Legacy of Lead: Report and Proposal for Legislative Action

    LEGACY OF LEAD: 
AMERICA’S 
CONTINUING 
EPIDEMIC OF 
CHILDHOOD 

LEAD POISONING 

 



  

LEGACY OF LEAD: 

AMERICA’S CONTINUING EPIDEMIC 
OF 

CHILDHOOD LEAD POISONING 

A Report 

and Proposal 

for Legislative Action 

Written by 

Karen L. Florini 

Senior Attorney 

Environmental Defense Fund 

George D. Krumbhaar, Jr. 

Consulting Author 

Ellen K. Silbergeld 

Senior Toxicologist 

Environmental Defense Fund 

March 1990 

Environmental Defense Fund 

Washington, DC 

 



  

© Copyright 1990, Environmental Defense Fund 
2" Printing. Printed on recycled paper. 

Acknowledgements 

The authors gratefully acknowledge the assistance of numerous 

individuals in preparing this report. Special thanks are due to Annemarie 

Crocetti, Ph.D., who prepared the regional data analysis in Appendix I; 

Stephanie Pollack, Esq., of the Conservation Law Foundation for her 

extensive comments on an earlier draft; and to Dr. Lawrence Goulder, 

Department of Economics, Stanford University, and Dr. Susan Cohen, 

Columbia University, for their assistance on economic issues. 

Additional extremely helpful comments were received from Eliza- 

beth Feuer, MD; Cheryl Burke, Esq., of Aiken, Gump; Herbert L. Needle- 

man, MD, of the University of Pittsburg Department of Psychiatry; Keith 

Winston; Mary Lynn Sferrazza; and Jerry McLaughlin. 

All errors are entirely the responsibility of the authors. 

Environmental Defense Fund 

1616 P st. NW 

Washington, DC 20036 
(202) 387-3500 

Document layout by Keith Winston. 

 



TABLE OF CONTENTS 

EXECUTIVE SUMMARY AND OVERVIEW 

Introduction 

The Toxicity and Pervasiveness of Lead 

Exposure Levels and the Environmental Reservoir of Lead 

Toward a Solution: A Proposal for Legislative Action 

PART I: UNDERSTANDING THE PROBLEM 

1. THE TOXICITY OF LEAD 

Neurotoxic Effects 

Cancer 

Reproductive Effects 

Effects on Blood Pressure 

2. EVALUATING EXPOSURES TO LEAD 

3. SOURCES AND PATHWAYS OF LEAD EXPOSURE 

Lead-Based Paint 

Gasoline 

Drinking Water 

Food 

Continuing Uses of Lead in Commerce 

Auto Batteries 

Other Uses 

4. NUMBERS OF INDIVIDUALS AFFECTED 

Children 

Fetuses 

Adults 

A Final Note 

5. TREATMENT AND PREVENTION OPTIONS 

Limitations of Conventional Treatment 

The Preventive Approach: Getting the Lead Out 

6. GOVERNMENT ACTION -- AND INACTION -- ON LEAD 

The Lead-Based Paint Poisoning Prevention Act 

Limits on the Use of Lead Paint 

Grant Programs 

Paint Abatement Efforts 

State and Local Action on Lead Paint 

Federal Controls on Other Lead Sources 

Lead in Air 

Lead in Soil 

Lead in Solid Waste 

Lead in Drinking Water 

Summary of Government Efforts  



  

  

PART lI: TOWARD A SOLUTION: 

A PROPOSAL FOR LEGISLATIVE ACTION 

7. SETTING GOALS AND PRIORITIES 

FOR FUTURE ACTION 

Identifying groups most at risk 

Establishing “least cost” methods 

Erecting administrative and budgetary safeguards 

Joining new efforts with secondary goals 

8. AN OUTLINE OF THE PROPOSAL 

The trust fund 
The excise fee 
Flexibility 
Administration 
Hiring Preferences 
Abatement Technology Development 
Abatement Oversight 

CONCLUSION: Future Concerns 

APPENDIX I: Geographical Distributions 

of Lead-Poisoned Children 

BIBLIOGRAPHY 

 



  

Introduction 

As a tragic legacy of the decades-long use of leaded products on a vast 

scale, lead today pervades America’s environment The result is a nation- 

wide epidemic of low-level lead poisoning, an epidemic that is causing 

permanent neurologic damage to millions of American children. Recent 

studies demonstrate that the long-term consequences of this disease are 

profound: children who had moderately elevated lead levels in early child- 

hood later exhibited seven-fold increases in school dropout rates, six-fold in- 

creases in reading disabilities, and lower final high school class standing.’ 

These effects occurred even though the inital exposures caused no overt 

symptoms. 

Although no precise national measurements have been collected, the 

federal government estimates that well over three million pre-school chil- 

dren -- more than 1 in every 6 -- have dangerously elevated lead levels. Poor 

and minority children are disproportionally affected, but the problem cuts 

across all socioeconomic lines. 

The consequences of low-level lead poisoning are devastating not only 

for the affected children and their families, but also for society as a whole. 

As the Secretary of Education observed earlier this year, reading and writing 

skills of the nation’s children remain “dreadfully inadequate” despite a 

decade of educational reform. The new data suggest that lead is partly to 

blame. By the same token, until children’s lead exposures are substantially 

curtailed, the nation will continue to fall short of its educational goals. 

The severity of the nation’s lead-poisoning crisis has gone generally 

unrecognized for decades largely because the great majority of cases have 

never been diagnosed. The effects of Jow-level lead poisoning, through 

severe, are not unique or obvious. Unlike the readily observable signs of 

chicken pox, for example, the impairment of intellectual ability caused by 

low-level lead poisoning is hard to pinpoint in individual children. Even 

when identified, such symptoms overlap with those of a variety of other 

biological and socioeconomic factors. Only recently, with the completion of 

sophisticated long-term studies, was the compelling association between 

childhood lead poisoning and significant neurologic impairmentrecognized. 

The Toxicity of Lead 

In the human body, lead is a potent poison that can affect individuals 

in any age group. Children and fetuses are particularly vulnerable, because 

their rapidly developing nervous systems are sensitive to lead’s potency as 

a neurotoxin. Moreover, children generally are exposed tomore lead thanare 

  

  

+ See HL Needleman, A Schell, D Bellinger, A Leviton, and EN Allred 

(1990), “The Long-Term Effects of Exposure to Low Doses of Lead In 

Childhood,” New Enaland Journal of Medicine, Vol. 322, pp. 83-88. 
  

EXECUTIVE SUMMARY 

AND OVERVIEW 

The federal government estimates 

that welloverthree million pre-school 

children -- more than 1 in every 6 -- 

have dangerously elevated lead 

levels. 

 



  

Many public health experts now be- 

lieve that lead presents a “continuum 

of toxicity,” in which the slightest 

exposure contributes to an adverse 

result somewhere in the body 

adults, and their absorption rates are substantially higher. 

Lead’s specific neurotoxic effects include impairments to IQ level, 

short-term memory, and reaction time; it also impairs the ability to concen- 

trate. In adults, low-level lead exposure has been associated with hyperten- 

sion in men and pregnancy complications in women, including minor birth 

defects. 

Once absorbed, lead is stored primarily in bone. To a lesser degree, 

I storage also occurs in the kidneys and the brain, while a small portion remains 

  

  

in circulation in the blood. Lead’s persistence in the body is unequalled by 

virtually any other toxin. Its “half life” in bone -- the time it takes half of a 

given dose to be removed -- exceeds twenty years. As a result, even small 

amounts of lead accumulate in the body, and can cause effects that endure 

long after exposure ends. Further, because stored lead can be released during 

pregnancy and readily transferred to the fetus, lead poisoning is, in effect, a 

heritable disease. 

In the early and middle decades of this century, lead was generally 

thought to be harmful only at high doses. Subsequent research, however, has 

uncovered a variety of effects at lower and lower levels. This trend has 

accelerated within the last few years, as increasingly sensitive analytic 

techniques allow investigators to document consequences that persist for 

years after initial exposure. Many public health experts now believe that lead 

presents a “continuum of toxicity,” in which the slightest exposure contrib- 

utes to an adverse result somewhere in the body. 

Because lead causes neurologic damage even atdoses that do not cause 

overt toxicity, levels of lead in blood are generally used in identifying lead 

exposures of concern. The federal government’s Centers for Disease 

Control (part of the Public Health Service) is currently reviewing its 

definition of “lead toxicity,” which is now set at 25 micrograms of lead per 

deciliter of blood (ug/dl); CDC is expected to adopt a new definition of 

between 10 and 15 ug/dl within the year. The U.S. Environmental Protection 

Agency, along with many public health experts, has already recognized that 

blood-lead levels of 10 to 15 ug/dl cause neurotoxic effects in children. This 

report uses the term “low-level lead poisoning” to denote these levels and the 

associated health effects. 

Even at the 25 ug/dl level, the very limited lead-screening programs 

now in place uncover over 10,000 previously unreported cases of poisoning 

each year. Indeed, though little recognized by the general public, the scale 

of this insidious epidemic makes it among the most common diseases of 

childhood.? It is also nationwide in scope, as an analysis of the estimated 

numbers of affected children throughout the country reveals. Exposures are 

  

  

2 Some common childhood illnesses and their reported 1988 incidence 

rates include: 

Lead Poisoning (25+ ug/dl) 11,793 
Viral meningitis 6,927 
Mumps 4,730 

Whooping cough 3,008 

Measles 2,933 

Source: Centers for Disease Control. The Centers’ records include 

only cases that were identified through screening programs and reported by 
health officials; therefore, these must be considered minimum figures. 

 



   
endemic in some urban regions, with over 50 % of children under 6 estimated 

to have blood lead levels over 10 ug/dl.? 

As a practical matter, prevention is the only realistic “cure” for lead 

poisoning. Available treatments are expensive and painful, do not com- 

pletely remove lead from the body, and are powerless to undo neurologic 

damage. But little has been done to prevent childrens’ exposures to lead 

already dispersed into existing environmental reservoirs. 

Exposure Levels and the 

Environmental Reservoir of Lead 
Most children are exposed to lead as a result of its presence in paint, 

plumbing, gasoline, solder, and other products. Over many decades, these 

uses have dispersed millions of tons of lead throughout the environment. 

And that reservoir continues to grow each year, as the United States uses 

another million-plus tons of lead in products such as automotive batteries, 

construction materials, gasoline, and other items. Because lead is an 

element, no force save a nuclear reaction can transform it into a more 

innocuous material; once excavated from the earth and distributed in 

commerce, lead can exert its inherent toxicity on the biosphere almost 

indefinitely. 

Of all the sources that make up the existing reservoir of environmental 

lead, one is responsible for especially intense exposures for many children: 

the three million tons of leaded paint remaining on the walls and woodwork 

of American homes. Though banned for most uses in 1977, leaded paint 

applied during the preceding decades continues to present a hazard. An 

estimated 1.2 million children under 6 absorb enough lead from deteriorated 

paint to elevate their blood-lead levels beyond 15 ug/dl, with a significant 

chance of subsequent neurologic impairment. 

Although the pronounced long-term consequences of childhood lead 

poisoning have only recently been identified, its more obvious manifesta- 

tions have been a focus of concern for decades. As early as 1904, reports of 

childhood lead intoxication appeared in the medical literature. Butdue to the 

limited diagnostic capabilities of the time, only the most obvious cases were 

identified -- those involving high doses of lead resulting in readily observable 

effects suchas convulsions, coma, and even death. With the advent of blood- 

lead determinations in the 1940s and ’50s, however, it became increasingly 

apparent that the problem was far greater in scope than had been recognized 

previously. 

Citing the “epidemic proportions” of childhood lead poisoning, 

Congress first took action in 1970 to eliminate a primary source of children’s 

exposures. The Lead-Based Paint Poisoning Prevention Act of 1971* 

authorized a wide range of actions designed to identify and treat those 

already harmed, to remove lead-based paint from federally-assisted homes, 

and to prohibit its use in areas thought to be accessible to children. Unfor- 

tunately, implementation of key provisions faltered badly almost from the 

start. As a result, two decades later the epidemic persists. 

  

  

3 Geographical distributions of lead-affected children are described in 

Appendix 1. 

1.42 U.S.C, sections 4801-4846. 

  
  

The reservoir continues to grow 

each year, as the United States uses 

another million-plus tons of lead in 

products such as automotive batter- 

ies, construction materials, gasoline, 

and other items. 

 



  

"Ideally, in keeping with the pre- 

cepts of primary prevention, lead 

should have been prohibited from 

ever having been dispersed in the 

modern environment." 

American Academy of Pediatrics 

  

  

The role of paint is even clearer today than it was twenty years ago, for 

many other major sources of lead have been at least partially controlled in the 

interim. For the American populace as a whole, the most. significant 

reductions in lead exposure have resulted from the phase-down in use of 

leaded gasoline over the last fifteen years. But while this step has provided 

important benefits in reducing lead exposures for many people, it has done 

little to aid those children whose primary source of lead is from paint. And 

these children -- many of them poor and/or minorities -- are precisely the 

same individuals who are most disadvantaged by a myriad of other social and 

economic factors. 

Toward a Solution: 

A Proposal for Legislative Action 

The massive amounts of information on lead’s toxicity -- bolstered by 

recent findings on low exposure level effects -- as well as indications of 

children’s current exposure levels, reveal an urgent need for an aggressive 

federal program to control America’s continuing epidemic of lead poisoning. 

To be effective, such a program must provide a mechanism not only to stop 

adding lead to children’s environments, but also to remove it from the areas 

where they are most heavily exposed: their homes. And, to be politically 

feasible, it must respond to current budgetary realities the nation now faces. 

The Environmental Defense Fund proposes creation of a National 

Lead Paint Abatement Trust Fund, to be financed by placement of a 

substantial excise fee on the production and importation of lead. Proceeds 

from the fund initially would be devoted to the removal of deteriorating lead- 

based paint from the group of highest-risk homes. In addition, a portion of 

the monies could be made available for research to develop more effective 

lead-removal methods. 

The program would be implemented jointly by the Environmental Pro- 

tection Agency and the Department of Health and Human Services. It would 

contain provisions to enable it to reflect market conditions and, where 

possible, accomplish secondary goals of improving housing and creating 

employment opportunities by hiring and training workers for abatement 

programs. In addition, by avoiding the slow and resource-intensive process 

of developing a regulatory approach to control continuing uses of lead in 

products, it would yield results far more quickly than would more traditional 

approaches. 

While the proposed program would not alleviate every aspect of the 

nation’s current lead poisoning epidemic, it would constitute a pragmatic and 

timely next step. Lead poisoning already burdens America with millions of 

dollars of costs each year -- both the direct costs of medical treatments, and 

the indirect social costs of special education, lost income, and a less 

productive citizenry. Italso imposes grave handicaps on individual children, 

their families, and their communities. For them and for the nation as a whole, 

these handicaps will only intensify as the transition to the twenty-first 

century’s “information age” continues. By creating a nationwide paint- 

abatement program funded by a lead excise tax, America can permanently 

reduce lead exposures and bring about a significant improvement in the 

health and abilities of the nation’s children -- now and for generations to 

come. 

 



1. THE TOXICITY OF LEAD’ 

Lead's primary effect of concern is neurotoxic 

damage to fetuses and preschool children, for this effect 

occurs at levels of exposure that are commonplace in con- 

temporary society. Low levels of lead exposure can also 

cause kidney damage and high blood pressure in adults. 

Upon entering the body, lead makes its way into the blood stream; into 

soft body tissue, including the brain and kidneys; and into the “hard tissues,” 

such as bone and teeth.? Biood-lead content is generally considered to be the 

most accurate measure of short-term lead exposure. The estimated half life 

of blood lead (i.e., the time required for one half of the lead to disappear) is 

35 days.?> While about 50 to 60 percent of the lead entering a person’s body 

is eliminated fairly rapidly ,* most of the remainder is stored in bone, where 

it stays for far longer periods. In fact, lead in bone has an estimated half life 

of about 20 years. 

Long thought to be inert, bone-based lead isnow looked on asa double 

threat to the body. Bone is a living tissue that is itself sensitive to toxic 

assaults.® Many conditions, moreover, can rapidly release bone-based lead 

back into the blood stream. For example, pregnancy and osteoporosis, both 

  

  

" The documentation of lead’s toxic effects is immense. Key sources 

include: Agency for Toxic Substances and Disease Registry (1988), The 

Nature and Extent of Lead Poisoning in Children in the United States: A 

Report to Congress (Atlanta: U.S. Dep't of Health and Human Services/Public 

Health Service), Doc. No. 99-2966, especially Chapters lll and IV; U.S. En- 

vironmental Protection Agency (1986a), Air Quality Criteria Document for 

Lead, Vols. I through IV; Centers for Disease Control (1985), Preventing Lead 

Poisoning in Young Children, (Atlanta: Dept of Health and Human Services/ 

U.S. Public Health Service). Excellent review articles include HL Needleman 

(1988a), “Why We Should Worry About Lead Poisoning,” Contemporary 

Pediatrics, pp. 34 - 56; JM Davis and DJ Svensgaard (1987), “Lead and Child 

Development,” Nature, Vol. 329, pp. 299-300; HL Needleman (1 988b), “The 

Persistent Threat of Lead: Medical and Sociological Issues,” Current Prob- 

lems in Pediatrics, Vol. XVIII, pp. 703-76; EK Silbergeld (1985), “Neurotoxi- 

cology of Lead,” in K Blum and L Manzo (eds.), Neurotoxicology (Amsterdam: 

Dekker). 

  

  

  

  

  

2 MB Rabinowitz, GW Wetherill, and JD Kopple (1976), "Kinetic 

Analysis of Lead Metabolism in Healthy Humans,” Journal of Clinical Inves- 

tigation, Vol. 58, p. 260. 
  

3 Ibid. 

4 Agency for Toxic Substances and Disease Registry (1988), p. I-7. 

5 Rabinowitz et al. (1976). 

¢ Agency for Toxic Substances and Disease Registry (1988), p. Il-7. 

PART I: 
UNDERSTANDING THE 

PROBLEM 

Lead makes its way into the blood 

stream; into soft body tissue, includ- 

ing the brain and kidneys; and into 

the “hard tissues,” such as bone and 

teeth. 

 



  

“At a sufficient level of lead expo- 

sure, virtually all body systems will 

be injured or have a high risk of in- 

jury.” 

  

  

of which cause demineralization of bone, have been associated with sharp 

rises in blood lead levels.” Indeed, lead moves from bone to other parts of the 

body readily enough that it may well be an “insidious source” of long term 

lead poisoning.® 

An important aspect of lead’s menace, therefore, is its cumulative 

effect. Even seemingly trivial exposures, if often repeated, can add up to 

doses that exert toxic effects.’ 
And virtually no part of the body is immune from lead. As one recent 

analysis put it, “At a sufficient level of lead exposure, virtually all body 

systems will be injured or have a high risk of injury.”'® While researchers 

have not yet discerned the exact biological mechanisms of lead toxicity, they 

have extensively documented its effects on a number of organ systems at the 

cellular level. 

The most important effects of lead involve disruption of energy 

metabolism at the cellular level and interference with neural cell function in 

the brain. Specifically, lead interferes with the formation of heme, the 

molecule that carries oxygen in all cells.!! In the nervous system, lead has 

a unique ability to inhibit communication and slow motor nerve conduction 

velocity? -- the speed at which nerves process signals. !? 

Neurotoxic Effects: Lead’s neurotoxic effects at relatively low 

exposure levels include decreased intelligence, short-term memory loss, 

reading and spelling under-achievement, impairment of visual-motor func- 

tioning, poor perceptual integration, poor classroom behavior, and impaired 

reaction time. Children and fetuses are especially susceptible to these 

effects, because their neurologic systems are rapidly developing.!* Growing 

  

  

7 EK Silbergeld, J Schwartz, and KR Mahaffey (1988), “Lead and Os- 
teoporosis: Mobilization of Lead from Bone in Menopausal Women,” Environ- 

mental Research, Vol. 47, p. 79. 
  

8 Environmental Protection Agency (1986a), Vol. IV, p. 13-16. 

® Centers for Disease Control (1985), p. 3. 

10 Agency for Toxic Substances and Disease Registry (1988), p. IV-3. 

'! Silbergeld (1985). 

'2 |bid.; see also, PJ Landrigan (1989), “Toxicity of Lead at Low Dose,” 

British Journal of Industrial Medicine, Vol. 46, pp. 593-4. 

3 In addition to these effects of low-level lead exposure, effects of high- 
level exposures are also varied, and include anemia, brain damage, muscle 
palsy, kidney failure, headache and vomiting, convulsions, and death. These 
high-dose effects have been known for centuries. The first known clinical ac- 
count of lead poisoning comes from the first century B.C., while Hippocrates 
offered unconfirmed descriptions two centuries earlier. See HA Waldron 
(1973), “Lead Poisoning in the Ancient World,” Medical History, Vol. 17, pp. 
391-99. In eighteenth century Massachusetts, lawmakers enacted one of the 

country’s first public health statutes after recognizing the health effects of 
drinking “rum and other strong liquors” from leaded containers. See CP 

McCord (1953), “Lead and Lead Poisoning in Early America: Benjamin 

Franklin and Lead Poisoning,” Industrial Medicine and Surgery, Vol. 22, p. 

397. 

4 Centers for Disease Control (1985), p.1.



  

evidence indicates that the effects of lead poisoning occur before any overt 

symptoms appear and often constitute a serious health problem even in the 

absence of obvious symptoms. 

Several key epidemiologic studies in recent years have compellingly 

demonstrated the range of lead’s effects on a variety of populations.’®* Most 

of these studies are retrospective, meaning that researchers identify a group 

of children, determine their lead levels, and evaluate their current health 

status in an attempt to ascertain the effects of prior lead exposure. Although 

lead poisoning is often viewed as primarily a disease of the poor, wealth and 

social status confer no immunity. Indeed, a recent government study 

concluded that children living above the poverty level comprise the largest 

category of people in danger of undue exposure.’ 

A series of landmark studies on lead neurotoxicity have been con- 

ducted by Dr. Herbert Needleman of the University of Pittsburgh and his 

colleagues. The researchers collected baby teeth -- which, like bone, serve 

as long-term storage sites for lead -- from over 2300 first and second graders 

in two suburban Boston school districts. They then categorized the children 

according to dentine (tooth) lead levels 7, and identified two. groups for 

further study: alow-lead group of 100 children who had extremely low levels 

and a high-lead group 58 children who had relatively high levels but who had 

no symptoms of overt lead poisoning.!®* Those 158 children were then 

evaluated using an array of standardized and some nonstandardized neurop- 

sychological tests. 

When the results were controlled for 39 other factors (such as socio- 

economic status, family size, and mother’s IQ), children in the high-lead 

group had a median IQ deficit of six points compared to their low-lead 

classmates, as well as shorter attention spans and imparied language skills. 

Even more striking was the effect on the overall distribution on IQ scores: the 

children in the higher-lead group were almost four times as likely to have an 

IQ below 80, while none of them scored above 125.1° 

Also striking were the results of evaluations by the children’s teachers 

(who did not know their pupils’ lead status). Using an 11-item scale that 

examined classroom behavior, attention, and overall functioning, teachers 

concluded that children with elevated lead levels scored significantly worse 

than the low-lead group. 

Five years later, the researchers re-examined these two groups of 

  

  

'5 Agency for Toxic Substances and Disease Registry (1988), p. 1-48. 

'® For an outline of epidemiological considerations, see sidebar below 
and Needleman (1990b), p. 677. 

'7 The high lead group had dentine levels above 24 parts per million 

(ppm); the low-lead group had dentine levels below 6 ppm. 

'® These 158 children were a subset of the 270 children with levels 

above 24 or below 6. Others were excluded to avoid possible confounding 
factors such as head injuries, acute lead poisoning, and variable lead levels 

in different teeth. 

' Needleman (1988a). 

20 Bellinger, D, HL Needleman, R Bromfield, and M Montz (1984), "A 
Follow-up Study of the Academic Attainment and Classroom Behavior of 

  

Although lead poisoning is often 

viewed as primarily a disease of the 

poor, wealth and social status confer 

no immunity. Indeed, a recent gov- 

ernment study concluded that chil- 

dren living above the poverty level 

comprise the largest category of 

people in danger of undue exposure. 

 



  

C
u
m
u
l
a
t
i
v
e
 
F
r
e
q
u
e
n
c
y
 

Di
st
ri
bu
ti
on
 

(%
) 

THE IMPORTANCE OF SMALL NUMBERS 

Figure 1 shows the frequency distribution 

of IQ scores between the “low lead” and “high 

lead” children, and indicates that high blood 

lead levels are associated with a left-ward shift 

in the overall IQ distribution curve. In addition 

to showing that the median IQ deficit is 6 

points, these data also illustrate two other key 

points: (1) High lead children in this case were 

almost four times as likely to have IQs of less 

than 80; and (2) five percent of the low lead 

group had IQs of more than 125, while none of | 

the high lead group did. 

In other words, lead’s effect on a population 

as a wholeis more dramatic than its effects on 

individuals, by affecting the frequency of high 

and low scores. The disadvantaged are further 

harmed, while the truly gifted are deprived of 

their potential. 

  

  

[remem 
High Leas ® ! 

(Lowieaa 4 | 

  

  

Tested Verbal IQ 

  

  

FIGURE 1 

DISTRIBUTION OF IQ SCORES   

children.®® The high-lead group had lower IQ scores, needed more special 

academic services, and had a higher rate of school failure. Eleven years after 

the initial study, a second follow-up was conducted, to determine whether 

lead’s effects persist into young adulthood.? The findings were dramatic: 

compared to the lower-lead classmates, the higher-lead group showed a 7.4 

increase in school dropout rates, and a 5.8 increase in reading disabilities 

(defined by scoring two or more grade levels below that expected for the 

highest grade completed). The higher-lead group also exhibited lower class 

rank and higher absenteeism. 

Other researchers have also found effects in epidemiological studies 

on lead-exposed children, though some have conducted similar studies and 

reported no effects. All studies published since 1972 were recently evaluated 

using meta-analysis, a technique thatallows investigators to pool data across 

studies and to draw conclusions as to the statistical reliability of the data 

taken collectively.? 
After eliminating studies that failed to meet key criteria such as 

adequate sample size, exclusion of acutely poisoned children, and controls 

for socioeconomic factors, data from the remaining twelve studies were 

pooled. The outcome strongly supports a linkage between low-dose lead 

exposure and intellectual deficits in children. 

Further evidence of lead’s neurotoxicity comes from a series of 

prospective studies, in which investigators measure variables over an ex- 

tended period of time into the future. Recent studies have found notable 

effects from prenatal lead exposures at very low levels. In fact, one study 

found effects from prenatal exposures as low as 6 to 7 ug/dL.% 

For example, in a study of several hundred children whose prenatal 

lead exposure had been determined from umbilical cord blood samples at the 

time of birth, investigators found that even moderate lead levels affected the 

  

  

Children with Elevated Dentine Lead Levels,” 

Besearch, Vol. 6, pp. 207-223. 

Biological Trace Elements 

21 Diagram adapted from HL Needleman (1988a). 

2 HL Needleman, et al. (1990a), “The Long-Term Effects of Exposure 
to Low Doses of Lead in Childhood,” New England Journal of Medicine Vol. 

322, pp. 83-88. Researchers were able to trace and evaluate about half of the 

original participants. The others could not be located or refused to participate. 

The group that was retested tended to have lower dentine levels, higher IQs, 

and better school behavior reports. As aresult, it seems likely thatthe 11-year 

follow-up may underestimate lead’s long-term effects, since a higher percent- 

age of the most severely affected individuals did not participate. 

22 HL Needleman, CA Gatsonis (1990b), “Low Level Lead Exposure 

and the IQ of Children,” Journal of the American Medical Association, Vol. 
263, pp. 673-678. 

24 For detailed discussion of these studies, see Agency for Toxic Sub- 
stances and Disease Registry (1988), pp. 1V-8 to IV-13. 

23 Bellinger, D, A Levitan, C Waternaux, HL Needleman, and M 

Rabinowitz (1989),"Low-level Lead Exposure, Social Class, and Infant 

Development,” Neurotoxicology and Teratology, Vol. 10, pp 497-503. 

 



children’s performance on mental-development tests up to two years later. 

Similar outcomes have been found in studies in Port Pirie, Australia and 

Cincinnati, Ohio.? In the words of the American Academy of Pediatrics, the 

available data have “shown conclusively” that reduction in intelligence and 

alteration in behavior occur in children with elevated blood lead levels.” 

In addition to these extremely disturbing findings on the consequences 

of lead exposure in children and fetuses, a growing body of research is 

showing that low levels of lead also exert toxic effects on adults, including 

cancer, reproductive effects, and high blood pressure. 

Cancer: The U.S. Environmental Protection Agency has classified 

lead as a “probable human carcinogen,” based on data from animal studies.” 

Recently, EPA’s Science Advisory Board, which is comprised of outside 

experts from industry and academia, formally reviewed EPA’s classification 

and endorsed it.?° Researchers are currently comparing lead’s potency as a 

carcinogen to its potency as a neurotoxin.*! 

Reproductive Effects: Experiments on laboratory animals give ample 

evidence of leads toxic effects on the reproductive system (e.g., failure of 

ovulation, delayed sexual maturity, impotence, sterility, spontaneous abor- 

tions).>? While there are fewer data on the reproductive effects in humans, 

there are numerous reports of an increase in spontaneous abortions, structur- 

ally abnormal sperm, and decreased fertility in lead-poisoned adults.* 

Effects on Blood Pressure: An additional threat to adult males is 

indicated by evidence showing a link between low-level lead exposure and 

    

26 D Bellinger, A Leviton, C Watermaux, HL Needleman, and M 

Rabinowitz (1987), “Longitudinal Analyses of Prenatal and Postnatal Lead 

Exposure and Early Cognitive Development, New England Journal of Medi- 

cine, Vol. 316, pp. 1037, 1039. ; 
  

27 AJ McMichael, PA Baghurst, NR Wigg, GV Vimpai, EF Robertson, 
RJ Roberts (1988), “Port Pirie Cohort Study: Environmental Exposure to 

Lead and Children’s Abilities at the Age of Four Years,” New England Journal 

of Medicine, Vol. 319, pp. 468-75; KN Dietrich, KM Krafft, RL Bornschein 
(1987), “Low Level Fetal Exposure Effect on Neurobehavioral Development 

in Early Infancy,” Pediatrics, Vol. 5, pp. 721-30. 

  

26 American Academy of Pediatrics (1987), “Statement on Childhood 
Lead Poisoning,” Pediatrics, Vol. 79, pp. 457. 

20 See 50 Fed. Reg. 46936 (Nov. 13, 1985). 

3% Environmerital Protection Agency, Scientific Advisory Board (De- 
cember 1989), “Report of the Joint Study Group on Lead: Review of LEad 
Carcinogenicity and EPA Scientific Policy on Lead,” (Doc. No. EPA-SAB- 
EHC-90-001), p. 1. 

31 Research underway at University of Maryland, Program in Toxicol- 
ogy. 

32 HL Needleman and PJ Landrigan (1981), “The Health Effects of Low 
Level Exposureto Lead,” Annual Review of Public Health, Vol. 1981, pp. 277- 
98. 
  

3 Ibid. 

  

  

DETERMINING CAUSE AND EFFECT 

THROUGH EPIDEMIOLOGICAL 

STUDIES 

In epidemiological studies, groups of people 

are studied in order to determine patterns of 

disease. Those patterns are then analyzed 

statistically in order to reveal links between a 

particular substance and certain health ef- 

fects. 

Scientists attempting to show cause and 

effect through epidemiological studies use 

five rules of thumb that, taken together, serve 

as a rigorous test of causality. There are: 

1. Order of precedence. The “cause” must 

precede the “effect.” 

2. Consistency. There must be broad con- 

sistency among data both internally, and 

among different studies. 

3. Dose-response. Causality can be more 

strongly inferred when variations inthe “cause” 

are associated with variations in the “effect.” 

4. Specificity. If the same effect can be 

produced by other means, the cause-effect 

relationship under scrutiny is weakened. Ifthe 

effect can be produced only by the cause, the 

relationship is strengthened. 

5. Biological plausibility. Put simply, this 

test asks whether, in light of current knowl- 

edge of human biology, the cause/effect rela- 

tionship seem likely. 

All five criteria are met for studies on the 

neurotoxicity of lead.  



Given the role of cardiovascular 

disease as the number one cause of 

death in America, even “small” in- 

creases in average blood pressure 

are of significant concern. 

  

high blood pressure.** Although differences between blood-pressure values 

were relatively small, the effect nonetheless is of concern from a public 

health perspective. Like lead’s effects on IQ distribution, the consequences 

of even a small shift in the distribution curve for blood pressures can be 

severe on a population-wide basis. Given the role of cardiovascular disease 

as the number one cause of death in America, even “small” increases in 

average blood pressure are of significant concern. 

  

  

3 In a statistical analysis based on a national health survey of 9,932 
persons of all ages, one researcher found a “robust relationship between low- 
level lead exposure and blood pressure” in aduit males. J Schwartz (1988), 

“The Relationship Between Blood Lead and Blood Pressure inthe NHANES 
Il Survey,” Environmental Health Perspectives, Vol. 78, pp. 15-22. Areanaly- 
sis of the same data for males between the ages of 12 and 74, using a different 

and rather conservative statistical technique, also found a significant linear 
association between blood lead levels and blood pressures. JR Landis and 

KM Flegal (1988), “A Generalized Mantel-Haenszel Analysis of the Regres- 

sion of Blood Pressure on Blood Lead Using NHANES Il Data,” Environ- 
mental Health Perspectives, Vol. 78, pp. 35-42. While the actual differences 

in blood pressure inthese and other studies are small, the consistency across 

studies is strong. W Victery, HA Tyroler, R Volpe, and LD Grant (1988), 

“Summary of Discussion Sessions: Symposium on Lead-Blood Pressure 

Relationships,” in U.S. Department of Health and Human Services, Environ- 

mental Health Perspectives, Vol. 78, pp. 139-155. 

   



2. EVALUATING EXPOSURES TO LEAD 

Most public health experts now agree that lead 

exhibits a “continuum of toxicity,” where the smallest 

exposure can have a consequence somewhere in the body. 

This marks a radical departure from the approach to the 

problem only a few years ago. 

Because most cases of lead poisoning have no overt symploms, 

screening programs are critically necessary 10 identify children in need of | 

treatment. Unfortunately, screening programs in many cities were curtailed 

or eliminated in the early 1980s after the federal government discontinued 

funding for such programs, and nationwide data-collection efforts were also 

dropped. As a result, estimates of numbers of affected children must be 

derived from limited sampling programs, and extrapolated using figures on 

other variables known to be related to lead poisoning. 

In measuring the amount of lead absorbed by an individual and 

determining whether treatment is needed, doctors generally rely on measure- 

ments of the amount of lead in the individual's blood.! Though such 

measurements do not reveal the individual's lifetime history of lead exposure 

or the amount that is currently stored in bone, blood-lead levels can provide 

a “snapshot” of recent lead exposures.® Results are generally expressed as 

micrograms of lead per deciliter of blood, or ug/dl. 

One practical way to obtain some longer-term data for children 

involves collecting children’s teeth as they are naturally shed (generally 

between ages five and nine). This approach, however, means that parents 

must be informed of the need to collect teeth and must agree to participate, 

and is obviously inapplicable to adults and older children. 

Prior to the mid 1960s blood lead levels of 60 micrograms of lead per 

deciliter of blood (ug/dL) or less were generally considered as not dangerous 

  

  

' Because analysis of blood samples takes up to two weeks, screening 

tests are sometimes used to give a preliminary indication of whether further 

testing is warranted. The so-called “EP” test, which is a finger-prick test that 

gives immediate results, was used as a screening tool for many years. The 

test measures the presence of a naturally occurring protein that is produced 

at higher levels in response to lead exposure. Unfortunately, the accuracy of 

the EP test is limited for blood-lead levels below 40 ug/dl. State of California, 

Department of Health Services (1989), Chil ad Poisoning in Calif 

nia: Causes and Prevention, p. 8, 14 (interim report). As a result, it is not 

useful in screening for exposures at current levels of concern. Researchers 

at the University of Maryland Department of Toxicology are attempting to 

develop a substitute test that will serve as a preliminary screening test for 

blood-lead levels around 10 ug/dl. 

2 While promising, methods of directly measuring the total amount of 

lead stored in an individual's body are still undergoing development and are 

not yet widely available. See, for example, JF Rosen etal. (1988), “L-Line X- 

ray fluorescence of Cortical Bone Lead Compared with the CaNa2EDTA Test 

in Lead-Toxic Children: Public Health Implications,” Proceedings of the 

National Academy of Sciences (USA), Vol. 86, pp. 685-689. 
  

  

  

Though such measurements do not 

reveal the individual's lifetime his- 

tory of lead exposure or the amount 

that is currently stored in bone, blood- 

lead levels can provide a “snapshot” 

of recent lead exposures. 

 



  

  80 

Bl
oo

d 
Le

ad
, 

Pb
-B
 

(u
g/
dl
) 

      
7071757885900 

Year 

FIGURE ll: RECOMMENDED BLOOD 

LEAD LEVELS FOR MEDICAL 

INTERVENTION 

Figure ll shows the erosion of the rec- 

ognized threshold for lead toxicity as 

new evidence has emerged through in- 

creasingly sophisticated scientific stud- 

ies. 

12 

  

enough to require monitoring or treatment.’ This became an official standard 

in October 1970 when the U.S. Surgeon General issued a report defining 60 

ug/dL asa level of “undue lead absorption.” Buteven within the year, further 

analysis prompted the Public Health Service to circulate a draft lowering that 

threshold for undue absorption by a third, to 40 ug/dL.* Within five years the - 

threshold fell again, to 30 ug/dL, while the threshold for outright lead 

poisoning was set at 80.’ 

In 1978, the Public Health Service revised its finding, with 30 ug/dL 

as the threshold for undue lead absorption and 70 ug/dL as the threshold for 

poisoning.’ In 1985 the Service’s Centers for Disease Control (CDC) issued 

a statement lowering its thresholds for both excessive lead absorption and 

lead toxicity to 25 ug/dL.” And in late 1989, CDC announced that it was 

convening an Advisory Committee to update its statement on preventing lead 

poisoning in young children, to reflect research findings since 1985. Public 

health experts interpret this action as portending another downward revision 

of the standard, probably to 15 ug/dl or lower.? 

The Environmental Protection Agency has also evaluated lead’s 

toxicity in developing regulations under a variety of environmental statutes, 

including the Clean Air Act, the Clean Water Act, and the Safe Drinking 

Water Act. A 1986 report prepared as a background document on air 

regulations cited 10-15 ug/dL as the range associated with “neurological 

  

  

3 Centers for Disease Control/Public Health Service (1985), p. 1 

4 Public Health Service, Bureau of Community Environmental 
Management, Control of Poisoning in Children - pr blication 

(Washington, U.S. Department of Health, Education, and Welfare, December 

1970), p. 2. 

5 Pu Health Service, anes Lead sa cn Lead Poison- 

ing i hildr for ntrol 
ry U.S. Department of rrr pan and Wears March 
1975), p. 1. That document used lead “poisoning” or “toxicity” to mean a 
condition showing acute or obvious symptoms; “undue lead absorption” or 
“elevated blood lead level” means a level warranting medical intervention but 
where obvious symptoms may not be present. 

® Public Health Service, Preventin d Poisoning in Young Children: 
m h for Di rol (Washington, U.S. Depart- 

ment of Health, Education, and Welfare, April 1978), p. 1. 

7 Centers for Disease Control/Public Health Service, (1985), pp. 1-2. 

Lead toxicity is defined by two factors: a blood lead level of 25 ug/dl together 
with an erythrocyte protoporphyrin (“EP”) of 35 ug/dl. EP is a naturally 

occurring protein that plays a key role in the manufacture of hemoglobin; an 

elevated EP level is one of the earliest and most reliable signs of impaired 

function due to lead. lbid., p. 3. 

® 54 Fed. Reg. 48026 (November 20, 1989). The CDC convenes such 

committees at irregular intervals, when it considers the evidence strong 
enough to warrant re-examination of the standard. 

 



deficits.” In its proposed regulations on lead in drinking water, the EPA 

again cited 10-15 ug/dL as an “appropriate range of concern for health effects 

that warrant avoidance.”® A December 1989 statement of EPA’s Science 

Advisory Board concludes that “...there is likely to be no threshold for lead 

neurotoxicity, at least within the contemporary range of blood lead levels 

(i.e., 1-10 ug/dl).”"! And as another EPA advisory group pointed out even 

more recently, "[t]he value of 10 ug/dl refers to the maximum blood-lead 

level permissible for all members of these groups, and not mean or median 

values."!? 

The steady erosion of the accepted threshold for lead’s toxic effects, 

coupled with lead’s known biochemical properties, has convinced many 

public health experts that lead has no threshold. Rather, the emerging view 

is that lead presents a “continuum of toxicity” in which traditional symptoms 

associated with high dosage, such as kidney failure and anemia, have their 

low dosage counterparts, such as IQ deficits and decreased nerve conduc- 

tion." 

Public health experts have also found that the same level of lead 

exposure may affect different people unequally. Among the chief variables 

appear to be dietary intake of essential trace minerals. Lead’s effects are 

aggravated in people who lack adequate dietary calcium, iron, zinc, or 

phosphorous.!* This places poor families, where malnutrition may be more 

common, at greater risk of adverse effects from lead. 

    

® Environmental Protection Agency (1986a), Addendum to Vol. 4, p. A- 

53 Fed. Reg. 31524 (August 18, 1988). 

Environmental Protection Agency, Science Advisory Board (1989), 

Environmental Protection Agency, Science Advisory Board (1990), 

Ibid. See also PJ Landrigan (198_), p. 593. 

Centers for Disease Control (1985), p. 3. 

  

"Because the ‘baseline’ level of 

lead in blood inthe U.S. population is 

apparently about 10 - 15 ug/dl, it is 

virtually impossible to demonstrate 

effects of lead at lower blood levels... 

the physiological states now defined 

as "normal" might actually be "ab- 

normal” conditions associated with 

typical levels of lead in the body. The 

hypothesis that people would be 

healthier in subtle ways if the aver- 

age blood lead level were 1 - 2 ug/dl 

(or less) deserves sober considera- 

tion..." 

National Research Council (1980), p.137 

 



3. SOURCES AND PATHWAYS OF 
LEAD EXPOSURE 

Lead can enter the environment directly, as from 

industrial emissions, or indirectly, as when automotive 

batteries are incinerated or when dust from lead paint 

forms part of household dust. The most critical source of 

lead exposure for most children isdeteriorating lead paint 

in dwellings; lead from gasoline and from drinking water 

are also significant. Additional exposures occur through 

continuing uses of lead. Each year industry produces, and 

consumers use and discard, products containing well over 

a million tons of lead. The lead in each of those products 

is indestructible. 

Because lead is an element, it cannot break down or decompose into 

something less toxic. Both pure lead and its compounds are harmful to 

humans. Once introduced into the biosphere -- that part of the earth’s surface 

and atmosphere where living organisms exist -- lead remains toxic indefi- 

nitely. 

Lead’s widespread usage and its resulting dispersal into the environ- 

ment have been no accident. Its convenient properties have been recognized 

from the earliest historical times. Itis malleable and easy to work. It insulates Figure Ill. Above, the medieval 

well and does not rust. It alloys readily. Lead compounds make excellent | chemical symbol for lead. Below, the 

pigments in paints that also weather especially well. Egyptians in the ime | modern equivalent. 

of the pharaohs used lead in ornaments and cosmetics.! Chalices made of 

lead-silver alloys carried wine for the ancient Greeks and lead piping still 

carries rainwater from the roofs of medieval cathedrals. Indeed, the word 

“plumbing” is itself derived from the Latin word for lead, “plumbum” (as is 

its chemical symbol, Pb). 

The United States currently consumes well over one million tons of 

lead per year.? A substantial fraction of that amount -- approximately 60% 

-- comes from secondary refining (recycling). About a third comes from 

primary refining of lead, while imports (primarily from Canada) slightly 

exceed exports.’ Almost 90% of U.S. lead mining occurs in Missouri, with 

some operations in Alaska, Colorado, Idaho, and Montana, as well as very 

limited mining in half a dozen additional states.* Major industrial sources 

alone dispose of or release 15,000 tons of lead wastes in the U.S. annually, 

in forms ranging from placement in landfills to fugitive emissions from fa- 

cilities.’ 
  

  

' See HA Waldron (1973), p. 392. 

2 Bureau of Mines (1989c¢) Mineral Commodity Summaries 1989, pp. 
90 - 91 (Washington: U.S. Dept of the Interior) (1988, data converted from 
metric tons to short tons; one metric ton equals about 2,200 pounds, while a 

U.S. or “short” ton equals 2,000 pounds). 

3 Ibid. 

‘ Ibid. 
  

5 Environmental Protection Agency, Office of Pesticides and Toxic 
Substances (1989), The Toxics Release Inventory: A National Perspective, |  



  

The prevalence of lead in the environment, and the public health 

problem it poses, is almost entirely the result of human activity. Ice layers 

in Greenland, far from industrial centers, reveal a record of increasing lead 

| use by humans, with certain phases (the industrial revolution, widespread use 

of leaded gasoline) clearly marked in the frozen strata.® The increased 

exposure to lead in our society is so pronounced that the skeletons of modern 

humans contain 200 times more lead than those of their preindustrial 

ancestors.’ 
From the standpoint of public health and environmental quality, 

therefore, the threat posed by lead is inescapably cumulative. Simply 

curtailing additional releases of lead does not solve the problem; it is also 

necessary to take action to remove existing sources of lead exposure. 

Reducing current lead usage can, however, slow the rate at which the 

cumulative exposure problem worsens. Ongoing releases of lead -- whether 

through a product’s manufacture, its use, or its disposal -- add to existing en- 

vironmental stockpiles. In sum, controlling lead exposures requires a two- 

fold approach of both limiting ongoing uses of lead and attacking stockpiles 

created by past uses. 

Because lead accumulates in the body, all sources that add lead to the 

environment contribute to lead poisoning. Some, however, play a far greater 

role than others, particularly for children’s exposures. Currently, lead in 

house paint is the most significant of these, especially for those children with 

Simply curtailing additional re- 

leases of lead does not solve the 

problem; it is also necessary to take 

action to remove existing sources of 

lead exposure. 

  

  

1987 (Doc. No. EPA 560/4-89-005), p. 59. The toxics release inventory 

program covers manufacturing in the industrial sector (as defined by Stan- 
dard Industrial Codes 20 through 39) that employ more than ten individuals 

and use more than certain amounts of specified chemicals, including lead 
compounds. TRI requires reporting the amounts of substances released 

directly to the environment or transferred   
  

  

      
  

      

rT to off-site locations, including gaseous or 

RES RR I RRR particulate emissions to air, discharges to 

0.20 p~ water, disposal of solid wastes in landfills, 

injection into underground wells, or trans- 

Shak fer to off-site treatment, storage, or dis- 
B46 p= posal facilities. | 

Worldwide, annual production of 

0.14 p= lead waste from industrial sources amounts 
3 to an estimated 1.3 milliontons. JO Nriagu, 

z 012 and JM Pacyna (1988), “Quantitative As- 

> sessment of Worldwide Contamination of 

P9101 Air, Water and Soils by Trace Metals,” 
g ote Nature, Vol. 333, p. 139. 

~ 0.06 b= ¢ Needleman and Landrigan (1981), 
p. 279. 

0.04 p= 
7 Environmental Protection Agency 

0.02 p— (1986a), Vol. I, p. I-81. This relationship 
5 14 rane dORTHI TOV TRC EY was first recognized by CC Patterson 

800 1750 1800 1850 1900 1950 (1980), An Alternative Perspective --Lead 

beg. la AD sy Pollution in the Human Environment: 
oad oe gd ih Origin, Extent, and Significance,” pp. 265- 

AGE OF SAMPLES 348, in National Research Council, Lead 

Figure IV. Lead concentration profile in snow strata of Northern in the Human Environment (Washington, 

Greenland. Source: Environmental Protection Agency (1986a), Vol. |, DC: National Academy of Sciences). 

p. 1-26. 

16 

 



  

moderate to heavy total lead burdens; indeed, a majority of the cases of lead 

poisoning that show up in clinics today are the result of paint that was applied 

to houses decades ago.® 

But other sources also make a notable contribution. Some of these -- 

such as leaded gasoline -- are products whose use has fallen in recent years, 

but their legacy of contamination persists. In addition, over a million tons of 

lead continue to be introduced into commerce in the form of new products 

each year; the manufacture, use, and disposal of those products adds still 

more lead to the environment. 

Lead-based paint 

During the early and middle decades of this century, lead-based paint 

was the preferred medium in millions of homes.” The lead content of such 

paint varied, with some -- particularly in earlier years -- containing as much 

as fifty percent lead by dry weight.'® Even as late as 1971, the New York City 

Health Department tested 76 different paints and found eight of them to 

contain lead concentrations between 3 and 11%.!! Today an estimated three 

million tons of lead from paint still remains in dwellings." 

At one time, the general consensus was that children were exposed to 

lead-based paint primarily when they actually ate flakes of the sweet-tasting 

product or chewed on readily accessible surfaces such as window sills. More 

recently, however, researchers have realized that the primary exposure route 

starts with the transformation of lead paint into ordinary household dust. 

Children absorb lead by playing in the dust that is contaminated with these 

fine particles of paint. Simply by behaving like children, they get dust 

particles on their clothes and hands, and into their mouths.!? 

Even a well-maintained home is likely to have some deterioration of 

paint on window sills, particularly in parts of the nation exposed to freeze- 

thaw cycles. Many older houses, however, have been poorly maintained. 

Paint from these dwellings can easily be converted into dust-size particles 

that pose an extra menace to any active child. Over 40 million houses 

  

  

8 Personal Communications with Dr. John Graef, Director, Boston Lead 
Screening Program, Boston, MA; Dr. J. Julian Chisholm, Director, John 
Hopkins School of Medicine Lead Program, Baltimore, MD. 

® Hearings before the Subcommittee on Housing and Community De- 
velopment of the House Committee on Banking, Finance and Urban Affairs, 
100th Cong., 2d Sess. (1988) (testimony of James Keck, Deputy Commis- 
sioner, Baltimore Department of Housing and Community Development). 
See also R. Rabin (1989), “Warnings Unheeded: A History of Child Lead 
Poisoning,” American Journal of Public Health, Vol. 79, pp. 1668-1674. 

10 HL Needleman and PJ Landrigan, (1981), p. 279. 

1" Rabin (1989). p. 1673. 

12 Agency for Toxic Substances and Disease Registry (1988), p. II-5. | 

13 Centers for Disease Control (1985), p. 7. 

  

Simply by behaving like children, 

they get dust particlesontheirclothes 

and hands, and into their mouths 

17 

 



  

Over 40 million houses containing 

leaded paint are the homes for each 

successive generation of American 

children, with 1.97 million of these 

houses particularly unsound from 

deteriorating paint. 

18 

  

containing leaded paint are the’ homes for each successive generation of 

American children, with 1.97 million of these houses particularly unsound 

from deteriorating paint.'* 

Lead based paint was also used extensively on exterior applications, 

and it too presents a hazard. Particles from exterior paint -- along with air 

borne lead from gasoline and other sources -- can settle on the ground. These 

particles then mix into the soil and accumulate with other falling particles 

year after year. A recent study in Oakland, California found that exterior 

paint had an even higher average lead content than paint on interior walls. 

The same study identified a strong correlation between the lead levels in a 

house’s exterior paint and the blood lead levels of children residing in that 

house. 

Lead in soil does not come solely from paint. The same sources that 

have deposited lead in measurable amounts on Greenland’s icecap spread 

dust in the nation's front and back yards each day. In some regions, total soil- 

lead levels are alarmingly high. Forexample, a majority of soil samples from 

Oakland exceeded 1000 parts per million -- a level that defines materials as 

hazardous waste under California law.!® The same study also found that a 

child’s blood lead level increased an average 4-5 ug/dL for every 500 ppm 

rise in front or back yard soil lead level.'” In light of the emerging consensus 

among public health experts that blood-lead levels above 10 or 15 ug/dl are 

associated with significant toxicity, this exposure source is of obvious 

concern. 

Gasoline 
Leaded gasoline was once a major source of lead releases, and lead 

from this source undoubtedly still remains in the soils of virtually every 

urban and suburban area throughout the country. EPA estimates that the lead 

level of soil alongside roadways can reach 10,000 ppm, or more than eight 

times the levels associated with elevated blood lead levels in the Oakland 

study.’ Areas alongside heavily traveled urban arteries -- such as sidewalks, 

parking lots, or street-front playgrounds -- may have even higher levels of 

lead in soil and dust.” Because farm vehicles long ran on leaded gasoline, 

and are still allowed to do so, lead is widely dispersed into agricultural soils 

as well. 

Data gathered during the first phasedown of leaded gasoline provides 

remarkable evidence of the strong association between blood lead levels and 

the use of leaded gas. The Environmental Protection Agency noted in a 1986 

  

  

4 Agency for Toxic Substances and Disease Registry (1988), pp. VI- 

13, VI-14, 

'5 State of California (1989), p. 19. 

16 Ibid. 

'® Environmental Protection Agency (1986a), Vol. IV, p. 13-5. 

'® bid, Vol. IV, p. 13-7. 

 



study that ambient air lead levels declined markedly during the changeover 

to nonleaded gasoline that started in 1978.2 While other factors were simul- 

taneously at work (e.g., a reduction in the use of leaded solder in food cans), 

physicians and epidemiologists observed a strong drop in blood lead levels 

attributable to the changeover. Between 1976 and 1980, the period covered 

by a national health survey of over nine thousand persons, the average blood 

lead level of all respondents fell by 5.8 ug/dL, from above to below the 

CDC’s current 25 ug/dL standard (itself soon to be revised as noted above). 

And in a study of umbilical cord blood lead in 12,000 newborn children in 

Boston, doctors charted a twenty percent drop in blood lead content between 

1979 and 1981.2 

While sales of leaded gasoline are but a small fraction of what they 

were at their height, they are nonetheless substantial. Current law still allows 

the use of leaded gasoline in pre-1975 vehicles, and in farm vehicles of any 

age.” Indeed, leaded gasoline still accounts for about 9 percent of total U.S. 

gasoline consumption.? During 1989, Americans burned approximately 9.8 

billion gallons of leaded gasoline containing a total of 880 million grams of 

lead.” Pending amendments to the Clean Air Act, if enacted, would ban the 
sale of leaded gasoline for motor vehicles by 1991 (with a two year extension 

available for farm vehicles). 

Drinking water 

Lead can enter drinking water in a number of ways. Atmospheric lead, 

or lead leached from solid waste sites, can accumulate in the water supply. 

By far the most significant source, however, is lead pipes or lead solder in the 

plumbing system. Lead pipes may be present in the water main, in the 

connecting service line, or within the home; lead solder may likewise be 

found in a variety of locations. Lead is more easily leached by water that is 

“soft” (has a low mineral content) and/or acidic (has a low pH). However, 

any water can leach lead, especially water that is hot or that sits in pipes for 

  

  

2 |bid., Vol. IV, pp. 13-4, 13-6. See also Agency for Toxic Substances 
and Disease Registry (1988), p. VI-19. 

21 American Academy of Pediatrics (1987), “Statement on Childhood 
Lead Poisoning,” Pediatrics, Vol. 79, p. 458. See also Environmental 

Protection Agency (1986a), Vol. |, pp. 1-87 through 1-95 for a detailed 
discussion of associations between blood lead levels and the reduction in use 

of leaded gasoline. 

2 Bellinger, et al. (1987). 

23 See 42 U.S.C. section 7550. 

24 Data from Environmental Protection Agency, “Lead in Gasoline,” for 
the quarter 1 July 1989 to 30 September 1989. 

25 bid. (extrapolated from quarterly data to annual basis). 

2 S.1630, 101st Cong., 1st Sess. section 216 (1989). Section 211 of 

the bill requires EPA to issue regulations prohibiting the sale of vehicle 
engines that require leaded gasoline as of 1992. This provision is designed 

to curtail production of farm machinery and small gasoline-powered engines, 

  

Leaded gasoline still accounts for 

about 9 percent of total U.S. gasoline 

consumption. 

 



Recently constructed or renovated 

housing may pose a problem because 

plumbing with freshly soldered joints 

can leach high levels of lead if lead 

solder was used. 

  

extended periods such as overnight. And, by contrast to paint-associated 

exposures that primarily occur in pre-1960 homes, recently constructed or 

renovated housing may pose a problem because plumbing with freshly 

soldered joints can leach high levels of lead if lead solder was used.” 

Food 

Adults consume an estimated 32-45 micrograms of lead each day 

through food. This is the major route by which lead enters adult bodies.? 

Lead contaminates food through a variety of routes. Atmospheric lead can 

land on crops at any stage of growth, harvest or food preparation. Lead-con- 

taminated water used in food preparation or cooking can contribute lead to 

the food. Finally, the same household lead dust that gets on children’s hands 

and faces can get into food during preparation. 3 

Lead also enters food from lead-soldered cans. In 1979, more than 

ninety percent of food cans had lead-soldered seams.” Subsequently, the 

Food and Drug Administration has been working with the National Food 

Processors Association, the Can Manufacturers Institute, and the major can 

manufacturers on a “voluntary phaseout” of leaded solder.>* According to 

industry statistics, the number of cans with leaded solder in 1988 fell to 5.8 

percent of total U.S. production.’ However, recent tests of canned tomato 

products by an independent consumers group found that about one quarter 

of the cans tested contained lead-soldered seams.** Even using the industry 

data, the problem remains extensive: Americans purchase more than twenty- 

eight billion cans of food and beverages yearly,” which at the 5.8 percent rate 

leaves more than 1.6 billion leaded cans passing through the nation’s grocery 

stores each year. The FDA effort, moreover, does not apply to imported 

canned foods. 

  

  

which are stillbeing manufactured to runon leaded gasoline. S. Rep. No. 101- 

228, 101st Cong., 1st Sess. 105 (1989). 

27 Agency for Toxic Substances and Disease Registry (1988), p. VI- 
37. 

28 Environmental Protection Agency (1986a), Vol. IV, p. 13-7. 

2 Agency for Toxic Substances and Disease Registry (1988), p. I-30. 
The statistics in this paragraph refer to food cans only; since 1983, soft drink 
cans have been made entirely without leaded solder. [Source: Food and Drug 
Administration] 

% Interview with Mr. Pat Lombardo, Associate Director for Contami- 
nants, Division of Contaminants Chemistry, Center for Food Safety and 
Applied Nutrition, Food and Drug Administration. 

3 Can Manufacturers Institute, letter dated March 28, 1989, to Mr. Jerry 
Burke, Acting Director, Office of Physical Sciences, Center for Food Safety 
and Applied Nutrition, Food and Drug Administration. 

2 Consumer Reports, July 1989, p. 473. 

3 Source: Can Manufacturers Institute.  



  

Continuing Uses of Lead in Commerce 

Currently, U.S. industries introduce approximately 1 million tons of 

lead into the economy each year. By far the largest use for lead today is in 

automobile starting/lighting/ignition batteries, with over 70% of lead de- 

voted to that one use.> But a wide variety of other products also continue to 

be made with lead. 

Many workers experience occupational exposures well above govern- 

ment standards, as do communities near primary and secondary smelters. 

Individuals living in the vicinity of such plants -- or of formerly operating 

plants -- may receive particularly high lead exposures. 
These continuing uses of lead are supported by federal tax policy: 

domestically mined lead has long benefitted from a 22% depletion allow- 

ance, and continues to do so today.” Interestingly, though lead consumption 

in the United States has decreased over the past decade, it has increased 

throughout much of the rest of the world. 

Auto batteries: The principal public health threat from lead in 

batteries stems from their manufacture and disposal, rather than from their 

use. While 80% of automobile batteries are recycled, the remainder forms 

the predominant source -- about 65% -- of the lead in municipal garbage, and 

an estimated 138,000 tons of automobile battery lead was discarded in 

1989.* Although States have begun enacting mandatory recycling laws for 

auto batteries, there are no federal regulations affecting disposal by individ- 

ual consumers; batteries continue to be dumped in the open, placed in 

landfills, and incinerated under conditions that allow environmental release 

of lead to occur.* 

Other: Other continuing uses of lead in commerce include ammuni- 

tion, brass, coverings for power and communication cables, in glass (primar- 

  
  

3 Bureau of Mines (1989b), p. 5, Table 5 (1988 annual data). This 
category includes other large storage batteries as well, such as for other 

vehicles and computers. 

% See Bureau of Mines (1988), Impact of Existing and Proposed 
Regulations on the Domestic Lead Industry, pp. 10-13. 

% Environmental Protection Agency (1986a), Vol. |, p. 1-49 (noting 
residence near a lead smelter as the single highest-intensity pathway for lead 
exposure by children). 

37 26 U.S.C. section 613. 

3 Bureau of Mines (1990b), “Mineral Industry Surveys: Lead Industry 
in November 1989,” p. 1 (citing statistics from the International Lead and Zinc 
Study group indicating the lead metal consumption in the “western world” 
increased for a seventh consecutive year to a record 4.41 million tons). 

3% Environmental Protection Agency (1989b), Characterization of 

  

Unit 2 ; 00: FinalF (Washington: u.s. ErvORMental 
Protection Agency), Doc No. EPA/530-SW-89-015A), pp. 1 & 81. 

40 Recently introduced federal legislation would bar disposal and 

instead mandate recycling of all lead-acid batteries. H.R. 3735, section 107, 

101st Cong., 1st Sess. (1989). 

  

An estimated 138,000 tons of auto- 

mobile battery lead was discarded in 

1989. 

21 

 



  

ily for color TV tubes), pipes and other extruded products, radiation shield- 

ing, and sheet lead as a sound-insulation material.*! Other uses included 

solders, pigments, and plastics.*? As with batteries, when lead-containing 

consumer items are discarded into municipal incinerators or landfills, that 

lead may be released into the environment. 

Finally, it is worth noting that although lead paint has been banned for 

household use, it still has many other applications. Lead paint’s durability 

and its rust inhibiting qualities have made it popular for traffic paints and for 

outdoor installations such as bridges, and it is still used extensively for those 

purposes. 

  

CRUSTAL - 
WEATHERING 

AUTO INDUSTRIAL 

EMISSIONS EMISSIONS 

         
  

  

  
  

              
  

  

  
  

  
  

  

                  

                          

    

                    

      

y | 
AMBIENT  |re——- SOI SURFACE AND | 

AIR RY ; »1 GROUND WATER | 

4 | 

PAINT PLANTS ANIMALS SOLDER 

| NL 

1 J J 

INHALED DRINKING pons Ll ee 

¥ 

MAN 
      

| 
J 

  

Figure V. Environmental pathways of lead. Adapted from Environmental Protection Agency (1986), Vol. 
l, p. I-12. 

  

  

4 Bureau of Mines (1989b), p. 4, Table 5. 

“2 Environmental Protection Agency (1989b). 

22 

 



4. NUMBERS OF INDIVIDUALS AFFECTED 

Millions of Americans are at risk of absorbing 

enough lead to trigger medically adverse outcomes. 

Because children. and fetuses absorb more lead than 

adults, theirs is a special danger. But adults are far from 

immune. 

Children 
Precise measurements of the numbers of U.S. children with elevated 

blood-lead levels are not available. However, a comprehensive set of 

estimates was compiled as part of a ground-breaking Report to Congress on 

Child Lead Poisoning. The report, which was prepared by the Agency for 

Toxic Substances and Disease Registry, or ATSDR -- a component of the 

U.S. Public Health Service -- used data from blood samples collected in the 

late 1970s.! Those data were then adjusted for changes in lead exposure in 

the intervening years, and extrapolated based on key factors known to affect 

blood-lead levels: age, race, family income, and age of housing. 

The ATSDR findings are remarkable. An estimated 3 to 4 million 

children under six have blood lead levels above 15 ug/dl.? Of those, about 
half -- 1.2 million children -- live in housing with deteriorating surfaces: 

peeling paint, broken plaster, or holes in walls.? Children who live in housing 

with peeling paint are particularly likely to absorb substantial amounts of 

lead. 

In addition to deteriorating paint, several other sources contribute to 

elevated blood-lead levels.* Lead in drinking water is estimated to account 

for approximately 240,000 cases.’ Available data do not allow calculation 

of directly comparable data for remaining major sources such as gasoline, 

dust/soil, smelters, and food.® For most children, however, those sources are 

less likely to cause significant increases in lead absorption than exposure to 

deteriorating paint. In the nation as a whole, exposure to paint-derived dust 

is the source of greatest concern. 

Moreover, many children have blood-lead levels well above 15 ug/dl. 

Over 200,00 children, about 1.5% of the nation's children, are estimated to 

have a blood lead level of 25 ug/dl or above.” At that level, observable IQ 

deficiencies, poor attention spans, and slow childhood development can be 

pronounced. Exposure rates are particularly high for poor, urban black 

  

  

' Agency for Toxic Substances and Disease Registry (1988). 

2 Ibid, p. 4. 

3 Ibid, p. I-19. 

‘4 Ibid, p. 6-8. 

* Ibid, p. 8. 

‘ bid 
7 |bid., p. 4. (extrapolating from SMSAs to the entire population).   

An estimated 3 to 4 million children 

under 6 have blood lead levels above 

15 ug/dl. 

 



  

While the national incidence of chil- 

dren with blood-lead levels over 15 

ug/dlis 17%, almost 70% of the urban 

black children from poor families are 

estimated to exceed that level, as are 

over 35% of white children in similar 

circumstances 

24 

    

  

children under age 6, an estimated 10% of whom have blood lead levels 

above 25 ug/dl.? 

Several observations are relevant. First, the data possibly understate 

the problem. Families move, and a new set of children can become exposed 

to the paint, dust and other contaminants in and around their new home. A 

California survey noted that 40 percent of the families in its survey moved 

every 15 months.’ The lead in the paint, dust and soil pose a continuing risk 

to each new resident. 

Second, the large numbers illustrate the magnitude of the problem 

from a public health perspective. Preventing exposure is the only appropriate 

approach, because available lead-poisoning treatments are fundamentally 

limited: they can neither remove all of the lead from target organs or long- 

term storage sites (i.., bone), nor undo neurological damage. Further, such 

treatments are both expensive and painful for the patient.!° 

Third, lead poisoning is not just a problem of poor children. While 

children from poorer families are at greater risk, in part because of other 

factors such as the greater incidence of malnutrition, millions of more 

affluent persons live in older housing. Indeed, the majority of children living 

in the nation’s oldest (pre-1950) homes come from families above the 

poverty level! 

The problem not only cuts across socioeconomic classes but also 

across regional boundaries. Appendix I of this report presents detailed 

estimates of the prevalence of elevated blood-lead levels in over 300 areas 

throughout the nation. 

Patterns revealed by this analysis are alarming. While the national 

incidence of children with blood-lead levels over 15 ug/dl is 17%, almost 

70% of the urban black children from poor families are estimated to exceed 

that level, as are over 35% of white children in similar circumstances. While 

these estimates are necessarily crude, given the limits of the available data, 

they compellingly indicate the breadth -- in the most literal sense -- of 

America’s lead-poisoning problem, and highlight the gravity of current ex- 

posure levels and the urgent need for action. 

Fetuses 
The ATSDR Report estimates that at current levels of environmental 

lead, more than four million individual fetuses will suffer toxic effects of 

cumulative lead exposure over the next ten years.!? Lead is especially 

harmful to the fetus because of the ease with which it passes through the 

placenta. As noted above, several studies have concluded that the fetus is 

sensitive to lead even at levels of absorption by the mother previously 

thought to be harmless.!? 
    

& Ibid. (1988), p. V-7. 

® State of California (1989), p. 25. 

10 See Section 5 of this report. 

'! Agency for Toxic Substances and Disease Registry (1988), p. 1-48. 

'2 Agency for Toxic Substances and Disease Registry, (1988), p. 1-49. 

'* Needleman (1988b). 

 



  

Adults 
A 1987 survey of occupational illness in New York, New Jersey and 

California found more than 1,000 workers with blood lead levels above 40 

ug/dL; 200 of these had levels of more than 50 ug/dL."* Exposure from 

occupational conditions presents the most serious hazard to adults. 

Contrary to the popular perception, however, several occupations 

present greater hazards than work at lead smelters. Table I sets forth the 

results of studies of actual lead exposure during various occupational 

activities. It indicates that persons working at steel cutting or welding risk 

exposure several times the level of those working in a primary or secondary 

lead smelter. Ironically, the current occupational standard for short-term 

exposure to lead -- now set at 50 micrograms per cubic meter of air (ug/m3) 

averaged over 8 hours -- does not apply to the construction industry.!s 

For males, risks from lead exposure include elevated blood pressure. 

The growing literature on the subject, establishing a statistically significant 

relationships between blood lead levels and blood pressure raises a public 

health concern in light of high blood pressure’s role in coronary disease -- the 

most common cause of death for adult males'®. 

The largest adult female population that is at risk from lead exposure 

is the child-bearing age group. This stems not only from the danger to the 

fetus itself, but also from the obstetrical complications that can accompany 

a non-normal childbirth. While available data are not conclusive, some 

studies suggest a connection between maternal blood lead levels and both 

pre-term delivery and premature membrane rupture.'’ 
  
  

Table I 

Maximum Observed Occupational Exposure to Lead (ug/m?) 

  

Activity Exposure 

Oxy-acetylene torch cutting of lead-painted 

structural steel, good ventilation 24.000 

Electric arc welding of zinc silicate-coated 

steel, poor ventilation 15,000 

Secondary smelter operation 4,800 

Lead smelter operation 4,000 

Alkyl lead manufacturing 1,249 

Battery manufacturing 1,200 

Can manufacturing 800 

Sanding indoor leaded paint surface for 5 min. 550 

Sanding outdoor leaded paint surface for 22 min. 510 

  

Source: Adapted from U.S. Environmental Protection Agency (1986a), Vol. 

I, pp. 1-45, 1-46; also Vol II, pp. 7-64 through 7-70. 
  

  

4 Landrigan (1989). 

5 29 C.F.R. Part 1910.1025 (“permissible exposure limit” for lead as 

established by U.S. Occupational Safety and Health Administration). 

6 See discussion in section 1 of this report. 

7 Environmental Protection Agency (1986a), Vol. |, p. 1-156. 

  

Ironically, the current occupational 

standard for short-term exposure to 

lead does not apply to the construc- 

tion industry. 

25 

 



  

A large target population -- namely 

children from poorer families -- may 

go undiagnosed because of inade- 

quate access to medical care. 

26 

  

  

A Final Note 

The fact that only a small fraction of the persons exposed to lead may 

be diagnosed as lead-poisoned does not indicate that the public health danger 

is slight.’® The symptoms of low-level lead poisoning are nonspecific, and 

may occur in many persons who escape diagnosis. A large target population 

-- namely children from poorer families -- may go undiagnosed because of 

inadequate access to medical care. From a public health standpoint, the 

strong statistical correlation between lead exposure and the onset of symp- 

toms in populations that are at risk is sufficient cause for alarm and action. 

The sad truth is that virtually every group surveyed for low level lead 

poisoning has turned up many cases that had previously gone undiagnosed. 

For reasons such as these, the American Academy of Pediatrics recommends 

that children whose life circumstance determines them potentially to be at 

high risk be screened when they are one year old." 

    

'® The Board on Toxicology of the National Research Council is prepar- 
ing a landmark report identifying critical populations at risk for low level lead 
poisoning. This report will include specific recomendations on exposure 
prevention and present for the first time a detailed analysis of the costs of 
source control and the health benefits of reducing lead toxicity. American 

Academy of Pediatrics (1987). 

'* American Academy of Pediatrics (1987). 

 



5. TREATMENT AND PREVENTION OPTIONS 

Treatment for lead poisoning is a partial cure at 

best. It is expensive, does not remove all the lead in the 

body, and cannot undo neurological damage. Nor does it 

address the conditions that caused the exposure in the first 

place. Removing lead from the environment is also 

expensive. Yet its results are more permanent, and proba- 

bly cheaper in both the short and long run. 

Lead poisoning is treated through the use of chelation, a process in 

which a drug binds itself to lead in the body and makes the lead easy to 

excrete. Candidates for possible chelation therapy generally spend a day in 

the hospital undergoing screening. If test results indicate that chelation is 

warranted, the patient spends an additional five days there for treatment and 

post-treatment testing. Not every child with an elevated blood-lead level 

requires chelation therapy: such treatment generally is considered warranted 

only in a relatively small fraction of cases, for chelation is not risk-free. 

Limitations of conventional treatment 
While chelation can substantially reduce lead levels, it has a number 

of significant limitations. The three major limitations of chelation are: 

1) Chelation cannot repair neurologic impairment, but rather can only 

keep further damage to the nervous system from occurring. Children treated 

for lead poisoning are still likely to require special education and other 

cognitive or behavior-related therapy long after their initial treatment.? 

2) Chelation generally cannot reach lead that has found its way to long- 

term storage sites in the hard body tissues (bone, teeth) or the brain and 

kidneys. As discussed above, lead can re-enter the soft tissues from bone at 

high levels. Chelation therapy does not prevent this. In fact, doctors have 

observed a “rebound” phenomenon in some patients, where blood lead levels 

rise after the cessation of chelation therapy? 

3) Finally, chelation has little effect when the patient, as is often the 

case, returns to the same lead-contaminated environment in which the 

  

  

! Centers for Disease Control (1985), p. 26. Using the 1985 definition 
for lead toxicity -- a level that, as discussed above, may soon be lowered 
based on more recent data -- EPA estimated that chelation therapy would be 
needed for about 5% of the children who have blood-lead levels above 25 ug/ 
dl, in orderto reduce theiroverall lead body burden. Environmental Protection 

Agency (1986b), Reducing Lead in Drinking Water: A Benefits Analysis, pp. 
I1-53 (Washington: U.S. Environmental Protection Agency), Doc. No. EPA- 
230-09-86-019. 

2 Bellinger et al. (1984). 

3 Centers for Disease Control (1985), pp. 16-17. In one documented 

case, the rebound took place a full five years after the initial treatment for lead 
exposure, with no additional exposure being observed during the interim 
period. See OJ David, S Katz, CA Arcolo, and J Clark (1987), “Chelation 
Therapy in Children as Treatment of Sequelae in Severe Lead Toxicity,” 

Archives of Environmental Health, Vol. 40, p. 113.   

Not every child with an elevated 

blood-lead level requires chelation 

therapy: such treatment generally is 

considered warranted only in a rela- 

tively small fraction of cases. 

 



"Medical treatment with chelating 

agents must not be considered a 

substitute for dedicated preventive 

efforts to eradicate controllable 

sources of lead..." 

Centers for Disease Control 

  
  

exposure occurred. Unless the source of exposure can be eliminated -- for 

example, by removal of accessible lead paint, or by substitution of bottled 

drinking water for lead-contaminated tap water -- itis likely that the problem 

will recur. In one reported case, a patient required nineteen chelation treat- 

ments over his childhood.* 
Moreover, the costs of chelation therapy are high. They include 

hospitalization, physician visits, laboratory tests, and psychological testing 

and evaluation. Using conservative assumptions, EPA estimates the cost for 

a single course of chelation treatment at $2,980, in 1988 dollars.® This 

estimate does not include the costs of multiple sessions, which EPA esti- 

mates may be needed for half of patients undergoing chelation. Nor does it 

include the costs of follow-up care such as remedial education and psycho- 

logical testing. 

The Preventive Approach: Getting the Lead Out 
Removing lead paint from homes is a complex task. It typically 

involves testing surfaces to determine where lead paint is present; replacing, 

encapsulating, or removing paint from woodwork or wall surfaces; careful 

cleanup of all dusts generated during the process; and post-removal testing 

to ensure that cleanup was properly completed. Because some of these 

operations can exacerbate the problem if not done properly, lead removal 

usually requires skilled labor and special equipment such as respirators and 

specialized vacuum cleaners. The Consumer Product Safety Commission 

wams flatly that “[c]onsumers should not attempt to remove lead-based 

paint.” 

Unfortunately, safe and effective removal of lead paint is not cheap. 

The City of Baltimore, which has an active lead abatement program, 

estimates the per unit cost of lead removal to run from approximately three 

thousand dollars, at the low end of the scale, toas high aseight to ten thousand 

dollars.” An urgent need exists for research aimed at developing abatement 

technologies that are fully effective but less expensive. 

  

  

“ S. Pollack (1989), “Solving the Lead Dilemma,” Technology Review, 

Oct. 1989, pp. 22-31. 
  

5 U.S. Environmental Protection Agency (1986b), p. l1I-53. Figures in 

the cited source are given in 1985 dollars. 

& Consumer Product Safety Commission (1989), “CPSC Warns About 
Hazards of ‘Do It Yourself’ Removal of Lead-Based Paint,” Consumer 

Product Safety Alert, p.1. 

7 Interview with James Keck, Deputy Commissioner, Baltimore 
Department of Housing and Community Development. The low number 
assumes abatement being carried out in tandem with other rehabilitation, and 
reflects abatement contractor costs on a specific modernization project in Bal- 

timore comprising 328 units; the high numbers assume “worst case” condi- 

tions of very deteriorated units where paint abatement alone is being carried 
out.  



  

6. GOVERNMENT ACTION -- AND INACTION -- 

ON LEAD 

To date, Congress has responded to the lead prob- 

lem on a number of fronts, enacting legislation to control 

lead in paint, ambient air, drinking water and solid waste. 

Initiatives to reduce lead in gasoline and lead-soldered 

food cans have made headway in “de-leading” the nation 

as a whole. But there have been only sporadic efforts to 

control the most stubborn and significant source of 

children’s exposure to lead: house paint. 

The Lead-Based Paint Poisoning Prevention Act 

The United States historically has been slow to respond to the health 

threats posed by lead paint. While most European countries signed a treaty 

banning the use of lead-based paint in the interior of buildings in 1921, the Merely prohibiting the use of addi- 

federal government took no action at all until 1971. That year, citing the tional lead-based paint in dwellings 

“epidemic proportions” of childhood lead poisoning in large cities, Con- has proven to be an Inadequate re- 

gress enacted the first national lead abatement legislation. The Lead-Based sponse to the problem. 

Paint Poisoning Prevention Act? sought to address three distinct aspects of 

the lead-paint problem. Specifically, the Act set some limits on the use of lead 

paint; created grants for lead-poisoning screening and treatment programs, 

and required the submission of a report on abatement methods. The three 

components have had notably different histories over the intervening two 

decades. 

Limits on the Use of Lead Paint: Contrary to general belief, the Act 

did not ban the production of lead paint or even all of its uses in dwellings. 

Rather, it merely prohibited the use of leaded paint on surfaces accessible to 

children. The Act also authorized the Secretary of Health, Education, and 

Welfare to issue regulations prohibiting the use of lead-based paint in Fed- 

eral construction or rehabilitation of residential housing. 

Recognizing the need to strengthen these provisions, Congress amended 

the Actin 1973 to prohibit the use of leaded paint (defined as paint containing 

0.5 percent lead by dry weight) in federally funded housing and extended the 

prohibition to toys and other articles.> Not until 1977 was the use of lead paint 

in housing actually banned -- and that ban was imposed by a regulation issued 

by the Consumer Product Safety Administration rather than by statute.* 

Grant Programs: The 1971 Act placed the administration of the grant 

program with the Secretary of Health, Education, and Welfare. A decade 

  

  

' 1921 Convention Concerning the Use of White Lead in Painting. 

2 Pub. L. No. 91-695, 84 Stat. 2087; current version at 42 U.S.C. 

sections 4801-4846.   
3 Pub. L. No. 93-151, 87 Stat. 560 (1973). | 

4 42 Fed. Reg. 44199 (Sept. 1, 1977), codified at 16 C.F.R. Part 1303. | 
Certain products were exempted, including agricultural and industrial coat- | 
ings, including building coatings, traffic paints, and artists paints. The 
regulations also revised the definition of lead paint to mean paint containing 

more than 0.06% lead by dry weight. 

20 

 



  

Today, fewer than one half of the 

States have active lead screening 

programs. 

30 

  

later, the Omnibus Budget Reconciliation Act of 1981 eliminated grants 

under the Lead-Based Paint Poisoning Prevention Act and several other child 

health-related grant-in-aid programs; in their place, the 1981 Act created the 

Matemal and Child Health Block Grants Program. 

Today, fewer than one half of the States have active lead screening 

programs.® Moreover, because the block-grant program contained far fewer 

reporting requirements, the changeover to block grants also had the effect of 

denying the Federal government ongoing information about the extent of 

lead poisoning in this country. The restoration of line-item funding for lead 

screening in the Lead Contamination Control Act of 1988 will help reinvig- 

orate screening programs by authorizing expenditures of $24 million for 

fiscal year 1991 and requiring grant recipients to report screening statistics.’ 

Paint Abatement Efforts: As its third and final component, the 1971 

Lead-Based Paint Poisoning Prevention Act directed the Secretary of Hous- 

ing and Urban Development (HUD) to prepare a report to Congress on “the 

nature and extent of the problem of lead-based paint poisoning” and methods 

for removal of paint to which children were exposed.®! Subsequent amend- 

ments directed HUD to eliminate “as far as practicable” the hazards of lead 

paint in existing housing,” and to promulgate regulations on lead paint 

abatement.” 

HUD’s implementation of these mandates can only be termed abys- 

mal. Asearlyas 1980, the U.S. General Accounting Office harshly criticized 

HUD'’s efforts in a report entitled “HUD Not Fulfilling Responsibility to 

Eliminate Lead-Based Paint Hazard in Federal Housing.”"! 

In subsequent litigation, the courts agreed, and ordered HUD to revise 

its regulations.’ The revised regulations were issued in 1986 and 1987.13 
  

  

* Prior to the 1981 Budget Act, the grant provisions of the Lead Paint 

Poisoning Prevention Act had been amended and transferred into section 
316 of the Public Health Service Act, codified as 42 U.S.C. section 247a. See 
Pub. L. No. 95-626, section 316, 92 Stat. 3551, 3586 (1978). The 1981 
Budget Act then repealed section 316 of the Public Health Service Act. Pub. 
L. No. 97-35 section 2193(b)(1), 95 Stat. 357, 827 (1981). See 42 U.S.C A. 
section 701, historical note. 

® See Agency for Toxic Substances and Disease Registry (1985) pp. 
V-24 through V-26. 

7 Pub. L. No. 100-572, 100th Cong. 2d Sess. (1988), section 566, 
codified at 42 U.S.C. 247b-1 (section 317A of the Public Health Service Act). 

8 Pub. L. No. 91-695, Sec. 301, 87 Stat. 2078. 

® Pub. L. No. 93-151, 87 Stat. 560 (1973), codified at 42 U.S.C. sec. 
4822. 

'° Pub. L. No. 94-317, 90 Stat. 695 (1976), codified at 42 U.S.C. sec. 
4821 et seq. 

'" (Washington: U.S. General Accounting Office), Doc. No. CED-81- 
31. 

2 Ashton v, Pierce, 541 F. Supp. 633 (D.D.C. 1982), affirmed, 716 F.2d 

56, modified, 723 F.2d 70 (D.C. Cir. 1983). 

B.24CF.R Pant 35. 

 



Responding to HUD’s intransigent failure to develop regulations fo- 

cused on preventing lead poisoning, Congress made major changes to the Act 

in 1988.'* Those amendments required HUD to promulgate regulations by 

June, 1988 that addressed lead paint on all surfaces and to conduct lead paint 

testing and abatement in housing receiving comprehensive modernization 

funds. The amendments also required HUD to conduct a demonstration 

program on the cost-effectiveness of different abatement methods and to 

prepare and submit to Congress two “comprehensive and workable” plans. 

One plan must address the abatement of public housing over a five year 

period and the other must address abatement of lead paint in private housing. 

This new HUD effort is moving ahead, albeit more slowly than Congress 

originally anticipated. 

In the almost twenty years since the passage of the Lead Based Paint 

Poisoning Prevention Act, several generations of children have occupied 

homes and apartments filled with lead paint. To date, however, the federal 

government has failed to craft an effective program that would reduce 

exposures to this source and thus prevent poisoning in the first place. A bold 

new initiative is needed to ensure that children are not still being poisoned 

by lead paint twenty years from now. 

State and Local Action on Lead Paint 
Housing quality issues such as lead paint have traditionally been 

regulated at the local or state level, rather that by the federal government. The 

federal Lead-Based Paint Poisoning Prevention Act applies only to housing 

that is owned, subsidized or the subject of mortgage guarantees by the federal 

government. Thus, the only regulation of lead paint in the vast majority of 

the U.S. housing stock occurs at the municipal or state level. 

Approximately twenty states and many cities and counties have laws 

or ordinances that regulate the use of lead paint in housing and require 

abatement under at least some circumstatnces. Many of these regulatory 

programs date to the 1970s and so do not reflect the past decade's research 

findings on the need to prevent low level lead poisoning from lead paint and 

dust. Three states, however, have recently enacted more comprehensive 

schemes to prevent childhood lead poisoning. 

Since 1971, Massachusetts law has required the removal of peeling 

paint and lead paint on certain accessible surfaces (such as window sills) in 

all dwellings occupied by a child under the age of six. The Massachusetts 

statute was amended and expanded early in 1988 and is now the most far- 

reaching state lead poisoning prevention law. One goal of the amended law 

is to screen all pre-school children for lead poisoning, by requiring doctors 

and health care providers to screen according to a prescribed schedule and by 

requiring day care providers to ensure that all two-year olds have been 

screened. Another goal is to make abatement safer by requiring training and 

licensing of lead paint inspecters and workers, requiring clean-up after abate- 

ment and prohibiting occupants from remaining in dwellings during abate- 

ment. To promote deleading in connection with property. transfers, the law 

requires home sellers to provide perspective buyers with information about 

  

  

* Pub. L. No. 100-242, section 566(a), 102 Stat. 1945, amended by 

Pub. L. No. 100-628, section 10288, 102 Stat. 3280 (1988), codified at 42 
U.S.C. 4822. 

  

In the almost twenty years since 

the passage of the Lead Based Paint 

Poisoning Prevention Act, several 

generations of children have occu- 

pied homes and apartments filled with 
lead paint. 

 



  
32 

  

  

lead paint and the lead law and to give buyers ten days to obtain a lead paint 

inspection. Finally, the law creates a $1,000 per unit state income tax credit 

to provide partial financial support for owners or tenants who pay for the 

removal of leaded paint or soil.'* 

California enacted the Childhood Lead Poisoning Prevention Program 

in 1986.'¢ The Program required the Department of Health Services to: 1) 

conduct screening programs in three geographical areas to determine the 

extent and causes of childhood lead poisoning; 2) analyze the information 

collected and implement a program to reduce childhood lead exposure; 3) re- 

quire laboratories to report cases of elevated blood lead levels; and 4) submit 

a policy report to the legislature with recommendations for future prevention 

of childhood lead poisoning. Preliminary findings from the screening 

programs show that 19-20% of children in these high risk areas had blood 

lead levels above 15 ug/dl and 1.5% had blood lead levels over 25 ug/dl." 

Of programs at the local level, Baltimore is the most extensive. 

Approximately 26,000 children are tested yearly. When a lead-poisoned 

child is identified, either by city health officials or by a private physician, the 

city health department is notified and an inspection of the child's home is 

ordered.'® Inspections are also required when a day care center that may have 

lead paint is reviewed for licensing or begins renovations which may disturb 

lead paint. A property owner who is concerned that a lead hazard may exist 

can also request an inspection. If the inspection shows a lead paint hazard 

to exist, a violation notice is issued to the landlord or owner of the premises, 

who must abate or remove the lead paint. 

Federal Controls on Other Lead Sources 
In addition to efforts to control lead from paint, other sources of lead 

have also come under government scrutiny. Most of these fall within the 

| jurisdiction of the U.S. Environmental Protection Agency (EPA). 

Lead in Air: Ironically, the nation’s most effective steps in preventing 

lead exposure were only partially prompted by concerns over lead toxicity. 

The Clean Air Act of 1970 set standards for auto emissions of certain 

pollutants (namely hydrocarbons, carbon monoxide and nitrogen dioxide)." 

To meet those standards, auto-makers developed the catalyuc converter, a 

device that happens to be rendered inoperative by leaded gasoline. As a 

result, the use of leaded gasoline in vehicles equipped with converters had to 

  

  

15 1987 Mass. Acts ch. 773 (codified primarily at Mass. Gen. Laws Ann. 
Ch. 111, ss 190-199). Implementing regulations have been promulgated by 
both the Department fo Public Health, Mass Admin. Code title. 105, s 460.000 
(1989), and the Department of Labor and Industries, Mass. Admin. Code titl. 

454, s 22:00 (1988. 

'® Cal. Health & Safety Code Section 309.7. 

'7 State of California (1989). 

'® Interview with M. Michael Wojotovycz, Baltimore City Health Depart- 
ment, Lead Poisoning Prevention Program (Feb. 2, 1990). 

'® Pub. L. No. 91-604, 84 Stat. 1676, 91% Cong., 2° Sess., codified at 

42 U.S.C. 1857 et seq. 

 



be prohibited.? 

As EPA moved to develop the necessary regulations, however, the 

Agency began evaluating lead-toxicity issues as well as the need to protect 

catalytic converters. But EPA found itself unable to resolve certain issues 

and deferred the adoption of health-based limits. Following litigation 

brought by environmentalists, EPA eventually adopted a health-based 

phasedown inleaded gasoline. Those regulations in turn were challenged by 

industry, but were upheld by a federal appellate court.” 

Efforts by the Reagan Administration to relax those standards in the 

early 1980s triggered a storm of protest by the public health community and 

were eventually abandoned. Indeed, EPA tightened the regulations some- 

what as a result of data presented during that process. Industry again 

challenged the regulations, and the courts substantially upheld them.z 

During that litigation, the court became so impressed by the strength of the 

scientific evidence that it took an unusual step: going beyond the scope of 

the regulations before it, the court remarked that the significant risk of 

adverse health effects from blood lead levels as low as 10-15 ug/dl would 

justify EPA in banning lead from gasoline entirely.” 

EPA subsequently lowered allowable levels in gasoline still further, 

effective January 1, 1986.% Overall, between 1975 and 1986, the amount of 

lead added to gasoline declined nearly 90 percent.” 

In addiuon to the substantial effects of the leaded-gas restrictions, the 

Clean Air Act also authorizes EPA to set ambient standards for pollutants 

“which may reasonably be anticipated to endanger public health or wel- 

fare.”? These standards, termed National Ambient Air Quality Standards or 

“NAAQS,” prescribe the maximum concentration of lead allowed in the air 

throughout the nation. In 1978, EPA set the current standard of 1.5 micro- 

grams of lead per cubic meters of air (“ug/m3”), averaged over a calendar 

  

  

20 For a detailed review of this topic, see EK Silbergeld and RV Percival 
(1987), “The Organometals: Impacts of Accidental Exposure and Experimen- 
tal Data on Regulatory Policies,” pp. 328-352 in S Sparber and H Tilson (eds.), 
Neurotoxicology of Organometals, New York: Wiley Interscience. 

2 Ethyl Corp. v. EPA, 541 F. 2d 1 (D.C. Cir. 1976) (en banc). 

22 ine hase n Kk r nvir | 

Protection Agency, 705 F.2d 506 (D.C. Cir. 1983) (upholding numeric 

statndards though remanding to correct procedural flaws). 

2 |bid,, 705 F.2d at 531. 

24 See 24 C.F.R. Part 80. The current limit for lead in leaded gasoline 
is 0.10 grams per gallon. 40 C.F.R. Section 80.20(a)(iii). 

2 The figures are: 1975 = 190 metric tons; 1986 = 29 metric tons. 
Sources: Bureau of Mines (1985), Mineral Facts and Problems, Lead Chap- 

ter, Table 4 (preprint); Bureau of Mines (1987), Minerals Yearbook, Lead 

Chapter, Table 11. Since 1986, figures for use of lead as a gasoline additive 
have been merged with other miscellaneous uses. 

2 42 U.S.C. section 7408(a).   

The court remarked that the signifi- 

cant risk of adverse health effects 

from blood lead levels as low as 10- 

15 ug/di would justify EPA in banning 

lead from gasoline entirely. 

 



  

One study acknowledges that 

nearly every primary smelter now in 

operation is violating current occu- 

pational and environmental lead stan- 

dards. 

34 

  

quarter.” Industry unsuccessfully challenged those regulations as well. 

The Act requires that a NAAQS be reviewed and, if needed, revised 

every five years.® EPA is still working on its first revision of the lead 

standard, and anticipates proposing it in October 1990.3° Given that EPA’s 

existing air quality standard was based on a target blood-lead level of 15 ug/ 

dl, it appears almost inevitable that the standard will be lowered. EPA’s 

preliminary analyses for a revised lead NAAQS were recently reviewed by 

a group of EPA-appointed outside experts, as mandated by the Clean Air 

Act® That group, known as the Clean Air Scientific Advisory Committee, 

noted that levels approaching the current standard provide “relatively little, 

ifany, margin of safety,” and urged “greater consideration be given to air lead 

values below 1.0 ug/m?3.”"? 

With the prevailing use of unleaded gasoline, the only parts of the 

country exceeding the current standard are those in the vicinity of lead 

smelters and refineries. While the technology exists to reduce these emis- 

sions, some familiar with the industry assert that the cost of cleanup is too 

high for the domestic industry to remain competitive against foreign im- 

ports.*® Indeed, one study acknowledges that nearly every primary smelter 

now in operation is violating current occupational and environmental lead 

standards.* 

Lead in Soil: There is no specific Federal program for soil-based lead 

removal. Under the authority granted in Title III of the 1986 amendments to 

the Superfund legislation®*, EPA has recently earmarked a small portion of 

Superfund money for long-term residual toxic deposits of lead in soil. 

Boston, Baltimore, and Cincinnati are currently using Superfund money for 

projects designed to test the health effects of removing high-lead soil in 

residential neighborhoods. 

    

27 40 C.F.R. section 50.12, 43 Fed. Reg. 46246 (Oct. 5, 1978). 

28 Lead Industries Association v. Environmental Protection Agency, 

647 F. 2d 1130 (D.C. Cir. 1980). 

28 42 U.S.C. section 7409(d). 

% EPA's projected schedule was stated in its semi-annual regulatory 

agenda of October 1989. 54 Fed. Reg. 45323 (Oct. 30, 1989). 

31 42 U.S.C. section 7409(d)(2). 

3 Environmental Protection Agency, Science Advisory Board (1990), 
p- 3 

3 See, e.g., Bureau of National Affairs, “Tighter Emission Controls at 
Lead Smelters Achievable But Costly, Bureau of Mines Says,” Environmental 
Beporter, Vol. 18, (December 18, 1987), p. 1931. 

  

3 Bureau of Mines (1988) pp. 9-10. 

35 Pub. L. No. 99-499, Superfund Amendments and Reauthorization 
Act of 1986, codified as ammendments to 42 U.S.C. 9601 et seq. 

% These projects are modest and aimed primarily at research on health 

effects of soil lead abatement. The three-year Baltimore effort is funded at 
$4.8 million and involves 160 dwellings, one half of which constitute a control 

 



  

Lead in Solid Waste: The primary federal statute governing control of 

solid waste is the Resource Conservation and Recovery Act of 1976 

(“RCRA”).*” Under RCRA and its implementing regulations, a waste 

qualifies as hazardous if it leaches lead above a certain threshold (namely 5 

parts per million).*® Hazardous wastes must be managed and disposed of 

according to detailed requirements.* Regulations for management of non- 

hazardous waste are virtually non-existent, though standards for municipal 

landfills were proposed in 1988.4 

The incineration of municipal waste presents another area covered by 

legislation. The Clean Air Act requires the EPA to set standards for air 

pollutants from solid waste incineration but EPA’s recently proposed stan- 

dards do not specifically address lead emissions.*! 

Lead in Drinking Water: Federal responsibility for control of lead in 

drinking water arises under the Safe Drinking Water Act,*? administered by 

EPA. EPA’s current standard for lead in drinking water is 50 micrograms per 

liter of water (50ug/L), but the Agency recently proposed a 10-fold lowering 

of the standard to 5 ug/L.* Because lead is contributed primarily by leaching 
of pipes and solder during distribution (rather than contamination at the 

wellhead or reservoir), EPA has proposed to set an “action level” that would 

require public water systems to reduce the corrosiveness of water if more 

than 5% of household water samples contain more than 20 ug/L of lead. 

EPA estimates that the drinking water of approximately 42 million 

Americans contains more than 20 ug/L of lead,* largely because many 

jurisdictions nationwide had used lead service lines and leaded solder in their 

  

  

group. Interview with Susan Guyaux, Technical Specialist for Lead, Center 

for Environmental Health, State of Maryland Department of the Environment. 

37 42 U.S.C. 6901 et. seq. 

3 40 C.F.R. section 261.24. Certain lead-containing wastes are also 
separately listed as hazardous wastes. 

% See generally 40 C.F.R. parts 260-270. 

40 53 Fed. Reg. 33314 (Aug. 30, 1988) (proposed municipal landfill re- 
quirements). 

“1 54 Fed. Reg. (Nov. 1989). For ash residues from such incineration, 
controversy exists as to whether ash that exceeds the threshold for leachable 
lead must be managed as hazardous waste. Although EPA has taken the 
position that it must, two district courts recently interpreted RCRA to provide 

an exception for ash under certain circumstances. See Environmental 

Defense Fund v. Wheelabrator, No. 88-0569 (S.D.N.Y. slip. op. Nov. 21, 
1989); EDF v, City of Chicago, No. 88-0769 (N.D. Ill. slip op. Nov. 29, 1989). 

“2 42 U.S.C. section 300f et seq. 

“ The current standard is found at 40 C.F.R. section 141.11(b); the 
revision was proposed on August 18, 1988, 53 Fed. Reg. 31516, 31571. 

“4 Environmental Protection Agency (1986b), p. 11-58.   

Under RCRA and its implementing 

regulations, a waste qualifies as 

“hazardous if it leaches lead above 

five parts per million. 

35 

 



  
36 

tings in any private or public potable 
(drinking) water supply system. 

  

  

water systems for years. Indeed, until recently the City of Chicago required 

the use of lead pipe in new service lines.*’ 
The 1986 Amendments to the Safe Drinking Water Act banned the 

further use of lead products in new public water systems and in new homes 

connected to them.*® The ban encompasses both leaded plumbing fixtures 

and leaded solder (containing more than 0.2% lead). Nonetheless, leaded 

solder continues to be sold for a variety of other uses. Unfortunately, it is far 

from clear that the small warming labels printed on solder packages serve as 

an effective means for deterring its use in drinking water systems, partcu- 

larly because unleaded solder is not carried by all hardware stores. 

Yet another source of lead in drinking water is found in the lead liners 

or solder in drinking fountains. Discovery of this problem in 1988 prompted 

enactment of the 1988 Lead Contamination Control Act, which banned the 

manufacture and sale of drinking water fountains containing lead that comes 

into contact with drinking water supplies.” The Act also directed EPA to 

compile lists of lead-containing water coolers, and assist schools in detecting 

lead in school drinking water.*® 

Summary of Government Efforts 
America has made significant progress in the battle to “de-iead” some 

aspects of its environment -- most notably air following the phase-down of 

leaded gasoline -- but has had woefully limited success in addressing other 

exposure sources. Chief among the latter is lead paint in older homes. This 

is ironic in view of the fact that the Lead-Based Paint Poisoning Prevention 

Act was enacted nearly two decades ago expressly to control this very source. 

But because leaded paint continues to be a highly accessible source of lead 

as long as it remains on the premises, merely prohibiting the use of additonal 

iead-based paint in dwellings has proven to be an inadequate response to the 

problem. The intractable features of this issue indicate that leaded paint 

represents a public health threat demanding extraordinary efforts, different 

in both degree and kind from those of the past. 

  

  

“ Ibid, p. I-15. 

“ Pub. L. No. 99-339, section 109, 100th Cong., 2d Sess. (1986), 

codified at 42 U.S.C. section 300g. 

47 Pub. L. No. 100-572, 102 Stat. 2884, 100th Cong., 2d Sess. (1988), 

codified to 42 U.S.C. section 300j-21 to 300j-25. 

“8 The final water cooler list was issued at 55 Fed. Reg. 1772 (Jan. 18, 
1990), while guidance for schools was published at 54 Fed. Reg. 14316 (April 

10, 1989). 

 



7. SETTING GOALS AND PRIORITIES 
FOR FUTURE ACTION 

Lead’s persistence and toxicity mandate efforts to minimize blood- 

lead levels for all Americans. At the same time, special attention must be 

directed to those who are most heavily exposed and most vulnerable. A new 

Federal effort should therefore aim at the two million high risk houses that 

have been and will be home to millions of children. It should also aim to cut 

the amount of lead being introduced into commerce. 

The vast amount of information available on lead’s persistence and 

toxicity, especially in light of new data on lead’s long-term neurologic 

effects provide a compelling basis for an aggressive Federal program of lead 
removal. Key factors include the following: 

€@ Lead in the body has no known biologic or physiologic value. Its 

only known effect is that of interfering with essential bodily functions. 
© Lead is indestructible. Virtually all of the reported cases of lead 

poisoning today stem from decades-old paint from the walls and woodwork 

of homes. 

© Lead’spresence inthe body is largely cumulative and its effects are 
largely irreversible. The half-life of lead stored in our bones and teeth is 
approximately twenty years; minute accumulations of lead in the body over 
time can produce toxic levels of blood lead, and bring about symptoms that 
last long after treatment. 

© New research continues to decrease the levels of human absorption 
that we deem to be dangerous. The federal government now recognizes 
adverse effects at levels that are a small fraction of the official standard in 
place twenty years ago. 

€@ While the exact number of persons with unduly high blood lead 
levels cannot be precisely calculated, the number far exceeds that reported 
through screening programs. That number includes millions of adults as well 

as children, and more affluent as well as poorer Americans. 

As a practical matter, society cannot immediately remove all the lead 
that may threaten the public health. In the words of one report, “Lead is toxic 

wherever it is found, and it is found everywhere.” 

As a result, priorities must be set. One approach is to (1) identify the 
group or groups who currently have the highest exposures to lead and sus- 
ceptibility to its effects, (2) establish a “least cost” method of minimizing 
those exposures, (3) erect administrative and financial safeguards to ensure 
the realization of policy goals, and (4) to the degree possible, join any new 
effort with other important policy goals, including stimulating the use of 
nonleaded products and environmentally responsible recycling of lead, and 

  

  

' Centers for Disease Control (1985), p. 1. 

2 Agency for Toxic Substances and Disease Registry (1985), p. I-1. 

  

PART II: 
TOWARD A SOLUTION: 

A PROPOSAL FOR 
LEGISLATIVE ACTION 

“Lead is toxic wherever it is found, 

and it is found everywhere.” 

 



An estimated 1.97 million homes 

with peeling lead-based paint house 

well over half a million children. 

  

  

increasing the supply of safe and affordable housing. 

Identify Groups Most At Risk 

As discussed above, children living in homes with deteriorating lead- 

based paint are at greatest risk of ingesting undue amounts of lead today. An 

estimated 1.97 million homes with peeling lead-based paint house well over 

half a million children today, and pose a continuing threat to additonal 

children in the future. The program could be structured so that the first areas 

addressed are those in which large numbers of lead-poisoned children have 

already been identified. By beginning lead abatement programs on this 

highest-risk segment of the population, resources will be spent where the 

potential public health benefits are the greatest, with concomitant economic 

benefits. In addition, millions of American families will avoid the financial 

and emotional costs of lead-induced school failure and reading disabilities. 

Establish “Least Cost” Methods 

The $3-10 thousand per unit cost of de-leading a house assumes 

current market conditions and current operating technology. The average 

cost could weigh in closer to the bottom end of this scale given a concerted 

effort to (1) maximize competition among contractors licensed to perform 

lead removal, (2) train additional workers in lead removal procedures, (3) 

encourage local governments and owners of multi-family housing units to 

couple paint abatement with other rehabilitation, and (4) develop new meth- 

ods of paint abatement. 

Erect Administrative and Budgetary Safeguards 

Congress enacted the 1970 Lead-Based Paint Poisoning Prevention 

Act with the best of intentions, but the Act’s effectiveness has been severely 

limited by HUD’s inaction and by inadequate funding. To avoid arecurrence 

of this problem, a program to combat the problem of lead-based paint should 

contain administrative and financial safeguards. These could include (1) 

guaranteed funding, (2) administrative responsibility vested in health and en- 

vironmental agencies whose expertise best comports with the goals of the 

program, and (3) a built-in policy approach that emphasizes prevention in 

addition to treatment. This third safeguard is particularly desirable given the 

irreversible effects of lead poisoning, for a policy consisting solely of treat- 

ment carries countless social, educational, and medical costs. 

Join New Efforts with Secondary Goals 

Any new Federal program takes its place beside others attempting to 

attain related goals. Where a new program can be constructed so as to 

reinforce the goals of existing programs, one achieves administrative effi- 

ciency and a better return on the taxpayer dollar. Over the years, some of the 

aims of Federal lead programs have included mandating or encouraging the 

use of substitutes for lead (e.g., the phase-down on leaded gasoline, the ban 

on leaded solders in drinking water systems, and FDA-National Food 

Processors Association program for use of non-leaded solder in food cans).  



  

8. AN OUTLINE OF THE PROPOSAL 

The Environmental Defense Fund (EDF) proposes 

a trust fund, to be financed by the creation of an excise fee 

on the production and importation of lead. Proceeds from 

the fund would be devotedfirst to the goal of paint removal 

in the high risk group of homes with peeling, lead-based 

paint. The program would be administered jointly by the 

Environmental Protection Agency and the Department of 

Health and Human Services; these agencies would also 

monitor the health effects of the lead removal actions. The 

program would contain extra provisions to enable it to 

adapt to market conditions and, where possible, accom- 

plish secondary goals. 

The Trust Fund 

EDF believes that earmarking funds in the budget within a specific 

trust fund is the preferred way to ensure that the goals of this program can be 

met.’ 

Congress has earmarked funds where it has determined that any 

inflexibility inherent in the earmarking process is more than offset by the 

need to accomplish specific policy goals, by the importance of generating 

secure and long-term funding, and where there is complementarity between 

the specific funding source, on the one hand, and the policy goals on the 

other. In the environmental arena, the Hazardous Substance Superfund,? the 

Nuclear Waste Fund,’ and the Leaking Underground Storage Tank Trust 

Fund,* each operate to achieve specific goals comparable to the one at hand.’ 

  

  

' It may be appropriate to adopt a means test or other eligibility test to 

ensurethattrustfund monies go to housing owners (whether public or private) 
who are not otherwise able to finance abatement of lead paint within their 

units. If such a restriction were adopted, it might be desirable to provide tax 

credits for abatement to homeowners not eligible for grants or loans. 

2 Established by the Comprehensive Environmental Response, Com- 

pensation, and Liability Act, Pub. L. No. 96-510, section 221, 94 Stat. 2767, 
2801 (1980), codified to 26 U.S.C. section 9631 (commonly referred to as 

“Superfund”). 

® Established by the Nuclear Waste Policy Act of 1982, Pub. L. No. 97- 
425, section 302, codified to 42 U.S.C. section 10222. Strictly speaking, this 

is a “special fund” rather than a trust fund, but it involves the same principles 

of earmarked funds. See General Accounting Office, Trust Funds and Their 
Relationship to the Federal Budget, (Washington, GAO, September 1988) 
GAO Document No. GAO/AFMD-88-55, p. 7. 

  

“ Established by the Superfund Act Amendments and Reauthorization 
Act of 1986, Pub. L. No. 99-499, section 522, 100 Stat. 1613, 1780, codified 

to 26 U.S.C. 9508. 

> Afourth environmental trust fund, the Oil Spill Liability Trust Fund, was 
established by the Omnibus Budget Reconciliation Act of 1986 (Pub. L. No. 
99-509, 100 Stat. 1874, and awaits authorization. 

  
39 

 



  40 

  

The Excise Fee 
Each of the trust funds mentioned in the previous paragraph is financed 

by a narrowly based excise or a series of excises that is closely related to the 

goal of the fund. Overall, on-budget federal trust fund receipts from excise 

and other levies in fiscal year 1989 were approximately $250 billion.® EDF 

proposes an excise on the introduction of new lead into commerce, including 

imported lead, for an initial period of seven years. 

The goal of de-leading two million homes, at an estimated average cost 

of $5,000 per unit, determines the total level of needed receipts as $10 

billion.” If the program is designed to have a seven year life, and to spend 

funds at aconstant rate, then the fee should be set to yield approximately $1.5 

billion annually (subject to adjustment for inflation). In 1988, the volume of 

new and imported lead entering U.S. commerce was approximately 600,000 

tons.® These data suggest that the fee initially should be set at approximately 

$2500 per ton, equivalent to $1.25 per pound of lead. Based on the 

November, 1989 average price of lead at 41.3 cents per pound,’ the excise 

would work out to approximately a four-fold increase in the price of lead." 

Imposition of a fee of this magnitude is not a novel concept. For 

example, the Budget Reconciliation Act of 1989 contains a per-pound feeon 

ozone depleting CFCs that rises to $4.90 per pound by the end of the decade.” 

A preliminary analysis suggest thal impacts on Consumers would 

generally be moderate. Assuming the fee has a linear effect on prices, anew 

automobile battery (which contains approximately 18 pounds of lead) would 

cost about $11 more if the battery contained 50% virgin or imported lead. 

Batteries range significantly in price, from about $50 to about $100, and 

typically carry a warranty of 5 years or longer.” The $11 initial price increase 

thus could be viewed as an incremental cost of about $2 per year over the 

guaranteed lifetime of the battery. Moreover, in practice the increase would 

probably be considerably smaller, since most batteries already contain more 

than 50% recycled lead. Price increases (in absolute terms) on other classes 

of products that use less lead by weight would be correspondingly lower. 

  

  

¢ Office of Management and Budget (1989), Budget of the United 

States Government, Fiscal year 1990: Special Analysis C (Washington, 

Government Printing Office), p. C-14. 
  

7 This brief analysis is not intended to be exhaustive or comprehensive, 

but rather only to provide a starting point for further discussion. 

® Figure derived from the Bureau of Mines (1989c) and converted from 

metric tons to short tons. 

® Bureau of Mines (1989b), Table 10. 

10 By way of comparison, during the last dozen years, lead prices have 

fluctuated from $0.202 per pound (1985) to $0.789 (1979) (based on constant 

1987 dollars). Bureau of Mines (1989a), Nonferrous Metal Prices in the 

United States Through 1988, (Washington: U.S. Dep't of the Interior), pp. 55- 

57. 

  

1 Budget Reconciliation Act of 1989, Pub. L. No. 101-238, section 

7506, 103 Stat. 2106, 2364, 101st Cong., 1st Sess. (1989). 

2 Consumer Reports, p. 103 (Feb. 1987). 

 



  

We propose that the level of the fee, the possibility of additional 

funding sources, and the duration of the program be carefully monitored in 

order to ensure the viability of the program as lead production levels 

fluctuate. 

We believe this narrow excise fully meets the test of complementarity 

between funding source and policy objective. Italso takes a policy approach 

to the issue that we believe maximizes the efficiency of the program, by ac- 

complishing a number of other important policy goals. 

First, it would use market signals, rather than cumbersome regulatory 

processes, to discourage new lead production. The proposed excise is 

intentionally large, so as to help begin to internalize the extraordinary social 

costs of lead exposure and thus create incentives to adopt safer substitutes. 

The excise fee approach avoids the current resource-intensive federal ap- 

proach to toxic substance control embodied in the Toxic Substances Control 

Act (TSCA). That approach, which involves a lengthy and expensive use- 

by-use investigation of the health effects of a particular substance, fails the 

pragmatic test. Since TSCA’s enactment in 1976, only a handful of 

substances have been regulated. The most far-reaching set of regulations — 

those banning many uses of asbestos — took almost a decade to develop and 

will not take effect for most asbestos products until 1997, almost two decades 

after the rulemaking process began.!* 

Moreover, TSCA’s regulatory approach as implemented to date ig- 

nores economic forces, while this proposal seeks to exploit them. Making 

new lead more expensive will provide a market incentive to use existing 

substitutes for lead, and to develop additional ones. This approach bypasses 

TSCA'’s inefficient reliance on bans coupled with use-by-use waivers, a 

process that is inherently cumbersome and that does nothing to encourage de- 

velopment of substitutes for any use that is initially granted a waiver. 

Second, the excise would promote the more responsible use and reuse 

of lead. Increases in the price of virgin lead would raise the price that smelters 

would be willing to pay for scrap, because they in turn will be able to receive 

higher prices for selling secondary lead. Because the excise would apply to 

virgin lead alone, there would be no corresponding direct increase in the costs 

of scrap lead. Thus, construction firms, salvage firms, and even individuals 

would have a strong economic incentive to sell their lead scrap. 

Third, the excise would direct needed attention to the dangers of lead 

in our environment. The failure of the 1970s lead-based paint legislation is 

attributable in part to the fact that lead poisoning slipped from the forefront 

of the nations's health policy concerns. As a result, competing budget 

priorities deprived the program of adequate funding. By placing a substantial 

fee on lead production and assigning specific responsibility for preventing 

lead poisoning in the nation’s health and environmental agencies, Congress 

would both create a stable funding source for a sustained response, and send 

a strong signal that lead poisoning is one of the country’s top environmental 

health priorities. 

Fourth, the program would increase the availability of safe housing 

for low income families. The deteriorated housing units targeted by the 

abatement program frequently house poor families with young children. By 

creating an external source of funding for abatement, the program will help 

  

  

13 54 Fed. Reg. 29460 (July 12, 1989). 

  
41 

 



  
42 

  

  

advance the goal of providing such families with housing that is both safe and 

affordable. 

Flexibility 

It is possible that market conditions will develop differently than 

predicted, so as to bring the trust fund income short of, or beyond, projec- 

tions. Therefore, the trust fund should be given sufficient flexibility in its au- 

thorizing legislation to (1) apportion trust fund disbursements in the form of 

both loans and grants, based upon timely income projections, so as to ensure 

a viable income stream; (2) adjust the excise upwards or downward, within 

specified limits, to correct for conditions that threaten an excessive deficit or 

surplus; (3) extend the life of the trust fund, within specified limits, to achieve 

the program goals; and (4) report on a regular basis to Congress on the need 

for additional legislation. 

Administration 
The success of this program will depend to a substantial extent upon 

our willingness to keep it oriented toward its major goals: improving the 

health of children and families who are today most likely to develop low- 

level lead poisoning, and developing a safe living environment for present 

and future generations of Americans. In this regard, we note that State lead 

abatement programs are routinely administered by departments of health or 

environment,’ and that the 1970 lead-based paint legislation placed admini- 

stration of the grant program in the Department of Health, Educauon and 

Welfare. 

We also note the classic conceptual basis of government organization 

into purpose, process, clientele, and place.” Consistent with these principles 

and with previous Federal and State experience, we recommend placing this 

program jointly under the jurisdictions of the Environmental Protection 

Agency and the Department of Health and Human Services (HHS). We 

believe that each of the four classic concepts points to these two entities. 

As stated above, the purpose of this program is to improve public 

health that is daily under assault from environmental factors. EPA and HHS 

are, quite simply, the federal government's primary agencies in the area of 

  

  

4 Maryland's lead abatement program is administered by the Toxics 

Operations Program, in the Department of the Environment (MDE). MDE 

drafted the regulations on lead paint abatement that all other departments 

(e.g., Department of Housing and Community Development, which oversees 

public housing) must follow when engaging in leaded paint abatement. The 

Childhood Lead Poisoning Prevention Program in Massachusetts is admini- 

stered by the Bureau of Environmental Health, in the Department of Public 

Health (DPH). Similarly, DPH's leaded paint regulations govern other 

programs (e.g., housing programs administered by the Executive Office of 

Communities and Development). Ohio's lead poisoning prevention program 

is administered by the State's Department of Health, through the Bureau of 

Environmental Health andthe Division of Maternal and Child Health. Sources: 

Toxics Operations Program, State of Maryland; Ohio Department of Health, 

State of Ohio; Department of Health, Commonwealth of Massachusetts. 

15 LH Gulick (1937), in L Gulick and L Urwick (eds.) Papers on the 
Science of Administration, Institute of Public Administration, Columbia Uni- 

versity (Concord NH, The Rumford Press), p. 15. 

 



environmental factors that affect our health. The process of paint abatement 

would have to take place under strict guidelines that, in view of the 

substantial health risk if performed improperly, have usually been drafted 

and enforced by departments of health or environment. Gauging the 

effectiveness of the process will require careful testing and monitoring 

procedures akin to those involved in other EPA programs. Bringing coun- 

seling and follow-up services to families affected by this program will 

require additional specialized resources that HHS has readily at hand. The 

clientele, i.e., children and families in danger of lead poisoning, come 

logically under the jurisdiction of HHS and EPA. And the place, the United 

States, is matched by the fact that both EPA and HHS have regional offices 

around the country.!® 

With EPA’s primary jurisdiction over environmental matters -- in- 

cluding environmental lead contamination -- and HHS’s expertise in public 

health services and programs affecting the family, the two agencies can bring 

a wide spectrum of resources to bear on this multifaceted problem. 

Hiring Preferences 

Many communities to be served by this proposal initially will not have 

sufficient labor to perform the specialized tasks of leaded paint removal. 

Paint removal projects covered by the trust fund could be required to give 

hiring preference to unemployed workers living in those communities. For 

example, the State of Maryland program initially carried an employment/job 

training component that emphasized technique and occupational safety. At 

one point, seventy-five percent of those working on leaded paint abatement 

in Baltimore came under the job training provision, which gave unskilled 

workers a one-week course of instruction before placing them on a project.” 

Bringing a similar feature into this program would help alleviate the 

serious unemployment that tends to afflict precisely the same areas in which 

deleading must be undertaken.'®* Workers would develop marketable skills, 

returning money to their communities from their paychecks. Such a feature 

might also help prevent the provision of these specialized services from 

becoming lodged in too few providers, a situation that can lead to price in- 

flation and poor quality. 

Abatement Technology Development 

Regulation of lead paint in housing is plagued by a “cost-quantity 

trade-off”: needed safety regulations that drive up costs are likely to reduce 

the number of units that can be abated.’ Conversely, lowering the unit cost 

  

  

'6 National Archives and Record Administration, Office of the Federal 

Register (1988), ni e ment Manual 1988/89, (Washing- 

ton: U.S. Government Printing Office), p. 293. 

'7 Interview with Ms. Susan Kleinhammer, Project Superintendent, 
Lead Paint Abatement Program, City of Baltimore. 

'® This concept was originally suggested by Dr. Herbert Needleman. 
See HL Needleman (1988b), p. 737-738. 

1° S Pollack (1989), “Solving the Lead Dilemma,” Technology Review, 
October 1989, p. 22. 

   



  44 

  

  

of safe abatement could greatly increase the number of homes that could be 

rendered lead-free with a given amount of resources. 

A less expensive way to remove or encapsulate lead paint would help 

to stretch trust fund (and other public or private) abatement dollars. For this 

reason, EPA and HHS should be authorized to devote a small percentage of 

the fund to research on, and evaluation of new abatement technologies. 

Abatement Oversight 
There are a number of areas in which EPA should play aregulatory and 

oversight role. For example, EPA (together with HHS and the Occupational 

Safety and Health Administration) should set safety regulations or guide- 

lines applicable to all abatement work financed by the trust fund. These 

regulations or guidelines should address issues such as worker protection, 

tenant relocation and re-occupancy clearance criteria. 

In addition, once the excise has been fully in place for a suitable period 

-- perhaps five years -- EPA should review whether the excise is having its 

intended purpose of prompting economic forces to shifting the market away 

from using lead in products where substitutes are available. In addition to 

submitting its findings in a Report to Congress, EPA should also be required 

to determine whether any remaining uses pose particular threats to health or 

the environment, and, if so, to use other existing statutory authorities to 

address those uses. 

Other oversight provisions should be included in the enabling legisla- 

tion such as regular reporting requirements of the progress of abatement 

programs. Both HHS and EPA should be given specific authority to collect 

statistics on lead screening and treatment programs. 

 



CONCLUSION: 

FUTURE CONCERNS 

At the close of the initial seven-year program, 

adjustments may need to be made to preserve the market 

conditions that foster lower lead usage in our economy. 

What is needed today, however, is the public will to apply 

pragmatic measures to a serious public health problem. 

Such steps will hasten the day when lead poisoning has 

become as rare a threat to this nation’s children and 

adults as polio is today. 

After completion of the initial de-leading program aimed at abatement 

of the two million units with deteriorating paint, the abatement program 

could be either retired or extended to begin addressing the 38 million hous- 

ing units with intact leaded paint -- a significant, though less immediate, 

source of concern. If the abatement program were terminated, the excise 

could either be repealed or the proceeds diverted to the General Fund of the 

Treasury. If the tax is discontinued, other constraints on increased use of lead 

may well be necessary to preserve the market conditions that foster lower 

lead usage in our economy. 

These, however, are issues for another day. Our primary concern at 

present is the millions and tens of millions of children who can be protected 

from actual lead poisoning by removing peeling paint immediately. 

Unlike the scientific breakthroughs that had to occur before conquer- 

ing diseases such as polio, effective solutions to this problem are at hand. 

Now, the major impetus for change must come from the realization that the 

current situation is both intolerable and unnecessary. As a society, we must 

translate that realization into the only truly effective response to lead 

poisoning: its prevention. We can choose to start on the road toward that goal 

or, through continued inaction, we can consign ourselves to the human 

misery and economic costs of ubiquitous lead contamination. The opportu- 

nity is ours. But the benefits will extend to our children and our children’s 

children for generations to come. 

   



The Local Prevalence of Lead Poisoning in the US 

This appendix presents estimates of the extent of lead expo- 

sure in American children on a local basis; such figures have not 

been available previously. These estimates clearly reveal the 
seriousness of lead poisoning for communities in many urban 

areas of the country: in many of these areas, a majority of 

children have unacceptable blood lead levels (i.e., above 10- 

15 ug/dl). And the prevalence of affected children is especially 

alarming among the urban poor in certain regions of the U.S. 

Urban areas (standard metropolitan statistical areas, or SMSAs) 

with older central cities and relatively small amounts of new 

housing -- the “Rust Belt”, the Northeast, and much of the Midwest 

--typically have higher prevalence rates. By contrast, urban areas 

in the “Sun Belt” and the West Coast generally have lower 

prevalence rates, because of their higher proportion of newer 

housing. 

Tables A-1 and A-2 contain summaries of the data on a 

national basis. The importance of key parameters -- family 

income, child’s age, race, and residence location -- are clear. 

Overall, in the central cities of large urban areas, almost 70% of 

poor Black children and about 35% of poor white children are at 

risk of lead toxicity. Tables A-3, A-4, and A-5 present a breakdown 

of these data on a local basis, by SMSA.! 

How the Estimates were Derived 
These estimates are based upon information collected and 

analyzed for the Agency for Toxic Substances and Disease Registry 
(ATSDR), a component of the US Public Health Service. In 1988 

the ATSDR published a comprehensive Report to Congress on 

childhood lead poisoning in the United States.? That report 

  

  

' Table A-3 contains estimates for SMSAs of over 1 million people. 

Tables A-4 and A-5 both contain estimates for SMSAs of under 1 million 

people, butthose in Table A-5 tend to be smaller. As an artifact of the census 
data from which the estimates were calculated, the residence location could 
be distinguished as “central city” versus “not central city” for SMSAs included 
in Table 4 but notin Table 5. As a result, the calculations in Table 5 are likely 
to be proportionally underestimated. 

2 Agency for Toxic Substances and Disease Registry (1988), The 
Nature and Extent of Lead Poisoning in Children in the United States: A 
Report to Congress (Atlanta: U.S. Department of Health and Human 
Services/Public Health Service), Doc. No. 99-2966. 

  

  

  

APPENDIX | 

GEOGRAPHICAL 
DISTRIBUTIONS OF 
LEAD-POISONED 

CHILDREN 

 



  
  

  

analyzed existing data on numbers of lead-exposed children 

throughout the U.S., including results from a national sampling of 

children in the late 1970s. Those data were adjusted (by linear and 

logistic regression techniques) to take into account the reductions 

in lead exposure following the phasedown in use of leaded gasoline 

since 1982. 

To derive the data set forth in this appendix, data from the 

ATSDR Report were used to take into account the distribution of 

children in housing units according to the age of the housing. 

Because levels of lead in paint are closely associated with the age 

of housing, residence by age of housingis an appropriate surrogate 

for apportioning the risk of elevated blood lead levels attributable 

to paint exposure. 

The ATSDR report presented aggregate data for the US as a 

whole. Because of the limitations of the national sampling data,? 

the ATSDR Report only dealt with white and Black children, aged 

six months to 5 years livingin the nation’s 318 standard metropoli- 

tan statistical areas (SMSAs). Omitted from the ATSDR analysis, 

and from the estimates presented in this appendix, are all children 

of other racial and ethnic groups, all children not living in these 

318 urban areas, and all children older than 6 years of age. 

Usingthe ATSDR data, one of the two principal authors ofthe 

' ATSDR Report, Dr. Annemarie Crocetti, has derived local esti- 

| mates of numbers of children with blood lead levels above the 

range of concern (i.e., 10 to 15 ug/dl). These local estimates reflect 

the impact of local differences in the age of housing and presence 

of lead paint in housing. 

| To calculate the local estimates, data used in the ATSDR 

| Report were categorized by housing unit, as pre-1950, 1950-1969, 

and post-1970. The data were further stratified to take into 

account variations in family income (less than $6000, $6000- 

14,999, and equal to or greater than $15,000), age (six months to 

2 years; 3-5 years), race (white or Black), and location (in central 

city or not in central city). 

These figures are estimates, not measurements. They 

are by no means definitive, and no margin of error can be 

calculated. However, these estimates are based upon reasonable 

| assumptions astotheimpact of exposure tolead painton children’s 

| blood lead levels. Data from recent lead screening programs in 

| Oakland and Baltimore have been compared to these estimates; 

the latter fall within 5% of the projections made by local public 

health officials, using actual screening data, of the number of 

children with elevated blood lead levels attributable to lead paint. 

    

3 The samples were collected and analyzed as part of the Second 
National Health and Nutrition Examination Survey, or NHANES II.  



  

Table A-1 Estimated percentages of children 6 months to 

5 years who are projected to exceed selected blood lead levels 

by strata and residence in SMSAs of 1 million or more. 

In Central City Not In Central City 

  

  

>10 >15 >10 >15 

Strata (ug/dl) (ug/dl) 

> $6,000 

White 

.5 - 2 years 79.9 36.6 69.7 28.4 
3 - § years 80.8 35.5 70.2 27.1 

Black 

.5 - 2 years 95.9 67.0 91.6 57.4 

3 -5 years 97.1 68.5 93.3 58.1 

$6,000 - 14,99 
White 

5 - 2 years 65.1 23.5 53.1 17.4 

3 - 5 years 65.1 22.2 52.6 16.1 

Black 

.5 - 2 years 91.4 53.6 84.6 43.9 

3 - 5 years 92.6 53.6 85.9 43.3 

> $15,000 

White 

5 - 2 years 47.7 12.5 35.4 8.6 

3 - 5 years 46.7 114 34.2 7.9 

Black 

.5 - 2 years 85.2 38.8 75.2 29.6 

3 - 5 years 85.7 37.7 75.4 28.3 

  

  

  

Young Black children living be- 

low the poverty level in urban ar- 

eas may have a greater than 95% 

chance of having a blood lead 

level in excess of 10 ug/dl. 

 



  

Table A-2. Estimated percentages of children 6 months to 

5 years who are projected to exceed selected blood lead levels 

by strata and residence in SMSAs under 1 million. 

  

  

In Central City Not in Central City 

| >10 >15 >10 >15 

| Strata (ug/dl) (ug/dl) 

> $6,000 

White 

5 - 2 years 67.2 26.3 55.8 19.8 

3 - 5 years 67.4 25.0 55.6 18.6 

| Black 

5-2 years 90.8 55.2 84.3 46.0 

| 3-5years 92.4 55.7 86.0 45.8 

$6,000 - 14,999 

White 

5 - 2 years 50.1 15.8 38.8 11.4 

3 - 5 years 49.5 14.6 37.7 10.3 

Black 

.5 - 2 years 82.9 41.5 73.7 33.0 

3 - 5 years 84.1 40.7 74.7 31.9 

>$15,000 

White 

.5 - 2 years 32.5 7.6 22.79 5.1 

3 - 5 years 31.2 6.7 21.4 4.4 

Black 

5-2 years 72.6 27.3 60.6 20.2 

3 - 5 years 72.7 26.0 60.2 13.9 

  

  

 



Table A-3. Estimated total number of children 6 months to 5 years who are projected to exceed selected 

blood lead levels for individual SMSAs with populations over 1 million. 

  
  

SMSA 

Anaheim-Santa Ana-Garden Grove, CA 

Atlanta, GA 

Baltimore, MD 

Boston, MA 

Buffalo, NY 

Chicago, IL 

Cincinnati, OH-KY-IN 

Cleveland, OH 

Columbus, OH 

Dallas-Fort Worth, TX 

Denver-Boulder, CO 

Detroit, MI 

Fort Lauderdale-Hollywood, FL 

Houston, TX 

Indianapolis, IN 

Kansas City, MO-KS 
Los Angeles-Long Beach, CA 

Miami, FL 

Milwaukee, WI 

Minneapolis- St. Paul, MN-WI 

Nassau-Suffolk, NY 

New Orleans, LA 

New York, N.Y-NJ 

Newark, NJ 

Philadelphia, PA-NJ 

Phoenix, AZ 

Pittsburgh, PA 

Portland, OR-WA 

Riverside-San Bernardino-Ontario, CA 

Sacremento, CA 

St. Louis, MO-IL 

San Antonio, TX 

San Diego, CA 

San Francisco-Oakland, CA 

San Jose, CA 

Seattle-Everett, WA 

Tampa-St. Petersburg, FL 

Washington, DC-MD-VA 

SMSA 
Population 

158969 

175183 

168837 

176957 

87443 

604862 

120413 

147225 

96246 

290019 

142197 

330694 

64944 

314479 

100752 

114924 

654692 

125378 

116685 

184637 

172248 

112345 

656937 

134614 

357534 

119152 

147585 

98903 

156291 

825689 

178984 

111714 

156162 

206937 

98287 

119113 

101611 

236578 

# 

52670 
82453 
98857 

122862 
54012 

371952 
65746 
95304 
48738 

124350 
51825 

186768 
25345 

124209 
50174 
58019 

380905 
64150 
66110 
82904 
61078 
64845 

490977 
95230 

221654 
38518 
86921 
44249 
63519 
33781 
99705 
48747 
62949 

114921 
34700 
47556 
41849 

122406 

14858 

28614 

42063 

42187 

20631 

154037 

23957 

40365 

17179 

41025 

16122 

77492 

8062 

40204 

17323 

21743 

137769 

24194 

25041 

24921 

16776 

29866 

222229 

40318 

94297 

12298 

30447 

13899 

18204 

10627 

41969 

17114 

19683 

40817 

9863 

14321 

14585 

46267 

  
   



Table A-4. Estimated total number of children 6 months to 5 years who are projected to exceed selected 

Jlood lead levels for individual SMSAs with populations of 1 million or less. 

  

  

SMSA 

Akron, OH 

Albany-Schenectady-Troy, NY 

Albuquerque, NM 

Allentown-Bethlehem-Easton, PA-NJ 

Ann Arbor, MI 

Appleton-Oshkosh, WI 

Austin, TX 

Bakersfield, CA 

Baton Rouge, LA 

Beaumont-Port Arthur-Orange, TX 

Birmingham, AL 

Bridgeport, CT 

Charleston-North Charleston, SC 

Charlotte-Gastonia, NC 
Chattanooga, TN-GA 

Colorado Springs, CO 

Columbia, SC 
Davenport-Rock Island-Moline, [A-IL 

Dayton, OH 

Des Moines, IA 

Duluth-Superior, MN-WI 

Erie, PA 

Eugene-Springfield, OR 
Evansville, IN-KY 

Flint, MI 

Fort Wayne, IN 

Fresno, CA 

Gary-Hammond-East Chicago, IN 

Grand Rapids, Mi 

Greenville-Spartanburg, SC 

Hartford, CT 

Honolulu, HA 

Huntsville, AL 

Jackson, MS 

Jacksonville, FL 

Jersey City, NJ 

Kalamazoo-Portage, Ml 

Knoxville, TN 

Lansing- East Lansing, MI 

Las Vegas, NV 

SMSA 
Population 

49485 

59747 

39071 

43276 

19647 

23728 

52468 

46461 

52065 

36925 

68266 

27682 

43296 

50445 

30889 

31351 

33221 

33983 

68605 

27196 

22088 

22830 

20898 

25042 

39017 

33846 

52133 

58072 

58978 

43837 

50646 

24296 

24900 

31228 

70984 

43551 

22318 

33976 

41420 

41774 

>10 ugdl 

# 

8242 
8847 
3120 
5461 
1925 
1915 
4473 
4364 
7229 
6479 

13265 
5394 
6290 
6575 
5207 
2647 
4476 
4456 

10425 
2766 
2608 
3198 
1533 
3164 
6707 
5229 
6210 

10310 
7426 
5464 
8404 
2170 
2950 

5639 

11630 

12739 

2854 

4201 

4595 

3316 

ugvd 

% 

18.7 

14.8 

8.0 

12.6 

0.8 

8.1 

8.5 

9.4 

13.9 

17.5 

19.4 

19.5 

14.5 

13.0 

168.9 

8.4 

13.5 

13.1 

18.2 

10.2 

11.8 

14.0 

73 

12.6 

17.2 

15.4 

11.9 

17.8 

12.6 

12.4 

16.6 

8.9 

11.8 

18.1 

16.4 

29.3 

12.8 

12.4 

11.43 

7.9 

Continued 

  

   



  

‘Table A-4 Continued 
  

  

SMSA >10 ug/dl >15 ug 
SMSA Population # % # % 

Lawrence-Haverhill, MA-NH 22355 11134 49.8 3391 15.2 

Lexington-Fayette, KY 26668 111563 41.8 3580 13.4 

Lorain-Elyria, OH 21713 8471 39.0 2687 12.4 

Louisville, KY-IN 73518 29203 39.7 10684 14.5 

Macon, GA 22100 10774 48.8 3926 - 17.8 

Madison, WI 23209 6783 29.2 1794 7.7 

Mcallen-Pharr-Edinburg, TX 39025 12771 32.7 3810 9.8 

Memphis, TN-AR-MS 87808 44671 50.9 18082 20.6 

Mobile, AL 43200 18308 42.4 6606 15.3 

Modesto, CA 24415 7628 31.2 2072 8.5 

Nashville-Davidson, TN 70665 26153 37.0 8475 12.0 

New Brunswick-Perth Amboy-Sayreville, N 40200 14721 36.6 4058 10.1 

New Haven-West Haven, CT 31415 15790 50.3 6049 19.3 

Norfolk-Virginia Beach-Portsmouth, VA-N( 76451 36210 47.4 14924 ° 19.8 

Oklahoma City, OK 79127 27265 34.5 8554 10.8 

Omaha, NE-IA 52525 19742 37.6 6392 12.2 

Orlando, FL 59118 19414 32.8 7050 11.9 

Oxnard-Simi Valley-Ventura, CA 46338 12672 27.3 3383 7.2 

Paterson-Clifton-Passaic, NJ 34954 20872 59.7 8723 25.0 

Peoria, IL 31382 12726 40.6 4162 13.3 

Providence-Warwick-Pawtucket, RI-MA 60958 30624 50.2 10317 16.9 

Raleigh-Durham, NC 38089 14458 38.0 5088 13.4 

Richmond, VA 48973 20881 42.6 8268 16.9 

Roanoke, VA 15271 5340 35.0 1707 11.2 

Rochester, NY 76623 35835 46.8 12130 15.8 

Rockford, IL 23738 9715 40.9 2794 11.8 
Salinas-Seaside-Montery, CA 29091 10804 37.1 3112 10.7 

Salt Lake City-Ogden, UT 129167 33147 25.7 8706 6.7 

Santa Barbara-Santa Maria-Lompoc, CA 21855 7497 34.3 1957 8.0 
Shreveport, LA 38986 19978 51.2 8130 . 20.9 

South Bend, IN 23745 11867 50.0 4054 17.1 

Spokane, WA 30870 9659 31.3 2759 8.9 
Springfield-Chicopee-Holyoke, MA-CT 37183 18126 48.7 6036 16.2 

Stockton, CA 32809 12488 38.1 3900 11.9 

Syracuse, NY 53313 24031 45.1 7479 14.0 

Tacoma, WA 47047 17782 737.8 5304 11.3 

Tuscon, AZ 45133 11819 .25.5 3174 7.0 

Tulsa, OK 62119 21785 35.1 6518 10.5 

Uticia-Rome, NY 23982 11736 48.9 3624 15.1 

Vallejo-Fairfield-Napa, CA 28569 8999 31.5 2717 9.5 

Waterbury, CT 18777 7110 45.1 2604 16.5 

West Palm Beach-Boca Raton, FL 39576 13666 34.5 4328 10.9 

Wichita, KS 41057 17830 43.7 5662 13.8 

Worcester, MA 25913 12244 47.3 3534 13.6 

Youngstown-Warren, OH 40084 18529 46.2 6654 16.6 

  

  

 



Table A-5. Estimated total number of children 6 months to 5 years who are projected to exceed selected 

blood lead levels for individual small SMSAs. 

  

  

SMSA 

SMSA Population 

Abilene, TX 14225 : 1645 

Albany, GA 11632 : 2171 

Alexandria, LA. 16306 ; 3054 

Altoona, PA 10151 ; 1101 

Amarillo, TX 17746 : 1980 

Anchorage, AK 21407 : 1445 

Anderson, IN 9632 . 1608 

Anderson SC 9616 : 1551 

Anniston, AL 9154 : 1628 

Asheville, NC 11197 : 1061 

Athens, GA 18196 : 2712 

Atlantic City, NJ 14555 . 2622 

Augusta, GA-SC 31646 : 4180 

Bangor, ME and Lewiston-Auburn, ME 11993 : 1610 

Battle Creek, Mi 14682 : 2549 

Bay City, Mi 10201 818 

Bellingham, Wa 7796 3 703 

Benton Harbor, Mi 14393 ; 2634 

Billings, MT 10159 . 806 

Biloxi-Gulfport, MS 18850 : 2336 

Binghampton, NY-PA 18656 : 2517 

Bismarck ND and Grand Forks,ND-MN 18443 . 1630 8.8 

Bloomington, IN and Owensboro, KY 14569 : 1897 

Bloomington-Normal, IL 9472 ; 729 7.7 

Boise City, ID 17230 . 1041 6.0 

Bradenton, FL 9790 : 994 10.2 

Bremerton, WA 11475 . 801 7.0 

Bristol, CT and Meriden, CT 8989 : 1082 12.0 

Brockton, MA 12103 : 1549 12.8 

Brownsville-Harlingen-San Benito, TX 26998 : 2422 9.0 

Bryan-College Station, Tex. And Sherman- [ 16515 : 1532 9.3 

Burlington, Vt. 9044 : 670 7.4 

Canton, OH 31219 : 4230 13.5 

Casper, WY and Great Falls, MT 16226 : 1083 6.7 

Cedar Rapids, IA 13168 ; 1179 9.0 

Champaigna-Urbana-Rantoul, IL 13291 : 1302 8.8 

Charleston, WV 19226 . 2190 11.4 

Charlottesville, VA 75083 ‘ 747 10.0 

Chico, CA 10771 : 879 8.2 

Clarksville-Hopkinsville, TN-KY 15972 ; 1684 10.5 

Columbia, MO 8618 . 553 6.4 

Continued 

  
   



Table A-5 Continued 

  

  
  

SMSA >10 ugdl >15 ugdl 

SMSA Population # % # % 

Columbus, GA-AL 21334 10793 50.6 3752 17.6 

Corpus Christi, TX 37248 14351. 38.5 4211 11.3 

Cumberland,Md.-WV 77%} 4117 53.4 1358 17.8 

Danbury, CT 9714 3233 33.3 1136 11.7 

Danville, VA 9090 3950 43.5 1576 17.3 

Daytona Beach, FL 18061 6758 37.4 2394 13.3 

Decatur, IL 10145 5073 50.0 2377 23.4 

Dubuque, IA and lowa City, IA 15991 5934 37.3 1615 10.1 

Eau Claire, WI 9989 3596 36.0 . 956 9.6 

El Paso TX and Las Cruces, NM 64306 32423. 50.4 10484 16.3 

Elkhart, IN 11804 4724 40.0 1491 12.6 

Elmira, NY 10935 3246 29.7 885 8.1 

Fall River, MA-RI 13069 6744 51.6 1927 14.7 

Fargo-Moorhead, ND-MN 12868 4002 31.1 1046 8.1 

Fayetteville, NC 27557 11285 41.0 3517. 12.8 

Fayetteville-Springdale, AR 14422 3736 25.9 980 6.8 

Fitchburg-Leominster, MA and Pittsfield, M 13068 6056 46.3 1736. 133 

Florence, AL 9916 3440 34.7 13671 11.7 

Florence, SC - 9486 3857 40.7 1351 14.2 

Fort Collins, CO 13130 2570 19.6 644 4.9 

Fort Myers-Cape Coral, FL 14925 4044 271 1262 8.5 

Fort Smith, AR-OK 15809 5229 33.1 1737 11.0 

Fort Walton Beach, FL and Panama City, FL 19921 6153 30.9 1960 9.8 

Gadsden, AL 8391 . : 3501 42.8 1355 “16.1 

Gainesville, FL 12528 3712 29.86 1186. 9.5 
Galveston-Texas City, TX 19484 8742 44.9 3274 16.8 

Glen Falls, NY 8144 4233 52.0 1202 14.8 

Greely, CO 12386 3456 27.9 888 7.2 

Green Bay, WI 12812 4283 33.2 1142 8.9 

Greensboro-Winston-Salem-High Point, NC 53487 20807 38.9 6439 12.0 

Hagerstown, MD 8009 3349 41.8 912 11.4 

Hamilton-Middietown, OH 22874 8546 37.4 2787 12.2 

Harrisburg, PA 24192 13004 53.8 5347 - 21.3 

Hickory, NC 8888 2797 -- 31.5 880 9.9 

Huntington-Ashland, WV-KY-OH 24931 10666 42.8 3313...:13.3 

Jackson,MI 11694 5201 44.5 1609 13.8 

Jacksonville, NC 15536 5723 36.8 1934 12.4 

Janesville-Beloit, WI 11476 4820 42.0 1418 12.4 

Johnson City-Kingsport-Bristol, TN-VA 27946 9044 32.4 2598 9.3 

Johnstown, PA 14308 7639. 53.4 2332... 18.3 

Joplin, MO 8539 4464 52.3 1274 14.9 

Kankakee, IL 9332 4235 45.4 1677 18.0 

Kenosha, WI 9103 4134 45.4 1182 13.1 

Killeen-Temple, TX 28554 9752 34.2 2809 9.8 

Kokomo,IN 17943 7964 44.4 2633. 14.7 

Continued 

  
  

 



Table A-5 Continued 
  

  

  

SMSA >10 ugdl >15 ugdl 

SMSA Population # % # % 

La Crosse, WI and Rochester, MN 15905 4679 29.4 1193 7.5 

Lafayette, LA 17473 5911 33.8 1940 111 

Lafayette-West Layafette, IN 8218 2582 31.4 744 9.1 

Lake Charles, LA 18245 8102 44.4 2845 156 

Lakeland-Winterhaven, FL 27123 10120 37.3 3425 = 12.6 

Lancaster, PA 23663 12473. 52.7 3743. 15.8 

Laredo, TX and Victoria, TX 22498 7877 35.0 2328 10.3 

Lawton, OK and Enid, OK 19245 8052 41.8 2841 14.8 

Lima, OH 20587 9481 46.1 2740 13.3 

Lincoln, NE 16369 4724 28.9 1386 8.5 

Little Rock-No. Little Rock, AR and Pine BI. 35625 15794 44.3 6674 18.7 

Long Branch-Asbury Park, NJ 34205 12666 37.0 4045....11.8 

Longview-Marshall, TX 13585 5723 42.3 2017 14.8 

Lowell, MA-NH 16114 6849 42.5 2093. -13.0 

Lubbock, TX 21505 7739 38.0 2208 10.3 

Lynchburg, VA 9762 3733: 38.2 1224. 12.5 

Manchester, NH 13545 6127 45.2 ¥723 112.7 

Mansfield, OH 10353 4553 44.0 1505 14.5 

Medford, OR 10376 3147 30.3 888 8.6 

Melbourne-Titusville-Cocoa, FL 19038 6126 32.2 1854 9.7 

Midland, TX and San Angelo, TX 20398 7038 34.5 1907 0.3 

Monroe, LA 11628 4612 39.7 1683 14.5 

Montgomery, AL 22645 11724 51.8 4709 20.8 

Munice, IN 8679 4058 46.8 1322. 18.2 

Muskegon-Norton Shores-Muskegon Heights, 14451 6440 44.6 2375 16.4 

Nashua, NH 8720 2558 ~ 29.3 630 7.2 

New Bedford, MA 12355 6168 49.9 1901 15.4 

New Britain, CT 8761 3578 4Q.8 946 10.8 

New London-Norwich, CT-RI 20995 8017... 42.5 2740-131 

Newark, OH 0029 4204 42.3 1206 12.1 

Newburgh-Middleton, NY 21434 9027 42.1 2576. 12.0 

Newport-News Hampton, VA 26886 10886 40.8 3220. :..12.0 

Northeast Pennsylvania 40080 15658 39.1 4389. 10.9 

Norwalk, CT 8057 3957 49.1 1454 18.0 

Ocala, FL 9539 3483 36.5 1416 14.8 

Odessa, TX 14966 4120 727.5 1073 7.2 

Olympia WA 10931 2377 21.7 630 5.8 

Parkersburg-Marietta, WV-OH 13332 4769 35.8 1499 11.2 

Pascagoula-Moss Point, MS 11402 3030 26.8 850 7.5 

Pensacola, FL 25674 90189 . 35.8 3122 12.2 

Petersburg-Colonial Heights-Hopewell, VA 9525 4232 44.4 1346 14.1 

Portland, ME 15075 6617 43.9 1842 12.2 

Portsmouth-Dover-Rochester, NH-ME 12840 6147 47.9 710: 13.3 

Poughskeepsie, NY 17870 7255 40.6 2265 12.7 

Provo-Orem, UT 39433 8736 22.2 2384 6.0 

Continued 
  
  

 



Table A-5 Continued 
  
  

SMSA >15 ug/l 

SMSA Population # % 

Pueblo, CO 10188 1052 10.3 

Racine, WI 15267 2291 15.0 

Reading , PA 18971 2702 14.7 

Reddina. CA 10303 721 7.0 

Reno, NV 15497 890 5.7 

Richland-Kennewick-Pasco, WA 15888 945 5.9 

Rock Hill, SC 8018 1163. 14.5 

Saginaw, MI 19585 3092 15.8 

St.Cloud, MN 17825 1341 72.5 

St. Joseph, MO 8029 8962 42.0 

Salem, OR 22225 1939 8.7 

Salisbury-Concord, NC 13781 2167 15.7 

Santa Cruz, CA 13799 1394 10.1 

Santa Rosa, CA 23936 2050 

Sarasota, FL 9681 635 

Savannah, GA 22997 4781 

Sharon, PA 9231 1309 

Sheboygan, WI 8437 1017 

Sioux City, IA-NE 11012 1047 

Sioux Falls, SD 9535 825 

Springfield, IL 15764 2521 

Springfield, MO 16944 1715 

Springfield, OH 14214 2434 

Stamford, CT 12672 1909 

State College, PA 6467 705 

Steubenville-Weirton, OH-WV 12249 1396 

Tallahasse, FL 12816 1659 

Terre Haute, IN 13280 1995 

Texarkana, TX-Texarkana, AR 10369 1457 

Toledo, OH-MI 64793 10634 

Topeka, KS and Lawrence, KS 17289 1480 

Trenton NJ 20327 4975 

Tuscaloosa, AL 10415 1333 

Tyler, TX 12801 1774 

Vineland-Millville-Bridgeton, NJ 11307 2079 
Visalia-Tulare-Porterville, CA 29095 2686 
Waco, TX 16268 2424 

Waterloo-Cedar Falls, [A 11890 1363 
Wausau, WI 8620 828 

Wheeling, WV-OH 12473 1644 
Wichita Falls, TX 12229 1862 

Williamsport, PA 8894 1244 

Wilmington, DE-NJ-MD 41065 5888 

Wilmington, NC 113151 1529 

Yakima, WA 13409 1531 

York, PA 20323 3194 

Yuba City, CA 9217 882 
  
   



  

Agency for Toxic Substances and Disease Boga? (1988), The 

a (Atlanta: U.S. De- 
partment of Health and Human Services/Public Health 

Service), Doc. No. 99-2966. 

American Academy of Pediatrics (1987), “Statement on Childhood 
Lead Poisoning,” Pediatrics, Vol. 79, pp. 457-64. 

Bellinger, D, A Leviton, C Watermaux, H L Needleman, and M 
Rabinowtitz (1989), “Low-Level Lead Exposure, Social 

Class, and Infant Development,” Neurotoxicology and 
Teratology, Vol. 10, pp. 497-503. 

Bellinger, D, A Leviton, C Watermaux, H L Needleman, and M 

Rabinowtitz (1987), “Longitudinal Analyses of Prenatal 
and Postnatal Lead Exposure and Early Cognitive 
Development, New England Journal of Medicine, Vol. 316, 

pp. 1037-43. 

Bellinger, D, HL Needleman, R Bromfield, and M Montz (1984), “A 

Follow-Up Study of the Academic Attainment and Class- 

room Behavior of Children With Elevated Dentine Lead | 

Levels,” Biological Trace Element Research, Vol. 6 pp. 
207-23. 

Bureau of Mines (1989a), Nonferrous Metal Prices in the United 

States through 1988 (Washington: U.S. Department of 
the Interior). 

Bureau of Mines (1989b), “Mineral Industry Surveys: Lead Indus- 
tryin November 1989,” (Washington: U.S. Department of 
the Interior). 

Bureau of Mines (1989c¢), Mineral Commodity Summaries 1989, 
(Washington: U.S. Department of the Interior). 

Bureau of Mines (1989d), Minerals Yearbook 1987 (Washington: 
U.S. Government Printing Office) 

Bureau of Mines (1988), Impact of Existing and Proposed Regula- | 

tions on Domestic Lead Industry. (Washington: U.S, 
Department of the Interior), Doc. No. OFR/55-88. 

Bureau of Mines (1985), Mineral Facts and Problems (Preprint 

from Bulletin 675) (Washington: U.S. Department of the 
Interior). 

  

BIBLIOGRAPHY 

B-1 

 



  B-2 

California, State of (1989), Interim Report to the California State 
Legislature: Childhood Lead Poisoning in California: 

Causes and Prevention, (Sacramento: California Depart- 

ment of Health Services), 38 pp. 

  

  

Can Manufacturers Institute, letter dated March 28, 1989, to Mr. 

Jerry Burke, Acting Director, Office of Physical Sciences, 

Center for Food Safety and Applied Nutrition, Food and 

Drug Administration. 

Centers for Disease Control (1985), Preventing LL Poisoningin 

Children (1985), (Atlanta: U.S. Department of Health and 

Human Services/Public Health Service). 

Consumer Product Safety Commission (1989), “CPSC Warns About 

Hazards of ‘Do It Yourself Removal of Lead-Based Paint,” 

Consumer Product Safety Alert (Washington: CPSC). 

David, OJ, S Katz, CG Arcolo, and J Clark (1985), “Chelation 

Therapy in Children as Treatment of Sequelae in Severe 
Lead Toxicity,” Archives of Environmental Health, Vol. 

40, pp. 109-13. 
  

Davis, JM and DJ Svensgaard (1987), “Lead and Child 
Development,” Nature, Vol. 329, pp. 297-300. 

Dietrich, KN, KM Kraft, RL Bornschein (1988), “Low Level Fetal 

Exposure Effect on Neurobehavioral Development in Early 
Infancy” Pediatrics, Vol. 5, pp. 721-730. 

Environmental Protection Agency, Office of Pesticides and Toxic 

Substances (1989a), The Toxics Release Inventory (1987): 

ANational Perspective, (Washington: U.S. Environmental 

Protection Agency), Doc. No. EPA 560/4-89-005. 

  

Environmental Protection Agency (1989b), Characterization of 

Products Containing Lead and Cadmium in Municipal 

Solid Waste in the United States, 1970 to 2000 (Washing- 

ton: U.S. Environmental Protection Agency), EPA Doc. 

No. EPA/530-SW-89-015A, 207 pp. 

  

  

  

Environmental Protection Agency (1986a), Air Quality Criteria 

for Lead (Research Triangle Park: U.S. Environmental 

Protection Agency/Environmental Criteria and Assess- 

ment Office), in four volumes, EPA Report Nos. EPA-600/ 

8-83/028aF through /028dF. 

  

Environmental Protection Agency (1986b), Reducing Lead in 

Drinking Water: A Benefit Analysis, (Washington: U.S. 

Environmental Protection Agency, Office of Policy, Plan- 
ning and Evaluation), Doc. No. EPA-230-09-86-019. 

  

 



  

Environmental Protection Agency, Science Advisory Board (1990), 

“Report of the Clean Air Scientific Advisory Committee: 

Review of the OAQPS Lead Staff Paper and the ECAO Air 

Quality Criteria Document Supplement,” (Washington: 

U.S. Environmental Protection Agency), Doc. No. EPA- 

SAB-CASAC-90-002. 

Environmental Protection Agency, Science Advisory Board (1989), 

“Report of the Joint Study Group on Lead: Review of Lead 

Carcinogenicity and EPA Scientific Policy on Lead” 

(Washington: U.S. Environmental Protection Agency), 

Doc. No. EPA-SAB-EHC-90-001. 

General Accounting Office (1988), Trust Funds and Their Rela- 

tionship to the Federal Budget, (Washington: U.S. Gen- 
eral Accounting Office) Doc. No. GAO/AFMD-88-55. 

General Accounting Difco (1980), HUD Not Fulfilling. Respon ag: 
in 

Housing I as DC: US General Accounting 2 

fice), Doc. No. CED-81-31. 

Gulick, L, and L. Urwick, eds., Papers on the Science of Admini- 
stration, Institute of Public Administration, Columbia 

University (Concord NH, The Rumford Press, 1937) 

Landis, JR, and KM Flegal (1988), “A Generalized Mantel-Haenszel 

Analysis of the Regression of Blood Pressure on Blood 
Lead Using NHANES II Data,” Environmental Health 

Perspectives, Vol. 78, pp. 35-41. 

Landrigan, PJ (1989), “Toxicity of Lead at Low Dose,” British 

Journal of Industrial Medicine, Vol. 46, pp. 593-96. 

McCord, CP (1953), “Lead and Lead Poisoning in Early America: 
Benjamin Franklin and Lead Poisoning,” Industrial 

Medicine and Surgery, Vol. 22. 

McMichael AJ, PA Boghurst, NR Wigg, GV Vimpai, EF Robertson, 

RJ Roberts (1988), “Port Pirarie Cohort Study: Environ- 
mental Exposure to Lead and Children’s Abilities at the 
Age of Four Years,” New England Journal of Medicine, vol. 
319, pp. 468-475. 

National Archives and Record Administration, Office of the Fed- 

eral Register (1988),_The United States Government 
Manual 1988/89, (Washington: U.S. Government Print- 

ing Office). 

National Research Council (1980), Lead in the Human Environ- 

ment, (Washington: National Academy of Sciences), 525 

pp.   
B-3 

 



  

Needleman, HL, A Schell, D Bellinger, A Leviton, EN Allred 

(19902) “The Long-Term Effects of Exposure to Low Doses 

of Lead in Childhood,” New England Journal of Medicine, 

Vol. 322, pp. 83-88. 

Needleman, HL, and CA Gatsonis (1990b), “Low-Level Lead 

Exposure and the IQ of Children: A Meta-analysis of 

Modern Studies,” rnal of meri Medical Asso- 

ciation, Vol. 263, pp. 673-678. 

Needleman, HL (1988b) “The Persistent Threat of Lead: Medical 
and Sociological Issues,” Current Problems in j 

Vol. 18, pp. 703-76. 

Needleman, HL (1988a), “Why We Should Worry About Lead 
Poisoning,” Contemporary Pediatrics, March 1988, pp. 34- 

56). 

Needleman, HL, and PJ Landrigan (1981), “The Health Effects of 
Low Level Exposure to Lead,” Annual Review of Public 
Health, Vol. XX, pp. 277-98. 

Nriagu, JO, and JM Pacyna (1988), “Quantitative Assessment of 

Worldwide Contamination of Air, Water and Soils by 
Trace Metals,” Nature, Vol. 333, pp. 134-9. 

Office of Management and Budget (1989), Budget of the United 

States Government, Fiscal vearXQ: Special Analysis C 

(Washington: U.S. Government Printing Office). 
  

Pollack, S (1989), “Solving the Lead Dilemma,” Technology Re- 

view, Oct. 1989, pp. 22-31. 

Rabin, R (1989), “Warnings Unheeded: A History of Child Lead 
Poisoning,” American Journal of Public Health, Vol. 79, 

pp. 1668-1674. 
  

Rabinowitz, MB, GW Wetherill, and JD Kopple (1976), “Kinetic 

Analysis of Lead Metabolism in Healthy Humans,” Jour- 

nal of Clinical Investigation, Vol. 58, pp. 260-70. 

Rosen, JF, ME Markowitz, PE Bijur, ST Jenks, L Wielopolski, JA 

Lalef-Ezra, and DN Slatkin (1988), “L-Line X-ray Flores- 
cence of Cortical Bone Lead Compared with the 

CaNa2EDTA Test in Lead-Toxic Children: Public Health 

Implication,” Proceedings of the National Academy of 
Sciences, Vol. 86, pp. 685-689. 
  

Schroeder, H, and IH Tipton (1968), “The Human Body Burden of 
Lead,” Archives of Environmental Health, Vol. 17, pp. 965- 

978. 
  

Schwartz, J (1988), “The Relationship Between Blood Lead and 

Blood Pressure in the NHANES II Survey,” Environ- 

mental Health Perspectives, Vol. 78, pp. 15-22.  



Silbergeld, EK (1985), “Neurotoxicology of Lead,” in K Blum and 
L Manzo (eds.), Neurotoxicology (Amsterdam: Dekker). 

Silbergeld, EK, and RV Percival (1987) “The Organometals: 
Impacts of Accidental Exposure and Experimental Data 

on Regulatory Policies,” pp. 328-352 in S Sparber and H 

Tilson (eds.), Neurotoxicology of Organometals (New York: 
Wiley Interscience). 

Silbergeld, EK, J Schwartz, and KR Mahaffey (1988), Lead and 
Osteoporosis: Mobilization of Lead from Bone in Meno- 

pausal Women,” Environmental Research, Vol. 47, pp. 79- 
94, 

Victery, W., H.A. Tyroler, R. Volpe, and L.D. Grant (1988), “Sum- 

mary of Discussion Sessions: Symposium on Lead-Blood 

Pressure Relationships,” Environmental Health Perspec- 
tives, Vol. 78, pp. 139-55. 

Waldron, HA, (1973), “Lead Poisoning in the Ancient World,” 

Medical History, Vol. 17, pp. 391-99.