCHEME S Thre e feasibl e screenin g strategie s are — 1
. Screenin g wit

h E P tests , followe dby bloo dlea d measurement s i

f indicated
. Thi s i s th e mos t commo n procedure
. 2
. Screenin g wit

h both E P an dbloo dleadtests . 3
. Screenin g wit

h bloo dlea dtests , followe db y E P measurement s i

f indicated
. Th e CD C recommend s E P tests , followe db y bloo d lea dmeasurement s fo

r al l childre n wit

h a n elevate dE

P level
. Th e E P tes t

ha s thes e advantages : 1
. Eas e o f measuremen t

by hematofluoromete r

or th e extractio n method
. 2
. Result s that

ar e no t affecte di

f specimen s ar e con taminate dwit

h environmenta l lead
. 3
. Mor e cos t

effectiv e tha n screenin g wit h th e bloo d leadtest . 4
. Abilit y t o detec t

achild' s metaboli c respons e t o th e toxicit y oflead
. 5
. Possibilit

y o f differentiatin g betwee n childre n wit h stabl e bloo dlea dlevel s an dthos e wit h declinin g levels
. 6
. Possibilit

y of identifyin g childre n wh o hav e iro n deficiency
. I n som e areas , wher e th e environmen t i s grossl y con taminate dwit

h lead , astrateg y o f

simultaneou s testin g fo r E P an dbloo dleadlevel s i s recommended
. I n thes e cases , venou s sample s shoul db e use dfo r measurin g lead
. When tt * i s th e primar y screenin g I'bSlilWO'appruai'nU! " ar e possible : 1
. E P measure do

n site
. A capillar

y bloo dspecime n i s collected , an

dwhile th e chil dwait s a

t th e screenin g site , E P i s determine db

y hematofluorometer
. Childre n foun

dto hav e E

P value s o

f 3 4 ug/d l or les s ar e discharge dunti l th e nex t routin e screening
. Fo r thos e wit h E P value s o f 3 5 ug/d l or

more , addi

tional bloo dsample s ar

e take n (preferabl y b

y veni

puncture ) fo

r laborator y analysi s o f

bloo dlead an d of EP—b y extraction , ifth e metho di s available
. 2
. E P measure dof

f site
. A venou s bloo dsampl e or duplicat e capillar

y sample s ar e collecte d a t th e screenin g sit e andsen t

t o th e laboratory fo

r mea suremen t o f EP , preferably b

y th e extractio n method
. Th e amoun t

o f bloo dcollecte dshoul db e sufficien t fo r confirmator

y tests . Unuse dspecimen s of bloo dfro mchildre n whos e E

P level s ar e 3 4 /xg/dl or les s ma y b e discarded
. Fo

r thos e childre n wit

h E P level s o f 3 5 ug/d l o

r more , th e bloo dlea

d level s an dhematocrit s or

hemoglobi n concentration s shoul db e determined
. O n site , E P i s nearly alway s measure db y hematofluo

rometer ; of

f site—preferably—it

i s measure db

y th e ex tractio n method
. I

f th e bloo dspecime n i s protecte dfro m temperatur e extreme s andlight , i t ma y b e store dfo

r a wee k t o 1 0 day s befor

e bein g analyze db

y th e extractio n method
. Bloodcollecte do n filte r paper ma y b e store dfo

r severa l week s befor

e i t i s analyzed
. 

### INTERPRETATIO NO F SCREENIN G RESULT S A singl e screenin g test , eithe r fo r E P or bloo dlead , canno t b e use dto categoriz e childre n fo r priorit y i n fol

lowup
. Bot

h E P andbloo dlea

dlevel s mus t

b e use dt o determin e th e potentia

l ris k o f lea dtoxicit y i n th e chil

dre n screened
. Childre n ca

n b e arbitrarily divide dint o fou r classe s on th e basi s o

f E P an dbloo dlea

dscreenin g results
. I

n vie w o f th e observe ddiscrepanc y betwee n result s fromth e hematofluoromete r

andextractio n methods , tw o table s ar e given : Table s 2. A an d2. B (derive dfromKaul e t al. , 1983)
. Thi s classification merel y suggest s th e relativ e ris k an dth e priorit

y fo r medica l evaluatio n an denviron

menta l intervention , an dth e table s shoul db e use donl y a s general guidelines
. Childre n 1 2 t o 3 6 month s old shoul db e give

n priorit y over older ones , an dchildre n whos e E P an dbloo dlea

dlevel s fal

l int o th e uppe r

rang e ofaclas s shoul db e give

n priorit y ove r thos e whos e level s fal l int o th e lowe

r range . For

example , th e urgenc y fo

r fol

lowup i s greater

fo r a1-year-ol

d whos e E P leve l b y extrac
tio n i s 10 9 ug/d l andwhos e bloo dleadleve l i s 4 9 ug/d l tha n fo r a5 1/2-year-old whos e E P level , b y th e extrac
tio n method , i s 3 6 ug/d l andwhos e bloo dlea dleve l i s 2 6 ug/dl
. Ye t bot h childre n fal

l int o clas s II
. Childre n i

n clas s IV—a

t urgen t ris k o f lea d toxicity—shoul d b e medicall y evaluate dwithi n 2

4 hours , P.2 0

1 2an di n n o cas e late r !W ah with'i \ Y

45J~'rr^u"fTsr"*bhiIdiidri-II H clas s II I ar e a t

hig h risk
. Thos e i n clas s I I ar e a t moderat e risk , an dthos e i n clas s I , a t lo w risk
. Clas s I ca n b e subdivide dint o tw o additiona l catego
ries
. Clas s I a(bloo dlead , 2 5 ug/d l o r less , an dEP , 3 5 ug/d l o r more ) include s childre n wit h iro n deficiency
. Thes e childre n shoul db e retested , wit h additiona l assess men t o f iro n status . Clas s l b (bloo dlead , 25-4 0 ug/dl , an dEP , les s tha n 3 5 ug/dl ) cover s childre n wh o appea r t o hav e transient , stable , declining , o r increasin g bloo d > r>lUkU»|,t!^1 1 W^-UJU i i j
_ th e childre n shoul db e carefull y foro^elf^fSmFcase's ^ th e btoo d lea dan dE P result s wil l differ
. Whe n th e E P valu e i s significantl y highe r tha n th e valu e suggeste db y th e bloo dlea dlevel , th e chil dprobabl y ha s bot h iro n defi

cienc y an dexcessiv e lea dabsorption
. Screenin g shoul dfocu s o n asymptomati c children
. Childre n wit h symptom s shoul db e referre dfo r immedi

at e evaluation , regardles s ofthei r ris k classification
. P.2 1

1 3

p.^l-jj^li. -•.-.•„•:..» ,

# V
. Diagnosti c Evaluatio n T l

Screenin g test s ar e no t

diagnostic
. Therefore , every chil dwit h apositiv e screenin g tes t shoul db e referre dto a physician fo

r evaluation , wit

h th e degre e of

urgenc y in

dicate dby th e ris k

classification
. A

t th e first diagnosti c evaluation , i

f th e screenin g tes t

wa s don e on capillar

y blood , avenous blood

lead level shoul db e determine din alaborator y tha t

participate s in CDC' s bloo dleadprofi

cienc y testin g program . Eve n whe n test s ar e don e by ex perience dpersonnel , bloo dleadlevel s ma y var y 10% t o 15% , dependin g o n th e leve l bein g tested
. Test s fo r th e sam e chil dma

y var y a s muc h a s ± 5 ug/d l in a24-hou r period
. Thus , difference s of 1 t o 5 ug/d l betwee n screen in g an ddiagnosti c level s i n eithe r directio n shoul dno t necessaril y b e interprete da s indicativ e o f actual change s in th e child' s lea dabsorptio n o r excretion
. Additiona l bloo dsample s ma y b e neede dfo

r test s suc h a s complet e bloo dcounts , seru miron , tota l iro n bindin g capacity , an dseru mferritin
. Th e amount s necessary fo r thes e tests , whic h usuall y excee dth e amoun t obtainabl e b y capillar

y sample , ca

n b e obtaine dwit

h asingl e venipuncture
. Symptoms , if

present , constitut e an urgen t risk , war rantin g promp t

hospitalizatio n (sectio n VI)
. Symptom s mus t b e looked

for, an dthe y ca

n b e misse d(Piomell i e t al. , 1984) : Acut e lea dencephalopath y i s characterize dclinicall y b y som e or

al l of thes e symptoms : coma , seizures , bizarr e behavior , ataxia , apathy , incoordination , vomiting , alteratio n in th e stat e o f consciousness , an d subtl e los s of

recentl y acquire dskills
. An y on e o r a mixtur e ofthes e symptoms , associate dwit h a n elevat

e dbloo dleadlevel , constitute s a n acut e medica

l emergency . Leadencephalopath y i s almos t alway s as sociate dwit

h abloo dleadleve l exceedin g 100 ug/dl , although , occasionally , i t ha s bee n reporte da

t bloo d lea dlevel s a s lo w a s 7 0 ug/dl
. Symptomati c leadpoisonin g withou t encephalopath y i s characterize db

y on e or severa l symptoms : decreas e i n pla y activity , lethargy , anorexia , sporadi c vomiting , intermitten t

abdomina l pain , an dconstipation
. I t i s usuall y associate dwit

h abloo dlea dleve l abov e 7 0 ug/dl , although , occasionally , case s ar e associate d wit h aleve l a s lo w a s 5 0 ug/dl
. Iftheblood lead level is below 50fig/dl, other

causes should

be' vigorously sought. Sinc e any symptomati c chil dma y develo p acut e lea

d encephalopathy , treatmen t an dsupportiv e measure s mus t b e starte dimmediatel y o

n a n emergenc y basis
. Whethe r o r no t symptomati c lea

dpoisonin g i s present , th e chil dshoul dhav e acomplet e pediatri c evaluation
. Specia l attentio n shoul db e given to — 1
. A detaile dhistory , includin g th e presenc e or ab

senc e o f clinica l symptoms , child' s mouthin g activi

ties , existenc e o

f pica , nutritiona l status , famil y his

tor y o f lea dpoisoning , possibl e sourc e o f exposure , an dpreviou s bloo dlea

dor E P determinations
. 2
. Th e physical.examination , especially th e neurologi c examination
. 3
. Nutritional statu s an dhematologi c evaluatio n fo r iro n deficiency
. Iro n deficienc y contribute s t o a n elevate dE

P andca n enhanc e lea

dabsorptio n an d toxicity
. 4
. Confirmator

y diagnosti c tests . 5
. Trend s i

n E P andbloo dlea

dlevels
. Sinc e trend s are importan t i n diagnosi s an dmanage ment , serial measurement s of bloo dleadan dE P (an d othe r measurement s a s indicated ) ar e fa r mor e valuabl e than dat aobtaine da

t on e time
. T

o b e comparabl e an d in

terpretable , seria

l E P level s shoul db e analyze db y th e sam e method
. Probabl y th e mos t

reliabl e metho dfo

r determinin g th e sourc e o f exposur e i s obtainin g acareful , complet e envi

ronmenta l histor

y (sectio n III) , inspectin g th e hom e fo r lea dhazards , andlearnin g abou t th e child' s hand

to-mout h behavio r

throug h carefu

l questioning
. Pica , th e Lati n wor dfo r "magpie, " describe s th e habitua l ingestio n of nonfoo dsubstances
. Thi s shoul dno t b e regarde da s synonymou s wit

h th e norma

l ora l behavior s o

f smal l chil

dren , suc h a s finge

r andthumb suckin g an dnai l biting , A n initial pla

n fo r managemen t

require s tha t

all inter

actin g factor s b e take n int o account . Th e pla n shoul db e modifie da s indicate db

y long-ter mtrend s in lead absorp

tion , exposure , an dclinica l status . TEST S In additio n t o confirmator y an dserial E P an dbloo d leaddeterminations , th e followin g test s ca n b e useful (i

f available ) i

n assessin g th e patient' s lea dabsorptio n status . 1 41 . Test s fo r Iro n Deficienc y Becaus e th e E P ca

n reflec t iro n deficienc y a s well a s lead'exposure , th e presenc e of iro n deficienc y mus t

b e es tablishe do r

rule dou t

if E P level s ar e t o b e properl y interpreted
. A commo n misconceptio n i s tha t a chil dwit

h a "normal " hematocri t

(33 % o r more ) o r hemoglobi n con centratio n (1 1 g/d l o r

more ) coul dnot

b e iro n deficient
. Thi s i s no t

true , particularl y wit

h respec t t o iro n deficien

c y sufficien t

t o affect.E P and , worse , t o enhanc e lea dab

sorptio n an dretention
. Thus , althoug h acomplet e bloo d coun t (CBC ) an dareticulocyt e coun t ar e indicate din th e evaluatio n oflea d toxicity , the y ar e no t sensitiv e enoug h t o rul e ou t

iro n deficiency
. O f th e re dbloo dcel l (RBC ) indices , adecrease dmea n corpuscula r

volum e (MCV ) i s ausefu l indicato r of iro n deficiency
. Norma l value s depen do n ag e (Dallman , 1982)
. Seru miro n an diro n bindin g capacity ar e mor e sensi

tiv e tha n th e MCV
. I

n general , a

n elevate diro n bindin g capacit y o f mor e tha n 35 0 ug/d l i s mor e likel y t o accurate
l y indicat e iro n deficienc y tha n anorma l o r lo w seru m iron , sinc e th e seru miro n i s quit e sensitiv e t o both di

etar y iro n an ddiurna l variation
. Thus , if achil dha s eate n an iron-ric h foo dwithi n 2- 4 hour s befor e th e bloo dfor th e tes t i s drawn , th e resul t

ma y b e close r

t o th e norma l leve l tha n i s actuall y th e case . Unde r standardize dcondi

tions , a n abnormall y lo w rati o o

f seru miro n t o iro n bind

in g capacit

y (transferri n saturation ) i s consisten t wit h iro n deficiency
. I n additio n t o th e leve l of E P itself , th e serum ferritin leve l i s a

n accurat e indicatio n o

f overal l iro n status . 2 . Fla tPlat e o

f th e Abdomen Radiologi c examinatio n (fia t plate ) of

th e abdome n ma y reveal radiopaqu e foreig n material , bu t only i f th e materia l ha s bee n ingeste ddurin g th e precedin g 24 t o 3 6 hours
. Sinc e lea dingestio n i s sporadic , thi s examinatio n i s significan t

onl y i f th e result s ar e positive ; negativ e re sult s d o not

rul e ou t lea dpoisoning
. Positiv e result s indi

cat e recen t

ingestio n o f

larg e amount s oflead
. 3
. X-ra y o

f Lon g Bone s X-ray s of th e lon g bones , usuall y th e knees , ma y hel p estimat e th e duratio n o f exposure . Line s o

f increase d densit y in th e metaphysea l plat e of th e distal femu r

an d proxima l libi aan dfibulaar e "growt h arres t lines. " The y ar e cause dby lead , whic h disrupt s th e metabolis mof th e bon e matrix
. A s aresult , area s of increase dmineraliza

tio n o r calcificatio n ma

y b e presen t

a t th e metaphyse s o

f th e lon g bones
. Thoug h sometime s calle d"lea dlines, " the y ar e no t

a n x-ra y shado w of

deposite dlead
. Althoug h definitiv e dat aar e no t available , thes e line s ar e though t

t o becom e visibl e afte r

a t leas t 4 t o 8 week s fro mth e tim e exposur e began ; th e length o f tim e depend s o n th e ag e of

th e chil dan dth e degre e of lea d exposure . Th e widt

h an dintensit y ofth e line s reflec t pro longe dpreviou s lea dabsorptio n bu t

3 6 rii'o t indicat e cur ren t ingestion
. The y ar e seldo msee n in childre n unde r 2 4 month s o

f age . Negativ e x-ray s d o no t rul e ou t lead poisoning
. 4 . Calciu m Disodium EDT

A Mobilizatio n (or Provoca - * tiv e Test ) Thi s tes t i s use dt o identif

y childre n wh o wil

l respon d t o chelatio n therap y wit

h abris k leaddiuresis
. Childre n whos e bloo dlea

dleve l exceed s 5 5 ug/d l shoul dno t re ceiv e aprovocativ e chelatio n test . Instead , appropriat e chelatio n therap y shoul db e started
. Th e mobilizatio n tes t i s particularly useful when th e screenin g tes t indicate s tha t th e chil dha s lea

dtoxicit y an dther e i s som e questio n a s t o whether

chelatio n therap y i s indicated
. Thi s tes t pro vide s a n inde x ofth e mobil e o

r potentiall y toxi c fractio n ofth e tota l bod y lea dburde n (Saenge

r e t al. , 1982)
. Sinc e CDC' s 197 8 statement , a n 8-hour mobilizatio n tes t ha s bee n show n t o b e a s reliabl e a s a24-hou r mobili

zatio n tes t

(Markowit

z an dRosen , 1984)
. Althoug h a n 8-hour tes t ma y b e don e o n a

n outpatien t

basis , th e pa tien t shoul dno t

leav e th e clinic
. Th e carefu l us e o f "lead

free " apparatu s i s mandatory. * 5 . Lumba r Puncture CAUTION : I f alumba r punctur e i s neede dt o rul e ou t meningiti s o r othe r seriou s disease , i

t shoul db e performe dcau tiously andonly afte

r acareful searc h fo

r sign s an d symptom s o

f increase dintracranial pressure . Th e flui d shoul db e obtaine ddro p b y drop , an dn o mor e than 1 millilite r (ml ) shoul db e removed
. Th e followin

g test s ar e no t

useful in diagnosin g lead toxicity
. 1 . Microscopi c Examinatio n o f Re d Cell s fo r Basophili c Stipplin g Sinc e basophili c stipplin g i s no t universall y foun di

n chroni c clinica

l lea dpoisonin g andi s relativel y insensitiv e t o lesse r degree s o

f leadtoxicity , i

t i s noi considere d useful i n diagnosis
. 2
. Test s o f Hai r an d Fingernail s fo

r Lea d Level s Th e level s oflea d in hai r

or fingernail s ar e no t

wel l cor relate dwit

h bloo dleadlevels ; therefore , test s fo r thes e level s ar e not considere duseful i

n diagnosis
. P.2 3

'Specia l lead-fre e collectio n apparatu s mus i b e use d i f vali d les tresult s ar e l o b e obtained . Th e laborator y performin g th e analysi s ma y suppl y th e proper collectio n apparatus . Preferably , urin e shoul d b e voide d directl y int o polyethylen e o r polypropylen e bottle s thathav e bee n cleane d b y th e usua l procedures , then washe d i n 1 % nitri c acid , an d thoroughl y rinse d with deionized , distille d waler . Fo r childre n wh o ar e no i toile ttrained , plasti c pediatri c urin e collectors , wit h doubl e com partments , ma

y b e used . Urin e collecte d i n thi s manne r shoul d b e transferre d directl y t o th e urin e collectio n bottles . Preservin g th e col lecte d urin e wil h hydrochlori c aci d wil l stabiliz e no i onl y lea d bu l als o S aminolevulini c aci d (ALA) . 1 5

# Y

L Clinica l Managemen

t P.2 4

Th e syste mdescribe di n sectio n I V i s fo r a n initial classification , t o b e modifie dby result s ofth e diagnosti c evaluation
. Thus , after

al l informatio n i s availabl e t o th e clinician , th e child' s tru e ris k classificatio n i s established
. Clinical managemen t

include s eliminatin g th e sourc e of th e child' s lea dexposure ; providin g genera l pediatri c care , family education , and , whe n appropriate , chelatio n therapy ; an dcorrectin g any nutritiona l deficiencies
. I n ad

dition , followup examination s mus t b e performe dunti l th e ris k of furthe r damag e i s minimal
. The single most important factor in pediatric management is to reduce the amount oflead ingested. Th e family mus t b e full y informe d of th e child' s conditio n an do f th e clinical an denviron

menta l action s t o follow
. On e recommende dapproac h t o th e treatmen t of chil

dre n wit h symptomati c an dasymptomati c lea dpoisonin g i s describe di

n detai l i n th e Appendix
. Th e major ne w fea

tur e o f thi s approac h i s a

n increase drelianc e o n calciu m disodiu mEDT A mobilizatio n testin g amon g childre n wit h moderat e bloo dlea dlevels
. Th e tes t result s ar e use d t o decid e whethe r

chelatio n i s indicated
. A ful l cours e of chelatio n therap y shoul dno t b e give n withou t

eithe r a confirme dbloo dlea dleve l equa l t o o r greate r tha n 5 6 ug/d l o r apositiv e mobilizatio n tes t i n childre n wit

h bloo dlea dlevel s o f

25-5 5 ug/dl
. Thi s approac h i s recom mende dby fou r

majo r medical center s i n whic h th e staff s hav e hadextensiv e experienc e in th e diagnosi s an dtreat
men t o f childre n wit

h lea dpoisoning
. Th e cornerstone s o f

clinical managemen t

ar e carefu l clinical an dlaborator y surveillanc e of th e chil dan dare ductio n in leadexposur e l o preven t furthe r accumulatio n o f lead
. Thi s approac h allow s previousl y absorbe dleadt o b e slowly excreted
. Mos t childre n wit

h lea dtoxicit y d o no t requir e chelatio n therapy , bu t thos e wh o d o ma

y nee dmor e tha n on e cours e o f treatment . Th e followup programfo r asymptomati c childre n depend s upo n th e degre e o f ris k determine ddurin g th e diagnosti c evaluation
. Fo r th e purpose s of

clinica l managemen t

an dfollowup , th e ris k categorie s ar e ranke dfromurgen t t o low
. Urgen t —Bloo dlea dlevel s of

7 0 ug/d l o r

mor e wit h o r withou t symptoms . Hig h —Childre n whos e repeat E P an dconfirmatory venou s bloo dlea dlevel s fal l in th e clas s I

I an dII I range s o f th e screenin g test , bu t

wh o als o hav e aposi

tiv e calciu mdisodiu mEDT A mobilizatio n les t

o r othe r confirmator

y diagnosti c test s o r

ris k factors
. Childre n in clas s II I wh o hav e no t hadconfirmator

y di

agnosti c test s shoul db e considere dhig h ris k unti l evi

denc e place s the mi

n anothe r ris k category . Moderat e —Childre n whos e repea t E P an dvenou s bloo dlea dlevel s fal

l int o th e clas s I

I rang e o f th e screenin g tes t

bu t whos e othe r

confirmator

y diagnosti c test s ar e negative
. Lo w —Childre n whos e repea t E P an dvenou s bloo d leadlevel s fal

l int o th e clas s 1 rang e of th e screenin g tests . Thes e childre n ar e usually no t give n othe r

diag

nosti c tests . Thi s categorizatio n i s arbitrar y an dca n b e adapte dt o a particula r child
. For

example , a20-mont

h oldwit h per sisten t pic awhos e environmenta l lea dhazar dcanno t

b e controlle dsatisfactoril y ma y b e considere d hig h risk , eve n i f hi s o r he r repea t E P an dvenou s bloo dlea

dlevel s fal l i n ih e rang e o

f clas s I I an dothe r

diagnosti c test s are negative
. URGEN T RIS K Childre n wit

h bloo dlea

dlevel s of

7 0 ug/d l or

more , regardles s of

th e presenc e o

r absenc e o

f clinica l symp toms , shoul db e treate dwit h th e sam e intensity a s chil

dre n wit h fran k neurologi c manifestations
. Th e highe r th e confirme dvenou s bloo dlead , th e greate r th e nee dfo

r chelatio n therapy
. Severe an dpermanen t brai n damag e ma y occu r in a s many a s 80 % o

f childre n wh o hav e acut e encephalopath y (Perlstei n an dAttala , 1966)
. Treatmen t befor e onse t

o f encephalopath y wil

l improv e thi s grim prognosis
. Lea dtoxicit y i s achroni c medica

l problem
. Childre n wh o requir e chelatio n therap y wil l nee dlong-termmedi

ca l surveillanc e andcare . Th e E P level s ca

n fluctuate durin g an dimmediatel y afte r chelatio n therapy
. Afte

r a n apparentl y successful cours e o f therap y wit

h calciu mdiso

diu mEDT

A (incorporatin g BAL , Britis h Anti-Lewisite , a s necessary) , th e "rebound " phenomeno n ma y b e observed
. First , th e bloo dlea

dlevel drop s durin g treatment . Thi s i s no t

areaso n to interrup t

therapy
. Then , afte

r treat
men t i s stopped , th e bloo dlea dleve l almos t

invariabl y rise s again
. Thi s phenomeno n reflect s areequilibratio n o f
1 6store dlead
. Th e decisio n t o repea t chelatio n therap y i s base don th e bloo dleadleve l afte r th e "rebound. "

, Reductio n of

leadintak e i s urgen t

fo r al l childre n i

n thi s category , both a s par t of immediat e therap y an da s par t of th e followup preventiv e procedure
. Childre n re ceivin g chelatio n therap y shoul dno t b e release dfromth e hospita l unti l lea dhazard s i n thei r home s an denviron ? men t ar e controlled
. Otherwise , suitabl e alternativ e hous

in g mus t b e arranged
. Thus , th e appropriat e publi c agenc y i n th e communit y mus t

b e notifie dimmediatel y s o tha t environmenta l investigatio n an dinterventio n ca n begin
. Afte r thei r hospitalizatio n an dafter lea dha s bee n re move dfromthei r

environments , thes e childre n ar e stil l a t hig h risk
. Clos e followup , wit h bloo dlea dan dE P mea surements , i s required
. A t first, thes e test s shoul db e don e every 1 t o 2 weeks
. Ifth e bloo dlea dleve l rebound s t o it s pretreatmen t

level , arepea t

ofth e chelatio n therap y shoul db e considered
. I f th e bloo dlea dleve l remain s stabl e o r show s acontinua l declin e afte r th e first fe w weeks , th e interva l betwee n testin g ma y b e incrementall y increase dfrom1 t o 6 month s unti l th e bloo dlea dan dE P level s retur n t o norma l o r th e chil dreache s 6 year s o f age . HIG H RIS K Man y childre n in th e high-ris k category wil

l hav e bee n give n acalciu mdisodiu mEDT A mobilizatio n tes t t o determin e whethe r

chelatio n therap y i s needed
. I f i t i s needed , inpatien t

chelatio n shoul db e performed
. Unde r som e conditions , however , childre n withou t urgen t ris k factor s ma

y b e treate da s outpatients
. Outpatien t treat
men t shoul db e reserved , however , for thos e center s capabl e o f providin g closel y monitore doutpatien t car e an dfollowup supervision , an din thos e center s i t shoul d b e provide donl y i

f th e child' s sourc e o

f lea dexposur e ha s bee n eliminate d(Piomell i e t al. , 1984)
. I

n addition , th e parent s shoul db e cooperativ e an dshoul ddemon

strat e that the y ca n follo w instructions
. Followu p of

high-ris k childre n shoul dconsis t

o f bloo d lea do r E P tests , o r

both , at leas t monthl y (especiall y i n th e summer) , unti l th e source s oflea d in thei r environ

ment s hav e bee n removed
. I f thei r bloo dlea

dor E P level s hav e decline dor

stabilized , th e interva l betwee n testin g ma

y b e incrementall y increased , excep t in summer , fro m1 t o 6 months , unti l th e bloo dleadan dE P level s retur n t o norma l o r th e chil dreache s 6 year s o f age . Carefu l neurologica l an dpsychological assessmen t i s ad

vise ds o tha t

any behaviora l o r

neurologica l deviatio n ca n B e Selecte d earl

y andprope r

th'eTap y afi d schoo l place

men t begun
. MODERAT

E RIS K Generally , childre n i

n thi s categor

y d o no t requir e che

latio n therapy
. Reducin g lea dintak e fromal l source s an d careful monitorin g ofth e chil dusuall y suffices
. Unti l th e lea

dhazard s are eliminate dfro mthei r envi

ronment , thes e childre n shoul db e teste dmonthl y i n th e summe r andever

y 2 month s i

n othe r seasons . I

f th e bloo dlea dan dE P level s remai n stabl e or

sho w acontinu

a l declin e afte

r th e first fe w months , th e interva l betwee n testin g ma

y b e incrementall y increase dfro m2 t o 6 month s unti l th e bloo dlea dan dE P level s retur n t o norma l o r th e chil dreache s 6 year s of age . NOTE : Al

l childre n i

n th e urgent- , high- , an d moderate-ris k

categorie s ma

y hav e concomitan t

nutri

tional deficiencies
. Thes e deficiencie s ma y increas e th e child' s ris k

fro mlea db y increasin g absorption , retention , an dtoxicity
. Al

l childre n i

n thes e categorie s shoul dre ceiv e acarefu

l nutritional evaluation , includin g appropri

at e laborator

y tests . I n additio n t o th e care given fo r lead toxicity , nutritional therap y shoul db e provided
. When in

crease dlea

dabsorptio n i s found , i

t ma y b e particularl y importan t t o correc t iro n deficienc y an dmaintai n a n ade

quat e calciumintake
. LOW RIS K When tested , childre n i

n thi s categor

y d o no t hav e sig

nifican t evidenc e o

f lea dtoxicity
. However , the y requir e periodi c screenin g unti l the y reac h thei r sixt h birthday
. Childre n whos e elevate dE P level s ar e no t

cause db y lead absorptio n shoul dreceiv e medica l attentio n an d care fo

r th e medica

l conditio n responsibl e fo r th e elevation
. Childre n wit

h elevate dbloo dlea

dlevel s bu t

n o evidenc e o f toxicit y shoul db e evaluate dmonthl y unti l lea d toxicit y ca n b e rule dout . Thi s ca n usuall y b e don e withi n 3 months
. I n conclusion , th e clinica l managemen t

o f childre n wit h lea dpoisonin g mus t

includ e appropriat e treatment , adequat e followup , environmenta l intervention , an d famil y education
. Chelatio n therap y i s indicate dfo r som e childre n wit

h lea dtoxicity
. Usin g i

t indiscriminantl y i s unwise , but

s o i s withholdin g or

delayin g i

t whe n i t i s in

dicated
. Th e physicia

n providin g clinica

l managemen t mus t kno w th e curren t

statu s o f th e child' s environment
. Th e optima

l frequenc y o

f followu p depend s o

n man y fac

tors , includin g th e child' s ag e an denvironmen t an dth e tren di n result s ofth e child' s tests . P.2 5

1 7

# VI

L Environmenta

l Evaluation and Lea dHazar dAbatemen

t

Environmenta l investigatio n an dinterventio n shoul d begi n a s soo n a s lea dtoxicity i s confirmed
. Leadhazard s mus t b e identifie dan dremove dfro mth e environment s of thes e children
. Prioritie s fo r actio n shoul db e deter

mine db y th e child' s ris k

classification
. Th e highe r th e bloo dleadleve l an dth e lowe r th e child' s age , th e highe r th e priority fo

r removin g th e lea dhazards
. Childre n wh o requir e hospitalizatio n an dchelatio n therap y ar e a t th e highes t ris k of permanen t

neurologi c damag e fro

mcon tinue dhigh-leve l exposur e an danothe r episod e o

f lea d toxicity
. Therefore , childre n in th e urgent
- an dhigh-ris k categorie s shoul dreceive first priorit y for

environmenta l investigatio n an dintervention
. I t i s strongl y recommend

e dtha t abatemen t

oflea d hazard s in ahospitalize dchild' s hom e b e complete ddurin g th e first fe w day s of

th e child' s hospitalization
. Childre n in th e moderate-ris k category ar e nex t

i n pri

ority
. Fo r them , identifyin g lea dhazard s an dreducin g lea dintak e ar e a s muc h amedica l necessity a s clinica l management . Th e effectivenes s o f environmenta l inter

ventio n i s judge dby th e child' s respons e an dno t b y th e service s performed
. Environmenta l managemen t i s no t successfu l o r

complet e unti l th e child' s E P an dbloo dlea

d level s hav e decline dan dstabilize dfo r a t leas t 1 2 months
. Th e identificatio n an dremova l of on e sourc e of

lead exposur e doe s no t

necessaril y mea n tha t

th e child' s expo sur e t o lea dha s ended
. Becaus e leadi s aubiquitou s an dpowerfu l toxin , wit h n o know n beneficial functio n i n th e huma n body , th e goa l o f preventio n i s t o reduc e children' s exposur e t o lea dt o th e maximu mextent . Lead-base dpain t i s th e mos t common , remediabl e sourc e o f lea dtha t

cause s symptomati c lea dpoisoning
. Detaile dprocedure s fo r removin g lea dpain t

fro mth e hom e environmen t ar e de

scribed , bu t

onl y genera l guideline s ar e give n fo r control

lin g othe r source s o f

lea ddiscusse di n sectio n III
. Ideal preventio n goal s ar e give n first; whe n thes e goal s canno t b e reache dimmediately , short-term , substitut e goal s ar e offered
. LEAD-BASE D PAIN T Th e ultimat e goa

l i s t o remov e all leade dpain t fro m housin g in th e Unite dStates
. Reachin g tha t goa l wil l b e expensive
. Short-termgoal s o f partia l removal help , bu t the y ten dt o postpon e effort s fo r complet e removal
. All painted interior and exterior surfaces should

be tested for lead. Portabl e x-ra

y fluorescenc e (XRF ) analyzer s ar e mos t convenien t

fo r identifyin g lead-base dpain t hazards
. Thes e instrument s ca

n measur e lea

dconten t in paint sur face s withi n ±0. 2 mg/cm 2 o f expose dsurface
. Reading s o f 0. 7 mg/cm 2 are considere dpositive
. Th e XR F analyzer i s aprobabilit

y samplin g device , an dreliabilit y depend s o n repeate dreadings
. I

f a n XR F analyzer

i s no t available , we t chemica l method s o

f analysi s mus t

b e used
. A lead-base dpaint

hazardexist s when (a ) th e XR F readin g i s positiv e an d(b ) th e surface s bein g teste dar e chewabl e o r

contai n damage d(cracked , chipped , loosened , chewed ) paint
. Lead-base dpaint o n intact walls , ceilings , o

r othe r surface s that

ar e no t chewabl e doe s riot constitut e a

n immediat e hazard
. Inspector s shoul dobtai n measurement s o n an y interio r or exterio r surfac e that

ma y constitut e alea

d hazard
. Thi s include s walls , doors , windo w frames , baseboards , guardrails , fences , an dsidings
. Outsid e inspectio n shoul dencompas s garage s andothe r

adjacen t structure s a s wel

l a s th e mai n building
. Next , th e inspecto r

shoul dclassif

y eac h interio r

an d exterio r par t o f th e buildin g where leadi s foun daccordin g t o th e degre e of

hazard
. I

f nonchewabl e surface s wit h lea dpaint ar e smooth an dintac t

an dth e supportin g struc
tur e i s sound , the y d o no t presen t a n immediat e hazard an dma y b e lef t alone
. Propert

y owner s an dresidents , however , shoul db e warne dtha t smooth surface s contain

in g lea dca n becom e hazardou s i

f the y ar e no t

properl y maintaine dan dar e allowe dt o fal l int o disrepair
. Al

l lead

painte dsurface s tha

t are identifie da s positiv e b y XR F (or we t chemica l analysis ) an dtha

t ar e i n unsoun dconditio n ar e classifieda s immediat e hazard s requirin g promp t abatement
. Thi s include s al l woodtri m—bot

h interio r an dexterior—wit

h blistering , scaling , peeling , or powder

in g paint an dwall s wit

h unsoun dpaint , painte dplaster , o r painted , peelin g wallpaper
. Floor s an dceilings , i f paint

e dwit h lead-base dpaint

andi f i n a n unsoun dcondition , ar e als o included
. New informatio n ha s reveale dth e importanc e o f lead

bearin g dus t

a s anothe r

majo r hazardfo r youn g children
.
1 8P.2 7

I n th e past , blistering , scaling , peeling , o r powderin g pain t wa s frequentl y remove donl y t o aleve l o f 4 or 5 fee t above-th e floor , because , usually , asmal l chil dca n reac h n o higher
. However , dus t o r pain t chip s fromunsoun d leadpain t abov e thi s leve l coul dfal l int o th e child' s pla

y area . CD C no w recommend s tha t all unsoun dleade d pain t b e remove dfromth e interior s of dwellings , includ

in g area s beyon dth e reac h o f children
. Likewise , exterio r leade dpain t

(o n porches , woodwork , an dwalls ) tha t eithe r i s in o r ca n fal l int o th e child' s pla

y are ashoul db e remove dimmediately
. Place s i n an dabou t th e hom e wher e youn g childre n spen dmuc h o f thei r time—namely , nea r

windows , doors , an dporches—ar e particularl y hazardous
. In summary , pain t

in unsoun dconditio n or o n chewa

bl e surface s i s classifie da s a n immediat e hazardrequirin g promp t abatement : othe r

lea dpain t

i n soun dconditio n ma y no t requir e immediat e attention , bu t i t mus t b e identifie da s apotentia l hazard
. Next , som e commo n method s fo r reducin g lead-base d pain t hazard s ar e outlined
. Phas e I —Emergenc y Interventio n A s soo n a s a

n elevate dbloo dlea dleve l i s confirmed , resident s shoul db e advise dt o remov e all scalin g pain t fromplace s suc h a s windo w sills , doo r frames , doors , an d porc h railing s tha t

ar e withi n eas y reac h of th e child
. A stif f brus h shoul db e use dfo r this
. Resident s shoul dals o b e advise dt o avoi dinhalin g th e dus t o r contaminatin g othe r areas . Th e debri s shoul db e vacuume dan dbagge d fo r saf e disposal
. The n th e are ashoul db e thoroughl y scrubbed , preferabl y wit h high-phosphat e detergent s suc h a s Spi c an dSpa

n (Mila r an dMushak , 1982)
. I

f acri b i s nex t t o asurfac e wit

h scalin g paint , th e cri b shoul db e move daway . Similarly , apiec e o f furnitur e shoul db e move dt o preven t

th e chil dfromreachin g area s of scalin g paint
. I n th e past , i

t wa s advise dtha t

windo w sill s an d othe r woo dtri mwit

h peelin g pain t

b e covere dwit

h mask

in g tap e o r

som e othe r

adhesive-backe dpaper . Thi s i s n o longe r recommended
. Inquisitiv e youn g childre n ofte n remov e thi s tape , thereb y renderin g th e techniqu e inef

fective
. Familie s shoul db e instructe do n way s t o kee p thes e area s fre e fromloos e o r flakin g paint

unti l mor e definitiv e step s ca

n b e take n t o reduc e th e hazard
. House

keepin g technique s suc h a s frequen t we t moppin g an d dam p dustin g ar e essentia l i n maintainin g areduce dleve l of hazard
. Phas e I I —Long-Ter

m Hazard Reductio n Onl y whe n a

n ol ddwellin g wit

h lead-base dpain t

i s gutte dan dcompletel y restore dca n th e leadhazard s b e considere d"permanentl y abated. " Les s extensive , com monl y use dprocedure s ma y b e calle d"lon g term" ; how

ever , ho w lon g th e hazar dwill remai n unde r contro l depend s o n suc h factor s a s th e thoroughnes s ofth e proce dure , th e soundnes s ofth e underlyin g structure , an dth e conditio n o

f th e plumbing
. Increase dmoistur e from leak y pipe s behin dwall s can quickl y caus e pain t tha t wa s smoot h an dintac t

t o bliste r an dscale
. Abatemententail s fou r steps : 1 . Removin g lea

dpain t fro mwoodtri mor

walls
. 2
. Thoroug h vacuumin g t o clea n u p th e debris
. 3
. We l scrubbin g fo

r maximu meliminatio n o f fine lead-bearin g particles
. 4
. Repaintin g th e are awit h lead-fre e paint

(thai is , paint containin g les s tha

n 0.06 % o f leadi n th e final drie dsolid)
. Th e propert

y owner' s responsibilit

y i s no t me t unti l all fou r step s hav e been completed
. Jus t prio r t o an ddurin g abatement , certai n precaution s ar e essential
. Carpets , rugs , upholstere dfurniture , bed

ding , clothing , an deatin g an dcookin g utensil s mus t b e seale da s tightly a s possibl e i n plasti c to protec t

the m fro mth e enormou s increas e i n lead-bearin g dus t

create d b y th e remova

l procedures
. Onc e item s suc h a s rug s are impregnate dwit

h fine, lead-bearin g particles , i t i s almos t impossibl e to remov e th e lea d(Mila r an dMushak , 1982)
. When feasible , thi s wor k shoul db e carrie dout

i n on e roo ma

t atime , wit

h th e roo mclose dof

f an dal l fur

nishing s removed
. Until step s 1 , 2 , an d3 ofth e cleanu p proces s ar e completed , all youn g childre n an dpregnan t wome n shoul dliv e elsewhere bot h da y an dnight
. I

f thi s i s no t possible , they , a s wel

l a s th e chil dwit

h th e inde x case , shoul dhav e seria

l bloo dlea

dtest s before , during , an dafter th e abatemen t

work
. Thos e doin g th e wor k shoul dcomply wit

h OSH A standards ; the y shoul d us e re spirator s an dwea

r coveralls , whic

h mus t no t b e take n t o th e workers ' home s fo

r laundering
. Wall s Removin g lea

dpaint fro mwalls , particularl y lea

dpaint applie dt o plaster , i s usually difficult
. I n mos t cases , abar

rier , suc h a s wallboard , hardboard , fiberglass , plywoo d panelin g o

r asimila r durable , fire-resistant

material , ca

n b e place dove r

th e lea dpaint o n th e walls
. Thes e material s mus t b e firml y nailed , cemented , or

glue di n plac e t o pre ven t th e chil dfro

mremovin g them
. Th e barrier s shoul d b e verminproo f

and , i n certai n area s ofth e dwellin g (tha t is , nex t t o furnace s an

dstove s andi

n commo n hallways) , fire retardant
. Wallpape

r painte dwit

h lea dpaint shoul d b e strippe dof

f t o th e maximu mexten t

possible
. Woodwor k Lead-base dpain

t i n unsoun dconditio n on bot h interi

o r an dexterio r

wood trim (fo r example , window units, door units, stair

risers, bannisters, and

railings) present s considerabl e danger

fo r children
. Pain

t ca n b e remove d fro mwoodsurface s b

y hea t (fro mga s torche s an dheat guns) , sanding , scraping , an dwit h liqui dpaint

removers . Al l o f thes e method s are hazardous
. Mos t solvent s i

n liqui dpaint

remover s evaporat e rapidly an dar e flammabl e an dtoxic
. Thes e remover s mus t b e use dwit

h th e utmos t cautio n an donly i

n well-ventilate darea s wit h prope r protectiv e clothin g andequipment
. When th e un derlyin g woodha s rotted , n o attemp t shoul db e mad e to remov e th e paint
. Instead , th e wood.shoul d b e replaced , including, 1 whe

n necessary , entir e windo w unit s an d door s or doo r frames
. Exterio r

rotte dwoo dshoul dals o
1 9b e replaced
. Whe n torches , hea l guns , an dsandin g

device s ar e use dl o remov e paini , ai r lea dlevel s increas e enormousl y i

n th e wor k area . Ofthese , sandin g i s b y fa r th e wors t offender
. I

t als o produce s th e greates t deposi

tio n oflea d i

n dusl , wil

h rate s a s hig h a s lOmgo f lead/s q ft/hou r (Inski p an dAttenbury , 1983)
. Therefore , fine sandin g dow n t o th e bar e woo dsurfac e i s no t recom mended
. Scrapin g ih e surfac e after aheat gun ha s bee n use dwil l probabl y produc e fewer fine particle s tha n sanding
. Th e abov e informatio n emphasize s th e urgenc y o f prope r cleanu p after

lead-base dpain t

ha s bee n removed
. Afte r th e dus l ha s settled , th e entir e area , includin g walls , floors , an dceiling , shoul db e vacuumed , preferabl y wit h a n industria l vacuu mcleaner
. Al l surface s shoul db e wet-scrubbe dwit

h phosphate-containin g detergents
. Im

mediatel y thereafter , al

l surface s fromwhich paint ha s bee n remove dshoul db e repainte dwit h lead-fre e paint
. Fo r saf e disposal th e debri s shoul db e place di n atoxi c wast e dum p approve db

y ih e Environmenta l Protectio n Agency , no t

i n a n ordinary landfil l o r

stor mor sanitary sewe r system . Fo r

bes t results , th e wel cleanin g proce dure s shoul db e repeale d(Mila r an dMushak , 1982)
. Worker s wh o remov e th e paint shoul db e responsibl e fo r ih e cleanup , inasmuc h a s man y of th e affecte dfamilie s hav e neithe r

th e equipmen t

no r th e resource s l o carr

y ou t a n adequat e cleanup
. Supplementa l Addresse s Childre n ofte n spen dsubstantia l amount s of tim e wit h relative s or

babysitter s wh o liv e a

t adifferen t

address
. I

f lead-base dpain t

i n unsoun dconditio n i s foun da t thes e addresses , i

t shoul db e remove di

n th e manne r

described. Similarly , day-car e center s an dothe r facilitie s ma

y b e locate di n ol d building s wit

h lead-base dpaint
. These , loo , shoul db e checke dan dhandle daccordingly
. Followu p Th e effectivenes s o

f th e initial abatemen t

ca n b e deter

mine donl y throug h coordinate dmedical an denviron

menta l followup
. Whe n th e initial abatemen t ha s bee n inadequate , ahig h recurrenc e ral e o f bloo dlea

dlevel s abov e 5 0 ug/d l ha s bee n foun d(Chisolm , 1983)
. Ideally , acommunitywid e code-enforcemen t progra mshoul db e develope di o remov e al

l lead-base dpain t

i n housing
. But , unti l then , th e appropriat e governmenta l uni t i n which th e chil dlive s i s responsibl e for identifyin g an dabatin g leadhazard s fo

r childre n wit

h leadtoxicity
. Removin g leadhazard s in housin g i s ihe majo r factor i n th e succes s ofalea dpoisonin g preventio n program . AIRBORN E LEA D Bloo dlea dlevel s ar e decreasin g a s th e us e o f leade d gasolin e decrease s (Annes t e t al. , 1983)
. I

n term s of reducin g backgroun dbloo dlea dlevels , removin g lea d fromgasolin e a s rapidl y a s feasibl e i s probabl y the mos t importan t publi c health measure . Emission s fromindustria l source s shoul db e reduce d sufficientl y t o achiev e th e curren t ambien t ai r lea dstan
dard
. Ne

w factories , a s par

t o f thei r licensin g specifica

tions , shoul db e require dt o hav e minimal lea demission s Th e publi c shoul db e informe dabou t th e hazard s asso ciate dwit h burnin g ol

d batler y casings , colore dnews print , wast

e oil , andlead-painte dwood
.
SOI L AN D DUS T Th e optima

l goa l i s t o preven t

lea d fro mbein g trans
ferre dfro man y sourc e t o soi l an ddust
. For th e goa l t o b e reached , ai

r lea d level s mus t

b e reduce dt o nea

r zero . For thos e area s where concentration s o f lea di n soil anddus t ar e high , large-scal e excavatio n o f soi l o r relocatio n o

f population s i s th e idea

l mean s o f reducin g th e exposur e o f childre n to lead
. Whe n th e lea dconten t o f househol ddus t

i s high , wet
moppin g andothe r

cleanu p measure s help reduc e chil

dren' s bloo dlea

dlevel s (Charne y e l al. , 1983)
. Thes e measure s provid e areasonable , short-ter mand mid-term solutio n t o th e proble mo

f contaminate dhous e dust
. I n severel y contaminate dresidentia l areas , unles s a n effectiv e barrier

ca n b e establishe dbetwee n th e childre n an dth e soil , surfac e soi l mus t b e remove dan dreplace d wit h soi l havin g alo

w lea d content . FOO D AN D WATE

R Th e lea dconten t o f air an dsoil , importan t

contributor s t o th e contaminatio n o

f foodandwater , shoul db e re duced
. Foo dcan s shoul db e mad e s o tha t lea ddoe s no t leac h fro msoldere dseams . Lea

di s als o adde dinadver

tentl y to food s durin g processin g an dhandlin g (Wolnik e t al. , 1983)
. Althoug h th e percentag e o f canne dfood s packagedi

n can s wit

h lead-soldere dsid e seam s ha s de

cline dsubstantially , som e ar e stil l package d thi s way . Thes e food s shoul dno t

b e store di

n th e opene dcan s be

cause , afte

r th e can s hav e been opened , even mor e lea d migrate s fro

mth e sid e sea

mint o th e food
. When feasible , lea

dplumbin g andlea

dwate r main s shoul db e replaced
. Wate

r fro mtap s i n th e hom e shoul d b e assesse dfo

r lea dcontent . I

f ahazar di s found , consum er s shoul db e educate dt o ru n wate r fo r several minute s befor e drinkin g i

t an dno t t o drink wate r fro mth e "hot " sid e ofth e lap
. Acidi c wate r supplie s shoul dbealkalinize d to help preven t

leaching
. OCCUPATIONAL Ideally , engineerin g feature s shoul dpreven t worker s fro mbein g expose dto lea

ddus t an dvapors . Whe

n work

er s are exposed , complianc e wit h Occupationa

l Safet y an dHealt h Administratio n (OSHA ) regulation s appear s t o b e effectiv e i

n protectin g the mandi

n preventin g the m fro mtransportin g lea

dhom e to children
. Under th e OSH A lea dstandard , factorie s tha

t us e lea dmus t provid e worker s wit

h facilitie s fo

r showerin g an d changin g 2 0P.2 9

clothe s an dshoe s befor e goin g hom e fromwork
. Thi s standar dno w applie s onl y t o industrie s covere db y OSHA regulations
. Fo r

th e protectio n of

children , i

t shoul db e extende dt o al l industrie s tha t us e lead
. Th e preventio n of lea dexposur e t o th e fetu s need s special emphasis
. Women^o f

childbearin g ag e shoul db e exclude dfrom workin g a t job s wher e significan t

lea dexposur e occurs . LEAD-GLAZE D POTTER Y Al l glaze dpotter

y use dfo r foodstuf f shoul db e free o f leachabl e lead
. Hobbyist s an dconsumer s shoul db e educate dt o th e risk s associate dwit h pottery glazes
. Consumer s shoul dno t

us e potter

y fo r cookin g o r

fo r stor
in g foo do r

beverage s unles s th e pottery ha s recentl y bee n determine dt o b e free o f leachabl e lead
.

2 1

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. Tf.VK^i'Xft-^a'i-'- 1

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# H
VIII
. Healt

h Educatio n

Th e communit y an despeciall y parent s o f preschoo l childre n wh o liv e in older , deterioratin g neighborhood s shoul db e informe da

t ever y availabl e opportunit y ofth e nee dt o hav e childre n screene dperiodicall y fo r lea d poisoning
. Basi c preventiv e measure s shoul db e empha

sized
. Thes e includ e frequen t wet moppin g an dvacuum in g of accessibl e pain t

flakes an ddus t

t o reduc e potentia l leadhazard s in th e child' s environment
. Th e dange r o f in

gestin g pain t

chips , dust , an dsoi l shoul db e stressed
. Olde r sibling s of

childre n a

t hig h ris k shoul dals o b e in

forme dabou t

th e source s an drisk s oflea d poisonin g becaus e the y ofte n tak e car e of younge r children
. I f achil di s screene dan dth e lea dleve l i s no t elevated , th e ris k remains , an dunti l th e sixth birthday , rescreenin g i s required , particularl y durin g th e summer . Unti l hazard

fre e housin g i s availabl e fo r al l an d othe r

high-ris k source s o

f lea dar e removed , periodi c screenin g wil l reduc e th e ris k

oflea d poisoning
. Educatio n shoul dstart

when th e chil di s screened , an d physicians , nurses , environmentalists , an daide s shoul d reinforc e i t a t ever y opportunity
. Whe n achil d i s foun dt o hav e lea dtoxicity , educatio n of

th e famil y i s essential fo

r successful followu

p ofth e child
. Th e famil

y mus t b e full y informe dabou t

th e conditio n an dth e clinica l an denvi

ronmental action s t o follow
. Healt h professional s mus t emphasiz e th e importanc e o f th e family' s understandin g th e child' s condition , it s cause , an dth e possibl e resul t of lea dtoxicity
. I

n addition , the y shoul dstres s th e impor

tanc e o f th e child' s havin g abalance ddie t tha t include s enoug h calciuman diron
. 

# IX
. Reportin g Lea

dToxicit y and Elevated
. Bloo

dLea dLevels

Primary car e physician s an d person s in charg e o f screenin g program s shoul drepor t both presumptiv e an d confirme dcase s oflea d toxicity t o th e appropriat e health agency , an dlaboratorie s performin g bloo dlea do r E P test s shoul drepor

t any abnormal result s t o th e appropri

at e healt h agency .

2 2

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# X
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2 4

WAj>y;T>f;v;v,;e :Piomell i S
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Pb an do f

F e deficiency
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. Manage

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tion
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JP , Lauwery s R , e t

al
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r Lead
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dChildNeuro l 1981;23:567-76
.

2 5

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

# Appendi x P.3 4
Reprinte d wit h permissio n b y th e U.S . DEPARTMEN T O F HEALT H AN D HUMA N SERVICE S

PUBU C HEALT H SERVIC E fro m th e Journa l o f Pediatrics , Volum e 105 , Octobe r1984 , Numbe r4
. pp . 523—53 2 

# SPECIA L ARTICL E Management

of childhood

lead poisoning Sergi o Piomelli , M.D. , Joh n F . Rosen, M.D. , J . Julia n Chisolm , Jr. , M.D. , an d Joh n W . Graef

, M.D . New York, New York, Baltimore, Maryland, and Boston, Massachusetts CHELATIO N TREATMEN T fo r childhoo d lea d poisonin g may b e life-savin g an d decrease s th e bod y burden o f lea d fa r mor e rapidl y than normal excretor y processe s can. 1 Furthermore , chelatin g agent s markedl y enhanc e remova l o f tha tfractio n o f

bod y lea d tha ti s readil y mobil e an d considere d t o b e th e mos ttoxic. 1 " * However , lea d poisonin g i s a wholl y preventabl e disorde r cause d b y th e wid e disseminatio n o f

lea d int o th e environment.'- ' Medica l treatmen twith chelatin g agent s mus tno tb e considere d a ' substitut e fo r dedicate d preventiv e effort s t o eradicat e controllabl e source s o f

lea d (e.g. , substandar d housin g tha t contain s lead-bearin g paints , combustio n o f leade d gaso line) . Althoug h repeate d course s o f chelatio n therap y may b e necessar y fo r medica l reasons , th e source(s ) o f environ menta l lea d mus tb e identifie d an d remove d fo r preventiv e reasons . Thi s revie w i s base d o n ou r experienc e in fou r differen t lea d poisonin g treatmen tclinic s an d reflects ou r consensu s o n curren tmanagemen tcriteria . PHARMACOLOGI C CONSIDERATION S Lea d poisonin g i s treate d wit h drug s capabl e o f bindin g (chelating ) lea d an d o f enhancing it s excretion . Thes e 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

ofPediatrics, 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-O9and 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. 630West 168th St.. New York. NY 10032. drug s deplet e th e sof ttissue s o f

lea d an d ma y thu s reduc e it s acut e toxicity . The y ar e als o used , i n asymptomati c children , to reduce a potentiall y dangerou s body burden o f lead . Al l drugs ar

e use d t o enhanc e th e slo w proces s o f natura l lea d excretion . Al l drugs hav e potentia l sid e effects and shoul d b e use

d carefully . A brie f

descriptio n o f

th e essentia l pharmacologi c aspect s o f th e variou s drug s fol lows . Detaile d guideline s fo r specifi c situation s ar e give n i n th e nex tsection . BA L Mechanism of

action. Tw o molecule s o f BA L combin e wit h on e atom o f

heav y metal t o for

m a stabl e complex . BA L enhance s feca

l a s wel l a s urinar

y excretio n o f

lea d an d diffuses well int

o erythrocytes . Itcan b e administere d i n th e presenc e o f

rena l impairmen tbecaus e i ti s predomi nantl y excrete d i

n bile. 1 BA L CaNa,-EDT

A E P G-6-P D (Britis

h anti-lewisite

) Dimercaptopropano

l Disodiu m calcium-edetat

e Erythrocyt e protoporphyri

n Glucose-6-phosphat

e dehydrogenas

e

' Route of

administration and

dosage. BA L i s availabl e onl y i n oi l fo r intramuscula r administration . I tmus tb e give n ever

y 4 hours' . Dosage s are discusse d below . Toxiciiy. Mil d febril e reaction s may occur , an d tran sien televatio n o f

hepati c transaminas e activitie s ma y b e observed . Othe r minor advers e effects include , in orde r o f frequency , nausea an

d occasional vomiting , headache , mild conjunctivitis , lacrimation , rhinorrhea , an d salivation . Mos tsid e effect

s are transien tan d rapidly subsid e a s th e dru g i s metabolize d and excreted . Precautions. I

n patient s wit

h G-6-P D deficiency , BA L shoul d b e use d onl y i

n life-threatenin g situations , becaus e i tmay induc e hemolysis . Medicinal iron shoul d neve r b e administere d during BA L therapy , becaus e th e combina tio n i s ver

y toxic . I f

iron deficiency coexists , it s manage men tshoul d b e postpone d unti l BA L therap y i s concluded . I n case s o f

extrem e anemi a bloo d transfusion s ar e prefer able . 2 6

'.•s.-;;--
. • *r.<&3r&iT'2

TjtuaT -aT^jt. CTTT

ft -? £
. y • ?^g , .-.r^'^-^.'-v-- , ?y.; < Bx' r •..j.'T.-«^y.'.y».<'»ygiB.\T,^^ ^P.3 5

CaNa 2-EDTA**' 6 ,0nly CaNa r

EDTA (calcium disodium versenate) should be used for treatment

of lead poisoning. Na r EDTA (endrate disodium) should never be used for treatment of lead poisoning, because it

may induce fatal hypocalcemia and

tetany. Mechanism of

action. CaNa 2 -EDT A increase s urinar y leadexcretio n 20

- t o 50-fold
. CaNa 2 -EDT A doe s not enter th e cells ; thu s i t

remove s leadfro

mth e extracellula

r compartment . Indirectly , lea di s reduce di

n th e sof t tissue , central nervou s system , an dre dbloo dcells. ' Route of administration and

dosage. CaNa2 -EDT A ma y b e give n intravenousl y o r

intramuscularly
. Th e pre ferre dan dmos t

effective rout e i s acontinuou s intravenou s infusion ; agive

n dos e i s mos t

effective i

f infuse dove r 6 hours. 1 0 CaNa,-EDT A shoul db e dilute dt o aconcentratio n <0.5 % i n dextros e an dwater

o r 0.9 % salin e solution
. Whe n administere dintravenousl y a s asingl e dose , i t shoul db e similarl y dilute dan dadministere dby slo w infusio n ove r 1 5 to 2 0 minutes
. Intramuscular administratio n o

f CaNa2 - EDT A i s extremel y painful an dshoul db e give n wit h procain e (0.5% ) b

y dee p injection
. CaNa 2 -EDT A shoul dnot

b e give n orally , becaus e i t

ma y enhanc e absorptio n o

f leadfro mth e gastrointestinal tract . Dosage s var

y i n differen t situation s andar e discussed below
. I n al l cases , course s shoul db e limite dto 5 days , followe db y a t leas t 2

- t o 5-da

y interval s t o allo w recover y fro mzin c depletion
. Toxicity. Th e kidne

y i s th e principal site o

f toxicity
. Rena l toxicit

y i s dos e related , reversible , an drarel y occur s a t dose s <150 0 mg/m 2

. Th e rena l toxicit y ma y b e reduced by assurin g adequat e diuresis
. CaNa 2 -EDT A shouldneve r b e give n i n th e absenc e o

f an adequat e urin e flow
. Befor e administerin g i t

intramuscularl y i

n childre n i

n goo dclini

ca l condition , adequat e oral intak e o f fluids mus t

be assured
. Precautions. Durin g chelatio n wit h CaNa2 -EDTA , urin e an dit s sediment , BUN , seru mcreatinine , an dlive r function test s mus t

b e carefully monitored
. Th e appear anc e o f protei n an dformedelement s i n urinary sediment , an drisin g BU

N andseru mcreatinin e value s signif y impendin g renal failure , th e seriou s toxicit y associate d wit h excessiv e o r

prolonge dadministratio n o f EDTA
. Inasmuc h a s CaNa 2 -EDT A ma y deplet e zin c store s and cellula r injur y ma y b e associate dwit

h zin c depletion , CaNa 2 -EDT A shoul db e use dwit h grea t caution
. CaNa 2 -EDTA , usedalon e withou t concomitant

BA L therapy , ma

y aggravat e symptom s i

n patient s wit

h ver y hig h bloo dleadlevels
. Thu s i t shoul db e usedexclusivel

y i n conjunctio n wit

h BA L whe n th e bloo dleadleve

l i s >7 0 /ig/d l o r

clinica l symptom s consisten

t wit h lea d poisoning ar e present . I

n such case s th e firs

t dos e o f BA L shoul d alway s preced

e th e first dos e o f CaNa 2 -EDTA b y a t leas t 4 hours
.

- D-PeniciUamine
. D-Penicillamin e i s not licensedb

y th e Foo dan dDrug Administratio n fo

r the treatmen t

o f lea d poisoning
. It s us e fo

r thi s indicatio n i s thu s t o b e consid

ere dexperimental
. I t

i s th e onl

y commerciall

y availabl e ora l chelating agent . I t

ca n b e give n ove r alon g perio d (days)
. Toxic sid

e effect s ma y occu r i n a s man y a s 20 % o

f patient s give

n th e drug. " Mechanism of

action. D-Penicillamin

e enhance s urinar

y excretio n o

f lead , althoug h not

a s effectivel

y a s CaNa2 - EDTA
. It s specifi

c mechanis mo

f actio n i s no t

wel l understood
. Route of administration and

dosage. D-Penicillamin

e i s administere dorally
. I t

i s currently availabl e i

n capsule s (12 5 and25 0 nig)
. Thes e capsule s ma y b e openedand suspendedi

n liquid , i f necessary . Th e usua

l dos e i s 3 0 mg/kg. Sid

e effect s ca n b e minimize

db y initiatin g therap y wit h smal l doses , fo r example , 25 % o

f th e desire dfinal dose , increasedafte

r 1 wee k t o 50 % an dagai n afte

r 1 wee k to th e ful l dose , while monitoring fo r possible toxicity
. Toxicity. Th e mai

n side effect

s o f D-penicillamin

e ar e reaction s resembling thos e o f penicilli n sensitivity , includ

in g fevers , rashes , leukopenia , thrombocytopenia , and eosinophilia
. Rarely , mor

e sever e an deve n life-threatenin g reaction s (autoimmun e hemolyti c anemia , Stevens-John

so n syndrome) hav e bee

n observed
. Anorexia , nausea , an d vomiting are infrequent
. O f mos t concern , however, ar e isolate dreport s o

f nephrotoxicity , possibl

y fro mhypersen

sitivit y reactions
. Fo

r thes e reasons , patient s shouldb e carefull y an dfrequentl

y monitoredfo

r clinically obviou s sid e effects , andfrequen

t bloo dcounts , urinalysis , an d rena l functio n test s shouldbe performed
. I n particular , bloo dcount s an

durinalysi s shoul

dbe don e twic e weekly , a

t leas t i n th e first 3 week

s o f treatment . I

f th e absolute neutrophi l coun

t fall s to <1500// d i t

shoul db e immediate

l y rechecked , an

dtreatmen t

shoul dbe stoppedi

f i t fall s t o <1200//zl
. D-Penicillamin

e shoul dtherefor e not b e give n o n a n outpatient

basi s i f there i s an

y questio n abou t complianc e wit

h appointments
. D-Penicillamine should

not be administered

in patients with known penicillin allergy. Ne w agents . Dimercaptosuccini c aci dand2-3-dimer

capto-propane-1-sulphonat e ar e bot h water-solubl e deriva

tive s o f BAL
. Althoug h bot

h appea r promising an dsaf

e andhav e bee n use dsuccessfull

y i n treatmen t

o f other heavy-meta

l poisoning , thes e drug s ar e presently i n th e investigativ e stag e fo

r th e treatment

o f lea dpoison

ing." " ,
2 7

•^^.^rrJWia?j?-j.~..^'jy'^?T-,;;.^-y^' j ~'£*i2*j~£'£"'*E*Ja£'£~i ^ iSgESB-gsaaIP.3 6

ACUT E LEA D ENCEPHALOPATH Y

' Acut e lea d encephalopath y i s characterize d clinicall y by som e o r al l o f

th e followin g symptoms : coma , seizures , bizarr e behavior , ataxia , apathy , incoordination , vomiting , alteratio n i n th e stat e o f consciousness , an d subtl e los s o f recentl y acquire d skills . An y on e o r a matri x o f thes e symptom s associate d with a n elevate d bloo d lea d concen tratio n constitute s a

n acut e medica l emergency . Lea d encephalopath y i s almos talway s associate d with a bloo d lea d concentratio n >10 0 /xg/dl , althoug h i tha s bee n reporte d a tbloo d lea d level s a s lo w a s 7 0 /ig/dl. M Genera l supportiv e management . Al l oral intak e i s pro hibite d initiall y unti l th e child' s conditio n ha s significanti y improved . Parentera l fluid therap y i s begu n immediately ; volum e i s restricte d to basal requirement s plu s a carefu l assessmen to f

continuin g losses . Excessiv e intravenou s fluid administratio n mus tb e avoided . Onc e urin e flo w i s establishe d b y administerin g dextros e i n wate r (1 0 to 2 0 ml/k g bod y weight) , chelatio n treatment , alread y begu n with BA L alon e fo r on e dose , i s continue d wit h simulta neou s administratio n o f CaNa 2 -EDTA . A n adequat e flow o f urin e mus tb e establishe d befor e intravenou s chelatio n therapy . Parentera l fluid therap y minimize s vomitin g tha t ma y accompan y administratio n o f BA L and ensure s promp texcretio n o f

CaNa 2 -EDTA , a dru g excrete d exclu sivel y b y th e kidney . Fo r initia l contro l o f seizures , diazepa m o r paraldehyd e i s th e preferre d drug . Barbitu rat e an d phenytoi n ar e reserve d fo r th e long-ter m manage men to f recurrin g seizures , onl y afte r th e acut e episod e i s manage d an d consciousnes s ha s bee n full y recovered . Althoug h i ti s desirabl e t o evacuat e an y residual lea d fro m th e bowel , thi s shoul d no tdela y th e star to f chelatio n therapy . Surgical decompressio n an d hypertoni c solution s t o reliev e intracrania l pressur e an d cerebra l edem a ar e contraindicated . Th e diagnosi s o f

acut e lea d encephalopath y ca n usuall y b e mad e withou tlumba r puncture , whic h i s extremel y risky becaus e o f

th e presenc e o f

increase d intracrania l pressure . I

n fulminan tlea d encephalopathy , increase d intracrania l pressur e may b e presen ti n th e absenc e o f any o f th e usual preliminary sign s (change s i n bloo d pressure , puls e o r respiration , retina l hemorrhag e o r edema) . If examinatio n o f

th e CS F i s absolutel y essentia l fo r th e differentia l diagnosis , th e ver y leas tamoun to f fluid, no t exceedin g a fe w drops , shoul d b e carefull y obtained . Chelatio n therapy . Treatmen ti s begu n wit h a primin g dos e o f 7 5 mg/m 2 BA L only , give n b y dee p intramuscula r injection ; BA L i s administere d a ta dos e o f 45 0 mg/m 2 /2 4 hours , i n divide d dose s o f 7 5 mg/m 2 ever y 4 hours . Onc e th e primin g dos e i s give n an d a n adequat e urin e flow i s established , administratio n o f CaNa 2 -EDT A i s begu n ata
2 8 dos e o f 150 0 mg/m 2 /2 4 hours . CaNa 2 -EDT A i s give n b y continuou s intravenou s drip i n dextros e an d wate r o r 0.9 % salin e solution . Th e concentratio n o f CaNa 2 -EDT A shoul d no texcee d 0.5 % i n th e parentera l fluid . (I n th e treatmen t o f acut e encephalopathy , restrictio n o f parenteral fluids take s precedence , s o tha tCaNa 2 -EDT A may hav e t o b e give n intramuscularl y i f fluid overload i s t o b e avoided. ) Combine d BAL-CaNa 2 -EDT A therap y i s give n fo r a to tal o f 5 days . Durin g treatment , rena l and hepati c func tio n and seru

m electrolyt e level s shoul d b e monitore d daily . A secon d cours e o f

chelatio n therap y wit h CaNa 2 - EDT A alon e or wit

h BAL , dependin g o n th e bloo d lea d concentration , ma

y b e required afte r a 2-da y interval . A third cours e i s required onl y ifth e bloo d lea d concentratio n rebound s to a valu e >5 0 /ig/d l withi n 4 8 hours afte r treatment . Unles s ther e ar e compellin g clinica l reasons , i t i s desirabl e t o wai ta tleas t5 t o 7 day s befor e beginnin g a third cours e o f

CaNa 2 -EDTA . SYMPTOMATI C LEA D POISONIN G WITHOU T ENCEPHALOPATH Y Symptomati c lea d poisonin g withou tencephalopath y i s characterize d by on e o r severa l o f th e followin g symptoms : decreas e in pla

y activity , lethargy , anorexia , sporadi c vomiting , intermitten tabdomina l pain , an d constipation . Symptomati c lead poisonin g i s usuall y associate d with a bloo d lea d concentratio n >7 0 /tg/dl , althoug h occasionall y ma y b e associate d wit

h a bloo d lead concentratio n a s lo w a s 5 0 fig/dl . Ifthe blood lead concentration is <50 ug/dl, otherdiagnostic possibilities should be vigorously sought. Becaus e all symptomati c childre n potentiall y hav e acut e lead encephalopathy , treatmen tan d supportiv e mea sure s mus tb e institute d immediatel y o n a n emergenc y basis.'- 4 Genera l supportiv

e management. Al l ora

l intak e i s pro hibite d and th e guideline s o f parentera

l fluid therap y ar e followe d a s noted abov e for th e treatmen to f lea d enceph alopathy . Intravenou s fluids ar e given a ta rate consisten t wit h basa l requirement

s plus ongoin g losses . Excessiv e fluid administratio n mus tb e avoided . Chelatio n therapy . Treatmen ti s begun wit h a primin g dos e o f 5 0 mg/m 2 BA L b

y dee p intramuscula r injection ; BA L i s administere d ata dos e o f 30 0 mg/m 2 /2 4 hours in divide d dose s o f

5 0 mg/m 2 ever

y 4 hours . Onc e th e primin g dos e i s give n an

d a n adequate urine flow i s established , administratio n o

f CaNa 2 -EDT A i s begun ata dos e o f 100 0 mg/m 2 /2 4 hours . CaNa 2 -EDT A i s give n b y continuou s intravenou s drip in dextros e and wate r or 0.9 % salin e solution . Althoug h continuou s infusio n o f CaNa 2 -EDT A i s preferable , i tma

y b e replace d by dose s o f

175 mg/m 2 ever

y

rrr..^\.apiwr-xr^i&v.-ra-ac%atv±:&>-riirt-f.-j--f-. r,rr.-'fr~ft'^*'*gyi , *:*^**'-'%^'"'''^ ^ HjBjflHHfifiififi BP.3 7

4 hours , give

n eithe r intravenousl y ove

r 1 5 to 2 0 minute s throug h ahepari n loc

k o r by dee p intramuscula

r injectio n mixedwit h procaine
. Th e concentratio n of CaNa 2 -EDT A shouldnot excee d0.5 % i n th e parentera l fluid. Combined BAL-CaNa 2 -EDT A therap y i s give n fo r atotal o

f 5 days
. Durin g treatment , renal an dhepati c function an dseru m electrolyte level s shoul db e monitore ddaily
. I t i s advisabl e t o measure th e bloo dlea

dconcentratio n daily
. (I t

wil l b e necessar y to interrup t

th e CaNa 2 -EDT A infusio n fo r 1 hou r befor e thi s sampl e i s obtained , to avoidaspuriously hig h value)
. I

f th e bloodlea

dconcentratio n reache s <5 0 /ig/dl , a s i t

ma y within 3 day s o

f combine dBAL

CaNa ; -EDT A therapy , BAL ma y b e safel y discontinue d an dCaNa 2 -EDT A continue dfo r aful l 5-da y cours e o

f treatment . I

f measurement s o

f bloo dlea

dcanno t be obtaine di n time , i t i s saf e t o continu e BA

L fo r th e ful l 5-da y course . Excep t

under highly unusual circumstances , CaNa 2 -EDT A shoul dnot

b e administere dfo

r mor e tha n 5 consecutiv e days
. A secondcours e o

f chelatio n therap y ma

y b e require d afte r a2

- to 4-da

y interval , t o b e starte dwit h CaNa ; - EDTA alon e o

r wit h concomitan t

BAL , dependin g o

n th e bloo dlea dconcentration
. A thir dcours e ma y be require di

f th e bloodleadconcentratio n rebound s to avalu e >5 0 Mg/d l withi n 7 t o 1 0 day s after

treatment . Unles s ther e ar e compellin g clinica

l reasons , i t

i s highly desirabl e t

o allow 5 to 7 day s befor

e beginnin g athir dcours e o f CaNa,

- EDTA
. ASYMPTOMATI C CHILDRE N WIT H INCREASE D BOD Y BURDE N O F LEA D Althoug h childre n wit

h increase dbod

y burde n o

f lea d ar e clinically asymptomatic , i t i s likely tha t

they have pervasiv e metaboli c effects involving hem e synthesis, 200

- ' re dcell nucleotid e metabolism, 24 vitami n D andCortiso l metabolism""' an drenal function,'- 4 an dsubclinica l neu robehaviora

l effects. 2 " 1 1 Som

e o f thes e profoundmetaboli c andcellula

r effect s o f lea dhav e bee

n observeda t

bloo d lea dconcentration s <2 5 ^g/dl. 20 '*'•-*<• • J 0 * ' Diagnosti c assessment . In asymptomati c childre n i t i s essential t o hav e afirmdiagnosi s base do n a n elevate d bloo dlea dleve l befor e treatmen t

i s initiated
. Measure

ment s o f bloodlea dconcentratio n i

n capillar y sample s ar e subjec t t o contaminatio n an dshoul dneve r be th e onl y basi s fo r treatment . Treatmen t

shoul db e initiate donl

y afte r a confirmator

y measuremen t

o f th e venou s bloodlea

dcon centration
. Eve

n whe n ther e i s stron g additional evidenc e o f lea dpoisoning , such a s pain t flakes i n th e abdome

n o r lea dline s i n th e bone s o

n x-ra y examination , i

t i s prefera

bl e to wai t

fo r aconfirmator

y measurement

o f venou s bloo dlead
. Althoug h measurement s of erythrocyte proto
porphyri n ma

y b e helpful i

n evaluatin g overal l toxicity , bloodlea dmeasuremen

t i s th e criterio n o

n whic h to bas e a decision a s t o whethe

r chelatio n therap y shouldb e consid

ered
. (Th e EP ma

y increas e initially durin g chelatio n therapy. ) Therapeuti c decision s shouldals o be basedo n th e result s o

f the CaNa

2 -EDTA provocative test . Chelation therapy Blood lead concentration >70pg/dl. I f th e bloodlea

d leve l i s *>7 0 fig/dl , BA

L andCaNa

2 -EDTA shouldb e given , i n the sam e dose s an dwit

h th e sam e guideline s a s fo r treatment

o f symptomati c lea

dpoisonin

g without encephalopathy
. A secon dcours e o

f chelatio n therap y wit

h CaNa : - EDT A alon e ma y be require di

f th e bloodlea

dconcentra
tio n rebound s to avalu e >5 0 jig/d l withi n 5 t o 7 day s after treatment . Unles s there ar e compelling clinica l reasons , i t i s highl y desirable to allow at

leas t 5 to 7 day s befor

e beginning asecon

dcours e o f CaNa 2 -EDTA
. Blood lead concentration 56

to 69pg/dl. I

f th e blood lea dvalue i s betwee

n 5 6 and6 9 /"g/dl , treatment shouldb e limitedto CaNa ; -EDT A only
. CaNa 2 -EDT A i s give n fo r 5 day s a t ados e o f 100 0 mg/m 2/day , preferabl

y b y continuou s infusio

n (or i n divide ddose s intravenousl

y a s above)
. Alternatively , how

ever , i f environmenta

l contro l o f the lea dhazard s ha s bee

n achieved , thi s treatmen t

ma y b e give n o n a n outpatien t basis , at adose o f 100 0 mg/m 2 /day , preferabl

y b y intrave

nou s infusio

n ove r 1 hour , wit

h adequate hydratio n (25 0 ml/m 2 )
. A s aleas t preferabl e option , CaNa 2 -EDTA ma

y be administere dintramuscularl y mixe dwit h procaine , at th e sam e single daily dos e o

f 100 0 mg/n r fo r 5 consecu tiv e days
. Thi s route o

f administratio n ma

y represent

a painfu l bu t practica l alternative , whe

n circumstance s dic

tat e it
. During treatment , rena

l an dhepati c functio

n an dserum electrolyt e levels shouldbe monitored
. A bloodlea d concentratio n shoul

dbe obtaine da t

7 2 hour s o

f treatmen t (i t wil l b e necessar

y t o interrup t

th e CaNa

2 -EDTA infu

sio n fo r 1 hou r befor e thi s sampl e i s obtained , to avoida spuriousl y hig h value ) to monito

r the effectivenes s o

f treatment . CaNa 2 -EDTA treatmen t

shouldb e continuedfo

r 5 days
. Excep t unde r highl y unusua l circumstances , i t

shouldnot b e administeredfo

r mor e tha n 5 consecutive days
. A secon dcours e o

f chelatio n therapy , wit

h CaNa2 - EDT A alone , ma

y b e require di

f the bloo dlea dconcentra
tion rebound s t

o avalu e >5 0 ug/d\ withi

n 5 t o 7 day s afte

r treatment . Unles s there ar e compelling clinica l reasons , i t i s highl y desirabl e t o allow aperio do f 5 t o 7 day s befor

e beginning asecon

dcours e o f CaNa2 -EDTA
. Blood lead concentration 25to 55iig/dl. Whe n th e bloo dlea d value i s persistently betwee n 2 5 an d5 5 Mg/d l an daccompaniedb

y E P persistently >3 5 Mg/dl , th e decision to procee

dwit h chelatio n therap y shouldb e base d 2 9

yr a **?."jf-.T > •«.*>

: \'-ra&&l;?*.^x*v* : i^w.&-ettJ^. !£j££lti££l£i-=Ss£siSgS ^"-TTr-irTTTT-YH" ' ^PH r '- P.3 8

Table . Choic e o f

chelatio n therap y base do n symptom s an dbloo dlea dconcentratio n Clinical presentation Treatment Comments Symptomati c childre n Acute encephalopathy

Othe r symptom s BA L 45 0 mg/m"/day Start wit h BA L 7 5 mg/m 1 I

M ever y 4 hours
. CaNa2 -EDT A 150

0 mg/m'/da y Afte

r 4 hour s star

t continuou s infusio

n o f CaNa 2 -EDTA 150

0 mg/m 2 /day
. Therap y wit

h BA L an dCaNa

2 -EDT A shoul db e continue dfo

r 5 days
. Interrup t therap y fo

r 2 days
. Treat fo r 5 additiona

l days , includin

g BA L i f bloo dP b remain s high
. Othe r cycle s ma y b e neede ddependin

g o n bloo dP b rebound
. BA L 300 mg/m'/da y Star t wit h BA L 50 mg/m

2 I M ever y 4 hours
. CaNa 2 -EDT A 100

0 mg/m"/da y Afte

r 4 hour s star

t CaNa 2 -EDT A 100 0 mg/m 2/day , preferably b y continuou s infusion , o

r i n divide ddose s I V (throug h a heparin lock)
. Therap y wit

h CaNa

2-EDT A shoul db e continuedfo

r 5 days
. BA L ma y b e discontinue

dafte r 3 day s i f bloo dP b <5 0 jig/dl
. Interrup t therapy fo

r 2 days
. Treat fo r 5 additiona

l days , includin

g BA L i f bloo dP b remain s high
. Othe r cycle s ma y b e neede ddependin

g o n bloo dP b rebound
. Asymptomati c childre n Before treatment, measure venous blood lead. Bloo dP b >7 0 /xg/d

l BA

L 300 mg/m'/da y CaNa2 -EDT A 100

0 mg/m*/da

y

Bloo dP b 5 6 t o 6 9 Mg/d

l CaNa,-EDT A 100

0 mg/m"/da y

Bloo dP b 2 5 t o 5 5 jig/d l Perform CaNa r

EDTA provocation test

to assess lead

excretion Start

wit h BA L 5 0 mg/m

2 I M ever y 4 hours
. Afte r 4 hour s star

t CaNa 2 -EDT A 100 0 mg/m'/day , preferabl

y b y continuou s infusion , o

r i n divide ddose s iv (throug h a heparin lock)
. Treatmen t wit h CaNa

2 -EDT A shoul db e continuedfo

r 5 days
. BA L ma y b e discontinue

dafte r 3 day s i f bloo dP b <5 0 Mg/dl
. Other cycle s ma y b e neede ddependin

g o n bloo dP b rebound
. CaNa 2 -EDT A fo r 5 days , preferabl

y b y continuou s infusion , o

r i n divide ddoses (throug

h ahepari n lock)
. Alternatively , i

f lea dexposur e i s controlled , CaNa 2 -EDTA ma

y b e give n a s asingl

e dail y outpatient

dose I M o r iv
. Other cycle s ma y b e neede ddependin

g o n bloo dP b rebound
. I T rati o >0.7 0 I f rati o 0.6 0 t o 0.6 9 Ag e < 3 year s o

f ag e Ag e > 3 year s o

f ag e I f rati o <0.6 0 ratio (see text)
.

CaNa2 -EDT A 100

0 mg/m 2 /da y Treat

fo r 5 day s i v o r IM , a s above
. CaNa2 -EDT A 100

0 mg/m"/da y Treat

fo r 3 day s i v o r IM , a s above
. N o treatmen t

Repea t bloo dP b an dCaNa,-EDTA provocatio n tes t periodically
. N o treatmen t

Repea t bloo dP b an dCaNa

2 -EDT A provocatio

n tes t periodically
.

o n positiv e findings o f acarefull y performe dCaNa 2 - EDT A provocatio n test . (I t mus t agai n b e emphasize dtha t chelatio n therap y shoul dcomplement , no t replace , abate

men t o f controllabl e lea dsources. ) CaNa,-EDT A PROVOCATIO N TEST
. First , arepeate dbase

lin e bloo dlea dleve l i s obtaine dan dth e patien t i s aske dt o empt y th e bladder
. The n CaNa 2 -EDT A i s administere da t ados e o f

50 0 mg/m 2 intravenousl y i n 25 0 ml/m 2 o f 5 % dextrose , infuse dove r

1 hour
. ( A painfu l bu t practica l alternativ e i s t o administe r th e sam e dos e intramuscularl y mixe dwith procain e an dt o encourag e th e chil dt o drin k a s muc h a s possibl e i n th e first 2 hours)
. Al l urin e mus t b e collecte dwit

h lead-fre e equipmen t

ove r 8 hours
. Th e urin e volum e shoul db e carefull y measured , an daliquot s shoul d b e sen t t o th e laborator y for

measuremen t

o f th e concen tratio n o f

lead
. Extrem e car e shoul dbe.exercise d t o us e onl y lead-fre e equipment
. I f thi s i s not

availabl e i n th e clinic , i t may b e bes t

tha t th e entir e urin e volum e b e sen t t o 3 0

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._J . " " 0 10. 0 20. 0 30. 0 40. 0 50. 0 60. 0 70. 0 Bloo d Lea d (#g/dl ) Figure . Lea d excretio n rati o a s a functio n o f bloo d lead . Dat

a expresse d a s decima l logarith m o f CaNa,-EDT

A excretio n rati o (\i% lea

d excreted/m g EDT

A administered

) versu s bloo d lead. Ther

e i s a significan

tcorrelatio

n ( r = 0.466 , P < 0.001) . wit

h a slope o

f 0.01 4 an d a n intercep to f -0.95 . Dat a show n wer e obtaine d b y differen ttechniques . A

tColumbi a University

. 7 7 childre n i n a n outpatien

tsettin g receive d CaNa

2 -EDT A a s a 20-minut

e intravenou

s infusio n a ta dos e o f 5 0 mg/kg . followe

d b y 25 0 ml/m2 5

% dextros e ove r 1 hour ; urin

e wa s collected fo

r 7 t o 8 hours. A

tAlber tEinstei n Colleg e o f Medicin e (Montefior

e Hospital) , 3

7 hospitalize d childre n receive d CaNaj-EDT

A intramuscularl

y wit h procain e a ta dos e o f 50 0 mg/m

2 ; urin e wa s collecte d fo r 8 hours. A tJoh

n Hopkin s Universit

y Schoo l o f Medicine

, 5 0 hospitalize

d childre n receive d CaNaj-EDT

A intramuscularl

y a ta dos e o f 2 5 mg/k g a t0 an d 1 2 hours ; urin

e wa s collecte d fo r 2 4 hours . A tChildren' s Hospita

l Medica l Center, 4 6 childre

n i n th e outpatien

tclinic receive

d CaNaj-EDT

A intramuscularl

y wit h procain e a ta dos e o r 5 0 mg/kg : urin e wa s collecte d fo r 6 t o 7 hours . Despit

e thes e differences, slope

s an d intercep to f regressio n line s wer e remarkabl

y similar : excretio

n rati o make s th e CaNaj-EDT

A provocatio

n tes tindependen

to f bot h th e dos e administere

d an d th e child' s ag e an d bod y weight . Therefore, dat

a coul d b e poole d togethe r i n a singl e regressio n line. Combine

d dat a represent

, t o th e bes to f ou r knowledge, th

e larges tserie s o f CaNaj-EDT

A provocatio

n test s i n children .

a laborator y wher e th e volum e ca n b e measure d with lead-fre e equipmen tan d aliquot s fo r lea d an d creatinin e measurement s ca n b e take n withou tcontaminatin g th e sample . INTERPRETATIO N O F CaNa 2 -EDT A PROVOCATIO N TEST . Th e concentratio n o f

lea d i n th e urin e (i n microgram s pe r milliliter ) i s multiplie d b y th e volum e (i n milliliters) , t o obtai n th e tota l excretio n (i n micrograms) . Th e tota l urinary excretio n o f

lea d (micrograms ) i s divide d b y th e amoun to f

CaNa 2 -EDT A give n (milligrams ) t o obtai n th e "lea d excretio n ratio" :

Lea d excrete d (jig) CaNa 2 -EDT A give n (mg) Th e CaNa 2 -EDT A provocatio n tes ti s considere d positiv e i f th e lea d excretio n rati o exceed s 0.60 . Th e recommendations o f th e author s ar e base d o n thei r experienc e wit h 21 0 provocatio n tests 1 " 1
- 6)2) J (Figure) . Inspectio n o f th e Figure show s tha ta rati o >0.6 0 i s neve r obtaine d i

n 1 2 children wit

h bloo d lea d leve l <3 0 jig/dl , an d i s alway s obtaine d in 1 9 childre n with bloo d lea d leve l >6 0 Mg/dl . A tbloo d lea d leve l 3 0 t o 3 9 ug/dl , th e rati o i s >0.6 0 i n six (11.5% ) o f

5 2 children ; atbloo d lea d leve l 4 0 to 4 9 jjg/d l th e rati o i s >0.6 0 in 2 5 (37.9% ) o f 6 6 children ; and a tblood leve l 5 0 t o 5 9 jxg/d l th e rati o i s >0.6 0 in 3 0 (49.2% ) o f

6 1 children . Itappears , therefore , tha ta rati o <0.6 0 represents a n appropriat

e cutof f poin tt o distinguis h childre n with "markedly increased " excretion . (I ti s no tpossibl e t o defin e a norma

l excretio n rang e becaus e n o dat a ar e availabl e an

d i twoul d b e unethica l t o obtai n the m in childre n wit

h bloo d lea d value s <2 5 Mg/dl . I n addition , even th e lower bloo d lea d level s observe d in childre n from industrialize d countrie s ar e significantl y highe r tha n thos e i n children fro

m remote area s uncontaminate d b y lead , which mos tlikel y representth e trul y norma l bloo d lea d level. 3 4 However , extrapolatio n fro m thes e dat a predicts , a t

3 1

K^-^ ; ^P?%;-A^:^ ^ l^rsSr^'g^Sa-g^e?:"; .P.4 0

bloo d lea d leve l 1 <jg/dl,-an excretio n rati o o f 0.1 , si x time s lowe r than th e propose d cutof f o f 0.60) . ' GUIDELINE S FO

RTREATMEN T BASE D O N CaNa 2 -EDT A PROVOCATIO N TEST . I f

th e lea d excretio n rati o i s >0.70 , a 5-day cours e o f

CaNa 2 -EDT A 100 0 mg/m 2 intramuscu larl y o r intravenousl y shoul d b e given , a s above . If th e lea d excretio n rati o i s betwee n 0.6 0 and 0.69 , (1 ) childre n younge r tha n 3 year s shoul d receiv e treatmen tfo r 3 consecutiv e day s wit h 100 0 mg/m 2 CaNa 2 -EDTA , a s discusse d above ; an d (2 ) i n childre n olde r tha n 3 year s th e tes tshoul d b e repeate d ever y 2 t o 3 month s an d treatmen t starte d i f th e lea d excretio n rati o increase s t o >0.7 0 (i n whic h cas e treatmen tshal l consis to f 3 day s wit

h 100 0 mg/m 2 CaNa 2 -EDTA , a s above) . I n childre n wh o hav e receive d chelatio n therapy , re peate d cycle s ar e indicate d i f th e bloo d lea d concentratio n rebound s t o withi n 5 /Jg/d l o f th e origina l value , 7 t o 1 0 day s afte r treatment . I n al l children , regardles s o f age , with elevate d bloo d lea d and E P value s bu twit h a n excretio n rati o <0.60 , bloo d lea d an d E P shoul d b e monitore d frequently . If th e elevatio n o f

bloo d lea d value s persists , th e CaNa 2 -EDT A provocatio n tes tshoul d b e repeate d periodicall y (ever y 2 t o 3 months) . IMMEDIAT E TREATMEN T FOLLOW-U P Th e goa l o f

chelatio n therap y i s t o permanentl y reduc e th e bloo d lea d leve l t o <2 5 /ig/d l an d tha to f EP t o <3 5 iig/dl . T o achiev e thi s goa l i tma y b e necessary to giv e severa l course s o f

treatment . I tcanno tb e overemphasized , however , tha trepeate d course s o f therap y are counterpro ductiv e unles s th e sourc e o f lea d ha s bee n identifie d an d eradicated . Childre n receivin g chelatio n therap y shoul d no tb e release d fro m th e hospita l unti l al l lea d hazard s in thei r home s an d elsewher e hav e bee n controlle d an d eliminate d and , i f

necessary , suitabl e alternativ e housin g ha s bee n arranged . Wit h vigorou s publi c health measure s complet e an d saf

e abatemen tshoul d b e achieve d durin g th e treatmen tperiod. ' I f a chil d with elevate d bloo d lea d concentratio n canno tb e move d t o ne w hpusing , multipl e repeate d course s o f

CaNa 2 -EDT A i n a clinicall y asymp tomati c chil d with stabl e bloo d lea d value s ma y b e coun terproductive ; parent s ma y despai r a tth e ineffectivenes s o f therap y an d fai l t o return t o th e clinic . Iti s mor e importan t in thes e unfortunat e situation s t o maintai n follow-u p s o tha ta ris e i n bloo d lea d concentration s i s detecte d prompt ly . A tth e en d o f

eac h treatmen tcycl e th e bloo d lea d concentratio n usuall y decline s t o value s <2 5 /.g/dl . How ever , withi n a fe w day s reequilibratio n take s plac e an d results i n a rebound ; thu s th e bloo d lea d leve l mus tb e rechecke d 7 t o 1 0 day s afte r th e en d o f treatment . If th e blood lea d level rebounds t o withi n 5 i-g/d l o f th e valu e befor

e th e las tcycle , additiona l treatmen tcycle s are indicate d (unles s th e concentratio n afte r reboun d i s <2 5 jig/dl) . A blood lea d concentratio n tha trebound s t o abov e th e pretreatmentvalu e i s evidenc e o f renewe d and exces siv e intake . If th e blood lea

d level remains low , it s measuremen t mus tb e repeated , initiall y biweekly , the n atmonthl y intervals , t o assur e tha tth e decrease d leve l i s permanent . Iron deficiency states , whic h ma y accompan y lea d poisoning , requir

e therapeuti c dose s o f

iron i n additio n to th e correctio n o f

othe r possibl e nutritiona l deficiencies . LONG-TER M CLINICA L FOLLOW-U P AN D MANAGEMEN T Th e vas tmajorit

y o f children wit

h lea d poisonin g no

w referred t o pediatrician s fro m screenin g clinic s are asymp tomatic . Acute lea d encephalopath y i s rare . Lead poison in g (wit h o r withou tclinica l symptoms ) shoul d b e re ported to th e local healt h authorities , wh o usuall y hav e prime responsibilit

y for environmenta

l investigatio n an

d abatemen to f

lea d hazard s in th e hom e o r elsewhere . Becaus e lea

d has bee

n widely disseminate d into th e environment , thereb y providing multipl e opportunitie s for repeate d overexposure , lead poisonin g shoul d b e manage d a s a chroni c disorder . A tea m approac

h involvin g publi c healt h personnel , pediatrician , pediatri c nurs e practitioner , an d social worke

r i s likel y t o b e th e mos teffective . Commonl y thi s ca

n b e accomplishe d bes ti f childre n wit

h lea d poisonin g ar

e referred for long-term follow-u p t o a special clini c wher

e al l phase s o f

clinical managemen tcan b e coordinate d an

d continuit

y o f car e i s maintained . A tth e outset , a long-ter m pla n o f managemen ti s developed . Age , th e intensit y o f hand-to-mout

h activity , pica , die tmodification , environmenta l exposure , an d serial laborator y dat a ar c taken int

o account . Th e objective s ar e t o reduce th e bod

y burde n o f lead and t o preventrecur rences . Al l preschool-age d housemate s o f inde x case s shoul d b e examined . Al l case s shoul d b e reporte d to socia l servic e fo r assistanc e in obtainin g saf e housing . Extende d follow-u p to a

tleas t6 years o f

ag e i s usuall y necessary . Identificatio n o f

lea d sourcefs) . I

n al l cases , firstpriorit

y i s give n to identificatio n o f importantsource s o f

exces s lea d in th e child' s environmentan d promp tseparatio n o f th e chil d therefrom. * A thoroug h histor y ca n facilitat e th e identificatio n an

d abatemen to f

th e mos timportant source s o

f lead . Althoug h thi s crucial par to f therap y (abatement ) i s usuall y performed b y health departmen t personnel , no

tuncommonl y informatio n obtaine d i n th e clini c provides clue s t o unsuspecte d sources . Th e environ menta l histor

y obtaine d in th e clini c shoul d includ e a lis to f al l dwelling s currentl y or recentl y visite d b y th e chil d 3 2

aatSSttr^.:'^

^Si^^^^^^3^T. A £%vv v -?:^ r *3i^^*^>> ^ >-„&> ? Ci'Ci'A V- ;P.4 1

(primar y residence , home s o f relative s an d bab y sitters , schools , daycar e centers ) an d evaluatio n o f eac h building' s ag e an d stat e o f

repair . I n th e Unite d State s a hig h proportio n o f

building s constructe d prio r t o 196 0 hav e lead-bearin g paint s an d putty o n both exterio r and interio r area s accessibl e t o th e child . Structure s in poo r repai r ofte n hav e lead-containin g chip s o r pulverize d fragment s in th e househol d dust . Pla y areas , especiall y urban playground s nea r vehicula r traffic , dir tplayground s an d dir tyards , painte d meta l fence s an d walls , an d vacan tlot s formerly containin g lead-painte d structure s shoul d b e identifie d a s potentia l lea d sources . Occupationa l historie s for al l adult s i n variou s dwelling s shoul d b e ascertaine d t o lear n i f an y ar e workin g i n lead-relate d industries . Lea d trade s include , bu tar e no tlimite d to , secondar y lea d smeltin g (recovery o f lea d from ol d storag e batteries) , lea d scra p smelting , storag e batter y manufacturin g an d repair , meta l founding , shi p breaking , automobil e assembl y an d bod y an d radiato r repair , demolitio n o f

painte d meta l structure s (suc h a s bridges) , an d demolitio n an d renovatio n o f ol d house s an d othe r structures . Adult s wh o work i n lea d industrie s mus t showe r befor e comin g hom e an d mus tleav e al l wor k clothes , includin g shoes , a tth e work place ; thes e clothe s mus tno tb e cleane d o r washe d a thome . Thu s lead-bearin g dus tfro m th e plac e o f

employmen twil l no tcontaminat e th e house . Additiona l source s ma y includ e ol d lead-painte d crib s an d bed s an d th e burnin g o f lead-painte d woo d i n wood-burnin g stoves . Proximit y t o lea d smelters , ingestio n o f lead-containin g dust , an d inhalatio n o f lea d fro m th e combustio n o f

gasolin e contribut e t o th e overal l body burde n o f

lea d i n children , bu tth e hig h concentratio n o f lea d tha tultimatel y result s i n clinica l lea d poisonin g i s mos tfrequentl y associate d with ingestio n o f lead-bearin g paint . Uncommo n cause s o f poisonin g includ e ingestio n an d retentio n i n th e stomac h o f metalli c lea d (fishin g weights , curtai n weights , shot , jewelr y painte d with lea d t o simulat e pearl) , contaminatio n o f acidi c food s an d bever age s from improperl y lead-glaze d cerami c pitchers , pots , an d cup s an d from opene d lead-soldere d food cans , and th e hom e burnin g o f

batter y casings . Inhalatio n o f fume s (sniffing ) from smal l leaded-gasolin e container s ha s occurre d i n olde r children . Poisonin g ha s als o bee n trace d t o orienta l cosmetic s (surma , a blac k eyeline r containin g u p t o 85 % lead ) an d t o Mexica n an d Oriental folk remedie s (azarcon , greta , paylooah) . Medica l managemen tdurin g abatemen to f lea d paint hazards . I f

th e sourc e o f

lea d i s limite d t o suc h item s a s retentio n o f

a metalli c lea d objec ti n th e stomac h or a n improperl y lead-glaze d foo d o r beverag e container , th e chil d ca n b e promptl y separate d fro m th e source . Suc h i s no tth e cas e whe n lea d pain ti n th e hom e i s th e principal source . Severa l method s ar e use d t o remov e ol d lead-base d pain tfro m wall s an

d woodwork . Som e methods , particu larl y remova

l b y burning and sanding , greatl y increas e th e amoun to f

ai r and dustborn e lea d i n th e home . Very fine lead-bearin g particulate s settl e ou tslowl y ove r man y hour s afte r burning an

d sandin g i s 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, an d shoul d no tretur

n unti l remova

l o f al l lead-bearin g pain t ha s bee n complete d an

d th e dwellin g has been thoroughl y vacuume d an

d scrubbed wit

h high-phosphate-detergen t solutions . Th e source s thathav e bee n denude d durin g th e abatemen tproces s shoul d b e repainte d t o sea l an y residua l lea d behin d th e surface . Childre n shoul d b e remove d fro m th e hom e during abatemen twhethe r o r no tthe y hav e increase d lea

d absorption . Whe n thi s procedure i s no t followed , i ti s notuncommon t o observe 3 0 t o 5 0 pg/d l increments in whol e bloo d lea d concentratio n withi n a matte r o f a fe w day s o r weeks . Long-rang e dus

tcontrol . It

must be understood

that dust control is not a substitute for

abatement. I

n area s heavil y contaminate d wit h lead , such a s deterioratin g ol d housin g and dwelling s adjacen tt o lead-emittin g industria l plant s o r heav

y vehicula r traffic , i tma y b e helpfu l t o institut e a regula

r progra m i n an d abou tth e hom e to contro l lead-bearin g dust , whic h constantl y reaccumulates . Becaus e hand-to-mout

h activity i s commo n in youn g children , parent

s mus tinstitut e a specifi c typ e o f cleanin g program ; vacuumin g an

d wetcleanin g ar

e recommended . Sweepin g wit

h a broom , althoug h i tma y remov e larg e fragments , serves onl y to sti r u p smalle r particulates . I ti s recommende d tha tal l floors an d woodwor k b e scrubbe d weekl y wit

h high-phosphate detergent s suc h a s Tid e o r Spi c an d Span . Fo

r al l surface s tha tth e chil d ca n touch , th e weekl y scrubbin g shoul d b e supplemente d wit h dail y dam p dustin g wit

h a cloth rinsed in a solutio n o f high phosphate detergent . Althoug h suc h cleanin g program s ma y b e helpful , th e definitive wa y to preven

trecurrence s i s for affecte d children an d thei r familie s to mov e int o housin g fre

e o f lead pain

thazards . Dietary factors . Althoug h reductio n in exposur e t o environmenta

l lea d mus treceiv e firstpriority , step s shoul d b e take n to identif

y an d correctdeficientdietar y intake , particularl y o

f calcium 25
- " and iron a s wel l a s excessiv e dietar y fat , eac

h o f whic h ma y increas e th e absorptio n and retentio n o f

lead . A die tadequate i

n mineral s an d limite d i n fa tshoul d b e assured . For thos e intoleran to f .co w milk , lactose-fre e mil

k product s such a s yogurtor som e alterna tiv e sourc e ar

e necessar

y t o ensure adequat e calciu m intake . Th e us e o f

low-fatmilk an

d th e avoidanc e o f

fried food s shoul d limi texcessiv e dietar y fat . .Acidi c food s suc h a s fruits , fruitjuices , tomatoes , sodas , an d col a drink s may 33

y , i »y.'iy % »w * T» i ^t'^-f*>>'g.g« » -J" ^ » - S*ISVTT
. .LV,':*. T?**r *-•••• 1-- ,leac h lea d fro m can s wit

h leaded-soldere d seams . Dietar y lea d intak e ma y b e reduce d i f th e abov e item s ar e purchase d fresh , frozen , o r package d i n aluminum , glass , cardboard , o r plasti c containers . Neurobehavioral considerations . A majo r problem i s presente d by th e hig h leve l o f hand-to-mout h activit y o f man y preschool-age d children . If hand-to-mout h activit y o r pic a (ingestio n o f

nonfoo d items ) i s particularl y severe , a behaviora l psychologis tca n b e helpfu l i n developin g a program t o reduc e th e activity . Fo r childre n give n an y combinatio n o f chelatin g agents , neurologi c an d psychologi c assessmen tshoul d b e obtaine d a tth e tim e o f

initia l diagnosi s an d durin g th e followin g years . Thi s wil l facilitat e appropriat e schoo l placemen tfor childre n with learnin g handicaps , i f the y ar e identifie d throug h thoroug h psychometri c evaluatio n prio r t o th e child' s entr y int o th e schoo l system . Fo r th e chil d wh o ha s had acut e lea d encephalopathy , long-ter m anticonvulsan t therap y wit

h phenytoi n (o r phenobarbital ) i s indicate d i f ther e wer e seizure s o r com a durin g th e encephalopathi c episode . Additiona l clinica l an d laborator y evaluatio n may b e indicate d t o detec tothe r sequela e o f chroni c lea d poisoning , suc h a s rena l impairment . Metaboli c disorder s associate d with acut e lea d poisonin g ar e reversibl e afte r chelatio n therap y an d substantia l reductio n o f lea d expo sure . Frequency o f

follow-up . Whe n th e result s o f initia l venou s bloo d lea d an d E P value s an d CaNa2-EDT A testin g indicat e th e nee d fo r chelatio n therapy , long-ter m follow-u p i s indicated . Fo r thos e childre n wh o hav e no t receive d chelatio n therapy , follow-u p a t3-mont h intervals , togethe r wit

h abatemen tan d dus tcontro l in th e hom e and correctio n o f

dietar y deficiencies , shoul d b e continue d unti l th e chil d ha s maintaine d normal bloo d lea d an d EP value s fo r 1 year . Thos e childre n wh o initiall y receive d a cours e o f chela tio n therap y requir e mor e intensiv e follow-up . Abatemen t o f environmenta l lea d hazard s i n th e hom e i s rarel y accomplishe d withi n a matte r o f a few days , s o tha ta s a genera l rul e th e firstcours e o f chelatio n therap y i s give n in th e hospital . Outpatien tchelatio n therap y whil e a chil d i s stil l overexpose d t o lea d i s counterproductiv e an d likel y t o b e associate d with enhance d absorptio n an d retentio n o f lead . I n childre n wh o hav e receive d a cours e o f chelatio n therapy , bloo d lea d an d E P determination s shoul d b e repeate d 5 to 7 day s afte r therap y an d the n afte r anothe r 1 t o 4 weeks , dependin g o n th e progress . I f som e improve men ti s observed , follow-u p may b e schedule d at2 - t o 4-wee k interval s for 6 months . Thereafter , bloo d lea d an d E P test s shoul d b e repeate d a t3-month interval s unti l th e chil d i s 6 year s o f

age . A teac h visi tth e environmenta l an d housin g situation s ar e update d an d reevaluate d an d dus t contro l and dietar e reviewed . If

seria l blood lea d and E P dat a sho w continue d improvement , i tma y b e assume d tha t ne w assimilatio n o f

ne w lea d i s notoccurring ; risin g bloo d lea d concentrations , which ma y b e followed by a risin g EP level , indicate increase d ingestio n o f lead . Often , reinvesti gatio n reveal s ne

w source s o f

environmenta

l lea d not previousl y detected . Whe n a chil d wit h earlie r elevate d bloo d lead concentration s approache s schoo l age , psycho metri c evaluatio n ma

y b e indicated , even though th e bloo d lea d concentratio n atth e tim e i s <2 5 pg/dl . Summary . Increase d body lea d burde n mus tb e manage d a s a chroni c disorder . Th e final evaluatio n and dispositio n o f eac h cas e mus ttak e int o accoun tth e entire prio r record . I ti s pruden

tto observ e mentall y or developmentall y handicappe d children wit h persisten tpic

a durin g schoo l years , becaus e recurrence s afte r th e ag e o f 6 year s are mos t likel y t o occu r i

n thes e children . Th e need t o remov e infants , youn g children , and pregnantwome n fro m a hom e durin g abatemen to f

lea d pain thazard s i s crucia l t o preventacute episode s o f sharpl y increased lead toxicity . W e than k Ms . Barbar a Cirella , P.N.P. , fo

r performin

g th e CaNa-EDT

A provocatio

n studies , an

d Ms . Caro l Seama n fo r statistica l analysi s o f th e data ; Dr . Morr i E . Markowitz

. an d th e CR C staf f a tAlber tEinstei n Colleg e o f Medicine : Ms. Barbar

a Mahan , an d th e nursin g staf f i n th e Pediatri c Lea d Clini c a t Children' s Hospital : an

d Ms. Victori

a Sadof f fo r carefu l an d painstakin g assistanc e wit h preparatio

n o f th e manuscript

. REFERENCE S 1. Chisol m J J Jr: Th e us e o f chelatin g agent s i n th e treatmen to f acut e an d chroni c lea d intoxicatio

n i n childhood

. J PEDIAT R 73:1 , 1968. 2 . Markowit

z ME. Rose

n JF : Assessmen

to f lea d store s i n children : Validatio

n o f a n 8-hou r CaNa

2 -EDT A provocatio

n test. J PEDIAT

R104:337. 1984 . 3 . Chisol m J J Jr , Mellit s ED . Barret

tMB : Interrelationshi

p amon g bloo d lea d concentration

, quantitativ

e dail y ALA-U an d urinar y lea d outpu tfollowin g calciu m EDTA. In Nordber g GF . editor : Effect

s an d dose-respons

e relationshi

p o f toxi c metals. Amsterdam

, 1976. Elsevie

r Scientific. 4 . Chisol m J J Jr , Barltro p D : Recognitio

n an d managemen

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