P.1 

OAR Box 1111 

Prepped by Ryan Dugan 

Document Number: 

-tT57ll-A-6 

Docket Number: 

A-83-22 

Printed 4/15/2008 1:25:18 PM Sheet 115 of 118 
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7Z-/*--*: 

«^9 

PEI ASSOCIATES 
P.3 

BLOOD LEAD LEVELS IN CHILDREN 

LIVING IN LEAD-BASED PAINTED 

HOUSING UNITS 

by 

Anne Pope 

PEI Associates, Inc. 

505 South Duke Street, Suite 503 

Durham, North Carolina 27701-3196 

Contract No. 68-02-4309 

Work Assignment No. 9 

PN 365.9-9 

Project Officer 

Richard B. Atherton 

Work Assignment Manager 

Jeff Cohen 

STRATEGIES AND AIR STANDARDS DIVISION 

U.S. ENVIRONMENTAL PROTECTION AGENCY 

RESEARCH TRIANGLE PARK, NORTH CAROLINA 27711 

January 1986 
P.4 

DISCLAIMER 

This report was prepared by PEI Associates, Inc., Cincinnati, Ohio, under 

Contract No. 68-02-4309, Work Assignment No. 9. It has been reviewed by the 

Strategies and Air Standards Division of the Office of Air Quality Planning 

and Standards, U.S. Environmental Protection Agency, and approved for publication. Approval does not signifiy that the contents necessarily reflect the 

views and policies of the U.S. Environmental Protection Agency. Mention of 

trade names or commercial products is not intended to constitute endorsement 

or recommendation for use. 

I I 
P.5 

CONTENTS 

Page 

. i v 

v 

Tables 

Acknowledgment 

1. Introduction 1 

2. Relationship of Blood Lead Levels in Children and Presence 

of Lead-Based Paints in Homes 2 

3. Distribution of Blood Lead Levels in Children 7 

4. Comparison of Blood Lead Levels of Children in the General 

Population and Children Living in Lead-Based Painted 

Homes 20 

References 24 

i i i 
P.6 

TABLES 

Number Page 

1 Characteristics of Studies on Distribution of Lead Levels 

in U.S. Children 9 

2 Distribution of Blood Lead Levels in U.S. Children 12 

3 Telephone Survey Participants 18 

iv 
P.7 

ACKNOWLEDGMENT 

This report was prepared for the U.S. Environmental Protection Agency by 

PEI Associates, Inc., Cincinnati, Ohio. Mr. Jeff Cohen was the EPA Work 

Assignment Manager. Mr. David Dunbar served as the Project Director; Mr. Ted 

Johnson was the Project Manager. The principal author was Ms. Anne Pope. 

The author would like to thank Mr. Jeff Cohen for his guidance and direction 

on this Work Assignment. The author also would like to acknowledge Mr. Ted 

Johnson, Ms. Alicia Ferdo, and Ms. Donna Sledge for their assistance and 

cooperation. 
P.8 

SECTION 1 

INTRODUCTION 

The U.S. Environmental Protection Agency (EPA) is currently assessing 

the exposure of children under 7 years of age to lead in the environment. 

High lead exposures Gan result in elevated blood lead levels (PbB's) in 

children. One important source of lead exposure in children is the ingestion 

of lead-based paint chips. Under Work Assignment No. 9, Contract No. 68-02-

4309, PEI Associates, Inc., (PEI) has estimated the distribution of PbB's in 

U.S. children living in lead-based painted housing units (LPH's). To determine the relationship between PbB's in children and residency of children in 

LPH's, PEI compared the distribution of PbB's in children residing in LPH's 

with that in children in the general population. This report also contains 

a review of the literature on PbB's in children living in LPH's and in children of the general population and summarizes the data in terms of percentiles, 

geometric means, and geometric standard deviations. 
P.9 

SECTION 2 

RELATIONSHIP OF BLOOD LEAD LEVELS IN CHILDREN AND 

PRESENCE OF LEAD-BASED PAINTS IN HOMES 

Clinical evidence indicates that young children are more likely to 

suffer from the effects of lead poisoning than adults because children tend 

to receive more exposure to environmental lead sources and to absorb 

greater amounts of lead than adults. This exposure is due primarily to 

the greater inclination of children to touch, mouth, and ingest objects in 

the environment. The EPA has determined that children under 7 years of age 

comprise the primary demographic age group at greatest risk from lead in 

the environment. 

Blood lead levels (PbB's) are the most widely used indices of exposure 

to lead in children. PbB's provide a reliable indicator of the amount of 

lead available in the exchangeable body pool and allow the evaluation of 

environmental lead exposure conditions. PbB, however, varies with time and 

provides only an indication of recent exposure because of the rapid 

1 2 clearance of absorbed lead from blood. ' The short-term ingestion of lead 

is not normally associated with severe lead toxicity, but it can cause 

large transitory increases in PbB's. Chelation treatments for lead 

poisoning also temporarily decrease PbB's in children. To avoid problems 

associated with the temporal variability of PbB's, PEI attempted to analyze 

data of investigations that collected random blood samples from children 

in quantities numerous enough to be representative and to minimize whatever 

variability exists in the measurements. 

Investigations of lead poisoning in children in various cities and 

States provided data on the number of children who had high PbB's. These 

data made possible early identification and treatment of children who had 

lead poisoning. In most investigations, large numbers of children who were 

assumed to be asymptomatic were screened to identify children who required 

further evaluation based on PbB. Children, whose tests were initially positive for lead toxicity, were further tested by obtai ning additional PbB and 
P.10 

free erythrocyte protoporphyrin (FEP) measurements to diagnose their conditions. Physicians use FEP measurements to validate PbB's in children. The 

FEP tests were performed to determine if the initially indicated PbB was the 

result of a single unusual ingestion of lead or of regular ingestion of lead 

over a prolonged period. In addition to PbB and FEP screening of children, 

most investigations also surveyed other individuals in the hauseholds of the 

children whose tests were initially positive for lead toxicity. These additional surveys were used to identify the sources of lead exposure and to 

examine the homes for the presence of lead-based paints. Currently 40 States, 

the District of Columbia, and Puerto Rico have some activities in childhood 

lead poisoning programs. 

Studies of PbB's in children are difficult to compare because screening 

methods vary among the different investigations and because of the 

decreases over time in "cut-off" or "clinically acceptable" PbB's and FEP's 

for purposes of classifying lead toxicity. Early screening programs in the 

late 1960's and early 1970's concentrated only on testing children who were 

at highest risk to lead exposure. Later programs such as the National Health 

and. Nutrition Examination Survey (NHANES) surveyed the general population. 

The "clinically acceptable" levels for lead toxicity have decreased as follows: in 1971 the PbB was. 40 ug/dl; in 1975 the PbB was 30 yg/dl and the 

FEP was 60 yg/dl; in 1978 the PbB was 30 yg/dl and the FEP was 50 yg/dl; and 

3 

in 1984 the PbB was 25 yg/dl and the FEP was 35 yg/dl. Currently, the 

average PbB's in children is 10 yg/dl and the "clinically acceptable" PbB's 

3 

is 25 yg/dl. In the review of the studies, PEI has indicated the cut-off 

PbB's for the threshold zone. 

Studies that measured the amount of lead in painted surfaces in homes 

of children with elevated PbB's defined the lead content of painted 

surfaces that constitutes a hazard to children in different terms. 

2 

Currently, homes in which painted surfaces contain >0.7 mg lead/cm are 

4 

considered hazardous to children. Many studies defined LPH's as homes in 

which the lead content of painted surfaces was 1 percent or more. The term, 

"one percent lead-based paint" has various meanings. The percentage of 

2 lead in paint does not correspond directly or indirectly to mg/cm as this 

would indicate the presence of lead in single and multiple layers of a 

5 

painted surface. Many older homes, however, contain layers of lead-based 
P.11 

2 paints coated by paints without lead; therefore, mg/cm is an appropriate 

unit of measure for potential exposure of children to other sources of lead. 

In its review of the literature, PEI indicated the criterion for defining a 

lead-based paint hazard in homes. 

Lead poisoning occurs in children under 7 years of age primarily in 

preschool age children. Many of the screened children who showed elevated 

PbB's reside in older deteriorating housing units that contain chalking, 

flaking., and/or peeling lead-based paints, and most of the children with 

results positive for lead toxicity are in the 6 month to 3 years age group 

and exhibit pica. ' Children who ingest lead-based paint chips or dust 

containing lead-based paint chips and who reside in deteriorated LPH's are 

at greatest risk of exposure to lead than other demographic groups of 

3 7 children. ' Children may also be exposed to lead in urban areas, areas 

near smelters, and in areas near roads with high average daily traffic 

volumes. Because cases of elevated PbB's have been reported among all socioeconomic groups, races, and sexes of children, lead poisoning is a national 

problem with the potential to affect a large number of young U.S. children. 

Numerous studies have attempted to identify the origins of elevated 

PbB's in children under 7 years of age. From 1930 to 1970, elevated PbB's 

were attributed to the presence of lead-based paints in homes and children's 

g 

pica for paint chips and dust. Recent investigations by Gilbert et al. 

and Galke et al. suggest that intact lead-based paint also contribute to 

9 10 elevated PbB's in children. ' The amount of lead per surface area of 

2 

painted surface (mg/cm ) , the integrity of the painted Surface, and the 

availability of paint chips to children determine the degree of lead-based 

paint hazard to children. In poorly maintained LPH's, peeling lead-based 

paint, weather powdered paint, and broken plaster are sources of lead 

exposure to children, especially children who reside in urban areas of the 

Northeast and Midwest. 

Although peeling and intact lead-based paints are implicated as major 

sources of elevated PbB's in children, no direct evidence exists, and the 

quantification of a specific dose-response relationship for lead-based paint 

exposure and PbB's has not been achieved. Because no single source of lead in 

the environment accounts for elevated PbB's in all children, the origins of 

C 11 1 p 

elevated PbB's in children is multifactoral . ' ' Sources of lead in the 
P.12 

blood include atmospheric lead from automotive and industrial emissions, soil 

lead, lead in street and house dusts, occupational dusts, food, drinking 

3 7 13 

water, and lead-based paints. ' ' Various studies relate PbB's to hand lead 

levels, lead concentration in house dust, lead concentration in outdoor dusts 

and soils, LPH's., and pica. 5 '

6 '8 '9 '10,12 *1 4 '1 5 '1 6 '1 7 Several investigations 

attribute elevated PbB's in children to lead in housedust, soil, and outdoor 

3 7 8 12 17 

dust. ' ' ' ' The lead in house dust and outdoor dust originates from automotive emissions, industrial emissions, secondary occupational sources, and 

lead-based paints. Pica is also a large contributing factor to elevated PbB's 

in children. Children with pica often engage in two types of lead ingestion--

regular or frequent hand-to-mouth transfer of dust and soil and irregular 

Q 

eating of paint particles. 

In their analyses of PbB's in children residing in LPH's and homes without lead-based paints, Urban and Gi1 sinn showed low correlations between residing in LPH's and PbB's but they demonstrated stronger correlations between 

the age of housing units and PbB's. ' The age of housing units and the 

lead content of painted surfaces are directly related. The lead content of 

20 paint used in homes built prior to 1940 was <_50 percent by weight. In 

1940, titantium oxide (Ti02) paints were used in addition to lead-based paints 

in homes. In 1955, the lead-content of interior paints was limited to <t 

percent lead by weight, and in 1971, the sale of all interior lead-based 

20 paints was banned in the United States. Today, the lead content of paints 

14 is limited to £ 0.06 percent by weight. Many of the homes built prior to 

1960 still contain lead-based paints on interior and exterior surfaces, plasters, 

and putties. Although the surfaces in older housing units may be coated with 

paints containing no lead, the underlying coats of lead-based paints still 

represent a large source of lead in a.child's environment. Based on the 

relationships between age of homes and PbB's in children and between the age 

of homes and amount of lead in paints, PEI assumes that elevated PbB's in 

children who reside in older homes constructed prior to 1960 result primarily 

from lead-based paint chips. 

Multiple sociodemographic factors in addition to multiple environmental 

factors enter into the explanation of why PbB's vary in children. In the 

multiple regression analyses by Stark et al., only 11.7 percent of the 

5 

variation in PbB's of children could be attributed to environmental factors. 
P.13 

The variables may, however, be intercorrelated with environmental lead exposure. Sociodemographic factors that influence PbB's of children include family income, age of children, location of child during the day, number of family 

members residing in housing units, marital status of parents, education of 

head of household, work status of head of household, race, ownership of housing units, age of housing units, condition of housing units, supervision of 

c iq in 11 

children, and cleaning practices in homes. ' ' ' Social characteristics 

associated with increased lead exposure in children are low socioeconomic 

status, disturbed mother-child relationships, frequent moves, single parent 

family, underemployment, large family size, and inadequate parental supervi22 

si on. Therefore, in addition to a reduction in environmental sources of 

lead, programs to educate individuals about lead toxicity and sources of lead 

in homes, social-welfare programs, and continued screening of children are 

needed to decrease lead exposure in children. 

No study has determined the individual effects of environmental and 

sociodemographic factors on PbB's in children, but the reduction of lead-based 

paints has been the prime method for prevention of lead poisoning in the 

United States. Although no relationship between PbB's and children's residency in LPH's has been established, a trend has been shown in the literature. 

Therefore, the relationship between PbB's and residency in LPH's needs to be 

described and quantified more fully. To help describe this relationship, PEI 

compares studies of PbB's in children who live in LPH's and PbB's in children 

of the general population in Section 4 of this report. 
P.14 

SECTION 3 

DISTRIBUTION OF BLOOD LEAD LEVELS IN CHILDREN 

The lognormal distribution has been shown to provide a good fit to PbB 

data for children, including, the upper tail of the distribution, which 

represents children who are at greatest risk of developing lead-related 

health effects. A lognormal distribution is completely specified if its 

geometric mean and geometric standard deviation are known. Consequently, 

these two parameters provide a convenient way of summarizing and comparing 

PbB data from different studies. 

Of principal interest to EPA were the geometric means and geometric 

standard deviations of PbB data for 1) children in LPH's, 2) children in 

the general population, and 3) children in non-LPH's. Finding studies 

appropriate for estimating these statistics was difficult. Many of the 

investigations reviewed by PEI only screened children in high-risk areas, 

reported the number of children who had PbB's above a specified amount, 

examined only the homes of children with elevated PbB's for the presence of 

lead-based paints, and reported the percentage of children with elevated 

PbB's who lived in LPH's. Because the screened high-risk children are not 

typical of children in the general population or of children living in 

LPH's,. PEI did not use PbB data obtained from studies of these high-risk 

children to determine the distribution of PbB's in either the children in 

LPH's or those in the general population. 

Many of the studies failed to. report geometric means and geometric 

standard deviations. Some reported only the percentage of children who 

had PbB's elevated above a specific level. Only 5 of the 20 studies PEI 

reviewed contained calculated geometric means and/or geometric standard 

deviations. PEI estimated geometric means and geometric standard deviations for 4 of these studies by graphically fitting lognormal distributions 

to selected percentiles. For one study, PEI estimated the geometric standard 

deviation under the assumption that the distribution is lognormal by using 

the following equation: 
P.15 

GSD = exp (ln [(ASD/AM)2 + 1]) 1 / 2 

where 

GSD = geometric standard deviation 

ASD = arithmetic standard deviation 

AM = arithmetic mean. 

Because the distribution of PbB's over a range of values was not reported 

in the other 11 studies, PEI could not estimate geometric means or 

geometric standard deviations for these studies. 

Table 1 provides a brief description of each of the 20 studies of 

PbB's in children of the general population and PbB's in children residing 

in LPH's. Table 2 summarizes the available data these studies contained on 

distribution of PbB's in children. This table includes: percentiles, geometric 

means, and geometric standard deviations of PbB's in children whenever they 

appeared in a report. In some cases, geometric means and geometric 

standard deviations were estimated by fitting a lognormal distribution to 

percentile data. For one study, PEI estimated the geometric standard deviation mathematically from the arithmetic mean and arithmetic standard 

deviation. 

In NHANES II, the first study listed in Tables 1 and 2, PbB samples were 

taken of 2372 children aged 6 months to 5 years and living in 64 sampling 

?3 ?4 ?6 

areas during 1976 to 1980. ' ' The children were selected to yield a probability sample representative of the U.S. civilian population. The PbB's in 

these children ranged from 2 to 66 yg/dl. No statistically significant 

correlation was found to exist between PbB's and age or between PbB's and 

the sex of children in this age bracket. Significant correlations between 

PbB's in children and race, urbanization, and family income were present, 

however, a potential source of bias in the NHANES II results could be the 

poor response rate. Initially, 5069 children were selected for PbB 

sampling. Of these, 4876 were interviewed and 4118 were examined. Blood 

samples were missing for 1634 of the 4118 children because of refusals to 

allow the blood tests or because of loss of blood samples during analy23 sis. Only 47 percent of the 5069 children in the original sample produced 

usable blood samples. 
TABLE 1. CHARACTERISTICS OF STUDIES ON DISTRIBUTION OF BLOOD LEAD LEVELS IN U.S. CHILDREN 

Reference 

NHANES 

jj23.24.25 

ASTHO and 

CDC3,21,26-28 

VO 

Billick and 

Gray6 

Stark et 

i 5 al. 

Simpson et 

i 29 al. 

Description of 

study 

General population 

General population 

General population 

LPH's 

General population 

General population 

Location 

Nationwide 

Nationwide 

Nationwide 

New York City 

New York City 

Cincinnati 

New Haven 

New Haven 

27 cities in 

23 states 

Year 

1976-1980 

1973-1983 

1975-1976 

1970-1976 

1976 

9/74-10/75 

12/75-02/77 

1971-1972 

Age of 

children 

6 mo-5.9 yr 

1 yr-6.9 yr 

Children 

1 mo-72 mo 

1 yr-6 yr 

Comments 

1973 data omit Boston, New York 

City, and Detroit 

1974 data omit New York City 

and St. Louis 

1973-1981 - CDC 

1982-1983 - ASTHO, omits Washington, D.C. 

In 1982-1983, 98.1% of children 

with PbB's _> 30 yg/dl lived in 

homes with lead-based paints 

1975 - HUD study, 58% children 

with PbB's _> 40 yg/dl live in 

lead-based painted homes 

Cincinnati - LPH's contain > 2 

2 

mg Pb/cm 

(continued) 
TABLE 1 (continued) 

Reference 

1 • r .30 Lm-Fu 

Hammond et 

, 31 al. 

Galke et 

, 10 al. 

Brunekreff 

14 

NASiH 

Barbara 

Todd32 

Cato Kirk33 

sey 

Joyce La34 PennJH 

Description of 

study 

General population 

General population 

General population 

General population 

General population 

General population 

General population 

'General population 

Location 

21 cities in 

U.S. 

Illinois - 14 

cities 

Rural Dutchess 

County, New 

York, and 

Litchfield 

County, Connecticut 

Cincinnati 

Charleston, 

South Carolina 

Dallas 

Omaha 

Nationwide 

Waterbury, 

Connecticut 

Chicago 

New York City 

Year 

1969-1971 

1971 

1971 

1980 

1973 

1976 

1971-1977 

1973-1978 

FY 1984 

FY 1984 

FY 1984 

Age of 

children 

1 yr-6 yr 

3 mo-3 yr 

0-5 yr 

1 yr-8 yr 

1 yr-5 yr 

0-6 yr 

0-6 yr 

0-6 yr 

Comments 

Study also gives data for the 

following age groups: 0-1 yr, 

1-2 yr, 2-3 yr, 3-4 yr, and 4-5 yr 

Screened high-risk children 

Screened high-risk children 

Screened high-risk children 

(continued) 
TABLE 1 (conti 

Reference 

Walter 3 5 

Sobolesky 

o-i • 19 Gilsinn 

ru 12 Charney 

Urban 

Shier and 

Hall3 6 '

3 7 

Yaffee et 

i 13 al. 

Gilbert et 

al.9 

Landrigan et 

al.3 8 

nued) 

Description of 

study 

General population 

LPH's 

General population 

General population 

LPH's 

Homes with nd leadbased paints 

General population 

LPH's 

Homes with no leadbased paints 

General population 

LPH's 

LPH's 

Homes with no leadbased paints 

LPH's 

Homes with no leadbased paints 

Location 

Philadelphia 

Nationwide 

New York City 

New Haven 

St. Louis 

Washington, DC 

Chicago 

Illinois - 12 

cities 

Baltimore 

Rochester, NY 

Pittsburgh 

California 

Springfield, 

Massachusetts 

El Paso 

Year 

FY 1984 

1972 

1970-1971 

1970 

1970-1971 

1971 

1968-1971 

1971 

1970 

1981 

1974-1975 

1979-1980 

1972 

Age of 

children 

0-6 yr 

0-6.9 yr 

18 mo-35 mo 

0-6.9 yr 

1-15 yr 

1-7 yr 

Comments 

Screened high-risk children 

Number of U.S. children living 

in LPH's who have PbB's _> 40 yg/ 

dl is estimated 

Controls: < 30 yg/dl 

Cases: To - 79 yg/dl 

Lead-based paints defined as > 

1% Pb in paint 

Lead-based paints contain > 1.2 

2 

mg Pb/cm 

Lead paints contain >_ 1% Pb 

—.—.—',..,.. 
TABLE 2. DISTRIBUTION OF BLOOD LEAD LEVELS IN U.S. CHILDREN 

ro 

Study 

NHANES II 

ASTHO and CDC 

1973 

1974 

1975 

1976 

1977 

1978 

1979 

1980 

1981 

1982 

1983 

Billick and Gray 

U.S. 1975 

U.S. 1976 

NYC 1970-76 

NYC 1976 

Cincinnati 

LPH's 

Stark et al. 

9/74-10/75 

12/75- 2/77 

Simpson etal. 

Lin-Fu (1973) 

21 U.S. cities 

14 IL cities 

2 rural co. in 

NY and CT 

Sample 

size 

2.372 

277,346 

371,955 

440,904 

404,818 

380,496 

397,963 

464,751 

502,925 

535,730 

552,235 

676,571 

440,650 

512,532 

766,967 

103,016 

81 

4,461 

2,313 

2,043 

344,657 

6,151 

230 

Percentage children with PbB's (yg/dl) < indicated level 

10 

12.2 

15 20 

75.5 

— 

25 

90.9 

30 

96 

91.7 

92.6 

93.5 

93.0 

94.7 

95.9 

98.0 

98.4 

100 

35 40 

99.5 

89.9 

94.6 

94.5 

93.5 

91.4 

75.6 

73.9 

81.4 

91.0 

45 50 

99.8 

• 

55 

99.0 

60 

99.9 

99.6 

99.0 

65 70 

100 

75 80 

100 

99.2 

PbB (ug/dl) 

Arithmetic 

Mean 

16.0 

sd 

0.42 

Geometric 

Mean 

14.9 

29.0 

24.9 

34.0a 

26.5a 

sd 

1.47 

1.26a 

1.58a 

Value 

Minimum 

2.0 

Maximum 

66.0 

70 

(continued) 

CO 
TABLE 2 (continued) 

00 

Sample 

Study size 

Hammond et al. 131 

Galke et al. 187 

Brunekreef 

Dallas 116 

Omaha 242 

NAS 2,380,942 

Barbara Todd 1,675 

Cato Kirksey 40,000 

Joyce LaPenn 145,000 

Walter Sobolesky 15,358 

Gilsinn . 

LPH's 2,400,000° 

General population: NYC 171,927 

New Haven 1,389 

St. Louis 5,048 

Washington, DC 1,821 

Baltimore 939 

Chicago 147,480 

12 IL cities 6,580 

Charney 

General population 99 

LPH's 36 

Homes with no 

lead-based 

paints 63 

Percentage children with PbB's (ug/dl) < indicated level 

10 15 20 

6.1 

25 30 

93.2 

92.5 

90.0 

99.3 

95.4 

41.1 

51.0 

58.7 

63.9 

35 40 

64.0 

75.0b 

73.8 

77.1 

69.5 

60.8 

68.5 

91.2 

80.6 

15 50 

88.5 

85.8 

83.3 

85.4 

89.7 

55 60 

98.0 

94.7 

92.6 

90.0 

92.4 

92.7 

97.6 

94.9 

65 70 

97.7 

96.4 

98.7 

96.9 

100 

100 

100 

75 80 

97.7 

98 

PbB 

Arithmetic 

Mean 

37.7 

sd 

pg/dl) 

Geometric 

Mean 

12.7 

37a 

16.0 

23.9 

32.5? 

27.5a 

31.0? 

36.5a 

33.0? 

16.5? 

24.5a 

sd 

1.24a 

1.46a 

1.58a 

1.64! 

1.41? 

1.48? 

1.91? 

1.76a 

Value 

Minimum 

2.2 

18.0 

Maximum 

46.5 

77.0 

(continued) 
TABLE 2 (continued) 

Study 

Urban, Shier 

and Hall 

General population 

LPH's 

Homes wi th no 

lead-based 

paints 

Yaffee et al. 

General population 

LPH's 

Gilbert et al. 

LPH's 

Homes with nu 

lead-based 

paints 

Landrigan et al. 

LPH's 

Homes with no 

lead-based 

paints 

Sample 

size 

456 

391 

65 

15,000 

10 

48 

12 

47 

85 

Percentage children with PbB's (ug/dl) < Indicated level 

10 15 

20.0 

20 

50.0 

25 30 

90.0 

99.3 

80.0 

37.5 

100 

35 40 

99.3 

99.0 

68 

61 

45 50 

100 

55 60 65 70 75 

100 

80 

PbB 

Arithmetic 

Mean 

21.9 

22.3 

19.5 

sd 

7.0 

7.1 

6.3 

Mg/dl) 

Geometric 

Mean 

20.7 

20.9 

18.3 

sd 

1.37c 

1.36^ 

1.37c 

Value 

Minimum 

0 

28 

Maximum 

73 

43 

Geometric mean and geometric standard deviation are estimated by graphically fitting lognormal distribution to selected percentiles. 

Estimated value by Judith Gilsinn. 

cEstimated from arithmetic mean, arithmetic standard deviation, and arithmetic mean under the assumption that the distribution is lognormal. 
P.22 

The Association of State and Territorial Health Officials (ASTHO) and 

Center for Disease Control (CDC) screened high-risk children l-to-6-yearsolds in the general population for elevated PbB's. 3 '

2 1 '26,27,2 8 The ASTHO 

and CDC studies only reported the percentage of children whose PbB's were 

elevated above a "clinically acceptable" value. From 1973 to 1975, the 

reported "clinically acceptable" PbB was 40 ug/dl; and from 1976 to 1983, 

it was 30 ug/dl. Because the distributions of PbB's were not presented in 

the study results, PEI could not estimate the geometric means or geometric 

standard deviations for these studies. From 1973 to 1981, CDC screened 

four million children in various cities in the United States. The reported 

results were incomplete for some cities in 1973 and 1974. For example, 

both the 1973 and 1974 data omitted New York City, where a major lead 

poison prevention program was screening approximately 100,000 children 

annually. From 1973 to 1975., the rate of children who had PbB's >_ 40 yg/dl 

varied regionally from 2 percent in EPA Region IX to 9.3 percent in EPA 

Region III.2 In 1982, ASTHO collected PbB data from 26 State health 

agencies; and in 1983, ASTHO collected PbB data from 33 State health 

agencies. The ASTHO data were incomplete and did not contain results of 

the lead poisoning program in Washington, D.C. During 1982 and 1983, the 

percentage of high-risk children with PbB's _> 30 yg/dl varied in different 

areas (0.2% in West Virginia, 1% in New York City, 2.5% in Boston and 

Chicago, 3.2% in Philadelphia, and 9.6% in St. Louis). 

The Billick and Gray study contained the results of national screening 

of high-risk children by the CDC, screening of high-risk children in New 

York City, and screening of children who resided in LPH's in Cincinnati. 

This study did not present any distribution of PbB's in children, but a 

clinically acceptable PbB was reported for each screening. During 1975 and 

1976, approximately 933,000 high-risk children were screened by the CDC. 

Forty to 45 percent of the high-risk children who had PbB's >_ 40 yg/dl 

resided in homes without lead-based paints. From March 1970 to December 

1976, 766,900 high-risk children were screened in New York City. During 

the course of the study, the mean PbB in children decreased, seasonal 

variations occurred with peaks in July and August, and 2- to 4-year-olds 

had the highest PbB's. In Cincinnati, 81 children who resided in LPH's 

2 

with >_ 2 mg lead/cm lead on painted surfaces were screened. All 81 

children had PbB's < 30 yg/dl. 

15 
P.23 

From 1974 to 1977, two investigations in New Haven, Connecticut, measured 

PbB's in children aged one month to 72 months. Stark et al. reported 

the geometric means for the two investigations and compared the PbB's of groups 

. 5 

of children with and without suspected risk factors. The characteristics 

associated with elevated PbB's were found to relate to the impaired ability of 

a family to provide adequate supervision of young children. 

During 1971 and 1972, 2309 children aged 1 to 6 years were screened in 

27 cities in 23 States to determine the percentage of children with PbB's >^ 

40 yg/dl who lived in older housing units. In all but four cities, some 

children were reported to have PbB's >_ 40 yg/dl. In the four cities where no 

children had elevated PbB's, only a limited number of children were screened. 

Using the PbB distribution data presented by Simpson et al., PEI estimated the 

29 geometric mean and geometric standard deviation. 

The distribution of PbB's in children surveyed by blood-screening pro30 

grams in 21 U.S. cities during 1969 to 1971 was discussed by Lin-Fu. The 

children resided in old, poorly maintained neighborhoods. The survey showed 

that 8.8 to 32.9 percent of the screened children had PbB's > 40 yg/dl, 0 to 

— 30 

19.4 percent had PbB's _> 60 yg/dl, and 0 to 7.6 percent had PbB's .> 80 yg/dl. 

Lin-Fu also reported the results of blood-screening programs that tested 6151 

children in 14 Illinois cities with populations of 10,000 to 150,000 and 230 

children in rural areas of New York and Connecticut. Table 2 shows the percentage of children with PbB's _> 40 yg/dl to decrease in less-populated areas. 

The percentage of children with PbB's _> 40 yg/dl decreased from 26.1 in large 

cities to 18.6 in moderate sized cities and down to 9 in rural areas. 

In 1980, Hammond et al. screened 131 Cincinnati children aged 3 months 

31 

to 3 years and related PbB's in children to environmental sources of lead. 

The PbB's. of the screened children ranged from 2.2 to 46.5 yg/dl with a geometric mean PbB of 12.7 yg/dl. The results of the study established a 

definite relationship between the age of housing units and elevated PbB's in 

children. The presence of lead in paint contributed only slightly to the 

elevated PbB's. 

In 1973, 187 newborn to 5 year old children in Charleston, South Carolina, 

were screened to determine if PbB's were related to residency in LPH's. 

Thirty-six percent of the children had PbB's > 40 yg/dl and 2 percent had 

PbB's > 60 yg/dl. Galke et al. found the PbB's in children to vary with soil 

16 
P.24 

lead, average daily traffic volume, and lead in exterior paint. The relationship between lead-based paints and elevated PbB's in the screened children, 

however, was not found to be significant. 

Brunekreef performed regression analyses on data from 19 studies conducted in Europe and North America to determine the relationship between PbB's 

and sources of lead in the environment. PEI has included the geometric mean 

PbB's obtained from screenings of 116 children in Dallas and 242 children in 

Omaha. The Dallas study showed a relationship between average daily traffic 

volume and PbB's in children. The increased geometric mean PbB of children 

screened in Omaha probably resulted from increased lead emissions from smelters 

located in the city and surrounding areas. 

The National Academy of Sciences (NAS) presented national results of 

14 urban screening programs in the United States. Approximately 2.4 million 

children were screened between 1973 and 1978 by local lead poisoning control 

rograms. Nationally, 6.8 percent of the screened children had elevated PbB's 

_> 30 yg/dl; in individual cities , the percentage of children with PbB's >_ 30 

yg/dl ranged from 3 to 20 percent. 

In a telephone survey, PEI contacted individuals in eight cities across 

the United States to obtain current information about lead poisoning prevention programs in the cities. Table 3 lists the individuals who were contacted. 

Only four of those contacted reported relevant information. In the four cities 

represented by this information, the percentage of screened children with PbB's 

_> 30 yg/dl ranged from 0.7 percent in New York City to 10 percent in Chicago. 

In 1972, Gilsinn estimated that of the 17 million U.S. children 6 years 

of age or younger, 2,400,000 resided in high-risk areas in LPH's and 600,000 

19 children had PbB's >_40 yg/dl. She calculated the number of children with 

elevated PbB's by analyzing previous data from blood-screening programs of 

high-risk children. The results of some of these blood-screening programs 

are presented in Tables 1 and 2. Gilsinn developed and tested a model for 

performing her estimate by using.census tract data for calibration of the 

model. When she used SMSA data during the application of the model, she 

experienced problems with aggregation. The Gilsinn model employed the following equation: 

17 
P.25 

TABLE 3. TELEPHONE SURVEY PARTICIPANTS 

Barbara Todd 

Program. Coordinator 

Lead Poison Prevention Program 

Waterbury, Connecticut 

Cato Kirksey 

Environmental Health Division 

Di rector 

Lead Poisoning Prevention Program 

Chicago* Illinois 

Walter Sobolesky 

Lead Abatement Program 

Philadelphia, Pennsylvania 

Ella Witherspoon 

Lead Poisoning Prevention Program 

Washington, DC 

David Nordmeyer 

Environmental State Specialist for 

Minnesota 

Minneapolis, Minnesota 

E. Billick 

Chicago, Illinois 

Margo Branson 

Environmental Assessment Program 

Dallas, Texas 

George Hansel 

Nashville, Tennessee 

Joyce LaPenn 

Bureau of Lead Poisoning 

New York City, New York 

, k, 0.2967 . 0.2484 

E-k6 (^)[0.747(-|) (j})" ] 

where 

E = 

c6 = 

H = 

P = 

d = 

the predicted number of children with elevated PbB's 

the number of children 6 years of age or younger 

the total number of housing units 

the total population 

the number of dilapidated and deteriorated homes. 

In a study of children 18 to 35 months of age, Charney et al. screened 

49 inner-city children in Rochester, New York, with PbB's of 40 to 70 yg/dl 

and FEP's > 59 yg/dl and 50 inner-city children with PbB's <_ 29 yg/dl and 

1? FEP's £5 9 yg/dl . Forty-six percent of the children with elevated PbB's 

and 26 percent of the children with low PbB's resided in LPH's. Because the 

children were preselected for correlating residency in LPH's and PbB, the 

18 
P.26 

Charney study did not provide an accurate distribution of PbB's in children 

who live in LPH's. 

For comparison with the NHANES II study, the Pittsburgh study conducted 

by Shier and Hall and analyzed by Urban produced the best results.1 8 '

3 6 '3 7 

During 1974 and 1975, children aged 6 years and younger in 4000 randomly 

selected homes in Pittsburgh were screened for elevated PbB's. Eight hundred 

children were identified as eligible to participate in the study. Because of 

reluctance of some parents to allow their children to be tested by the public 

health department and lack of lead-based paints in some homes, however, only 

456 children were actually screened, and only 391 of these children lived in 

2 

LPH's with > 2 mg lead/cm on interior painted surfaces. Room-by-room comparison of lead in painted: surfaces of housing units showed that the screened 

children resided in dwellings with greater amounts of lead than the total survey population. Therefore, children not screened probably had lower PbB's 

than the screened children. In the Pittsburgh study, if a relationship existed 

between elevated PbB's in children and residency in LPH's, the bias was in the 

direction of higher PbB's in children. 

An investigation by Yaffee et al. compared the PbB's of 10 children who 

lived in a California duplex with an average paint lead concentration of 63,000 

13 

ppm. Because of the small sample size, however, results of the Yaffee study 

were not compared with those of the other 19 investigations. 

Gilbert et al. examined.48 children who lived in LPH's with >_ 1.2 mg 

2 

lead/cm on painted surfaces and 12 children who resided in homes that cong 

tained no lead-based paints. Thirty of the children, who had PbB's _> 50 yg/dl, 

were designated as case children, and the other 30 children, who had PbB's 

£ 3 0 yg/dl, were classified as controls, the results showed that 18 of the 

controls (60%) lived in LPH's and 30 of the case children (100%) lived in 

LPH's. Because this investigation did not screen the general population of 

children who resided in LPH's, the results of the Gilbert et al. study were 

not compared with the NHANES II results. 

In 1972, Landrigan et al. screened the PbB's in children who resided in 

38 three areas of El Paso that were near a smelter. Forty-seven children who 

lived.in LPH's having paint with > 1 percent lead.content and 85 children who 

lived in homes with no lead-based paints were screened. Thirty-two percent 

of the children who resided in LPH's and 39 percent of the children who 

resided in homes with no lead-based paints had PbB's >_ 40 yg/dl. 

19 
P.27 

SECTION 4 

COMPARISON OF BLOOD LEAD LEVELS OF CHILDREN IN THE 

GENERAL POPULATION AND CHILDREN LIVING IN 

LEAD-BASED PAINTED HOMES 

The PbB screening programs presented in Tables 1 and 2 were yery difficult to compare because most programs screened only high-risk children who 

were more likely to be exposed to lead. The PbB's in high-risk children were 

usually higher than PbB's in children of the general population. Of the 

reviewed studies of PbB's in children of the general population, NHANES II 

used a random screening process, whereas the other studies screened high-risk 

children. The latter studies included ASTHO and CDC, Billick and Gray, Stark 

et al., Simpson et al., Lin-Fu, Hammond et al., Galke et al., Brunekreef, NAS, 

Barbara Todd, Cato Kirksey, Joyce LaPenn, Gilsinn, and Yaffee et al. 

NHANES II, ASTHO and CDC, Billick and Gray, Simpson et al., Lin-Fu, and 

NAS summarized data from national screening programs. The percentage of highrisk 1 to 6 years olds with PbB's j^ 40 ug/dl was greater in national screening 

programs conducted from 1969 to 1972 than NHANES II. Lin-Fu and Simpson et a1. 

reported that approximately 25 percent of the high-risk children screened during 1969 to 1972 had PbB's > 40 yg/dl, and NHANES II reported only 0.5 percent 

of children screened randomly had PbB's _> 40 yg/dl. The significant difference 

between the results of NHANES II and Lin-Fu and Simpson et al. probably occurred because of differences in the characteristics of the sample populations 

of the studies. Between 1973 and 1976, approximately 6 percent of the highrisk children screened nationally by CDC and Billick and Gray had PbB's _> 40 

yg/dl; the number ranged from 5.4 to 10.1 percent. Because CDC, Billick and 

Gray, Lin-Fu, and Simpson et al. screened only high-risk children, the percentages of children with PbB's >_ 40 yg/dl were probably not representative 

of the general population and were greater than the actual percentage of the 

children in.the general population with PbB's 2: 40 yg/dl. Therefore, the 

reported percentage of children with PbB's,2: 40 yg/dl in NHANES II is probably 

more reasonable. 

20 
P.28 

Between 1976 and 1981, CDC screened 1.6 million high-risk children 

nationally, and the percentage of children with PbB's >_ 30 yg/dl ranged from 

8.3 percent in 1976 to 4.1 percent in 1981. From 1973 to 1978, NAS reported 

that 2.38 million high risk children were tested, and 6.8 percent had PbB's 

14 

>_ 30 yg/dl. Although CDC and NAS studies showed similar percentages of highrisk children with PbB's _> 30 yg/dl, NHANES II reported that 4 percent of the 

2372 children randomly selected for screening had PbB's >_ 30 yg/dl. In 1982 

and 1983, approximately 2 percent of the children screened by ASTHO had PbB's 

_> 30 yg/dl. The CDC and ASTHO screening programs produced results similar to 

those of the NHANES II study. 

Other investigations screened high-risk children of the general population in the following areas: New York City, Cincinnati, Dallas, Omaha, 

Chicago, Philadelphia, Baltimore, New Haven, St. Louis, Waterbury, Charleston, 

South Carolina, mid-size cities in Illinois and two rural counties in New York 

and Connecticut. Most of these studies (especially the investigations conducted prior to 1977) showed higher geometric means and geometric standard 

deviations than the NHANES II study. Most of the screening programs in individual cities reported that greater percentages of children had PbB's 21 30 

yg/dl and PbB's 2: 40 yg/dl than children screened during the NHANES II survey. 

In 1980, Hammond showed.a lower geometric mean (12.7 yg/dl) for 131 children 

31 

screened in Cincinnati than children screened in the NHANES II study. Data 

are not available to determine if the Hammond value differs significantly 

from the NHANES II value. In fiscal year 1984, the percentage of children 

screened by lead poisoning prevention programs in Waterbury, Chicago, Philadelphia, and New York City who had PbB's >_ 30 yg/dl ranged from 0.7 percent 

in New York City to 10 percent in Chicago, The percentage of children with 

PbB's >_ 30 yg/dl for these four screening programs were in agreement with the 

percentages reported by NHANES II. 

Of the seven studies that measured the PbB's in children residing in LPH's, 

the Pittsburgh study conducted by Shier and Hall and analyzed by Urban was the 

10 oc 

only investigation that randomly screened children who resided in LPH's. ' 

Studies performed by Charney et al., Yaffee et al., Gilbert et al., and Landrigan et al. compared the PbB's in children and levels of lead on painted 

9 12 13 18 surfaces of homes for case and control groups. ' ' ' Because the four 

studies did not screen the general population of children who resided in LPH's, 

21 
P.29 

the results did not provide an accurate distribution of PbB's in children who 

lived in LPH's and the studies were not compared with results of either the 

Pittsburgh study or the NHANES II study. Billick and Gray measured PbB's in 

81 children living in LPH's in. Cincinnati, and found that all of them had 

PbB's < 30 yg/dl. Because the Cincinnati study sampled fewer children than 

the Pittsburgh study and presented no information concerning sample selection, 

the results of Billick and Gray were not compared with the results of NHANES 

II. The Gilsinn model estimated that 24 percent of children residing in 

19 

LPH's in the United States had PbB's 2: 40 yg/dl. Because Gilsinn's results 

were not based on random screening of children who reside in LPH's, the study 

was not compared with NHANES II. Based on the elimination of six of the studies 

and on the sampling methodology used in the Pittsburgh study, PEI compared 

the results of the NHANES II study with those of the Pittsburgh investigation. 

In Pittsburgh, 0.7 percent of all screened children who resided in LPH's 

and in homes with no lead-based paints had PbB's >_ 40 yg/dl, and 0.5 percent 

of children screened by NHANES II had PbB's ^4 0 ug/cji .

1 8 »2 3 '2 4 '2 5 '3 6 '3 7 The 

geometric mean PbB of the NHANES II study (14.9) was lower than the geometric 

mean PbB of all children screened in Pittsburgh (20.7). In Pittsburgh, 1 percent of the screened children who lived in LPH's had PbB's >_ 40 yg/dl. The 

percentage of children with PbB's >_ 40 yg/dl was not significantly different 

for children screened in the NHANES II study, screened children who lived in 

homes with no lead-based paint in Pittsburgh, and screened children who resided in LPH's in Pittsburgh. Compared with the NHANES II study results, the 

geometric mean PbB's were higher both in Pittsburgh children who resided in 

LPH's and homes with no lead-based paints. The reported geometric mean PbB 

in children screened during NHANES II was 14.9 yg/dl, and the geometric standard deviation was 1.47 yg/dl. For the Pittsburgh study, the reported geometric mean PbB's of children were 20.7 yg/dl in LPH's and homes with no 

lead-based paints, 20.9 yg/dl in LPH's, and 18.3 yg/dl in homes with no leadbased paints. 

Although PEI compared the results of the NHANES II study with the Pittsburgh study, the results of the comparison may be misleading because of the 

different years that the studies were conducted. From 1975 (the year of the 

Pittsburgh study) to 1980 (the final year of the NHANES II study), lead exposure declined. Therefore, the results of the two studies cannot be compared 

22 
P.30 

accurately from the available literature. PEI provided the best comparison 

of the data. To provide a better comparison of PbB's in children of the 

general population and in children who reside in LPH's, additional studies 

of randomly selected samples of children living in LPH's are needed, 

especially in large metropolitan areas of the United States. 

23 
P.31 

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P.32 

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26