P.1 

OAR Box 1126 

Prepped by Ollie Stewart 

Document Number: 

122)11-1-336 

Docket Number: 

A-83-22 

Printed 4/18/2008 9:58:26 AM Sheet 122 of 182 
Psycho-Social 

Factors, Lead 

Exposure, 

___andI 9 

•AMM^^^: :•.'•••-J' 

•-.-••:. ;!;.--.<v.-; .'•„ •.••• 

The history of research on lead is instructive. The effects of lead 

encephalopathy on mental retardation and deficits in motor function have 

been known for centuries. The amount of ambient lead in the 

environment increased sharply with the advent of the Industrial 

Revolution in the nineteenth century, so that now the average blood lead 

level considered acceptable in a highly industrialized nation like the U.S. 

may be up to 30 M-gMl (U.S. Environmental Protection Agency (EPA), 

1986). This is seven times as high as average blood lead levels in Nepal, an 

acculturated but nonindustrialized, society (Piomelli et al., 1980). 

Nevertheless, concern over asymptomatic lead exposure without the 

signs of encephalopathy began only about 50 years ago, when the 

sociopolitical climate set the stage for concern about overpopulation, 

abuse of natural resources, and environmental poUution. Lead then 

became the prototype for research on many environmental poUutants. 

Research emphasis focused on adverse health effects, that is, lead toxicity 

on organ systems of the body. Experimental prospective research was 

perforce done primarily on laboratory animals. Human research focused 

on medically oriented epidemiological studies that attempted to locate 

sources of exposure, at-risk populations, and environmental ecological 

conditions that could be used to set standards for public policy. The main 

question addressed by this research was finding the threshold level of lead 

1

 Now at the Nisonger Center, Ohio State University. 

1

 Now at Chapel HUI Pediatrics PA., North Carolina. 

Acknowledgements. We wish to acknowledge NIEHS Grant #flMt EPA Grant 

CR809992-01-9; USPHS Grant ""HI"" to the Child Development Research Institute; 

•B^tf-MPaa-n-prt^^Wn the Division for Disorders of Development and Learning, where the 

children were evaluated. Thanks are also due to the Department of Pediatrics, North 

Carolina Memorial Hospital and the Health Effects Research Laboratories of the 

Environmental Protection Agency for their countless examples of support and collaboration 

in these projects. 

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S3 To«IC SUBSTANCES 

burden in the body that signals an unacceptable risk for retardation of 

cognitive and adaptive behavior, as measured by intelligence tests, and for 

minimal brain dysfunction (MBD), as exemplified by hyperactivity, 

attention deficit disorders, fine motor skills, reaction time, etc. 

LEAD EXPOSURE LEVELS 

A vast body of clinical, epidemiological, and experimental data has 

accumulated over recent decades to show that young children, particularly 

preschoolers, are most at risk for the adverse effects of lead (National 

Academy of Sciences (NAS), 1980; U.S. EPA, 1986). The basis for this 

risk-effect relationship has its genesis in both the physiological status of 

the developing child and the relationship of the child to a given exposure 

setting. Young children, as developing organisms, have metabolic 

characteristics quite distinct from the adult human and these differences 

are such that they augur a deleterious outcome when a general toxicant 

such as lead is introduced into the picture. For example, children have an 

incompletely developed blood-brain barrier to movement of lead to the 

central nervous system. Secondly, demands of rapid growth require 

nutrient assimilation rates that often result in deficiencies in these factors, 

one result of which is that lead absorption and/or retention is enhanced 

(Mahaffey & Michaelson, 1980; NAS, 1976; NAS, 1980; U.S. EPA, 1986). 

Children are also fundamentally distinct from adults with respect to 

exposure status. First, children assimilate lead in food and water at a 

higher rate than do adults on a body-weight or surface-area basis (NAS, 

1980), absorb a greater fraction of the ingested element, and retain a 

greater portion of the absorbed amount (Alexander, Delves, & Clayton, 

1972; Ziegler, Edwards, Jensen, Mahaffey, & Fomon, 1978). Secondly, in 

crawling babies the ingestion of nonfood items, such as lead contaminated 

dust and soil, normally occurs as part of nonnal behavior such as 

mouthing activity. In older children who frequently engage in rough-andtumble outdoor play, lead in dust or soil is transferred to their hands and 

to food they hold in their hands, and is thus eventuaUy ingested. In a 

setting where there is significant contamination of dust and soil, this route 

may dominate the dietary pathways (National Academy of Sciences, 1976, 

1980). 

From a historical perspective, it is quite clear that the acceptable level 

of exposure of children to lead and our understanding of the nature of the 

adverse effects engendered have been undergoing constant change. With 

respect to exposure, concern has shifted from such evidence of internal (or 

systemic) exposure as blood lead values of 60 ug/dl and higher to values 

considerably below this. In its 1978 statement on lead poisoning in young 

chUdren (U.S. Centers for Disease Control (CDC), 1978), and directed to 

PSYCHO-SOCIAL FACTOOS «9 

. ^TM~ -^~,i»f«»d various risk categories, 

the pediatric community, the CDC artocu utea - , bloo d fead when 

predicated upon an initial action level oi * i*» d agai n t o 25 

Ireatment should begin. ^^tog^ J | rotectio n 

Ug/dl (U.S. CDC, 1985). Similar y the U&**TM> base d o n 

Agency established an ambient -'"JXo f ead expos e in chUdren, 

what the agency took to be acceptable levels oi ie- r 

which were below the older value of 60 W^1: { ^ , constitutes 

The compelling rationale behind a rethinkingM* wlui ^ 

society acceptable levels of P^ « ^^tiat o concern 

constellation of subclinical or more *"*'%X ^ exposure levels, on 

have been the effects of lead, reported at rather ^P ° rf hera l 

heme biosynthesis, erythropoiesis, and botn

 c " \ 1980- NAS, 

nervous system functions (Moore, Mered.th * Gold ~[£TM^ ' " & 

1980; Needleman U Landrigan, 1981; Piomelli, »*J X 

Davidow, 1982; U.S. EPA, 1977). It is the issue of lead neurotoxicity at low 

levels of exposure that is the central focus

 ol fu

^

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r '^T L r w m S 

In the update of the EPA document Air QM'\CntTMt Z»So*c 

EPA. 1986), we reviewed 20 of the best known stud.*i o the-eurotox* 

effects of low levels of lead exposure where the <*^ **£**££*£ 

symptoms of lead encephalopathy. Table 1 shows some of the weaknesses 

and/or inconsistencies of these studies: „«^»«, „f iMd 

1. WhUe several studies show statistically significant effects of lead 

exposure on IQ test performance, the group effects are usuaUy smaU that 

is/less than 6 IQ points, which is near the standard error for *ese tarts. 

(ClinicaUy significant IQ effects would be nearer to 15 IQ PTM*-*«• * 

one standard deviation.) The IQ test, like other standardized V>V*TM*TM 

performance tests (fine motor, reaction time, perceptual-motor * W ^ 

be too blunt an instrument to reliably tap subtle neurobehavioral effects ot 

moderate lead exposure. . . 

2 Only a few studies used a standardized rating scale tor 

hyperactivity. However, few significant effects of asymptomatic lead 

exposure were found. Our group also found no effect on chUdren age 

12-72 months. (MUar, Schroeder, Mushak, & Boone, 1981.) 

3. Neurological examinations yielded few lead effects below 40 »ig/dl. 

Apparently, more sensitive neurometric measures are needed. Our group 

(Otto, Benignus, MuUer, & Barton, 1981) demonstrated significant 

amplitude changes in slow wave potentials of children aged 12-47

 m°TMTML 

with 6-59 (ig/dl, whUe this effect did not appear in older chUdren (48-/5 

mos.). . . . . 

4. No study has evaluated children's intelligent or social behavior 

based on a theoretical hypothesis as to the nature of the cognitive, 

attentions, and perceptual-motor deficits that have often been found on 

IQ tests and attention deficit questionnaires. 
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TABLE 1 

Summary of Studies on Neurobehavioral Functions of Lead-Exposed Children* 

..,„,.. 

Population 

•tudted N^povxp 

Clink-type Stadia of Cfeildrca with Hijb Lead Level* 

delaBurdeand 

Cham (1972) 

d« to Buidt and 

Rummo (1974); 

Rummo rl al. 

<1979) 

KttokflTO) 

Inner dty 

^ (Ridunond, VA) 

Follow-up 

urn* subject) 

Inner dry 

(Providence, RI) 

Inner dty 

(New Haven, CT) 

C-7 2 

Pb-70 

C-67 

Pb-70 

C-4 5 

Pb,-15 

Pt»-20 

C-2 5 

Pb-2« 

HfU 

ltstifis,jrr 

(range! 

4.0 

4.0 

7-8 

7-< 

3.8(4-8) 

5.6 

5.6 

2.7(1.1-8.3) 

2.8(1.0-5.1) 

Blood had, 

W/dl 

(range oe ± S.D.I 

r 

58O0-100)-

PbT-lHi^/1 

2Q2|ig/g 

D(»8 ) 

61(17) 

M(»13) 

88(x41) 

38(30-55) 

81 (58-137) 

rtychooietric 

tcsti employed 

IQ (StanfordBinet) 

Rnc motor 

Crou motor 

Concept formation 

Behavior profile 

WBC Full Stale 

IQ 

VettallQ 

Performance IQ 

Bender.Ge--.talt 

Reading 

Spelling 

Arithmetic 

Goodenough-Harria draw teat 

Auditory vocal aaaoc. 

Tactile recognition 

Behavior profile 

McCarthy Scale!: 

Gen. cognitive 

Verbal 

Perceptual 

Quantitative 

Memory 

Motor 

Parent rating! 

Neurologic event 

Denver Developmental: 

Grau motor 

Fine motor 

Language 

Score: 

% aubnonnal: 

Score 

% aubnonnal:' 

C 

93 

46 

48 

45 

47 

52 

8 

Norm 

1.00 

1.00-

1.00-

7/12 

Sunmary of multa 

C 

94 

26 

7 

10 

10 

27 

7 

11 

13 

3 

3 

Pb, 

94 

49 

44 

46 

52 

10 

meaauree alg 

C 

1.02 

.82 

.82 

Pb 

89 

45 

16 

15 

30 

87 

49 

12 

16 

31 

15 

25 

88 

41 

43 

50 

10 

differen 

Pb 

1.06 

.81" 

.73-

Pb. 

77 

35 

36 

IS 

level, of 

aignlficance'-' 

<.05 

N.S. 

N.S. 

<01 

.01 

N.S. 

.01 

N.S. 

N.S. 

N.S. 

.01 

.05 

.001 

<01 

<05 

<01 

N.S. 

•<.01 

•<.01 

%.&'. 

wi<yr 

vVftft'j 

•R*'-

•&r 

!S5!H.i 

a??Jt"r. :'-• m 

- - T.a^aft-a.a 

•a.-:1*:JlS.-! 

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TABLE 1 

Summary of Studies on Neurobehavioral Functions of Uad-Exposed Children* (Continued) 

Summary of multa 

Reference 

Ko-ok.i.l 

(1977) 

Population 

atudied 

Inner city 

(Rochciter, NY) 

Wfmf 

C-3 6 

Pb-31 

Age at 

teeting,yr 

(range) 

3.6(1.9-5.6) 

3.611.7-5.4) 

Blood Uad, 

(range or ± S.D.) 

28(11-40) 

80(61-200) 

Ptychometn-c 

teeu employed 

IQ Equivalent: 

Social 

Spatial 

Spoken vocal 

ln to-cooiprehcnaion 

Visual attention 

Auditory memory 

Sinelt----r Area Studiee 

Landriganetal. 

(1975) 

McNeil etal. 

(1975) 

Dateline (1977) 

Smelter area 

(El Paao. TX) 

Smelter area 

(El Paao, TX) 

Smelter atea 

(Mar-cheater. UK) 

C-78 

Pb-46 

a-" 3 7 ! (1.8-18) 

Pb-101 91 

<40 WISC Full Scale IQ1 

40-68 WPPS1 Full Scale IQ* 

WISC + WPPSI Combined 

WISC * WPPSI Subecalea 

Mod.Fb-23 

HiPb-24 

4.7(4.1-5.6) 

4.8(4.2-5.4) 

29(14-39) 

58(4043) 

28(18-35) 

44(36-64) 

Neurologic tearing 

McCarthy General 

Cognitnre 

WISC-W AE Full Scale IQ 

Oaeretaky Motor Level 

California Pertonality 

Frootig Perceptual 

Quotient 

Finger-Thumb Appoeition 

Griffith! Mental Dev. 

Froatig Viaual Perception 

PegboardTcat 

Dominant hand 

Nondominant hand 

93 

ICC 

C 

93 

91 

93 

90 

93 

Pb 

89 

86 

88 

C > Pb on 13/14 acalea 

7/14 Kale! aig 

C > Pb on 

1/8 teiti aig. 

C 

82 

89 

101 

. different 

7/8 teata 

different 

Pb 

81 

87 

97 

C > Pb, 6/10 itctne 

100 

27 

Mod. 

108 

14.3 

17.5 

19.5 

103 

29 

High 

102 

11.8 

17.3 

19.8 

Levelaof 

aignifi-

>.10 

<.!0 

>.10 

>.10 

>.10 

>.10 

N.S. 

N.S. 

N.S. 

N.S. 

N.S. 

•e0.05 

N.S. 

N.S. 

N.S. 

N.S. 

N.S. 

N.S. 
P.5 

TABLE 1 

Summary of Studies on Neurobehavioral Functions of Lead-Exposed Children* (Continued) 

(range) 

Blood lead, 

pg/dl 

(rangtor tS.D.) 

Wlnnckt, Hrdina. Stnettcrarca 

4 Bnxkhaus (Durjberg, FRC) 

(1982) 

Per-ino and Inner Qty LowPb-50 

Emhart (197<)" (New York, KY) Mod.Fb-30 

FbT-2.4ppm* German WBC Full Scale 

PbT-9.2ppm Verbal IQ 

No PbB PerfonnancelQ 

Bender Gettalt Teat 

Standard Neurological Testa 

Conner* Teacher Rating! 

Follow-up »J 

subjccti 

General Population Studio 

Needleman et al. Urban 

(1979)- (Boston, MA) 

LowPb-31 

Mod.Pb-32 

10-30 

40-70 

21 (*4) 

32(*3) 

PbT^lOppm1' 

> 20 ppm 

McCarthy Scaler 

Gen. cognitive 

Verbal 

Perceptual 

Quantitative 

McCarthy Scaler 

Gen. cognitive 

Verbal 

Perceptual 

Quantitative 

Reading teets 

Conner* teacher ratinga 

Varkw experimental test* 

WBC PuD Scale IQ 

VerballQ 

PerfonnancelQ 

Seashore Rhythm Te*t 

Token Teat 

Sentence Repetition Tett 

Delayed Reaction Tune 

Teacher Rating* 

c 

122 

130 

130 

17.2 

2.7 

? 

Low 

90 

44 

44 

48 

45 

46 

Low 

94 

ts 

43 

43 

44 

49 

Pb 

117 

124 

123 

19.6 

7.2 

? 

Mod. 

80 

39 

37 

44 

42 

42 

Mod. 

82 

41 

40 

38 

39 

46 

Not Reported 

Not Reported 

Not Reported 

106.6 

103.9 

100.7 

21.6 

24.8 

12.6 

102.1 

99.3 

104.9 

19.4 

23.6 

11.3 

C > Pbon3/4 Uodta 

s 

c: • / 

-•wB>W*»v -

Summaiy 

TABLE 1 

of Studies on Neurobehavioral Functions of Lead-Exposed 

Population 

•tudled 

Age at 

teettafryr 

(range) 

^ 4 1 

n o r ±S.D.) 

McBrideetal. 

(1982) 

Yule et al. 

(1981) 

Yule etal. 

(19M) 

Urt»nfeuburban Low ft - >100 

(Sydney, Australia) Mod. Pb - >10O 

Urban 

(London, UK) 

Group 1 - 34 

Group I-* 8 

Group 3-4 9 

Croup 4-3 5 

2-9 ug/dl 

19-29 g/dl 

8.8* (7-10) 

11.6(11-12) 

14.5 (1V16) 

1M(1M » 

Same subjecta 

in Yute etal. (1981) 

Yule and Lanadown Urban 

(1963); Yule (London, UK) 

et al. (1983) 

teeta employed 

Children' (Continued) 

Stan-nary of reattlta 

Peabody Picture 

Vocab. Tett 

Rne Motor Tracking 

Pegboard 

Tapping Te*t 

Beam Walk 

Standing Balance 

Rutter Activity Scale 

W1SC-R Pun Scale IQ 

Verbal IQ 

Performance IQ 

Vernon Spelling Teat 

Vernon Math Tew 

Neale Reading Accuracy* 

Neak Reading Compre.k 

Needleman Teacher 

Ratings 

Conner* Teacher 

Rating* 

Rutter Teacher 

Rating*, including 

•Qwractivtty*'factor 

WBC-RPuD Scale 

Verbal IQ 

Performance IQ 

Neale Reading Accuracy 

Ntilt Reading Comprehension 

Vcmort Spelling 

Vernon Math 

Group: 

Low 

-105 

Mod. 

-104 

C > Pb 1/4 comperiaona 

-20 

-30 

- 5 

-20 

-31 

- 4 

C < Pb IM comperiaona 

-1.9 

1 2 

103 103 

101 101 

106 03 

104 98 

97 97 

121 110 

117 110 

1 2 

1-53 1.34 

-2.1 

3 

96 

9S 

96 

92 

93 

96 

95 

3 

2.4S 

4 

96 

94 

99 

89 

95 

89 

88 

4 

2.63 

N.S. 

-C0.05 

N.S. 

N.S. 

N.S. 

-C0.05 

N.S. 

.007 

.043 

.102 

.001 

N.S. 

.001 

.001 

.096 

(4/11 Hems tig. different) 

.26 .37 

(3/4 factor* aig. at p <.0S) 

(2/26 items tig. at pS-05) 

(5/26 item* differ at .05<p<.10) 

6% 4% 20% 17% 

Low 

107 

104 

108 

Hinh 

105 

103 

106 
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TABLE 1 

Summary of Studies on Neurobehavioral Functions of Lead-Exposed Children" (Continued) 

Population 

studied N/group 

Aje •! 

tating, jr 

(range) 

Blood lead, 

HSM1 

(range or xS.D.) tcata employed Stmutar^ of rcanlta 

Smith etal. 

(1983) 

Urban 

(London, UK) 

HI-155 

Mad-103 

Low-145 

Urban 

(Bim-Jnghim. UK) 

PM>8.0 

PbT-5-3.5 

PbT <2.5 

(All in ug/g) 

SPM-13.1 

ug/dl 

15.5(6-30) 

WBC-RPuB Scale 

Verbal IQ 

PerfonnancelQ 

Word Reading Teat 

Seaahore Rhythm Teat 

Viaual Sequential Memory 

Sentence Memory 

Shepe Copying 

Mathctnaba 

Mean Viaual RT(aea) 

Cmn m Teacher Ratinga 

Britidi Ability Scale. 

Naming 

Recall 

Comprvhenaion 

Recognition 

IQ 

Stanford-Binet Items 

Shape* 

Block* 

Bead* 

Playroom Activity 

Low 

107 

103 

108 

45 

21 

20 

9 

14 

16 

.37 

11 

Med 

105 

103 

106 

42 

20 

19 

9 

14 

15 

.37 

11 

High 

105 

103 

106 

40 

20 

20 

9 

14 

15 

.39 

13 

Smelter area 

(Sto&urg, FRC) 

PbT:6.16ppm» 

PbB: 14.3 ug/dl 

m ii i iiiumiimmtat0mmsH0nmmm 

TABLE 1 

Summary of Studies on Neurobehavioral Functions of Lead-Exposed Children' (Continued) 

Population 

aMdlad 

Age at 

tearing, )T 

trasgel 

Wtnnesaetal. 

(1984) 

Smelter area 

(Nocdenham. FRC) 

• Abbreviation! C-control aubiectl Pb - leed-e.poied eubjecta. N.S. - nonaignificant (p>.05); PbT-tooth lead; WISC - Wecheler Intelligence Scale lor Children; WPPSI - Wechaler 

IWoo l and Prim.TM Scale ol IMeUg-mc RT-ReKtion Tone. ---Sgnltance Wveta .. . tho - found aiu. p-urialing out confounding covamte.JUnn.ty cop»pon>hyrintad. wa . 

TMTeZ ^ -Some with po*,TM ndM^ c finding, .ugg«ting ..*••» rtpoaur, in «« . <X 4M0 *g/dl. -IWn t ofeach^ p .conn, -bord.rt,n«r-.«»p«,- -detam..- 0, 

Tbnonn.1- 'U-d fo. childTM over 5 y« n of «. . X M for childTM und., 5 y» » of .g.. 'Main tneaaur. , » tkntm. tad (PbT). Dm.-tad . -^^-^^W^Mon. . 

•Blood lead level, laken 9-12 month, prior to icing, none .bov. 33 «MI. 'Data not comct-rf lor age. ton.^o^» by Endur, conecrmg te mMhodol-^ prthm . m 

oioou ...o rv * j . di d M MbMnhat. aignificanl difference, between control .nd Pb-opoeed children indicated In Uu two column, to the nght (tee 

Z%r^^!^7^ Z Zt£ £ Z m-hodo^ l prob,TM in e*» r pubbd-d .iuly » connmwd Ignihcn, «* — b«w« „ «udy g^p . indict* 

in U.t two righthand column, for WISC IQ Mat reault. (Me chapter text). 
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106 Toxic SUBSTANCES 

5. Epidemiological studies have not followed up on these children to 

evaluate the cumulative clinical effects of lead exposure or reversibility 

upon removal of lead from his/her home environment. 

6. The long-term clinical neurotoxic effects of moderate lead exposure 

on children's development largely remain to be investigated. 

7. Epidemiological studies that have been done point to the presence 

of a hazard caused by lead and the need for guidelines to regulate 

exposure in the general population. But they are of limited help in 

predicting the outcome of individuals with specific deficits that vary along 

continuous behavioral dimensions interacting with social and developmental factors. 

RESEARCH DIFFICULTIES 

Biological Indices 

In addition to the above, there are some general, pervasive difficulties 

in lead research. The first is the highly controversial issue of the best 

biological index of internal, or systemic, exposure to lead. A growing data 

base dealing with lead toxicokinetics provides some useful guides in 

considering a choice of exposure index. 

Blood lead measurement, to the extent that it can be accurately 

determined in a given laboratory, is dependent for its usefulness on the 

nature of the exposure being sustained by the study population. Lead 

absorbed into the bloodstream is cleared from blood to tissues on the 

order of weeks or several months (Chamberlain, Heard, Little, Newton, 

Wells, & Wiffen, 1978; Rabinowitz, Wetherill, & Kopple, 1977). Hence, it is 

most useful with chronic elevated exposure and less so with episodic 

bouts of lead intake. Measurement of lead in an accessible, accumulating 

matrix such as shed dentition pushes back the exposure period to years, 

but this measure is by its nature retrospective (see Needleman et al., 

1979). One analyzes shed dentition to ascertain whether lead exposure 

occurred, rather dian is occurring. 

Hence, while dentition analysis is more appropriate in defining 

aggregate exposure and its relationship to health measures, it does not 

provide a useful regulatory metric for monitoring lead exposure in real 

time or concurrent lead intake versus change in outcome measure 

assessment. In the absence of available methods for in situ measurement 

of lead in children during their most vulnerable stage of development, the 

best compromise seems to be serial blood lead measurements, for example, 

quarterly. Such serial measurements would, of course, increase the 

reliability of using blood lead as the exposure index because increases in 

f 

s&m 

PSYCHO-SOCIAL FACTORS 107 

chronic exposure would be ascertainable while the occurrence of episodic 

intake of large amounts of lead would be more likely to be captured in 

laboratory analysis with frequent sampling. 

Exposure indicators that directly reflect a biological lesion are also of 

value when taken in tandem with blood lead values (CDC, 1978). At 

present, the indicator of most utility of this type is free erythrocyte 

protoporphyrin (FEP), a heme precursor whose elevation is related more 

to chronic than to episodic exposure. 

Social Factors 

The second chaUenge is a growing understanding of and concern over 

the interrelationships among social factors, lead, and child IQ. 

The contribution of maternal inteUigence to the child's intelligence 

must also be evaluated in carefully controUed studies of lead effects on 

intelligence. Heber (1970) found a high concordance between maternal 

and child inteUigence. A majority of the children with IQs in the retarded 

range have mothers with IQs of less than 80. He also found a decline in IQ 

range for lower socioeconomic status (SES) chUdren with increasing age. 

For mothers with IQs less than 80, the percentage of their children with 

IQs less than 80 increased from 20% for ages under 6 years of age to 90% 

for those over 13. If mothers of lead exposed chUdren have IQs less than 

80, then inteUectual differences previously attributed to lead might also be 

explained by maternal IQ. 

Most studies have attempted to control for possible covariates (Table 

2) such as social class, age, maternal IQ, pica, and parents' attitude toward 

education, but not for the quality of the caregiving environment. 

Studies examining the relationship between socioeconomic status and 

intelligence and academic achievement have yielded mixed results. In a 

meta-analysis of 200 studies relating SES to academic achievement. White 

(1982) found that home atmosphere correlated to a much higher degree 

with academic achievement than any other combination of SES indicators. 

The more important variables were the childrearing practices and 

stimulation of learning at home and school, and not parents' occupation, 

income, or education. In general, SES seems to be a broad but crude 

measure of factors such as caregiving practices, resources, etc., that may 

be better examined individuaUy. 

The Influence of Caregiving 

The results of previous research have suggested that there might be 

deficiencies in the caregiving environment of chUdren who evidence increased 

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108 TOXIC SUISTANCSS 

TABLE 2 

Evaluation of Control of Confounding Variables of the Twenty Major Studies 

on Low to Moderate Blood Lead Levels in ChUdren 

Poaaibla Confounding Variabtee ControUed (Indicated by + 

Blind Home Mai 

SES Age Pica Evil. Envir. Race IQ 

ExposuR 

Hiitoiy 

de la Burde & Choate (1972) 

Kotok(1972) 

Lansdownetal. (1974) 

Perino & Emhart (1974) 

de la Burde & Choate (1975) 

Landrigan etal. (1975) 

McNeil etal. (1975) 

Kotoketal. (1977) 

Ratcliffe (1977) 

Needleman etal. (1979) .. 

Rummoetal. (1979) 

Emhart etal. (1981) 

Yule etal. (1981,1984) 

McBrideetal. (1982) 

Winneke, Hrdina, & 

Brockhaus(1982) 

Haivey etal. (1983) 

Smith etal. (1983) 

Winneke etal. (1983) 

Yule etal. (1983) 

Winneke & Kraemer (1984) 

lead burden (Chatterjee & Gettman, 1972; Lansdown, Sheperd, Clayton, 

Delves, Graham, & Turner, 1974; MilUcan, Lourie, & Layman, 1956; 

Rennert, Weiner, & Madden, 1970; Rummo, Routh, Rummo, & Brown, 

1979). 

Milar, Schroeder, Mushak, Dolcourt, and Grant (1980) compared two 

groups of chUdren, 12-30 months of age and 31-78 months of age, 

showing increased lead burden with a sample of chUdren matched for age, 

sex, and socioeconomic status, but showing no evidence of increased lead 

burden. The quality of the caregiving environment of these children was 

assessed with the Home Observation for Measurement of the Environment (HOME) Inventory developed by CaldweU, Heider, and Kaplan 

(1966) A measure of maternal intelligence was also obtained. For younger 

children in the sample, significant deficits in maternal IQ and quaUty of 

the caregiving environment were associated with increased lead burden. 

Subscales of the HOME Inventory dealing with emotional and verbal 

responsivity of the mother and maternal involvement with the child 

showed significant deficiencies in the caregiving environment of the 

chUdren with increased lead burden. For older chUdren, the HOME 

PsrcHoSociAt FACTOKS 109 

Inventory also showed deficiencies in the caregiving environment with 

increased lead burden, but the differences were statisticaUy not 

significant. 

Research has only recently begun to document the powerful 

influences of the early caregiving environment on subsequent development of the duld. Studies by Bradley and CaldweU (1976a, b) used the 

HOME Inventory to identify factors in the chUd's environment during the 

first two years of life that are related to mental test performance at 36 and 

54 months of age. Two of the subscales of the HOME Inventory that were 

strongly related to later inteUectual development were emotional and 

verbal responsivity of the mother and maternal involvement with the 

child. These are the two subscales identified by Milar et al. (1980) showing 

significant deficiencies in the environment of chUdren with increased lead 

burden. 

Traditionally, the interpretation of the research on lead effects in 

humans has been that increased lead burden directly results in deficits in 

cognitive functioning. However, alternative hypotheses are equaUy 

plausible. First, the results of Milar et al. (1980) suggest the possibility that 

deficits found in chUdren exposed to lead may be a direct result of 

deficiencies in the caregiving environment and may not be related to lead 

at all. The research of Bradley and CaldweU (1976a, b) tends to support 

this conclusion. 

Second, it is possible that deficiencies in the caregiving environment 

are responsible for increased lead burden and that the deficiencies are 

caused by lead. A child in an environment where lead is available would 

be much more Ukely to ingest significant amounts of lead if left 

unsupervised by his/her caregiver. The poor caregiving environment may 

be an antecedent to the lead ingestion, but the neurotoxic effects of lead 

may be responsible for observed deficits in cognitive functioning. This 

situation may be analogous to malnutrition in chUdren. Severe malnutrition can lead to cognitive deficits (Dobbing, 1970), but Cravioto and 

DeUcardie (1972) have also documented that aspects of the caregiving 

environment may place chUdren at risk for malnutrition. 

A third hypothesis is that the caregiving environment and lead 

combine to affect inteUectual development adversely. This would be 

similar to the relationship found by Werner, Honzik, and Smith (1968) 

between perinatal complications and later psychological development. At 

20 months of age IQ differences between chUdren with and without 

perinatal complications were only 5-7 points for chUdren from a favorable 

social background; but for infants living in a low socioeconomic 

environment, the IQ differences ranged from 19-37 points. Apparently, 

perinatal insult and the quaUty of the child's environment both affected 

development. Similarly, even with low lead levels, we might anticipate a 
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combined effect of SES, maternal IQ, the caretaking environment, 

inadequate nutrition, and lead, each of which by itself is not significant, 

but when combined with the others poses a cumulative risk of handicaps 

in the development of cognitive and adaptive behavior. 

THE DEVELOPMENTAL 

PERSPECTIVE 

The epidemiological studies presented earUer on the toxicology of lead 

have been very valuable for dealing with the acute effects of lead 

exposure, but they have been only modestly helpful in addressing its 

chronic effects. A developmental perspective, in addition to defining who 

is at risk, what is wrong, and how the disease can be corrected, also asks 

what the cumulative risks on functioning at a later age are within one's 

ecological context ~and how these adverse effects can be compensated for, 

reversed, or at least minimized. 

Focusing investigative efforts on younger populations has other 

advantages when one considers that possible neurological insult resulting 

from lead takes place within a developmental context. Sameroff and 

Chandler (1975) pointed out that that even serious insults such as anoxia 

and prematurity often have transient effects. If the exposure to lead 

occurred many years before, a robust deficit may not still be present 

because of the reversibility of effects. They also pointed out that the 

severity of effect could be lessened by a favorable home environment. In 

addition, during the first two years of life, brain growth is very rapid and 

the brain is more vulnerable to insult (Dobbing, 1970). The possibUity of 

differential effects of lead dependent on the age at exposure has not been 

carefully investigated. 

The majority of chUdren evaluated in studies investigating possible 

subclinical effects of lead were more than five years old. It has been 

documented (CDC, 1978) that chUdren between 1 and 3 years of age are 

most susceptible to lead poisoning. The subsequent evaluation of chUdren 

two or more years after exposure to lead makes it difficult to 

retrospectively determine the extent and duration of a cluld's lead 

exposure. By studying younger populations of chUdren, the influence of 

uncontroUed and unknown events affecting development is reduced 

because of the recency of the lead exposure. 

By adding the developmental perspective and recognizing the ethical 

Umitations of doing prospective lead studies on chUdren, it seems that 

lead investigators should take a lesson from related fields Uke nutrition. 

Decades of research attempts in nutrition have failed to clarify a causal 

relationship between malnutrition and specific psychological developmental variables in chUdren (Read, 1982). As with malnutrition, it may be 

PSYOCO-SOOAL FACTODS 111 

impossible to isolate the causal effects of lead independent of the social 

conditions in which they occur. Perhaps we should move beyond the 

assumption that there is a direct causal relationship between lead 

exposure, altered brain development, and impaired behavioral functioning and focus instead on: (a) more systematic analysis of the ways in 

which the child's lead exposure, social environment, and early experience 

interact in jointly to influence the course of his psychological development, with more precise assessment of lead exposure and behavioral 

development; (b) a fuller understanding of the mechanisms through 

which lead exposure may affect inteUectual and adaptive behavior 

development; and (c) evaluation of the effectiveness of systematic efforts 

to prevent or reverse the detrimental consequences of early lead exposure. 

This latter strategy has been pursued by studies that have tried to 

evaluate the effects of lead chelation therapy (see Rutter, 1980, for review). 

We took a similar strategy with a longitudinal and cross-sectional study of 

the inteUectual, social, and neurobehavioral development of preschool 

chUdren exposed to low (10-30 (ig/dl) or moderate (30-60 (ig/dl) blood lead 

levels. We asked two questions: (a) Does cross-sectional comparison show 

a significant interaction between age and blood lead levels, between age 

•and type of exposure (occupational vs. nonoccupational), or between age 

and the important behavior covariates of lead exposure (socioeconomic 

status, maternal IQ, and quaUty of the caregiving environment); and (b) 

, Upon regular five-year reevaluations, is there a change in these children's 

inteUectual, social, and neurobehavioral developnesnt that can be related 

to current blood levels or to cumulative previous Wood lead levels after 

removal of lead from their home environments? 

GENERAL METHODOLOGY 

Populations Sampled 

Several sources were utilized to recruit subjects for this project. These 

sources included: (a) referrals from the statewide Early and Periodic 

Screening, Diagnosis, and Treatment (EPSDT) Program; (b) referrals from 

local lead screening programs in Wake, Lencor, and New Hanover 

counties, and (c) direct recruitment of chUdren from, families employed or 

residing near lead-related industries. Direct contact, recruitment, and 

scheduling of subjects were done by the Patient Coordinator through local 

or county health departments under the aegis of the North Carolina 

Statewide Lead Screening Advisory Committee. A. description was sent to 

all county health departments to inform them, of the objectives and 

resources of the research project and to encourags referrals as new cases 
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112 Toxic SUBSTANCES 

of elevated PbB levels are discovered. Descriptions of recruitment sources 

foUow. 

EPSDT Program 

The North Carolina EPSDT Progam, implemented under Title XIX of 

the Social Security Act (Medicaid Law), provided general medical 

screening for lower income families. AU Medicaid eligible familes were 

informed that screening is avaUable, but participation in the EPSDT 

program was voluntary. Screening was performed by county health 

departments and local well-baby clinics. One component of the screening 

program was a lead poisoning test performed between 12 and 60 months of 

age. This test determined the free erythrocyte protoporphyrin (FEP) level 

using a hematofluorimeter and capillary blood sample (fingerprick). If the 

level of FEP, a measure of heme synthesis, was greater than 50 p-g/dl, a 

venipuncture blood sample was drawn and sent to the North Carolina 

Division of Health Services (NCDHS) for blood lead analysis. If the PbB 

levels were > 50 ug/dl, chUdren were referred to appropriate medical 

facUities for chelation treatment to reduce PbB levels. If PbB levels were 

between 30 and 50 (ig/dl, the county health department was instructed to 

send periodic blood samples to the state lab to monitor PbB levels. A home 

visit team was also sent to identify the source of lead and to initiate 

appropriate abatement procedures to eliminate the source of contamination. A flow diagram of the screening, treatment, and abatement 

procedures implemented in Wake County is shown in Figure 1. 

NCDHS provided data from screening probes by the Environmental 

Epidemiology Branch for the purpose of determining the frequency of 

occurrence of elevated FEP/PbB cases by county during 1981 and previous 

years. This procedure permitted the identification of "hot spots" for study 

purposes and the evaluation of county compliance with the EPSDT Pb 

screening program. A list of potential subjects for the proposed studies 

was also obtained in this manner. Available data from NCDHS records 

included birthdates, sex, race, county, FEP, PbB, and the date that the 

blood sample was drawn from each child. Contact with individual families 

was arranged and coordinated through county or local health agencies 

participating in the EPSDT Program. NCDHS has perfomed about 10,000 

PbB analyses during each of the past five years. Elevated PbBs have been 

found in 1-12% of the samples analyzed from the screening probes. The 

highest incidences were found in Lenoir and New Hanover counties, 

which were selected for one of our studies. 

Local Screening Programs 

Pb screening in most areas of North Carolina is carried out as an 

optional part of the EPSDT Program. Lenoir, Cabarrus, New Hanover, 

PSYCHO-SOCIAI FACTORS 113 

SCREENING PBOCEDUBK 

FIGURE 1. Screening procedures for the Uad Screening Program. 

and Wake Counties, however, have organized aggressive screening, 

intervention, and abatement programs in response to recent outbreaks of 

Pb poisoning in these areas. Subjects for our early studies were referred 

primarily by the Wake County Health Department and we continued to 

study these chUdren. We also studied chUdren from more remote parts of 

the state by means of a mobUe laboratory in Lenoir and New Hanover 

counties. 

Pb-Industry Target Populations 

A variety of major Pb industries are located in North Carolina. 

Children whose parents work in these industries constitute a discrete 

population with increased risk of lead poisoning. Permission was obtained 

to continue the study of chUdren from famiUes employed by one of these 

Pb industries. About haU of the subjects who participated in our initial 

study were obtained from this source. These chUdren constituted a large 

part of the five-year foUow-up study. It should be noted that the study 

population consisted of a self-selected sample from the lower income 

segment of the general population; we felt that concentration on the lower 

income group was appropriate in this project because lead poisoning is 

most prevalent in this target group (see U.S. EPA, 1977, 1986). 

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Experimental Design and Statistical Methodology 

These were not experimental studies, but rather used a cross-sectional 

observational epidemiologic design. No manipulation of independent 

variables was made. In other words, we assumed for purposes of 

hypothesis testing a random sample representative of chUdren Ukely to be 

considered for screening for lead exposure in the EPSDT population. 

The principal approach to analysis involved multiple regression 

modelling with age and PbB as predictors for Central Nervous System 

(CNS) outcomes. When considering IQ as the outcome, the regression 

models controUed for age, SES, Home Environment Score, and maternal 

IQ. The general strategy fbr determining the best model paraUeled the 

approach of Kleinbaum, Kupper, and Morgenstem (1982). 

Lead Analysis Procedures 

An essential part of toxicology research is the assessment of the 

amount of a toxic substance present in a given system. In this research, 

blood lead level was the key predictor variable under study. Measurements of blood lead and lead in house paint and house dust were the 

responsibUity of the Heavy Metals Analysis Laboratory, Department of 

Pathology, University of North Carolina at Chapel HUI (UNC-Chapel HUI). 

The laboratory had a variety of trace analytical equipment, including 

atomic absorpting spectrometers (AAS) that permit both flame and 

flameless atomic absorption analysis. 

Lead in Blood 

The Delves Cup micro procedure (Delves, 1970) with the modification 

by Ediger and Coleman (1972) was employed for whole blood (and 

plasma) lead determinations. The Delves Cup procedure was selected on 

the basis of speed, minimal sample manipulation, and concomitant low 

contamination risk and a good "track record" in our hands and in other 

laboratories. Speed was a critical factor because of the large volume blood 

analysis requirements and relative instabUity of blood. Direct insertion of 

blood samples into Delves Cups foUowed by drying, preignition, and 

atomization of the contained lead is rapid and relatively free from 

contamination problems. A number of interlaboratory method comparison 

studies have shown the Delves Cup micro procedure to be as good as or 

better than other atomic absorption or nonatomic absorption techniques. 

Furthermore, this procedure is used by many laboratories in the CDC 

proficiency screening program. 

•i-Uii 

PSYCHO-SCCIAI. FACTOOS 115 

Special precautions were taken to minimize sample contamination 

prior to analysis. AU glassware that came in contact with samples was 

washed and chemically debrided of metal contaminants by low-metal acid 

washing foUowed by repeated deionized water rinsing. Reagents, solvents 

for reagents, and other assay materials were selected for very smaU or 

undetectable metal contaminant content. With human subjects, blood 

was coUected into B-D low-lead vacutainer tubes via puncture. 

QuaUty control was maintained by both internal and external means. 

Frequent preparation and testing of aqueous and matrix-matched 

standards on a daUy or weekly basis was employed to assess changes in 

day-to-day precision and accuracy. External monitoring of laboratory 

performance was achieved by participation of our laboratory in the CDCs 

proficiency testing for blood lead determination. Further methodology 

evaluation was done using certified blood samples of known metal 

content and provided either by a commercial source (Kaulson Laboratories) or by the New York State Health Department. In the CDC program, 

three month bovine samples were airmailed to our laboratory and 

analyzed and the results forwarded to CDC. Our results were then 

compared both with overaU participant performance and with the mean 

values for the reference laboratories. Our overaU performance has been 

quite good over the range of blood lead levels encountered in the 

proficiency survey. 

Instrument and Test Battery Development 

This project had several unique features: the development of a mobue 

neurotoxicity testing laboratory that permitted the assessment of chUdren 

in remote cachement areas with sophisticated behavioral and electrophysiological, measures; a cooperative arrangement with federal, state, county, 

and local health agencies and industry that permitted the coordinated 

screening and assessment of at risk chUdren across the state; and an 

opportunity to obtain valuable longitudinal data on the long-term effects 

of early Pb exposure on neurobehavioral and cognitive development. This 

project was based on a productive collaboration among the EPA, the 

University of North Carolina School of Medicine, the North Carolina 

Division of Health Services, and private industry. The addition of a 

sophisticated mobile laboratory for the assessment of exposure significantly enhanced the research capabUities of the team. 

Behavioral and medical evaluations were carried out by professional 

staff from the Division for Disorders of Development and Learning 

(DDDL). DDDL is a clinical training faciUty that is part of the Quid 
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116 TOXI

C SUISTANCES 

Development Research Institute and Biological Sciences Research Center 

(BSRC) at the University of North Carolina. 

Daily Test Protocol and Home Visit 

Collection of electrophysiological data was done at DDDL or in the 

field mobUe laboratory. Demographic, psychometric, and medical data 

were obtained in an auxiliary trailer or in space provided by local health 

agencies. 

FamiUes were seen for a testing protocol that took approximately four 

hours to complete. Informed consent was obtained from the parent(s), 

who also were asked to sign a volunteer's statement. At the time of 

testing, the examiner was blind as to the child's lead exposure. A 

maximum of four chUdren per day could be evaluated in die mobile 

laboratory. 

After evaluation day a home visit was made for several reasons. If 

behavior problems were assumed to be related to lead exposure, control 

assessments of the home environment would have to be made to estimate 

its contribution to the child's hyperactivity or any other problem behavior. 

The CaldweU HOME Inventory is a standardized rating scale used for this 

purpose. The home was evaluated as a vehicle for continued lead 

exposure; the lead, if discovered, had to be removed by cleaning 

supervised by the county health department. Dust samples from the living 

room carpet, bedroom, and inside the front door were obtained by suction 

on preweighed glass filters and analyzed for lead by x-ray fluorescence 

using a portable unit. Home water supply was also analyzed for lead by 

AAS. These analyses have led to clean up of several homes and a resultant 

reduction of PbB levels of the lead-exposed chUdren (Milar Sc Mushak, 

1982). Once aU the clinical data were gathered and evaluated, the chUdren 

were reviewed at a staffing conference and any problems discovered 

during evaluation, whether they were lead related or not, were referred to 

the appropriate local community resources for foUow-up. ChUdren with 

PbB > 50 M-g/dl and FEP > 190 jig/dl were referred to a hospital for further 

evaluation and treatment of elevated lead levels. 

Medical, Psychometric, and Behavioral Measures 

Table 3 summarizes the blood lead chemistry and medical, electrophysi-

ological, psychometric, behavioral, and demographic measures that were 

coUected from children and parents who participated in this project. These 

measures were chosen to provide convergent information from several 

different perspectives in order to elaborate more clearly the subtle and 

complex effects of asymptomatic lead exposure on CNS development. 

PSVCHO-SOOAI. FACTORS 117 

TABLE 3 

Summary of Evaluations 

I. Exposure Evaluation A. Fantus Lead Poisonin

g Questionnaire 

B. Blood lead (PbB): flameless atomic absorption spectrometry 

C. Free erythrocyte protoporphyrin (FEP) 

II. Medical Evaluation A. Medical history B. Pediatric neurologica

l examination 

C. Growth: height, weight, head circumference 

D. Lab tests: BDS, WBC, RBC, Hgb, HCT, MCV, MCH, MCHC 

ID. Electrophysiological Evaluation A. Slow Cortical Potentials during Sensor

y Conditioning 

. B. Brainstem Auditory Evoked Potentials 

C. Pattern-Reversal Visual Evoked Potentials 

IV. Psychometric-Behavioral Evaluation A. Stanford-Binet Intelligence Test—Revised B. Bayley Scales of Infant Development (<30 mos

. of age) 

V. Demographic Covariale Evaluation A. Maternal IQ: Ammons Quick Test o

r Peabody Picture Vocabulary Test Revised 

B. Socioeconomic status: Hollingshead Two-Factor Index 

C. Quality of caregiving environment: Caldwell's Home Observation for Measurement 

of the Environment 

D. Chronological age 

E. Sex 

Several tests were selected on the basis of guidelines that were later 

adopted at an International Symposium on Neurobehavioal Methodology 

in Pediatric Lead Research held in Cincinnati in September, 1981. These 

guideUnes included: (a) use of standardized, age-normed tests with 

documented vaUdity and reUabUity when avaUable; (b) use of experimental 

measures to evaluate areas of function for which standardized measures 

are not avaUable; and (c) use of instruments with cross-cultural 

comparison data. An extensive medical histoi

y was taken on each chUd to rule out a 

variety of problems related to mental retardation but not attributable to 

lead, and to evaluate lead exposure history. The instrument we used was 

the Lead Poisoning Study Questionnaire developed at the Fantus Lead 

Screening Clinic at Cook County Hospital in Chicago. This 28-page 

questionnaire examines pertinent demographic history, prenatal history, 

cluld developmental mUestones, past medical history, lead poisoning 

symptomatology, dietary history, famUy history, immunizations, Ulnesses, vital signs, and chelation therapy and side effects. 
i? 

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SUDSTANCSS 

STUDY I: COMPARISON OF 

CHILDREN OCCUPATIONALLY 

AND NONOCCUPATIONALLY 

EXPOSED TO LEAD 

From 1975 to 1980, we conducted an interdisciplinary lead screening ' 

program as part of a program project grant from the National Institute of 

Environmental Health Sciences (ES-01104). Our strategy was to screen a 

population not only with traditional psychometric measures, but also for 

subclinical dose related effects of lead using direct longitudinal observations of children's behavior, for example, home observations, parent/child 

interactions, activity level, and slow wave brain potentials that might be 

developmentaUy related to subclinical lead levels and the children's 

behavior. Such a strategy, with appropriate design, might aUow a search 

for behavioral threshold effects of lead while avoiding the criticisms of 

previous studies. 

A North Carolina Memorial Hospital case report of lead poisoning in a 

family from Raleigh uncovered a highly stable and cooperative population 

associated with a battery factory in Wake County, where the relatives 

were employed. The chUdren were exposed to lead dust brought home 

and deposited in the house dust and in the carpets, which placed toddlers 

at the crawling stage at risk (Dolcourt, 1977; Dolcourt, Hamrick, OTuama, 

Wooten, & Baker, 1978). From 1977 to 1979, we evaluated over 115 

chUdren, 42 of whom were chUdren of employees in that plant and 104 of 

whom met criteria for study. We continue to foUow them longitudinaUy. 

Methods 

Subjects 

One hundred and four chUdren in Wake County aged 10 months to 6 

1/2 years at the time of initial testings who met inclusion criteria served as 

subjects. They were mostly black (94%) from lower social classes—that is, 

x=4.5 on the Hollingshead Two-Factor Index (Hollingshead, 1957). 

ChUdren previously evidencing CNS disease or insult or having 

undergone chelation therapy for lead poisoning and chUdren with 

ptediagnosed language delay or mental retardation were excluded from 

data analysis. Approximately half of the chUdren were less than 30 months 

of age and half ^ere over 30 months of age. Half of the subjects were 

EPSDT children and half were chUdren of battery factory workers referred 

from a local county health department to the lead screening program at 

North Carolina Memorial Hospital as part of a statewide screening 

program. 

PSYCHO-SOCIAL FACTOOS 119 

Procedures 

Subjects were evaluated at DDDL in the protocol described above in 

General Mtthodolgy, except that the only electrophysiological measures 

they received were Slow Cortical Potentials during Sensory Conditioning 

(see Otto et al., 1981, for a report of results). 

Results and Discussion 

A preliminary forward stepwise regression analysis of the relationship 

of lead to IQ and 18 of the covariates showed no effect of occupational 

exposure among the present cohort of chUdren (Hawk & Schroeder, 1983). 

Therefore, further analysis of occupational exposure was dropped and the 

number of confounding variables was reduced to HOME, SES, maternal 

IQ, age, sex, test (Bayley versus Stanford-Binet), presence of the father in 

the home, and number of siblings, in order to avoid overcontrol and Type 

II errors. The main statistical model used a multivariate regression analysis 

in which a set of aU the interaction terms was tested first. If the set were 

nonsignificant, aU interactions were dropped from the model. The second 

step was to test the main effects of the confounding variables. FinaUy, the 

test for the main effects of lead was performed. Any significant result was 

then further reduced in a stepwise manner for individual or linear 

combinations of variables for inclusion in the final model (Kleinbaum et 

al., 1982). 

The main result was that there was a significant linear relationship 

between blood lead level (range 6-59 ug/dl) and IQ (F = 7.689; df 1, 96, p 

< .01) (Figure 2). None of the interaction terms nor any of the quadratic or 

cubic effects was significant. Of the confounding variables only SES was 

significant (F = 20.159; df 1, 96, p < 001) and remained in the model. 

Nevertheless, the main effect of lead on IQ remained significant. 

The faUure of HOME, maternal IQ, and age to reach significance as 

thev had in other studies was Ukely the result of multicollinearity with 

SES. Table 4 shows that the intercorrelation of these variables was high. It 

seems that whichever of these variables enters the regression equation 

first is Ukely to render the effects of the others less significant. While SES 

and HOME shared a great deal of variance, one would ordinarily expect a 

direct measure of caregiving environment Uke the HOME to be a more 

accurate measure than an indirect one based on parental occupation 

and education Uke SES. Order of entry of multicoUinear covariates into the 

regression equation was important in determining which were significant 

and which were not. We wUI return to the matter of separating the effects 

of social factors on the relationship between lead and IQ in the Study ill: 

Replication Study. 
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6 12 18 24 30 36 42 48 54 

INITIAL BLOOD LEAD LEVEL (yug/dl) 

FIGURE 2. Initial IQ as a function of initial blood lead levels of children 

screened from 1977-1979. 

TABLE 4 

Correlation Matrix of Blood Lead Level and Child IQ (1977) and 

Comcomitant Variables 

VARIABLES 

Blood lead level (PbB) 

Child IQ 

CaldweU HOME 

Maternal IQ (MatlQ) 

Chronological age (CA)

 4 

Sex 

Socioeconomic status (SES) 

Father present (FaPr) 

Number ot siblings (Sibs) 

PbB 

-.27 6 

-.26 9 

-.19 3 

-.06 8 

-.07 2 

.183 

-.01 0 

.314 

IQ 

.451 

.379 

.254 

.130 

-.449 

.165 

-.284 

HOME 

.522 

.089 

.123 

-.62 4 

.433 

-.202 

MatlQ 

.029 

-.028 

-.47 5 

.178 

-.177 

CA 

.062 

-.143 

.161 

.116 

SEX 

-.064 

.054 

-.003 

SES 

-.49 5 

.161 

FaPr 

-.064 

PSVCHO-SOOAI FACTOHS 121 

STUDY II: FIVE-YEAR 

FOLLOW-UP STUDY 

The basic objective of this study (Schroeder, Hawk, Otto, Mushak, & 

Hicks, 1985) was to determine whether asymptomatic lead exposure in 

early childhood resulted in residual altered CNS function in chUdren 

when they reached school age. There might be latent or cumulative 

effects, even though their blood lead levels would be lower because they 

had grown out of the toddler stage. 

Methods 

Subjects 

Eighty of the 104 chUdren from Study I were located through county 

health department and school records five years later in 1983. Of the 80, 50 

agreed to reevaluation. 

Procedures 

ChUdren were seen at the Wake County Health Department in the 

mobUe laboratory using the same protocol as in Study I, described under 

General Methodology, except that the home visit was not repeated. Most of 

their blood lead levels had come down (Figure 3). 

Results and Discussion 

The same logistic backward multiple regression analysis was used as 

in the initial study except that initial blood lead level was used as the 

independent variable, current blood lead level was added to the Ust of 

covariates, and test and age were dropped as covariates because aU of the 

chUdren received the Stanford-Binet IQ test this time. The two lead scores 

were highly correlated (r = 0.74); the correlation of initial lead to 

foUow-up IQ was also significant (r = 0.34, p < .05). 

The main result in this study was that in the regression analysis lead 

no longer had a significant effect after the confounding variables were 

added to the model (F < 1). Apparently, the decUne in lead levels, whUe 

not appreciably disturbing the relation of social factors to lead and IQ, did 

negate lead's relation to IQ when confounding factors were controUed. 

This was not caused by self-selection bias at follow-up because the 

demographic characteristics of the families who participated were very 

similar to those who did not. 

In conclusion, in the present cohort of mainly low SES black famiUes, 

the covariance matrix among social factors and the relationship of lead to 
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122 Toxic SUISTANCES 

O INITIAL BLOOD LEAD 

• FIVE-YEAR BLOOD LEAD 

5-10 11-20 21-30 31-40 41-50 51-60 61-70 

BLOOD LEAD LEVELS (pg/dl) 

FIGURE 3. Frequency distribution of blood lead levels of chUdren seen from 

1977-1978 and in follow-up five years later. 

IQ seemed to be fairly stable over a five-year period. SES seemed to 

capture much of the variance related to the other covariates because of 

multicollinearity with HOME, maternal IQ, and age. 

STUDY III: REPLICATION STUDY 

The primary objectives of this study were to replicate the previous 

studies in a more homogenous group (all-black low SES chUdren aged 3-7 

years) and to find the best regression model based on both accuracy and 

precision that described the relationship of lead and IQ (Hawk et al., 

1985). Regression analyses typicaUy eliminate or incorporate control 

PSYCHO-SOCIAL FACTORS 123 

variables on the basis of precision, that is, whether significant additional 

variation in one's outcome variable is explained by adding one or more 

control variables to the model comprised of outcome and predictor 

variables. Alternatively, an unforced backward regression would eliminate 

all variables that do not account for a significant amount of variance with 

the outcome variable. Precision is concerned with random error, that is, 

the size of the confidence interval around the estimated parameter, that 

can occur when estimating effects. Confounding, on the other hand, is 

concerned with systematic error that can occur when estimating effects. 

Confounding is said to exist (Kleinbaum et al., 1982) if a meaningfuUy 

different interpretation of the relationship of interest wiU result, 

depending on whether an extraneous variable is ignored or included in 

one's data analysis. 

Confounding, then, is concerned with the issue of validity, that is, 

whether one has the right answer. Kleinbaum et al. (1982) suggested an 

analogy to target shooting: validity (confounding) is concerned with 

whether or not one is aiming at the correct buU's eye, while precision is 

concerned with individual variation from shot to shot, given the actual 

bidl's eye involved. According to Kleinbaum et al. (1982), while both 

precision and confounding must be considered and incorporated during 

the modeling process, for etiologic questions (such as the questions 

addressed in this study) confounding, or validity, usually takes final 

precedence over precision in the determination of the final model. These 

issues were addressed in the replication. 

Methods 

Subjects 

Eighty black chUdren aged 3-7 were recruited from high risk 

neighborhoods in Lenoir and New Hanover counties in cooperation with 

county health agencies and the Environmental Epidemiology Branch 

(EEB) of the North Carolina Division of Health Services. Most of the 

members of the New Hanover sample were enrolled in the Headstart 

Program. A Ust of criteria that defined the eUgibUity of individual chUdren 

for inclusion in the study was provided to referring health agencies. 

Eligibility criteria are specified below. 

1. Age 

2. Race 

3. Health status/history 

3-7 years 

Black 

Subjects could not have any current 

acute or chronic Ulness or be unde r 

medication of any sort. Perinatal his-
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124 Toxic SUBSTANCES 

4. Lead exposure histoiy 

5. Socioeconomic status 

6. IQ 

tory should be free of complications. 

Subjects should not have any history of 

neurobiological insults. 

Child should be asymptomatic and 

never have received chelation therapy 

or been treated for lead poisoning. A 

range of PbB levels from 5-60 p.g/dl was 

desired. 

Only low income families defined as 

Class IV or V (Hollingshead Scale) were 

Included. EPSDT famiUes were included in this group. 

In order to exclude any chUdren who 

were clearly mentally retarded, a minimum subject IQ of 60 was required. 

Procedures 

The same procedures as outlined in the General Methodology section 

were performed. Based on the results of our previous studies, covariates 

in the present study were restricted to HOME, SES, maternal IQ, age, and 

gender. 

Results and Discussion 

Of the 80 chUdren screened, 75 met the inclusion criteria and were 

used for analysis. Their demographic characteristics are given in Table 5. 

The mean socioeconomic status of this group was lower than other groups 

that we have studied. Also, the low maternal inteUigence scores reflect the 

TABLE 5 

Demographi c Characteristics of Children in the Replication Study 

DEMOGRAPHIC CHARACTERISTICS MEAN SCORE SD RANGE 

Mean blood lead level (|tg/dl) 

High blood lead level (jig/dl) 

Most recent blood lead level (|ig/dl) 

Most recent FEP (iig/dl) -

Home caregiver practices (Bradley fc Caldwell, 

1976a, 1979b) 

Maternal IQ (Dunn fc Dunn. 1981) 

Chronological age (mos.) 

Socioeconomic class (Hollingshead Tvwj-Factor Index) 

21.80 

26.71 

20.65 

32.74 

59.84 

63.41 

58.40 

4.91 

9.76 6.00-39.00 

14.11 6.2O-56.00 

9.73 6.20-47.40 

14.03 8.0 -193.0 

15.08 

11.29 

11.74 

0.20 

20-47 

40-94 

39-91 

4-5 

PSYCHO-SOCIAI FACTORS 125 

new revised norms for the Peabody Picture Vocabulary Test, Revised 

(PPVT-R) (Dunn & Dunn, 1981), which are less comparable to the more 

common adult inteUigence tests such as the Wechsler Adult InteUigence 

Scale (WAIS), but which are perhaps more vaUd than the Ammons Quick 

Test. 

STATISTICAL ANALYSIS 

STRATEGY FOR ASSESSING 

INTERACTION AND 

CONFOUNDING OF SOCIAL 

FACTORS 

The main objective of the statistical analysis strategy was to find the 

model that best described the relationship between lead and IQ. The 

principal approach to analysis involved multiple regression modeling with 

blood lead level as a predictor variable, child IQ as the outcome variable, 

and age, SES, HOME score, gender, and maternal IQ as control variables. 

The control variables were restricted to those five that had proven 

sigruficant in our earlier studies in order to reduce Type II errors caused by 

overcontrol. Type I errors were controUed by focusing on one confirmatory hypothesis-that blood lead levels would be significantly related to 

chUd IQ-whUe controUing for SES, maternal IQ, HOME (caregiving 

environment), gender, and age. Exploratory analyses were performed to 

find the most accurate and precise model that described the relationship 

between lead and IQ and their covariates. 

Methods 

TT,e general strategy for determining the best regression model was 

the same hierarchical logistic modeling strategy of Kleinbaum et al (1982) 

as was used before. This strategy incorporated the assessment of 

confoundmg, "Inaction, and precision into the selection of variables for 

the final model. A backward stepwise multiple regression approach was 

used m which interactions (PbB x age, PbB x SES PbB x MIO PbB x 

HOME) were tested first followed by the set of possible confounding 

covanate effects, followed by examination of main effects of lead and IQ 

This approach involved testing for a set of variables (e.g., aU the 

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126 Tone SUISTANCIB 

regression) tests to identify specific variables that should be retained in the 

final model to increase its precision. If the overaU test results were not 

significant, these terms were dropped from the final model. However, 

simply using stepwise regression to obtain a best regression model can 

lead to misleading interpretation of data because the issue of confounding 

is not automaticaUy addressed by such analyses (Kleinbaum et al., 1982). 

Exploratory analyses were then performed to find the most accurate 

and precise model. A variable (e.g., age, SES, etc.) determined to be a 

nonconfounder might stUl be retained in the model to increase precision; 

that is, the variable might significantly contribute to the total variability in 

IQ over and above what is contributed by the other variables remaining in 

the model. Similarly, even though confounding may be present within a 

set of variables, it may be that some smaUer subset is aU that is required for 

control, whUe providing increased precision in estimating the association 

of interest. 

Procedures 

Finding the model that best described the data in terms of both 

precision and confounding was accomplished in the foUowing way. A gold 

standard, that is, a baseline or standard adjusted estimate of association, 

was compared with adjusted estimates of association that accounted for 

other combinations of the extraneous variables. The gold standard was the 

model obtained in the backward regression analysis that controUed for aU 

interactions but kept aU the control variables ih the model. A subset of 

these variables that gave nearly the same adjusted estimates of the 

regression coefficient (p) for PbB was then a candidate for selection. 

The first model to be compared to this gold standard was obtained in 

the backward regression that eliminated control variables in terms of 

precision (finding the factors that explained the most variabUity in the 

dependent variable). This answered the question of whether the most 

precise model was also the most vaUd model. If the two models were not 

the same (i.e., the most precise model was not the most vaUd model), 

other models were chosen based on logic, predictions from past Uterature, 

and examination of the steps of the original backward elimination. The fl 

coefficients obtained from these various general linear models were 

compared to the gold standard and those most similar were then used to 

calculate confidence intervals for each model. The formula used for this 

calculation was as foUows: £ -1- (T64, .975) (Sfl). The model with the 

smaUest confidence interval is the model with the greatest precision, that 

is, die most accurate and precise model. 

PSYCHO-SOOAI. FACTORS 127 

Results and Discussion 

IQ Results 

Results of the confirmatory univariate analysis of the relation of 

current blood lead level to IQ are shown in the summary table (Table 6) 

below. Since the chunk test of interactions and control variables were 

nonsignificant, each set was dropped from the model. Exploratory tests 

using maximal (historically highest level obtained from PubUc Health 

Department records) and mean PbB levels were also done to further clarify 

the effect. Table 6 shows that there was a very strong negative linear 

relationship between blood lead levels and IQ, irrespective of which PbB 

index was used. Results of tests for quadratic and cubic components were 

not significant. Figure 4 shows a smooth Unear relationship between the 

highest (47.4 ug/dl) and the lowest (6.3 p-g/dl) blood lead levels. 

Results of the Exploratory Analyses 

Although the multiple regression analysis for the interaction terms 

using the overaU chunk test was not significant, the one for control 

variables approached significance, suggesting that a more accurate and 

precise model could be found. Furthermore, inspection of Table 7 shows 

that, while the regression model with lead and IQ alone (including no 

covariates) was the most precise, that is, had the smaUest confidence 

interval, the coefficient for lead differed considerably from that of the gold 

standard, that is, the model that included lead, IQ, SES, HOME, maternal 

IQ, age, and gender. Therefore, stepdown backward regression analyses 

were performed in which each variable was considered individuaUy. No 

interaction variables were found to be significant, even when considered 

individuaUy in the backward stepwise regression. When backward 

regression continued using aU single independent variables (e.g., PbB and 

control variables) with no forcing, SES was the first variable to be 

eliminated, foUowed by age, gender, and then HOME, whUe maternal IQ 

TABLE 6 

Summary Table of the Confirmatory Analysis of the Relation of Blood Lead & 

IQ Univariate F, p 

EFFECT USING CURRENT PbB 

STANFORD-BINET IQ TEST 

USING MEAN PbB USING HIGHEST PbB 

Interactions 

Control 

Uad PbB 

R 

0.55, 0.74 

1.82, 012 

12.31, 0.0008 

0.144 

1.01, 0.42 

1.86, 0.11 

10.08. 0.002 

0.121 

1.34. 0.26 

1.76, 0.13 

10.55, 0.0018 

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128 Toxic SUBSTANCES 

remained in the model with lead. Lead and maternal IQ were found to be 

significant variables in relationship to child IQ. That is, the model that 

included only those variables sharing a significant amount of variance 

with the' dependent variable was the model comprised of lead and 

maternal IQ. 

However, comparison of the coefficient for lead in this model (IQ, 

lead, and maternal IQ) with the gold standard (from the stepwise 

regression that eliminated all interactions but kept aU single variables) 

indicated that there was a discrepancy between their values that seemed 

to be substantial (Table 7). Therefore, other models employing different 

combinations of terms were examined (IQ, PbB, SES, maternal IQ, 

HOME; IQ, PbB, age, maternal IQ, HOME, gender; IQ, PbB, maternal IQ, 

HOME; IQ, PbB, maternal IQ, HOME, gender). Similarity of their 

coefficients for lead to that of the gold standard were assessed and sizes of 

the confidence intervals were calculated for each. The model with the 

smaUest difference in & coefficient for lead from that of the gold standard 

that stiU maintained a smaU confidence interval was IQ, PbB, maternal IQ, 

HOME, and gender. That is, the model that best controUed for 

confounding with the greatest precision (i.e., the most accurate and 

120 

«. no O 

100 

o 

_| 90 

^ 80 

O 

70 

60 

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• 

-

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• 

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• • 

• 

• •• • S aaa-a M ^ 

• , • 

• 

1 1 

5 10 4 15 20 25 30 35 40 45 50 

BLOOD LEAD LEVEL (jig/dl) 

FIGURE 4. Child IQ as a function of blood lead levels of children screened in 

the replication study. 

PSYCHO-SOOAI. FACTOBS 129 

precise model) contained lead, maternal IQ, HOME, and gender. 

Nevertheless two other models (IQ, PbB, age, gender, HOME, and 

maternal IQ; IQ, PbB, gender, HOME, and maternal IQ) gave acceptable 

accuracy and precision. AU the models in Table 7 were significant beyond 

the p<.01 level. 

The exploratory analyses demonstrated two important points: the 

most precise regression model may not always be the most accurate one in 

the assessment of confounding social factors on the lead-IQ relation; and if 

both precision and accuracy are considered, then HOME environment was 

more precise and accurate than SES in the population studied. SES is a 

rather crude measure that may not accurately reflect the heterogeneity of 

caregiving practices among lower SES families (Dietrich et al., 1985; 

Elardo, Bradley, & CaldweU, 1975; Ramey, Farran, & CampbeU, 1979; 

White & Watts, 1973). Indeed the relation of HOME score to SES may be 

different for different social classes. Recently, BeUinger, Needleman, 

Leviton, Watemaux, Rabinowitz, and Nichols (1984) found that HOME 

scores were positively related to umbiUcal cord blood lead levels in upper 

middle and upper class inner city Boston families, just the opposite of 

what has been found with lower SES families. Therefore, SES and HOME 

are not interchangeable measures. Considerably more study of their 

interrelationships is needed. The present study suggests that assessments 

TABLE 7 

Accuracy and Precision of Different Models of Regression of Blood Lead Levels 

on IQ Including Different Combinations of Variables as Candidates for 

Control Variables 

CANDIDATE SUBSET P COEFFICIENT* 

93% CONFIDENCE 

INTERVAL 

l$xit*i,mnsb»i 

1. Age,SES,Cender,HOME,MlQ.PbB,IQ* 

2. Age, Cender,HOME.MIQ.PbB.lQ 

3. SES, HOME.MlQ.PbB.lQ 

4. Cender,HOME,MIQ,PbB,IQ, 

5. HOME,MlQ.PbB,IQ 

6. MIQ.PbB.IQ 

7. PbB.lQ 

-0.254 

-0.248 

-0.282 

-0.255 

-0.273 

-0.396 

-0.456 

0.049" 

0.051 

0.021 

0.043 

0.026 

-0.102 

-0.196 

-0.558-a 

-0.548 

-0.585 

-0.554 

-0.572 

-0.637 

-0.715 

0.607* 

0.598 

0.606 

0.597 

0.598 

0.535 

0.520 

'This is the f) coefficient fbr lead 

'Lower bound of the confidence interval 

cUpper bound of the confidence interval 

^Absolute difference between the lower and upper bounds of the confidence interval 

•TT-ie baseline model or gold standard with all control variables included 

The match to the gold standard with least confounding (p coefficient for lead that is 

closest to that in the gold standard) while maintaining good precision (small confidence 

interval) 
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130 Toxic SUBSTANCES 

of their precision and accuracy are important criteria to consider in 

choosing the best regression model for lead and IQ. 

GENERAL DISCUSSION 

Lead Exposure an d IQ in Children 

Considerable controversy exists concerning the effects of low to 

moderate Pb exposure on cognitive function, as indexed by standard IQ 

tests, in chUdren (U.S. EPA, 1986). Results of the repUcation study provide 

very strong evidence (p < .001) in young chUdren of a continuous linear 

decrease in IQ (Stanford-Binet FuU Scale) with increasing blood lead level 

across a wide range (5-47 p-g/dl). This confirmatory finding is particularly 

compelling because the potentially confounding factor of socioeconomic 

status was effectively controUed by selecting a very homogeneous group 

of chUdren (mostly SES Class V). 

Results of the five-year follow-up study provided further clarification 

of the long-term effect of Pb exposure on IQ. Initial assessment of these 

chUdren aged 1-6 in 1977-1978 showed the same inverse linear 

relationship of PbB and IQ as found in the repUcation study. In addition, 

a dissociation of maternal and child IQ (Perino & Emhart, 1974) was found 

(r = 0.058) in chUdren below 30 months of age with elevated PbB levels (a 

30 tig/dl). Five years later the PbB levels of all chUdren retested had 

dropped to £ 30 p.g/dl. After controlling for possible confounding 

variables (SES and HOME caregiver scores), no significant Pb effect on IQ 

was apparent and the previously observed dissociation of maternal and 

chUd IQ was no longer present (r = 0.451). These observations suggest 

that IQ decrements associated with undue Pb absorption in the low to 

moderate range may be reversible if appropriate abatement procedures are 

taken to reduce body Pb burdens in young chUdren. However, these 

chUdren must be foUowed into adulthood to seriously test this hypothesis. 

Assessing the Effects of the Caregiving Environment 

and Other Social Factors 

In aU of the present studies, socioeconomic status, maternal IQ, and 

HOME scores were highly interrelated. The combination of these three 

covariates seems to bd at the source of multiple pathways that affect the 

relationship between lead exposure and IQ. It seems that a variety of 

social factors must be considered for a given population and that a 

considerable amount of additional research wiU be needed before the 

pieces can aU be fitted into the mosaic that will yield a coherent picture of 

PSVCHO-SOCIAI FACTOIS 131 

these interrelationships. Below we consider some of the main interrelationships of the social covariates of lead exposure in chUdren. 

HOME Scores 

In the current research HOME scores were consistently related to 

maternal IQ, SES, and presence of the father in the home (see Table 4). 

This last variable was also highly related to SES. Father absence was 

probably more of a socioeconomic variable in that it was related to the 

mother's receiving public assistance. A related effect was that single 

mothers and their chUdren often Uved with relatives as part of an 

extended family resource network. Families who lacked these other 

breadwinners tended to be more indigent and more sociaUy isolated. 

The relation of HOME scores to blood lead level also seems to vary 

with age. Milar et al. (1980) found a significant relationship of HOME 

scores to blood lead levels and Bayley MDI scores in the 11-30 month age 

range, but not in the 31-72 month range. Dietrich et al. (1985) found, in a 

comparable inner city population in Cincinnati, a significant relationship 

of neonatal umbilical cord blood lead levels and HOME scores, which 

tended to increase from 1 to 15 months of age. However, this is just the 

opposite of what Bellinger et al. (1984) found in an upper middle and 

upper class white population in a renovated inner city Boston area. So it 

seems that there may be a complex age x SES x race interaction with 

HOME scores that may be related to exposure to lead and its relationship 

toIQ. 

Socioeconomic Status 

Does SES protect or compensate for developmental risk caused by preand perinatal neurotoxic insults Uke lead exposure? In the present 

experiments, and certainly in most of the experiments discussed in Table 

1, SES tended to account for a great deal of the variance found in the 

relationship between lead and IQ. However, as discussed above, this 

seems to depend greatly on the age, sex, and race of the population 

studied. SES is a passive, rather crude measure of caregiving environment. Studies by Sameroff and Chandler (1975) indicate that SES can 

indeed buffer physiological insults in the pre- and perinatal period. 

However, this may not always be the case, given the nature of some 

neurotoxic risks. For example, Bellinger et al. (1984) found a positive 

relationship between HOME score and umbilical cord lead in an upper 

middle and upper class .white population living in a newly renovated 

inner city Boston area. Thus, in this case high SES placed children at a 

higher risk for lead exposure (from the dust from the lead paint on old 

buildings that had been torn down or sandblasted). Further, caregiving 
:' -'M?:^'?^^ ^ • 

:!&*:• 

132 Toxic SUBSTANCES 

practices per se may be overshadowed in such a setting by the risks 

associated with housing environments chosen as a result of having a high 

socioeconomic status. On the other hand. White (1982), in a meta-analysis 

of 200 studies relating SES to academic achievement, found that a much 

higher correlation between home atmosphere and academic achievement 

than in any other combination of SES indicators. The more important 

variables were childrearing practices and stimulation of learning at home 

and at school, and not parents' occupation, income, or education. 

ChUdren living in socially disadvantaged settings may have fewer 

opportunities for such experiences, but this does not automaticaUy confer 

adverse risk upon them. Rather, the risk seems to Ue in the combination of 

HOME, SES, and maternal IQ. 

Maternal IQ 

In the presenf studies maternal IQ was highly related to HOME 

scores, SES, and child IQ in Experiments I, U, and UI and with blood lead 

level in experiment HI (r = 0.314, p < .007). There was a great deal of 

heterogeneity among the mothers of the chUdren in the current studies, 

both in inteUectual level and in childrearing practices. Many of the 

mothers were very conscientious, but others engaged in harsh disciplinary 

practices and provided only a minimum of stimulation for their chUdren in 

the home. HOME scores ranged from 20-87 in Study Ul, for instance (see 

Table 5). In particular, the most indigent mothers displayed depression, 

showing Uttle positive affect toward their chUdren. Dietrich et al. (1985) 

also reported a lack of emotional responsivity of caregivers, which was 

related to lack of child supervision and to lead exposure. 

Maternal IQ may also be related to neglect of chUdren's nutritional 

needs. In the present studies nutrition was controUed by excluding from 

study those subjects with nutritional deficiencies, such as iron deficiencies. But in everyday life there are many ways in which borderline 

nutritional deficiencies may affect lead exposure (Milar & Schroeder, 

1983): (a) by serving as a nutritional basis for pica (Snowdon, 1977); (b) by 

altering susceptibiUty to lead intoxication because of deficiencies in iron, 

copper, chromium, zinc, calcium, and Vitamin D, aU of which compete 

with lead for protein binding sites (Mahaffey & Michaelson, 1980); (c) 

because of persistence of mouthing and pica of people with mental 

retardation or autism into adulthood (Danford & Huber, 1982). 

Multiple Paths and Expressions of Neurotoxic 

Effects of Lead 

There are many paths by which social factors can affect the 

relationship between lead and IQ. Certainly IQ is by far the most weU 

PSYCHO-SOCIAL FACTO-RS 133 

studied neurotoxic effect of lead exposure in chUdren. However, there are 

other effects of lead exposure, such as fine motor, perceptual-motor, 

reaction time, sensory-neural, and evoked and slow wave potential 

electrophysiological effects, which have also been demonstrated and for 

which the effects of social factors have hardly been studied. There are also 

many other stressful biological effects of lead, for example, hematological, 

nephrological, cardiovascular, endocrine, and gastroenterological effects, 

whose interaction with neurotoxic effects have not been addressed at aU. 

Such a complex view of neurotoxicity renders it difficult to study (Weiss, 

1980). Indeed Bornschein (1985) has criticized traditional main effects 

models as inadequate for reflecting the complexity of human neurotoxicity. In his view, a dynamic interactional longitudinal model as Ulustrated 

in the use of structural equations is preferable. However, such models will 

also have to cope with such sources of error as sampling, attrition, history, 

maturation, different test instruments for different age groups, statistical 

regression, heterogeneity of covariates over time, etc. (Baltes & 

Nesselroade, 1979). For instance, SES might be fairly stable over time in a 

low SES group caught in the poverty cycle, but quite different in an 

upwardly mobUe middle class group. Such a change might easUy affect the 

relationship of lead exposure to IQ over time. Nevertheless, longitudinal 

studies wUI Ukely provide more conclusive answers to the many questions 

concerning the neurotoxic effects of lead on retardation of cognitive and 

adaptive development. 

REFERENCES 

Alexander. F.W., Delves, H.T., * Clayton, B.E. (1972). The uptake and excretion by 

children of lead and other contaminants. In D. Barth et al. (Eds.), Environmental health 

aspects of lead: Proceedings of tn international symposium (pp. 319-330). Amsterdam: 

Commission of the European Communities. 

Baltes, P.B., fc Nesselroade, J.R. (1979). History and rationale of longitudinal research. In J.R. 

Nesseboade fc P.B. Baltes (Eds.), longitudinal research in the study of behavior and 

development (pp. 1-39). New York: Academic Press. 

Bayley, N. (1970). Development of mental abilities. In L. Carmichael (Ed.), Manual of chili 

psychology (3rd ed.). New York: Wiley. 

Bellinger, D.C, Needleman, H.L., Leviton, A., Watemaux, C , Rabinowitz, M.B., * 

Nichols, M.L. (1984). Early sensory-motor development and prenatal exposure to lead. 

Neurobehavioral Toxicology and Teratology. 6. 387-402. 

Bornschein, R.L. (1985). Influence of social factors on lead exposure and child development. 

Paper submitted for pubUcation. 

Bradley, R., fc CaldweU, B. (1976a). Early home environment and changes in mental test 

performance in children from 6 to 36 months. Developmental Psychology. 12, 93-97. 

Bradley, R. fc CaldweU, B. (1976b). The relation of infants' home environments to mental test 

performance at fifty-four months: A foUow-up study. -Child Development, 47, 1172-1174. 

Bradley. R., fc CaldweU. B. (1979a). Early home environment and changes in mental test 

performance in children from 6-36 months. Developmental Psychology, 12, 93-97. 

Bradley, R., fc CaldweU, B. (1979b). Home Observation for Measurement of the 
d^Sn^- ? z j^Ar. -• J- r^^^^^mw^ i^Tiiea-iiyi-r-'xtiia&iJfir.,' •Jj-^m 

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134 Toxic SUBSTANCES 

Environment: A revision of the preschool scale. American Journal of Mental Deficiency, 84, 

235-244. 

CaldweU, B., & Bradley, R. (1979). Home observation for measurement of the environment: 

Administration manual. University of Arkansas at Litde Rock. 

CaldweU, B.. Heider, I., Kaplan, B. (1966). The Inventory of Home Stimulation. Paper presented 

at die meeting of the American Psychological Association, Washington, DC. 

Centers for Disease Control. (1978). Preventing lead poisoning m young children. Adanta: U.S. 

Department of Health, Education and Welfare. 

Centers for Disease Control. (1985). Pmxntin; laaf prisoning in young children. Atlanta: U.S. 

Department of Health, Education and Welfare. 

Chamberlain, A.C., Heard, M.J.. Uttle, P., Newton, D , Wells, AC , fc Wiffen, R.D. (1978). 

Investigation into lead from motor vehicles. Harwell, United Kingdom: United Kingdom 

Atomic Energy Authority, Report No. AERE-R9198. 

Chatterjee, P., fc Cettman, J.H. (1972). Lead poisoning: Subculture as a facilitating agent? 

American Journal of Clinical Nutrition, 25, 324-330. 

Cravioto, 1. fc DeUcardie, E. (1972). Environmental correlates of severe malnutrition and 

language development in survivors from Kwashiorkor and Marasmus. In Nutrition: The 

nervous system and behavior. Scientific Publication No 251. Washington, DC.: Pan 

American Health Organization, 

de la Burde, B., & Choate, M.S. (1972) Does asymptomatic lead exposure in children have 

latent sequelae? Journal of Pediatrics, 81, 1088-1091. 

de la Burde, B., fc Choate, M.S. (1975) Early symptomatic lead exposure and development at 

school age. Journal of Pediatrics, 87, 638-642 

Delves, H. (1970). A micro sampling method for the rapid determination of lead by atomic 

absorption spectrometry. Analyst, 95, 431-438. 

Dietrich, K.N., Krafit. K.M., Pearson, D.T., Harris. L.C. Bornschein, R.L., Hammond, P.B., 

& Succop, P.A. (1985). The contribution of social and developmental tutors to lead 

exposure during the first year of life. Pediatrics, 75, 1114-1119. 

Dobbing, I. (1970). Undernutrition and die developing brain. In W.A. Hamwick (Ed.), 

Developmental neurology. Springfield, IL: Thomas. 

Dolcourt,). (1977). Lead poisoning in chUdren of battery plant employees in North Carolina. 

Mortidity out Mortality Weekly Reports. September 30. 

Dolcourt, )., Ham-rick, H.. OTuama, L., Wooten. J.. & Baker, E.L. (1978). Increased lead 

burden in chUdren of battery workers. Pediatrics, 62, 561-563. 

Dunn, L.M., fc Dunn, A.M. (1981). Peabody Picture Vocabulary Test, Revised. Qrde Pines, 

MN: American Guidance Service. 

Ediger, R.D., & Coleman, R.L. (1972). Modified Delves Cup atomic absorpting procedure for 

determination of lead in blood. Atomic Absorpting Newsletter, 11, 33. 

Elardo, R-, Bradley, R , & CaldweU, B.M. (1975). The relation of infants' home environments 

to mental test performance bom six to thirty-six months: A longitudinal analysis. OiHd 

Development, 46. 71-76. 

Emhart, C.B., Landa, B.. ScheU, N.B. (1981). Subclinical levels of lead and development 

defidt-A multivariate foUow-up reassessment. Pediatrics, 67, 911-919. 

Harvey, P., Hamlin, M., Kumar, R. (1983). The Birmingham blood lead study. Paper read at 

the Annual Conference of the British Psychological Society, York Univ., UX 

Unpublished manuscript. 

Harvey, P.G., Hamlin, M.W., Kumar, R., fc Delves, H.T. (1984). Blood lead, behavior and 

intelligence test performance in preschool chUdren. Tke Science of tht Total Environment, 

40,45-60. 

Hawk, B., fc Schroeder, S.R. (1983). Factors interactive with IQ and blood lead levels in 

children. Paper presented at die XVIth Annual Conference on Mental Retardation and 

Developmental Disabilities, Gadinburg, TN. 

Hawk, B.A., Schroeder, S.R., Robinson, G , Otto. D, Mushak, P., Kleinbaum, D„ & 

Dawson, C. (1985). Relation of lead and social factors to IQ of low SES children: A 

partial repUcation. Manuscript submitted for publication. 

Heber, R. (1970). Epidemiology of mental retardation. Springfield, IL: Thomas. 

PSYCKO-SOOAI FACTOaS 135 

Hollingshead. A.B. (1957). Two-factor index of social position. Unpublished manuscript. 

(Available from A.B. Hollingshead, 1965 Yale Station, New Haven Connecticut). 

Kleinbaum, D., Kupper. L., & Morgenstem, H. (1982). Epidemiologic research: Principles and 

quantitative methods. London: Lifetime Learning Publications. 

Kotok, D. (1972). Development of chUdren with elevated blood levels: A controlled study. 

Journal of Pediatrics, 80, 57-61. 

Kotok, D., Kotok, D., fc Heriot. J.T. (1977). Cognitive evaluation of chUdren with elevated 

blood lead levels. American Journal of Diseases of ChUdren, 131, 791-793. 

Landrigan. P.J., Whitworth, R.H., Baloh, R.W.. Staehling, N.W., Barthel, W.F., & 

Rosenblum, B.F. (1975). Neuropsychological dysfunction in children with chronic 

low-lead absorpting. lancet, I, 708-712. 

Lansdown, R.G., Sheperd, J., Clayton, R.E., Delves, H.T., Graham, P.J., & Turner, W.C. 

(1974). Blood lead levels, behavior, and intelligence: A population study. Lancet. 1, 

538-541. 

Mahaffey, K.R.. fc Michaelson, LA. (1980). The interaction between lead and nutrition. In H. 

Needleman (Ed.), Low level lead exposure: the clinical implications of current research (pp. 

159-200). New York: Raven Press. 

McBride, W.C., Black, B.P., fc English, BJ. (1982). Blood lead levels and behavior of 400 

preschool children. Medical Journal of Australia. 2, 26-29. 

McNeil, J.L.. Ptasnik, J. A., fc Croft. D.B. (1975). Evaluation of congestion effects of elevated 

Mood lead concentrations in asymptomatic children. Archines of Industrial Hygiene and 

Toxicology, 21, Supplement. 

Milar, C, fc Mushak, P. (1982). Lead-contaminated housedust Hazard, measurement, and 

decontamination. In ). Chisholm and D. O'Hare (Eds.), Management of increased lead 

absorption in children: Clinical, social, and environmental aspects. Baltimore: Urban fc 

Sdiwarzenburg. 

Milar, C.R., fc Schroeder, S.R. (1983). The effects of lead on retardation of cognitive and 

adaptive behavior. In J.L. Matson and F. Andrasik (Eds.), Treatment issues and 

innovations in mental retardation (pp. 129-158). New York: Plenum Press. 

Milar, C.R., Schroeder, S.R., Mushak, P., & Boone, L. (1981). FaUure to find hyperactivity in 

preschool chUdren with moderately elevated lead burden. Journal of Pediatric Psychology 

6. 85-95. 

Milar, C.R., Schroeder, S.R., Mushak, P., Dolcourt. J.L., & Grant, L.D. (1980). Contributions 

of the caregiving environment to increased tead burden in children. American Journal of 

Mental Deficiency. 84. 339-344. 

MiUicon, F.K., Lourie, R.S., fc Layman. E.M. (1956). Emotional factors in the etiology and 

treatment of lead poisoning. American Journal of Diseases of Children, 91,144-149. 

Moore, M.R., Meredith, P.A., & Goldberg, A. (1980). Uad and hemebiosynthesis. In P.L. 

Singhal & J.A. Thomas (Eds.), Lead toxicity (pp. 79-118). Baltimore: Urban and 

Swarzenburg. 

National Academy of Sciences. (1976). National Research Council, Recommendation fer the 

prevention of lead poisoning in children. National Academy of Sciences Washington DC 

AvaUable bom NTIS, Springfield, VA: PB257645. ' 

National Academy of Sciences. (1980). Laid in Me human environment. Committee on Lead in 

die Human Environment. National Academy of Sciences, Washington. DC. 

Needtsman, H.L., Gunnoe, C, Leviton, A., Reed, R., Peresie, J., Maher, C, & Barrett, B.S. 

(1979). Deficits in psychologic and classroom performance of chUdren with elevated 

dentine levels. Nea England Journal of Medicine, 13. 689-695. 

Needleman, H.L., fc Landrigan, P.J. (1981). The health effects of low level exposure to lead. 

Annual Review of Public Health, 2, 277-298. 

Otto, D.A., Benignus, V.A., MuUer, K.E., & Barton, CN. (1981). Effects of age and body 

lead burden on CNS function in young chUdren. I. Slow cortical potentials. EEC Clinical 

Neurophysiology, 52, 229-239. 

Pernio, J., fc Emhart, CB. (1974). The relation of subclinical lead level to cognitive and 

sensorimotor impairment in black preschoolers. Journal of Learning Disabilities. 7, 26-30. 

Piomelli, S., Corash, L., Corash, M., Seaman, C, Mushak, P., Glover, B., & Padgett, R. 
titogt-nknii a 

% 

:-f- •'-'•iajiJ^S**'*,*1 

A<AA7m% 

A77')<:'•• 

m°4 

:

:

:

^M^iJJJ7 

136 Toxic SUISTANCES 

(1980). Blood lead concentrations in a remote Himalayan population. Science, 210, 

1135-1137. 

Piomelli, S., Seaman, C , ZuUow, D., Curran, A., fc Davidow, B. (1982). Threshold for lead 

damage to heme synthesis in urban children. Procmiinxs of Ihe National Academy of 

Sciences. 79, 3335-3339. 

Rabinowitz, M.B., WetheriU, G.W., fc Kopple, J.D. (1977). Magnitude and lead intake bom 

respiration by nonnal man. Journal of Laboratory and Clinical Medicine, 90, 238-248. 

Ramey, CT., Farran, D.C , fc CampbeU, F.A. (1979). Predicting IQ from moUter-chUd 

interactions. Child Development, SO, 804-814. 

Ratcliffe, J.M. (1977). Developmental and behavioral functions in young chUdren widi 

elevated blood lead levels. British Journal of Preventive Social Medicine. 31, 258-264. 

Read, M.S. (1982). Malnutrition and behavior. Applied Research in Mental Retardation, 3, 

279-291. 

Rennert, O.M., Weiner, P., fc Madden, J. (1970). Asymptomatic lead poisoning in 85 Chicago 

chUdren. Clinical Pediatrics, 9, 9-13. 

Rummo, J.H. (1974). Intellectual and behavioral effects of lead poisoning in chUdren. 

Unpublished doctoral dissertation. University of North Carolina. 

Rummo, J.H., Routh, D.K., Rummo, H.J., & Brown, J.F. (1979). Behavioral and neurological 

effects of symptomatic and asymptomatic lead exposure in children. Archives of 

Environmental Health, 34, 120-124. 

Sameroff, A.J., fc Chandler, M.J. (1975). Reproductive risk and die continuum of caretaking 

casualty. In F.D. Horowitz (Ed.), Review of -Child Development Research (Vol. 4) (pp. 

187-244). Chicago: The University of Chicago Press. 

Schroeder, S., Hawk, B., Otto, D., Mushak, P., fc Hicks, R. (1985). Separating die effects of 

lead and social factors on IQ. Environmental Research, 38. 144-154. 

Smith. M , Delves, T., Lansdown. R., Clayton, B., fc Graham, P. (1983). The effects of lead 

exposure on urban chUdren: The Institute of Child Health/Southampton Study. 

Developmental Medicine and Child Neurology, 26, Supplement No. 6. 

Snowdon, CF. (1977). A nutritional basis for lead pica. Physiology and Behavior. 18, 888-893. 

U.S. Environmental Protection Agency. (1977). Air QuaUty for Lead. EPA-600/8-77-017. 

Washington, DC. 

U.S. Environmental Protection Agency (1986). Air QuaUty' Criteria for Lead, Vol. IV, 

EPA-600S-83-028A. Washington, DC. 

Weiss, B. (1980). Conceptual issues in die assessment of lead toxicity. In H. Needleman 

(Ed.), Low level lead exposure: The clinical implications of current research. New York: Raven 

Press. 

Werner, E., Honzik, M., fc Smith, R. (1968). Prediction of inteUigence and achievement at ten 

years from twenty months, pediatric and psychological examinations. Oiiki Development, 

39, 1063-1075. 

White. K.R. (1982). The relation between socioeconomic status and academic achievement. 

Psychological Bulletin, 91(3), 461-481. 

White. B., & Watts, J.C. (1973). Experience and environment: Major influences on the development 

of the young chad. Englewood Cliffs, NJ: Prentice-Han. 

Winneke, C , Hrdina, KG., fc Brockhaus, A. (1982). Neuropsychological studies in chUdren 

- with elevated tooth-lead concentration. Part 1: Pilot study. International Archives tf 

Occupational Environmental Health, 51. 169-183. 

Winneke, C , Kramer, U., Brockhaus, A., Ewers, U., Kujanek. C , Lechner, H., fc Janke, W. 

(1983). Neuropsychological studies in children with elevated tooth-lead concentrations. 

Part D: Extended study. International Archives of Occupational Environmental Health, 51, 

231-252. 

Winneke. C . fc Kraemet U. (1984). Neuropsychological effects of lead in chUdren: 

Interactions with social background variables. Neuropsychabiology, II, 195-202. 

Yule. W., Lansdown, R., Millar, LB., fc Ur-banowicz, M.A. (1981). The relationship between 

blood lead concentrations, intelligence and attainment in a school population: A pilot 

study. Developmental Medicine and Child Neurology, 23, 567-576. 

Yule, W., fc Lansdown. R. (1983). Lead and children's development: Recent findings. In 

•Proceedings of Heidelberg Conference on heavy metals in the environment. Heidelberg, FRG. 

PSYCHO-SOCIAI. FACTO«S 137 

Yule, W., Lansdown, R., Hunter, J., Uibanowicz, M.A., Clayton, B-, fc Delves, I. (1983). 

Blood lead concentrations in school age chUdren: InteUigence, attainment, and 

behaviour. Paper presented at die Annual Conference of the British Psychological 

Society, York, England, April. 

Yule, W , Uibanowicz, M.A., Lansdown. R , fc Millar. l.B. (1984). Teachers' ratings of 

children's behavior in relation to blood lead levels. British Journal of Developmental 

Psychology, 2, 295-305. 

Ziegler, E.E., Edwards, B.B., Jensen. R.C, Mahaffey, K.R., fc Fomon, S.J. (1978). Absorption 

and retention of lead by infants. Pediatric Research, 12, 29-34. 

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