Declarations of Rosen, Mushak, Reigart and Lnnn Lee
Public Court Documents
November 23, 1992
276 pages
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Case Files, Thompson v. Raiford Hardbacks. Declarations of Rosen, Mushak, Reigart and Lnnn Lee, 1992. b9f00973-5c40-f011-b4cb-002248226c06. LDF Archives, Thurgood Marshall Institute. https://ldfrecollection.org/archives/archives-search/archives-item/f3102f1c-fa9c-4b8e-af71-d092f24c23d9/declarations-of-rosen-mushak-reigart-and-lnnn-lee. Accessed June 18, 2025.
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. AFFIDAVIT OF JOHN F. ROSEN
AFFIDAVIT OF JOHN F. ROSEN, M.D.
STATE OF NEW YORK )
ye 8g,
COUNTY OF BRONX )
JOHN F. ROSEN, M.D., being duly sworn, states as follows
under oath:
1. I am Professor of Pediatrics and Head of the Division
of Pediatric Metabolism at Albert Einstein College of Medicine;
Attending Pediatrician at Montefiore Medical Center, Bronx, New
York; and Chairperson of the Childhood Lead Poisoning Prevention
Advisory Committee of the Centers of Disease Control (CDC),
United States Department of Health and Human Services. I have
also been appointed to a committee formed by the National Academy
of Sciences that is writing an extensive report on measuring lead
exposure in sensitive populations. My statements in this
Affidavit are based on my own personal knowledge.
PROFESSIONAL BACKGROUND
2 My entire professional career has been dedicated to
research and writing on mineral and heavy metal metabolism. In
particular, my research focuses on the pathophysiology,
metabolism, and consequences of lead toxicity in children.
3. Since 1984, I have served as Chairperson of CDC’s
Childhood Lead Poisoning Prevention Advisory Committee. The
Centers’ Statement, Preventing Lead Poisoning in Young Children,
issued in 1985 and again in 1991, sets forth the standards of the
medical profession and the United States Public Health Service on
the medical testing for and management of lead poisoning and is
jfraff tom i
2.1
recognized as the definitive federal statement on prevention and
treatment of lead poisoning in children. The Public Health
Service issues this statement every 6-7 years.
4. In October 1991 our CDC Committee issued a new
statement on Preventing Lead Poisoning in Young Children,
attached as Exhibit 1 to the Declaration of Sue Binder, M.D. As
stated in the Preface to that statement, "it reflects the vision
expressed in the Department of Health and Human Services’
Strategic Plan for the Elimination of Childhood Lead Poisoning,
which calls for a concerted, coordinated societywide effort to
eliminate this disease." U.S. Dep’t of Health & Human Services,
Pub. Health Serv., Centers for Disease Control, Preventing Lead
Poisoning in Young Children iii (Oct. 1991) (CDC Statement). The
Strategic Plan (Feb. 1991) is attached as Exhibit B. I served as
a Peer Reviewer of that federal report.
Se I also served as a Peer Reviewer for the Agency for
Toxic Substances and Disease Registry (ATSDR) of the Public
Health Service. Pursuant to § 118(f) of the Superfund Amendments
and Reauthorization Act (SARA) of 1986, 42 U.S.C. § 9618(f),
ATSDR was required to prepare a study of lead poisoning in
children. This report, titled The Nature and Extent of Lead
Poisoning in Children in the United States: A Report to Congress
(ATSDR Report), was completed and submitted in July 1988. The
Report’s most salient conclusions are that childhood lead
poisoning is a pervasive disease; shockingly, it is the most
common preventable childhood disease. Over 5,000,000 children in
jfraff.tom 2
7 2%
the United States were found at high risk of lead poisoning. The
report further emphasizes that lead at a level once considered
safe does impair neurobehavioral and cognitive development in
children. (The ATSDR Report is attached as an Exhibit to the
accompanying Declaration of Paul Mushak, Ph.D.)
6. Also at the federal level, I served on the Peer Review
Panel for the United States Environmental Protection Agency’s
Lead Criteria Document and as a consultant and author for the
agency’s Air lead Quality Criteria Document.
7 At the Division of Pediatric Metabolism of the Albert
Einstein College of Medicine and Montefiore Medical Center, I am
the Director of the Lead Poisoning Prevention Project, which
tests and treats approximately 10,000 children annually for lead
toxicity. The vast majority of these patients are Medicaid
recipients. The Division assesses the sources of this disease in
our patients, and we provide medical, environmental, and
nutritional intervention. Twelve years ago we also set up our
own laboratory capacity and reporting system to handle the blood
lead samples from our Lead Poisoning Prevention Project Clinic.
8. In addition to my contributions to the recent federal
reports mentioned above, my most recent studies and publications
include the following. CDC used one of these studies in the
Strategic Plan’s cost-benefit analysis. Sequential Measurements
of Bone Lead Content by X-Ray Fluorescence in CaNa2EDTA-Treated
Lead-Toxic Children, 93 Envtl. Health Perspectives 271 (1991).
This study showed that when children were detected with high
jfraff tom 3
2
blood lead levels and then removed from leaded environments or
returned to lead-abated environments, significant accumulation of
lead in the children’s bodies ended. Id. at 274. The children
in this study were representative of the majority of children
attending lead-toxicity programs nationally. Id. at 273. An
extension of that study is now in press, to be published in the
medical journal Neurotoxicology. Trends in the Management of
Childhood Lead Poisoning. This further demonstrates the
effectiveness of environmental intervention alone, without costly
medical intervention, if lead poisoning is detected early.
9. CDC restricted its cost-benefit calculation to children
whose blood lead levels are held to 25 ug./dl., even though
additional benefits are now conclusively known at lower blood
lead levels. Another of my recent publications draws together
and analyzes all the recent, rigorously performed studies that
all converge on the strong, unequivocal conclusion: No blood
lead threshold is too low to be disassociated with the adverse
effects on IQ and cognitive and central nervous system
functioning. Health Effects of Lead at Low Exposure Levels:
Expert Consensus and Rationale for Lowering the Definition of
Childhood lead Poisoning, 146 Am. J. Dis. Child. 1278 (1992).
Lead exposure well below 10 pg./dl. is directly related to
neurobehavioral and cognitive deficits. The impairments in
intellectual performance are currently considered irreversible.
These consistent findings result in the following societal
effects: at least 50% more children falling into the borderline
jfraff.tom 4
9 UY
&
IQ range and an absence of children in the superior range.
10. I have authored numerous other articles on the etiology
and treatment of lead toxicity in children. These articles
include: Rosen, Metabolic and Cellular Effects of Lead: A Guide
to Low-Level Lead Toxicity in Children, Dietary and Environmental
Lead Exposure 157-85 (K. Mahaffey ed. 1985); Piomelli, Rosen &
Chisolm, Treatment Guidelines for the Management of Childhood
Lead Poisoning, 105 J. Pediatrics 523 (1984); and Rosen, The
Metabolism and Subclinical Effects of Lead in Children,
Biogeochemistry of Lead in the Environment 151-72 (J. Nriagu ed.
1978). Articles reporting my original research on the effects of
lead toxicity in children include Markowitz & Rosen, Assessment
of L.ead Stores in Children: Validation of an 8-Hour CaNa2-EDTA
Provocation Test, 104 J. Pediatrics 337 (1984), and Saenger,
Rosen & Markowitz, Diagnostic Significance of Edetate Disodium
Calcium Testing in Children with Increased Lead Absorption, 136
Am. J. Dis. Child. 312 (1983). Several other articles are listed
in my curriculum vitae relating to the pathophysiology of lead
toxicity.
11. I am a Fellow of the American Academy of Pediatrics and
a member of the American Pediatric Society, the New York Academy
of Sciences, the Society for Pediatric Research, the Society of
Toxicology, and the American Institute of Nutrition. I graduated
from Harvard College in 1957 and the Columbia University College
of Physicians and Surgeons in 1961. I attach a copy of my
curriculum vitae to this affidavit as Exhibit A.
jfraff tom 5
725
THE RISK OF LEAD POISONING
12. As can be gleaned from all the publications and studies
cited above, lead particles ingested by the human body cause
severe damage to the brain and central nervous system. Children
from birth through age six years are by definition at risk of
lead poisoning. Their normal hand-to-mouth activity causes more
frequent ingestion of such particles. More significantly,
children’s brains and nervous systems are particularly vulnerable
in their developmental stages. Environmental factors may cause
older children to be at risk also. See ATSDR Report 1, 10, III-
12, Iv-7; CDC Statement 7-12.
13. Ingestion of lead particles by pregnant women also
causes damage to the developing fetus. The 1988 ATSDR Report
estimated that nationwide, 400,000 fetuses per year are at risk
of being born lead poisoned. ATSDR Report 16. It should be
noted that all the statistics on frequency of lead poisoning
before 1992 are based on a lead poisoning threshold of 25 ug./dl.
In 1991, CDC lowered the threshold to 10 ug./dl. CDC Statement
1. Thus many more children are considered at risk today.
14. Lead paint is the greatest source of lead exposure to
young children. Id. at 12. The problem stems primarily from
peeling or chalking lead paint in aging or damaged housing. Id.
at 18. For much of this century lead paint was used in homes on
both exterior and interior surfaces. Although the federal
government virtually prohibited the manufacture of household lead
paint in 1977 (allowing only a narrow class of exemptions), lead
jfraff.tom 6
2b
paint remains in more than 57,000,000 households nationwide; 74%
of all homes constructed before 1980 contain lead paint. 16
C.P.R. pt. 1303; CDC Statement 18.
15. Because of these risks, and because lead poisoning’s
effects are so severe--impacting all the skills critical for
educational success--children age 0-6 years, the age range most
at risk, should be tested for lead poisoning a minimum of once
per year. Environmental and other risk factors may require more
frequent testing.
16. In the majority of cases, lead poisoning is
asymptomatic. In the rare instances when symptoms are present,
they are the same as many other childhood diseases and
impairments. Severe cases cause coma, convulsions, kidney
damage, and even death. According to currently published data,
all cases cause some irreversible brain damage, reduced IQ,
delayed cognitive development, and other physical and mental
impairments. Such effects occur at blood lead levels above and
even below 10 ug./dl. In fact there is no apparent threshold.
Lead causes adverse effects even below 2 ug./dl.
17. Lead toxicity produces altered behavior such as
attention disorders, learning disabilities, and cognitive
disturbances. Symptoms and signs of severe toxicity are fatique,
pallor, malaise, loss of appetite, irritability, sleep
disturbance, sudden behavioral change, and developmental
regression. Even more serious symptoms include clumsiness,
ataxia, weakness, abdominal pain, constipation, vomiting, and
jfraff.tom 7
2.7
changes in consciousness (coma) due to early encephalopathy,
which may lead to death. Mental retardation is a frequent
result. See CDC Statement 7-15.
DETECTING LEAD POISONING
18. The only way to determine the presence of lead
poisoning is to test for the level of lead in the blood.
According to the 1991 CDC Statement, only direct measurement of
the blood lead concentration has the clinical and diagnostic
capability to determine whether a child has lead poisoning. See
id. at 41.
19. Verbal questioning about a child’s possible exposure to
lead cannot elicit complete, definitive, or accurate data to
indicate a child’s blood lead level. Many patients, especially
Medicaid recipients, simply may not know all the answers to the
verbal assessment questions. Furthermore, medical histories are
not substitutes for clinical laboratory measurements, when such
measurements by definition have the capability to establish a
medical diagnosis.
20. A blood test that does not test for the level of lead
in the blood does not elicit complete, definitive, or accurate
enough data either. The erythrocyte protoporphyrin (EP) test is
such a test. The federal Health Care Financing Administration
(HCFA) concedes the EP test is not sensitive to blood lead levels
under 25 ug./dl., and therefore the EP test will miss all
children at risk for elevated blood lead levels between 10 and 25
po. /41.
jfraff.tom 8
29
21.. The EP test not only falls to detect levels of lead in
blood below 25 ug./dl.; the EP test also fails to detect blood
lead concentrations above 25 ug./dl. This is because the EP test
does not test for the level of lead in blood at all. In fact, it
is only an indirect reflection of iron or lead status. For lead
status, this test is an insensitive index of any blood lead
values below 40 ug./dl. At blood lead values between 10 and 30
Kg./dl., EP measurements will totally fail as a screening method
to identify the overwhelming majority (over 95%) of children
whose blood lead levels fall in this danger zone. As a result,
the EP test only identifies a child with an elevated blood lead
in about one out of seven or eight cases.
22. In our clinic alone, where we perform blood lead tests
and EP tests together, we have seen a significant number of cases
where the EP test result was normal, and the blood lead level was
above 25 pug./dl. This is not only a known occurrence in our own
Lead Poisoning Prevention Program; such occurrences were
demonstrated nationally by the Second National Health and
Nutrition Examination Survey (NHANES II), in 1976-80. See, e.q.,
ATSDR Report V-31.
23. For a pediatrician pursuing a diagnosis, the only
responsible course of action is to carry out a test that provides
safe and definitive results for all children, according to
Survent Standards of pediatric practice. A blood lead test
provides definitive information concerning to what extent a child
has been recently exposed to lead. An EP test provides, at best,
jfraff.tom
marginal information only for the one child out of seven or eight
indicating that a child may be lead poisoned. For a pediatrician
pursuing a conclusive diagnosis, to perform such an unreliable
test for lead poisoning is irresponsible pediatric practice.
24. Unfortunately average American pediatricians must be
encouraged to engage in responsible practice regarding lead
poisoning, because many are unfamiliar with this area of
practice. That being so, everything must be done to safeguard
children’s health, rather than to give license to do otherwise.
The 1991 CDC Statement explicitly recognizes this point. The
Statement was prepared with primary medical care providers
foremost in mind, so they could glean the current, essential
standards of pediatric practice in a readily digestible form.
See especially CDC Statement ch. 4 & app. II.
THE RESOURCES FOR BLOOD LEAD TESTING
25. I cannot fathom why, more than a year after the CDC
Statement dictated blood lead tests as the reasonable standard of
medical practice, a state’s medical care providers’ capacity for
performing the tests, particularly if reimbursable under the
Medicaid program, would be limited.
26. The laboratory capacity certainly exists among the
large commercial laboratories, such as Roche, MetPath, or Smith
Kline. Similar capacity must exist at state and local public
laboratories. The large commercial laboratories are located
around the country and routinely assess blood samples of Medicaid
patients in-state or out-of-state. These laboratories can
jfraff.tom
zZ0
process the blood lead results of any children in the Medicaid
program and be reimbursed by the Medicaid program. See
Declaration of William Hiscock ¢Y 15, 18.
27. CDC’s 1991 Statement did allow a "grace period" for
transition from EP to blood lead testing. As Chairperson of
CDC’s Advisory Committee, I can state that our intent was to
provide a transition of up to a year for state and local agencies
to order proper equipment and implement blood lead measurements
as the diagnostic test for childhood lead poisoning. One year is
more than twice the time required to mount such a laboratory
capability de novo, including the time required to order an
instrument, train a technician, and set up a reporting systen.
The transition period was not intended to be a bureaucratic
vacation to extend until the next CDC Statement is issued. The
next CDC Statement, like the last, may not be issued for another
SiX years or more.
28. If CDC envisioned a further transition period to
universal blood lead testing anywhere, it would be outside the
Medicaid program, where reimbursement may not be available.
29. Although HCFA’s policy to reimburse any blood lead
tests that are performed eliminates cost as a factor, blood lead
testing is not expensive anyway. Throughout the Montefiore
Medical Center-Albert Einstein College of Medicine complex,
including all their satellite clinics, we have established that
the total cost per blood lead test does not exceed $12-13.
Colleagues’ findings in Pennsylvania, West Virginia, and North
jfraff.tom 11
Carolina confirm these results. One need only check the rates
from the commercial mass laboratories to find their charges in
the same range.
30. Even if these nationwide resources were somehow not
available in a particular area, it is not overly difficult or
costly to develop independent laboratory capacity, as we did
years ago at Montefiore Medical Center. The laboratory can be
staffed with a laboratory technician and a clerk-typist with a
computer. The required instrumentation currently runs
approximately $60,000-75,000, plus $10,000 in consumables per
year. This country certainly has the technology to perform
universal blood lead tests for all Medicaid eligible children.
THE RISKS FOR MEDICAID ELIGIBLE CHILDREN IN PARTICULAR DICTATE
BLOOD LEAD TESTING.
31. Medicaid eligible children are virtually by definition
at high risk for lead poisoning. Their low income by itself is
an indicator that they live in older, deteriorated or recently
rehabilitated housing that has exposed them to lead paint. The
ATSDR Report shows the incidence of lead poisoning is 2-3 times
higher among Medicaid eligible children than among the same aged
children in general. HCFA concedes this point. Hiscock
Declaration q 20.
32. Lead poisoning is the most common, preventable
childhood disease. For Medicaid children, even in an urban
setting, visits to the doctor may be limited. These factors make
it all the more nonsensical not to require the proper blood lead
test for all Medicaid children, when they do visit a doctor, and
Jfraff tom 2
2
when we know how to detect the onset of this most common
preventable disease in the pediatric age group.
33. Too much attention is being paid to the possibility of
risk when among this population there is only likelihood, not
possibility, of exposure to lead paint or other sources of lead.
Under these circumstances anything other than a blood lead test,
like the EP test, for lead testing, is a waste of time and money
for the Medicaid program. Even more importantly, the
alternatives present unacceptable clinical and medical risks of
not arriving at the correct diagnosis of lead poisoning in
Medicaid eligible children.
34. Furthermore, as Chairperson of CDC’s Advisory
Committee, I can state that it was not our intent to suggest to
Medicaid providers that the use of a questionnaire should
determine whether children, particularly in the most vulnerable
age group of 6-36 months, should receive a blood lead test. The
CDC Statement is unequivocal that for this population, a blood
lead test must be conducted at least once by the time a child
reaches 12 months and again by 24 months of age, even if the
responses to the assessment questions indicate the child is at
"low risk" of lead poisoning. CDC Statement 43. The CDC
screening schedule is based on the fact that children’s blood
lead levels increase most rapidly at 6-12 months and peak at 18-
24 months. Id. at 42. The incidence of high blood lead levels
among this population is so high, it makes little sense to try to
ascertain with a questionnaire who within this group is at "high
jfraff tom 13
oR.
FD
risk.” See id. at Figure 6-1. The CDC Statement explicitly
states that for this group the questionnaire is not a substitute
for a blood lead test. Id. at 42.
35. HCFA states that its revised guidelines incorporate
CDC’s methodology of using verbal assessments to determine risk
categories and in this regard its methodology is consistent with
the 1991 CDC Statement See Hiscock Declaration q 14. Contrary
to Mr. Hiscock’s statement, and as stated above, the use of
questionnaires to determine risk for children age 6-36 months is
indisputably inconsistent with the CDC Statement.
36. Clearly the current state of medical knowledge and
standards of pediatric practice dictate measurements of blood
lead levels on a frequent periodic basis for all Medicaid
eligible children. Moreover, if the Medicaid Early Periodic
Screening, Diagnosis and Treatment program is supposed to be
preventive, then it is only proper pediatric medical practice to
err on the side of considering all Medicaid children at high
risk. If Congress’ 1989 amendment was intended to remedy HCFA’s
past failures to require blood lead tests, then clearly the blood
lead test should be given to all Medicaid children who fall
within the age range at risk, birth through age six. Older
jfraff tom 14
oe
children should also be tested if they have not been previously
tested or are otherwise at risk.
JOHN F. ROSEN, M.D. /
Sworn to before me
on November 18, 1992
Lv] Aine rilings
NOTARY PUBLIC
pr
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Be ie 24,1443
jfraff.tom 15
COSEN
EXHIBIT A
CURRICULUM VITAE
JOHN FRIESNER ROSEN, M.D.
BORN: JUNE 3, 1935, NEW YORK CITY
EDUCATION:
Harvard College, 1953-1957, B.A.
Columbia University College of Physicians and Surgeons
1957-1961, M.D.
GRADUATE TRAINING:
Montefiore Hospital and Medical Center
1961-1962, Internship
Columbia-Presbyterian Medical Center
1962-1965, Resident in Pediatrics (Babies Hospital)
Rockefeller University, 1965-1967, Guest Investigator (Post
Doctoral Fellow) (Mineral Metabolism and Peptide Chemistry)
Intern - Montefiore Hospital and Medical Center, 1961-1962
Junior Resident - Babies Hospital, New York City, 1962-1964
Senior Resident - Babies Hospital, New York City, 1964-1965
PROFESSIONAL EMPLOYMENT AND HOSPITAL APPOINTMENTS:
Assistant Physician - The Rockefeller University, 1965-1969
Guest Investigator - The Rockefeller University, 1965-1967
Research Associate - The Rockefeller University, 1967-1969
Research Collaborator - Brookhaven National Laboratory
(Departments of Medicine and Physics), 1975-Present
Chairman, Research Advisory Committee - Tandem - Van de
Graaff Facility, Brookhaven National Laboratory
Department of Physics), 1979-Present
Director, Metabolism Services
Montefiore Medical Center, 1969-Present
Head, Division of Pediatric Metabolism, Albert Einstein
College of Medicine, 1980-Present
Adjunct Attending Physician —- Montefiore Hospital and Medical
Center, 1969-1974
Associate Attending Pediatrician - Montefiore Hospital and
Medical Center, 1974-1978
27]
Attending Pediatrician - Montefiore Hospital and Medical
Center, 1978-Present
Assistant Professor of Pediatrics - Albert Einstein College of
Medicine, 1969-1975
Associate Professor of Pediatrics - Albert Einstein College of
Medicine, 1975-1980
Professor of Pediatrics - Albert Einstein College of Medicine,
1980-Present
BOARD CERTIFICATION: Diplomate, American Board of Pediatrics, 1966
PROFESSIONAL SOCIETY MEMBERSHIPS:
American Chemical Society, 1967-Present
Sigma XI, 1967-Present
American Association for the Advancement of Science, 1967-
Present
American Federation for Clinical Research, 1969-Present
Fellow of the American Academy of Pediatrics, 1966-Present
Harvey Society, 1966-Present
New York Academy of Sciences, 1971-Present
Society for Pediatric Research, 1972-Present
Lawson Wilkins Pediatric Endocrine Society, 1975-Present
American Pediatric Society, 1979-Present
American Institute of Nutrition, 1979-Present
American Society for Bone and Mineral Research, 1979-Present
Society of Toxicology, 1984-Present
OTHER PROFESSIONAL ACTIVITIES:
Research Committee - Montefiore Hospital and Medical Center,
1980-Present
Committee on Appointments and Promotions to Rank of Full
Professor - Albert Einstein College of Medicine, 1982-1984
Peer Review Panel, Health Effects Chapters, Lead Criteria
Document, EPA - 1982-1984
Consultant and Author, E.P.A. (Washington). Writing of
Air Lead Quality Criteria Document - 1981, 1985.
Ad Hoc Member, Toxicology Study Section, Division of
Research Grants, N.I.H. - 1982-1984
Chairman, Centers for Disease Control Advisory Committee on
Childhood Lead Poisoning Prevention. CDC, 1984
Member, Toxicology Study Section, Division of Research Grants,
N.I.H., 1985-1989
2
23
Member, National Academy of Science, National Research Council
Committee on Low Level Exposure in Susceptible Populations.
1989-
Chairman, Centers for Disease Control Advisory Committee on
Childhood Lead Poisoning Prevention. CDC, 1990-
Peer Reviewer, Centers for Disease Control's Strategic Plan
For The Elimination Of Childhood Lead Poisoning, 1991.
CURRENT GRANT SUPPORT:
1. The metabolism of lead in bone.
NIH #ES 01060-12-16
Dr. J.F. Rosen - Principal Investigator
12/01/86-11/30/96 (MERIT AWARD)
Treatment outcomes in moderately lead toxic children.
NIH #ES 04039-02-06
Dr. J.F. Rosen - Principal Investigator
3/1/86-4/30/92 (Renewed to 1997)
A Nutritional Survey in Homeless Children.
Diamond Foundation
Dr. J.F. Rosen - Principal Investigator
1988-1992 (Renewed to 1994)
Lead Poisoning Prevention Project.
Aron/JC Penney and Robert Wood Johnson Foundations
Dr. John F. Rosen - Principal Investigator
1987-1992 (Renewed to 1994)
MERIT AWARDEE of the National Institute of Environmental
Health Sciences - 1986-1996 (ES 01060)
SAFE House (Transition Housing) For Successfully Treated
Lead Poisoned Children and Their Families.
Robert Wood Johnson Foundation
Dr. John F. Rosen - Principal Investigator - 1990-1993.
REVIEWER FOR:
American Journal of Physiology
Annals of Internal Medicine -
Journal of Clinical Endocrinology and Metabolism
Journal of Laboratory and Clinical Medicine
Journal of Neurochemistry
Journal of Pediatrics
Life Sciences
New England Journal of Medicine
Pediatric Research
Pediatrics
Science
Toxicology and Applied Pharmacology
3
54
ARTICLES: (Selected)
1.
io.
13%
32.
Haymovits, A.H. and Rosen. J.F.: Human thyrocalcitonin.
Endocrinology 81:993-1000, 1967.
Rosen, J.F., and Haymovits, A.H.: Liver lysosomes in
congenital osteopetrosis: A study of lysosomal function,
calcitonin, parathyroid hormone, and 3!',5' AMP, J. Peds.
81:5138-527, 1872.
Rosen, J.F. and Finberg, L.: Vitamin D dependent rickets:
Actions of parathyroid hormone and 25-hydroxycholecalciferol.
Ped. Res. 6:1552-562, 1972.
Rosen, J.F.: The microdetermination of blood lead in children
by flameless atomic absorption. The carbon rod atomizer. J.
Lab. and Clin. Med. 80:567-576, 1972.
Rogen, J.F. and Finberg, L.: Vitamin D dependent rickets:
Actions of parathyroid hormone and 25-hydroxycholecalciferol.
In, Clinical Aspects of Metabolic Bone Disease. Frame,
Parfitt and Duncan (Eds)., Excerpta Medica Foundation, 1973,
Pp. 388-393,
Rosen, J.F.: The microdetermination of blood lead in children
by nonflame atomic absorption spectroscopy. In, Proceedings of
the Institutional Consortium on Endemic Lead Poisoning.
Clinical Toxicology Bulletin 3:111-118, 1973.
Daum, F., Rosen, J.F. and Boley, S.J.: Parathyroid adenoma,
parathyroid crisis, and acute pancreatitis in an adolescent.
J. Peds, 83:275-277, 1973.
Rosen, J.F., Zarate-Salvador, C. and Trinidad, E.E.: Plasma
lead levels in normal and lead-intoxicated children. J. Peds.
84:45-48, 1974.
Lamm, S. and Rosen, J.F.: Lead contamination in milks fed to
infants: 1972-1973. Pediatrics 53:137-141, 1974.
Rosen, J.F., Roginsky, M., Nathenson, G. and Finberg, L.: 25-
hydroxyvitamin D: Plasma levels in mothers and their premature
infants with neonatal hypocalcemia. Amer. J... Dis. Child.
127:220-223, 1974.
Regen, J.F., and Trinidad, E.E.: The significance of plasma
lead levels in normal and lead-intoxicated children. Environ.
Health Perspect. 7:139-144, 1974.
Rosen, J.F. and Lamm, S.H.: Further comments on the lead
content of milks fed to infants. Pediatrics 53:144-145;, 1974.
4-0)
15.
14.
15,
ls.
17.
i8.
19.
20.
21.
22.
23.
24.
Sorell, M. and Rogen, J.F.: Ionized calcium: Serum levels
during symptomatic hypocalcemia. J. Peds. 87:67-70, 1975.
Daum, F., Rosen, J.F., Roginsky, M., Cohen, M. and Finberg,
L.: 25-hydroxycholecalciferol in the management of rickets
associated with extrahepatic biliary atresia. J. Peds.
88:1041-1043, 1975.
Bosen, J.F. and Wexler, :E.E.: .Studies of lead transport in
bone organ culture. Biochem. Pharm. 26:650-652, 1977.
Rosen, J.F. and Sorell, M.: Interactions of lead, calcium,
vitamin D, and nutrition in lead-burdened children. In,
Clinical Chemistry and Chemical Toxicology of Metals. Brown,
S.5. (Fd.), Elsevier, 1977, pp. 27-31.
Rosen, J.F., Fleischman, A.R., FPinberg, 1.., Eisman, J. and
DeLuca, H.P.: 1,25-dihydroxycholecalciferol: Oral
administration and sterol levels in the long-term management
of idiopathic hypoparathyroidism in children. In, Vitamin D:
Biochemical, Chemical and Clinical Aspects Related to Calcium
Metabolism. Norman, A.W. et al (Eds.) Walter de Gruyter,
Berlin, 1977, pp. 827-830.
Sorell, M., Rosen, J.F., and Roginsky, M.: Interactions of
lead, calcium, vitamin D and nutrition in 1lead-burdened
children. Arch. Environ. Health 32:160-164, 1977.
Rosen, J.F., Fleischman, A.R., Finberqg, L., Eisman, J., and
DeLuca, H.F.: 1,25-dihydroxyvitamin D;: Its use in the long-
term management of idiopathic hypoparathyroidism in children.
J. Clin. Endocrinol. Metab. 45:457-468, 1977.
Rosen, J.F., Wolin, D. and Finberg, L.: Immobilization
hypercalcemia after single limb fractures in children and
adolescents. Amer. J. Dis. Child. 132:560-564, 1978.
Fleischman, A.R., Rosen, J.F., and Nathenson, G.: 25-
hydroxyvitamin D: Serum levels and oral administration in
neonates. . Arch. Int. Med. 138:869-873, 1978.
Fleischman, A.R., Rosen, J.F., and Nathenson. G.: Oral 25-
hydroxycholecalciferol for the prevention of early neonatal
hypocalcemia 1n premature neonates. Aner. J. Digs. Child.
132:973-977, 1978.
Rosen, J.F., Fleischman, A.R., Finberyg, L., Hamstra, A., and
DeLuca, H.F.: Rickets with alopecia: An inborn error of
vitamin D metabolism. J. Peds. 94:729-735, 1979.
leischman, A.R., Rosen, J.F., Nathenson, G. and Finberg, L.:
Oral 25-OHD in preventing neonatal hypocalcemia. In,
Pediatric Diseases Related to Calcium. Anast, DeLuca
{(Eds.) Elsevier, 1980, pp. 345-354.
od
25.
26.
27
28.
29.
30.
3].
32.
33.
34.
35.
Chesney, R.W., Rosen, J.F., Hamstra, A. and Deluca, H.F.:
Serum 1,25-dihydroxyvitamin D levels in normal children and in
vitamin D disorders. Amer. J. Dis. Child. 134:135-139, 1980.
Rosen, J.F., Chesney, R.W., Hamstra, A., Deluca, H.FP. and
Mahaffey, K.R.: Reduction in 1,25-dihydroxyvitamin D in
children with increased lead absorption. New Engl. J. Med.
302:1128-1131, 1980.
Rosen, J.F., and Markowitz, M.: D-Penicillamine: Its actions
on lead transport in bone organ culture. Ped. Res. 14:330-
335, 1980.
Fleischman, A.R., Rosen, J.F., Smith, C.M. and Deluca, H.F.:
Maternal and fetal levels of 1,25-dihydroxyvitamin D levels at
term. J. Peds. 97:640-642, 1980.
Sorell, M., Rosen, J.F., Kapoor, N., Kirkpatrick, D., Raju
S.K., ‘Chaganti, Good, R.A., and O'Reilly, R.J.: Marrow
transplantation for juvenile osteopetrosis. Amer. J. Med.
70:1280-1287, 1981.
Chesney, R.W., Rosen, J.F., Smith, C.M. and Deluca, H.F.:
Absence of seasonal variation in serum concentrations of 1,25-
dihydroxyvitamin D despite a rise in 25-hydroxyvitamin D in
summer. J. Clin. Endocrinol. Metab. 53:139-142, 1981.
Bil, C., Liberman, U.A., Rogen, J.F., and Marx, 8S.J.: A
cellular defect in hereditary vitamin D-dependent rickets Type
ITI: Defective nuclear uptake of 1,25-dihydroxyvitamin D in
cultured skin fibroblasts. New Engl. J. Med. 304:1588-1591,
1981.
Rosen, J.F., Chesney, R.W., Hamstra, A., and Deluca, H.F.:
Reduction in 1,25-dihydroxyvitamin D in children with
increased lead absorption. In, Chemical Indices and
Mechanisms of Organ-Directed Toxicity. Brown, S.8. {(Ed.),
Pergamon Press, 1981, pp. 91-95.
Rosen, J.F.: The metabolism of lead-210 in isolated bone
cells. In, Chemical Indices and Mechanisms of Organ-Directed
Toxicity. Brown, S.S. (Ed.), Pergamon Press, 1981, pp. 305-
310.
Saenger, P., and Rosen, J.F.: 63~hydroxycortisol: A non-
invasive probe to evaluate inhibitory effects of lead on drug
metabolism in children. In, Chemical Indices and Mechanisms
of Organ-Directed Toxicity. Brown, S.S. (Ed.), Pergamon
Press, 1981, pp. 297-303.
Markowitz, M.E., Rotkin, “L., and Rosen, J.¥.: Circadian
rhythms of blood minerals in humans. Science 213:672-674,
1381.
6 4L)
[ &~
36.
37.
38.
3%.
40.
41.
42.
43.
44.
45.
46.
Rosen, J.F., Kraner, H.W., and Jones, X.W.: Effects of
CaNa,EDTA on lead and trace metal metabolism in bone organ
culture. Tox. Appl. Pharm. 64:230-236, 1982.
Saenger, P., Rosen, J.F., and Markowitz, M.E.: The diagnostic
significance of EDTA testing in children with increased lead
absorption. Amer. J. Dis. Child. 136:312-315,6 1982.
Wielopolski, L., Rosen, J.F., Slatkin, D., and Cohn, S.: Non-
invasive L-X-ray fluorescence analysis of lead in the human
tibia. Medical Physics 10:248-251, 1983.
Wisniewski, X.E., French, J.H., Rosen, J.F., Kozlowski, P.,
Tenner, M. and Wisniewski, N.H.: Basal ganglia calcification
(BGC) in Down's syndrome (DS)-another manifestation of
premature aging. Annals New York Acad. Sci. 396:179-192,
1982.
Mahaffey, K.R., Rosen, J.F., Chesney, R.W., Peeler, J.R.,
Smith, C.M. and DeLuca, H.F.: Association between age, blood
lead concentration, and serum 1,25-dihydroxycholecalciferol
levels in children. Am. J. Clin. Nutrition 35:1327-1331,
1981.
Markowitz, M.E., Rosen, J.F., Smith, C.M., and Deluca, H.P.:
1-25-Dihydroxyvitamin D;-treated hypoparathyroidism: 35
patient years in 10 children. J. Clin. Endocrinol. Metab.
55:727-733, 1982.
Rosen, J.F.: The metabolism of lead in isolated bone cell
populations: Interactions between lead and calcium.
Toxicology and Applied Pharmacology 71:101-112, 1983.
Liberman, U.A., Eil, C., Holst, P., Singer, F., Rogen. J.F.,
and Marx, S.J.: Hereditary resistance to 1,25-
dihydroxyvitamin D: Defective function of receptors for 1,25-
dihydroxyvitamin D in cells cultured from bone. Jd. Clin.
Endocrinol. 57:958-962, 1983.
Rogen, J.F,: Interactions between lead and calcium in
isolated bone cell populations. In, Clinical Chemistry and
Chemical Toxicity of Metals. Bronx, 8.8. (FEd.), AcadenicC
Press, 1983, ‘pp. 247-250.
Saenger, P., Markowitz, M.E., and Rosen, J.F.: Depressed
excretion of 6B8-hydroxycortisol in lead-toxic children. J.
Clin. Endocrinol. Metab. 58:363-367, 1984.
Markowitz, K M., Rosen, J.F., and Mizruchi, M.: Circadian and
ultradian rhythms of blood minerals during adolescence.
Pediatr. Res. 18:456-462, 1984.
7 1%)
47.
48.
49.
50.
51.
52.
53.
54.
55.
56.
57.
Markowitz, M.E. and Rosen, J.F.: Assessment of body lead
stores in children: Validation of an 88-hour CaNa,EDTA
provocative test. J. Peds. 104:337-342, 1984.
Gundberg, C., Markowitz, M.E., and Rosen, J.F.: Osteocalcin
in human serum: A circadian rhythm. J. Clin. Endocrinol.
Metab. 60:737-739, 1985.
Markowitz, M.E., Rosen, J.F. and Mizruchi, M.: Circadian
variations in serum zinc concentrations: correlation with
blood ionized calcium serum total calcium and phosphate in
humans. Amer. J. Clin. Nut. 41:689-696. 1985.
Markowitz, M.E.; Rosen, J.F. and Mizruchi, M.: Effects of
1,25-dihydroxyvitamin D; administration on circadian minerals
rhythms in humans. Calcif. Tiss. Internat. 37: 351-356, 1985,
Markowitz, M.E. Rosen. J.F., Holick, M.F., Hannifan N. an
Endres, D.: Time-related variations in serum 1,25-
dihydroxyvitamin D concentrations in humans. In, Vitamin D:
Biochemical Chemical and Clinical Aspects. Normal, A. (Ed.),
W. de Gruyter, Berlin, 1985, pp. 249-251.
Pounds, J.G. and Rosen, J.F.: The cellular metabolism of
lead: A kinetic analysis in cultured osteoclastic bone cells.
Tox. Appl. Pharmacol. 83:531-545, 1986.
Markowitz, M.E., Gundberg, C., and Rosen, J.F.: A rapid rise
in serum osteocalcin following 1,25-(OH),D; administration in
normal adults. Calcif. Tiss. Internat. 40:179-183, 1987.
Rosen, J.F. and Pounds, J.G.: The cellular metabolism of lead
and calcium: A kinetic analysis in cultured osteoclastic bone
cells. Contributions to Nephrology 64:64-71, 1988.
Pounds, J.G. and Rosen, J.F.: Cellular Ca'* homeostasis and
Ca'*-mediated cell processes as critical targets for toxicant
action; Conceptual and methodological pitfalls. Toxicology and
Applied Pharmacology 94:331-341, 1988.
Morris, V., Markowitz, M.E., and Rosen, J.F.: Serial
measurements of ALA dehydratase in lead toxic children. J.
Pediatrics 112:916-919, 1988.
Markowitz, M.E., Rosen, J.¥., Arnaud, S.B., Therpy, M. and
Laxminarayan, S.: Temporal interrelationships between the
circadian rhythms of serum parathyroid hormone and calcium
concentrations. J. Clin. Endocrinol. Metab. 67:1068-1073,
1988.
8
ks
53.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69 .
Rosen, J.F., Markowitz, M.E., Bijur, P.E., Jenks, S.T.,
Wielopolski, L., Kalef-Ezra, J.A. and Slatkin, D.N.: L-x-ray
fluorescence of cortical bone lead compared with the CaNa,EDTA
test in 1lead-toxic children: Public health implications.
Proc. Nat. Acad. Sci. (USA). B6:685-689, 1989.
Rosen, J.F, and Pounds, J.G.: Quantitative interactions
between lead and calcium in osteoclastic bone cells. Toxicol.
Appl. Pharmacol. 98:530-543, 1989,
Wielopolski, L., Kalef-Ezra, J., Slatkin, D.N. and Rosen,
J.F.: Polarized L-x-ray fluorescence to measure cortical bone
lead. Medical Physics 16:521-529, 1989.
Markowitz, M.E., Fishman, X., Rosen, J.F., and Saenger, P.:
Effects of growth hormone therapy on circadian osteocalcin
rhythms in idiopathic short stature. J. Clin. Endocrinol.
Metab. 69:420-425, 1989.
gchanmne, PF.A.X., Dowd, T.L., Gupta, R.K. and Rosen, J.F.:
Lead increases free Ca‘ concentration in cultured osteoblastic
bone cells: Simultaneous detection of intracellular free Pb?
by Fr NMR. Proc. Natl. Acad. Sci. (USA). §£6:5133-5135, 1989.
long, G.J., Rosen, J.F., and Pounds, J.G.: Cellular lead
toxicity and metabolism in primary and clonal osteoblastic
bone cells. Toxicol. Appl. Pharmacol. 102:346-36], 1990.
Fullmer, C.S. and Rosen, J.F.: Effect of dietary calcium and
lead states on intestinal calcium absorption. Environ. Res.
51:91-99, 1990.
Markowitz, M.E., Bogen, J.F., and Bijur, P.E.: Effects of
iron deficiency on lead metabolism in moderately lead toxic
children. J. Pediatr. 116:360-364, 1990.
Kalef-Ezra, J.A., Slatkin, D.N., Rosen, J.F. and Wielopolski,
L.: Radiation risk to the human conceptus attributable to
measurement of maternal tibial bone lead by L-line x-ray
fluorescence. Health Physics 58:217-219, 1990.
Schanne, F.A.X. Dowd, T.L., Gupta, R.K. ‘and Bosen, J.F.:
Development of pg NMR for measurements of [Ca?*] and [Pb®*] in
cultured osteoblastic bone cells. Environmental Health
Perspectives, 84:99-106, 1990.
Long, G.J., Pounds, J.G. and Rosen, J.F.: Lead impairs the
hormonal regulation of osteocalcin in rat osteosarcoma (ROS
17/2.8) cells. Toxicol. Appl. Pharmacol. , 106:270-277, 1990.
Schanne, F.A.X., Dowd, T.L., Gupta, R.J., and Rogen, J.F.:
Differential effects of lead on parathyroid hormone-induced
changes in clonal osteoblastic bone cells using 9F NMR.
Biochim. Biophys. Acta., 1054:250-255, 1990.
45
70.
71.
72.
73.
74.
75.
76.
77.
78.
Dowd, 'T-L., ‘Rosen, J.F., and Gupta, R.K.: Pp NMR and
saturation transfer studies of the effect of lead on cultured
osteoblastic bone cells. J. Biol.’ Chem., 265:20833-20838,
1990.
Rosen, J.F., Markowitz, M.E., Bijur, P.E., Jenks, S8.T.,
Wielopolski, L., Kalef-Ezra, J.A. and Slatkin, D.N.:
Sequential measurements of bone lead content by L-x-ray-
fluorescence in CaNa,EDTA-treated lead-toxic children.
Environmental Health Perspectives, 93:271-277, 1991.
Slatkin, D.N., Kalef-Ezra, J.A., Balbi, K.E., Wielopolski, L.
and. Rogen, J.F.: Radiation risk from L-line x-ray
fluorescence of tibial lead: Effective dose equivalent.
Radiation Dosimetry, 37:111-116, 1991.
Markowitz, M.E. and Rosen, J.F.: Need for the lead
mobilization test in children with lead poisoning. J.
Pediatr. 119:305-310, 1991.
Long, G.L., Pounds, J.G. and Rosen, J.F.: Lead intoxication
alters basal and parathyroid hormone-regulated cellular
calcium homeostasis in rat osteosarcoma (ROS 17/2.8) cells.
Calcif. Tiss. Int. 50:451-453, 1992.
Rosen, J.FP.: Trends in the management of childhood lead
poisoning. Neurotoxicology, In press, 1992.
Long, G.L. and Rosen, J.F.: Lead perturbs epidermal factor
modulation of intracellular calcium metabolism and collagen
synthesis in clonal rat osteoblastic (ROS 17/28) cells.
Toxicol. Appl. Pharmacol. 114:63-70, 1992.
Schanne, F.A.X., Gupta, R.K. and Rosen, J.F.: Lead perturbs
1,25-dihydroxyvitamin D; modulation of intracellular calcium
homeostasis 1n clonal osteoblastic bone cells. Biochim.
Biophys. Acta, In press, 1992.
Rosen, J.F., Crocetti, A.M., Balbi, K. et al.: Bone lead
content assessed by L-line x-ray fluorescence in lead-exposed
and non-lead exposed suburban populations in the United
States. In Press, 1992 or early 1993.
1.
REVIEWS:
Haymovits, A.H. and Rosen, J.F.: Calcitonin: Its nature and
role in man. Pediatrics 45:133-149, 1970.
Haymovits, A.H. and Rosen, J.F.: Calcitonin in metabolic
disorders. In, Advances in Metabolic Disorders. Levine, R.
and Luft. R. (Pds.), 6:177-212, 1972.
Rosen, J.F. and Finberg, L.: The real and potential uses of
new vitamin D; analogues in the management of metabolic bone
disease in infants and children. In, Nutritional Imbalances
in Infant and Adult Disease. Seelig, M. (Ed.), Spectrum,
1977, pp. 87-102.
Rosen, J.F.: The metabolism and subclinical effects of lead in
children. In, The Biogeochemistry of Lead in the Environment.
Nriagu, J.0. (Ed.), Elsevier/North Holland, 1978, pp. 151-172.
Chesney, R.W., Rosen, J.F.,, Hamstra, A., Mazess, R.B. and
Deluca, H.F.: The use of serum 1,25-dihydroxyvitamin D
(Calcitriol) concentrations in the clinical assessment of
demineralizing disorders in children. In, Hormonal Control of
Calcium Metabolism. Excerpta, 1981, pp. 252-260.
Markowitz, M.E. and Rosen, J.F.: Mineral interactions in
health and disease. In, Pediatric Update. Moss, A. (Ed.),
Elsevier, 1982, pp. 97-114.
Rosen, J.F. and Chesney, R.W.: Circulating calcitriol
concentrations in health and disease. J. Peds. 103:1-17, 1983
(Medical Progress Article).
Chesney, R.W., Rosen, J.F., and Deluca, H.F.: Disorders of
calcium metabolism in children. In, Recent Progress 1in
Pediatric Endocrinology, Raven Press, 1983, pp. 5-24.
Rosen, J.F.: Nuclear analytical methods and heavy metals -
real and potential applications in the biomedical sciences.
Neurotoxicology 4:218-219, 1983.
Piomelli, S., Rosen, J.F., and Chisolm, J.J. Jr.: “Treatment
guidelines for the management of childhood lead poisoning. J.
Pediatrics 105:523-532, 1984.
Rosen, J.F.: Lead and the vitamin D-endocrine system. In,
Air Quality Criteria For Lead. Grant, 1.. and Davis, M.
(Eds.), Volume 4, Chapter 12, 1984, pp. 42-47.
Rosen, J.F.: Metabolic and cellular effects of lead: A guide
to low level lead toxicity in children. In, Dietary and
Environmental Lead Exposure. Mahaffey, K.R. (Ed.), Elsevier,
1985, pp. 157-185.
13.
14.
15.
16.
17.
18.
19,
20.
Rosen, J.F.: An overview of metabolic effects of lead in
children. In, Health Effects of Lead. Hotz, M. (Ed.}, Royal
Society of Canada, Commission on Lead in the Environment,
1986, pp. 203-224.
Needleman, H.L., Rosen, J.F., Piomelli, S., Landrigan, P. and
Graef, J.: The hazards of benign neglect of elevated blood
lead levels. Amer. J. Dis. Child. 141:941~942, 1987.
Rosen, J.F.: The toxicological importance of lead in bone:
The evolution and potential uses of bone lead measurements by
x-ray fluorescence to evaluate treatment outcomes in
moderately lead toxic children. In, Biological Monitoring of
Toxic Metals. Clarkson, T. (Ed.), Plenum Press, 1988, pp.
603-621.
Rosen, J.F.: Metabolic abnormalities in lead-toxic children:
Public health implications. Bull. New York Acad. 65:1067-1084,
1989.
Rosen, J.F., Novak, R.P. and Galvin, M.J.: The calcium
messenger system: Implications for toxicological research.
Environmental Health Perspectives, 84:3-5, 1990.
Pounds, J.G., Long, G., and Rosen, J.F.: The cellular and
molecular toxicity of lead in bone. Environ. Health
Perspectives, 21:17-32, 1991.
Rosen, J.F., and Pounds, J.G. The metabolism of lead in bone.
CRC Review in Toxicology, In Press, 1992.
Rosen, J.F.: Health effects at low exposure levels: Expert
consensus and rationale for lowering the defination of
childhood lead poisoning. Amer. J. Dis. Child., In Press,
1992.
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ih
STRATEGIC PLAN FOR THE
ELIMINATION OF CHILDHOOD
LEAD POISONING
February 1991
bh
STRATEGICPLAN FOR THE
ELIMINATION OF CHILDHOOD LEAD POISONING
TABLE OF CONTENTS
Summary of Chapters
Chapter 1.
Chapter 2.
Chapter
Chapter
Chapter 5. Research Agenda
Chapter 6. Funds Needed for Implementation of the Strategic Plan
Chapter 7. Suna of Recommendations
References
APPENDICES
L Lead exposure and its effects on children and fetuses
II. Benefits of preventing lead exposure in the United States and costs and
benefits of lead-based paint abatement
History of childhood lead poisoning prevention programs
Organizations and agencies that could help promote awareness of childhood
lead poisoning
Infrastructure development for abatement of lead hazards in housing
bd
PREFACE
Three striking conclusions about childhood lead poisoning have emerged in the past
several years: 1) the effects of exposure to even moderate amounts of lead are more
pervasive and long-lasting than previously thought, 2) significant impairment of
intelligence and neurobehavioral function is being reported at increasingly lower levels of
lead in blood, and 3) mullions of children in the United States have blood lead levels in
this new range of concern. These findings have been reviewed mn great detail elsewhere,
and they are summarized here. They are not, however, the main subject of this report.
The main subject 1s the public health response to our new understanding of childhood
lead poisoning.
In this report, we set forth a strategy for eliminating childhood lead poisoning as a public
health problem. Essential actions inciude increased support of programs that prevent
childhood lead poisoning, increased abatement of lead-based paint and paint-
contaminated dust in high-risk housing, reductions in other sources and pathways of lead
exposure in children, and national surveillance for children with elevated blood lead
levels. Finding and treating children with lead poisoning is critical, but not sufficient.
Preventive actions must be taken to remove sources of lead in the child's environment
before poisoning occurs.
Any plan to eliminate childhood lead poisoning in the United States must address the
formidable problems posed by lead-based paint. lead-based paint abatement has been
rcither widespread nor effective. Developing an effective, long-term lead-based paint
ahatement effort is probably the most cntical factor in eliminating childhood lead
poisoning. In this plan, approaches to developing this effort receive most attention.
From a national viewpoint, the relative contribution from different sources of lead for
children with high blood lead levels (that is, those with or likely to get lead poisoning) is
different from that for children with low or moderate blood lead levels. For children
with the highest blood lead levels, lead-based aint is a particularly important source.
Stategies will need to be developed to focus abatement efforts on the highest priority
groups (especially children with lead poisoning severe enough to require medical
intervention, e.g., blood lead levels > 25 ug/dl). Inital screening efforts will also have
to be focused on areas where there are the greatest numbers of children with the highest
blood lead levels (e.g., > 25 ug/dL).
This plan also calls for reducing lead in other major sources and pathways of exposure.
Ongoing regulatory and voluntary protective actions are important and must be
strengthened. Lead is widely distributed in water, food, and air, but this lead is less
likely to produce lead poisoning than lead m such concentrated sources as lead paint.
Reducing the amount of lead in these environmental media, however, can have a
profound effect on blood lead levels throughout the entire United States. This was
demonstrated when lead was removed from gasoline. Reducing the amount of lead in
water, food, and air would help reduce the prevalence of lead poisoning and would help
protect children with blood lead levels below the current definition of lead poisoning
from adverse effects.
The role of exposure to soil lead, both directly and through the contribution of soil lead
to lead in housedust, is still being investigated. The nature and degree of soil lead
abatement that would be appropnate 1s unclear. The research needed to resolve the soil
lead issues will take years. However, since so many children are being poisoned by
lead-based paint, significant action on lead-based paint abatement should not be delayed
while we await the results of research. Decisions on how to set up rational soil lead
abatement programs will have to be made separately as more data become available.
(However, 1t is critical not to further contaminate the soil during lead-based paint
abatement efforts.)
We have made substantial progress in reducing exposure to lead; deaths and severe
illness from lead poisoning (e.g., encephalopathy) are now rare. The results of recent
studies indicate, however, that blood lead levels previously believed to be safe are
adversely affecting the health of children. Millions of children in the United States are
believed to have blood lead levels high enough to affect intelligence and development.
The need to deal with preventing exposure at these lower levels will require increased
efforts. The Administration is responding to this problem with increased resources. In
FY 1992, the President’s budget calls for $14.95 million for the lead poisoning prevention
program at the Centers for Disease Control and $25 million for the new HOME
abatement program of the Department of Housing and Urban Development.
In many ways, the tone of this report is one of understatement. The enormity of the task
of eliminating childhood lead poisoning and the extensive public health benefits to be
gained are very clear. This strategic plan is at best a first step. More detailed plans for
implementation must follow, and then the work itself must be done.
Childhood lead poisoning has already affected millions of children, and it could affect
millions more. Its impact on children is real, however silently it damages their brains
and limits their abilities. Deciding to develop a strategic plan for the elimination of
childhood lead poisoning is a bold step, and achieving the goal would be a great
advance.
AUTHORS, CONTRIBUTORS, PEER REVIEWERS, AND ACKNOWLEDGEMENTS
PRINCIPAL AUTHORS
Sue Binder, M.D.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atlanta, Georgia 30333
Henry Falk, M.D, M.P.H.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atanta, Georgia 30333
CONTRIBUTORS
FEDERAL
Max Lum, E.D.
Agency for Toxic Substances and Disease Registry
Division of Health Education
1600 Clifton Road, NE
Atlanta, Georgia 30333
Susanne Simon
Agency for Toxic Substances and Disease Registry
Division of Health Education
1600 Clifton Road, NE
Atlanta. Georgia 30333
James L. Pirkle, M.D, Ph.D.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Adanta, Georgia 30333
Joel Schwartz, Ph.D.
Environmental Protection Agency
401 M Street, SW, PM-221
Washington, D.C. 20460
bo
CONTRIBUTORS (cont'd)
William McC. Hiscock
Health Care Financing Administration
Program Initiatives Branch
P.O. Box 26678
Baltimore, Maryland 21207
Jane Lin-Fu, M.D.
Health Resources and Services Administration
Matemal and Child Health Bureau
S600 Fishers Lane
Rockville, Maryland 20857
Dopald T. Ryan
National Institute of Environmental Health Sciences
727 S. 26th Place
Arlington, Virginia 22202
STATE AND LOCAL
Charles G. Copley
Office of the Health Commissioner
City of St. Louis
Department of Health and Hospitals
634 N. Grand
St. Louis, Missoun 63178
PRIVATE SECTOR
Anne Elixhauser, Ph.D.
Human Affairs Research Center, Battelle
370 L Enfant Promenade, SW, Suite 900
Washington, D.C. 20024-2115
Mark S. Kamlet, Ph.D.
Camegic Mellon University
Department of Social and Decision Sciences
Pittsburgh, Pennsylvania 15213
50
CONTRIBUTORS (cont'd)
Paul A. Locke, Esq.
Environmental Law Institute
1616 P Street, NW, Suite 200
Washington, DC 20036
Stephanie Pollack, Esq.
Conservation Law Foundation of New England
3 Joy Street
Boston, Massachusetts 02108-1497
PEER REVIEWERS
Anita S. Curran, M.D.
Robert Wood Johnson Medical School
University of Medicine and Dentistry of New Jersey
One Robert Wood Johnson Place
New Brunswick, New Jersey 08903
Richard J. Jackson, M.D.
California Department of Health Services
Hazard Identification and Risk Assessment Branch
2151 Berkeley Way, Room 619
Berkeley, California 94704-1011
James C. Keck
Baltimore City Health Department
Lead Poisoning Prevention Program
303 East Fayette Street
Baltimore, Maryland 21202
John F. Rosen, M.D.
Albert Einstein College of Medicine
Montefiore Medical Center
111 East 210th Street
Bronx, New York 10467
ACKNOWLEDGEMENTS
We appreciate the assistance of the following individuals who reviewed and commented
on drafts of this report:
FEDERAL
Yernon N. Houk, M.D.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atlanta, Georgia 30333
Robert W. Amler, M.D.
Agency for Toxic Substances and Disease Registry
1600 Clifton Road, NE
Atlanta, Georgia 30333
Elizabeth Cochran
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atlanta, Georgia 30333
Gene Freund, M.D.
Centers for Disease Control
National Institute for Occupational Safety and Health
4676 Columbia Parkway
Cincinnati, Ohio 45226
Teri Guilmette
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atlanta, Georgia 30333
Daniel A. Hoffman, Ph.D.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Adanta, Georgia 30333
Lg vii
Robert S. Murphy, M.S.P.H.
Centers for Disease Control
National Center for Health Statistics
Hyattsville, Maryland 20782
Daniel C. Paschal, Ph.D.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atlanta, Georgia 30333
Jeffrey J. Sacks, M.D, M.P.H.
Centers for Disease Control
Center for Environmental Health and Injury Control
1600 Clifton Road, NE
Atlanta, Georgia 30333
Sandra C. Eberkee
Consumer Product Safety Commission
5401 Westbard Avenue
Bethesda, Maryland 20816
Brian C. Lee, Ph.D.
Consumer Product Safety Commission
5401 Westbard Avenue
Bethesda, Maryland 20816
Robert W. Elias, Ph.D.
U.S. Environmental Protection Agency
Office of Research and Development
Research Tnangle Park, North Carolina 27711
Renate D. Kimbrough, M.D.
U.S. Environmental Protection Agency
Office of the Administrator
401 M Street, SE, A-101
Washington, DC 20460
Ronnie Levin
U.S. Environmental Protection Agency
Office of Research and Development
401 M Street, SE, H-8105
Washington, DC 20460
1 vill
Dave E. Schutz, M.S., M.P.P.
U.S. Environmental Protection Agency
Office of Toxic Substances
401 M Street, SE, TS-798
Washington, DC 20460
P. Michael Bolger, Ph.D, D.A.B.T.
U.S. Food and Drug Administration
Division of Toxicological Review and Evalunation
200 C Sueet, SW, HFF-156
Washington, DC 20204
Ellis Goldman, M.C.P.
U.S. Department of Housing and Urban Development
Office of Policy Development and Research
451 7th Street, SW
Washington, DC 20410
Ronald J. Morony, P.E.
U.S. Department of Housing and Urban Development
Office of Policy Development and Research
451 7th Street, SW
Washington, DC 20410
Steve Weitz, M.U.P.
U.S. Department of Housing and Urban Development
Office of Policy Development and Research
451 7th Street, SW
Washington, DC 2041G
Kathryn Mahaffey, Ph.D.
National Institute of Environmental Health Sciences
3223 Eden Avenne, Room 13
Cincinnati, Ohio 45267-0056
Mary McKnight
U.S. Department of Commerce
National Institute of Standards and Technology
Gaithersburg, Maryland 20399
oO
®
STATE AND LOCAL
Mary Jean Brown
Massachusetts Department of Public Health
Childhood Lead Poisoning Prevention Program
State Laboratory Institute
305 South Street
Jamaica Plain, Massachusetts 02130
Mark Matulef, Ph.D.
Massachusetts Executive Office of Communities and Development
Office of Program and Policy Development
100 Cambndge Street
Boston, Massachusetts 02202
Lewis B. Prenney
Massachusetts Department of Public Health
Childhood Lead Poisoning Prevention Program
State Laboratory Institute
305 South Street
Jamaica Plain, Massachusetts 02130
PRIVATE SECTOR
John B. Moran
Laborers’ National Health and Safety Fund
Occupational Safety and Health
905 16th Street, NW
Washington, DC 20006
Herbert L. Needleman, M.D.
University of Pittsburgh School of Medicine
3811 O'Hara Steet
Pittsburgh, Pennsylvania 15213
Margery Turner
The Urban Institute
2100 M Steet, NW
Washington, DC 20037
STRATEGIC PLAN FOR THE
ELIMINATION OF CHILDHOOD LEAD POISONING
EXECUTIVE SUMMARY
The U.S. Public Health Service Year 1990 and Year 2000 Objectives for the Nation aim
for progressive declines in the numbers of lead-poisoned children in the United States,
leading to the elimination of this disease. We believe that a concerted society-wide
effort could virtually eliminate this disease as a public health problem in 20 years.
This plan, developed for the Committee to Coordinate Environmental Health and
Related Programs of the U.S. Department of Health and Human Services, provides an
agenda for the first 5 years of a comprehensive society-wide effort to eliminate childhood
lead poisoning. The results and experience from this 5-year program will lead to the
agenda for the following 15 years.
Lead is a poison that affects virtually every system of the body. Results of recent studies
have shown that lead’s adverse effects on the fetus and child occur at blood lead levels
previously thought to be safe; in fact, if there is a threshold for the adverse effects of
lead on the young, it may be close to zero.
Lead poisoning remains the most common and societally devastating environmental
disease of young children. Enormous strides have been made in the past 5 to 10 years
that have increased our understanding of the damaging, long-term effects of lead on
children’s intelligence and behavior. Today in the United States, millions of children
from all geographic areas and socioeconomic strata have lead levels high enough to
cause adverse health effects. Poor, minority children in the inner cities, who are already
disadvantaged by inadequate nutrition and other factors, are particularly vulnerable to
this disease.
Childhood lead exposure costs the United States billions of dollars from medical and
special education costs for poisoned children, decreased future earnings, and monality of
newboms from intrauterine exposure to lead. Childhood lead poisoning continues in our
society primarily because of lead exposure in the home environment, with lead-based
paint being the principal high-dose source. It is the most important source for the
highest-risk children (e.g., those with blood lead levels > 25 ug/dL); preventive actions
for such exposures should receive the highest priority.
x1
Federal regulatory actions have significantly reduced or eliminated lead from many
consumer products, including pew paint and gasoline. Federal agencies continue to take
actions further to reduce lead exposure from water, food, soil, air, and the workplace.
Unfortunately, we are making litle progress in eliminating the major source of high-dose
lead poisoning, leaded paint from older housing.
In a new benefits analysis based on data from three studies, we estimate that the
abatement of lead from all pre-1950 housing containing lead-based paint over the next
20 years would result in societal benefits of $62 billion. This anticipated economic
benefit is an additional incentive to society, since even if no economic benefits of
abatement could be demonstrated, prevention of childhood lead poisoning would still be
a worthwhile public health activity.
This plan contains recommendations for program and research activities. The four
immediately essential elements of this effort are:
1) Increased childhood lead poisoning prevention programs and activities.
2) Effective abatement of leaded paint and lead paint-contaminated dust in
high-risk housing.
3) Continued reduction of children’s exposure to lead in the environment,
particularly from water, food, air, soil, and the workplace.
4) Establishment of national surveillance for children with elevated blood lead
levels. i
Increased childhood lead poisoning prevention activities and national surveillance for
elevated lead levels are essential parts of a national strategy to eliminate childhood lead
poisoning for several reasons. Children should be screened for elevated blood lead
levels so that affected children will receive appropriate medical attention and
environmental follow-up. Initally, screening activities must focus on those areas with the
greatest prevalence of children with the highest blood lead !svels. Screening and
surveillance data are also important for defining those areas in greatest need of intensive
abatement programs and for evaluating the success of the national abatement program in
eliminating this disease In targeted areas.
Effective lead-based paint abatement is essential for the elimination of childhood lead
poisoning. lead-based paint is the most concentrated source of lead to children and,
historically, is the source most closely linked to lead poisoning in children. Many sources
of lead, for example, food and soil, contribute to overall exposure of U.S. children to
lead, but for children with the highest blood lead levels, that is, children with lead
poisorung, lead-based paint is of particular importance.
X11
LD
The development of a national strategy to abate lead-based paint is critical to the success
of the effort to prevent lead poisoning. At present, far too few homes are being abated.
To achieve maximum impact in the shortest time, lead-based paint abatement programs
need to be closely linked with public bealth programs.
We recommend development of a national strategy for lead-based paint abatement that
includes actions by both the private and the public sectors. Since the public health
benefits and costeffectiveness of lead-based paint and dust abatement are greatest in the
housing most likely to contribute to lead poisoning, in the early years the emphasis
should be on abating the housing units of affected children and the units likely to poison
children in the near future.
To eliminate completely this disease, however, will require that all housing with
lead-based paint eventually be addressed. A prioritized program will allow the
highest-risk housing to be abated first, while enhanced programs, infrastructure, and
technology continue to be developed. This national lead-based paint abatement program
must include an evaluation component to ensure efficacy and safety for occupants as well
as workers and their families.
This strategic plan focuses heavily on lead-based paint because of its key role in lead
poisoning and because of the limited nature of previous efforts to reduce this source of
lead. A national plan to eliminate childhood lead poisoning, however, must also focus
on other widespread sources and pathways of lead exposure to children. Lead in water,
food, soil, and air, in particular, may affect large numbers of children and may contribute
to overall levels of lead in the population. Continued efforts to reduce these sources and
pathways of lead exposure will result in lower average blood lead levels in the United
States and will thereby further diminish the likelihood of lead poisoning developing even
in children exposed to a high-dose source.
Childhood lead poisoning usually does not cause distinctive clinical symptoms, but the
effects of childhood lead poisoning on intellectual and neurobehavioral funciioning are
pronounced and may persist for life. Furthermore, lead poisoning is entirely preventable.
We understand the causes of lead poisoning and, most importantly, how to eliminate
them. This plan establishes priorities and identifies steps toward that end.
p 838
of
SUMMARY OF CHAPTERS
Chapter 1. Introduction
Lead poisoning, the most common and societally devastating environmental disease of
young children, is entirely preventable. We understand the causes of childhood lead
poisoning and, most importantly, how to eliminate them. A concerted societal effort
could virtually eliminate this disease in 20 years.
Chapter 2. Health Effects of Lead and Lead Exposure
Lead is a dangerous and pervasive environmental poison. particularly harmful to fetuses
and young children. The threshold for some of lead’s health effects may be close to
zero. The Agency for Toxic Substances and Disease Registry (ATSDR) estimated that
between 3 and 4 million children in the US. (17% of all children) had blood lead levels
above 15 ug/dL in 1984, levels high enough to adversely affect intelligence and behavior.
Lead in the home environment, principally from lead-based paint, is the major source of
lead poisoning. (See Appendix I for more details on the material in this chapter.)
Chapter 3. Benefits of Preventing Lead Exposure of Children and Fetuses
A benefits analysis was performed for this report, taking into account recent data on the
effects of lead on children and fetuses. (In addition, an example of a cost-benefit
analysis of a national lead-based paint abatement program, along with the detailed
benefits analysis, appears in Appendix II.) For this analysis, the benefits of preventing
children and fetuses from being exposed to lead are the costs that would have been
associated with exposure had it occurred. On the basis of this analysis, the average
benefits of preventing a child's blood lead level from exceeding 24 ug/dL (the level at
which medical evaluation is necessary) are $4,631 for avoided medical and special
education costs. For all children, including those with blood lead levels below 25 ug/dL,
the average increased wages to be expected from preventing each 1 ug/dL increase in a
child's blood lead level are $1,147. The average benefits of preventing a 1 ug/dL
increase in the blood lead level of a pregnant woman are $300. Based on data from
three programs (see Appendix II), the benefits of abating all pre-1950 housing with
lead-based paint over a 20-year period would be $62 billion, discounted to the present.
Chapter 4. Program Agenda
The four essential programm components of a strategy to eliminate childhood lead
poisoning are:
1) Increased childhood lead poisoning prevention programs and activities.
62
2) Increased abatement of leaded part and paint-contaminated dust in housing.
3) Continued reduction of children’s exposure to lead in the environment,
particularly from water. food. air. soil. and the workplace.
4) Establishment of national surveillaxe for children with elevated blood lead
levels.
Increased childhood lead poisoning prevenzion activities include both funding of public
lead poisoning prevention programs and inreased awareness and action by private
physicians. Increased ahatement should also result from a combination of efforts by the
private and public sectors. Before we can safely and effectively conduct as many
abatements as are needed, the infrastructure for abatement must be developed.
(Appendix V discusses infrastructure development in more detail.) Other environmental
sources of lead should also continue to be addressed as part of the strategic plan;
reductions of lead in water, food, soil. air. 2nd the workplace are of most importance.
National surveillance for elevated blood lead levels is needed to target areas requiring
increased lead poisoning prevention activites and abatement, to track our progress in
eliminating childhood lead poisoning, and to evaluate lead exposure in abatement
workers and workers in other lead-comiamizaied environments.
Chapter 5. Research Agenda
Research activities to complement the four essential program components are described
in this chapter.
Chapter 6. Funds Needed for Implementation of the Strategic Plan
Significant Federal, State, local, and privaiz resources must be committed to meet the 5-
year goals. Preliminary estimates indicate that as much as $974 million in combined
resources may be required to implement the first 5 years of this Strategic Plan.
Chapter 7. Summary of Recommendations
The five most urgent recommendations of this plan include increased prevention
activities, increased abatement, reduced exposure to other sources of environmental lead,
national surveillance, and research.
Xv
CHAPTER 1. INTRODUCTION
INTRODUCTION
® CHILDHOOD LEAD POISONING IS EXTREMELY
WIDESPREAD.
®¢ ALTHOUGH SUBSTANTIAL PROGRESS HAS
BEEN MADE IN THE PAST 20 YEARS, KEY
ENVIRONMENTAL SOURCES OF LEAD REMAIN.
THIS DOCUMENT PRESENTS A STRATEGIC
PLAN FOR THE ELIMINATION OF CHILDHOOD
LEAD POISONING.
Lead poisoning remains the most common and societally devastating environmental
disease of young children. Millions of U.S. children from all geographic areas and
socioeconomic strata have blood lead levels high enough to be associated with adverse
health effects. Poor, minority children in the inner cities, who are often already
disadvantaged by inadequate nutrition and other factors, are particularly vulnerable to
this disease. The pervasiveness of childhood lead poisoning was well described in The
Nature and Extent of Childhood Lead Poisoning in Children in the United States: a
Report to Congress, prepared by the Agency for Toxic Substances and Disease Registry
(ATSDR, 1988).
Page 1
Childhood lead poisoning is entirely preventable. We understand the causes of lead
poisoning and, most importantly, how to eliminate them. We believe that a concerted
societal effort could virtually eliminate this disease as a public health problem
in 20 years.
Important progress has been made in reducing some sources of lead in the past 20 years.
Federal regulatory actions have significantly reduced or eliminated lead from many
consumer products, including new paint and gasoline. Voluntary programs, such as the
work by the Food and Drug Administration (FDA) with can manufacturers to reduce
lead in canned food, have also been highly successful in reducing exposure to lead.
Federal agencies continue to take actions to further reduce lead exposure from water,
food, air, and the workplace. Unfortunately, limited progress has been made in
eliminating lead-based paint from older housing--the major source of high-dose lead
poisoning in children. Abatement of lead-painted homes is an essential part of both the
prevention of childhood lead poisoning and the treatrnent of poisoned children.
LEAD-BASED PAINT ABATEMENT IS AN INTEGRAL PART
OF THE TREATMENT OF CHILDHOOD LEAD POISONING
AND THE PREVENTION OF NEW CASES. WE HAVE MADE
LITTLE PROGRESS IN ELIMINATING LEAD-BASED PAINT
IN OLDER HOMES AS A CAUSE OF CHILDHOOD LEAD
POISONING.
The lack of progress in eliminating childhood lead poisoning is due to several factors.
For example, lead poisoning has been improperly considered by many to be a disease of
the poor that could be remedied by better housekeeping and childrearing; another source
of confusion is that many people believe the disease was eliminated when the
manufacture of lead-based paint for residential use was banned. The logistical
difficulties and high costs of abating lead-based paint in homes have also been a major
problem.
Page 2
Dunng the past 20 years, scvere, symptomatic lead poisoning in children (c.g.,
encephalopathy with coma) has been markedly reduced. However, new and increased
knowledge and awareness of the health effects of exposure to lead in childhood,
especially at lower levels once considered safe, have dramatically increased concem
about this problem in recent years. The fact that childhood lead poisoning is a societally
devastating, yet totally preventable disease has focused attention on the need for a
strategic plan to eliminate it.
— =D, ae
EEE IE ae PTET
rr et EE Sr 7 SR A ICS
DEATHS AND ACUTE, SEVERE ILLNESS FROM LEAD
POISONING ARE NOW RARE. HOWEVER, WE NOW KNOW
THAT LARGE NUMBERS OF CHILDREN MAY SUFFER
ADVERSE HEALTH EFFECTS AT BLOOD LEAD LEVELS THAT
WERE ONCE CONSIDERED SAFE.
Several recent government documents have extensively reviewed health and
environmental data related to childhood lead exposure (ATSDR, 1988; Environmental
Protection Agency, 1986). This strategic plan discusses these data briefly, but focuses on
a detailed benefits analysis and major agenda items. The plan consists of chapters on
exposure to lead and its effects on children and fetuses, a benefits analysis of reducing
lead exposure, a program agenda, a research agenda, and a discussion of the funds
needed for implementation. Several appendices provide the background and justification
for the material in the plan.
This document has been developed at the request of Dr. James O. Mason, Assistant
Secretary for Health, U.S. Department of Health and Human Services, for the
Committee to Coordinate Environmental Health and Related Programs. It has been
developed with the help of contmbutors from other Federal, State, and local agencies and
the private sector. It does not, however, necessarily reflect the policies of these
individuals and agencies.
Page 3
0°)
CHAPTER 2. HEALTH EFFECTS OF LEAD AND LEAD EXPOSURE
(See Appendix I for more details on material in this section.)
DE A EE YL EO LS wp py LAR ET NA PWT Feri DE ee PL TRYRIIE CL AL SEE OG EE a nie I: ie EST el ES RS Te Mav ant ed SPR EE Lae a PA Ne a TES al Sandy 13 eB
JRE = Ee aE IIR le NN AST RRS LL A Se ame a SE NE eS LE SU NR eh Sr LATER SRE Eran A BL
EFFECTS OF EXPOSURE
e HEALTH EFFECTS
LEAD AFFECTS EVERY SYSTEM IN THE BODY.
EFFECTS ON INTELLIGENCE AND BEHAVIOR
ARE MOST IMPORTANT.
¢ [EAD EXPOSURE
CHILDREN ARE EXPOSED TO LEAD FROM
MANY SOURCES AND PATHWAYS.
LEAD-BASED PAINT IS THE SOURCE OF
GREATEST CONCERN.
Lead is an extremely dangerous and pervasive environmental poison. In 1984, at least 3
to 4 million children in the United States (17% of all children) had blood lead levels
high enough to cause neurobehavioral and other adverse health effects (ATSDR, 1988).
The large number of children with blood lead levels in the toxic range shows that
existing environmental lead levels in the United States provide no margin of safety for
the protection of children.
The risks of lead exposure are not based on theoretical calculations. They are well
known from studies of children themselves and are not extrapolated from data on
laboratory animals or high-dose occupational exposures. Whereas conservative
approaches are used to estimate risk from low level exposures to many chemicals,
especially carcinogens, this is not the case for lead.
Page 4
uD
HEALTH EFFECTS OF LEAD
ADVERSE EFFECTS OF LEAD ON
CHILDREN AND THE FETUS
© Neurobehavioral
Decreased intelligence
Developmental delays
Behavioral disturbances
Seizures (at very high levels)
Coma (at very high levels)
Growth
Decreased stature
Endocrinologic
ARered vitamin D metabolism
Hematologic _.
Elevated rye Jroloponpimy levels
Anemia
On the totes
Decreased gestational weight
Decreased gestational age
Miscarriage and stillbirth (at very high levels)
Lead is a poison that affects virtually every system in the body. It is particularly harmful
to the developing brain and nervous system; therefore, lead exposure is especially
devastating to fetuses and young children.
Very severe lead exposure (blood lead levels > 80 ug/dL) can cause coma, convulsions,
and even death. It is currently estimated that there are about 250,000 children under ©
years of age whose blood lead is 25 ug/dl and greater. The adverse effects on these
children are great. They need to be identified as soon as possible to remove them from
the source of lead and provide appropriate medical care. This is the highest prionty.
Blood lead levels as low as 10 ug/dL, which usually do not cause distinctive symptoms.
are associated with decreased intelligence and slower neurobehavioral development.
Other effects that begin at blood lead levels as low as 10 ug/dL include behavioral
disturbances, reduced stature, and effects on vitamin D metabolism. Matemal and cord
blood lead levels of 10 to 15 ug/dL appear to be associated with reduced gestational age
Page 5
/
and reduced weight at birth (ATSDR, 1988). Blood lead levels of 10 ug/dL and above
at age 2 years have been shown to result in a reduction of the General Cognitive Index
at age 57 months. Most of the children studied had blood levels below 15 ug/dL
(Bellinger, 1991). Although researchers have not yet completely defined the impact of
blood lead levels <10 ug/dL on central nervous system function, it may be that even
these levels are associated with adverse effects that will be more clear as our research
instruments become better.
The neurobehavioral effects of childhood lead exposure
appear to be longlasting.
In a recent long-term follow-up study (Needleman, 1990), for children who had been
exposed to moderate lead levels in preschool years, the odds of those children dropping
out of high school were seven times higher, and the odds of a significant reading
disability were six times higher than for children exposed to lower lead levels. In
addition, the children exposed to higher lead levels had lower class standing, increased
absenteeism, and lower vocabulary and grammatical-reasoning scores, even after
investigators controlled for other covariates. The apparent persistence or irreversibility
of many of lead’s neurobehavioral effects intensifies concen over exposure of fetuses
and children to lead.
Blood lead levels considered elevated by CDC
50
7s
> 40 }
3 |
© 30 Ft :
2 bcs
L 20 F .
KY 2*
2 10}
=
on
0 BY 2 1 1 1
1970 1975 1980 1985 1990
Aa RR I SE RR RP RE AAR BE IE I I ER A RE SB A LS EV ATE mae <F ren
*Currently undergoing revision
Page 6
7,
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or)
j
Studies on the health effects of lead over the past 20 years have produced a consistent
trend: the more that is leamed about kad’s effects on children and fetuses, the lower the
blood lead level at which adverse effects can be documented. In the first half of the
20th Century, medical care providers were concemed about blood lead levels > 80
ug/dL; by the 1960s, they were concemed about levels > 60 ug/dL; in the 1970s, as
studies began showing effects at lower and lower levels, the level of concen was at 40
ug/dL; and by the middle 1980s, t was lowered to 25 ug/dL. A current reassessment
will likely place the level at which interventions are recommended at 10-15 ug/dL.
Blood lead levels formerly considered safe have now been clearly associated with adverse
effects. If there is a threshold for lead’s effects on health, it is probably near zero.
The definition of childhood lead poisoning requires a blood
lead level of =25 pg/dL. This definition is being reconsidered
and the blood lead level is being revised downward.
The current definition of childhood lead poisoning requires a blood lead level > 25
ug/dL (CDC, 1985). This definition is being reevaluated and, as a result of recent
research on the effects of low-level lead exposure in children, it will undoubtedly be
lowered to 10-15 ug/dL. A Federal advisory committee is currently meeting and working
on these changes.
LEAD EXPOSURE
OTHER SOURCES AND PATHWAYS
TO BE ADDRESSED
Paint ced
Industrial Gasoline \
Air
Solder
Sources
Dust
Stationary sources, like smelters
Lead has some unusual characteristics that cause special concem about exposure. First,
lead deposited in the environment does not biodegrade; it remains there and
accumulates. Second, lead exposure is pervasive, sparing no segment of the U.S.
populace. Third, lead accumulates over months and years in the bodies of children.
Therefore, chronic exposure to small sources of lead can result in a large long-term
accurnulation in a child, increasing that child’s risk of adverse health effects. During
pregnancy, a woman's bone lead stores may be mobilized, exposing the fetus to lead.
Thus, childhood lead exposures in one generation may result in prenatal exposure in the
next generation. .
Page 8
-
oY
i
e
]
Children are exposed to lead from many sources (for example, paint, gasoline, solder,
and stationary sources like smelters) via multiple pathways (for example, air, dust, soil,
water, and food). A child's particular environment determines the relative importance of
cach source and pathway.
Today, lead-based paint is the source of greatest public health concem. It is the most
common cause of high-dose lead exposure. Exposure occurs not only when children
ingest chips and flakes of paint (which often contain as much as 50 percent lead by
weight), but also, and probably more commonly, when children ingest lead-based
paint-contaminated dust and soil during normal mouthing activities.
In the mid-1980s, about 13.6 million children under 7 years of age lived in homes with
lead-based paint. An estimated 1.8 to 2.0 million children lived in deteriorated
lead-painted housing with unsound paint (for example, peeling paint and other damage
to walls), which placed them at high nisk of excessive lead exposure from this source:
about 1.2 million of these children were estimated to have blood lead levels above 15
vg/dL, mainly because of exposure to lead paint (ATSDR. 1988). ATSDR has assessed
existing lead paint in U.S. housing and public buildings to be an "untouched and
enormously serious problem.”
LEAD-BASED PAINT IS THE SOURCE OF GREATEST PUBLIC
HEALTH CONCERN. OTHER SOURCES OF LEAD ALSO CAN BE
IMPORTANT CONTRIBUTORS TO CHILDREN’S BLOOD LEAD
LEVELS.
Estimates of numbers of children exposed to other sources and pathways of lead appear
in Appendix I. The removal of lead from gasoline during the last decade, as well as
reductions in other widespread sources and pathways such as lead in food, has
contributed to a major drop in the mean blood lead levels of children. By lowering the
average, or baseline, level of lead in children, the nisk of lead poisoning is reduced, even
from exposure to concentrated sources such as lead paint, because higher doses are
necessary to produce lead poisoning. It is, therefore, important to continue to reduce
children’s exposure to lead from air, water, food, soil, and the workplace; there will also
be occasions where these sources and pathways result in lead poisoning. Efforts to
reduce these exposures are not a substitute for lead-based paint abatement, however,
because in the geographic areas where lead-based paint and dust are a prominent
hazard, they alone can, as noted above, produce childhood lead poisoning.
Page 9
45
CHAPTER 3. BENEFITS OF PREVENTING LEAD EXPOSURE OF
CHILDREN AND FETUSES (The methods and assumptions on which
this benefits analysis are based are detailed in Appendix IL Numerical
estimates are included only for those benefits which we believe are
defensible by good, quantative data. Not factored in the benefits analysis
are those which are not able to be quantified. Appendix II also contains a
detailed cost-benefit analysis, in which the benefits of reducing lead
exposure are compared to the costs of lead-based paint abatement, based
on the three currently available studies for which we had data both on the
costs of abatement and the resultant changes in blood lead levels.)
BENEFITS OF PREVENTING LEAD EXPOSURE
THE BENEFITS WE QUANTIFIED ARE:
® REDUCED MEDICAL COSTS
eo REDUCED SPECIAL EDUCATION COSTS
® INCREASED FUTURE PRODUCTIVITY
® REDUCED INFANT MORTALITY
Lead exposure in U.S. children is estimated to cost society billions of dollars a year (for
example, Levin, 1986). These estimates have included costs of medical care. special
education and institutionalization. and decreases in productivity and lifetime eamings
resulting from impaired cognition.
Page 10
16
For this strategic plan, we have developed a new benefits analysis. The analysis is
detailed in Appendix II and is focused on the benefits of preventing exposure to lead in
children and fetuses. The benefits of reducing lead exposure in persons already being
exposed are likely to be substantial, but they are difficult to quantitate. For example, we
do not know how long lead levels must be elevated before a child develops cognitive
deficits or before these deficits become irreversible. We, therefore, did not include
already exposed individuals in the main benefits analysis.
For this analysis, the benefits of preventing children and fetuses from being exposed to
lead are the avoided costs that would have been associated with exposure. The four
benefits for which we provide monetary values for prevention are 1) reduction in medical
care costs of poisoned children, 2) reduction in special education costs for poisoned
children, 3) reduction in future lost productivity from cognitive deficits in children, and
4) reduction in neonatal mortality from prenatal lead exposure. These are but a few of
the benefits of preventing lead exposure. We did not evaluate the benefits related to
children’s stature, hearing, vitamin D metabolism, and blood production; the benefits of
preventing the effects of lead on adults; or nonhealth-related benefits such as reduced
personal injury court cases and improved property values.
The benefits we evaluated fall into two categories: 1) The first category consists of
benefits achieved only for children whose blood lead levels are prevented from rising
above a certain threshold; avoided medical and special education costs are estimated
only for those children prevented from developing blood lead levels >25 ug/dL. 2) The
second category consists of the benefits of preventing increased blood lead levels in
children no.matter what their initial levels are. For example, intellectual deficits result
over a broad range of blood lead levels. Estimates of costs saved by reducing the effects
of lead on intellectual functioning were made for preventing increases of 1 ug/dL in
blood lead level, regardless of the starting blood lead levels. The benefits of reducing
maternal blood lead levels, which results in decreased infant mortality, are included in
the second category.
REN ELI) —— ESR REE ECS
Average benefits of preventing
Blood lead levels from rising above 24 pg/dL:
Avoided medical costs $1,300 per child
Avoided special education costs $3,331 per child
A 1 pg/dL increase in blood lead level, regardless of
starting blood lead level:
Increased lifetime earnings $1,147 per pg/dL per child
Reduced infant mortality $ 300 per pg/dL per newborn
The average total medical cost avoided by preventing a child's blood lead level from
nsing above 24 ug/dL is $1,300 per child. (This amount is lower than the cost per
cpisode for chelation, because not all children with elevated blood lead levels will be
chelated.) On the average, $3331 per child is saved in special education costs. By
preventing an increase of 1 ug/dL in a child's blood lead level, a net present value
benefit of §1,147 per child from increased future income is saved. Clearly, the greater
the prevented increase in blood lead level. the greater the benefits; for the individual
child. preventing the blood lead level from exceeding 24 ug/dL results in maximum
benefits. Preventing a 1 ug/dL increase in the blood lead level of a pregnant woman
saves an average of $300 from reduced infant morality. (Assumptions used in
quantifying these benefits, including the monetary benefits of preventing infant mortality,
are in Appendix II.)
EXAMPLE:
The benefits of preventing a child’s blood lead level
from rising from 24 pg/dL to 34 pg/dL are:
Avoided medical costs $ 1,300
Avoided special education costs $ 3,331
Increased lifetime earnings
($1,147 per pg/dL * 10 pg/dL) $11,470
$16,101
When these figures for the individual (average) child are applied nationally, the benefits
of eliminating childhood lead poisoning are striking. For example, based on data from 3
programs (See Appendix II), the benefits of abating all pre-1950 housing with lead-based
paint over a 20-year period would be $62 billion, discounted to the present.
FEIN THEA VN en TT eT 3
SEE APPENDIX II FOR
® Detailed benefits analysis
CHAPTER 4. PROGRAM AGENDA
THE PROGRAM AGENDA FOR THE NEXT
5 YEARS CONTAINS FOUR MAIN ITEMS
INCREASED CHILDHOOD LEAD POISONING
PREVENTION ACTIVITIES
INCREASED ABATEMENT OF LEADED PAINT
AND PAINT-CONTAMINATED DUST IN
HOUSING
REDUCTIONS IN OTHER SOURCES AND
PATHWAYS OF LEAD EXPOSURE
NATIONAL SURVEILLANCE
The program agenda for the first § years of the effort to eliminate childhood lead
poisoning has four essential components: 1) increased childhood lead poisoning
prevention activities, 2) increased abatement of leaded paint and paint-contaminated
dust in housing, 3) continued efforts to reduce other widespread sources and pathways of
lead exposure, and 4) national surveillance for elevated blood lead levels. Education and
public awareness are essential to success in implementing all of these components.
PROGRAM AGENDA ITEM I. INCREASED CHILDHOOD LEAD POISONING
PREVENTION ACTIVITIES
INCREASED CHILDHOOD LEAD POISONING
PREVENTION ACTIVITIES MEANS
® INCREASED FUNDING FOR FEDERALLY-
SUPPORTED PROGRAMS |
e OTHER EFFORTS TO INCREASE SCREENING
AND EDUCATION
® DEVELOPMENT OF INFRASTRUCTURE
TO SUPPORT INCREASED PROGRAMS
For this document, childhood lead poisoning prevention activities are defined as the
screening of children for elevated blood lead levels, referral of poisoned children for
medical and environmental mterventions, and education about childhood lead poisoning.
Such education is not limited to increasing public and medical provider awareness of
lead poisoning. It also includes the education of children with elevated blood lead levels
and their families about nutritional and other interventions. Expansion of childhood lead
poisoning prevention activities should first focus oa those children with the highest blood
lead levels (e.g., blood lead levels > 25 ug/dL).
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SR PR
Most children with lead poisoning are never identified.
An estimated 250,000 children had blood lead levels >25 ug/dL in 1984 (ATSDR, 1988).
(More up-to-date estimates will be available in the next couple of years from the Third
National Health and Nutnticn Examination Survey.) Available data indicate that the
majority of such lead-poisoned children are never identified. The screening of children
for elevated blood lead levels must be increased so that poisoned children can receive
appropnate medical attention and environmental follow-up. (Environmental follow-up
varies widely among programs and includes the measurement of lead in paint and often
other potential media and interventions to prevent further exposure.) Screening data are
also important for defining those areas in greatest need of intensive abatement programs
and for evaluating the success of abatement programs in eliminating this disease in
targeted areas.
Federally-Supported Childhood Lead Poisoning Prevention Programs
FEDERALLY-SUPPORTED PROGRAMS
© Federal programs began in 1972,
® Programs are administered by several agencies.
® Programs are directed at children
at highest risk for lead poisoning.
® Programs screen only a small percentage of
children at risk.
Page 15
The history of childhood lead poisoning prevention programs in the United States is
summarized in Appendix II. State and local childhood lad poisoning prevention
programs perform many functions. They screen large numbers of children for lead
poisoning and accept referrals of poisoned children from other practitioners for
follow-up. They ensure that appropnate investigations are conducted of the homes and
other environments of poisoned children. They may issue orders for abatement and may
work with other government agencics to have abatements done. They also make sure
that children receive appropriate medical treatment and that any other young children in
the family or household are screened for lead poisoning. They educate parents and
health care providers about lead poisoning and ways of preventing it.
Door-to-door screening in high-risk neighborhoods generally is the most productive
method of identifying children with lead poisoning. Early in the 1970s, community
outreach and door-to-door screening efforts were an essential component of programs.
However, these activities are labor-intensive and costly. Consequently, most programs
now screen children in fixed-site facilities.
The national effort to identify children with lead poisoning and abate the sources of lead
in their environments began with the passage of the Lead-Based Paint Poisoning
Prevention Act of 1971. Federally-funded screening began in Fiscal Year 1972 with
blood lead testing, but in 1975 the Centers for Disease Control (CDC) recommended
screening with erythrocyte protoporphyrin (EP) instead. (EP levels are elevated in the
presence of elevated blood lead levels. Although useful for identifying children with
blood lead levels above about 30 ug/dL and for detecting iron deficiency, EP is not a
sensitive test for identifying children with blood lead levels below 25 ug/dl..) For most
of the early years of this program, Federal funds appropriated under this Act were
administered by the CDC. More than $89 million were distributed, and over a quarter
of a million children were identified with lead poisoning and received referrals for
environmental and medical intervention. The improvement in the health status of
children identified with lead poisoning in this program was documented in an evaluation
by F.D. Kennedy (1978).
Current major sources of Federal funding for screening programs are thz Matemal and
Child Health (MCH) Block Grant Program, administered by the Health Resources and
Services Administration (HRSA), and the Categorical Grant Program, administered by
the CDC.
A A Ee AE Eh AS eras
A a rN a Sa el
SOURCES OF FEDERAL FUNDING
© Maternal and Child Health Block Grants
® (Centers for Disease Control Categorical Grant
Program
® Early and Periodic Screening, Diagnostic,
and Treatment Program (EPSDT)
® Supplemental Food Program for Women,
Infants, and Children (WIC)
© Head Start
The MCH Block Grants serve as the principal means of Federal support to States to
maistain and improve the health of mothers and children, including children with special
needs. These grants are made to State health agencies to assure access to MCH
services, especially for those with low mmcome who live in areas with limited health
services, and to reduce the incidence of preventable diseases and handicapping
conditions in children. After assuming administrative responsibility for the Lead-Based
Paint Poisoning Prevention Act in Fiscal Year 1982, HRSA issued a policy statement to
all State MCH and Crippled Children’s Services recommending routine periodic EP
screening for all preschool children. Althcugh pot all States use MCH block grant funds
for childhood lead screening. a 1984 survey indicated that 40 States, the District of
Columbia, and Puerto Rico had screening activities.
Page 17
The CDC Categorical Grant Program was authorized by the Lead Contamination
Control Act of 1988. This program provides for childhood lead screening by State and
local agencies, referral of children with elevated blood lead levels for treatment and
environmental interventions, and education about childhood lead poisoning prevention.
Money for this program was first appropriated in FY 1990. The President’s budget for
FY 1992 contains $14.95 million for this program, an increase of $7.16 million from FY
1991.
Other government-funded child health programs also conduct some childhood lead
screening. These programs include Medicaid’s Early and Penodic Screening, Diagnostic,
and Treatment Program (EPSDT); the Supplemental Food Program for Women, Infants,
and Children (WIC); and Head Start
EPSDT is a comprehensive prevention and treatment program available to
Medicaid-eligible persons under 21 years of age. In 1989, of the 10 million eligible
persons, more than 4 million received initial or periodic screening health examinations.
These are provided at a variety of sites (for example, physician offices, public health
clinics, and community health centers) by private or public sector providers. Screening
services, defined by statute, must include a blood lead assessment "where age and risk
factors indicate it is medically appropnate.” (The requirements for a blood lead
assessment are not further defined.) In additon, the EP test is recommended for
children ages 1 to S years to screen for iron deficiency. Because this test is also useful in
identifying children with blood lead levels > 25 ug/dL, many children being screened for
iron deficiency are screened for lead poisoning at the same time. The guidelines for
States indicate that environmental investigations for lead-poisoned children are covered
under EPSDT, although abatement is not. However, specific critena for screening and
the determination of what Medicaid will cover are decided on a State-by-State basis.
Thus, many States do not conduct much screening or do pot pay for environmental
investigations for poisoned children. National data are not available on the numbers of
children screened for lead poisoning through EPSDT, since State-reported Medicaid
performance and fiscal data are not broken down to such specific elements.
The U.S. Department of Agnculture’s WIC program serves pregnant and postpartum
women and children under § years of age in low-income households. Program benefits
include supplemental food, nutrition education, and encouragement and coordination for
the use of other existing health services. As of March 1988, an estimated 1.63 million
children ages 1 to 4 years were participating in WIC. Although children must undergo a
medical or nutritional assessment or both to be certified to receive benefits, Federal
WIC regulations permit States to establish their own requirements for WIC certification
examinations. These regulations permit the use of an EP test for certification and define
lead poisoning as a nutritionally-related medical condition that can be the basis of
certifying a child to receive WIC benefits. Most WIC programs that perform EP tests
use them to screen for iron deficiency, although hematocnt or hemoglobin measurements
are most commonly used for this purpose. The nutritional education and supplemental
food provided by WIC are undoubtedly important in reducing lead absorption in many
children and pregnant women.
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34
Limited data on EP screening of children being seen for WIC certification or follow-up
are available from CDC's Pediatric Nutntion Surveillance System (PedNSS). For
calendar year 1989, 2,231,939 WIC visits for children 6 months through 4 years of age
were reported to PedNSS (provisional data). Six States reported performing EP tests on
44 852 children; of these children, 10.8% had EP levels > 35S ug/dl.. Data are not
available on how many of the children with elevated EP levels had blood lead levels
measured.
Head Start provides a comprehensive developmental program for low-income children
between the ages of 3 and 5 years. About 24 percent of U.S. 3- and 4-year-olds living in
poverty are served by 229 Head Start programs. Although Head Start is mainly known
as an education program, 99 percent of the enrolled children receive medical screening
(54 percent through EPSDT). This screening can include screening for lead poisoning, if
lead poisoning is prevalent in the community. National data on how much lead
screening 1s conducted through Head Start are not available.
In 1985-86, about 785,000 children were screened through childhood lead poisoning
prevention programs (ATSDR, 1983). In Fiscal Year 1938, according to data collected
by the Public Health Foundation, State and local health agencies screened 970,768
children and identified 18,912 that had positive screening tests requiring diagnostic
confumation (Jane Lin-Fu, personal communication). (These latter numbers include
some children screened through EPSDT, WIC, and Head Start. but they may
underestimate the numbers of children screened under the MCH Block Grant Program.)
Given that an estimated 250,000 children had blood lead levels above 25 ug/dL in 1984
(ATSDR, 1988), it is apparent that most lead-poisoned children are never identified.
REASONS TO INCREASE ACTIVITIES
Increase the number of children screened
Increase the use of intensive screening
methods
Ensure prompt investigations of the
environments of poisoned children
Assure proper follow-up of poisoned
children
More childhood lead poisoning prevention activities are needed to 1) increase the
number of children screened, particularly in communities with the highest levels of
blood lead in children and rates of childhood lead poisoning, 2) increase the use of
intensive screening methods, such as community outreach and door-to-door screening, 3)
ensure prompt investigation of the environments of poisoned children, and 4) assure
proper follow-up of poisoned children. Increasing the number of States that require of
encourage EP or blood lead testing through MCH Block Grant activities, EPSDT, WIC,
and Head Start would probably be an efficient way of increasing screening in high-nsk
populations. Outreach and educational activities from the Federal level to regional and
State offices and local agencies and programs could increase recognition of the
importance of such screening. Better information about the amount and efficacy of
screening children in EPSDT, WIC, and Head Start would be helpful in developing
strategies for increasing testing through these programs where appropnate.
Other Efforts to Increase Screening and Education
OTHER EFFORTS NEEDED
e Increased outreach to children
without a usual source of care
e Increased screening by health
care providers
®
Increased public awareness
Page 20
Outreach to Children Without a Usual Source of Medical Care
On the basis of 1988 data from the National Health Interview Survey, it has been
estimated that 8 percent of children less than 5 years of age do not have a regular source
of medical care. Intensified childhood lead poisoning prevention activities must be
duected at these children, many of whom are at high risk for lead poisoning. Some of
these children could be reached by increasing enrollment in EPSDT and other programs.
Others could be identified through intensified (for example, door-to-door) screening by
childheod lead poisoning prevention programs. Additional strategies, such as screening
children using emergency rooms in high-risk neighborhoods for primary or semiemergent
care, should be evaluated for cost-effectiveness.
Screening by Health Care Providers
Education is of vital importance in increasing the amount of screening conducted by
health-care providers. The American Academy of Pediatrics issued its most recent
statement en lead poisoning prevention, diagnosis, and treatment in 1987. Nevertheless.
many providers do not consider screening for childhood lead poisoning to be a part of
routine pediatric care.
Several strategies are available for increasing health-care provider awareness. The first
is to disseminate educational materials and do outreach through existing professional
organizations and medical schools. (A partial list of relevant professional organizations
is in Appendix IV, Table 1). A second strategy is to develop and disseminate training
modules that can be completed for Continuing Medical Education credits, such as the
Case Study in Environmental Medicine developed by ATSDR. A third is to provide
conferences for medical care providers on childhood lead poisoning, either through the
private sector (such as those held in 1989 at the University of Maryland and the
University of Virginia) or through federally funded centers (such as the Health
Education Centers of the Health Resources and Services Administration, the Education
Resource Centers of the National Institute for Occupational Safety and Health, and the
occupational and environmental clinics with activities funded by ATSDR).
Increased Public Awareness
Campaigns to increase public awareness of childhood lead poisoning and its prevention
are likely to increase the amount of screening conducted. Such campaigns will not only
educate medical care providers, they will also increase the public’s demand for lead
screening of children. Some lead poisoning cases may be prevented, for example. by
informing homeowners of the potential dangers in renovating older homes. The
National Matemal and Child Health Clearinghouse is a source of publications about
childhcod lead poisoning. This Clearinghouse and other resource centers could expand
their activities, including operating a toll-free hotline and developing and disseminating
simple materials about lead poisoning prevention in different languages. Information
centers could also supply information on Federal, State, and local resources for dealing
with childhood lead issues.
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148
State and local health departments and childhood lead poisoning prevention programs
should also be encouraged to increase public awareness of childhood lead poisoning.
The categorical grants program authorized by the Lead Contamination Control Act of
1988 specifically allows funds to be used for educational activities conducted by State and
local childhood lead poisoning prevention programs.
Several private sector organizations have sponsored educational activities about
childhood lead poisoning. Other organizations should be encouraged to follow suit.
Because childhood lead poisoning 1s associated with decreased intelligence and ability to
leam, coalitions between organizations promoting lead poisoning prevention and
organizations promoting educaticn and the prevention of mental retardation should also
be encouraged. Organizations that might be interested in such activities are listed in
Appendix IV, Table 2.
Development of Infrastructure to Support Increased Childhood Lead Poisoning
Prevention Programs
DEVELOPMENT OF INFRASTRUCTURE
TO SUPPORT PROGRAMS MEANS INCREASED
® Training programs
® Laboratory services
® laboratory proficiency testing programs
Page 22
The expansion of screening programs will result in a demand for training programs on
childhood lead screening and the investigation of environmental sources. The Louisville,
Kentucky. training program can serve as a model for other such programs. This program
provides methods for assessing lead poisoning in high-risk populations and demonstrates
the integration of lead screening with basic child health services and the technical and
management skills needed for an effective and efficient childhood lead poisoning
prevention program.
In addition, increased screening will lead to a demand for increased laboratory services.
In 1991 CDC will likely issue new recommendations suggesting that screening programs
attempt to identify children with blood lead levels below 25 ug/dl.. This change will
mean that blood lead measurements must be used for childhood lead screening instead
of EP measurements. When this happens. the demand for increased blood lead testing
will far exceed current capacity. In addition, cheaper, easier to use, and portable
instrumentation for blood lead testing will need to be developed. Furthermore, existing
programs for proficiency testing and certification of laboratories will have to be
expanded. With concem about health effects at low blood lead levels, laboratories will
be called upon to do better measurements in the 4 to 5 ug/dL range. As a result. major
efforts will be needed to improve laboratory quality assurance and control at these lower
levels. Reference matenals for laboratories performing blood lead measurements and
technical assistance will be required to improve laboratory quality.
Page 23
PROGRAM AGENDA ITEM 2. INCREASED ABATEMENT OF LEADED PAINT
AND PAINT-CONTAMINATED DUST IN HOUSING
INCREASED ABATEMENT REQUIRES
Setting priorities for which homes are to
be abated first
Strategies for increasing the number of
abatements conducted
Assuring the safety and effectiveness
of abatement
Development of infrastructure for
abatement
Development of a national implementation
plan
Lead-based paint abatement is an integral part of the treatment of childhood lead
poisoning and a crucial step in the preventuon of pew cases. Many sources besides
lead-based paint are contributors to the exposure of children to lead, but we have four
reasons for focusing on abatement of lead paint in this plan. First, lead-based paint and
paint-contaminated house dust are sull the major cause of high-dose lead poisoning in
U.S. children. Second, we have known of the dangers of lead paint since the beginning
of the century. The greatest concentrations of lead m paint occur in housing built before
1950. Although the Consumer Product Safety Commission has required paint
manufactured for residential use to be almost lead-free since 1977, we have made little
progress in eliminating paint previously applied as a cause of childhood lead poisoning.
This problem may get worse with time, as houses painted with lead-based paint
deteriorate further. Third, abatement of paint is expensive, and a successful effort to
eliminate poisoning from leaded paint will require a coordinated effort from the
Page 24
U D
government and private sectors. Fourth, leaded paint abatement is difficult and
potentially dangerous. Poorly performed abatements have poisoned workers and their
families and people living in the homes being abated. In recent years, numerous families
have been poisoned while renovating homes that were not tested for lead. Until this
environmental source of lead is eliminated, the United States will continue to have a
significant childhood lead poisoning problem.
Setting Priorities for Lead-Based Paint Abatement
PRIORITIES FOR ABATEMENT
® Homes of children identified with lead
poisoning
® Homes at high risk of housing children
with lead poisoning
® Homes with lead-based paint that are
being renovated or remodelled for other
reasons
An estimated 30 to 40 million residences in the United States contain leaded paint
(ATSDR, 1938), although not all of them pose an rmminent hazard. Priorities for
abatement should be based largely on public health concems; therefore, abatement
programs must work im tandem with childhood lead poisoning prevention programs to
ensure the most efficient use of resources.
Page 25
i
-
Three prionty groups of housing for abatement can be identified: homes of children
identified with lead poisoning, homes at high risk of housing children with lead poisoning
(but in which poisoned children have not yet been identified), and homes with lead-
based paint that are being renovated or remodelled for other reasons. Although not
specifically discussed in the following, day care centers and other buildings frequented by
young children are also a high pnonty.
The first prionty for abatement is the homes of children identified with lead poisoning.
This is important not only to protect these children from continued exposure, but also to
prevent children who will live in these dwellings in the future from being poisoned. In
particular, children with lead poisoning severe enough to require medical intervention
(i.e., > 25 ug/dL) should be the utmost prionty.
The second priority for abatement is the homes with a large potential for poisoning
children. These are homes that are likely to be causing unrecognized lead poisoning or
to poison children in the near future. This category includes housing in areas with a high
prevalence of lead poisoning, but could include older housing in areas where there is
little or no childhood lead screening. Screening, housing, socioeconomic, environmental,
and other data should be used to identify those areas where housing is most likely to
poison children. Abatement of housing in this category is a crucial part of the lead
poisoning prevention strategy. Within this second priority group, decisions will have to
be made about which specific homes and areas should be abated first. These decisions
should be based on a combination of environmental and demographic data. A "hazard
ranking scheme” should be developed and validated. The more efficient the
identification of homes likely to contain poisoned children and to poison children in the
future, the more cost-effective the abatement will be.
Opportunistic abatements, the third priority, involve those homes that can be efficiently
abated because they are being worked on anyway or have other special characteristics.
An example of opportunistic abatement is the removal of leaded paint from public
housing during comprehensive modernization. The comprehensive modemization
program is effective because 1) the Federal government has authority over the housing
to be abated and 2) lead abatement adds only a relatively small amount to the cost of
ongoing modernization activities.
Data from several evaluations show that abatement of lead-based paint decreases
children's blood lead levels (Kennedy, 1978; Rosen, 1990; Copley, unpublished data;
Amitai et al., unpublished data). The data from these studies indicate that even less
than complete abatements reduce children’s blood lead levels. In general, the most
thorough abatements are believed to be the most effective in reducing blood lead levels
and residual lead in the eavironment. Given the limited resources for abatement,
however, a balance must be struck between doing the best possible abatements in fewer
units and using reasonably good, less expensive methods in more units. The cost-
effectiveness of alternative paini abatement methods should be evaluated, and the cost of
abatement should be reduced through the development of new methods and matenals
and the establishment of a larger infrastructure for abatement
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47
An important issuc is that some of the housing stock. particularly in the inner cities, is
deteriorated past the point of rehabilitation or may be in neighborhoods that are so
economically depressed that buildings rapidly deteriorate and are abandoned. Extremely
deteriorated buildings in declining neighborhoods with large numbers of abandoned units
are very likely to be abandoned or razed in the next 5 years. Requiring complete
abatement in such situations would be futile and could lead to families being dislocated.
In such circumstances, the efficacy of preventive maintenance—leaning and partial
abatement with frequent environmental and blood lead testing—should be determined,
and its role should be defined. In addition, when low-income units are abated,
safeguards will be required to ensure that they remain available as low-income housing.
Strategies for Increasing the Number of Abatements
STRATEGIES FOR INCREASING ABATEMENTS
Incentives
Demonstration programs
Testing and disclosure requirements
Education and public awareness
Increasing the number of abatements performed will require a mixture of public and
private sector efforts. Housing can be divided imto several different sectors—for example,
public housing, public-assisted rental units, privately owned rental units, and
owner-occupied homes. Different strategies will be required to increase abatements for
different kinds of housing. These strategies include positive and negative incentives,
demonstration programs, and the use of test and disclosure requirements.
Page 27
Positive and ncgative incentive strategies confer a financial benefit or other advantage,
or withdraw a financial benefit or advantage, to promote or discourage certain behaviors.
Incentive programs can be used to encourage testing for lead-based paint or abatement
of identified hazards. Demonstration area programs would set aside entire
neighborhoods that would be abated to serve as a model to encourage abatement
elsewhere.
Another possible strategy would require testing for lead levels in housing and the
disclosure of the test results. (These results would be recorded, so that units undergoing
multiple transactions would not be repeatedly tested.) Requiring the abatement of units
with high lead levels could be an additional option. Testing and disclosure could be
required for all housing units or it could center around transactional "trigger events,”
such as renovation or remodeling, renting, sale, or transfer.
Education and public awareness strategies are critical to the success of abatement
programs. They are designed to inform the general public, the housing industry, and
other relevant parties about preventing childhood lead poisoning and the role of
lead-based paint. These strategies are designed to mobilize the community to act
voluntanly to address the problem of leaded paint in housing. Public education and
awareness will prompt the market to encourage abatement by placing a higher value on
an abated house or rental unit than on a nonabated dwelling. Without increased
awareness of the dangers of lead-painted housing, incentive strategies will be ignored,
and regulatory approaches will be less acceptable to the public.
The President’s budget for FY 1992 includes $25 million for the HOME program which
will be administered by the Department of Housing and Urban Development (HUD).
This program will assist low- and moderate-income private residential property owners,
abate lead-based paint, and will be directed to homeowners with young children in high-
risk housing. This program could provide a knowledge base for evaluating the effects of
abatement.
Federal, State, and local govemments and the private sector have roles in many of these
strategies; different groups ar: appropriate for implementing different strategies. How
these strategies should be used to ensure the abatement of homes in the three prionty
groups and the roles of different levels and agencies of government and the private
sector should be dealt with in an implementation plan.
Page 28
Development of Infrastructure for Abatement (See Appendix V for More Details on the
Material in this Section.)
INFRASTRUCTURE DEVELOPMENT MEANS
e Developing testing and abatement guidelines
o Developing worker training and certification
programs
e Evaluating emerging abatement technology
e Developing laboratory accreditation programs
® Ensuring the availability of insurance for
contractors
® Arranging relocations for residents during
abatement
® Developing guidelines for disposal of
abatement debris
Although enough is known to start an effective national abatement program, the capacity
to undertake large-scale abatement does not currently exist. Regulations to ensure the
safety of workers and occupants and the quality of the abatement work are limited. Very
few inspectors, abatement contractors, Of workers have been trained to perform the
needed work properly. Both contractors and property owners can have difficulty getting
insurance. These deficiencies in the infrastructure for abatement must be corrected as
quickly as possible so that a national abatement program can be developed. This section
briefly describes the steps that must be taken to increase the national capacity to do safe
and effective abatements. More details on infrastructure development appear in
Appendix V.
Page 29
Guidelines for testing for lead-based paint and performing safe and cffective abatements
are essential. In Apnl 1990, HUD issued the first national set of comprehensive
technical guidelines (the HUD Intenm Guidelines) for lead paint testing and abatement.
These guidelines were developed by a committee of government and nongovemment
experts for public and Indian housing authorities. Since the guidelines were developed
for housing that is to be extensively modified during modernization by the Federal
Government, they should be modified for use by States, localities, and individuals in
situations where funds are not as available, time is a critical factor, and the unit is not
being gutted for other reasons.
The development of guidelines should be followed by the development of
government-sanctioned model training programs for assuring the quality and consistency
of worker training. As the amount of leaded paint abatement increases, market forces
will meet the growing demand for training programs. Government involvement may be
necessary, however, to control the quality of instruction and to assure the competence of
trainees. In addition, mandatory requirements for the certification of contractors and
their workers, testers, and inspectors should be established either by government or trade
organizations.
Lead-based paint abatement will probably not evolve exclusively as a separate industry
and skill specialty. It is an integral and inevitable part of a variety of existing building
trades: painting, plastering, masonry, flooring, cabinetry, carpentry, electrical, plumbing,
insulation, and door and window replacement. Some home renovation contractors will
probably specialize in lead paint abatement. Thus, lead-based paint abatement should
be integraied into the various building trades. Because abatement is a potentially
hazardous activity, all workers involved in home renovation and repair should be familiar
with the special safeguards and techniques required.
Another potential benefit of a national abatement program is increased employment. As
persons with litle training develop the skills needed for lead-based paint abatement. they
will be likely to vacate jobs that do not require training. Because this abatement work
will require a large work force, often in neighborhoods with high rates of unemployment,
the training and employment of local persons will have local economic and social
benefits.
Lead exposures of persons performing abatement and other workers, especially of
pregnant women and of women and men who have or are planning to have children,
should be reduced. At present, abatement workers are not covered by the Occupational
Safety and Health Administration (OSHA) general industry standard regulating worker
exposure to lead. Instead, they are covered under the safety and health standards for the
construction industry, which regulate lead exposure far less strictly. A standard is needed
that takes into account new data showing adverse effects of lead on adults at lead levels
below the current OSHA general industry standard. Abatement workers and their
families should be protected by medical monitoring and medical removal provisions. as
are potentially lead-exposed workers in general industry.
Page 30
ho
During the past few ycars, private firms have developed a variety of new products to
reduce the costs of lead-based paint abatement. Standards and performance criteria
must be established to assure the effectiveness of new products. Standards for
laboratories evaluating environmental samples should also be developed.
Other constraints to rapidly expanding lead-based paint abatement programs are the
unavailability of liability insurance for contractors and building owners performing
abatement, the lack of programs for quality assurance of lead-based paint and dust
laboratory analysis, and the lack of suitable temporary housing for families whose homes
are being abated. Another constraint is uncertainty about the proper disposal of
abatement debris. When lead is removed from buildings, it is, in effect, being
concentrated; if lead is to be kept from being dispersed in the environment, there must
be rules and regulations for its safe disposal.
Development of a National Implementation Plan for Abatement
AN IMPLEMENTATION PLAN FOR ABATEMENT
SHOULD FOCUS ON
® Increased abatements by the private
and public sectors
® Increased safety and efficacy and
decreased cost of abatement
® Targeting of high-risk housing
® Best use of available funds
A well-designed national implementation plan for increasing the number of abatements
performed should be developed immediately. Although there is an immediate need for
increased resources for abatement, a phased approach to increasmg abatement should be
designed. The implementation plan should focus on three main issues: 1) how to
increase private and public sector abatements; 2) how to increase the safety and efficacy
and decrease the costs of abatements through technology development and evaluation
and worker training and certification; and 3) how best to use available funds to quickly
reduce the number of children poisoned by lead-contaminated hceasing.
During the early years of the national abatement strategy, an evaluation component will
be essential. This evaluation should include measurements of efficacy and safety through
postabatement environmental and human testing, and the inspection and collectica of
data on numbers of abatements being funded by the private and public sectors.
Page 32
PROGRAM AGENDA ITEM 3. REDUCTIONS IN OTHER SOURCES AND
PATHWAYS OF LEAD EXPOSURE
OTHER SOURCES AND PATHWAYS
TO BE ADDRESSED
So I | Diet
Industrial
\
Sources
Water
Air
Housewares
Food
Workplace and hobbies
Lead-based paint and paint-contaminated dust account for most cases of lead poisoning
in the United States. Other sources of lead will also have to be addressed, however, to
eliminate this disease. For example, lead-contaminated soil is probably an important
source for a large number of children. However, adequate information is not yet
available on which to base recommendations for a national soil abatement strategy.
Federal agencies are proceeding with or are evaluating further regulation of
environmental lead mm water, air, and housewares. In this section, some current and
needed activities are summarized.
Page 33
Although lead-based paint and paint-contaminated
dust account for most cases of childhood lead poisoning
in the United States, other sources of lead will also
have to be addressed.
The Environmental Protection Agency (EPA) is evaluating the need for more stringent
standards for lead in drinking water and air. EPA is also conducting a demonstration
project in three cities to evaluate the benefits of removing lead-contaminated soil from
yards of homes where children live.
The Food and Drug Administration (FDA) has proposed new regulatory standards for
lead in ceramic pitchers and other types of ceramic foodware. FDA is also attempting to
identify sources of lead in the diet other than those that have already been identified,
such as lead in wine bottle cap wrappers and in calcium supplements. Mechanisms
should be established so that potters and other crafts people either clearly indicate that
their wares are not for food service or have their wares tested to ensure that they do not
contain lead.
In coordination with FDA, domestic manufacturers of food cans have markedly reduced
their use of solder with a high lead content. This change has resulted in large reductions
in the lead levels in canned foods in the United States. Nevertheless, a total ban on the
use of solder with high lead content in domestically produced canned goods should be
seriously considered. The frequency of use of solder with high lead content in imported
food cans is unknown; a ban on the use of solder with high lead content in imported
food cans should also be considered.
Childhood exposures from parental occupations and hobbies involving lead should be
reduced. This can be done through a combination of good work practices and education.
The use of folk remedies containing lead continues to be a problem in certain ethnic
populations. Educational activities, intensified lead screening, and intervention strategies
could reduce exposure to this source of lead.
Page 34
PROGRAM AGENDA ITEM 4. NATIONAL SURVEILLANCE FOR ELEVATED
LEAD LEVELS
USES OF SURVEILLANCE DATA
To target interventions
To track progress
To evaluate worker exposures
The only national data available for estimating the number of children who may have
elevated blood lead levels are derived from national surveys of nutritional and health
status that, in the past, have been conducted about once a decade. These data are
extremely valuable for providing unbiased estimates of the blood lead levels of children
and workers in the United States. In the future they will be conducted more often, and
this will make it possible to evaluate national and regional blood lead levels more
frequently. As these data are now collected, however, they cannot be used to monitor
short-term trends over several months or a few years. They cannot be used to
characterize geographic distributions of poisoning in the community of to target
interventions where they are most needed. A national surveillance program for elevated
blood lead levels in children and workers is essential for the development of a “lead
priority list™ for targeting interventions, for tracking our progress in eliminating childhood
lead poisoning, and for evaluating lead exposure in abatement workers and workers in
other lead-contaminated environments.
Several sources of data could be used for surveillance. These include childhood lead
poisoning prevention programs, other government programs that conduct or reimburse
for screening for lead poisoning, and laboratories that perform blood lead testing.
The development of better systems for managing data in childhood lead poisoning
prevention programs should be a high priority. Data from childhood lead poisoning
prevention programs could be extremely important for evaluating the yield of screening
in specific areas, the yield of alternative screening strategies, and the efficacy of
interventions. Since screening takes place in only limited geographic areas, however,
data from screening programs cannot provide national information. Furthermore,
although many areas that need targeted abatement programs could be identified through
screening data, areas that have no screening programs cculd not be evaluated. In
addition, many large programs have not yet computerized their data, and those computer
systems that exist are often cumbersome or cannot link data on screening and medical
follow-up with data on environmental investigations and interventions.
Data from other government programs conducting or reimbursing for screening, like
EPSDT. could also be useful, but these data have serious limitations. They would
provide information on only a small segment of the population being tested for lead
poisoning. and they would not include follow-up data.
The optimal model for national surveillance is the notifiable disease system that CDC
has used since 1961. Through this system, cases of illnesses are reported electronically to
CDC by State epidemiologists. Since lead poisoning is diagnosed on the basis of
laboratory tests, reporting for lead would depend upon laboratories sending their data on
persons with elevated blood lead levels to State health departments for transmission to
CDC. The State health department would also be responsible for ensuring that multiple
tests on the same individual are identified as such and that persons needing follow-up
are referred appropriately. An evaluation component is essential for determining that
the data collected are complete and representative. The Amencan Academy of
Pediatrics, the American Medical Association, and the Council of State and Temtonal
Epidemiologists have endorsed the development of such surveillance.
Page 36
KEY ORGANIZATIONS ENDORSING
NATIONAL SURVEILLANCE
® American Academy of Pediatrics
@ American Medical Association
® Council of State and Territorial
Epidemiologists
The feasibility of developing national surveillance for elevated lead levels is illustrated by
the National Institute for Occupational Safety and Health (NIOSH) efforts to develop a
_ system for reporting elevated blood lead levels in workers. NIOSH receives reports from
eight State health departments that provide data about numbers of workers with elevated
blood lead levels and industries in which lead poisoning is occurring. The States with
surveillance systems also ensure follow-up of the affected workers. In 1988, 4,804
workers in seven States were reported to have blood lead levels > 25 ug/dL.
Page 37
CHAPTER 5. RESEARCH AGENDA
meer. gu Wwe a . - PUTS rT ap - ih My ad, vai Et -, iar PEL I ons LR GT reas: nl C agh a EIR END 2T % oe a ha a nelae Ee. 3 - .
nS a NT Se i Te et Ea RT pT SAND dah ms ty 2 A at ene oT i Re CSS I ep A ny Sa Te SSS i SN LH > >
BC Sl A LA a Da ON er 03 Ea a Tr a Be a Th Ae A BIT ip A Tem BI EE SO Spe aos ral LTS Y
RESEARCH [IS NEEDED FOR
© [INCREASED PREVENTION ACTIVITIES
INCREASED ABATEMENTS
® REDUCTIONS IN OTHER SOURCES
Enough is already known to start an effective campaign to eliminate childhood lead
poisoning, and intensified efforts to prevent this disease should get under way
immediately. There are, however, several questions that must be answered if this disease
is to be successfully eradicated in the most costeffective manner. The following are key
elements of a research agenda designed to provide essential information for future years
of a program to eliminate childhood lead poisoning. Many of these elements appeared
in the Committee to Coordinate Environmental Health and Related Programs ad hoc
committee report on the implementation of the ATSDR report to Congress.
Page 38
The results of basic research have shown the
need for a strategic plan for the elimination
of childhood lead poisoning.
This research agenda does not include a discussion of or a budget for many basic
research activities. Such activities include evaluating the amount of lead absorbed by
children and adults, identifying new biomarkers for lead exposure, and determining the
impact of pharmacological treatment of lead poisoning on children’s cognitive
functioning. Although these activities are not essential for the first 5 years of the
Strategic Plan, they are important. The findings of basic research have made a plan such
as this necessary, and they make it possible to develop a program agenda at this time.
These research activities should receive financial support
RESEARCH AGENDA ITEM 1. RESEARCH FOR CHILDHOOD LEAD POISONING
PREVENTION ACTIVITIES
RESEARCH FOR INCREASED CHILDHOOD LEAD
POISONING PREVENTION ACTIVITIES
Cost-effectiveness of screening strategies
Better instruments for blood lead testing
Evaluation of capillary blood collection
devices
Evaluation of educational and nutritional
interventions
A A ON SP A OS RAE RE POT HES
Studies should be conducted on the cost-effectiveness of different strategies for
childhood lead screening. These strategies include screening in inner-city emergency
rooms to reach children who have no ongoing source of care and “cluster testing” of all
children in multiple dwelling units where cases of childhood lead poisoning have been
identified. The usefulness of screening in day care centers and nursery schools should
also be evaluated. In addition, Federal programs now funding childhood lead screening
should be evaluated to see how they can work together for a most efficient use of
resources.
At present it is much cheaper and easier to perform an EP test than a blood lead
measurement; however, the EP test is not a useful screening test for blood lead levels
below 25 ug/dL. Both because of the expected increase in screening and because of the
concem about the health effects of lower blood lead levels, the demand for blood lead
testing is likely to increase. The development of portable, easy-to-use, cheaper
instrumentation for blood lead measurement is extremely important.
Because capillary (or fingerstick) blood samples may be easily contaminated with lead on
the skin, venous blood must be used to confirm lead poisoning in children. Several
capillary blood collection devices now on the market purport to collect blood free of
surface finger contamination from lead. These devices should be evaluated for ease of
use and ability to collect an uncontaminated sample.
The education of families about lead poisoning by childhood lead poisoning prevention
programs often includes information about the importance of nutrition. Because of our
growing concem about the adverse effects of low blood lead levels, nutritional
interventions are likely to be recommended for more children. A number of nutritional
factors have been shown experimentally to influence the absorption of lead and its
concentrations in tissues. Intervention studies or clinical trials should be conducted to
establish that increasing the regularity of meals and ensuring adequate dietary intake of
iron and calcium can reduce blood lead levels.
Educational strategies for increasing medical care provider and public awareness of lead
poisoning should also be evaluated for their efficacy in reducing childrea’s blood lead
levels and preventing lead poisoning.
RESEARCH AGENDA ITEM 2. RESEARCH ON LEAD-BASED PAINT AND
PAINT-CONTAMINATED DUST ABATEMENT
RESEARCH ON ABATEMENT
Long-term follow-up postabatement
Efficacy of abatement methods
Better methods for measuring lead in paint
and dust
Evaluation of worker exposures
Abatement of forced air ducts, rugs,
furniture, etc. ud
Determination of safe ShYifamentl levels
The techniques recommended in the HUD Interim Guidelines have been shown to be
cffective in abating lead-based paint and reducing dust levels. However, no long term
evaluations have been conducted to ensure that dust lead levels and children’s blood
lead levels remain low once abated units have been reoccupied. Long-term follow-up of
units abated under these guidelines and their occupants should be conducted.
Few childhood lead poisoning prevention programs performn as rigorous an abatement as
that recommended in the HUD Inteom Guidelines. Better data on the long-term
efficacy of less stringent abatement methods should also be collected, and the
cost-effectiveness of alternative methods of lead-based paint abatement should be
evaluated. These analyses should be used to determine how best to spend resources,
Page 41
given that more complete and expensive abatements probably result in greater reductions
of blood lead levels but may result in fewer units being abated.
Current methods for measuring lead in paint and dust are sometimes inaccurate,
expensive, or both. Accurate, inexpensive methods for such measurements would
decrease the cost and increase the reliability of preabatement and postabatemement
testing. These methods include improved X-ray fluorescence (XRF) devices and
chemical spot tests. Preferred methods are those that can be used onsite, instead of
requiring offsite laboratory analysis, and those that do not destroy surfaces.
All abatement methods should be evaluated to determine worker exposures to lead and
other hazards. Laboratory and field studies should be conducted, when appropriate,
before new methods are recommended for widespread use, and they should include
evaluations of worker safety. HUD, EPA, and other agencies have already started some
of these evaluations.
Methods for abating such items as forced air ducts, rugs. and fumiture have not been
evaluated adequately. Furthermore, there is no consensus on whether such abatement is
appropriate. For example, discarding lead-contaminated rugs and upholstered fumiture
has been advocated.
Environmental lead levels used for determining whether a home needs abatement or if
an abated unit can be reoccupied are based on limited scientific data. These levels
should be evaluated to ensure that they are both adequate to protect health and do not
result in unnecessary abatements. Included in this work would be the paint lead
concentration at which paint abatement is recommended; the dust lead concentration at
which dust abatement is recommended, even in the absence of lead-based paint; and the
soil lead concentration at which abatement should occur. In addition, a system for
estimating the total lead hazard in a building or housing unit, combining information on
household demographics, paint lead concentration, quantity, and condition, and dust and
soil lead levels should be developed. The lead levels of paint, dust, and soil that are to
be considered safe after abatement should be evaluated. One important outcome of this
work would be algorithms for identifying which housing units are most likely to poison
children in the future.
Because of the limited money available for abatement, imexpensive interim methods must
be developed and evaluated for preventing children from being exposed to high
environmental lead levels in units awaiting abatement. Such interventions may include
regular professional cleaning with high-efficiency vacuum cleaners and scraping and
repainting small areas of peeling paint. Outcome measurements should include
measurement of lead in house dust and children's blood Such preventive maintenance
strategies should be evaluated over several years.
Page 42
RESEARCH AGENDA ITEM 3. RESEARCH ON REDUCTIONS IN OTHER
SOURCES AND PATHWAYS OF LEAD EXPOSURE
RESEARCH ON REDUCTIONS IN OTHER
SOURCES AND PATHWAYS
Relative contributions of different sources
Cost-effectiveness of soil abatement
Drinking water lead levels and treatments
Sources of dietary lead
Improved food lead measurement
Bioavailability | on
Mobilization of lead during pregnancy
Studies should be conducted to determine the relative contributions of various sources
and pathways of lead to children’s blood lead levels. These studies should also
investigate the relationship between lead in the various environmental compartments to
which children are exposed. Sources and pathways to be investigated should include
paint, dust, soil, air, food, water, and exposure from parental occupations and hobbies.
Current methods for remediating soil are expensive, and their efficacy under varying
conditions has not been proven, particularly in urban areas. Studies should be conducted
to examine the efficacy and costeffectiveness, in terms of blood lead level reductions, of
various methods of remediating soil (such as removing soil and planting ground cover).
These efforts should complement EPA’s ongoing efforts.
Page 43
Lead levels in drinking water in the United States, including levels in water fountains,
should be assessed more completely. Alternative treatment approaches aimed at
reducing lead in drinking water should be evaluated.
While a great deal is known about many dietary sources of lead, others have not been
identified or evaluated. Lead in calcium supplements is of particular concern because of
the many pregnant women taking these preparations. Other inadequately studied
sources of lead include wine (from lead in the wine itself or in caps or seals), coffee
produced in institutional coffee ums, infart foods, and bottled waters. Surveys of lead
ingested by special populations should also be conducted. These surveys should focus on
canned foods, housewares, and folk remedies used by special populations, such as ethnic
groups. For these evaluations, analytical procedures will have to be improved.
The bioavailability of lead probably varies according to the substrate (for example, paint,
dust, sol, food) and the chemical form and particle size of the lead. Criteria for cleanup
may need to vary according to the probable bioavailability of lead at a given site.
Animal feeding studies and collection of data on human populations are needed to
provide information on how bioavailability issues should be considered when decisions
on remediation and clearance are made.
Studies should be conducted on the mobilization of bone stores of lead during pregnancy
and on the biokinetics of fetal lead exposure. If bone stores prove to be an important
determinant of blood lead levels during pregnancy, interventions to reduce lead
mobilization in pregnancy should be developed and studied.
Page 44
CHAPTER 6. FUNDS NEEDED FOR IMPLEMENTATION OF THE
STRATEGIC PLAN
SUMMARY OF FUNDS PROJECTED TO BE NEEDE
FOR THE FIRST 5 YEARS OF THE STRATEGIC PLAN*
(millions of dollars)
Increased childhood
lead poisoning
prevention activites
$164.68
5
£.
Increased
abatement
$729.95
Research
$61.55
Fa
x 2
L : =
>
-*
National
surveillance
$18.10
os Sar SRE oA Tm ER
*Costs reflect the amount of money needed to implement the program agenda and a
shared commitment of the public and private sectors.
Our estimate of the cost of implementation for the first S years of the Strategic Plan is
expected to be $974 million. Ninety-four percent of this money is for program activities
six percent is for research. The source of funds is not discussed m this report; these
costs reflect a shared commitment of the public and private sectors.
Page 45
Funds Needed for Implementation of the Program Agenda
Implementation of the program agenda will require the efforts and cooperation of many
Federal, State, and local agencies. The first five years of this agenda will cost $913
million. This budget does not include funds for program activities needed to reduce
sources and pathways of exposure other than lead-based paint and paint-contaminated
dust. Many of these are already being addressed through Federal and other actions.
The estimate of the additional costs for increased abatement requires further discussion.
Because of the lack of baseline data, it is difficult to project how many more housing
units should be abated as part of a strategic plan to eliminate childhood lead poisoning.
Furthermore, development of cheaper abatement methods and of an infrastructure for
abatement is an essential part of the first years of any national abatement strategy.
Therefore, a phased increase in the number of abatements performed is proposed, with
an emphasis on research and development and the testing of strategies and materials in
the first 2 years of the program. Within 3 years, resources should be made available to
perform 20,000 to 30,000 more abatements annually than are currently being performed.
These resources would be enough to abate the homes of all lead-poisoned children
currently being identified by childhood lead poisoning prevention programs who have no
other source of funding for abatement. (As the amount of screening increases, the
estimate of additional units to be abated annually will also need to be increased.) These
resources would also make it possible to have demonstration projects and to abate units
in the second priority group, homes that have a large potential for poisoning children.
At this rate, eliminating all lead paint from housing stock in the United States will take a
long time, but it is important to make a start--to eliminate lead-based paint from those
units that have the greatest potential to adversely affect health.
The costs of abatement vary greatly according to the size and kind of housing unit, the
region of the country, and other factors. For this plan, we assumed that an average
abatement costs around $6,500. This estimate was developed by Anne Elixhauser,
Battelle, under a contract with CDC through interviews with screening programs. (The
abatement methods used in the three studies whose data form the basis of the benefits
anulysis and the cost-benefits analysis in Appendix II were much cheaper and less
comprehensive; however, data are not available on how much blood lead levels might be
reduced by more expensive methods. We assume that the reduction would be
correspondingly greater. Information on the costs and benefits of abatement will need to
be continually updated as new information becomes available.) Thus, the abatement of
20,000 to 30.000 units a year could be expected to cost around $130 to $195 million a
year. Since it will take a couple of years to build up the infrastructure for abatement
and increase the number of abatements performed, we estimate that the increased
abatements needed to complete the first 5 years of this Strategic Plan would cost a total
of $710 million. The unit cost of abatement is likely to decrease over the next several
years as new abatement methods are developed and the infrastructure for abatement
increases.
Increasing the amount of abatement conducted will also require development of a
national abatement plan and infrastructure development, as described in Chapter 4. We
estimate that the costs of such development work will be between $3 and 6 million a
year for the first 5 years of the Strategic Plan, and will total $19.95 million over $ years.
Following are detailed budgets for increased childhood lead poisoning prevention
activities and national surveillance.
PROJECTED ADDITIONAL COSTS PER YEAR FOR INCREASED
CHILDHOOD LEAD POISONING PREVENTION ACTIVITIES* ——
Cost per Year Total
(millions of dollars) Cost
Year 1 2 3 4 5
Increased funding for programs 25 25 25 35 45 155
Increased screening through
EPSDT, WIC, and Head Start 025 025 025 0.25 025 1.25
Educational materials and
ouireach 0.5 0.3 0.01 0.01 0.01 0.83
Federal campaign to increase
awareness 8.3. '05 05 05.065 125
Clearinghouse 0,75. 05 02 07 005 16
Infrastructure development for
prevention activities 1.5 0.8 0.8 0.2 0.2 35
Total 28.50 27.35 26.76 36.06 46.01 164.68
eT ht onthe —————. TT Tn PE TERS 5h mint >
*Costs reflect the amount of money needed to implement the program agenda and a shared commitment of the public and private sectors. |
PROJECTED ADDITIONAL COSTS PER YEAR
FOR NATIONAL SURVEILLANCE*
(millions of dollars)
6.00
5.00
4.00
3.00
2.00 Develo pment
of surveillance
systems
1.00 Be
Evaluati
of ies
systems
0.00
*Costs reflect the amount of money needed to implement the program agenda and a
shared commitment of the public and private sectors.
Funds Needed for Implementation of the Research Agenda
Implementation of the research agenda will cost $62 million. The next three tables
summarize the budgets for the three main categories of research needed to support the
program agenda.
PROJECTED ADDITIONAL COSTS PER YEAR FOR RESEARCH FOR
CHILDHOOD LEAD POISONING PREVENTION ACTIVITIES*
Cost per Year
(millions of dollars)
Year 1 2 4
Cost-effectiveness of alternative
screening strategies 0.5
Capillary collection
evices
New instrumentation for
measuring blood lead levels
Nutritional interventions
Educational strategies
- Total
II Ea HOHE lS RTT FEERS ER I ES TE
*Costs reflect the amount of money needed to implement the research agenda and a
shared commitment of the public and private sectors.
Page 49
PROJECTED ADDITIONAL COSTS PER YEAR FOR
RESEARCH ON ABATEMENT?
Cost per Year
(millions of dollars)
Efficacy of abatement
AHlernative abatement methods
Measurement of lead in paint
and dust
Worker exposure studies
Abatement of air ducts, etc.
Safe levels of lead in paint,
dust, and soil
Preventive maintenance
*Costs reflect the amount of money needed to implement the research agenda and a
shared commitment of the public and private sectors.
ee
PROJECTED ADDITIONAL COSTS PER YEAR FOR RESEARCH
ON REDUCTIONS IN OTHER SOURCES
Cost per Year
(millions of dollars)
Sources of children's exposure
Cost-effectiveness of soil abatement
Drinking water lead levels
Treatment for lead in water
Sources of dietary lead
Food lead measurement
Bioavailability studies
Lead biokinetics in pregnancy 05 034"
Total : 565 4.5 275 28.7
EEG RETR
*Costs reflect the amount of money needed to implement the research agenda and a
shared commitment of the public ana private sectors.
CHAPTER 7. SUMMARY OF RECOMMENDATIONS
In summary, childhood lead poisoning is a preventable discase with a huge societal cost.
This plan outlines several steps that must be taken to eliminate sources of lead exposure
for children. These steps will require a combination of government financial assistance
and strategies to maximize the role played by the private sector.
The most urgent elements of the plan are the following:
) Increased childhood lead poisoning prevention activities —These activities are
essential to identify poisoned children and assure appropriate interventions are
conducted. They are also important for targeting neighborhoods that need more
intensive, communitywide interventions for preventing lead poisoning.
0 Increased abatement --A nationwide lead-based paint abatement program must be
designed that will maximize the number of children benefited, given the fixed
resources for abatement, using safe and effective methods.
0 Reductions in other sources and pathways--Ongoing efforts to limit children’s
exposure to lead from water, food, air, soil, and the workplace require continued
attention.
0 Surveillance —A national surveillance system for elevated blood lead levels should
be developed for tracking progress in eliminating childhood lead poisoning,
identifying areas in need of further evaluation or interventions, and evaluating
exposures of persons performing abatement and other workers.
0 Research - Research on lead should focus on developing and evaluating
cost<ffective methods for screening children, testing paint and dust for lead, and
reducing the sources of lead to which children can be exposed as much as
possible.
Agency for Toxic Substances and Disease Registry (ATSDR). 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, 1988.
Bellinger D, Sloman J, Leviton A, Rabinowitz M, Needleman H, Watemaux C. Low-
level exposure and children’s cognitive function in the preschool years. Pediatrics
1991:57:216-22].
Centers for Disease Control (CDC). Preventing lead poisoning in young children: a
statement by the Centers for Disease Control. Adanta: U.S. Department of Health and
Human Services, 1985; CDC report no. 99-2230.
Environmental Protection Agency (EPA). Air quality criteria for lead. Research
Triangle Park, N.C.: Office of Health and Environmental Assessment, 1986; EPA repon
no. EPA/600/8-83/028aF.
Kennedy FD. The childhood lead poisoning prevention program: an evaluation. A
report for the Centers for Disease Control. 1978.
Levin R. Reducing lead in drinking water: a benefit analysis. Washington, DC:
Environmental Protection Agency. 1986; EPA report no. 230-09-86-019.
Needleman HL, Schell A, Bellinger D, et al. The long-term effects of exposure to low
doses of lead in childhood: an 11-year follow-up report. N Engl J Med 1990;322:83-8.
Rosen JF, Markowitz ME, Bijur PE, et al. Sequential measurements of bone lead
content by L-X-ray fluorescence in Ca, EDTA treated lead-toxic children.
Environmental Health Perspect (in press).
APPENDIX 1
LEAD EXPOSURE AND ITS EFFECTS ON CHILDREN
AND FETUSES
The problem of human exposure to lead has been extensively studied, probably more
than exposure to any other toxic substance. For public health policy, the following
summary findings are especially important:
0 Lead is an extremely dangerous and pervasive environmental poison.
0 Today, far too many children are still exposed to excessive levels of lead: most
recent national estimates indicate that in 1984, between 3 and 4 million children
had lead in their bodies at levels which justify significant public health concem
and which have been associated with neurobehavioral and other adverse health
effects.
0 Our children have not been effectively protected from the major sources of lead
exposure—especially leaded paint and lead-contaminated dust and soil.
LEAD EXPOSURE
Lead has some unusual characteristics that cause special concem. First, lead deposited
in the environment remains there and accumulates. Therefore, lead distributed in the
areas where we live from paint, gasoline, and stationary Sources remains there. As long
as lead continues to be added to our environment, more lead will accumulate.
Second, lead exposure 1s pervasive, sparing no socioeconomic segment of the United
States. Since lead is dispersed into air, food, soil, dust, and water, children of all
socioeconomic backgrounds in all geographic . areas experience unacceptably high lead
exposures. Overall, children living in or around old, dilapidated inner city housing are at
highest risk for lead poisoning.
Third, lead accumulates over months and years in the bodies of children. Therefore,
chronic exposure to small amounts of lead can lead to a large long-term accumulation in
a child, increasing that child's risk of adverse health effects. In addition, it is believed
that, during pregnancy, women's body lead stores may be mobilized, exposing the fetus to
lead. Therefore, childhood exposures in one generation may result in prenatal exposure
for the next generation.
APPENDIX 1- PAGE 1
Measurement of Lead Exposure
All Americans are exposed to some amount of lead. The amount of exposure has most
often been quantified by measuring lead in blood (common units are ug/dL). Lead in
blood reflects exposure during the previous weeks or months, whereas bone (or tooth)
lead is a measure of cumulative lead exposure over months and years.
In most studies of the health effects of lead, measurements of outcome (such as IQ or
behavioral changes) have been compared with blood lead measurements, and most
public health decisions have been based on blood lead levels. Developing more practical
methods to measure bone lead may substantially increase the use of such methods 1n
assessing lead exposure; but at present, blood lead measurements remain the most
generally used method of assessing human exposure to lead. The current definition of
childhood lead poisoning is a blood lead level >25 ug/dL with an erythrocyte
protoporphyrin (EP) level >35 ug/dL (Centers for Disease Control, 1985). This
definition is currently being reevaluated, and the blood lead level will be revised
downward to the level of 10-15 ug/dL.
Sources and Pathways of Lead Exposure
Children are exposed to lead from multiple sources such as paint, gasoline, solder,
batteries, and stationary Sources via multiple pathways such as air, dust, dirt, water, and
food. The distinction between SOUICES and pathways 1s not always clear. For example,
dust and dirt are pathways for lead exposure. Because so much lead has been deposited
in dust and dirt, they are sometimes also considered sources of lead exposure. In
addition, in some discussions of lead exposure, water, food, and air are classified as
sources of lead, although lead in these media comes almost totally from other sources.
The important public health point is that lead comes from known sources and moves
through and is deposited in identified pathways to enter children. Although accurately
tracing lead through all the complex pathways once it has left the source (e.g. leaded
paint on a wall) may be difficult, it is not difficult to establish that reducing the amount
of lead coming from the source will reduce the amount of lead going nto children. For
example, it is difficult to accurately trace all the pathways by which lead from gasoline
enters children. Nonetheless, children’s blood lead levels are well-correlated with
gasoline usage pattems, and these levels have fallen dramatically in response to the
reduction of lead in gasoline.
Children are exposed, therefore, when lead moves from its source through environmental
pathways to be ingested or inhaled by a child. Reducing the amount of lead coming
from these primary sources of lead (e.g. leaded paint on 2 wall) will reduce children’s
exposure to lead.
APPENDIX 1 - PAGE 2
¢ +7
\ 4 L
For the fetus, exposure comes from the mother's blood lead burden. The placental
barrier is not effective in stopping lead from crossing over to the fetus (ATSDR, 1988).
Generally, prenatal exposure is assessed by measuring the mother’s blood lead level.
The role of mobilization of maternal bone lead stores in prenatal exposure is yet to be
determined.
For an individual child, the particular environment in which the child lives determines
the relative importance of each lead source. For example, for a child living in a home
with deteriorating lead paint, the paint will almost certainly account for a significant
portion of exposure.
Although the immediate environment determines the importance of various lead sources
for an individual child, estimates can be made of the overall relative importance of lead
sources to U.S. children as a group. The Agency for Toxic Substances and Disease
Registry (ATSDR) recently reviewed the available information on childhood lead
exposure by source. The following are ATSDR's estimates of the number of children
exposed by lead source (ATSDR, 1988). As noted in that report, these estimates are
based on the best available information, and the estimation errors are difficult to
quantify. The assumptions involved in the calculations differ for each source. Some
numbers are for children potentially exposed and some for children actually exposed.
Lead in paint: Currendy, leaded paint is the source of greatest public health concem. It
is the most common Cause of high-dose lead exposure. Exposure occurs not only when
children ingest chips and flakes of paint (which often contain as much as 50% lead by
weight) but also when children ingest lead paint-contaminated dust and soil, usually
during normal mouthing activities. ATSDR has assessed that existing leaded paint in
U.S. housing and public buildings .s "an untouched and enormously serious problem.”
About 13.6 million children under 7 years of age are potentially exposed in their homes
to paint that contains lead at concentrations of 0.7 mg/cm? or higher. About 1.8 t0 2.0
million children live in housing with unsound lead-based paint (e.g. holes in walls,
peeling paint), which places them at high risk of excessive lead exposure; about 1.2
million of these children are estimated to have blood lead levels above 15 ug/dL, mainly
due to exposure to leaded paint.
Lead-based paint abatement has been an essential part of all lead poisoning prevention
programs in high-risk areas, despite cost constraints which limit the extent of such
abatements. Historically, many studies have shown that the risk of lead poisoning 1s
related to the presence of lead-based paint, and also to deteriorated or dilapidated
housing (Gilbert et al, 1979); lead in dust is undoubtedly an important pathway for such
exposures. Bomschein et al. and Chisholm have shown that children living in of
retuming to rehabilitated lead-free or lead-reduced housing after medical treatment for
lead poisoning have significantly lower lead levels than children living in similar,
non-rehabilitated housing (Bornschein et al., 1986; Chisholm, 1988). Three studies cited
APPENDIX 1 - PAGE 3
25
VL
in Appendix II demonstrate decreased blood lead levels in children with lead poisoning
after the abatement of lead-based paint in their homes. (There may also be additional
input to dust lead from lead in outdoor soil. Exposure to soil lead may occur from direct
exposure to soil of indirectly as a result of its contribution to dust lead indoors. Lead in
soil may arise from past usc of exterior lead-based paint or from other external sources
(see below). The value and role of soil abatement in addition to lead-based paint and
dust abatement are currently being investigated in an Environmental Protection Agency
(EPA) demonstration project; this issue will probably not be clarified for at least several
years.)
Lead in gasoline: Since the introduction of lead as a gasoline additive in the mid-1920s,
millions of tons have been used for this purpose (EPA, 1986). The recent reduction in
the amount of lead in gasoline In the United States has been of major benefit to
children. In the 13 years between 1976 and 1989, the amount of lead used in gasoline
was reduced by more than 99% (EPA, 1990). Because of this, the blood lead levels in
the U.S. population have decreased substantially.
Lead from primary and secondary smelters: About 230,000 children live near enough to
a primary or secondary smelter to be exposed to lead from that source. Up to 13,000 of
these children are estimated to bave blood lead levels above 20 ug/dL from exposure to
smelting by-products.
Lead in drinking water: In the United States, lead in water comes predominantly from
lead in plumbing such as lead-soldered joints in copper Pipes. The EPA maximum
contaminant level (MCL) for lead is currently SO ug/L. EPA estimated that in 1988,
about 3.8 million children were exposed to water with a lead concentration higher than
20 ug/L. In 1988, EPA proposed that the allowable level for lead in drinking water be
reduced. A revised lead standard is currently under consideration.
Lead in food: EPA estimated that about 42% of lead in food comes from lead-soldered
cans or other metal sources, about 45% is deposited from the atmosphere, and the
remainder comes from unidentified sources (EPA, 1986). Thus, almost 90% of lead in
food comes from sources external 10 the food. Because of major decreases in the
production of lead-soldered food and beverage cans and decreases in air lead levels due
to decreases in gasoline lead, food lead levels are declining. The most obvious means of
reducing lead in food is to reduce further lead in soldered cans and reduce lead
emissions into the air (this has essentially been accomplished for mobile sources, ie.
automobiles, but not yet for stationary SOUICES, such as smelters, incinerators, and other
industrial sources).
I ead in dust and soi}: Dust and soil act as a pathway to children for lead deposited by
primary lead sources such as leaded paint, leaded gasoline, and stationary lead emitters.
Since lead does not dissipate, biodegrade, or decay, the lead deposited into dust and soll
becomes a long-term source of lead exposure for children. For example, although lead
APPENDIX I - PAGE 4
®
1
!
emissions from gasoline are much reduced, gasoline lead deposited in years past remains
in the dust and soil, and children continue to be exposed to it. The samc is true for
lead-based paint used in previous years. ATSDR (1988) has concluded that the “actual
number of children exposed to lead in dust and soil at concentrations adequate 10
clevate blood lead levels cannot be estimated with the data now available.”
Other sources and pathways of lead exposure: Several other sources and pathways are
also important Causes of elevated lead levels in many populations. These include lead in
ceramic ware, folk remedies, hobbies or craftware, and childhood exposure to lead
brought home by parents from their workplaces. As battery recycling increases, €Xposufc
to lead from this activity should be limited by control of emissions and lead levels in the
workplace.
ADVERSE EFFECTS OF LEAD EXPOSURE
The adverse health effects on children from exposure to lead are a major public health
concern. The risks associated with many chemicals, especially carcinogens, are extremely
uncertain; for such chemicals, conservative approaches are used to extrapolate risks from
animal or human occupational studies to estimate the upper limit of the risk posed to
children and other populations. The adverse effects and risks of lead are well-known
from studies of children themselves, and risk assessment calculations, with their inherent
uncertainties, are not needed. Moreover, environmental lead levels in the United States
provide no margin of safety to protect children; this 1s well-illustrated by the large
number of children with lead levels in the toxic range. These effects of lead have been
reviewed elsewhere in detail (ATSDR, 1988; EPA, 1986; EPA, 1989) and are only briefly
summarized in this discussion.
High levels of lead in the body cause encephalopathy manifested by convulsions, mania,
confusion, somnolence, or coma, if untreated, lead poisoning often results in death.
Encephalopathy has been reported in persons with blood lead levels as low as 80 ug/dL
(EPA, 1986). Since blood lead levels of 80 ug/dL can cause frank encephalopathy, it is
not surprising that lower levels cause adverse effects on the central nervous system. In
addition, lead affects the kidrzy, reproductive system, hematopoietic system, and virtually
all other systems of the body.
Particularly disturbing are the following effects of lead exposure: 1) neurobehavioral
effects of lead (including electrophysiologic changes) that occur at blood lead levels at
least as low as 10 to 15 ug/dL; 2) reduced gestational age and reduced weight at birth
that occur at levels at least as low as 10 to 15 ug/dL; 3) reduced growth rates up 10 7 to
8 years of age that occur at levels at least as low as 10 to 15 ug/dL: 4) effects on heme
metabolism starting at levels of about 15 to 20 ug/dL; and 5) effects on vitamin D
APPENDIX 1-PAGE 5
metabolism starting at levels of about 15 to 20 ug/dl. (ATSDR, 1988; EPA, 1986; EPA,
1989). Some studies have even indicated effects at levels below 10 ug/dL; some effects
appear to have no threshold. Millions of children have blood lead levels above or near
these values.
In addition, studies on health effects of lead exposure during the past 20 years have
produced a consistent trend: the more that is learned about lead's effects on children
and the fetus, the more concem is generated by lower and lower blood lead levels. The
lowest observed adverse effect level (LOAEL) continues to drop. Blood lead levels
formerly considered safe, or without adverse effect, have now been clearly associated
with adverse effects.
Although other health effects are of significant concem, 2 dominant focus of recent
studies of lead is the effect of lead on central nervous: system cognitive function (e.2.,
intelligence). When the results are viewed collectively, a ceries of both prospective and
cross-sectional studies provide persuasive evidence of lead’s effects on children’s
cognitive function at blood lead levels as low as 10 ug'dL (ATSDR, 1988; EPA, 1986;
EPA, 1989). Blood lead levels of 10 ug/dL and above at age 2 years have been shown
to result in a reduction of the General Cognitive Index at age 57 months. Most of the
children studied had blood lead levels below 15 ug/dL (Bellinger, 1991). Although
researchers have not yet fully defined the impact of blood lead levels <10 ug/dL on
central nervous system function, it. may be that even these levels are associated with
adverse effects that will be more clear as our research mstruments become better. If
there is a threshold for lead’s effects, it is near zero.
In a recent long term follow-up study (Needleman, 1990), for children exposed to
moderate lead levels during preschool years, the odds of dropping out of high school
were seven times higher and the odds of a significant reading disability were six times
higher than for children exposed to lower lead levels. In addition, these children had
lower class standing, increased absenteeism, and lower vocabulary and
grammatical-reasoning scores, even after controlling for other covariates. The magnitude
and persistence of these impacts on ability to leam and perform well in school suggest
that lead exposure may have a significant deletencs effect on how well a child will
function in society.
REFERENCES
Agency for Toxic Substances and Disease Registry (ATSDR). The nature and extent of
lead poisoning in children in the United States: a report to Congress, 1988. Atlanta:
U.S. Department of Health and Human Services, 19838.
APPENDIX 1-PAGE 6
Bellinger D, Sloman J, Leviton A, Rabinowitz M, Needleman H, Watemaux C. Low-
level exposure and children's cognitive function in the preschool years. Pediatrics
1991;57:219-2217.
Bomschein RL. Succop PA, Krafft KM, et al. Exterior surface dust lead. interior house
dust lead and childhood lead exposure in an urban environment. In: Hemphill DD, ed
Trace substances in environmental health. Columbia, Mo: University of Missouri, 1986:
322-32.
Centers for Disease Control (CDC). Preventing lead poisoning in young children: a
ctatement by the Centers for Disease Control. Atlanta: U.S. Department of Health and
Human Services, 1985; CDC report no. 99-2230.
Chisholm JJ, Jr. Interrelationships among lead in paint, housedust, and soil in childhood
lead poisoning: The Baltimore experience. In, Davies BE, Wixson BG, eds. Lead In
soil: issues and guidelines. Northwood, U.K.:Science Reviews Limited, 1988: 185-93.
Environmental Protection Agency (EPA). Air quality criteria for lead. Research
Triangle Park, N.C. Office of Health and Environmental Assessment, 1986; EPA repon
no. EPA/600/3-83/028aF.
Environmental Protection Agency. Lead in gasoline (Quarterly summary of lead
phasedown reporting data), March 8, 1990.
Environmental Protection Agency (EPA). Supplement to the 1986 EPA air quality
criteria for lead - volume 1 addendum. Research Triangle Park, N.C.: Office of Health
and Environmental Assessment, 1989; EPA report no. EPA/600/3-89/04%
Gilbert C, Tuthill RW, Calabrese EJ, et al. A comparison of lead hazards in the housing
environment of lead poisoned children versus nonpoisoned controls. J Environ Sci
Health 1979;A14(3), 145-68.
I evin R. Reducing lead in drinking water: a benefit analysis. Washington, DC: Office
of Policy, Planning and Evaluation, 1986: EPA report no. EPA/230/09-86/019.
Needleman HL, Schell A, Bellinger D, et al. The long-term effects of exposure to low
doses of lead in childhood: an 11-year follow-up report. N Engl J Med 1990;322:83-8.
APPENDIX I - PAGE 7
APPENDIX II
BENEFITS OF PREVENTING LEAD EXPOSURE IN THE
UNITED STATES AND COSTS AND BENEFITS OF
LEAD-BASED PAINT ABATEMENT
Lead exposure among U.S. children has been estimated to cost society billions of dollars
annually (e.g.. Levin, 1986). For this Strategic Plan, we have developed a new benefits
analysis, taking into account recent data on the effects of lead on children and fetuses.
In addition, we have developed an example of a cost-benefit analysis for the abatement
of lead-based paint in pre 1950 housing. We based this analysis on data from three
studies conducted between 1983 and 1988; information on the costs and benefits of
abatement will have to be continually updated as newer information becomes available.
The Departmeni of Housing and Urban Development and others are attempting to
develop new and more effective abatement practices.
THE BENEFITS OF PREVENTING LEAD EXPOSURE AMONG CHILDREN
AND FETUSES
This analysis will focus on the benefits of preventing exposure to lead among children
and fetuses. The benefits of reducing lead exposure of persons already being exposed
are likely to be substantial, but they are difficult to quantify. For example, we do not
know how long a child needs to have an elevated blood lead level to develop cognitive
deficits, although presumably longer durations of exposure have greater and possibly
more longlasting effects. Therefore, the benefits of reducing exposure in already-exposed
persons will not be included in the main portion of this analysis, although they will be
included in the sensitivity analysis. For purposes of this analysis, the benefits of
preventing exposure to lead in children and fetuses are the avoided costs that would have
been incurred had exposure occurred. The benefits for which we provide monetary
values are 1) reduction in medical care costs incurred by poisoned children, 2) reduction
in special education costs for poisoned children, 3) reduction in future lost productivity
due to cognitive deficits in children, and 4) reduction in neonatal mortality due to
prenatal lead exposure.
The above benefits are only a few of the benefits of preventing lead exposure. Many
benefits cannot be described in monetary terms, (e.g., avoiding the emotional costs to
families of having a lead-poisoned child). Other benefits, such as preventing lead’s
effects on children's stature, hearing, vitamin D metabolism, and blood production, will
not be explored in this analysis. The reason is not that they are unimportant, particularly
when summed over millions of children; rather, it reflects the absence of methods for
estimating appropriate monetary values for these effects. We also have not evaluated
the potential contribution of lead to juvenile delinquency (Needleman, 1989), the
administrative costs of personal injury lawsuits, the improvement in property values from
APPENDIX 5 - PAGE 1
improved housing conditions resulting from abatement, or the effects of lead on adults,
such as increased rates of hypertension, stroke, and cardiovascular disease. By not
including these effects, we grossly underestimate the costs of lead exposure to society.
The benefits evaluated in this analysis fall into two categories. The first category consists
of only the benefits that will be achieved for children whose blood lead levels are
prevented from rising above a certain threshold; avoided medical and special education
costs are estimated only for those children who would have had blood lead levels >25
ug/dL. These costs are presented as the average cost for each child in this category; the
figure derived takes into account that not all children with blood lead levels >25 ug/dL
will need chelation therapy or special education. The second category consists of
benefits of preventing increased blood lead levels in children no matter what their initial
levels are. For example, intellectual deficits result over a broad range of blood lead
levels. We estimated the avoided costs due to the effects of lead on intellectual
functioning for preventing increases of 1 ug/dL in blood lead level, regardless of the
child's starting blood lead level. The benefits of reducing maternal blood lead levels
(ie., decreased infant mortality) are also included in this latter category.
The Benefits of Preventing Children from Developing Blood Lead Levels >25 ug/dL
Medical costs: We assume, per the 1985 statement by the Centers for Disease Control,
Preventing Lead Poisoning in Young Children, that children identified with blood lead
levels >25 ug/dL. will receive medical attention. Estimates of the medical care these
children would need are based on data from Piomelli et al. (1984). We updated cost
data from the regulatory impact analysis prepared by the Environmental Protection
Agency (EPA) for reducing lead in gasoline (Schwartz et al., 1985) to 1989 using data
from the medical care component of the Consumer Price Index.
Follow-up tests and administrative expenditures for all children whose blood lead levels
are >25 ug/dL will total $148 per child. Previous benefit analyses have used data from
Piomelli et al. indicating that 70% of children with blood lead levels >25 ug/dL will
have erythrocyte protoporphyrin levels >35 ug/dL and will receive provocative disodium
calcium-edetate (EDTA) testing and follow-up. Provocative chelation requires a one-day
hospitalization and one physician visit and is assumed to cost $740. These same children
will require a further series of follow-up tests and physician visits totaling $444.
Five percent of children with blood lead levels >25 ug/dlL will receive chelation therapy
(Schwartz et al, 1985), requiring five days of hospitalization, several physician visits,
laboratory testing and a neuropsychological evaluation. Half of these (2.5%) will require
a second chelation therapy because their blood lead levels will rebound to >25 ug/dL.
Half of these (1.25%) will require a third round of chelation therapy. (Therefore, an
average of .0875 chelation therapies will be required for every child with a blood lead
level >25 ug/dL.) The cost of each chelation therapy is esumated to be $3,700.
APPENDIX II - PAGE 2
To estimate the average medical cost per child with a blood lead level >25 ug/dL, the
costs are multiplied by the associated probabilities by using the following equation:
AMC = PFU($FU) + PEDTA(SEDTA) + PCHEL(SCHEL)
= 1.0(3148) + 0.703740 + $444) + 0.0875(83,700) = $1,300
where AMC = Average medical costs for children >25 ug/dL
PFU = Probability of follow-up testing for children >25 ug/dL
SFU = Cost of follow-up testing
PEDTA = Probability of receiving provocative EDTA testing and
follow-up
$EDTA = Cost of EDTA testing and follow-up
PCHEL = Probability of receiving chelation therapy
SCHEL = Cost of chelation therapy
Therefore, the total medical cost that can be avoided by preventing a child from
developing a blood lead level above 24 ug/dL is $1,300.
Costs of special education: Children with high blood lead levels are more likely to have
decreased school performance and require reading or speech therapy or psychological
assistance. The costs of such treatment can be substantial. In a 3-year follow-up of
children with high and low blood lead levels, de la Burde and Choate (1975) reported a
relative risk of 7 for poor academic progress and a relative risk of 4 for repeating a
grade. In addition, they reported that cognitive effects persisted for at least 3 years.
Bellinger et al. (1984) reported that an excess of 17% of children with high blood lead
levels were receiving daily assistance outside the classroom. Needleman et al. (1990)
recently reported an odds ratio of 5.8 for reading disability among the children in their
high lead group. Lyngbye et al. (1990) reported an odds ratio for learning disability of
4.3 for children with tooth lead levels above 16 parts per million (ppm).
On the basis of these reports and previous benefits analyses (Schwartz et al, 1985), we
assume that 20% of children with blood lead levels >25 ug/dlL will require special
education (defined as assistance from a reading teacher, school psychologist, or other
specialist) for an average of 3 years. Costs for part-time special education have been
estimated by Kakalik et al. (1981) to be $5,827 per year (updated to 1989 by using the
Consumer Price Index). Becanse costs would be incurred over 3 years, costs in years 2
APPENDIX 1 -PAGE 3
[27
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i X
and 3 are discounted at 5% to the year special education begins. The average special
education costs for children with blood lead levels >25 ug/dL in year 1 are computed by
using the following equation:
ASEC = (PSEXSSE)
= (0.20%35,827) = $1,165
ASEC = Average special education costs
PSE = Probability of requiring special education
$SE Cost of special education
Discounting years 2 and 3 by 5% results in total special education costs of $3,331 per
child with a blood lead level >25 ug/dL.
The Benefits of Preventing a 1 ug/dL Increase in the Blood Lead Levels of Children
Most children with lead-related cognitive deficits do not require special education or
other assistance; however, their losses can still be substantial in monetary terms.
Impaired cognitive functioning and IQ decrements can reduce a person's productivity in
socicty. In this benefits analysis, we use this loss in productivity as a proxy for the cost to
society of cognitive impairment. This cost is clearly an underestimate because it puts po
value on the losses sustained by the individual that are not reflected by decreased
economic productivity. In addition, this analysis does not consider uneamed income
(c.g., interest, dividends), which would presumably be affected as the wage rate. We
assume for this analysis that the benefits of reducing lead exposure on the cognitive
functioning of children exhibit no threshold.
Figure 1 depicts the relationship between lead exposure and eamings. The first way lead
exposure affects earnings is through its effect on IQ.
Lead has a direct effect on cognitive functioning, as measured by changes in IQ (pathwzy
a). This reduction in IQ then has a direct effect on wage rate (pathway b), which affects
"When costs or benefits occur in the future, they should be adjusted by discounting. The
principle behind discounting is that there is a social as well as a personal preference fot
postponing costs and obtaining benefits as soon as possible. Therefore, dollars available
in the future are less valuable than those available today. Mathematically, discounting
future dollars can be thought of as the opposite of computing a retum on an investment
Discounting, therefore, has the effect of reducing the numerical value of benefits or costs
occurring in the future. For all calculations, we use a discount rate of 5% real (ie., 5%
above the rate of inflation).
APPENDIX IH - PAGE 4
lg
. »
lifetime camings. Lead also affects camings through its effect on educational attainment
by reducing IQ and by other effects, such as decreased attention span (pathway c). The
effect of educational attainment on eamings is traceable through two main pathways.
First, educational attainment 1s directly associated with wage rates and, therefore, with
lifetime eamings (pathway d). Second, educational attainment is also associated with
labor force participation (pathway e), which again has an effect on lifetime eamings.
The relationship between lead exposure and IQ (pathway a): Needleman and Gatsonis
(1990) reported on a meta-analysis of the recent studies associating lead exposure with
cognitive deficits. Although they reported only joint p values and partial r values, we
used this information to perform a meta-analysis on effect size. We computed the
estimated change in IQ for a 1 ug/dl. change in blood lead for the six studies for which
regression coefficients relating blood lead levels to IQ decrements were reported.
Weighting by the inverse of the variance of each estimate, we estimate that each 1 ug/dL
change in blood lead level results in a 0.25 point change in IQ.
The direct effect of IQ on wage rate (pathway b): A large body of literature exists on
the relationship between IQ and wage rate. For example, in studies that examined the
economic impact of increased schooling, it was important to control for differences in
IQ: thus, the marginal impact of IQ on wage rate was estimated. In a review of the
literature, estimates of the direct effect of IQ on wage rate (pathway b) ranged from a
0.2% to a 0.75% change in wage rate for each one IQ point change (Barth et al., 1984).
Structural equations modeling can be used to estimate the impact of multiple variables
on an outcome of interest. Griliches (1977) used structural equations modeling and
estimated the direct effect of IQ on wage rate to be slightly more than 0.5% per IQ
point. Because this method has conceptual advantages and 0.5% is roughly the median
estunate in the review by Barth et al. (1984), we used this value in these benefits
estimates. |
The impact of lead exposure on educational attainment (pathway ¢): From Needleman
et al. (1990) and Needleman and Gatsonis (1990), it is possible to estimate the change in
years of schooling attained per | IQ point change. The regression coefficients for the
effect of tooth lead on achieved grade in those studies provide an estimate of current
grade achieved, not of expected grade. Some of the children in those studies were,
however, in college at the time of data collection and were expected to attain a higher
grade. After adjusting the published results for the fact that a higher than reported
percentage of the children with low tooth lead were likely to be attending college, we
estimated a 0.59 year difference in expected maximum grade achieved between the high
and the low exposure groups. We assumed that educational attainment scales with blood
lead levels in proportion to IQ. The difference in IQ score between the high and the
low exposure groups was 4.5 points. By dividing .59 by 4.5, we estimate that, the increase
in blood lead level that reduces 1Q by one point, reduces years of schooling achieved by
0.131 years.
APPENDIX II - PAGE 5
ge3
=
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ir ert
Education and wage rate (pathway d): Studies that allow estimates of the relationship
between educational attainment and wage rate (pathway d) are less common than those
assessing the direct effects of IQ on wage rate. Chamberlain and Griliches (1977)
estimated that a one year’s increase in schooling would increase wages by 6.4%. In a
model with similar specifications, Olneck (1977) reported a 4.8% increase. In a
longitudinal study of 799 subjects for 8 years, Ashenfelter and Ham (1979) reported that
an extra year of education mxreased the average wage rate by 8.8%. We have taken 6%
as a reasonable and slightly conservative estimate of the effect of a year of schooling on
wage rate.
Education, labor force participation, and earnings (pathway e): In addition to affecting
wages, lead exposure is likely to affect participatton in the labor force for several
reasons. Labor force participation is correlated with failure to graduate from high
school, principally through higher unemployment rates and earlier retirement ages. Lead
exposure is also strongly correlated with arientica span deficits and other effects which
would also be likely to reduce labor ferce particpation.
The differences in labor force participation betwesn high school graduates and
nongraduates were obtained from an analysis of the data in the 1978 Social Security
Survey of Disability ‘and Work by Cropper and Krupnick (1989), which controlled for
age, mantal status, number of children, race, region, and other socioeconomic and
medical variables. We have estimated. using their regression coefficients, that average
participation in the labor force is reduced by 105% for persons who fail to graduate
from high school (pathway e). It is possible that this analysis overcontrols for other
factors in estimating the effect of schooling. For example, high school drop-outs are
more likely to have occupations with a higher nsk of disability, which was also included
as an independent variable in the regression analysis. Using the 1978 Current
Population Survey, stratified by age groups betwzen 25 and 65 years, we found that the
mean number of hours worked in the previous vear was 20% lower for persons with less
than a high school education than the number worked by those with a high school
education and those who graduated from high school. This difference results from
reduced participation in the labor force and reduced hours worked by participants, and
suggests that lead exposure sufficient to cause 2 1 IQ point decrease would decrease
expected earnings by about twice as much as repoited by Cropper and Krupnick. To be
conservative, we have used the results derived by using the regression models in Cropper
and Krupnick as the estimate in this analysis. Using the study of Needleman et al.
(1990), we estimate that lead exposure sufficient to cause a 1 point reduction in IQ
would result in a 4.5% increase i the risk of faillmg to graduate (pathway c’).
Lifetime earnings: Annual lifetime-eamings benefits achieved by preventing a 1 ug/dL
increase in a child’s blood lead level are computed as the net present value of the
increased earnings expected from preventing the mcrease, discounted to age 6. To
calculate the net present value of lifetime earings, a number of assumptions are
required. First, dollars available in the future must be discounted (see footnote, page 4).
APPENDIX II - PAGE 6
pt fe)
The second assumption is that the real wage growth in the future will be 1% per annum
from the 1987 distribution of incomes. (Historically, real wage rates have increased
approximately 2% per annum; however, in the last decade that growth rate has fallen.)
This assumption is conservative because (1) it assumes that the same percentage of the
work force will have a college education in the future as in 1987, and (2) it assumes the
1987 ratio of female to male eamings will remain unchanged, whereas the ratio has
increased from 0.6 to 0.7 in the past 15 years and is expected to continue to increase in
the future. On the other hand, this assumption is not conservative because it assumes
that women will participate m the labor force at the same rate as in 1987, whereas their
participation is likely to increase. If women continue to eam less than men, the real
overall wage rate may pot grow as quickly as 1% per year.
A third assumption made in calculating the net present value of lifetime eamings
concems labor force participation and the value placed on the productivity of
nonparticipants. Many adults do not participate in the work force at all during ther
potential working years. The largest group are women who remain at home doing
housework and child reanng. There is no consensus on how to put a monetary value on
this nonmarket productivity. Work in the home has been valued in economic studies by
using either the opportunity cost (the value of foregone income) or the market value of
substitute labor for this work. The opportunity cost is usually taken as the average wage
eamed by persons of the same age, sex, and educational level. This may be too high, as
the employed members of these cohorts tend to have more work experience, more
training, and more relevant education than those who remain at home. The estimate
based on the market value of substitute labor is often too low, as many of the substitute
workers have less educztion than the persons they would replace. The most appropriate
value is likely to be between these two estimates.
Given an estimate of the value of this nonmarket work, an additional assumption must
be made about whether the impact of lower IQ on nonmarket productivity is the same as
on market wages. There appears to be an association between maternal IQ and child’s
IQ, which is unlikely to be entirely hereditary. Moreover, m recent lead studies the
Home Observation for Measurement of the Environment (H.O.M.E.) score (a measure
of the quality of the home rearing environment) has been positively correlated with the
mother’s and the child's IQs (Bellinger et al., 1984). These findings suggest that IQ has
an impact on nonmarket work, at least on the child-rearing component. For this
analysis, we have taken the value of lost productivity due to lead exposure for
nonparticipants in the labor force as half the value for employed workers.
Data for calculating the values of the expected lifetime earnings of an average child in
the United States, under these assumptions, were obtained from 1987 eamings profiles
from the U.S. Bureau of the Census. To compute the average lifetime eamings, we
assumed that the numbers of men and women in the population would be equal, and
part-time workers and pon-labor force participants would earn half as much as average
full-time workers. The pet present value of average lifetime earnings per child,
APPENDIX H - PAGE 7
i a
discounted to age 3, is estimated to be $260,000. The average child bom into a housing
unit 1 year after abatement is 4 years younger than the child currently occupying the
unit; discounting that child’s lifetime eamings to today’s value yields a net present value
of $223,000.
Total earnings benefits: Figure 1 shows the pathways through which lead exposure
affects total eamings benefits. The lower case letters a to e¢ correspond to the pathways
on Figure 1., on page 25.
We used the following equations to calculate the total lost wages attributable to
reductions in eamings because of lead exposure:
I. The estimated change in wage rate for a 1 ug/dL change in blood lead level can be
expressed as follows:
a*b = 25*5% = .125%
where a = estimated change in IQ for each 1 ug/dL. change in blood lead level
(.25 IQ points per 1 ug/dL. change in blood lead level)
b= estimated percentage change in wages for a 1 IQ point change (5%
wage change per IQ point)
2. The average change in wage rate from the decreased educational attainment resulting
from lead exposure can be expressed as follows:
a*c*d = .25*.131*6% = .197%
where c= estimated change in grade attained for a 1 IQ point change (.131
years schooling per 1 IQ point change resulting from lead exposure)
d = estimated percentage change in wage rate for a 1 years change in
grade attained (V% per year of schooling)
3. The average change in wage rate from decreased labor force participation from
failure to graduate from high school can be expressed as follows:
a*cC'tc = 25%45%*10.5% = 118%
where c'= estimated change in the probability of graduating from high school
for a 1 1Q point change resulting from lead exposure (45%
increased probability of failure to graduate for each 1 point
decrease in IQ)
APPENDIX YI -PAGE §
a | fd
Ps
~~”
]
¢ = estimated percentage change in labor force participation because of
failure to graduate from high school (10.5% decrease in labor force
participation because of failure to graduate)
4. Therefore, the change in the expected present value of lifetime eamings from a I
ug/dL change in blood lead levels can be expressed as follows:
AE = E[(ab) Hcd) + (c’e)]
= $260,000[(.125% + .197% + .118%)]
= $260,000* 441% = $1,147
where AE = the expected change in lifetime earnings from exposure to lead
E = the pet present value of lifetime eamings
We estimate, therefore, that prevention of an’ increase of 1 ug/dL in a child's blood lead
level will produce a net present value benefit of $1,147 per child. We again note that
lost income is a clear underesimate of cognitive impairment, reduced educational
attainment, and reduced labor force participation.
The Benefits of Preventing Prenatal Exposure to Lead
Prenatal lead exposure has been linked with reduced gestational age, lower birth weight,
and decreased cognitive functioning, even in children exposed to low-to-moderate
matemal blood lead levels (Dietrich et al., 1987). In this analysis, we assess only the
impact on mortality of low gestational age due to lead exposure, since the data
supporting the relationship between prenatal lead exposure and gestational age are
stronger than the data supporting the relationship between lead exposure and low birth
weight. In addition, to avoid the possibility of counting some infants in both prenatal
and postnatal estimates, we did not assess the consequences of cognitive damage.
Prenatal exposure has also been linked to stillbirths in a number of studies (Vimpani et
al., 1990), but we have not computed any benefits of avoiding fetal loss because the
evidence is not complete and no study provides a dose-response function. We also have
not computed costs from hospitalizations for prematue and low birthweight infants.
These omissions result in an underestimate of the benefits of reducing prenatal exposure
to lead.
The impact of prenatal exposure on mortality: We used data from the Linked Birth and
Infant Death Record Project (National Center for Health Statistics) to estimate infant
The numbers shown are based on calculations using the most precise numbers possible.
Because of rounding, there may be small differences between the numbers shown and
those obtained by performing the calculations described.
APPENDIX UI - PAGE 9
por
Plata ef ir
mortality as a function of gestational age. The impact of prenatal lead exposure on
gestational age is obtained from Dietrich et al. (1987). These estimates yield a predicted
reduction of 10° (or 0.0001) in risk of infant mortality for each 1 ug/dL reduction in
maternal blood lead level. In this analysis, we assume that the relationship between
neonatal mortality and low gestational age is the same whether it results from prenatal
lead exposure or from all other casses of low gestational age.
Valuing reductions in mortality: Placing a monetary value on reductions in mortality is
highly controversial. The U.S. Department of Transportation has used lifetime wages
(human capital approach) as a proxy, an approach common in litigation as well. This
approach has obvious faults. For example, the value of reducing early mortality among
retired persons or housewives is not zero, even though they may not be expected to eam
wages. Because this approach underestimazes the value of human life by approximating
its value with the economic productivity of an mdividual, most economists prefer the
willingness to pay method for valuing reductions in mortality.
Numerous methods for valuing people’s willingness to pay for reducing their risk of
mortality have been employed The two most common methods include surveys that
present realistic scenarios of trade-offs between expenditures and mortality risks or
contingent valuation studies (Jones-Lee et al, 1985; Gegax et al, 1985) and assessments
of market transactions that reveal implicit trade-offs between risk and dollars (e.g.,
Thaler and Rosen, 1976; Smith, 1976; Viscusi, 1978; Viscusi and O'Connor, 1984).
Estimates resulting from these studies range from $500,000 to $9 million per statistical
life, with most estimates falling between $1 millicn and $5 million (Violette and
Chestnut, 1989). We have taken $3 millica per statistical life as the best estimate of the
willingness to pay to avoid excess mortality risk.
Under these assumptions, the monetary benefit associated with reducing infant mortality
is (0.0001) ($3,000,000) or $300 per ug/dL. increase in blood lead level prevented for
each pregnant woman.
Total Benefits of Preventing Lead Exposure
On the basis of the above analyses, the benefits of preventing a child's blood lead level
from reaching 25 ug/dL are $4,631 for aveided medical and special education costs. The
increased productivity to be expected from preventing a 1 ug/dL increase in a child's
blood lead level is $1,147. Clearly, the greater the prevented increase in blood lead
level, the greater the benefits; for the individual child, preventing the blood lead level
from exceeding 24 ug/dL results in maximum benefits. The average benefits of
preventing a 1 ug/dL increase in the blood kad level of a pregnant woman are $300.
ABATEMENT OF HOMES
In this section we describe the costs and effectiveness of lead-based paint abatement.
APPENDIX 1 - PAGE 10
Effectiveness of Lead-Based Paint Abatement in Reducing Lead Exposure
Studies have shown that abatement of lead-based paint in housing is effective in reducing
children’s blood lead levels (Kennedy, 1978), but quantitative data on these reductions
are limited. We obtained both cost of abatement and effectiveness data for three
evaluations of the efficacy of abatement--a study by Rosen et al. in New York City (in
press), a study from St. Louis (G. Copley, unpublished data), and a study from
Massachusetts (Y. Amitai et al, unpublished data). These data are not necessarily
representative of abatements as they are currently performed. However, because of the
lack of other data, we used them for our cost-benefit analysis.
In a study on the use of bone lead measurements in New York City children, Rosen et
al. (in press) reported on children who did not receive chelation therapy but who did
have their homes abated. At 24 weeks, the children’s blood lead levels had declined
from an initial mean level of 29 ug/dL to 21 ug/dL.. Abatement methods used in this
study included scraping, spackling and repainting surfaces with deteriorating lead paint.
An unpublished study from the City of St. Louis Division of Health (G. Copley,
unpublished data) reported that children who did not receive chelation and whose homes
were abated experienced a mean reduction of 9.3 ug/dL in blood lead levels (from 43.9
to 34.2 ug/dL) measured 6 to 12 months after the abatement. Abatement consisted of
scraping or encapsulating deteriorated surfaces.
An evaluation of data collected in 1984 and 1985 by the Massachusetts Childhood Lead
Poisoning Prevention Program (Y. Amitai et al., unpublished data) examined the
intraabatement and postabatement blood lead levels of children who received no
chelation therapy. The purpose of the study was to examine the impact of abatement
method on intraabatement blood lead levels when children were not relocated dunng
abatement. Several abatement methods were employed, including dry scraping, sanding,
and encapsulation. Mean blood lead levels 8 months postabatement decreased by 10.2
ug/dL (from 35.7 ug/dL to 25.5 ug/dL).
In these three studies, the approximate mean decrease in blood lead levels after
abatement was 9 ug/dL for children in lead-contaminated housing and with initial blood
lead level >25 ug/dL.
These studies only included children with blood lead levels >25 ug/dl. No data are
available on the effects of abating homes of children with lower blood lead levels. In the
studies, the mean decrease in a child's blood lead level with abatement was 25%. For
the cost-benefit analysis presented here, we assume that the reduction in blood lead
levels from abatement of homes of children with initial levels <25 ug/dlL will be
proportional to the reduction for children with higher blood lead levels. Thus, children
with blood lead levels <25 ug/dL will experience a 25% decrease in blood lead levels
APPENDIX 11 - PAGE 11
~~ x
from lead-based paint abatement. Using estimates from models developed by EPA and
others, we estimate that the mean blood lead level for children whose preabatement
levels are between 10 and 24 ug/dL is 1S ug/dL (J. Schwartz, personal communication).
For children whose blood lead levels are between 10 and 24 ug/dL, the mean decrease
in blood lead levels expected from abatement is 3.75 ug/dL.
Costs of Lead-Based Paint Abatement
We contacted individuals associated with the abatement programs in New York City, St.
Louis, and Massachusetts to ascertain the nature and approximate costs of the abatement
methods used at the time that data for these studies were compiled. All three programs
relied extensively on scraping, spackling, and repainting areas with deteriorated
lead-containing paint. Encapsulation was less frequently used (only in Boston and St.
Louis), and there was no replacement of doors, windows, or woodwork. Only
deteriorated or damaged lead-containing surfaces were abated routinely in New York
City and St. Louis, while Boston abatements included stripping of all chewable,
accessible surfaces below § feet (e.g., window sills, baseboards, door frames), regardless
of condition, if they contained lead. Costs for abating an average unit of 5 to 6 rooms
for each of the cities were as follows: St. Louis - $2,000, New York City - $2,500, and
Boston - $1800 (inflated when necessary to 1989 prices by using the Consumer Price
Index). These prices include abatement of common areas and exteriors when necessary
and costs of materials, labor, insurance, overhead, whatever worker protection was
employed, preparation of the unit before abatement, and cleanup. An average cost of
$2,100 will be assumed for these studies.
It should be noted that some currently recommended abatement methods and
procedures are much more expensive than those discussed above. A cost-benefit analysis
was not conducted for these more rigorous abatements because data on associated
changes in blood lead levels are not available.
The investigators in New York City. St. Louis, and Massachusetts were questioned about
the longevity of the effectiveness of these abatement methods--that is, about how long a
relatively "lead-free environment would be maintained in the home. In all three cases,
the investigators reported that repoisoning after abatement was very infrequent
(considerably less than 1% within a year). This does not address the problem of
long-term effectiveness of the abatement, for example, 5 to 15 years after the original
abatement is completed.
The average charge for home inspections in several lead poisoning prevention programs
is $97 per unit (K. O'Connor, C. Tomes, H. Billingsly, personal communications), which
we round to $100. If we assume that 80% of pre-1950°s housing contains leaded paint
(Shier and Hall, 1977), the cost for an investigation per positive home is $125.
Therefore, the total cost of abatement is $2225 per unit. Several costs are not included
in these estimates because they are more difficult to quantify or are extremely variable.
APPENDIX HH - PAGE 12
One source of costs is court proceedings, for example, when notices to landlords are
challenged; another is for the dislocation of families from their homes and the effects on
neighborhoods when landlords refuse to ahate marginally viable housing. An additional
cost results if families are relocated to alternative housing at program expense.
COST-BENEFIT ANALYSIS
In the following section, we present a cost-benefit analysis for abatement of an average
house with lead-based paint built before 1950. In the analysis, we will use the data
presented earlier on the costs and effectiveness of abaternents performed in St. Louis,
New York City, and Boston.
The benefits used in this analysis are likely to be substantial underestimates of the true
benefits of abatement. In addition to the reasons for underestimation already discussed,
a very important component of underestimation in this analysis is that we will not assign
monetary value to the benefits of abating homes of children and pregnant women who
already are currently being exposed to lead. This assumption may be unjustified for
several reasons. First, children remaining in a lead—<ontaminated environment may need
repeated courses of medical treatment for continued elevations in blood lead levels.
Second, the blood lead levels of some of these children will increase further as a result
of living in leadcontaminated homes, thereby increasing the probability that they will
need medical care and special education and further reducing their future eamings.
Third, decreasing the amount of time children and pregnant women have elevated blood
lead levels will probably decrease the adverse effects from lead. Data are not available,
however, to allow these benefits to be quantified. Therefore, this cost-benefit analysis is
conducted under the assumption that we target homes for abatement in a high-risk area
based on the home’s containing lead-based paint and having been built before 1950. All
benefits are accrued by children who will enter a high-risk age group in the house in the
future and by fetuses potentially exposed to lead in the future. No attempt is made to
target abatement to the homes of curmrentiy lead-poisoned children.
For this cost-benefit analysis, we use the following assumptions:
Assumptions:
Assumption 1: In general, children’s exposure to lead-based paint and
paint-contaminated dust and soil begins to increase when they become mobile and
decreases as they practice less mouthing behavior. We will assume that children less
than 10 months and greater than 6 years of age are unlikely to be poisoned by
lead-based paint, regardless of their housing. Therefore, quantitative benefits can be
assessed for children who are less than 10 months of age and are now living in the unit,
for children who are likely to be bom into or move into the abated unit, and women who
will become pregnant while living in the abated unn.
APPENDIX H- PAGE 13
} 2.
be
Assumption 2: On average, there are 0.287 children per house built before 1950 (Pope,
1986). The average number of children less than 10 months old per pre-1950 housing
unit is (0.287 children x (9/72 months)) = 0.036 children.
Assumption 3: This analysis is performed fce the average home built before 1950 which
is painted with leaded paint.
Assumption 4: The average overall loss rate of housing, both rental and owner-occupied,
built before 1950 is 1% per year (D. McGoczh. Department of Housing and Urban
Development, personal communication). On the basis of this assumption, the median
remaining life of existing housing stock built before 1950 is 68 years.
Assumption 5: A targeting strategy is emplcyed that abates homes built before 1950 that
contain lead-based paint, whether or not these hemes currently contain children.
Assumption 6: Were the targeted homes nx abated, some of the children who occupied
them would have become lead poiscned. For these children the increase in blood lead
level prevented by abatement is 9 ug/dl. For children who would not have become
poisoned, the average prevented crease in blood lead level is 3.75 ug/dL.
Assumption 7: On the basis of data from Cincinnat, the difference in blood lead levels
among pregnant women in lead-contaminated 1%th century housing and those in
lead-free public housing is 2.13 ug/dl. (R. Bomschein, personal communication). On the
basis of these data, we assume that abating a unit results in the prevention of a 2.13
ug/dL increase in the blood lead levels of pregnant women.
Assumption 8: Almost 6 million children under 7 years of age live in pre-1950 housing
with high levels of lead in paint (ATSDR. 1288). Of these, 0.2 million, or 3.4%, have
blood lead levels above 25 ug/dL. Thus. for this analysis we will assume that abatement
will prevent blood lead levels >25 ug/dL m the 3.4% of children who would be expected
to develop them otherwise and will prevent levels between 10 and 24 ug/dL in the rest.
Thus, the average prevented increase in bled lead level for a child living in a house
contaminated with lead-based paint is:
(0.034) (9 ug/dL) + (0.966) (3.75 ug. dL) = 3.93 ug/dL
Assumption 9: An average of 0.045 infant's below age 1 year are present in housing units
built before 1950 (Pope, 1986). We will therefore assume that 0.045 children are bom
into each unit each year after abatement and that 0.045 represents the proportion of
pregnant women in such houses each year. Ahatement preveats an increase of 2.13
ug/dL in the blood lead level of a pregnant woman. Thus, the average prevented
increase in blood lead levels in pregnant women in abated housing is:
(0.045) (2.13) = 096 ug/dL
APPENDIX H - PAGE 14
\ $C
{
Assumption 10: The medical costs avoided by preventing a child bom into a unit the
year after abatement from developing a blood lead level >25 ug/dL is $1,069
(discounted to 4 years into the future, since we assume costs are incurred at age 3 years).
The avoided special education costs are $2,365 (discounted to 7 years into the future).
For each 1 ug/dL blood lead level increase prevented in a child, $1.085 in lost eamings
is avoided.
Assumption 11: Each avoided increase of 1 ug/dL blood lead in a pregnant woman by
abating the unit the year before she becomes pregnant, when discounted to 1 year in the
future, results in an average savings of $286 from the prevention of infant mortality.
Assumption 12: A discount rate of 5% is used.
Assumption 13: Analysis is done for a set time. Both benefits and costs are discounted
to that year.
Assumption 14: Benefits can be assessed for each cohort of children entering the home.
Because we assume that the average remaining lifespan of housing units built before
1950 is approximately 68 years, benefits are calculated for 68 cohorts of children, with
benefits being discounted appropriately.
Assumption 15: The discounted total value of benefits for children is equal to the sum
of the benefits accruing for current resident children less than 10 months of age and the
benefits accruing to children who will move into or be bom into the residence in the
future. These are the benefits of avoiding medical and special education costs and
increasing earnings.
Assumption 16: Benefits are also accrued by reducing blood lead levels in pregnant
women who will live in the house in the future.
The following equations summarize this information. In these calculations, figures are
only presented up to 4 decimal places. As a result, an attempt to duplicate the
calculations performed will result in rounding errors; final values are based on the most
precise figures possible. |
1. The proportion of children now living in the home who will accrue benefits from the
avoidance of medical and special education costs can be expressed as follows:
f= g*h
= .034*.036 = .0012
where f= average number of children per house less than 10 months of age
living in pre-1950 housing whose blood lead levels would be
expected to rise above 24 ug/dL
APPENDIX HO - PAGE 15
14
I
v
average proportion of children with blood lead levels above 24
ug/dL (.034; sec Assumption 8, page 14)
average number of children less than 10 months of age per housing
unit built before 1950 (0.036; see Assumption 2, page 14)
2. The proportion of future children who will accrue benefits from avoidance of medical
and special education costs can be expressed as follows:
i= g*)
034* 045 = .0015
where average number of children per house who will be bom into the
average pre-1950 house each year of the house's remaining lifespan
and whose blood lead levels would be expected to nse above 24
ug/dL without abatement
j= average number of pregnant women per house per year (.045; see
Assumption 9, page 14)
3. The net present value of medical costs avoided through abatement is the sum of the
avoided costs for children currently living in the unit plus the avoided costs for 67
cohorts of future children.
MED = f*AMC + i*[AMC, + AMC, + .. + AMC]
0012*$1,300 + .0015%$21,605.23
$1.59 + $33.06 = $34.65
AMC average medical costs for children with blood lead levels
above 24 ug/dL. the present year ($1,300: see page 3)
AMC, average medical costs for children with blood lead levels
above 24 ug/dL in year, discounted to the present year
4. The net present value of special education costs avoided through abatement is the sum
of the avoided costs for children currently living in the unit plus the avoided costs for 67
cohorts of future children.
SEC = f*ASEC + i*[ASEC, + ASEC, + ...+ ASEC]
0012#$3,331 + .0015%$347,783.47
= $4.06 + $73.11 = $77.17
ASEC = average special education costs for children with blood lead
levels above 24 ug/dL in the present year ($3331; sce page 4)
APPENDIX 11 - PAGE 16
ASEC = average special education costs for children with blood lead
levels above 24 ug/dL in year, discounted to the present
year
5. The average net present value of lost earnings prevented by abatement for children
less than 10 months of age currently living in the home is:
INC, = h*k* AE
= .036*3.93*$1,147 = $161.65
where INC, = lost earnings prevented for current children less than 10
months of age living in lead-painted homes
k= average decline in blood lead levels of children from
abatement (3.92 ug/dL; see Assumption 8, page 14)
AE = change in eamings that can be attributed to a 1 ug/dL
change in blood lead level ($1,147; see page 9)
6. The net present value of lost earnings prevented through abatement for future
children is the avoided costs for 67 cohorts of future children.
INC, = J*k*[E, + E, + ..+ Eg)
= .045*3.93*319,781 = $3,497
where ING; = net present valde of lost eamings prevented for future
children who would live in pre-1950 homes
E = average present value decrease in eamings for each cohort,
discounted to tix present year
7. The net present value of lives saved from avoided mortality from reducing prenatal
lead exposure can be expressed as follows:
LIFE = *[M, + M, + __ + M]
= .096*$5,571.72 = $553.22
where 1 = average prevented increase in a pregnant woman's blood lead level
from abatement (.096 uvg/dL; see Assumption 9, page 14)
M, = average benefits from reduced fetal mortality of preventing a 1
ug/dL increase in blood lead level in year n, discounted to the
present year
APPENDIX IH - PAGE 17
8. The total benefits of abatement are:
MED + SEC + INC_ + INC, + LIFE
= $34.65 + $77.17 +3161.65 + $3,497.00 + $553.22 = $4,323.70
Costs Versus Benefits of Abatement
We estimate that abating an average pre-1950 lead-painted home using the methods
employed for the three studies described above earlier costs $2,225, and the benefits over
the lifetime of the home are $4,323. Thus, abatement of a home results in a net benefit
of $2,098. This net benefit does not take into account any benefits sustained by a child
who is already poisoned in the unit or the numerous benefits to which we could not
assign monetary values.
This cost-benefit analysis provides an economic justification for a national program of
abating lead-contaminated housing to prevent childhood lead poisoning. This analysis is
conservative because a number of important benefits remain unquantified. Moreover,
prevention of lead poisoning would be an important public health activity, even if no
economic benefits could be demonstrated.
This analysis indicates what is needed for a rational national abatement program.
Obviously, the better a plan for setting priorities for abatement can be targeted to homes
likely to house children in the future, the greater the net benefits. Furthermore, if
strategies can be developed for determining which homes are most likely to poison
children, the efficiency and benefits of any abatement program will be markedly
increased.
Sensitivity Analysis
Changing certain values may have an impact on the conclusions that are drawn from an
analysis; consequently, we perform sensitivity analysis to test the impact of changing our
assumptions. In this section, we repont the results of sensitivity analyses aimed at testing
whether the values of key variables significantly alter the conclusions that can be drawn
from the study. Table 1 displays the results of the base case analysis along with the
sensitivity analyses. Benefits are expressed in terms of net benefits--that is, the
difference between the total benefits and the cost of abatement.
Changing the number of children per home: In the base case analysis, we assumed that
abatement would not be targeted to homes with children; therefore, the average number
of children per pre-1950 home was used in estimating the benefits of abatement. In this
variation, we assume that abatement is conducted in communities with more children
than the average. For this analysis, we assume that the average unit to be abated houses
three times more children than the national average. Thus, we assume that, on the
average, 0.108 (or 0.287*3*{9/72]) children less than 10 months of age now occupy the
APPENDIX II - PAGE 18
\
! i
44
: \
unit and, for future cohorts, we assume that an average of 0.135 (or 0.045*3) children
will be bom into each unit each year. Under these assumptions, the net benefits are
$10,747 per urut. Altematively, if we assume that five times the average number of
children occupy these units than is the average for the nation, the net benefits are
$19,395 per unt.
Changing the discount rate: In the base case analysis we assumed a discount rate of S%.
If we discount all future benefits and costs by 3% the net benefits are approximately
$6,357. When all future benefits and costs are discounted by 7%, net benefits become
$404.
Changing the lifespan of houses: Assuming a 50-year lifespan rather than the median of
68 years reduces net benefits to $1,866, and decreasing the lifespan of houses to 30 years
reduces net benefits to $1,212 per abated unit.
Changing the effectiveness of the abatement (ug/dL reduction): In the base case
analysis, we assumed that children with blood lead levels >25 ug/dL experience a 9
ug/dL blood lead decline after abatement and that children with lower levels will have a
3.75 ug/dL decline. In this vanation, we will assume that abatement is more effective
than in the three studies from which we obtained data. We will assume that children
with blood lead levels >25 ug/dL experience a 21.6 ug/dL decline (60% of the average
baseline blood lead level) and that children with lower blood lead levels experience a 9
ug/dL decline. We also assume a proportionately greater decrease in the blood lead
levels of pregnant women (5.11 ug/dL). Under this scenario, net benefits increase to
$7,992. This analysis implies that a more effective abatement method that results in an
approximate average decline in the blood lead level of 9.4 ug/dL could cost as much as
$10,000 per unit and we could still expect to see net benefits from abatement.
Changing assumptions about the impact of abatement on children 9 months of age or
older currently in lead-painted homes: In the base case analysis we estimated benefits
only for those children currently living in the home who were less than 10 months of age.
No benefits were assumed in the analyses for children above that age. In this vanation,
we will assume that all children 6 years of age and under living in an abated home will
experience full benefits. In this case, the net benefits are $3,290. If we assume that
children between 10 months and 6 years of age receive only half the benefits of children
less than 10 months, the net benefits are $2,693.
These analyses show that targeting abatement to homes with children and improving the
efficacy of abatement will result in greater net benefits. Furthermore, if strategies can
be developed for determining which homes are most likely to poison children, the
efficiency and benefits of any abatement program will be markedly increased.
APPENDIX II - PAGE 19
THE BENEFITS OF A NATIONAL EFFORT TO ABATE ALL PRE-1950
HOUSING UNITS WITH LEAD-BASED PAINT
In this analysis, we estimate the benefits from abating all homes in the United States.
I. Results of a study by Shier and Hall (1977) show that 80% of pre-1950 housing
contains lead-based paint. Since there are 28,971,000 occupied pre-1950 housing
units in the United States (U.S. Bureau of the Census, 1989), we estimate that
there are 23,176,800 occupied pre-1950 housing units containing lead.
2. For this analysis, we use a cost estimate of $2,225 per abatement. Therefore,
the cost of abating all 23,176,800 units today would be $51,568,380,000. Were the
abatement conducted over the next 20 years (performing an equal number of
abatements each year), the total present cost of abatement would be
$33,739,550,000.
3. We have estimated that the total benefits of abatement are $4,323 per
housing unit. If all abatements were performed now, the total benefits would be
$100,193,306,000. If abatements were conducted over the next 20 years, the total
present value of the benefits would be $61,742,270,000. (This number takes into
account the fact that a house abated in the future has a shorter lifespan as a
lead-free dwelling than a unit abated today; therefore, fewer cohorts of children
would benefit.)
4. We have estimated that the pet benefits of abatement (total benefits of
abatement - costs of abatement) are $2,098. If all pre-1950 lead-painted housing
units in the United States were abated today, the net benefits of abatement would
be $48,624,926,000. If units were abated over the next 20 years, the present valve
of the net benefits would be $28,002,830,000.
REFERENCES
Agency for Toxic Substances and Disease Registry (ATSDR). 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, 1988.
Ashenfelter O, Ham J. Education, employment and earings. Journal of Political
Economy 1979,87:S99-S131.
Barth MC, Janney AM, Amold F, Sheiner L. A survey of the literature regarding the
relationship between measures of IQ and income. Washington, D.C: ICF Inc, 1984.
APPENINX IF - PAGE 20
fo: Z
fit : ‘ i ‘
i £3 id & he
SE
fA
Bellinger DC, Needleman HL, Leviton A, et al. Early sensory-motor development and
prenatal exposure to lead. Neurobehavioral Toxicol Teratol 1984:6:387-402.
Centers for Disease Control (CDC). Preventing lead poisoning in young children: a
statement by the Centers for Disease Control. Atlanta: U.S. Department of Health and
Human Services, 1985; CDC report no. 99-2230.
Chamberlain G, Griliches Z. More on brothers. In: Taubman P, ed. Kinometrics:
determinants of socioeconomic success within and between families. Amsterdam: North
Holland Publishing, 1977:97-124.
Cropper M, Krupnick AJ. The social costs of chronic heart and lung disease. Discussion
paper QE 89-16. Quality of the Environment Division, Resources for the Future,
August, 1989.
de la Burde B, Choate MS Jr. Early asymptomatic lead exposure and development at
school age. J Pediatr 1975;87:63742.
Dietrich KN, Krafft KM, Bomshein RL. et al. Low level fetal lead exposure effect on
neurobehavioral development in early infancy. Pediatrics 1987:80:721-30.
Deitrich KN, Krafft KM, Shukla R, Bemnschein RL, Succop P. The neurobehavioral
effects of early lead exposure. In: Schroeder SR, ed. Toxic substances and mental
retardation: neurobehavioral toxicology. Washington, D.C.: American Association of
Mental Deficiency, 1987:71-95 (Mocograph No. 8).
Gegax D, Gerking A, Schulze W. Perceived risk and the marginal value of safety.
Report to the U.S. Environmental Protection Agency. 1985.
Griliches Z. Estimating the retums to schooling: some econometric problems.
Econometrica 1977;45:1-22.
Jones-Lee MW, Hammerton M, Phillips PR. The value of safety: results of a national
sample survey. Economic Journal 1985:95:49-72.
Kakalik JS. The cost of special education. Rand Corporation Rep. 1981, N-1791-ED.
Kennedy FD. The childhood lead poisoning prevention program: an evaluation. A
report for the Centers for Disease Control. 1978.
Levin R. Reducing lead in drinking water: a benefit analysis. Washington, DC:
Environmental Protection Agency (EPA), 1986; EPA report no. 230-09-86-019.
APPENDIX II - PAGE 2}
Lyngbye T, Hanson O, Trillingsgaarb A, Beese I, Grandejcan P. Leaming disabilities in
children: significance of low-level lead-exposure and confounding factors. Acta Paediatr
Scand 1990;79:352-60.
Needleman, HL. The persistent threat of lead: a singular opportunity. Am J Public
Health 1989;79:643-45.
Needleman HL, Gatsonis CA. Low-level lead exposure and the IQ of children. JAMA
1990;263:673-78.
Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long-term effects of
exposure to low doses of lead in childhood: an 11-year follow-up report. N Engl J Med
1990;322:83-8.
Olneck M. On the use of sibling data to estimate the effects of family background,
cognitive skills, and schooling: results from the Kalamazoo Brothers Study. In: Taubman
P, ed. Kinometrics: determinants of socioeconomic success within and between families.
Amsterdam: North Holland Publishing Company 1977:125-62.
Piomelli §, Rosen J, Chisolm JJ, Graef J. Management of childhood lead poisoning. J
Pediatr 1984:4:523-32.
Pope A. Exposure of children to lead-based paints. Research Trnangle Park, N.C: US.
Environmental Protection Agency (EPA), 1986; EPA report no. 63-02-4309.
Rosen JF, Markowitz ME, Bijur PE, et al. Sequential measurements of bone lead
content by L-X-ray fluorescence in CaNa,-EDTA treated lead-toxic children.
Environmental Health Perspect (in press).
Schwartz J, Pitcher H, Levin R, Ostro B, Nichols AL. Costs and benefits of reducing
lead in gasoline: final regulatory impact analysis. Washington, D.C.: U.S. Environmental
Protection Agency (EPA), 1985; EPA report no. 230-05-85-006.
Shier DR, Hall WG. Analysis of housing data collected in a lead-based paint survey in
Pittsburgh, Pennsylvania, Part 1. Washington, D.C.: National Bureau of Standards, 1977.
Smith RS. The Occupational Safety and Health Act. American Enterprise Institution
for Public Policy Research, 1976.
Thaler R, Rosen S. The value of saving a life: evidence from the labor market. In:
Taleckji NE, ed. House production and consumption. New York: Columbia University
Press, 1976.
APPENDIX HI - PAGE 22
U.S. Bureau of the Census. Statistical abstracts of the United States: 1989. 109th ed.
Washington, D.C., 1989.
Vuinpani G, Baghurst P, McMichael AJ, Robertson E, Wigg N, Roberts R. The effects
of cumulative lead exposure on pregnancy outcome and child development during the
fust four years. Presented at advances in lead research: implications for environmental
health conference. Research Triangle Park, NC: National Institute of Environmental
Health Sciences, 1990.
Violette DM, Chestnut L. Valuing risks: new information on the willingness to pay for
changes in fetal risks. Washington, D.C.: U.S. Environmental Protection Agency (EPA).
1989; EPA report no. 230-06-86-016.
Viscusi WK. Labor market valuations of life and limb: empirical evidence and policy
implications. Public Policy 1978;26:359-86.
Viscust WK, O'Connor CJ. Adaptive response to chemical labeling: are workers Bayesian
decision makers? American Economic Rev 1984:;74:942-56.
APPENDIX 11 - PAGE 23
Table 1. Results of the base case cost-benefit analysis and sensitivity analysis, expressed
as net benefits for abatement of the average pre-1950 home with lead-based paint,
discounted to the present. (Net benefits = total benefits - cost of abatement.)
Description of Analysis Net Benefits
Base case analysis (see text for assumptions) $ 2,098
Sensitivity analyses
Number of children per home
If increased 3-fold 10,747
If increased 5-fold 19,395
Discount rate of 5%
If decreased to 3% 6,357
If increased to 7% 404
Life span of houses is 68 years
If decreased to 50 years 1,866
If decreased to 30 years 1.212
Effectiveness of the abatement
With 60% decrease in blood lead levels 7,992
Benefits accrue to children 10-72 months
With 100% benefits 3,290
With 50% benefits 2,693
APPENDIX HI - PAGE 24
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Labor force participation
Educational attainment
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Lead exposure —t IQ =r Wage rate ———p Earnings
Figure 1. Effect of lead exposure on earnings.
APPENDIX mI
HISTORY OF CHILDHOOD LEAD POISONING
PREVENTION PROGRAMS
The first cases of childhood lead poisoning from lead paint in housing were reported in
1892 in Australia. Although many severe cases of the disease were reported in
subsequent decades in the United States, little effort was made to find additional cases
until the 1950s, when caseworkers in a few large cities attempted to find lead-poisoned
children. In 1966, Chicago began the first mass screening program, followed shortly by
New York and other cities (Lin-Fu, 1980).
The Lead-Based Paint Poisoning Prevention Act, passed in 1971, initiated a national
effort to identify children with lead poisoning and abate the scarces of lead in their
environments. For most years of this program, Federal funds appropriated under this
Act were administered by the Centers for Disease Control (CDC). More than $89
million were distributed, and over a quarter of a million children were identified with
lead poisoning and received referrals for environmental and medical intervention.
In 1981 the Omnibus Budget Reconciliation Act amended Trle V of the Social Security
Act, which had authorized the Matemal and Child Health (MCH) Services Program
since 1935. The amendment created the MCH Services Block Grant Program and
consolidated many categorical programs, including that for childhood lead poisoning
prevention, into the Block Grant. In 1982, the administrative responsibility for the
Lead-Based Paint Poisoning Prevention Act was transferred to the Office of Matemal
and Child Health (now the Matemal and Child Health Bureau) of the Health Resources
and Services Administration.
Under the provisions of the MCH Services Block Grant Act, each State decides how to
use these Federal funds. Data on whether these funds are used to support childhood
lead poisoning prevention activities has not been reported to the Federal govemment.
The 1989 Omnibus Reconciliation Act includes a requirement for State MCH Block
Grant Programs to be consistent with the Public Health Service Year 2000 Objectives for
the Nation and to submit an annual report with specified coatent in a standardized
format. Since reduction of the numbers of children with lead poisoning is likely to be
included as a Year 2000 Objective, more information oa childhood lead poisoning
prevention activities funded by the MCH block grant is anticipated.
The Lead Contamination Control Act of 1988 authorized $20 million for Fiscal Year
1989, $22 million for Fiscal Year 1990, and $24 million for Fiscal Year 1991 for CDC to
administer a childhood lead poisoning prevention grant program. Under this law, $4
APPENDIX III - PAGE 1
| £577
a’ i
million were appropriated in Fiscal Year 1990, and $8 million were appropriated in 1991.
The President’s budget for 1992 includes $14.95 million for this program. The majority
of this money will be provided as grants for State and local agencies to perform
childhood lead screening, referral for medical and environmental follow-up, and
education about lead poisoning in those communities with children with the highest
blood lead levels. This moocy is directed at communities with large numbers of children
with higher blood lead levels (e.g.. > 25S ug/dL). Although clearly many more States and
communities need comprehensive programs to address childhood lead poisoning, CDC's
current grant program is an mmportant step m our effort to eliminate childhood lead
poisoning.
The President’s budget for FY 1992 also mcludes $25 million for the HOME program,
which will be administered by the Department of Housing and Urban Development
(HUD). This program will assist low- and moderate-income private residential property
owners to abate lead-based paint, and will be directed to homeowners with young
children in high-nsk housing. This program could provide a knowledge base for
evaluating the effects of abatement
REFERENCES
Lm-Fu J. Lead and children: a historical review. In: Needleman HL, ed. Low level
lead exposure: the clinical implications of current research. New York: Raven Press,
1980:3-16.
APPENDIX II - PAGE 2
APPENDIX IV
ORGANIZATIONS AND AGENCIES THAT COULD HELP
PROMOTE AWARENESS OF CHILDHOOD LEAD POISONING
Table 1. Professional Organizations That Could Increase Practitioner Awareness of
Childhood Lead Poisoning
Primary Care Physicians (family practice, internal medicine,
pediatrics, and emergency medicine)
Ambulatory Pediatric Association
American Academy of Pediatrics
American Association of Family Physicians
American Board of Pediatrics
American College of Emergency Physicians
American College of Physicians
American Medical Association
American Medical Student Association
American Osteopathic Association
American Pediatric Society
American Society of Intemal Medicine
Association of American Physicians
Association of American Indian Physicians
Association of General Practitioners/Family Physicians
Association of Medical School Pediatric Department Chairmen
Association of Program Directors in Internal Medicine
Federal Physicians Association
National Association of Residents and Interns
National Medical Association
North American Primary Care Research Group
Society of Teachers of Family Medicine
Society of General Intemal Medicine
Public Health Physicians
American Association of Public Health Physicians
American College of Preventive Medicine
American Osteopathic College of Preventive Medicine
Association of Teachers of Preventive Medicine
Association of Preventive Medicine Residents
APPENDIX IV - PAGE 1
ig”
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to
Table 1 (continued). Professional Organizations that Could Increase Practitioner
Awareness of Childhood Lead Poisoning
Other Physician Speciality Organizations
American Association of Obstetrics and Gynecology
American College of Occupational Medicine
Nurses
American Society of Pediatric Hematology /Oncology
American Nursing Association
American Academy of Nursing
American Association of Neuroscience Nursing
American Association of Occupational Nursing
American College of Nurse-Midwives
American Licensed Practical Nurses Association
American Nurses’ Association
American Organization of Nursing Executives
Assembly of Hospital Schools of Nursing
Association of State and Territorial Directors of Nursing
Frontier Nursing Service
National Association of Hispanic Nurses
National Association of Pediatric Nurse Associates and Practitioners
National Association of Physician Nurses
National Association of Registered Nurses (State Associations)
National Association of School Nurses
National Association of Black Nurses
National Board of Pediatric Nurse Practitioners and Associates
Nurses Association of the American College of Obstetricians and
Gynecologists
Physician Assistants
American Academy of Physician Assistants
Association of Physician Assistant Programs
Pharmacists
American Pharmaceutical Association
American Society of Hospital Pharmacists
National Association of Retail Druggists
National Pharmaceutical Association
National Pharmaceutical Foundation
State Boards of Pharmacy
State Pharmaceutical Associations
APPENDIX IV - PAGE 2
Table 1 (continued). Professional Organizations that Could Increase Practitioner
Awareness of Childhood Lead Poisoning
Public Health Professionals
American College of Epidemiology
American Industrial Hygiene Association
American Public Health Association
Association of Schools of Public Health
Association of State and Territorial Directors of Public Health Education
Association of State and Territorial Health Officers
Association of State and Territorial Public Health Laboratory Directors
Association of University Programs in Occupational Health and Safety
Conference of Public Health Laboratorians
Conference of State Health and Environmental Managers
Council of State and Territorial Epidemiologists
Council on Education for Public Health
National Association of County Health Officials
National Coalition of Hispanic Health and Human Services Organizations
National Conference of Local Environmental Health Administrators
National Environmental Health Association
National Foundation of Rural Medical Care
National Rural Health Association
Society for Occupational and Environmental Health
United States Conference of Local Health Officials
World Federation of Public Health Associations
Other Health Organizations
American Indian Science and Engineering Society
American Industrial Health Council
Asian American Health Forum
Association of American Medical Colleges
Association of Minority Health Professions Schools
National Association of Community Health Centers
Society for Pediatric Research
APPENDIX IV - PAGE 3
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Table 2. Other Organizations that Would be Interested in Educating the Public About
Childhood Lead Poisoning
Matemal and Child Health
American Association of University Affiliated Programs for Persons with
Developmental Disabilities
Association of Matemal and Child Health Programs
Be Healthy, Inc.
Healthy Mothers, Healthy Babies Coalition
March of Dimes
National Association for the Education of Young Children
National Black Women's Health Project
National Center for Education in Matemal and Child Health
National Matemal and Child Health Clearinghouse
Safe Kids Coalition ;
Health Education, Information, and Promotion Organizations
American Hospital Association, Health Promotion Center
American Dietetic Association
American Lung Association
American Red Cross
Association for the Advancement of Health Education
Consumer Health Information Resource Institute
Consumer Information Center
Environmental Defense Fund
Health Education Center
Health Education Foundation
Health Insurance Association of America
Health Media Education
HealthWorks Northwest
The Henry J. Kaiser Family Foundation
National Health Information Center
The National Health Network
National Information System for Health Related Services
National Public Health Information Coalition
Patient Education Resource Center
Society for Public Health Education
Women’s Occupational Health Resource Center
APPENDIX IV - PAGE 4
Table 2 (continued). Other Organizations that Would be Interested in
Educating the Public About Childhood Lead Poisoning
Civic Organizations
Federation of Women's Clubs
Kiwanis
Knights of Columbus
League of Women Voters
Shriners
Young Mens’ Chnstian Association
Young Womens® Christian Association
Housmg and Finance Organizations
Association of Local Housing Finance Agencies
Building Owners and Managers Association
Council of State Governments
Federal National Mortgage Association
Housing Assistance Council
Mortgage Bankers of America
National Apartment Association
National Association of Counties
National Association of Governments
National Association of Home Builders
National Association of Housing and Redevelopment Officials
National Association of Realtors
National Community Development Association
National Council of State Housing Agencies
National Council of State Legislatures
National Housing Conference
National Leased Housing Association
National Low Income Housiag Coalitions
Advocacy Groups
Alliance to End Childhood Lead Poisoning
Amencan Association on Mental Retardation
Association for Retarded Citizens of the United States
American Federation of Teachers
Child Welfare League of America
Children's Defense Fund
Citizen's Cleannghouse for Hazardous Waste
Coalition on Human Needs
APPENDIX [IV - PAGE 5
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Table 2 (continued). Other Organizations that Would be Interested in
Educating the Public About Childhood Lead Poisoning
Advocacy Groups (continued)
Foundation for Child Development
The Lead Coalition
Legal Services Corporation
National Association for Rights, Protection, and Advocacy
National Education Association
National Parent-Teacher Association
Artist Safety Organizations
Arts, Crafts and Theatre Safety (ACTS)
Center for Safety in the Arts
APPENDIX IV - PAGE 6
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APPENDIX V
INFRASTRUCTURE DEVELOPMENT FOR’ ABATEMENT OF LEAD
HAZARDS IN HOUSING
In the past two decades progress has been limited in reducing childhood lead poisoning
caused by lead-based paint and dust in homes. Only a small fraction of the housing units
with lead-based paint have had the lead abated. To make matters worse, improper
techniques were used in many past abatement projects. The high levels of lead in dust
generated during abatement resulted in poisoning of workers and their families, and
children left in their homes during abatement had exacerbations of lead poisoning.
Inadequate abatement and cleanup procedures also resulted in children being repoisoned
upon returning to their "deleaded” homes.
Great strides have been made in the past few years in improving abatement technology
and protecting workers and their families. Although further improvements in abatement
technology and practice are needed. we now have the tools to start a national abatement
program. This section details the steps that must be taken to increase the national
capacity to do safe and effective abatement work.
GUIDELINES DEVELOPMENT
The first set of comprehensive technical guidelines for lead-based paint testing and
abatement, developed by a committee of government and nongovernment experts, were
issued on an interim basis in April 1990, by the Department of Housing and Urban
Development (HUD) for public and Indian housing authorities (the HUD Interim
Guidelines). The HUD Interim Guidelines emphasize lead abatement of large blocks of
units at the same time that other renovation work is done (comprehensive
modemization). These guidelines were developed for housing that is to be extensively
modified during modemization by the Federal government. These guidelines must be
modified for use by States, localities. and individuals in situations where funds are scarce
time is critical, or the unit is not being gutted for other reasons.
WORKER TRAINING AND CERTIFICATION
Worker Safety
Lead-based paint abatement is a potentially hazardous occupation. Exposures among
abatement and other workers, especially among pregnant women and among women and
men who have or are planning to have children, should be reduced. Currently, lead
abatement workers are not covered by the Occupational Safety and Health
APPENDIX V - PAGE 1
Administration (OSHA) gencral-industry standard regulating worker exposure to lead.
Instead, they are covered under the safety and health standards for the construction
industry, which regulate lead exposure less strictly. A standard is needed that takes into
account new data showing adverse effects of lead on adults at levels well below the
current OSHA general industry standard. Abatement workers should be protected by
medical monitoring and medical removal provisions, as are potentially lead-<xposed
workers in general industry. Since many companies performing abatement are likely to
have only a few employees, all companies, regardless of size, must be required to
conform with Federal standards.
Curriculum Development
Federally developed or sanctioned model training programs are a method for assuring
the quality and consistency of worker training. Basic course curricula must be developed
to meet the training needs of different groups: HUD staff, public housing authorities,
individual homeowners and landlords, contractors, workers, architects, designers, testers,
and inspectors. Since such courses are a prerequisite for all other training activities,
developing these course curricula should be given highest priority. Some curriculum
development has already begun for implementation of the HUD Interim Guidelines.
Course Delivery Mechanisms
As the amount of lead paint abatement increases, market forces will meet the growing
demand for training programs. In the short term, however, government involvement may
be necessary. Ope option, establishing govemment-funded pilot training centers, was
used successfully to deliver training to asbestos workers quickly. This approach offers a
high degree of quality control and assures that training is available in all geographic
areas. Pilot training centers, however, are expensive and could discourage centers
without government funding from entering the market. Alternatively, the govemment
could establish core curricula or curriculum requirements for each course. Federal or
State governments or some other group could then evaluate private instruction programs
and certify their adequacy. This approach would encourage the immediate involvement
of universities, labor organizations, and others and would probably provide the greates:
training capacity in the long run. Although low in cost, this alternative does require
government personnel or contract staff to review and approve each training program. In
any event, mechanisms to control the quality of instruction and assure the competence of
trainees are essential.
Certification
Institutionalizing lead paint abatement training will be difficult without mandatory
requirements for certifying contractors and their workers, testers, and inspectors. At a
minimum, individual training programs must be approved by a Federal or State agency
or some other body, such as a trade organization. The Environmental Protection Agency
APPENDIX V - PAGE 2
(EPA) uscd this approach--certifying training materials and approving course
providers—in the initial phase of its asbestos program. Another altemative 1s for the
certifying body to require that workers simply pass a standardized test. EPA is using this
general approach to license radon-testing personnel. A third approach is
performance-based accreditation, as in Massachusetts.
Institutionalizing Abatement Training
Lead-based paint abatement will probably not evolve exclusively as a separate industry
and skill speciality. Lead-based paint abatement is an integral and inevitable part of a
variety of existing building trades: painting, plastering, masonry, flooring, cabinetry,
carpentry, electrical, plumbing, insulation, and door and window replacement.
Therefore, lead-based paint abatement should be integrated into the various building
trades, and all workers involved in home renovation and repair should be familiar with
the special safeguards and techniques required.
A potential benefit of a national abatement program is increased employment. Most of
the neighborhoods that will be targeted for lead abatement have high unemployment
rates. As persons with little training develop the skills needed for leaded-paint
abatement, they are likely to leave jobs that do not require training. Because this
abatement work will require a large work force, training and employing local persons will
have local economic and social benefits.
LABORATORY ACCREDITATION
Although laboratory testing protocols and quality assurance mechanisms currently exist
for analysis of lead in air, water, and blood, no similar program, either mandatory or
voluntary, exists for the analysis of lead in paint film or dust. Currently, EPA is
distributing detailed instructions on standard test procedures for laboratories. However,
within the next 18 to 24 months, some laboratory accreditation program is clearly needed
to assure that consistent and reliable laboratory results are obtained. Options include a
direct Federal laboratory certification program, a new independent voluntary
accreditation. program, or an expansion of existing accreditation programs for analyzing
lead in other media to include tests of paint and dust.
EVALUATING EMERGING ABATEMENT TECHNOLOGY
During the past few years, private firms have developed a variety of new products to
reduce the costs of lead-based paint abatement. Currently, more than a dozen new
encapsulants and chemical strippers are being marketed across the country.
Unfortunately, few independent standards have been developed or tests conducted to
evaluate the effectiveness of these products or substantiate the claims made by
manufacturers. Standards must be set and performance critena established to assure the
effectiveness of emerging products, either by the Federal government or by
APPENDIX V - PAGE 3
nongovemnment consensus. Such standards would allow private laboratories to test new
lead abatement products at the manufacturer's or vendor's expense.
DISPOSAL OF ABATEMENT DEBRIS
At present, a significant impediment to broad scale abatement of lead-based paint in
housing is uncertainty about whether the debns generated can go in regular municipal
landfills as solid waste or must be disposed of as hazardous waste, at substantially greater
expense. When lead is removed from buildings, it is, in effect, being concentrated;
therefore, rules and regulations for its safe disposal are critical to prevent widespread
dispersal throughout the environment. Although at present disposal is not an issue for
the individual homeowner because of a household exemption, it is a problem for society.
Certain wastes, such as stripping agents and cleanup materials with high dust
concentrations, may be subject to hazardous waste classification and disposal
requirements. Most abatement debns, especielly bulky items, such as old window and
door frames painted with lead-based paint, are likely to be considered not hazardous.
Nevertheless, contractors are having difficulty finding laboratories to do toxicity testing,
and insurance companies are wary of these requirements which place the responsibility
and burden of proof on the unit owner and contractor. The situation is further confused
by the conversion to a new toxicity test method planned for the summer or autumn of
1990. As soon as requirements for the new toxicity tests are finalized, clear and practical
guidance must be given to contractors and owners of multifamily units as to how they
should segregate waste debris so that as moch of the debris as possible will not be
classified as hazardous.
RELOCATION DURING ABATEMENT
Under most circumstances, residents and their pets should not occupy their housing
during abatement. One of the most serious problems faced by local abatement programs
is the lack of suitable temporary housing for families while their homes are being abated.
Although relatives and friends have traditionally provided such housing, consideration
should be given to special provisions in government-subsidized or other housing
programs to deal with this special problem. Since most abatement projects take only a
week or two, each unit provided for relocation purposes could be used for 25 to 50
families per year.
INSURANCE FOR CONTRACTORS
Another constraint to rapidly expanding lead-based paint abatement programs is the lack
of insurance for contractors and building owners performing abatement work. As in the
case of asbestos, improper abatement techniques used in the early years raised concerns
among insurance companies about providing liability coverage. With the availability of
guidelines on safe practices, the marketplace can be expected to respond with coverage
at reasonable prices. Comprehensive coverage is already being provided by the
APPENDIX V - PAGE 4
<3
® »
self-insurance risk retention pool established by many large public housing authorities. It
is hoped that private insurers will soon recognize this market and provide coverage at
competitive rates. Federal, State, and local agencies should take steps to encourage or
require such coverage.
APPENDIX V -PAGE 5
DECL. OF PAUL MUSHAK
27
28
DECLARATION OF PAUI, MUSHAK, Ph.D.
I, Paul Mushak, Ph.D., declare as follows:
1. The matters stated herein are true of my own personal
knowledge. If called as a witness, I would competently and
truthfully testify consistent with the following.
2. I am a principal at PB Associates, a scientific
consulting firm in health and exposure assessment of toxic
metals and metalloids -- particularly lead. I am a senior
scientific and health hazards consultant to the U.S.
Environmental Protection Agency, the U.S. Department of
Justice, the U.S. Public Health Service, the World Health
Organization, and the Ontario, Canada, Environment Ministry.
I serve as an adjunct professor of environmental/chemical
pathology at the University of North Carolina School of
Medicine in Chapel Hill, North Carolina. Formerly, I was a
tenured medical school faculty member at the University of
North Carolina and was director of the Heavy Metals
Laboratory, an internationally recognized research and
consulting facility involved in various functions, including
blood lead research.
PROFESSIONAL BACKGROUND
3. As a chemical toxicologist and environmental health
scientist, I have more than 20 years’ professional experience
researching and writing on the toxicology, biology, and
environmental/biological chemistry of pollutant metals and
other agents, especially lead. My curriculum vitae is attached
as Exhibit A hereto.
4. I have published extensively in the national and
international scientific and public health literature with over
130 papers, abstracts, and book chapters, plus more than 15
authored/co-authored federal and international public health
risk assessment documents on metal pollutants that have served
as scientific blueprints for regulatory and legislative
actions. I have authored/co-authored numerous articles and
papers dealing specifically with lead, including: Mushak,
"U.S. Agency for Toxic Substances and Disease Registry’s Report
to Congress on Childhood Lead Poisoning in America Review and
Update," Proceedings of the First National Conference on
Laboratory Issues in Childhood Lead Poisoning Prevention 79-104
(1991); Mushak, Davis, Crocetti and Grant, "Prenatal and
Postnatal Effects of Low-Level Exposure: Integrated Summary of
a Report to the U.S. Congress on Childhood Lead Poisoning," 50
Environmental Research 11-36 (1989); Mushak and Crocetti,
"Determination of Numbers of Lead-Exposed American Children as
a Function of Lead Source: Integrated Summary of a Report to
the U.S, Congress on Childhood Lead Poisoning," 50
Environmental Research 210-29 (1989); Mushak and Crocetti,
"Methods for Reducing Lead Exposure in Young Children and Other
Risk Groups: An Integrated Summary of a Report to the U.S.
Congress on Childhood Lead Poisoning," 89 Environmental Health
Perspectives 125-35 (1990); Crocetti, Mushak, and Schwartz,
"Determination of Numbers of Lead-Exposed U.S. Children by
Areas of the United States: An Integrated Summary of a Report
to the U.S. Congress on Childhood Lead Poisoning," 89
Environmental Health Perspectives 109-20 (1990); Crocetti,
Mushak, and Schwartz, "Determination of Numbers of Lead-Exposed
Women of Childbearing Age and Pregnant Women: An Integrated
Summary of a Report to the U.S. Congress on Childhood Lead
Poisoning," 89 Environmental Health Perspectives 121-24 (1990).
5. I have been extensively involved as a principal author
and evaluator of a number of public agency health risk
assessment documents. I was a principal co-author of the EPA’s
4-volume 1986 criteria document for lead, generally considered
to be one of two federal "bibles" for lead. I was an external
expert reviewer for the U.S. Public Heath Services/U.S. Centers
for Disease Control Advisory Committee on Preventing Childhood
Lead Poisoning’s October 1991 Statement on Preventing Lead
Poisoning in Young Children ("Statement"). This Statement sets
forth the standards of the medical profession and the U.S.
Public Health Service on the medical testing for and management
of lead poisoning and is recognized as the definitive federal
statement on prevention and treatment of lead poisoning in
children.
6. I was a senior advisor to the committee preparing the
CDC’s 1985 Statement on Preventing Lead Poisoning in Young
Children and actively assisted in its preparation.
7. In 1988, I served as the senior author and scientific
manager of the Agency for Toxic Substances and Disease
Registry’s report, The Nature and Extent of Lead Poisoning in
Children in the United States: A Report to Congress (July
1988) ("Report to Congress"), which is the second of the two
federal "bibles" for lead. The Report to Congress was prepared
in compliance with Section 118(f) of the 1986 Superfund
Amendments and Reauthorization Act, 42 U.S.C. &§ 9618(f). Upon
completion, the Report to Congress was presented to the House
of Representatives’ Committee on Energy and Commerce. The
Report represents the first systematic effort to quantify the
extent of the U.S. child lead-poisoning problem and to place
such numbers in some context of distribution of the children,
the lead sources, the adverse health responses, and strategies
for lead reduction. As discussed below, two of the "take home"
messages of the Report to Congress are: (1) exposure to even
low levels of lead can have serious, persistent effects on
children and (2) lead toxicity must be measured using a blood
lead test. Excerpts from the Report to Congress are attached
as Exhibit B hereto.
8. I am a member of the American Chemical Society,
American Association for the Advancement of Science, American
Public Health Association, Association of Clinical Scientists,
International Society for the Study of Xenobiotics, New York
Academy of Sciences, Society for Environmental Geochemistry and
Health, Society for Occupational and Envivoniental Health,
Society for Risk Analysis (national, N.C.), and the Society of
Toxicology (national affiliation & N.C. chapter).
THE EFFECTS OF LEAD POISONING
9. Lead affects virtually every body system; however, in
its early stages, lead poisoning is often asymptomatic. Toxic
effects may range from subtle to profound. See Report to
Congress at Executive Summary ("Ex. Summ.") 9-11.
10. The primary target organ for lead toxicity is the
brain or central nervous system, especially during early child
development. Very severe lead poisoning (associated with lead
levels at or above 80 ug/dL) can result in coma, convulsions,
profound mental retardation, and even death. At lower
concentrations, lead mainly interferes with normal development
of IQ and other neurobehavioral measures in children; with the
body’s heme-forming system, which is critical to the production
of heme and blood; and with the vitamin D regulatory system,
which involves the kidneys and plays an important role in
calcium metabolism.
11. Effects of lead on children’s IQ and other neural
measures appear to persist. The evidence is quite compelling
that these persistent effects exist at even low levels of lead
exposure (10 ug/dL or lower). I am familiar with at least
three longitudinal studies of young children in Boston,
Cincinnati, and Australia -- all are showing that prenatal and
early childhood exposure to lead has adverse effects at low
exposure levels on a child’s IQ and other neurobehavioral
measures and that these effects persist into the school-aged
years. Thus, one of the "take home" messages of our Report to
Congress and later papers is that even low levels of lead
absorption can have persistent, adverse effects on the highly
vulnerable central nervous systems of young children.
SOURCES OF LEAD POISONING
12. Lead 1s pervasive in the environment. Children are
27
28
exposed to lead from six environmental sources, three of which
still persist as major sources or pathways: paint, dust/soil,
and water. Lead in gasoline, foods, and stationary sources is
declining in importance. Paint is the major source of lead
poisoning. Although residential use of lead-based paint is now
banned, lead paint in existing housing remains the most
widespread and dangerous high-dose source of lead exposure for
young children. Lead paint continues to be used on the
exteriors of painted steel structures, such as bridges and
expressways. Children living near such sites as expressways
have been shown to have elevated blood lead levels.
13, Lead deposited in soil or as dusts does not
biodegrade or decay since lead is a chemical element. Children
playing around contaminated dusts and soils will remain exposed
indefinitely.
14. The water distribution system can also pose a lead
risk. Contamination of drinking water occurs in or near
residences and schools when lead leaches into the water from
lead connectors, service pipes, lead-soldered joints, or lead-
lined water coolers.
15. Lead entering the body from different sources and
through different pathways presents a combined toxicological
threat. Thus, multiple, low-level inputs of lead can result in
significant aggregate exposure. See Report to Congress, 6-8,
Chapters VI and VIII.
THE EXTENT OF LEAD POISONING IN YOUNG CHILDREN
16. Lead poisoning is the major environmental threat to
27
28
the health of children. In the Report to Congress, we
concluded that, in 1984, 2.4 million white and African-American
preschool U.S. children -—- 17% of all such children -- in
metropolitan areas had projected blood lead levels exceeding 15
ug/dL. See Report to Congress, at Ex. Summ. 3-4. While some
progress has been made to reduce some sources of lead toxicity,
scientific determinations of what constitutes "safe" levels of
lead exposure are concurrently declining even further. The
history of" research in this field has, in fact, shown a
progressive decline in the lowest exposure levels at which
adverse health effects can be reliably detected. Since the
Report to Congress was published, the 1991 CDC statement on
Preventing Lead Poisoning in Young Children has identified a
blood lead level of 10 ug/dL as the new value of concern.
Notably, any subsequent declines in the prevalence of elevated
blood lead for our 1984 base year in the Report to Congress
have been offset by more children having blood lead at or above
the new CDC action level.
17. For my recent presentation to the First National
Conference on Laboratory Issues in Childhood Lead Poisoning
Prevention (Exhibit C hereto), I used additional 1984
prevalence projection data from the Second National Health and
Nutrition Examination Survey (NHANES II) to calculate the
prevalence of elevated blood lead concentrations and associated
early adverse effects at the new CDC 10 ug/dL level.
Prevalences for 5 pg/dL were estimated as well. The NHANES II
data were used heavily in the Report to Congress. NHANES III
data will not be available until sometime in 1994.
18. These new calculations show that the elevated blood
lead levels and early poisoning risks in America’s poor
communities are astounding. In smaller cities (population less
than one million), 79% of all children with family incomes
below $6000 -- 91.6 percent of African-American children --
were projected to have lead levels exceeding the new CDC action
level of 10 pug/dL in 1984. In larger cities, 88 percent of all
children with family incomes below $6000 -- 96.5 percent of
African-Americans -- were projected to be affected. For
children living in smaller cities and whose families earn
between $6000 and $14,999, approximately 67% had blood lead
levels associated with early toxicity; 83.5 percent of African-
American children in this category were affected. In larger
cities, 78.5 percent of all children whose families earn
between $6000 and $14,999 -- 92 percent of African-American
children -- had lead levels at or exceeding the 10 pg/dL level.
Prevalence of blood lead levels above 5 ug/dL, a level only
one-half that for early toxicity, in poor children was
virtually 100 percent. While corresponding prevalence for the
current year, 1992, will be lower overall (that is, over all
national strata), it is likely that inner-city, poor children
will show the smallest declines.
19. As noted in the CDC’s 1991 Statement (page 39),
almost all U.S. children are at risk for lead poisoning, and
some children are at higher risk than others. Clearly, the
statistical findings quoted in this declaration show that poor 2 hl
7
gar
27
28
children in the U.S. are at the highest risk for lead poisoning
and are virtually assured of experiencing elevated lead
absorption. Lead poisoning in its early stages is often
asymptomatic, so these children must be screened for lead
poisoning using a test. Neither the exposure setting itself
nor an oral risk questionnaire is capable of assessing blood
lead levels.
THE APPROPRIATE TEST
20. To confirm, i.e. reliably measure, the amount of
toxic lead in body fluid, a blood lead test must itself be
used. See Report to Congress at II-8, 9. The blood lead (Pb-
B) test directly measures the level of lead in whole blood.
Blood for measuring lead content can be taken from a vein in
the arm (venous blood) or from puncture of a finger tip
{Capillary blood). If the latter type of test is used,
contamination protocols must be followed and an elevated Pb-B
confirmed by venous puncture. A blood lead measurement should
not be confused with an "EP test."
21. During the early and mid 1970s, the erythrocyte
protoporphyrin (EP) test became a popular (low cost, high
volume) test for predicting whether a child was lead poisoned.
The EP test does not directly yield a specific blood lead
concentration. In children exposed to elevated concentrations
of lead, the lead interferes with the body’s ability to make
the important substance, heme. Heme is used to carry oxygen
when in the form of hemoglobin. Lead retards formation of heme
from the protoporphyrin molecule and protoporphyrin builds up
27
28
in the blood. The EP test measures this build up of
protoporphyrin. The EP test does not give directly discreet
blood lead concentrations; rather, protoporphyrin levels are a
surrogate indicator for the likelihood of elevated blood lead
levels. The test, in brief, is used to predict lead
absorption.
22. The EP test is not unique for predicting lead
exposure. It can also be used to determine iron deficiency
anemia. Therefore, one must take account of the iron
nutritional status to avoid confounding.
23. The EP test is a reasonably reliable predictor of
lead absorption at blood lead levels around 40 ug/dL. As lead
levels dip below this amount, the EP level begins to "uncouple"
from the blood lead level. Uncoupling means that the EP level
is losing its predictive value. That is, EP can occur within
the normal limits while the blood lead level is actually
elevated and toxic. By 25 ug/dL, the uncoupling is quite
significant, and there are unacceptable numbers of false
negatives. The uncoupling occurs quite steeply as the blood
lead level moves farther downward, from 25 pug/dL to 10 ug/dL.
At 10 pg/dL, the new CDC action level, there is probably total
uncoupling, and the EP test cannot be used as a predictive
surrogate for lead poisoning.
24. Data contained in the Report to Congress illustrate
this problem with false negatives. Of 118 children with Pb-B
levels above 30 pug/dL (the CDC criterion level at the time of
the NHANES II study), 47% had EP levels at or below 30 ug/dL,
10
aot A pr
\ z
27
28
and 58% had EP levels less than an EP cutoff value of 35 ug/dL.
Report to Congress at II-9. Of course, the CDC has revised the
criterion level to 10 pg/dL, an action which introduces even
more false negatives into the EP test results.
25. With respect to lead poisoning, then, the EP test
does not act as a preventive test which allows the health care
provider to detect lead poisoning at its early, more manageable
stages. Rather, the EP test can only accurately predict that
unacceptably high lead exposure and greater risk of more severe
poisoning have already occurred.
26. In July 1988, the Report to Congress formally
recommended to the Energy and Commerce Committee of the United
States House of Representatives that accurate screening tests
replace the continued use of the EP test (see Report to
Congress Recommendation 2(b), at XI-8). The Report repeatedly
told Congress of the problems associated with continued use of
the EP test to test for lead poisoning and noted that the rate
of false negatives using the EP test is considerable. See
Report to Congress at I11-8-9, V-20, V—-47, X1-8.
27. The health delivery system has responded often with
concern over changes to lead screening and testing protocols.
There had been complaints to the 1991 CDC Statement advisory
group regarding increased work requirements that will result
from lowering the definitions of lead poisoning, for example.
Experience has shown us, however, that any predicted chaos does
not occur. The system has been able to handle the change.
28. Cost is not an adequate justification for continued [J
use of the EP test in testing young, Medicaid-eligible children
for lead poisoning. Because of its unreliability for
accurately predicting elevated Pb-B around the new CDC action
level, the EP test -- which I estimate to cost somewhere under
$10 (depending on economies of scale and type of testing) is
probably a waste of money for lead absorption prediction. EP
testing for iron deficiency, of course, remains appropriate.
I estimate the cost of the blood lead tests in public health
laboratories at somewhere between $10-$15, depending on volume
and other economies of scale. Private laboratories may be able
to provide the test even more cheaply if large volumes of
screening samples were contractually guaranteed.
29. As noted in the Report to Congress, screening
programs, especially blanket screening, are particularly cost-
effective. This is demonstrated by comparing data on the costs
of treating children who are poisoned because early lower
levels of lead intoxication were not detected by screening with
the costs of testing. In the example used in the Report, the
ratio of medical costs to child screening costs was about 50:1
in 1986 dollars. Given this highly favorable cost-
effectiveness, the issue of a somewhat more expensive blood
lead test over an EP test is relatively trivial in terms of
overall costs of lead poisoning to the health system and
society. See Report to Congress at IX-21-22.
30. Delaying blood lead testing of Medicaid-eligible
children is also not justified by concerns regarding laboratory
capacity. Recent legislation should already have moderated to
12.
[= L
27
28
some extent the effect of any stated concerns regarding quality
control. In 1988, the Clinical Laboratory Improvement Act was
amended to tighten quality assurance and quality control in all
laboratories and for all measurements, not just blood lead.
So, laboratories should already be operating with more of the
stringent quality control measures than before and, implicit in
this, be able reliably to measure Pb-B at or around the CDC 10
pug/dL value. Public laboratories exist in every state and
territory, and there are huge private laboratories (e.g. Roche,
MetPath) that can be mobilized in a big way to share the test
volume. These private laboratories already adhere to tight
confidentiality and quality control standards in their use of
tests for employers and some public entities in, e.g., drug use
screening. Both public and private laboratories can react
quickly to an increased volume of blood lead tests -- the
laboratories and their administrative infrastructures already
exist, so the expansions needed are horizontal, i.e., lateral
in nature (to expand staff and equipment) rather than vertical
(to build new infrastructures and create new facilities).
31. In summary, then, the question of an appropriate test
for lead exposure and lead poisoning in Medicaid children is
not arguable on cost or other logistical grounds but on such
technical merits as accuracy and freedom from under-reporting
the prevalence of lead poisonings. Using the example from our
Report, the averted medical cost would be about $20,000 to
$25,000 per child in 1992 health care dollars. The unit child
costs for expanding or setting up more accurate blood lead
2 [screening would itself be a trivial fraction of the medical
3 |costs that are averted through use of the appropriate test.
4 I declare under the penalty of perjury that the foregoing
5|is true and correct, this #0 day of November 1992 in Durham,
6 [North Carolina.
7 Se a
Paul Mushak, Ph.D.
MOSHAK
EXHIBIT A
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NAME:
ADDRESS:
PHONE:
DATE/PLACE OF BIRTH:
MARITAL STATUS:
MILITARY SERVICE:
EDUCATION:
EMPLOYMENT HISTORY:
Present Position:
Past Positions:
11/23/86-6/5/87
7/1/77-12/31/85
CURRICULUM VITAE
Paul Mushak SSN:208-28-8852
811 Onslow St.
Durham, N.C. 27705
(919) 286-3854
Dec. 9, 1935; Dunmore, Pa.
m. Elizabeth W. Mushak
U.S. Army (Medical Corps), 8/54- 8/57;
Honorable discharge
B.S. Chemistry (Magna Cum Laude), University of Scranton,
Scranton, Pa., 1961
Ph.D. Metalloorganic/organic chemistry and biochemistry,
University of Florida, Gainesville, Fla., 1970.
Research assistant/associate, clinical toxicology/clinical chemistry, Pathology Department, University of Florida School of Medicine,
1/67-11/69.
Dissertation Title: Addition and Rearrangement Reactions
Involving Various Organopalladium Compounds.
Postdoctoral Study: Fellow, Department of Molecular Biophysics and Biochemistry, School of Medicine, Yale University, New
Haven, Conn., 11/69-6/71.
Principal, PB Associates; Consulting toxics scientist: toxicology, risk assessment, and relevant chemical aspects of pollutant metals and metalloids :
Adjunct Professor, Department of Pathology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, N.C.
Special appointment as expert adviser, U.S. Public Health Service, Agency for Toxic Substances and Disease Registry, Atlanta, Ga.
Associate Professor, Department of Pathology, School of Medicine,
University of North Carolina, Chapel Hill, N.C.
7/77-12/31/85 Research Scientist, Biological Sciences Research Center, University
of North Carolina.
7/1/71-7/11177 Assistant Professor, Department of Pathology, University of North
Carolina, Chapel Hill, N.C.
8/75-6/76 Consultant, Environmental Health Hazard Project, American
Public Health Association, Washington, D.C.
1/67-11/69 Research Assistant/Associate, Department of Pathology, University
of Florida School of Medicine, Gainesville, Fla.
9/62-11/69 Predoctoral Research Fellow, Chemistry Department, University of
Florida.
6/61-7/62 NIH Trainee, Biochemistry Department, University of Florida
School of Medicine.
PROFESSIONAL SOCIETIES: -
American Chemical Society
American Association for the Advancement of Science
American Public Health Association
Association of Clinical Scientists
International Society for the Study of Xenobiotics
Society for Environmental Geochemistry and Health
Society for Occupational and Environmental Health
Society of the Sigma Xi
Society for Risk Analysis (National & N.C.)
Society of Toxicology (National affliliation & N.C. Chapter)
PROFESSIONAL SERVICE:
Consultancies:
1/1/77- Senior Scientific and Health Hazards Consultant, Environmental
Protection Agency, Environmental Criteria and Assessment Office,
Research Triangle Park; N.C., and Cincinnati, Ohio.
1/1/81- Health Effects Consultant, Office of Carcinogen Standards, Occupational
Safety and Health Administration, U.S. Department of Labor,
Washington, D.C.
6/1/75- National Institute of Environmental Health Sciences, P.O. Box 12233,
Research Triangle Park, N.C.
4/1/85- External Review Committee, Hazardous Substances Branch, Ontario
1% |
Ministry of the Environment, Toronto, Ontario, Canada.
Committees of the National Academy of Sciences:
Committee on Measuring Lead Exposure in Infants, Children and Other Sensitive
Populations, National Academy of Sciences/National Research Council
Joint Workshop Committee: National Academy of Sciences and Councils of
Academies of Sciences and Arts of Yugoslavia: Exposure to Heavy Metals in the
Environment
Zinc Panel, Medical and Biological Effects of Air Pollutants, National Academy
of Sciences/ National Research Council
Committees of the World Health Organization:
Advisor and Rapporteur, Air Quality Guidelines Program, Regional Office for
Europe, World Health Organization, 8 Scherfigsvey, DK 2100 Copenhagen,
Denmark.
Member, Interim Working Group, International Programme on Chemical Safety,
Environmental Health Criteria 101 Methyl Mercury. December 1988/ June 1989.
Other Public Committees:
North Carolina Child Lead Poisoning Advisory Committee
Lead Exposure Subcommittee, Clean Air Scientific Advisory Committee, U.S.
Environmental Protection Agency
Corresponding Member, Subcommittee on Nickel, International Union of Pure
and Applied Chemistry, 6/79-1/88
Other Professional Activities:
Testimony before the U.S. Congress:
U.S. House Subcommittee on Health and the Environment, Rep. Henry
Waxman (D-Calif.), Chairman, Dec. 10, 1987, Washington, D.C., Lead in
Drinking Water of Schools and Other Public Facilities;
U.S. House Subcommittee on Health and the Environment, Rep. Henry
Waxman (D-Calif.), July 13, 1988, Washington, D.C., testimony in
support of H.R. 4939 to regulate lead in drinking water.
Expert Witness for the U.S. Department of Justice:
A principal expert witness, United States vs, Sharon Steel Corp. et al..
Midvale, UT; action under CERCLA (Superfund).
A principal expert witness, United States vs, Apache Chemical Co, et al.,
California Gulch, Leadville, CO; action under CERCLA (Superfund).
Service in various capacities for the U.S. Environmental Protection
Agency, including Clean Air Act pollutants, health assessment documents
for hazardous pollutants, toxic substances, and Superfund scientific
activities. These activities include numerous workshop reviews, 1977-
present.
ADMINISTRATIVE ACTIVITIES:
1975-1985: Co-Principal Investigator, Neurobiology of Environmental Pollutants, NIEHS.
1971-1985: Director, Heavy Metals Laboratory, University of North Carolina School of
Medicine.
1/86-Current: Owner and Principal, Scientific consulting firm in health and exposure
assessment of toxic metals, metalloids, and organic pollutants for Federal and
international agencies
5/88-6/90: Owner and technical director, TRUE-TEX, laboratory services to the
historical and decorative fiber arts
HONORS:
Undergraduate research scholarships, 1958-1960. Joint Program, University of Scranton,
Jefferson Medical College, and Health and Welfare Fund, United Mine Workers of
America.
NSF Undergraduate Research Program, 1960-1961.
Research Award, University of Southern California- Continental Oil Co., Annual
National Contest in Surface and Colloid Chemistry, 1961.
NIH Trainee, University of Florida, 1961-1962.
American Cancer Society Institutional Fellowship, University of Florida, 1962-1963.
NSF and U.S. Air Force AFOR Research Assistantships, University of Florida, 1963-
1967.
Yale Corporation Fellow, Yale Medical School, 1969-1971
Award for Meritorious Service, U.S. EPA, Cincinnati, Ohio- January 1981.
RESEARCH INTERESTS:
Toxicological chemistry and toxicology of metals/organometals; toxic metal/metalloid
monitoring; metal toxicokinetics and metabolism; toxicokinetics of environmental metals
in large populations.
PUBLICATIONS
P. Mushak, J. Weiss and W. Haab: Some in-vitro relationships with reference to surface activity
and cholesterol. Proc, Penna, Acad. Sci. 35: 169-173 (1961).
J. Savory, P. Mushak,, N.O. Roszel and F.W. Sunderman, Jr.: Determination of chromium in
serum by gas-liquid chromatography. Fed, Proc,, 777 (1968).
J. Savory, N.O. Roszel, F.W. Sunderman, Jr., and P. Mushak: An improved procedure for the
determination of serum ethanol by gas-liquid chromatography. Clin, Chem, 14: 132 (1968).
J. Savory, N.O. Roszel, P. Mushak and F.W. Sunderman, Jr.: Measurements of thallium in
biological media by atomic absorption spectrometry. Amer, J, Clin, Path, 50: 505 (1968).
P. Mushak and M.A. Battiste: A novel palladium (II) Chloride-catalyzed reaction of terminal
olefins with diphenylacetylene. Chem. Comm., 1146 (1969).
P. Mushak and M.A. Battiste: The reaction of 1,2,3-triphenylcyclopropene with palladium (II)
chloride. A novel ring-opening reaction in the cyclopropene series. J, Organometal, Chem, 17:
P46 (1969).
J. Savory, P. Mushak and F.W. Sunderman, Jr.: Measurement of chromium in urine. In:
Laboratory Diagnosis of Toxic Agents, F.W. Sunderman, Sr. and F.W. Sunderman, Jr., Eds.
W.H. Green Co., St. Louis, 1970.
J. Savory, P. Mushak, F.W. Sunderman Jr., R.H. Estes and N.O. Roszel: Determination of
chromium in biological media by gas chromatography. Anal. Chem. 42: 294 (1970).
J.S. Taylor, P. Mushak and J.E. Coleman: Electron spin resonance studies of carbonic
anhydrase. Transition metal ions and spin-labeled sulfonamides. Proc. Nat. Acad. Sci._(USA)
67: 1410 (1970).
P. Mushak and J.E. Coleman: Hydrolysis of a stable oxygen ester of phosphorothioic acid by
alkaline phosphatase. Biochemistry 11: 201 -205 (1972).
P. Mushak and J.E. Coleman: Electron spin resonance studies of spin-labeled carbonic
anhydrase. J. Biol. Chem, 247: 373-380 (1972).
P. Mushak, J.S. Taylor and J.E. Coleman: Proton hyperfine splitting in the ESR procedure for
alkaline phosphatase. Biochem. Biophys. Acta 261: 332-338 (1972).
P. Mushak: Gas-liquid chromatography in the analysis of mercury (II) compounds. Environ,
Health Perspect. 2: 55-60 (1973).
P. Mushak: Fluoro-B-diketones and metal fluoro-B-diketonates. Fluorine Chemistry Reviews.
Vol. 6, P. Tarrant, Ed., Marcel Dekker, Inc., New York, 1973, pp. 43-133.
P. Mushak, F.E. Tibbetts, III, P. Zarnegar and G.B. Fisher: Perhalobenzenesulfinates as
reagents in the determination of inorganic mercury in various media by gas-liquid
chromatography. J. Chromatog, 87: 215-226 (1973).
P. Zarnegar and P. Mushak: Quantitative measurements of inorganic mercury and
organomercurials in water and biological media by gas-liquid chromatography. Anal, Chim,
Acta 69: 389-401 (1974).
A.W, Fitchett, P. Mushak and R.P. Buck: Direct determination of heavy elements in biological
media by spark-source mass spectrometry. Anal, Chem, 46: 710-713 (1974).
M.R. Krigman, D.T. Traylor, E.L. Hogan and P. Mushak: Subcellular distribution of lead in
the brains of intoxicated and control rats. J. Neuropath, Exper. Neurol. 33: 176 (1974).
B.A. Fowler, G.W. Lucier and P. Mushak: Phenobarbital protection against methylmercury
nephrotoxicity. Proc, Soc, Exp, Biol, Med. 149: 74-79 (1975).
T.W. Bouldin, P. Mushak, L.A. O’Tuama and M.R. Krigman: Blood-brain barrier dysfunction
in acute lead encephalopathy: A reappraisal. Environ, Health Perspect, 12: 81-88 (1975).
E.H. Daughtrey, Jr., A.W. Fitchett and P. Mushak: Quantitative measurements of inorganic
and methyl arsenicals by gas-liquid chromatography. Anal. Chim, Acta 79: 199-206 (1975).
A.W. Fiichett, E.H. Daughtrey, Jr., and P. Mushak: Quantitative measurements of inorganic
and organic arsenic by flameless atomic absorption spectrometry. Anal, Chim, Acta 79: 93-99
(1975).
R.A. Fiato, P. Mushak and M.A. Battiste: Intramolecular cyclization of pi-1-chloro-3-
phenylallylpalladium (II) compiexes. Novel route to stable indenyl complexes of palladium (II).
J. Chem. Soc., Chem. Comm. 869-871 (1975).
L.A. O’Tuama, C.S. Kim, J.T. Gatzy, M.R. Krigman and P. Mushak: The distribution of
inorganic lead in guinea pig brain and neural barrier tissues. Observations in control and lead-
poisoned animals. Toxicol. Appl. Pharm. 36: 1-9 (1976).
G.T. Barthalmus, J.D. Leander, D.E. McMillan, P. Mushak and M.R. Krigman: Chronic
effects of lead on schedule-controlled pigeon behavior. Toxicol. Appl. Pharmacol. 42: 271-284
(1977).
R.A. Goyer and P. Mushak: Lead Toxicity: Laboratory Aspects in Toxicology of Trace
Elements, R.A. Goyer and M.A. Mehlman, Eds., Vol. II, John Wiley and Sons/Halsted Press,
New York, 1977, pp. 41-77.
M.R. Krigman, P. Mushak and T.W. Bouldin: An appraisal of rodent models of lead
encephalopathy. Neurotoxicology, L. Roizin, H. Shiraki and N. Greevic, Eds. Raven Press, New
York, 1977, pp. 299-302.
P. Mushak: Advances in the analysis of toxic heavy elements having varying chemical forms. J.
Aniul. Toxicol. 1: 286-291 (1977).
P. Mushak: The Gas-Liquid Chromatography of Metals Via Chelation and Non-Chelation
Techniques. In: Handbook of Derivatives for Chromatography, K. Blau and G.S. King, Eds.
Heyden and Son, Ltd., London, 1977.
P. Mushak: Chapter 13- Analysis of Zinc in Various Media. In: Zinc. National Academy of
Sciences/National Research Council, Washington, D.C., 1977.
P. Mushak, K. Dessauer and E.L. Walls: The bioanalysis of arsenic using gas-liquid
chromatography and flameless atomic absorption spectrometry. Environ, Health Perspect, 19: 4-
10 (1977).
R.B. Mailman, M.R. Krigman, R.A. Mueller, P. Mushak and G.R. Breese: Lead exposure
during infancy permanently increases lithium-induced polydipsia. Science 201: 637-639 (1978).
D.K. Routh, P. Mushak and L. Boone: A new syndrome of elevated blood lead and
microcephaly. J, Ped, Psychol, 4: 67-76 (1979).
P. Petrusz, C.M. Weaver, L.D. Grant, P. Mushak and M.R. Krigman: Lead poisoning and
reproduction: Effects on pituitary and serum gonadotropins in neonatal rats. Environ, Res, 19:
383-391 (1979). :
D.D. Dietz. D.E. McMillan and P. Mushak: Effects of chronic lead administration on acquisition
and performance of serial positional sequences by pigeons. Toxicol. Appl, Pharmacol, 47: 377-
384 (1979).
M.R. Krigman, P. Mushak and T.W. Bouldin: Lead Neurotoxicity. In: Experimental and
Clinical Neurotoxicity, P.S. Spencer and H.H. Schaumburg, Eds., Williams and Wilkins Co.,
New York, 1980, pp. 490-507. :
C.R. Millar, S.R. Schroeder, P. Mushak, J.D. Dolcourt and L.D. Grant: Contributions of the
care-giving environment to increased lead burden of children. Amer. J. Mental Def, 84: 339-344
(1980).
P. Mushak: Metabolism and Systemic Toxicity of Nickel. In: Nickel in the Environment, J.
Nriagu, Ed., J. Wiley and Sons/ Interscience, New York, 1980, pp. 499-523.
S. Piomelli, L. Corash, M.B. Corash, C. Seaman, P. Mushak, B. Glover and R. Padgett. Blood-
lead concentrations in a remote Himalayan population. Science 210: 1135-1137 (1980).
W.D. Blaker, M.R. Krigman, D.J. Thomas, P. Mushak and P. Morell: Effect of triethyl tin on
myelination in the developing rat. J. Neurochem, 36: 44-52 (1981).
C.R. Millar, S.R. Schroeder, P. Mushak and L. Boone: Failure to find hyperactivity in
preschool children with moderately elevated lead burden. J. Pediatric Psvchol. 6: 85-95 (1981).
D.A. Otto, S.R. Schroeder, P. Mushak, K. Muller and M. Crenshaw: Prospective studies of
electrophysiological assessment of central nervous system function in children with elevated body
lead burden. In: Proc. International Conference on Prospective Studies of Lead Toxicity.
Cincinnati, Ohio. In press.
S.R. Schroeder, R.C. Kanoy, C.R. Millar, P. Mushak and D.A. Otto: Child-caregiver
interactions with lead exposure. In: Proc. International Conference on Prospective Studies of
Lead Toxicity Cincinnati, Ohio. In press. ;
E. Anders, C.R. Bagnell, Jr., M.R. Krigman and P. Mushak: Influence of dietary protein
composition on lead absorption in rats. Bull, Environ, Contam. Toxicol, 28: 61-67 (1982).
P. Mushak, M.R. Krigman and R.B. Mailman: Comparative organotin toxicity in the
developing rat: Somatic and morphological changes and relationship to accumulation of total tin.
Neurohehav, Toxicol. Teratol, 4: 209-215 (1982).
E. Anders, D.D. Dietz, C.R. Bagnell, Jr., J. Gaynor, M.R. Krigman, D.W. Ross, J.D. Leander
and P. Mushak: Morphological, pharmacokinetic and hematological studies of lead-exposed
pigeons. Environ, Res, 28: 344-363 (1982).
C.R. Millar and P. Mushak: Lead-Contaminated Housedust: Hazard, Management, and
Decontamination. In: Proceedings of the Conference on Management of Increased Lead
Absorption in Children: Management, Clinical, and Environmental Aspects. J.J. Chisolm, Jr.,
and D.M. O’Hara, Eds., Urban and Schwartzenberg, 1982, pp. 143-152.
D.J. Thomas, H.L. Fisher, L.L. Hall, and P. Mushak: Effects of age and sex on retention of
mercury by methylmercury treated rats. Toxicol. Appl, Pharm, 62: 445-454 (1982).
P. Mushak. Mammalian biotransformation processes involving various toxic metalloids and
metals. In: Chemical Toxicology and Clinical Chemistry of Metals, (S.S. Brown and J. Savory,
Eds.), Academic Press, London, 1983, Pp. 227-245. :
D. Otto, V. Benignus, K. Muller, C. Barton and P. Mushak. Event-related slow brain potential
changes in asymptomatic children with secondary exposure to lead. In: Neurobehavioral
Methods in Occupational Health: Advances in the Biosciences, V. 46, Pergamon, New York,
1983, pp.295-300.
A.D. Toews, W.D. Blaker, D.J. Thomas, J.J. Gaynor, M.R. Krigman, P. Mushak and P.
Morell. Myelin deficits produced by early postnatal exposure to inorganic lead or triethyltin are
persistent. J. Neurochem, 41: 816-822 (1983).
P. Mushak: Analysis of Total and Form-Variable Tin in Various Media. Proceedings:
International Conference on Neurotoxicology of Selected Chemicals. Neurotoxicology 5: 163-176
(1984).
P. Mushak: Nickel Metabolism in Health and Disease. In: Clinical Laboratory Annual, Vol. 3.
H.A. Homberger and J.G. Batsakis, Eds. Appleton-Century-Crofts, Norwalk, Ct., 1984, pp.
249-269.
T.W. Bouldin, M.E. Meighan, J.J. Gaynor, W.D. Gaines, P. Mushak and M.R. Krigman: Lead
neuropathy: Differential vulnerability of mixed and cutaneous nerves in lead neuropathy. J,
Neuropathol. Exp. Neurol. 44: 384-396 (1985).
R.A. Goyer, J. Bachmann, T.W. Clarkson, G.F. Ferris, Jr., J. Graham, P. Mushak, D.P. Perl,
D.P. Rall, R. Schlesinger, W. Sharpe and J.M. Word: Potential Human Health Effects of Acid
Rain: Report of a Workshop. Environ, Health Perspect, 60: 355-368 (1985).
P. Mushak: The Potential Impact of Acid Precipitation on Arsenic and Selenium. Environ,
Health Perspect, 63: 105-113 (1985).
D.A. Otto, G. Robinson, S. Baumann, S. Schroeder, P. Mushak, D. Kleinbaum, C. Barton and
L. Boone. Five-year follow-up study of children with low-to-moderate lead absorption:
Electrophysiological evaluation. Environ, Res, 38: 168-186 (1985).
G.S. Robinson, S. Baumann, D. Kleinbaum, C. Barton, S.R. Schroeder, P. Mushak and D.A.
Otto. Effects of low to moderate lead exposure on brain stem auditory evoked potentials in
children. WHO Regional Office for Europe, Copenhagen, Denmark (Environmental Health
Document 3), pp. 177-182 (1985).
S.R. Schroeder, B. Hawk, D.A. Otto, P. Mushak and R.E. Hicks. Separating the effects of lead
and social factors on IQ. Environ. Res. 38: 144-154 (1985).
D.K. Orren, J.C. Caldwell-Kenkel and P. Mushak. Quantitative analysis of total and trimethyl
lead in mammalian tissues using ion exchange HPLC and atomic absorption spectrometric
detection. J. Anal, Toxicol. 9: 258-261 (1985).
M.R. Krigman, T.W. Bouldin and P. Mushak. Metal toxicity in the nervous system. In: The
Pathologist and the Environment, (D.G. Scarpelli, J.E. Craighead and N. Kaufman, Eds.),
International Academy of Pathology Monograph, Williams and Wilkins, Baltimore, 1985, pp.
58-100. |
B.A. Hawk, S.R. Schroeder, G. Robinson, D. Otto, P. Mushak, D. Kleinbaum and E. Dawson.
Relation of lead and social factors to IQ of low SES children: a partial replication. Am. J. Ment.
Defic. 91: 178-183 (1986).
D.K. Orren, W.M. Braswell and P. Mushak. Quantitative analysis of ethyltin compounds in
mammalian tissue using HPLC/FAAS. J. Anal. Toxicol. 10: 93-97 (1986).
D.J. Thomas and P. Mushak. Effects of Cadmium exposure on zinc and copper distribution in
neonatal rats. Arch. Toxicol. 58: 130-135 (1986).
D.J. Thomas, H.L. Fisher, M.R. Sumler, A.H. Marcus, P. Mushak and L.L. Hall. Sexual
differences in the distribution and retention of organic and inorganic mercury in
methylmercury-treated rats. Environ. Res. 41: 219-234 (1986).
D.J. Thomas, H.L. Fisher, M.R. Sumler, P. Mushak, L.L. Hall. Sexual differences in the
excretion of organic and inorganic mercury by methylmercury-treated rats. Environ. Res, 43:
203-216 (1987).
P. Mushak. The quantitative measurement of methyl mercury. In: The Toxicity of Methyl
Mercury, C.U. Eccles and Z. Annau, Eds, Johns Hopkins University Press, Baltimore, MD,
1987, pp. 1-12.
P. Mushak. Interactive relationships as modifiers of metal toxicity with special reference to those
of lead and those of selenium. In: Selected Aspects of Exposure to Heavy Metals in the
Environment, National Academy Press, Washington, D.C., 1987, pp. 36-41.
P. Mushak. co-editor, Air Quality Guidelines for Europe ( The Non-Carcinogenic Metals
Cadmium, Lead, Manganese, Mercury and Vanadium). WHO Regional Publications: European
Series No. 23, World Health Organization, Regional Office for Europe, Copenhagen, 1987.
D.J. Thomas, H.L. Fisher, M.R. Sumler, L.L. Hall, P. Mushak. Distribution and retention of
organic and inorganic mercury in methyl mercury-treated neonatal rats. Environ, Res., 47: 59-
71, 1988.
P. Mushak. Biological monitoring of lead exposure in children: overview of selected biokinetic
and toxicological issues. In: M. Smith, L.D. Grant and A. Sors, Eds., Lead Exposure and Child
Development: An International Assessment. Lancaster, United Kingdom. Kluwers Academic
Press, 1989, pp. 129-145.
P. Mushak, J.M. Davis, A.F. Crocetti, and L.D. Grant. Prenatal and postnatal effects of
low-level lead exposure: Integrated summary of a report to the U.S. Congress on childhood lead
poisoning. Environ. Res, 50: 11-26, 1989.
P. Mushak and A.F. Crocetti. Determination of numbers of lead-exposed American children as
a function of lead source: Integrated summary of a report to the U.S. Congress on childhood
lead poisoning. Environ. Res. 50: 210-229, 1989.
L.D. Grant and P. Mushak. Specification of metals and metal compounds: Implications for
biological monitoring and development of regulatory approaches. Toxicol. Indust. Health 5: 891-
897 (1989).
A.F. Crocetti, P. Mushak, and J. Schwartz. Determination of numbers of lead-exposed U.S.
children by areas of the United States: An integrated summary of a report to the U.S. Congress
on childhood lead poisoning. Environ. Health Perspect. 89: 109-120, 1990.
A.F. Crocetti, P. Mushak and J. Schwartz. Determination of numbers of women of child-
bearing age and pregnant women by areas of the United States: An integrated summary of a
report to the U.S. Congress on childhood lead poisoning. Environ, Health Perspect, 89: 121-124,
1990.
P. Mushak and A.F. Crocetti. Methods for reducing lead exposure in young children and other
risk groups: An integrated summary of a report to the U.S. Congress on childhood lead
poisoning. Environ. Health Perspect. 89: 125-135, 1990.
P. Mushak. The monitoring of human lead exposure, In: (H.L. Needleman, ed.) Human Lead
Exposure, CRC Press, Boca Raton, Fla., 45-64, 1991.
P. Mushak. Gastrointestinal absorption of lead in children and adults: Overview of biological
and biophysico-chemical aspects. Chemical speciation and Bioavailability 3: 87-104, 1991.
P. Mushak. The Agency for Toxic Substances and Disease Registry’s Report to Congress on
childhood lead poisoning in America: Overview and Update. Proceedings of the First National
Conference: Laboratory Issues in Childhood Lead Poisoning Prevention, Association of State
and Territorial Public Health Laboratory Directors, Washington, D.C., 79-104, 1991.
P. Mushak. Perspective: Defining lead as the premiere environmental health issue for children in
America: Criteria and their quantitative application. Environ, Res. 59: in press, 1992.
P. Mushak. New directions in the toxicokinetics of human lead exposure. Neurotoxicology, in
press.
P. Mushak. Commentary. The landmark Needleman study of childhood lead poisoning:
Scientific and social aftermath. PSR Quarterly, 2: 165-170.
Driscoll, W., Mushak, P., Garfia, J., and Rothenberg, S.J. Public health benefits of gasoline
lead reduction: Mexico’s experience. Environ, Sci, Technol, 26: 1702-1705.
ABSTRACTS
P. Mushak and M.A. Battiste: The reaction of 1,2,3-triphenylcyclopropene with palladium (II)
chloride. Synthesis of a novel Pi-allyl palladium (II) complex. 1968 Meeting, Florida Section,
American Chemical Society, Orlando, Florida, May 1968.
P. Mushak, J. Savory, N.O. Roszel and F.W. Sunderman, Jr.: Determination of chromium in
serum by gas chromatography. 1bid,
J. Savory, P. Mushak, N.O. Roszel and F.W. Sunderman, Jr.: Measurements of chromium in
urine. Association of Clinical Scientists’ Applied Seminar on the Laboratory Diagnosis of Toxic
Agents. Washington, D.C., November 1968.
J. Savory, P. Mushak, N.O. Roszel and F.W. Sunderman, Jr.: Measurements of chromium in
biological media. Fifth International Symposium on Advances in Chromatography, Las Vegas,
Nevada, January 1969.
R.C. Elser, P. Mushak and J. Savory: Determination of lead in blood by atomic absorption
spectrometry. 1969 Meeting, American Association of Clinical Chemists, Denver, Colorado,
Aug. 10, 1969.
M.T. Glenn, P. Mushak and J. Savory: Arylperfluorohexane-1,3-diones as chelating agents,
GLC and mass spectral studies of selected divalent metal derivatives. 1970 Meeting, Florida
Section, American Chemical Society, Cypress Gardens, Fla., May 1970.
P. Mushak: Measurement of mercury compounds in biological media by GLC. Symposium:
Mercury, Biology and Analysis. Interuniversity Consortium for Environmental Studies, Chapel
Hill, N.C. Sept. 26-27, 1972. :
P. Mushak, G.B. Fisher, P. Zarnegar, G.W. Lucier and R. Klein: Levels and distribution of
inorganic and methylmercury in rats and mice administered methylmercury. 24th Annual
Southeastern Regional Meeting, American Chemical Society, Birmingham, Ala., Nov. 2-4, 1972.
D.L. Leonard and P. Mushak: Comparative effects of equivalent dose administration of NTA
and EDTA salts on blood glucose and selected metal levels in rats. Ibid.
| 410
P. Zarnegar and P. Mushak: Quantitative determination of inorganic mercury and
organomercurials in biological media using gas-liquid chromatography. Ibid.
F.E. Tibbetts, P. Zarnegar and P. Mushak: Perhalobenzenesulfinates as reagents in the gas-
liquid chromatographic determination of inorganic mercury in biological media. Ibid.
G.W. Lucier, P. Mushak, B.A. Fowler, M.D. Folsom and C. Wratten: Methylmercury-induced
changes in rat liver microsomes. Symposium: Heavy Metals in the Environment, March 8-9,
1973, Research Triangle Park, N.C. Environ. Health Perspect. 5: 95 (1973).
B.A. Fowler, G.W. Lucier, M.D. Folsom, H.W. Brown and P. Mushak: Phenobarbital
protection against methylmercury nephrotoxicity. Ibid.
P. Mushak: Gas-liquid chromatographic techniques in the estimation of inorganic mercury. Ibid.
B.A. Fowler, H.W. Brown, G.W. Lucier and P. Mushak: Ultrastructural evaluation of
protection against methylmercury toxicity by sodium phenobarbital. Fed, Proc, 32: Abs. 2440
(1973).
A.W. Fitchett, P. Mushak and R.P. Buck: The direct determination of heavy metals in
biological media by spark-source mass spectrometry. 1973 Southeastern Regional Meeting,
American Chemical Society, Charleston, S.C., Nov. 7-9, 1973, Abs. 64.
D.L. Leonard, P.R. Maulden and P. Mushak: Measurements of chromium in hair and soft
tissue using flameless atomic absorption (FAA) spectrometry. Ibid. Abs. 71.
W.H. Bobbitt and P. Mushak: The determination of tetra- and triethyl lead in biological media
by gas-liquid chromatography. Ibid. Abs. 70.
D.L. Leonard and P. Mushak: Equivalent dose effects of NTA and EDTA salts on selected
essential element levels in rats. Ibid. Abs. 151.
P. Mushak, M. Cates, M.R. Krigman, D.T. Traylor and E.L. Hogan: Distribution of lead in
various fractions of brain in control and lead-treated rats. Ibid. Abs. 173.
P. Zarnegar and P. Mushak: The use of arylboron (III) and alkylcobalt (III) reagents in the
GLC analysis of water and biological media for inorganic and organic mercury. Ibid. Abs. 76.
L.A. O’Tuama, J.L. Howard, P. Mushak and M.R. Krigman: Distribution of *°Pb in choroid
plexus, brain and meninges of normal and lead-poisoned guinea pigs: modification by a cardiac
glycoside. Symposium: Heavy Metals in the Environment, Durham, N.C., May 9-10, 1974.
Environ. Health Perspect. 1C: 266 (1975).
J.F. Moore, P. Mushak and M.R. Krigman: Selected subcellular distribution studies of lead in
the rodent central nervous system. lbid. 265 (1975).
A.W. Fitchett, C. Ku and P. Mushak: Evaluation of arsenic in urine and water using flameless
atomic absorption spectrometry and an electrodeless discharge lamp. Ibid. 265 (1975).
P. Mushak and A.W. Fitchett: Preliminary gas-liquid chromatographic studies of inorganic and
organic arsenicals. Ibid. 166 (1975).
M.R. Krigman, J.F. Moore and P. Mushak: Distribution of lead in glial and neuronal fractions
of rat cerebral cortex. J, Path, 78: 17 (1975).
L.D. Grant, G.R. Breese, J.L. Howard, M.R. Krigman and P. Mushak: Neurobiology of lead
intoxication in the developing rat. Fed. Proc. 35: 503 (1976).
G.T. Barthalmus, J.D. Leander, D.E. McMillan, P. Mushak and M.R. Krigman: Effects of
chronic lead ingestion on the schedule-controlled behavior of pigeons. Environ, Health Perspect.
17: 290 (1976).
M.R. Krigman, P. Mushak, J.C. Hayward, A.D. Toews and P. Morell: Ac:te lead
encephalopathy in the suckling rat: A study of isolated capillaries. Am. J, Fath, 86: 40 (1977).
R.B. Mailman, M.R. Krigman, P. Mushak, R.A. Mueller and G.R. Breese: Lead enhances
lithium-induced polydipsia. Pharmacologist 19: 37 (1977).
D.D. Dietz, D.E. McMillan and P. Mushak: Effects of chronic lead administration on acquisition
and performance of serial positional sequences by pigeons. Toxicol. Appl. Pharmacol. 45:
(1978).
S. Piomelli, C. Seaman, L. Corash, M. Corash and P. Mushak: The "normal" blood Pb level of
children reflects environmental pollution. American Pediatric Society Annual Meeting, Atlanta,
Ga., May 1979.
D.J. Thomas, H.L. Fisher, L.L. Hall and P. Mushak: Comparative Hg distribution following
methylmercury administration in neonatal and adult rat. The Toxicologist 1: 122, Abs. 443,
1981.
G.J. Harry, J.F. Goodrum, P. Mushak, M.R. Krigman and P. Morell: CNS damage resulting
from inorganic lead is not directly related to blood lead level. Fed. Proc., Vol. 41, p. 1561 (Abs.
7544), 1982.
D. Otto, G. Robinson, S. Baumann, D. Kleinbaum, C. Barton, S. Schroeder and P. Mushak:
Effects of low to moderate lead exposure on brainstem auditory evoked potentials in chiidren.
Second International Symposium on Neurobehavioral Methods in Occupational and
Environmental Health, Copenhagen, June 1985.
D.A. Otto, S.B. Baumann, G.S. Robinson, S.R. Schroeder, D.G. Kleinbaum, C.N. Barton and
P. Mushak: Auditory and visual evoked potentials in children with undue lead absorption.
Annual Meeting, Society of Toxicology, San Diego, CA, March 1985.
B.A. Hawk, S.R. Schroeder, S. Robinson, D.A. Otto, P. Mushak and C.N. Barton: Effects of
lead on cognitive function of black children from low socioeconomic status (SES) families: a
replication. Annual Meeting, Society of Toxicology, San Diego, CA, March 1985.
S.B. Baumann, G.S. Robinson, D.A. Otto, C.N. Barton, P. Mushak and S.R. Schroeder: Late
positive brain waves (P3) elicited by auditory stimuli in lead exposed children. Annual Meeting,
Society of Toxicology, San Diego, CA, March 1985.
P. Mushak: Interactive relationships as modifiers of metal toxicity with special reference to
those of lead and those of selenium. Second National Academy of Sciences— Council of the
Academies of Yugoslavia Joint Workshop: "Selected Aspects of Exposure to Heavy Metals in
the Environment: Monitors, Indicators and High Risk Groups," Washington, D.C., April 29-
30, 198s.
L.D. Grant and P. Mushak: Speciation of metals and metal compounds: Implications for
biological monitoring. International Workshop on the Biological Monitoring of Toxic Metals,
University of Rochester, Rochester, N.Y., June 6-9, 1986.
P. Mushak: Biological monitoring of lead exposure in children: overview of selected biokinetic
and toxicological issues, International Symposium on Lead Exposure and Child Development,
Edinburgh, Scotland, September 6-11, 1986.
P. Mushak: Gastrointestinal absorption of lead in children and adults: Overview of biological
and biophysico-chemical aspects. Symposium on the Bioavailability and Dietary Uptake of Lead,
Chapel Hill, N.C., September 24-27, 1990.
P. Mushak: Defining lead as the premiere environmental health issue for American children:
Criteria and their quantitative application, Getting the Lead Out: Priorities for the 1990s. 12th
Annual Universities Occupational Safety and Health Educational REsources Center Symposium,
Rutgers University, Piscataway, NJ, May 8-9, 1991.
P. Mushak: Newer Directions in Toxicokinetics and Assessment of Lead Toxicity, Ninth
International Neurotoxicology Symposium, Little Rock, Ark., October 28-31, 1991.
P. Mushak: The U.S. Agency for Toxic Substances and Disease Registry’s report to congress on
childhood lead poisoning in America, First National Conference: Laboratory Issues in Childhood
Lead Poisoning Prevention, Association of State and Territorial Public Health Laboratory
Directors, Columbia, MD, October 31-November 2, 1991.
P. Mushak: Child lead toxicity and new directions in biological monitoring. Werkshop on Lead
Investigation and Abatement, University of North Carolina School of Public Health and the
North Carolina Department of Health, Environment and Natural Resources, Winston-Salem,
NC, December 4-6, 1991.
P. Mushak. Analytical approaches to monitoring lead levels. CLINCHEM 92, American
Association for Clincial Chemistry, Tarrytown, NY, October 15-16, 1992.
PUBLIC HEALTH DOCUMENTS & REPORTS
Principal co-author: Air Quality Criteria for Lead. Criteria and Special Studies Office, U.S.
Environmental Protection Agency, Research Triangle Park, N.C. EPA Report No. EPA-600 18-
77-017. Available from NTIS: PB 280411.
Principal co-author: Health Assessment Document for Cadmium. U.S. Environmental Protection
Agency, Research Triangle Park, N.C. EPA Report No. EPA-600 18-79-003 and final report,
1981.
Principal co-author: Health Assessment Document for Nickel. (Multi-Media Source Document).
U.S. Environmental Protection Agency, Research Triangle Park, N.C. April 1979.
Principal co-author: Health Assessment Document for Antimony (Multi-Media Source
Document). U.S. Environmental Protection Agency, Research Triangle Park, N.C. April 1979.
Principal co-author: Ambient Water Quality Criteria for Nickel. U.S. Environmental Protection
Agency, Office of Water Regulations and Standards, Criteria and Standards Division,
Washington, D.C. EPA Report No. 440/5-80-060, October 1980.
Principal co-author: Ambient Water Quality Criteria for Antimony. U.S. Environmental
Protection Agency, Office of Water Regulations and Standards, Criteria and Standards Division
Washington, D.C. EPA Report No. 440/5-80-020, October 1980.
’
Principal co-author: Multi-Media Environmental Pollutants. A Report to The National
Commission on Air Quality, Washington, D.C. December 1980. Summarized in: To Breathe
Clean Air, Report of The National Commission on Air Quality, Washington, D.C. March 1981.
Principal co-author: Health Assessment Document for Inorganic Arsenic. Final Report. U.S.
Environmental Protection Agency, Environmental Criteria and Assessment Office, Research
Triangle Park, N.C. EPA Report No. 600/8-83-021F, March 1984.
Principal co-author: Health Assessment Document for Nickel and Nickel Compounds. U.S.
Environmental Protection Agency, Environmental Criteria and Assessment Office, Research
Triangle Park, N.C. External Review Draft No. 1, EPA 600/8-83-012, May 1983.
Ibid. Final Report, September 1986.
Principal co-author: Air Quality Criteria for Lead. U.S. Environmental Protection Agency,
Environmental Criteria and Assessment Office, Research Triangle Park, N.C. External Review
Draft No. 1, October 1983.
Ibic External Review Draft No. 2, September 1984.
i¢. Draft Final, September 1986. In
u
Principal co-author: Health Assessment Document for Selenium. Various drafts, November,
1987 [and later]. U.S. Environmental Protection Agency, Environmental Criteria and
Assessment Office, Research Triangle Park, N.C. 27709.
Senior author: The Nature and Extent of Lead Poisoning in the United States: A Report to
Congress. Agency for Toxic Substances and Disease Registry, U.S. Public Health Service,
Atlanta Ga. Submitted to Congress, July 12, 1988.
Co-author: Update: Health Assessment Document for Chromium, chapter 4, U.S.
Environmental Protection Agency, Environmental Criteria and Assessment Office, Research
Triangle Park, N.C. 27709.
Rapporteur/principal author: International Strategies, Mechanisms and Recommendations for
Risk Reduction for Lead. A Report of the Expert Committee on Risk Reduction Policies for
Lead to the Commercial Chemicals Office/ Office of Toxic Substances, U.S. Environmental
Protection Agency, and Chemicals and Management Group, Organization for Economic
Cooperation and Development, Paris, France.
MOSHAK
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THE NATURE AND EXTENT OF LEAD POISONING
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AUTHORS AND CONTRIBUTORS
Principal Authors
Paul Mushak, Ph.D.
Consultant and Adjunct Professor
University of North Carolina/Chapel Hill
811 Onslow Street
Durham, NC 27705
Annemarie F. Crocetti, Dr.P.H.
Consultant and Associate Adjunct Professor
New York Medical College
Apt. 11-A
31 Union Square West
New York, NY 10003
Contributors
Michael Bolger, Ph.D.
Center for Food Safety and Applied
Nutrition (HFF-156)
Food and Drug Administration
Washington, DC 20204
Jeanne Briskin
Office of Drinking Water (WH-550)
U.S. Environmental Protection Agency
Washington, DC 20460
Jeffrey Cohen, M.S.P.H.
Office of Air Quality Planning
and Standards (MD-12)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
J. Michael Davis, Ph.D.
Environmental Criteria and
Assessment Office (MD-52)
U.S. Environmental Protection Agency
Research Triangle Park, NC 27711
Henry Falk, M.D.
Center for Environmental
Health and Injury Control
Centers for Disease Control
Atlanta, GA 30333
TABLES
FIGURES
AUTHORS AND CONTRIBUTORS
ACKNOWLEDGMENTS
CONTENTS
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PART 1
EXECUTIVE SUMMARY Ma i GE an a a i TER SE VES aE ORE SUR a a
A. RESPONSE TO DIRECTIVES OF SECTION 118(f) OF SARA ® 8 6 8 0 0 0 00 8 0 0
phn Sd die, WE 8 J JE SF BR TE 0 TE TE EE a IE ar a sen EE
3,
2. Section 118(f)(1)(B)
3. Section 118(f)(1)(C)
4.
5.
wat ELI Boob J2 TEN ALT I UE SE i RT TN Te EE Or I A a a rs
dais en de Bb 5 REG, BE GEE Se SEE TE TF I ESP IE gh Re eR a SM
Section 118(f)(1)(D)
Section 118(f)(2)
BANDS 0.068.400.0990 0688 85808900000 060
vd le a TOE SEE on 5 el TE ME ER BR BRE Gr ar le Sa SA Sei
B SUMMARY -OF REPORT RECOMMENDATIONS .,........ co... n't
C ISSUES, DIRECTIONS, AND THE FUTURE OF THE LEAD PROBLEM. .......
1 Issues ........ GABLE a ary OER LP Sn a IR
2 Directions and Future of the Lead Problem ..............
PART 2
CHAPTER I. REPORT FINDINGS, CONCLUSIONS, AND OVERVIEW ® 8 0 © 0 00 0 0 0 0 0 0 ¢ 0
A. BACKGROUND INFORMATION TO THE REPORT al a SE HN ME FR AE Ser WE Rr TNE TE TE RY SS ES Ger Te Ge
1. Historical Perspectives and Discussion of
Important Issues ..... 00 ita i ai
2. Lead Metabolism and its Relationship to Exposure,
Risk Population Identification and Adverse Health
ite Sie Ri ein el SEED IL Baa
3. Adverse Prenatal and Postnatal Effects of Lead in
Children: Relationship to Public Health Risk
and Their Relative Persistence .:............... . 0.
B. MAIN REPORT: QUANTITATIVE EXAMINATION OF LEAD EXPOSURE AND
TOXICITY RISK IN CHILDREN AND PREGNANT WOMEN AND STRATEGIES
POR ABATEMENT er rer ee a ET
1, Ranking of Lead-Exposed Children by Geographic Area ..
2. Numbers of Lead-Exposed Children by Lead Source
3. Number of Women of Childbearing Age and Pregnant
AIG SRT a a BLA SEL SE NE Ge TN CR NY RS 0 Se Pa I MR ed re oe LN
4. The Issue of Low-Level Lead Sources and Aggregate Lead
© eo eo 6 0° 0 0 o
® @ ee 6 ee 2 0 ee 0 0 0
5, Lead Exposure Abatement Strategies and Alternatives ...
lead dmPaint oo. oat EE
lead An Ambient Bir... i
Lead in Dust and Soil
Lead in Drinking Water
Lead in Food
i anTanel AL RE IY 0 Te I ME JRO Re 0 BT er I
lee A J TH Se J, BEL RE iE RR SR BS RE TER RY IRE SEA SRE ay Fa A Cs
RT I EE RE AT de SS EE OE EDS ob J SI Be Se er I tar Sse te a ee
CONTENTS (continued)
Page
Secondary Exposure Prevention Measures ...........ccc0en I-31
Secondary Nutritional Measures .......c.scesnscssvasrenn 1-34
Extra-Environmental Prevention Measures ................ 1-34
6. A Review of Environmental Releases of Lead Under
SUPRTEUNG wiv sss srstisnnasrsnnsseavnrvausninnsunynsess I-34
bf Information Gaps, Research Needs, and Recommendations .. 1-36
Information GBPS . voyuer srsssnvrsninnverssansasssrsnas 1-37
Research Needs ...... .5 csc rsesasssmensnsnassenzssnnnss 1-38
Recommentations v.. ic ev essnininssirsssdssssganssssnstnnny 1-34
1. Lead in the Environment of Children ................ I-39
2. {ead in the Bodies of Children ......svecvasrscncvss 1-41
Ce CONCLUSIONS AND OVERVIEW .... ivoire sosnnsansssssasnssvsnnens 1-42
}. Lead as a Public Health Issue .......ccvesasvssrrrsrenns 1-42
2. Lead in the Environment.of Children .............cccenenn 1-43
3. Lead in the Bodies of Children ...........oeeuvennnnn.e 1-45
4 The Extent of Lead Poisoning in Children in the
Undted SLates uses vnsssissonssmnssosavsnvasionnssnns 1-46
5 The Problem of In Utero Lead Toxicity: The Extent of
Feta: Lead Exposure in the United States ............. 1-48
6. Removal or Reduction of Lead in the Child's
ERVITONMENT, +c vcecncsvrrnsnnervrns ay ahi wet ta A 1-49
7. Future Directions of Lead as a Public Health Problem ... 1-50
PART 3
CHAPTER II. INTRODUCTION AND DISCUSSION OF TERMS AND ISSUES ......... 11-1
A. INTRODUCTION oot cite nsssinnssnsnsensiocssnsnssnasesnansenins
11-1
B. DISCUSSION OF TERMS AND ISSUES .. civ versrsevicnrnenanasnsnnenn 11-6
1 Young Children and Other Groups at Greatest Risk for
Lead Exposure and Adverse Health Effects ............. 11-6
2. Monitoring Lead Exposure in Young Children and Other
Risk POPUIBLIONS «vevsnsressionssnasnnnsacanesexrnntsse
11-7
3. Environmental Sources of Lead in the United States with
Reference to Young Children and Other Risk Groups .... 11-9
4. Adverse Health Effects of Lead in Young Children and
Other Risk Groups and Their Role in Health Risk
ABsecememt es neva ssa eraser esas naan 11-11
CHAPTER III. LEAD METABOLISM AND ITS RELATIONSHIP TO LEAD EXPOSURE
AND ADVERSE EFFECTS OF LEAD ....ccenvereavrrsracvnnnnn 111-1
A. LEAD ABSORPTION IN HUMAN POPULATIONS ..........ccccevecnvnnn. 311-1
i. Respiratory Absorption of Lead in Human Populations .... 111-1
2: Gastrointestinal (GI) Absorption of Lead in Human
Populations oi sst resins erases asta nie Ji1-2
3. Percutaneous Absorption of Lead in Human Populations ... 111-4
4. Transplacental Transfer and Fetal Uptake of Lead in
Pregnant Women ......vivsstssssaunssrarecsannrnnannny:
111-4
B. DISTRIBUTION OF ABSORBED LEAD IN THE HUMAN BODY oui. ves viin ae 711-5
x. Lead Uptake in Soft Tissue ... a. sueurucnscnnrnnanprenss 111-6
2. {ead Uptake in Mineralizing Tissue .........corrnsrnenre 311-7
vi
70]
CONTENTS (continued)
LEAD EXCRETION AND RETENTION IN HUMAN POPULATIONS
So
J
gl
Ldn ieee ons ER iid 1. Lead Metabolism and the Nature of Lead Exposure and ToniOiy aN aE 2. Lead Metabolism and the Identification of Risk
TEE A SEN WAR wk eee ti eee eae a ie ie 3. Lead Metabolism and Biological Exposure Indicators .... .
CHAPTER IV. ADVERSE HEALTH EFFECTS OF LEAD: RELATIONSHIP TO PUBLIC HEALTH RISK AND SOCIETAL WELL-BEING ..... 00 oa A. THE EXPOSURE (DOSE) INDEX IN ASSESSMENT OF THE ADVERSE HEALTH EFFECTS OF LEAD IN HUMAN POPULATIONS... . 00... B. MAJOR ADVERSE HEALTH. EFFECTS OF LEAD IN CHUOREN. ..... 3. Effects of Lead on Heme Biosynthesis, Erythrocyte
Physiology and Function, and Erythropoietic
Pyrimidine Metabolism .,....... os co 2, Neurotoxic Effects of Lead in Chiddren oo... .......... 3. Other Adverse Effects of Lead on the Health of
. e
ARI LR i ah ETE SR SI
EA Se aR Te RB a Ss EE BE SE ae PR eS ad
CHAPTER V. EXAMINATION OF NUMBERS OF LEAD-EXPOSED CHILDREN BY AREAS OF THE UNITED STATES eee ra LO A. ESTIMATED NUMBERS OF LEAD-EXPOSED CHILDREN IN SMSAs BY SELECTED BLOOD LEAD CRITERION VALWES . .......0. ~~ «© 3. Estimation Strategies and Methods ............... .
2. Results
oe
RE RE LE RR DE RET
SENN ANS ce et a
3. Lead Screening Programs ......... aa 2. The NHANES 11 BLUBY ee a a C. RANKING OF CHILDREN WITH POTENTIAL EXPOSURE TO PAINT LEAD Leh Tee oon deal a a Gd 3. Strategies and Methows ©... .., 0 Noland 2. Results... 0... oo ©
D. SUMMY AND OVERVIEW... 0, RT ee 1. Lead-Evposed Children in SMSAs .....,. i orn 2. Numbers of Lead-Exposed Children Detected by Screening
PIOGENS de ea a TT
3. Comparison of Prevalences Found in NHANES 11 Updated
Prevalences and U.S. Screening Programs ....... .
ARLE Rl Sn Ct VEE TR I SR re an Sl a Re NE
rad
Vii :
ee ee te elle 8 ee. METABOLIC INTERACTIONS OF LEAD WITH NUTRIENTS AND OTHER ACTIVE FACTORS IN HUMAN POPULATIONS
E. LEAD METABOLISM AND SOME KEY ASPECTS OF LEAD EXPOSURE AND
pea adn ad 20 A EE SE EL Be SF HE BR ee a
*
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« a
CRY
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°
CONTENTS (continued)
4. Children with Potential Exposure to Lead Paint in the
5.
CHAPTER VI. EXAMINATION OF NUMBERS OF LEAD-EXPOSED U.S. CHILDREN
A.
BY LEAD SOURCE
GENERAL ISSUES
3. The Level of Exposure Risk in Human Populations by
Lead Source
2, Relationships of External to Internal Lead Exposure
on a Total Population Basis
3; Human Behavior and Other Factors in Source-Specific
Population Exposures to Lead
4, Organization of the Chapter
NUMBERS OF CHILDREN EXPOSED TO LEAD IN PAINT
1. Estimation Strategies and Methods
2. Results
NUMBERS OF CHILDREN EXPOSED TO
1 Estimation Strategies and
2. Results
NUMBERS OF CHILDREN EXPOSED TO
EMISSION SOURCES
x. Estimation Strategies and
2. Results
NUMBERS OF CHILDREN EXPOSED TO LEAD IN DUSTS AND SOILS
1 Estimation Strategies and Methods
2. Results
NUMBERS OF CHILDREN EXPOSED TO
1. Estimation Strategies and
2. Results
NUMBERS OF CHILDREN EXPOSED TO
: Estimation Strategies and
2. Results
Paint Lead as an Exposure Source
Gasoline Lead as an Exposure Source
Lead from Stationary Sites as an Exposure Source
Lead in Dust and Soils as an Exposure Source
Lead in Drinking Water as an Exposure Source
Lead in Food as an Exposure Source
Ranking of Lead-Exposed Children by Source
CHAPTER VII. EXAMINATION OF NUMBERS OF LEAD-EXPOSED WOMEN OF
A.
CHILDBEARING AGE AND PREGNANT WOMEN
STRATEGIES AND METHODS
]. Methods
2 Results
CONTENTS (continued)
CHAPTER VIII. THE ISSUE OF LOW-LEVEL LEAD SOURCES AND AGGREGATE
LEAD EXPOSURE OF U.S. CHILDREN ......c on vvesnanannasns
A. NATIONAL/REGIONAL SURVEYS OF BLOOD LEAD LEVELS: BASELINE
LEVELS AND SOURCE-RELATED CHANGES IN SURVEY BASELINES .......
USE OF SOURCE-SPECIFIC TRACING METHODS ...............c..nn.
THE USE OF SOURCE-BASED DISTRIBUTIONS OF LEAD INTAKE AND
SOURCE-BLOOD LEAD RELATIONSHIPS IN ASSESSING AGGREGATE
INTAKE AND POPULATION RISKS cnc visa cnnsrsvnsinssnnnisnsns
D. BIOKINETIC MODELS OF THE IMPACT OF LEAD SOURCES ON
BLOOD LEAD oss viasisiiis vastness sss dwn tren ns snimltainsie ain,
E. GUMMY i i ss ih a wr a my ae ee ede
B.
C.
CHAPTER IX. METHODS AND ALTERNATIVES FOR REDUCING ENVIRONMENTAL LEAD
EXPOSURE FOR YOUNG CHILDREN AND RELATED RISK GROUPS .....
A. PRIMARY PREVENTION MEASURES FOR LEAD EXPOSURE ...............
2 i Primary Prevention Using Environmental Measures ........
2. Primary Prevention Using Combined Environmental and
Biological Measures ......«<...-.c ounnransvrrsssrssniness
B. SECONDARY PREVENTION MEASURES FOR LEAD EXPOSUEZ .............
1 Environmental Lead Control ...... conven nssssnvamsarnns
2. Environmental/Biological Prevention Measures ...........
3 Extra-Environmental Prevention Measures ................
CHAPTER X. A REVIEW OF ENVIRONMENTAL RELEASES OF LEAD AS EVALUATED
UNDER SUPERFUND oo. os stun insure enn als sap amensans vasa
A. NPL SITES -- PROPOSED AND FINAL .....cuuivnseinsnnnason
Exposure of Children to Lead at NPL Sttes . 0...
B.. URBAN AREA SITE . vies cine vvmnisssdnn=nsramanasseit
HRS Scoring at the Boston Urban Site .................
C. REVISION OF THE HAZARD RANKING SYSTEM ................
Do CUMMARY is sd en aia se ee a ee me a aes
CHAPTER XI. LEAD EXPOSURE AND TOXICITY IN CHILDREN AND OTHER RELATED
GROUPS IN THE UNITED STATES: INFORMATION GAPS, RESEARCH
NEEDS, AND REPORT RECOMMENDATIONS .......................
HEORMATION GAPS ray vii an Rn sian Te nda asinine nies
RESEARCH NEEDS i. o.. veisneicvsrncerstannsvn nnnsesnrinnn Sei
C. RECOMMENDATIONS ...... Coes Bn VR a Ra mal a SS Bre
l. Lead in the Environment of DE rR RL Te EL el
2. Lead in the Bodies of Children ....... ca oivnsnnsanssss
1
Bl
REFERENCES i dem iiss a ee nian wie hein lpia ane fe aie Re
APPENDIX A. TABLES OF INDIVIDUAL SMSAs WITH A POPULATION OF OVER
ONE MI! LION SHOWING NUMBERS OF YOUNG CHILDREN BY
THE AGE OF THEIR HOUSING AND FAMILY INCOME ............-
ix
V11ll-5
VIII-6
Viii~13
1X-1
I1X-4
1X-4
I1X-18
1X-20
I1X-20
1%-24
1X-24
CONTENTS (continued)
APPENDIX B. TABLES OF INDIVIDUAL SMSAs WITH A POPULATION OF LESS
THAN ONE MILLION SHOWING NUMBERS OF YOUNG CHILDREN BY °
THE AGE OF THEIR HOUSING AND FAMILY INCOME
APPENDIX C. TABLES OF INDIVIDUAL AND MERGED SMSAs WITH POPULATIONS
OF LESS THAN 500,000 SHOWING NUMBERS OF YOUNG
CHILDREN BY THE AGE OF THEIR HOUSING AND FAMILY
INCOME
APPENDIX D. SMSAs RANKED BY NUMBER OF YOUNG CHILDREN IN PRE-1950
HOUSING AS OF 1980
APPENDIX E. LEAD-CONTAMINATED SOIL CLEANUP, DRAFT REPORT
APPENDIX F. FINAL AND PROPOSED NATIONAL PRIORITIES LIST WASTE SITES
WITH LEAD AS AN IDENTIFIED CONTAMINANT
APPENDIX G. METHODOLOGICAL DETAILS OF BLOOD LEAD PREVALENCE
PROJECTIONS FROM NHANES II DATA
J
In 1981, Federal resources for screening were put under the program of
the Maternal and Child Health Block Grants to States. Although the States’
use of Federal funds for lead screening programs was estimated by one source
to have been reduced initially by 25% (Farfel, 1985), a precise figure cannot
be readily given since allocations of the block grant funds for particular
projects are determined by the States according to their priorities, and data
are not systematically collected on these State funding allocation decisions.
The evidence of the national impact of this initial reduction in Federal
resources appears to be mixed. While it appears that the total number of
screening program units in the nation has decreased from 60 to between 40 and
45 (Chapter V), there is also evidence in some States and localities that the
number of children currently being screened has increased since 1981 (CDC,
1982; Public Health Foundation, 1986). However, a study of data from Newark,
NJ for a nine-year period prior to implementation of the block grants showed
that the rate of high-lead exposures in asymptomatic children increased about
fourfold after funding for lead screening and public education programs was
reduced (Schneider and Lavenhar, 1986). Based upon this report, it is likely
that those areas that choose to decrease the efficiency of their lead screening
services can expect to experience increases in the number of children with lead
poisoning.
A key point in the Schneider and Lavenhar (1986) report and additional
information given below is that screening programs, especially those supported
at a level that allows blanket screening, are particularly cost-effective.
This is demonstrated by comparing data on the costs of treating children who
are poisoned because early lower levels of lead intoxication were not detected
by screening with the costs of community screening programs. According to
O'Hara (1982), the cost of repeat admissions to Baltimore hospitals for 19
lead-poisoned children in 1979 was $141,750, or at least $300,000 in 1986
dollars. In summary statistics submitted to ATSDR for the 1985-13986 program
year, St. Louis listed budgetary support of $303,453 from the city and $100,000
from the State of Missouri. During that funding year, all agencies in the
St. Louis program tested 12,308 children, of whom 1,356 or 11.02% tested posi-
tive for lead exposure using CDC classifications. Of these positives, 8489
tested as (lass 11, 445 as Class 111, and 62 as Class IV, the most severe level
of toxicity. The new CDC guidelines of 1985 were implemented midway through
the 1985 screening year (July 1, 1985), so these figures represent a low
boundary for the number of positives.
a
en ih
bat
In St. Louis, the entire screening program cost $403,453 and identified
1,356 cases of toxicity; that is just under $300 per poisoned child. In
Baltimore, the multiple hospital admissions required for only some of the
poisoned children cost about $16,000 per child in 1986 dollars. This does not
account for additional essential costs for adequate management of severe toxic
cases. These additional huge costs stem from medical follow-up care and treat-
ment, remedial education, etc. The monetized costs of the sequelae in signifi-
cant toxicity cases are spelled out in U.S. EPA (1985 and 1986b). The effec-
tiveness of screening children for lead poisoning is well demonstrated in
terms of deferred or averted medical interventions, and in most settings. is
quite cost-effective.
In March 1987, the Committee on Environmental Hazards, American Academy of
Pediatrics, issued its “Statement on Childhood Lead Poisoning." It includes
this statement:
“...to achieve early detection of lead poisoning, the Academy recom-
mends that all children in the United States at risk of exposure to
lead be screened for lead absorption at approximately 12 months of
age.... Furthermore, the Academy recommends follow-up...testing of
children judged to be at high risk of lead absorption."
These guidelines from America's pediatric medicine community probably cannot
be effectively implemented or coordinated with the current levels or existing
type of program support at local, State, and Federal levels.
Environmental Hazard Identification and Abatement for Severe Poisoning
Cases
When cases of toxicity were found, mass screening programs for lead
poisoning routinely made efforts to find the sources. A careful examination of
the information on reducing lead exposure by completely or partially removing
leaded paint clearly shows that, at best, the effect is debatable. At worst,
the approach may not work. In a prospective study, Chisolm et al. (1985)
observed that when children return to "lead abated" structures, their Pb-B
levels invariably return to unacceptable levels. This is not a case of
endogenous Pb-B increase from the release of bone lead, because children
heavily exposed before treatment will respond better when placed in lead
paint-free housing.
1X-22
20
PART 1
EXECUTIVE SUMMARY
Exposure to lead continues to be a serious public health problem --
particularly for the young child and the fetus. The primary target organ for
lead toxicity is the brain or central nervous system, especially during early
child development. In children and adults, very severe exposure can cause
coma, convulsions, and even death. Less Severe exposure of children can produce
delayed cognitive development, reduced IQ scores, and impaired hearing -- even
at exposure levels once thought to cause no harmful effects. Depending on the
amount of lead absorbed, exposure can also cause toxic effects on the kidney,
impaired regulation of vitamin D, and diminished synthesis of heme in red blood
cells. All of these effects are significant. Furthermore, toxicity can be
Persistent, and effects on the central nervous system (CNS) may be irreversible.
In recent years, a growing number of investigators have examined the
effects of exposure to low levels of lead on young children. The history of
research in this field shows a progressive decline in the lowest exposure
levels at which adverse health effects can be reliably detected. Thus, despite
some progress in reducing the average level of lead exposure in this country,
it is increasingly apparent that the scope of the childhood lead poisoning
problem has been, and continues to be, much greater than was previously
realized. -
The “Nature and Extent of Lead Poisoning in Children in the United States:
A Report to Congress" was prepared by the Agency for Toxic Substances and
Disease Registry (ATSDR) in compliance with Section 118(f) of the 1986
Superfund Amendments and Reauthorization Act (SARA) (42 U.5.C. 9618(T)). This
Executive Summary is a guide to the structure of the document and, in partic-
ular, to the organization of the responses to the specific directives of
Section 118(f). It also provides an overview of issues and directions to the
U.S. lead problem.
=
ST 7
ig) 1
The report comprises three parts: Part 1, consisting of the Executive
Summary; Part 2, consisting of Chapter I. “Report Findings, Conclusions, and
Overview," which provides a more detailed overview of information and conclu-
sions abstracted from the main body of the report; and Part 3, consisting of
Chapters II through XI, which constitute the main body of the report.
Before addressing the specific directives of Section 118(T), it is
important to point out that childhood lead poisoning is recognized as a major
public health problem. In a 1987 statement, for example, the American Academy
of Pediatrics notes that lead poisoning is still a significant toxicological
hazard for young children in the United States. It is also a public health
problem that is preventable.
In recognition of evolving scientific evidence of the harmful effects of
lead exposure, Congress directed ATSDR to examine (1) the long-term health
implications of low-level lead exposure in children; (2) the extent of low-
level lead intoxication in terms of U.S. geographic areas and sources of lead
exposure; and (3) methods and strategies for removing lead from the environment
of U.S. children.
The childhood lead poisoning problem encompasses a wide range of exposure
levels. The health effects vary at different levels of exposure. At low
levels, the effects on children, as stated subsequently in this report, may not
be as severe or obvious, but the number of children adversely affected is
large. Moreover, as adverse health effects are detected at increasingly lower
levels of exposure, the number of children at risk increases. At intermediate
exposure levels, the effects are such that a sizable number of U.S. children
require medical and other forms of attention, but usually they do not need to
be hospitalized, nor do they need conventional medical treatment for lead
poisoning. For these children, the only appropriate solution, at present, is
to eliminate or reduce all significant sources of lead exposure in their
environment. At high levels, the effects are such that children require
immediate medical treatment and follow-up. Various clinics and hospitals,
particularly in larger cities, continue to report such cases.
Lead exposure may be characterized in terms of either external or internal
concentrations. External exposure levels are the concentrations of lead in
environmental media such as air or water. For internal exposure, the most
widely accepted and commonly used measure is the concentration of lead in
blood, conventionally denoted as micrograms of lead per deciliter (100 ml) of
whole blood -- abbreviated pg/dl. For example, when ATSDR estimated the number
3 ia 0
L 2 ga /
Lo
of children considered to be at risk for adverse health effects, the Agency
used blood lead (Pb-B) levels of 25, 20, and 15 pg/d1 to group children by their
degree of exposure.
These levels are not arbitrary. In 1985 the Centers for Disease Control
(COC) identified a Pb-B level of 25 ug/dl along with an elevated erythrocyte
protoporphyrin level (EP) as evidence of early toxicity. For a number of
practical considerations, CDC selected this level as a cutoff point for medical
referral from screening programs, but it did not mean to imply that Pb-B levels
below 25 pg/dl are without risk. More recently, the World Health Organization
(WHO), in its 1986 draft report on air quality guidelines for the European
Economic Community, identified a Pb-B level of 20 pug/dl as the then-current
upper acceptable limit. In addition, the Clean Air Scientific Advisiory Commit-
tee to the U.S. Environmental Protection Agency (EPA) has concluded that a Pb-B
level of 10 to 15 pg/dl in children is associated with the onset of effects that
“may be argued as becoming biomedically adverse". In this connection, the
available evidence for a potential risk of developmental toxicity from lead
exposure of the fetus in pregnant women also points towards a Pb-B level of 10
to 15 ug/dl, and perhaps even lower. These various levels represent an evolving
understanding of low-level lead toxicity. They provide a reasonable means of
quantifying aspects of the childhood lead poisoning problem as it is currently
understood. With further research, however, these levels could decline even
further.
A. RESPONSE TO DIRECTIVES OF SECTION 118(f) of SARA
Section 118(f) and its five directives give ATSDR the mandate to prepare
this report. These directives are identified in the five subsections below.
1, Section 118(f)(1)(A)
This subsection requires an estimate of the total number of children,
arrayed according to Standard Metropolitan Statistical Area (SMSA) or other
appropriate geographic unit, who are exposed to environmental sources of lead
at concentrations sufficient to cause adverse health effects. Chapter V,
"Examination of Numbers of Lead-Exposed Children by Areas of the United
States,” and Chapter VII, "Examination of Numbers of Lead-Exposed Women of
Childbearing Age and Pregnant Women," respond to this directive.
pi 7 H 3
21D 3
Lr
ee ete ees inn tn
Valid estimates of the total number of lead-exposed children according to
SMSAs or some other appropriate geographic unit smaller than the Nation as a
whole cannot be made, given the available data. The only national data set for
Pb-B levels in children comes from the National Health and Nutrition Examina-
tion Survey II (NHANES II) of CDC's National Center for Health Statistics. The
NHANES II statistical sampling plan, however, does not permit valid estimates
to be made for geographic subsets of the total data base.
In this report, the numbers of white and black children (ages 6 months to
5 years) living in all SMSAs are quantified according to selected blood lead
levels and 30 socioeconomic and demographic strata. Within large SMSAs (those
with over 1 million residents each) for 1984, an estimated 1.5 million children
had Pb-B levels above 15 pg/dl. In smaller SMSAs (with fewer than 1 million
residents), an estimated 887,000 children had Pb-B levels above 15 pg/dl.
In short, about 2.4 million white and black metropolitan children, or
about 17% of such children in U.S. SMSAs, are exposed to environmental sources
of lead at concentrations that place them at risk of adverse health effects.
This number approaches 3 million black and white children if extended to the
entire U.S. child population. If the remaining racial categories are included
in these totals, between 3 and 4 million U.S. children may be affected. The
numbers of children in SMSAs with blood lead levels above 20 and 25 pg/dl are
715,000 (5.2%) and 200,000 (1.5%), respectively. These figures, however, are
for all strata combined; many strata (e.g., black. inner-city, or low-income)
have much higher percentages of children with elevated Pb-B levels.
Although these projected figures, based on the NHANES II survey, provide
the best estimate that can now be made, they were derived from data collected
in 1976-1980 (the years of NHANES II) and extrapolated to 1984. With respect
to bounds to the above projections, variables in the methods used to generate
these figures contribute to both overestimation and underestimation. The major
source of overestimation is the unavoidable omission of declines in food lead
that may have occurred in the interval 1978-1964 and that would have affected
the results of the projection methodology. On the other hand, two significant
factors contribute to underestimation. One is the restriction of the estimates
to the SMSA fraction of the U.S. child population, some 75% to 80% of the total
population. The other is the unavoidable omission of children of Hispanic,
Asian, and other origins in the U.S. population. In a number of SMSAs in the
West and South west, children in such segments outnumber black children. In
balancing all sources of overestimates and underestimates, including variance
in the projection model itself, the projections given are probably close to the
actual values.
A breakdown of the above estimates according to national socioeconomic and
demographic strata shows that no economic or racial subgrouping of children is
exempt from the risk of having Pb-B levels sufficiently high to cause adverse
health effects. Indeed, sizable numbers of children from families with incomes
above the poverty level have been reported with Pb-B levels above 15 pg/dl.
Nevertheless, the prevalence of elevated Pb-B levels in inner-city, underprivi-
leged children remains the highest among the various strata. Although the
percentage of children with elevated Pb-B levels is not as high in, for example,
the more affluent segment of the U.S. population living outside central cities,
the total number of children with these demographic characteristics is much
greater than the number of poor, inner-city children. Consequently, the
absolute numbers of children with elevated Pb-B levels are roughly equivalent
for some of these rather different strata of the U.S. child population.
In this report, ATSDR has also used data from lead screening programs and
1980 U.S. Census data on age of housing to estimate SMSA-specific numbers of
children exposed to lead-based paint. In December 1986, ATSDR conducted a
survey of lead screening programs. Of 785,285 children screened in 1985,
11,739 (1.5%) had symptoms of lead toxicity by one of two definitions. Because
COC criteria for lead toxicity changed in 1985, some programs were still using
the 1978 CDC criteria (Pb-B 230 pg/dl and EP 250 pg/dl) in 1985, whereas others
used the new 1985 CDC criteria (Pb-B 225 pg/dl and EP 235 pg/dl).
Differences in the estimates of children with lead toxicity become
apparent when using the NHANES II data and the childhood lead screening program
data. Estimates derived from screening program data very likely underestimate
the actual magnitude of childhood lead exposure by a considerable margin. This
is especially evident when the percentages of positive test results from
screening programs are compared with the much higher NHANES II prevalences of
elevated Pb-B levels in strata corresponding to screening program target
groups, for example, poor, inner-city children in major metropolitan areas.
An analysis of 318 SMSAs, based on 1980 Census data on age of housing,
showed that 35 SMSAs had 50% or more of the children living in housing built
before 1950. A total of 4,374,600 children (from these 318 SMSAs alone) lived
in pre-1950 housing. The percentage of these children with lead exposures
sufficient to cause adverse health effects could not be estimated, but the
older housing in which they live is likely to contain paint with the highest
levels of lead and is, therefore, likely to pose an elevated risk of dangerous
lead exposure. A noteworthy finding concerns the distribution of children in
older housing according to family income. Actual enumerations (not estimates)
show that children above the poverty level constitute the largest proportion of
children who reside in older housing. The implication, consistent with the
conclusion based on projections from NHANES II data that was stated above, is
that children above the poverty level are not exempt from lead exposure at
levels sufficient to place them at risk for adverse health effects. Children
above the poverty level are the most numerous group within the U.S. child
population.
Although Section 118(f)(1)(A) does not explicitly request such information,
an accurate description of the full childhood lead poisoning problem requires
an estimate of the number of fetuses exposed to lead in utero, given the
susceptibility of the fetus to low-level lead-induced disturbances in develop-
ment that first become evident at birth or even some time later during early
childhood. Accordingly, in a given year, an estimated 400,000 fetuses (within
SMSAs alone) are exposed to maternal Pb-B levels of more than 10 pg/dl and are
therefore at risk for adverse health effects. This number pertains to a single
year; the cumulative number of children who have been exposed to undesirable
levels of lead during their fetal development is much greater, particularly in
view of the higher average levels of exposure that prevailed in past years.
2. Section 118(fY{1)(B)
This subsection requires an estimate of the total number of children
exposed to environmental sources of lead arrayed according to source or source
types. Chapters VI ("Examination of Numbers of Lead-Exposed Children in the
United States by Lead Source") and VIII (“The Issue of Low-Level Lead Sources
and Aggregate Lead Exposure of Children in the United States") respond to this
directive.
The six major environmental sources of lead are paint, gasoline, stationary
sources, dust/soil, food, and water. Dust/soil is more properly classified as
a pathway rather than a source of lead, but since it is often referred to as a
source, it is included. (Figure 11-1 in the main report shows how lead from
these sources reaches children.) The complex and interrelated pathways from
UND
these sources to children severely complicate efforts to determine source-
specific exposures. Consequently, exact counts of children exposed to specific
sources of lead do not exist.
The first step in approximating the number of children exposed to lead
from each of the six major sources is to define what constitutes exposure. For
each lead source, approximate exposure categories are defined and range from
potential exposures through actual exposures known to cause lead toxicity.
Because the type and availability of data for each lead source vary consider-
ably, definitions of exposure categories also differ for each lead source. The
total numbers of children estimated for each source and category are therefore
not comparable and cannot be used to rank the severity of the lead problem by
source of exposure in a precise, quantitative way. Furthermore, because of the
nature of methods used to calculate the numbers of children in these exposure
categories, it is not possible to provide estimate errors. Some numbers are
best estimates, but others may represent upper bounds or lower bounds.
One should not overlook the limitations and caveats for these calculations,
lest the estimates be misinterpreted and misapplied. In addition, source-based
exposure estimates of children have different levels of precision. The
estimated number of children potentially exposed to a given lead source at any
level is necessarily greater than the number actually exposed at a level
sufficient to produce a specified Pb-B value. Source-specific estimates of
potentially and actually exposed children, based on the best available informa-
tion and reasonable assumptions, are summarized as follows:
0 For leaded paint, the number of potentially exposed children
under 7 years of age in all housing with some lead paint at
potentially toxic levels is about 12 million. About 5.9 million
children under 6 years of age live in the oldest housing, that
is, housing with the highest lead content of paint. For the
oldest housing that is also deteriorated, as many as 1.8 to
2.0 million children are at elevated risk for toxic lead expo-
sure.
The number of young children likely to be exposed to enough
paint lead to raise their Pb-B levels above 15 pg/dl is esti-
mated to be about 1.2 million.
0 An estimated 5.6 million children under 7 years old are poten-
tially exposed to lead from gasoline at some level.
Actual exposure of children to lead from gasoline, was projec-
ted, for 1987, to affect 1.6 million children up to 13 years of
age at Pb-B levels above 15 pg/dl.
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0 The estimated number of children potentially exposed to U.S.
stationary sources (e.g., smelters) is 230,000 children.
The estimated number of children exposed to lead emissions from
primary and secondary smelters sufficient to elevate Pb-B concen-
trations to toxic levels is about 13,000; estimates for other
stationary sources are not available.
0 The number of children potentially exposed to lead in dust and
soil can only be derived as a range of potential exposures to
the primary contributors to lead in dust and soil, namely, paint
lead and atmospheric lead fallout. This range is estimated at
5.9 million to 11.7 million children. ;
The actual number of children exposed to lead in dust and soil
at concentrations adequate to elevate Pb-B levels cannot be ;
estimated with the data now available. |
0 Because of lead in old residential plumbing, 1.8 million chil-
dren under 5 years old and 3.0 million children 5 to 13 years
old, are potentially exposed to lead; for new residences (less
than 2 years old), the corresponding estimates of children are
0.7 and 1.1 million, respectively.
Some actual exposure to lead occurs for an estimated 3.8 million
children whose drinking water lead level has been estimated at
greater than 20 ug/l.
E
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EPA, in a recent study, estimated that 241,000 children under
6 years old have Pb-B levels above 15 pg/d1 because of elevated i
concentrations of lead in drinking water. Of this number, 100 ,
have Pb-B levels above 50 pg/dl, 11,000 have Pb-B levels between i
30 and SO pg/dl, and 230,000 have Pb-B levels between 15 and
30 pg/dl.
0 Most children under 6 years of age in the U.S. child population
are potentially exposed to lead in food at some level.
Actual exposure to enough lead in food to raise Pb-B levels to
an early toxicity risk level has been estimated to impact as
many as 1 million U.S. children.
Despite limitations in the precision of the above estimates, relative
judgments can be made about the impact of different exposure sources. Some key
findings are:
0 As persisting sources for childhood lead exposure in the United
States, lead in paint and lead in dust and soil will continue as
major problems into the foreseeable future.
oe
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«
0 As a significant exposure source, leaded paint is of particular
concern since it continues to be the source associated with the
severest forms of lead poisoning.
0 Lead levels in dust and soil result from past and present inputs
from paint and air lead fallout and can contribute to signifi-
cant elevations in children's body lead burden {i.e., the
accumulation of lead in body tissues).
[ 0 In large measure, paint and dust/soil lead problems for children
are problems of poor housing and poor neighborhoods.
0 Lead in drinking water is a significant source of lead exposure
in terms of its pervasiveness and relative toxicity risk. Paint
and dust and soil lead are probably more intense sources of
exposure.
0 Greater attention must be paid to lead exposure sources away
from the home, especially lead in paint, dust, soil, and drink-
ing water in and around schools, kindergartens, and similar
locations.
0 The phasing down of lead in gasoline has markedly reduced the
number of children impacted by this source as well as the rate
at which lead from the atmosphere is deposited in dust and soil.
0 Lead in food has been reduced to a significant degree in recent
years and contributes less to body burdens in the United States
than in the past. :
0 Significant exposure of unkown numbers of children can also
occur under special circumstances: renovation of old houses
with lead-painted surfaces, secondary exposure to lead trans-
ported home from work places, lead-glazed pottery, certain folk
medicines, and a variety of others unusual sources.
3. Section 118(F){1)(C)
This subsection requires a statement of the long-term consequence for
public health of unabated exposure to environmental sources of lead.
Chapters III ("Lead Metabolism and Its Relationship to Lead Exposure and
Adverse Effects of Lead") and IV ("Adverse Health Effects of Lead") address
this issue.
Infants and young children are the subset of the U.S. population considered
most at risk for excessive exposure to lead and its associated adverse health
effects. In addition, because lead is readily transferred across the placenta,
the developing fetus is at risk for lead exposure and toxicity. For this
reason, women of childbearing age are also an identifiable, albeit surrogate,
'} :
subset of the population of concern, not because of direct risk to their
health, but because of the vulnerability of the fetus to lead-induced harmful
| effects.
Direct, significant impacts of lead on target organs and systems are
evident across a broad range of exposure levels. These toxic effects may range
from subtle to profound. In this report, the primary focus has been on effects
that are chronic and that are induced at levels of lead exposure not uncommon
in the United States. Cases of severe lead poisoning are, however, still being
reported, particularly in clinics in.our major cities.
The primary target organ for lead toxicity is the brain or central nervous
system (CNS), especially during early child development. Other key targets
in children are the body heme-forming system, which is critical to the
production of heme and blood, and the vitamin D regulatory system, which
involves the kidneys and plays an important role in calcium metabolism. Some
of the major health effects of lead and the lowest-observed-effect levels (in
terms of Pb-B concentrations) at which they occur can be summarized as follows:
0 Very severe lead poisoning with’ CNS involvement commonly
includes coma, convulsions, and profound, irreversible mental.
retardation and seizures, and even death. Poisoning -of this
severity occurs in some persons at Pb-B levels as low as
80 ug/dl. Less severe but still serious effects, such as
peripheral neuropathy and frank anemia, may start at Pb-B levels
between 40 and 80 pg/dl.
0 Numerous epidemiologic studies of children have related lower
levels of lead exposure to a constellation of impairments in CNS
function, including delayed cognitive development, reduced IQ
scores, and impaired hearing. For example, peripheral nerve
dysfunction (reduced nerve conduction velocities) have been
found at Pb-B levels below 40 pg/dl in children. In addition,
deficits in IQ scores have been established at Pb-B levels below
25 pg/dl. Preliminary data suggest that effects on one test of
children's intelligence may be associated with childhood Pb-8
levels below 10 pg/dl.
0 Adverse impacts on the heme biosynthesis pathway and on vitamin
D and calcium metabolism, all of which have far-reaching physio-
logical effects, have been documented at Pb-B levels of 15 to
20 pg/dl in children. At levels around 40 pg/dl, the effects on
heme synthesis increase in number and severity (e.g., reduced
hemoglobin formation).
0 Of particular concern are consistent findings from several
recent longitudinal cover a period of years epidemiologic
studies showing low-level lead effects on fetal and child
development, including neurobehavioral and growth deficits.
7)
7 _4+10
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§
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i
These effects are associated with prenatal exposure levels of 10
to 15 pg/dl.
With regard to the long-term consequences of lead exposure during early
development, the American Academy of Pediatrics (1987) has noted that utmost
concern should be given to the irreversible neurological consequences of
childhood lead poisoning. Recent findings from longitudinal follow-up studies
of infants starting at birth (or even before birth) show persistent deficits in
mental and physical development through at least the first two years of life as
a function of low-level prenatal lead exposure. It is not yet known, however,
whether deficits in later childhood development will continue to show a signif-
icant linkage to prenatal exposure or whether, at older ages, postnatal lead
levels will overshadow the effects of earlier exposure. Human development is
quite plastic, with well known catch-up spurts in growth and other aspects of
development. On the other hand, even if early lead-induced deficits are no
longer detected at later ages, this apparent recovery does not necessarily
imply that earlier impairments are without consequence. In view of the complex
interactions that figure into the cognitive, emotional, and social development
of children, compensations in one facet of a child's development may exact a
cost in another area. Very little information is available for evaluating such
interdependencies and trade-offs, but at this point even "temporary" develop-
mental perturbations cannot be viewed as inconsequential.
In addition, given the poor prospects for immediate improvements in the
environments of many children (e.g., deteriorated housing occupied by under-
privileged, inner-city children), lead exposure and toxicity often are, in
practice, irreversible. Thus, the issue of persistence must encompass the
reality of exposure circumstances as well as the potential for biological
recovery.
4, Section 118(f)(1)(D)
This subsection asks for information on the methods and options available
for reducing children's exposure to environmental sources of lead. Chapter IX
("Methods and Alternatives for Reducing Environmental Lead Exposure for Young
Children and Related Risk Groups") addresses this issue. Abatement methods
include primary as well as secondary measures. Primary abatement refers to
reducing or eliminating lead's entrance into pathways by which people are
71% 11
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exposed; secondary abatement refers to ways of dealing with lead after it has
already entered the environment or humans. Biological approaches such as
improved nutrition may fall into either of these two categories, depending on
whether they are intended primarily as prophylactic or treatment measures.
Extra-environmental approaches to prevention (e.g., legal actions and stric-
tures) are also discussed.
Here are some key points on the abatement of childhood lead exposure and
poisoning :
] 0 Efforts in the United States to remove or reduce human lead
; exposure have produced notable successes as well as notable
failures.
0 Effective primary lead abatement measures have included EPA's
phase-down regulations for gasoline lead, EPA's national ambient
air quality standard for lead, and cooperative actions between
the Food and Drug Administration and the food industry to reduce
lead in food.
0 A number of new initiatives are being implemented by EPA to
reduce lead in the drinking water of children and other popula-
: tion segments. Of particular interest is water as it comes from
the tap not only in homes but in public facilities such as
; kindergartens and elementary schools. The schools, in partic-
ular, present special exposure characteristics that have not yet
been adequately assessed.
) Existing leaded paint in U.S. housing and public buildings
remains an untouched and enormously serious problem despite some
regulatory action in the 1970s to limit further input of new
leaded paint to the environment. For this source, corrective
actions have been a clear failure.
0 Lead in dust and soil also remains a potentially serious exposure
source, and remediation attempts have been unsuccessful.
0 Secondary prevention measures in the form of U.S. lead screening
programs for children at high risk still appear to require
improved standardization of screening methodology (criteria for
populations, measurement techniques, data collection, data
reporting and statistical analysis) and central coordination.
0 The effectiveness of screening children for lead poisoning is
well demonstrated in terms of deferred or averted medical
interventions, and in most settings is quite cost-effective.
0 Extra-environmental measures, such as comprehensive good nutri-
tion programs, have a role in mitigation of lead toxicity, but
they cannot be used as substitutes for initiatives to reduce
lead in the environment.
4
0 At present, legal sanctions do not appear to be very effective;
to be effective, sanctions have to be both meaningful and
rigidly enforced. So long as it is cheaper to pay a fine than
to remove lead from the child's environment, little progress is
likely to be made on this front.
) The "easiest" steps to lead abatement have already been taken or
are being taken. These steps, not surprisingly, have involved
reducing lead in large-scale sources, such as gasoline and food,
with more-or-less centralized distribution mechanisms.
0) Enormous masses of lead remain in housing and public buildings,
along with large amounts of lead in dust and soil. If these
highly dispersed sources are to be abated, huge efforts will be
required.
5. Section 11B(f)(2)
Chapter X ("A Review of Environmental Releases of Lead as Evaluated under
Superfund") was prepared by the U.S. Environmental Protection Agency (EPA)
in response to Section 118(f)(2). The National Priorities List (NPL) of
September 30, 1987, was reviewed to identify those sites containing lead. Of
the 457 sites, 307 have lead as an identified contaminant and 174 have an
observed release of lead to air, to surface water, or to ground water. In
addition to describing facilities and lead releases for which remedial action
was designed under the Comprehensive Environmental Response, Compensation, and
Liability Act of 1980 (CERCLA), EPA has also gathered data for an urban,
non-CERCLA site in Boston where children are exposed to soil contaminated by
lead-based paint. This site scored 3.56 under the current Hazard Ranking System
(HRS). (The minimum HRS score needed for a site's listing on the NPL is 28.5.)
Revisions of the HRS by EPA could change the urban site's score, depending on
what revisions are made.
B. SUMMARY OF REPORT RECOMMENDATIONS
The report concludes with Chapter XI (“Lead Exposure and Toxicity in
Children and Other Related Groups in the United States: Information Gaps,
Research Needs, and Report Recommendations"), an overview of information gaps,
research needs, and recommendations. Of key importance are the various general
and specific recommendations of the report.
7 ig 13
In view of the multiple sources of lead exposure, an attack on the problem
of childhood lead poisoning in the United States must be integrated and
coordinated, if it is to be effective. In addition, such an attack must
incorporate well-defined goals so that its progress can be measured. For
example, the lead exposure of children and fetuses must be monitored and
assessed in a systematic manner if efforts to reduce their exposure are to
succeed. A comprehensive attack on the lead problem in the United States
should not preclude focused efforts by Federal, State, or local agencies with
existing statutory authorities to deal with different facets of the same
problem. Indeed, it is important that all relevant agencies continue to
respond to this important public health problem, but they should do so with an
awareness of how their separate actions relate to the goals of a comprehensive
attack.
Specific recommendations, by category, are summarized below:
0 Coordinated efforts to reduce lead levels in sources that remain
as major causes of lead toxicity, particularly paint and
dust/soil lead, are strongly recommended.
0 Scientific assessments of lead levels in these sources, through
strengthening of existing programs to monitor environmental
levels of lead, should accompany removal/reduction efforts.
: 0 Major improvements in the collection, interpretation, and
¢ dissemination of environmental lead data on a national level are
needed. In particular, lead screening data should be compiled
in a uniform manner on a nationwide basis.
0 Precise and sensitive methodologies for environmental monitoring
and in situ measurement of lead concentrations in various media
are required.
0 An integrated assessment of all exposure sources for children is
required, including those that are obvious and others that are
not. Attention should be given to the lead exposure of children
away from the home: paint lead, dust/soil lead, and lead in
drinking water in schools, day-care centers, custodial care
institutions, and similar sites. Particular attention should be
given to the investigation of lead leaching into the drinking
water of children in schools.
0 The report strongly recommends that lead abatement initiatives
include careful consideration of lead movement to avoid simply
shifting the lead problem from one part of the environment to
another. :
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a
lo} The report strongly recommends that much more attention be paid
to exposure of the fetus with screening of Pb-8 levels in all
high-risk pregnant women.
0 Key initiatives recommended by the American Academy of Pediat-
rics (1987) should be adopted. These initiatives include
screening of every child in the United States at risk of expo-
sure to lead.
o) The report recommends a careful examination of the role of
improved nutrition in ameliorating lead toxicity.
|
|
0 Continuing large-scale assessments of lead burdens in children,
including further national surveys and more regionally focused
studies are required.
: 0 Continued support should be given to the highly productive
: prospective epidemiological studies now under way and to the
development and refinement of metabolic models that are used to
examine the quantitative relationship between source-specific
lead exposure levels and the resulting lead levels in blood or
other body compartments.
C. ISSUES, DIRECTIONS, AND THE FUTURE OF THE LEAD PROBLEM
1. Issues
A number of key scientific issues concerning lead as a major health
problem are of special concern for the establishment of public health policy in
the United States. These issues include:
0 The Indestructibility of the Problem. As an element, inorganic
lead cannot be processed by current technology and destroyed.
It will continue to be a potential problem in some form forever.
0 The Relative Non-Transferability of the Problem. Lead cannot be
easily shifted from a hazardous setting to a nonhazardous
setting without some concomitant increased potential risk
elsewhere. Once removed from its geologically bound forms by
human activities, lead poses a toxic threat for which there are
no natural defense mechanisms.
0 The Environmental Accumulation Factor. Lead accumulates
indefinitely in the environment so long as input continues -- no
matter in how small a quantity.
0 The Human Body Accumulation Factor. The human body accumulates
lead over the individual's active lifetime and does so even with
"small" intakes from common sources. For hazards to exist,
major exposures at given points in time need not occur.
AN
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1) The Risk Population Accumulation Factor. Estimates of exposure
and toxicity based on data from particular points in time, such
as the estimates provided in this report, greatly understate the
cumulative risk for a population posed by a uniquely persistent
and pervasive pollutant such as lead. This cumulative toll over
extended time is of much greater magnitude, and hence concern,
than the prevalence or total exposure estimates for any given
year.
(a) An individual fetus is never counted more than once in any
survey examining populations. In the absence of effective
abatement of lead exposure, the estimate of 400,000 indivi-
dual fetuses at risk for lead toxicity in a single year
becomes 4 million individual fetuses in 10 years, or
20 million in 50 years, of lead exposure.
(b) Within a given time period, successive sets of preschool
children are likely to move into the same housing unit,
particularly in the case of deteriorated inner-city tenant
housing. Thus, the number of infants and toddlers at risk
for the exposure associated with such conditions (espe-
cially paint and dust/soil lead) is much greater than the
number of deteriorated houses. If one assumes 3 to 5 years
as the average period of residency, then perhaps 10 times
as many children would be exposed to such conditions over a
30- to 50-year period.
0 The Pervasiveness of the Problem. As a pervasive toxicant, lead
is shown in this report to affect totals of children that are
high in all socioeconomic/demographic strata. The U.S. lead
problem is not simply a problem of a generally neglected segment
of society. At present, little or no margin of safety exists
between existing Pb-B levels in large segments of the U.S.
population and those levels associated with toxicity risk.
0 Absence of a Truly Optimal Blood Lead Level. As a ‘toxicant
serving no known physiological requirement, the presence of
lead at any level in the body is less than optimal. Current
average Pb-B levels in some U.S. population segments are 15- to
30-fold higher that the theoretical value of 0.5 pug/dl calcu-
lated for early, pre-industrial humans.
2. Directions and Future of the Lead Problem
At the same time that progress is being made to reduce some sources of
lead toxicity, scientific determinations of what constitute "safe" levels of
lead exposure are concurrently declining even further. Thus, increasing
percentages of young children and pregnant women fall into the “at-risk”
category as permissible exposure limits are revised downward. Accompanying
these increases is the growing dilemma of how to deal effectively with such a
|
J
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widespread public health problem. Since hospitalization and medical treatment
of individuals with Pb-B levels below approximately 25 pg/dl is neither
appropriate nor even feasible, the only available option is to eliminate or
reduce the lead in the environment.
In large measure, the more tractable part of the lead abatement effort in
the United States is already underway, because the reduction of lead in
gasoline, food, and drinking water is amenable to centralized control
strategies. Lead in old paint, dust and soil, however, is pervasive and
dispersed, and fundamentally different approaches to abatement will be needed.
If the Nation is to solve these difficult facets of the lead problem, society
must make a strong effort to do so. Without this effort, large numbers of
young children in present and future generations will continue to be exposed to
persistent and massive sources of lead in their environment.
2. Monitoring Lead Exposure in Young Children and Other Risk Populations
Health professionals determine the degree of lead exposure of children and
other risk populations in three ways. The traditional method is to measure
lead in external or environmental media (ambient air, workplace air, food,
water, dust, soil, etc.) that are pathways for human exposure. Surveying lead
in these media, termed environmental or ambient monitoring, provides informa-
tion about the lead exposure sources and the potential risk for persons so
exposed to lead. Environmental monitoring does not indicate the actual
internal level of lead for any given individual, because individuals may
respond differently to an external source of lead exposure. On a group basis,
however, one can determine the probable internal exposure level, given
knowledge of the concentrations in the external media and the mathematical
relationship between the two variables (different levels in the media and
different responses in groups of people). In many cases, one must use environ-
mental monitoring, either because other types of exposure assessment cannot be
carried out or because a more direct, systemic measure of exposure is
considered unnecessary.
Lead exposure is also commonly assessed through biological monitoring and
effects monitoring. Biological monitoring is the measurement of the concentra-
tion of lead in a biological sample, e.g., blood, from an exposed person.
Effects monitoring involves measuring some endpoint, e.g., the amount of
certain proteins or enzymes associated with lead exposure. For a more compre=
hensive examination of monitoring exposure to lead, see Elinder et al. (1987).
Biological monitoring and effects monitoring have advantages for assessing
re3lth effects, giving an integrated picture of a person's uptake of lead from
all external sources.
To assess lead exposure in children and other risk groups, the level of
fo in whole blood (Pb-B) is the most practical biological measure of ongoing
lead absorption. This measure is used throughout Chapters IV-VIII as a means
of relating lead exposure levels to adverse health effects. A Pb-B level is
generally regarded as reflecting relatively recent exposure. However, Pb-B
levels also give information on the relative level of exposure at more remote
time points. In other words, a child who had the highest Pb-B level at one
time will probably have the highest Pb-B level at a future retesting. Pb-B
levels do not, however, indicate cumulative past exposure, as do lead levels
of mineralizing tissue such as tooth or bone. Such cumulative measures cannot
275 ares
&r”
yet be routinely employed in screening programs. The kinetic, toxicological,
and practical aspects of biological monitoring and other approaches to assess-
ing lead exposure have been extensively discussed by U.S. EPA (19863).
In young children, effects monitoring for lead exposure is primarily based
on lead's impact on the heme biosynthetic pathway, as shown by (1) changes in
the activity of key enzymes delta-aminolevulinic acid dehydratase (ALA-D) and
delta-aminolevulinic acid synthetase (ALA-S), (2) the accumulation of copropor-
phyrin in urine (CP-U), and (3) the accumulation of protoporphyrin in erythro-
cytes (EP). For methodological and practical reasons, the EP measure is the
effect index most often used in screening children and other population groups.
Effects monitoring for exposure in general and lead exposure in particular
has drawbacks (Friberg, 1985). Effects monitoring is most useful when the
endpoint being measured is specific to lead and sensitive to low levels of
lead. Since EP levels can be elevated by iron deficiency, which is common in
young children, indexing one relationship requires quantitatively adjusting for
the other.
An elevated Pb-B level and, consequently, increased lead absorption may
exist even when the EP value is within normal limits, now £35 micrograms (ng)
EP/deciliter (d1) of whole blood. We might expect that in high-risk, low
socioeconomic status (SES), nutrient (including iron)-deficient children in
urban areas, chronic Pb-B elevation would invariably accompany persistent EP
elevation. Analysis of data from the second National Health and Nutrition
Examination Survey (NHANES II) by Mahaffey and Annest (1986) indicates that
Pb-B levels in children can be elevated even when EP levels are normal. Of Y
118 children with Pb-B levels above 30 ug/dl (the CDC criterion level at the
time of NHANES II), 47% had EP levels at or below 30 ug/dl, and 58% (Annest
and Mahaffey, 1984) had EP levels less than the current EP cutoff value of 35
ug/dl (CDC, 1985). This means that reliance on EP level for initial screening
can result in a significant incidence of false negatives or failures to detect
toxic Pb-B levels. This finding has important implications for the interpreta-
tion of screening data, as discussed in Chapter V.
3. Environmental Sources of Lead in the United States with Reference to
Young Children and Other Risk Groups
As graphically depicted in Figure II-1, several environmental sources of
lead exposure pose a risk for young children and fetuses. Many sources not
7 11-6
2/6
Analysis (J. Schwartz and H. Pitcher) performed a statistical procedure called
logistic regression analysis to update estimates of prevalences to 1984 and
produce prevalences at the selected criterion values of >15, >20, and >25 pg/d1
for SMSA populations of children in the required strata. A detailed discussion
of this logistic regression/projection methodology is presented in the second
part of Appendix G.
2. Results
Tables V-1 and V-2 give estimated prevalences of Pb-B levels in children
above three selected levels; 15, 20, and 25 pug/dl within the strata. Tables V-1
and V-2, respectively, show these rates for "Inside Central City" and "Qutside
Central City" categories. Shown are three family income levels to indicate
relative poverty, and each income category has two classifications by race.
Each of these 6 strata is further divided into "SMSA with population 21 million"
and "“SMSA with population <1 million." In 122 SMSAs, we had 12 strata available
to us, and each strata gave us three prevalence estimates.
TABLE V-1. PROJECTED PERCENTAGES OF CHILDREN 0.5-5 YEARS OLD ESTIMATED
TO EXCEED SELECTED Pb- 3B CRITERION VALUES (ug/dl1) BY FAMILY INCOME, RACE,
AND URBAN STATUS, 4 WHO LIVE “INSIDE CENTRAL CITY" OF SMSAs, 1984
Family Income/ >15 ug/dl >20 ug/d1l >25 pg/dl
Race <1 M 21 M <1 M 21 M <1 M 21 M
<$6,000
White 25.7 36.0 7.6 11.2 2.1 3.0
Black 55.5 67.8 22.8 30.8 7.7 10.6
$6,000-14,999
White 15.2 22.9 4.0 6.1 1} 1.5
Black 4}.1 53.6 14.1 19.9 4.1 5.9
2$15,000
White 7-1 11.9 1.5 2.5 0.4 0.5
Black 26.6 38.2 6.8 10.4 1.5 2.2
3SMSA with population <1 million (<1 M) and SMSA with population 21 million
(21 M).
TABLE V-2. PROJECTED PERCENTAGES OF CHILDREN 0.5-5 YEARS OLD ESTIMATED
TO EXCEED SELECTED PbZB CRITERION VALUES (ug/d1) BY FAMILY INCOME, RACE,
AND URBAN STATUS,“ WHO LIVE "OUTSIDE CENTRAL CITY" OF SMSAs, 1984
Family Income/ >15 pg/dl >20 ug/dl >25 pg/dl
Race <1 M 21 M <1M 21 M <1M 21 M
<$6,000 ;
White 19.2 27.7 5.6 8.4 1.6 2.3
Black 45.9 57.8 17.9 24.5 6.1 8.4
$6,000-14,999
White 10.9 16.8 2.9 4.5 0.8 1.2
Black 32.4 43.7 10.7 15.4 3.2 4.6
2$15,000
White 4.7 8.1 1.96 1.7 0.2 0.4
Black 19.5 28.9 4.9 7.6 3.1 1.7
4SMSA with population <1 million (<1 M) and SMSA with population 21 million
(21 M).
Table V-3 shows the more limited number of strata and the relevant sets of
prevalence estimates when Inside/Outside Central City status could not be
ascertained. This applied to 196 SMSAs: 34 paired, 161 with populations below
200,000 (with very few exceptions), and Nassau-Suffolk, NY, with a population
over 1 million but no central city.
The NHANES II Pb-B levels reported and used in calculating prevalences for
criterion levels are based on Pb-B determinations for all cases--they are not
influenced by initial erythrocyte protoporphyrin (EP) determinations and, for
cases with elevated EP levels, subsequently selected Pb-B determinations.
In earlier analyses, we attempted to apply the national, urbanized compos-
ite prevalences to each of the SMSAs with the appropriate qualifications as to
their reliability. This approach was attempted to best respond to the directive
of Section 118(f) that asked for ranking of individual SMSAs. When the scien-
tific community was reviewing this approach, however, problems were found with
the level of permissible disaggregation due to the sample design of the
NHANES II survey. For example, the national source-based differences that were
implicit but not specific in the original analytic process could not be broken
out and reassigned in disaggregation.
— 3
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TABLE V-3. PROJECTED PERCENTAGES OF CHILDREN 0.5-5 YEARS OLD ESTIMATED
TO EXCEED SELECTED Pb-B CRITERION VALUES BY FAMILY INCOME AND RACE WHO
LIVE IN SMALL SMSAs,~ 1984
Family Income/
Race >15 pg/dl >20 ug/dl >25 pg/dl
<$6,000
White 23.9 6.9 i.8
Black 56.5 22.9 7.4
$6,000-14,999
White 13.2 3.4 0.9
Black 40.3 13.6 4.0
2$15,000
White 5.8 1.2 0.3
Black 25.4 6.3 1.4
ASMsAs with less than 1 million population.
In a second attempt to geographically specify lead exposure, projected
prevalence estimates were calculated for the four major regions used in the
original NHANES II survey: Northeast, Midwest, West, and South. However,
statistical projection data could not be established for these regions. This
was due in part to the small numbers of children with higher Pb-B/levels in
some regions, such as the West. If these small numbers had been used to calcu-
late prevalences in the region, some prevalences would have had unacceptable
margins of estimating error. Consequently, in this report, we provide the
updated Pb-B prevalence calculations for selected Pb-B levels and the nation's
urbanized childhood lead-exposure status for each of the 30 socioeconomic/
demographic strata described earlier.
Tables V-4, V-5, and V-6 present the results of applying the estimated
prevalences of the 30 strata of children in all SMSAs. Table V-4 depicts chil-
dren living inside central cities for the SMSAs where such division was
possible, and Table V-5 shows the children outside central cities in these
SMSAs. Table V-6 shows the findings for smaller and paired SMSA child popula-
tions. A partial summary of these three tables for children with Pb-B levels
above 15 pg/dl is presented in Table V-7. Table V-8 presents overall summary
data.
of the SMSAs. But the ubiquity of the exposure to lead at >15 pg/dl is the
striking finding. There are no strata of children totally free of this poten-
tial health risk, which holds true for higher Pb-B levels as well.
B. NUMBERS OF LEAD-EXPOSED CHILDREN BY COMMUNITY-BASED SCREENING PROGRAMS
In the previous section; the number of lead-exposed children was identi-
fied and categorized by socioeconomic-demographic variables and prevalence
of selected Pb-B levels. In this section, we will discuss U.S. communities
that have screening programs for identifying young children at risk. Elevated
Pb-B level plus elevated erythrocyte protoporphyrin (EP) in blood is the measure
used for assessing this risk. Because these screening programs are defined
geographically as to city, county, or state, these programs and their locales
come within the general meaning of the directives of Section 118(f)(1)(A) of
SARA. In general, children living in these screening sites are considered to
be at highest risk for lead exposure/toxicity, as we presently understand it.
This section briefly discusses the Second National Health and Nutrition
Examination Survey (NHANES II) to compare with the lead screening efforts used
over the years.
1. Lead-Screening Programs
Before examining in detail the results of the various lead exposure
screening programs operating in U.S. communities it is useful to consider how
the screening programs developed and their current status for interpreting the
results of these programs. An additional overview of the U.S. screening
process is also presented later, in the chapter dealing with exposure abatement
and related issues. A comprehensive history of the public health aspects and
operational characteristics was presented by Lin-Fu (1985a,b).
Screening activities were first mandated and supported by the 1971 Lead-
Based Paint Poisoning Prevention Act, and the actual project started in Fiscal
Year (FY) 1972. Shortly thereafter, the U.S. Centers for Disease Control (CDC)
was given administrative responsibilities for these activities. By FY 1981,
under CDC's guidance, screening in the United States had expanded to more than
60 programs and represented eight regions of the Department of Health and Human
Ned fs
rt >
H
ya
/
Services (DHHS). Part of CDC's overall efforts included establishing a labora-
tory proficiency testing service for Pb-B and EP measurements in screening and
other child medicine services. This was under the aegis of the Center for
Environmental Health.
In FY 1982, screening and other grant programs were incorporated into the
Maternal and Child Health (MCH) Block Grant Program and administered by the
Maternal and Child Health Division, Bureau of Health Care and Delivery Assis-
tance, Health Resources and Services Administration, DHHS. Although Farfel
(1985) proposes that this change was attended by funding reductions, it is not
possible to identify an actual reduction figure. As noted by Lin-Fu (1987),
each state receiving the block grant portion of money determined its own
priorities within the MCH programs, including lead screening. Furthermore, in
many cases lead-screening costs are included in budgets for comprehensive
pediatric services (Lin-Fu, 1987).
At present, the Association of State and Territorial Health Officials’
(ASTHO's) administrative unit, the Public Health Foundation, is collecting data
on childhood lead-poisoning prevention efforts from the various states; however,
participation is voluntary. A number of states and constituent programs within
the states have attempted to maintain the same level of effort that prevailed
under CDC administration of the programs. In general, this is the case for the
major programs in New York City, Chicago, Baltimore, and Massachusetts.
In FYs 1982 and 1983, the numbers of reporting states were 26 and 33,
respectively. Has the number of programs decreased? This question cannot be
answered very well without detailed canvassing. During the present administra-
tive period, each state agency reports their results, and a given state may
have more than one program unit as defined under the former CDC system. In
December 1986, ATSDR canvassed reporting states and other jurisdictions;
41 program units responded with usable data. For all responding programs, the
count was over 45 units. This tally included the MCH projects in Massachusetts
and counted the rest of the state as one screening unit.
Screening data for different geographic areas have been tabulated. For
several reasons, including continuity across time and differences in program
characteristics, shown are: (1) data for the final year of the original program
administered by CDC, FY 1981; (2) screening results from the programs under the
Maternal and Child Health Block Grant as reported under the ASTHO program
(FY 1983); and (3) survey results gathered by ATSDR in December 1986. The ATSDR
survey include results from agencies reporting by fiscal and calendar years,
reported within 1985 or 1986 or both, and from independent programs within the
various states.
Within each program period and between program periods, several factors
have influenced, and continue to influence, screening results. (1) The screen-
ing risk classifications have changed since the results set forth in the
following tables were gathered. These various classification schemes are shown
in Tables V-9, V-10, and V-11. (2) Targeting high-risk populations has proba-
bly changed over the years. From FY 1972 to 1981, the strategies for screening
~ populations, under CDC guidance, were uniform. The main goal was to screen
groups of children in the community judged at high risk and having high preva-
lence rates for elevated Pb-B levels and for lead poisoning serious enough to
warrant medical or public health action. Although this screening may give the
number of children exposed in high-risk areas, it does not necessarily reflect
the nationwide status of the lead problem. This screening was appropriate for
the original purpose, that is, to concentrate attention on those children who
most urgently need screening.
TABLE V-9. CDC LEAD SCREENING CLASSIFICATION SCHEME, 1978-19852
Blood Lead Erythrocyte Protoporphyrin (ug/dl Whole Blood)
(pg/dl) 50-109 110-249 >250
30-49 II III ITI
50-69 ITI 111 IV
270 b Iv IV
Classification numbers increase with increased "toxicity" risk and need for
diagnostic evaluation. A given class, e.g., Class III, can represent a com
bination of Pb-B/EP results. See CDC (1978) statement for more details.
Pot commonly encountered in screened populations.
Fall V-18 |
TABLE V-10. CDC LEAD SCREENING CLASSIFICATION SCHEME AS OF JANUARY 1985,
USING THE HEMATOFLUOROMETER®
Blood Lead Erythrocyte Protoporphyrin (ug/dl Whole Blood)P
(pug/dl) <35 35-74 75-174 2175
Not Done -C =C
12 74
Instrument for field measurement of EP, see CDC (1985) statement.
bine protoporphyrin measured with hematofluorometer and free EP with chemical
method.
“Requires a Pb-B measurement.
Not usually observed.
®Erythropoietic protoporphyria (EPP), a genetic disease, is a possibility.
TABLE V-11. CDC LEAD SCREENING CLASSIFICATION SCHEME AS OF JANUARY 1985,
USING CHEMICAL ANALYSIS OF EP :
Blood Lead Erythrocyte Protoporphyrin (ug/dl Whole Blood)?
(pg/dl) <35 35-10% 110-249 2250
Not Done -¢
<24 a
25-49
See CDC (1985) statement for more details.
"Free" erythrocyte protoporphyrin measured by chemical method.
Requires a Pb-B measurement.
a
b
Cc
d
Not usually observed.
€Erythropoietic protoporphyria (EPP), a genetic disease, is a possibility.
Screening programs are now conducted with methods that tend to under-
report the true screening prevalences of Pb-B levels. Since an EP level is the
first step in assessing lead exposure in young children, children who have a
“normal” EP level but an elevated Pb-B level will not be counted as a subject
risking toxicity. The rate of these "false negatives" was reported to be con-
siderable (see earlier quantitative discussion in Chapter II). Furthermore,
the true rate may be even higher than when the prevalence of lead exposure is
determined mainly at the time of clinic visits or the equivalent, compared with,
for example, intensive, door-to-door canvassing.
Tables V-9, V-10, and V-11 show changes in risk classifications that
consist of lowering the Pb-B level for the lowest category by 5 ug (from 30 to
25 ug/d1) and lowering the EP level in whole blood by 15 units (from 50 to 35).
As noted elsewhere, these changes represent a trade-off between the lead levels
the pediatric health community sees as harmful and the logistics of screening
and the technical limits of the EP measuring methods routinely used. In other
words, Pb-B levels below the CDC level of 25 pg/dl for whole blood should not
necessarily be viewed as "safe." :
In Table V-12, we have presented groups of children screened in the CDC
program for FY 1981 and have given the number of children positive for lead
toxicity based on the older action levels of 30 pg/dl Pb-B and 50 ug/dl EP.
The numbers of responses currently defined as positive are separated further
into two risk groups, Class II and combined Classes III and IV. Data in
Table V-12 are as reported in the Morbidity and Mortality Weekly Report (CDC,
1982).
Table V-13 shows a summary of the more recent screening results that ASTHO
collected from state health agencies. Twenty-seven state agencies provided
numbers of young children screened for lead toxicity, but only 24 provided
data on confirmed cases of toxicity (Public Health Foundation, 1986).
To determine the current scope and outcomes for various lead screening
programs, ATSDR asked all state and known county or city screening units for
information on the numbers screened, the numbers of confirmed lead toxicity
cases, and the relevant time periods. Data from this ATSDR survey are in
Table V-14. The survey period covers the time during which CDC distributed its
January 1985 lead statement. Data in this table therefore represent numbers
from some combination of the former and present screening classification
schemes (For schemes see Tables V-9 through V-11.)
2% V-20
exposure cases was .1.5%. In terms of numbers, more children appear to be
screened at present, although statistical comparisons with the older CDC
framework would be difficult.
Toxicity responses for 1985-1986 ranged from 0.3% for four programs to
11.0% for the City of St. Louis program. The five highest prevalences are
11.0% (St. Louis), 9.0% (Augusta and Savannah, GA), 4.9% (Harrisburg, PA), 3.5%
(Washington, DC) and 3.5% (Merrimac Valley, MA, a program within a MCH pro-
ject). Most of the rates for confirmed toxicity cases were below 2%.
Prevalences reported for earlier years include those from state agencies,
as summarized by the Public Health Foundation. For FY 1983, reporting agencies
screened 675,571 children and recorded a prevalence of 1.5%. Similarly, the
CDC data for FY 1981 indicated that 535,730 children were screened, with 21,897
meeting the toxicity risk criteria then in use--a prevalence of about 4%. For
the reasons noted above, we cannot closely compare these three sets of results.
Trends in prevalences over time, at least in the years under CDC control,
suggest a moderate decline in toxicity risk from 1973 on. Data from two
programs for 1973 to 1985, and data from the St. Louis, MO, program show
downward shifts, even with changes in risk classifications.
With the 1985 change in the CDC toxicity risk classifications, we might
expect the number of toxicity risk positive results to increase, and the New
York City screening program results show such an increase. In future years,
then, the prevalences will reflect this change in classification, but they will
also reflect the impact of reduced levels of lead in gasoline and food.
Comparison of Prevalences Found in NHANES II Updated Prevalences and
U.S. Screening Programs
Because the NHANES II prevalences, and therefore the updated adjusted
rates, are based on Pb-B determinations for the subjects, there is consequently
no intervening problem of first determining EPs. These rates are not subject
to systematic underreporting due to false negative results found when EP deter-
minations are used to classify the initial population group being evaluated and
identify who will then be tested for Pb-B levels. Screening programs, however,
test for EP first.
Other factors in screening programs probably produce lower prevalences com-
pared with those that can be predicted on the basis of results from NHANES II
- SEE
uae V-47
and other surveys. Screenings are not always intensive, for example, house-
to-house; in most cases, they are conducted in clinics. Any factor that
affects the characteristics of clinic visits also affects Pb-B prevalences.
For example, the mothers who bring children to clinics may be more concerned,
informed, and motivated than those who do not bring their children.
Finally, communities with the highest prevalences may not have unique
situations. Their approach to the problem simply may be more systematic than
in other communities, and therefore, they report the highest rates. The more
appropriate question may well be why all communities do not have higher rates
rather than why certain communities have high rates. This type of question
cannot be answered unless the screening programs are again centrally
administered.
4. Children With Potential Exposure to Leaded Paint in the SMSAs
This section summarizes an attempt to identify potential lead exposure by
each SMSA and by a specific source, leaded paint. It therefore combines
approaches dealing with source-specific exposure described earlier in Chapter V
and those in Chapter VI.
The number of children living in pre-1950 housing was obtained from the
actual 1980 Census enumeration. Table V-20 and Appendix D present the ranking
of SMSAs by the number of children in pre-1950 housing and show that young
children are least often found in the newest housing, built in 1970-1980. This
is probably due to the fact that young families are least able to afford newer
housing and particularly newer units inside central cities. While children in
families with the lowest incomes were found disproportionately in the older
housing, large proportions of children in the highest income families were also
found living in the oldest housing stock. Furthermore, the children with
family incomes above the poverty levels frequently constituted the largest
proportion in the oldest housing.
While there is no perfect correlation between the age of the housing and
the presence of a leaded paint hazard, note that weathering and chalking occur
even when there is no dilapidation or deterioration of the housing. We do not
know how many pre-1950 housing units have been renovated or had high lead-
content paint removed, but we can say with some confidence that the fraction is
quite low, given data for Massachusetts cities described in Chapter IX.
c)-CF a
750 V-48
* »
Equally, we do not know the consequences of such paint removals in terms of
increasing the raw lead content of the sites' dusts and soils within reach of
these young children.
Another factor to consider when examining the significance of housing age
is the presence of lead in plumbing and the potential contamination of the
drinking water. Older housing may contain lead plumbing, and the most recent
stock may contain lead in the solder used for copper piping. In either case,
lead may leach into the drinking water, which is discussed more fully in
Chapter VI.
The environment in which young children are housed, which depends on the
income of young families at the start of the family phase of the life cycle as
well as the availability of housing units of different ages, exposes a large
_ proportion of young children regardless of family income to the older housing
stock that in turn is likely to contain the paint with the highest lead
content. The ubiquity of Pb-B levels representing health risks found by the
NHANES II survey is supported by the finding that young children frequently
live in the type of housing most likely to contain sources of lead: in paint,
drinking water, and dust/soil.
Finally, one significant but often unrecognized point about childhood
exposure sources such as leaded paint deserves emphasis. Until leaded paint
and contaminated dust and soil are removed from young children's environment,
the number of young children at risk for adverse health effects will accumulate
over time and continue to present a serious public health problem since each
new cohort of children will in turn be exposed to lead in the environment. In
other words, the cumulative tally of exposed children becomes much larger as
time passes than the specific counts given at one point in time. This is due
to both the high mobility within the high leaded paint zones in which the
high-risk families live and the sociological fact that poor families may be
“locked" into such housing for many years.
5. Conclusions and Overview
This report represents the first systematic effort to quantify the extent
of the U.S. child lead-poisoning problem and to place such numbers in some
context of distribution of the children, the lead sources, the adverse health
responses, and strategies for lead reduction or removal. This chapter is a key
i
ie 3 ~~ / 5 77 v-49
ir
component of this effort and is important both for the numbers provided and for
helping answer the obvious questions "Which children have the problem?" and
"What can we start to do about it?"
From the key findings of Chapter V, we conclude that the total number
of U.S. children exposed to lead at unacceptable levels (Pb-B >15 pg/dl),
2.4 million SMSA children or 17% of the SMSA child total, arise from many
different socioeconomic and demographic strata.
It was to be expected that the "traditional" high-risk groups, e.g., poor,
inner-city black children, would have figured prominently in the estimation
outcomes, and they do. These high-risk groups are usually defined as such in
terms of high prevalence rates of elevated Pb-B levels. Less well understood,
perhaps, is the fact that the totals for exposed strata in this chapter are
derived from both a prevalence for a given Pb-B and the base population by
which the prevalence fraction is multiplied to give a stratum final total.
The consequences of an estimating exercise, across strata, for exposure
totals is simply that large numbers in a stratum's base population can have
quite low prevalences for certain Pb-B levels and still yield numbers that are
comparable to those obtained from high-risk strata that have smaller base
populations of children but quite high prevalences of elevated Pb-B levels. In Chapter V, a variety of estimating strategies were employed, and
provide quite different numbers for exposure estimates. These differences were
explained earlier in the summary. Furthermore, some of the totals complement
each other, providing different views of the same total population of U.S.
children. For example, examining the very detailed U.S. Census Bureau counts
(not estimates) of children in the 318 SMSAs reported in terms of housing age
and family income (Section C) produces the unexpected finding that more
children in older housing (high paint-lead levels) were also in noncentral-
city, nonpoverty families than were children associated with the typical risk
groups. This observation corresponds to this report's projected Pb-B distribu-
tions in the nation's children.
These distributions in high-risk housing might account for why certain
Pb-B prevalences in the otherwise lower-risk strata of U.S. SMSA children are
as high as they are. In other words, distribution of the nation's children
into high lead-exposure risk housing is uniform enough that all strata of such
children, when examined by means of a national composite survey such as NHANES
II, will produce significant prevalences. Clearly, however, other sources also
have an impact on Pb-B levels and their prevalences in the general child popula-
tion, and this point is established in Chapter VI.
At present, the third national survey of its type, NHANES III, is in the
planning stage, and eventually results of this survey (expected in the mid-
1990s) will produce more precise numbers for prevalences of Pb-B levels in
strata used in NHANES II and in this report. In the interim, the 1990 U.S.
Census will also be conducted. For the present, however, the estimates and
U.S. Census counts of children in Chapter V are the best that can be done with
the available data.
X. A REVIEW OF ENVIRONMENTAL RELEASES OF LEAD AS EVALUATED UNDER SUPERFUND
Section 118(f)(2) of the Superfund Amendments and Reauthorization Act
(SARA) of 1986 requires this report to "score and evaluate specific sites at
which children are known to be exposed to environmental sources of lead due to
releases, utilizing the Hazard Ranking System of the National Priorities List."
EPA has carried out this requirement in two ways: (1) by identifying proposed
and final sites on the National Priorities List (NPL) that have been numeri-
cally scored under the Hazard Ranking System (HRS) and at which lead has been
released into ground or surface waters or air, highlighting those sites where
children are known to have been exposed to lead; and (2) by gathering data at
an urban area in Boston where children are known to be exposed to lead in soil,
and scoring one residence as a site under the HRS.
The HRS was designed to respond to section 105(a)(8)(A) of the Comprehen-
sive Environmental Response, Compensation and Liability Act of 1980 (CERCLA).
This section requires that the National Contingency Plan (NCP) include
“criteria for determining priorities among releases or threatened releases
throughout the United States for the purpose of taking remedial action,...."
Section 105(a)(8)(B) requires that the criteria be used to prepare a list of
national priorities for sites with known or threatened releases of toxic
substances throughout the United States. This use of the HRS to form the NPL
is a means of directing EPA response resources to those facilities believed to
present the greatest magnitude of potential harm to human health and the
environment.
The HRS is a means of comparing one site against others based on the
estimated relative threat to human health and the environment. Relative threat
is determined by assessing the likelihood of release or migration of waste
contaminants from a facility, along with the consequences of such a release,
such as effects on people. Migration of contaminants from a site occur through
air, surface water, and groundwater. Consequences of such a release are
determined by the toxicity and other characteristics of the wastes and whether
the release has affected or will affect people.
The HRS is not an assessment of the risks found at a facility. Such an
assessment occurs only after a great deal of additional data have been gathered
and is used to help determine the type and degree of cleanup necessary to
reduce the risk to human health to an acceptable level.
A. NPL SITES--PROPOSED AND FINAL
To be listed on the NPL, a site must score at least 28.5 out of a possible
score of 100 under the HRS in effect September 30, 1987. (EPA is now revising
the HRS; see discussion later in this chapter.) Of the 957 proposed and final
NPL sites as of September 30, 1987, 307 have lead as an identified contaminant,
and 174 have an observed release of lead to air, to surface water, or to
groundwater. An observed release is documented by monitoring data showing such
a release from the site. The sites with only an identified contaminant had no
data showing release of the contaminant from the site. All proposed and final
NPL sites with an observed release of lead are listed (with their HRS scores)
in Appendix F.
Exposure of Children to Lead at NPL Sites
EPA reviewed site files to obtain data regarding the exposure of children
at each NPL site with an observed release of lead. In only a few cases was the
Agency able to document exposure of children to lead from the site, since no
records are kept that separate children from the general population exposed to
releases from a site. In some cases, however, studies had been conducted
around sites that showed that children were exposed to lead from the sites.
These are documented below.
The Interstate Lead Company, an NPL site in Leeds, AL (HRS score 42.86),
is a battery recycling and secondary lead smelting operation. Results of a
March 1984 study of lead contamination conducted by the Jefferson County
Department of Health and Bureau of Communicable Diseases, showed that children
under 10 years of age living less than one-half mile from the lead plant had
higher blood lead levels than children the same age living farther from the
plant. Blood lead levels of all children ranged from 6 to 29 pug/dl.
R
E
RA
RO
A
R
ON
D
y
n
The East Helena, MT, site (HRS score 61.65) is a primary lead and zinc
smelter where 8.4 square miles of land have been contaminated, with lead in
soil measuring more than 1,000 ppm. In a random sample of 90 children living
near the smelter, blood lead levels of 6 to 25 ug/dl were detected. In 1975
and 1978, cattle reportedly died from lead poisoning.
At the NL Industries/Taracorp Lead Smelter, an NPL site in Illinois (HRS
score 38.11), the ITlinois EPA measured high lead levels in the soil of
residential areas near the smelter. Two soil samples exceeded 5,000 ppm lead.
The I11inois EPA recommended that small children living nearby be restricted
from playing in the dirt, from eating outside, and from placing dirt or dirty
objects in their mouths.
The Sharon Steel Smelter, in Utah, has been proposed for the NPL (HRS
score 73.49). It is an inactive smelter with 10 million tons of tailings piled
on the site. People have taken some of the waste from these piles to use in
sandboxes and gardens. Analyses by the State of Utah indicate elevated levels
of lead and other heavy metals in edible portions of food grown on soil to
which the waste from this site has been added.
At the Harbor Island Battery Recycling site in Washington State (HRS score
34.60), elevated levels of lead have been reported in workers and their chil-
dren.
At the Brown's Battery Recycling site in Pennsylvania (HRS score 37.34),
the Pennsylvania Department of Health measured elevated blood lead levels in
four children. One child received treatment to reduce his body burden of lead.
Soil from three residences adjacent to the primary disposal area had lead
levels ranging from 1,120 to 84,200 ppm.
At the Bunker Hill Mining and Metallurgical site (HRS score 54.76), a lead
smelter in Idaho, the Idaho Department of Health and Welfare found an epidemic
proportion of children (98%) living within 2 miles of the smelter who had
blood lead levels exceeding 40 pg/dl.
The Lackawanna Refuse site in Pennsylvania (HRS score 36.57) is a former
strip mining site. It is near a residential area of 9,500 people, and local
children use the site as a recreational area. EPA and the Pennsylvania Depart-
ment of Environmental Resources found concentrations of 12,000 ppm lead in the
waste contained in the thousands of drums found at the site.
As can be seen from the descriptions of the foregoing cases, the sites on
the National Priority List with observed releases of lead consist of sites
where manufacturing, processing, or disposal of lead has taken place. This can
be seen graphically in Table X-1, relating the twelve most common activities at
NPL sites with observed lead releases from waste. Actual disposal of waste
accounts for the largest proportion by number of sites, with manufacturing, ore
processing, and battery recycling at the bottom of the list.
B. URBAN AREA SITE
EPA has carried out a preliminary assessment and site investigation of
a Boston area to prepare an HRS package for scoring the site. The site
consists of a rectangular area encompassing approximately 5 square miles where
children are believed to be exposed to lead from both interior and exterior
paint and from elevated lead concentrations in the soil surrounding the houses.
This site was chosen because it contains areas that have been designated by the
City of Boston as Emergency Lead Poisoning Areas (ELPAs). An ELPA is an area
of one or more city blocks where a higher than average number of children were
found to have elevated blood lead levels.
The areas consist mostly of triple-story houses of frame construction.
Most have been converted to six apartments, causing a high population density
in the area. Because the houses are separated by only a few feet, lack of
sunlight inhibits the growth of grass or a suitable cover for the soil, and the
lead is available to children playing in the dirt in these areas.
Data were gathered for two housing units within the area specifically to
be evaluated under the HRS. Scoring was done for the unit expected to score
highest under the HRS. This unit has greatly elevated soil lead levels both in
front and behind the house, but no evidence of peeling paint. The lead concen-
trations in the front of the house near the street exceed the concentrations in
the back of the house, indicating that a portion of the lead may have resulted
from auto emissions.
The data for this area have been processed through the Hazard Ranking
System as if it were a hazardous waste disposal site to be evaluated for the
NPL. The data were collected by Region I personnel and scored prior to
transmission to headquarters. This original scoring package passed through the
quality assurance and quality control process without revisions, and the
assigned score of 3.56 was affirmed. The minimum HRS score needed for listing
on the NPL is 28.5.
1 TABLE X-1. MOST COMMON ACTIVITIES ASSOCIATED WITH LEAD WASTE AT NPL SITES WITH LEAD RELEASE®
ug With Observed A11 NPL Sites
Lead Release Percentage
Activity of Number Number With Lead NPL Site Rank of Sites Rank - of Sites Release
Landfill, 1 75 2 349 21 commercial/
industrial
Surface 2 66 } 350 19 impoundments
Containers/drums 3 49 3 261 19
Landfill, 4 35 4 158 22 municipal
Waste piles 2 27 10 89 30
Spill 6 21 oo B 139 15
Other 7 18 5 142 13 manufacturing/
industrial
Chemical process/ 8 18 i 104 17 manufacturing
Battery recycling 9 15 24 17 88
Tank, above 10 14 9 94 15 ground
Leaking 11 10 8 95 11 containers
Ore processing, 12 9 19 29 La 3] refining,
smelting
The release of lead is not necessarily attributed to the specific activity indicated. Sites often have more than one activity and EPA reporting requirements do not identify the activity to which the release of a specific substance is attributable. These activities are present at 162 of the 167 sites with an observed release of lead.
(a) Field studies on the efficacy of broader lead removal from child
environments, e.g., at a tract or neighborhood level or larger.
Such efforts would include before-and-after evaluation of Pb-B
levels, done with careful statistical and quality control/
quality assurance protocols. In response to SARA, EPA is now
addressing this problem systematically via three demonstration
projects.
(b) Field studies of the type detailed above with designs stratified
to permit assessment of how such procedures relate to primary
contributors, for example, lead paint versus urban air fallout
of lead. Here, also, the EPA demonstration projects will be
helpful, if sub-studies are made of these variables. : (c) Further development of field methods is necessary to test lead
i in various exposure media. Of particular importance are
i improved in situ methods for lead in painted surfaces.
(d) Assessment of the actual physical removal technology for removal
of leaded paint , dust, and the like. A related examination of
practical disposal plans is also necessary. As noted earlier,
leaded paint consists of an aggregate burden of millions of
tons, while other inputs also add up to millions of tons.
Therefore, disposal is not inconsequential to the lead abatement
problem. Moving the lead may also inadvertently shift exposure
to another population. A draft report for a model site in
Boston (Appendix E), discusses various scenarios and associated
problems.
(e) Further examination of the efficacy of lead screening programs
for high-risk populations both for their scope and effectiveness
and for the relationship between public financial support of
screening and the ability to identify children at risk is
needed.
(f) Assessment of the relative costs of effective, if expensive,
alternatives to the piecemeal abatement, the piecemeal enforce-
ment, and the piecemeal follow-up for reexposure that appears to
be the present status of remedial actions. Is it less expen-
sive, in human and resource terms, to consider such measures as
relocation?
(g) Research that explores the feasibility of better biochemical
screening measures beyond the use of erythrocyte protoporphyrin
(EP) since this measure is not reliable and yields too many
false negatives. Failure to detect positive cases makes such
research urgent.
L. RECOMMENDATIONS
In view of the multiple sources of lead exposure, an attack on the pro-
blem of childhood lead poisoning in the United States must be integrated and
Ey Ii 1.52
7.3) I=
er 3 a
Zz i
coordinated to be effective. In addition, such an attack must incorporate
well-defined goals so that its progress can be measured. For example, the lead
exposure of children and fetuses must be monitored and assessed systematically
if efforts to reduce their exposure are to succeed. A comprehensive attack on
the U.S. lead problem should not preclude focused efforts by Federal, state,
or local agencies with existing statutory authorities to deal with different
facets of the same problem. Indeed, all relevant agencies should continue to
respond to this important public health problem, but do so with an awareness
of how their separate actions relate to the goals of a comprehensive attack.
The following specific measures are recommended to support the general
objective of eliminating childhood lead poisoning.
1, Lead in the Environment of Children
(a) We recommend that efforts be implemented to reduce lead levels in sources
that remain major causes of childhood lead toxicity.
(1) Leaded paint continues to cause most of the severe lead
poisoning in U.S. children. It has the highest concentration of
lead per unit of weight and is the most widespread source, being
found in approximately 21 million pre-1940 homes.
(2) Dust and soil lead, derived from flaking, weathering, and chalk-
ing paint plus airborne lead fallout over the years, is the
second major source of potential childhood lead exposure.
(3) Drinking water lead is of intermediate but highly significant
concern as an exposure source for both children and the fetuses
of pregnant women. Food lead also contributes to exposure of
children and the fetuses.
(4) Lead in drinking water is a controllable exposure source and
state and local agencies should be encouraged to enforce
strictly the Federal ban on the use of leaded solder and plumb-
ing materials. Stronger efforts should also be made to reduce
exposure to lead-based paint and dust/soil lead around homes,
schools, and play areas.
7
(b) We recommend that efforts to reduce lead in the environment be accom-
panied by scientific assessments of the amounts in each of these sources
through strengthening of existing programs that currently attempt such
assessment. The largest information gap exists in determining which
> // PUY x1-6 /
rbd
(c)
(d)
(e)
housing, including public housing, contains leaded paint at hazardous
levels. A similar information gap exists for information in distribu-
tions of soil/dust lead on a regional or smaller-area basis. Systematic
monitoring of lead exposures from food and water is urgently needed.
Programs, such as the FDA's Total Diet Study, must be supplemented. The
data currently collected with the resources available do not yield
sufficient information on the high risk strata of the population to
support intervention measures. Water monitoring programs suffer from a
paucity of systematically collected data.
Use of precise and sensitive methodologies is essential for environmental
monitoring of source specific lead. More sensitive and precise techniques
are required for in situ field testing of lead in painted surfaces.
Major improvements in the collection, interpretation, and dissemination
of environmental lead data on a national basis are required and recom-
mended to assess the extent of remaining lead contamination and to identify
trends. Data from screening programs should be compiled nationally and
made uniform so that geographic differences in lead toxicity rates can be
determined.
The need to examine fully the extent of lead contamination in all parts of
the child's environment remains. We recommend emphasis on examining the °
presence of lead in schools, day care centers, nurseries, kindergartens,
etc., particularly the lead in paint, in drinking water, and in soil and
dust in such facilities.
(1) We recommend that all attempts at source-specific reduction in
children's environments be accompanied by assessment of the
long-term effectiveness and efficiency of such actions (see
Section 2 of Recommendations also).
(2) Lead is both a ubiquitous and persistent pollutant. Planned
lead reductions in any environmental compartment must be
evaluated in terms of impacts on other compartments so that
fruitless shifting of the problem from one source or medium
to another is avoided. For example, when leaded paint or soil
is removed from a child's environment, ultimate, safe disposal
must be considered.
(3) The evidence is strong that in utero exposure of the developing
fetus occurs at potentially toxic levels in some proportion of
pregnant U.S. women. This risk population needs close attention
to assess and reduce thelr most significant lead exposure
sources, which should especially include occupational exposures.
UE
2] X1-7
2.
(a)
(b)
{c)
(d)
(e)
(f)
(9)
(h)
(4) Lead pollution is a health problem that involves almost all seg-
ments of U.S. society. Extra-environmental or legal measures
should be explored to reduce lead levels in the environment by
both public and private sectors.
Lead in the Bodies of Children
Children are being exposed to and poisoned by lead while environmental
lead reduction is under way. Screening programs with sufficient funding
to make a real and measurable impact are urgently needed.
There is a need to maintain screening programs extant in some states that
currently identify children at risk from lead exposure at or above blood-
lead levels of 25 pg/dl. Since current EP tests, used as the initial
screen, cannot accurately identify children with blood lead levels below
25 pg/dl, screening tests that will identify children with lower blood-
lead levels must be developed.
The 1987 statement of the American Academy of Pediatrics calling for lead
screening of all high risk children should be supported by assistance in
implementation.
Use of in vivo cumulative lead screening methods is recommended as soon
as available. A quick, accurate, noninvasive screening test would be bet-
ter accepted by parents, resulting in many more children being screened.
We recommend that screening be extended to all high-risk pregnant women,
with particular emphasis on urban teenaged pregnant women, and that
prenatal medical care providers be involved in this effort.
We recommend determination of the prophylactic role of nutrition in
ameliorating systemic lead toxicity.
Further use should be made of metabolic models already developed and
research to refine them should be done. This will enable their use to
predict total body burden contributions from varying environmental sources
of known lead levels.
Long-term prospective studies of lead's effects during child growth and
development should continue to be supported through appropriate support
mechanisms, beginning with the relationship of maternal lead burden to
in utero toxicity and including children with neurological disabilities
and genetic disorders, such as sickle cell anemia.
LL
24 XI-8
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(i) Nationwide assessments of lead toxicity status in U.S. children on a con-
tinuing basis are recommended. Efforts such as the planned NHANES III
survey should be supported to maximize the data collected about lead expo-
sure levels. Support as well should be provided for more geographically
focused surveys, e.g., on the level of Metropolitan Statistical Areas
(MSAs).
MOSHAK
EXHIBIT GC
2%: PROCEEDINGS #
of the
First National Conference
on Laboratory Issues in
Childhood Lead Poisoning
Prevention
October 31 - November 2, 1991
Jointly Sponsored By:
Association of State and Territorial Public Health Laboratory Directors
Centers for Disease Control -- National Center for Environmental Health
and
Environmental Protection Agency
U.S. Agency for Toxic Substances ~nd Disease Registry’s
Report to Congress on Childhood Lead Poisoning in America
Review and Update
Paul Mushak, Ph.D.
Consultant and Adjunct Professor
University of NC School of Medicine
SUMMARY
Lead poisoning is the major environmental threat to the health of children. The explosion in
research documenting lead’s status has been recorded and interpreted in a number of expert
consensus documents. In response to mandate, the U.S. ATSDR sent to Congress in 1988 a key
document of this type and a review with update is presented here. The ATSDR report set forth
methodologies and results that answered the questions: How many U.S. children are at risk for
lead poisoning by area? What are the sources of child Pb exposures? What are the health effects
and their persistence? How effective are exposure reduction methods?
In 1984, 2.4 million metropolitan Black and White U.S. children had a projected Pb-B > 15
pg/dL. The national total for all races was 3 to 4 million. For children with Pb-B >5 ug/dL and
>10 pg/dL, post-report analysis yielded corresponding numbers (% of SMSA total) of 12.5
million (91) and 6.4 million (46). In 1984, 400,000 pregnant women were projected to have Pb-B
levels >10 pg/dL, a level linked to fetal toxicity risk. Numbers of children in screening
programs show a 1.5% toxicity rate. The number of children <6 years old in old housing, an
indirect index of lead paint exposure, was 4.3 million in 1980.
The report to Congress quantified numbers of children exposed by source. Source-specific tallies
are difficult for a multi-media contaminant like lead. Major sources and pathways are lead in
paint, lead in dust and soil, airborne lead fallout, and lead in drinking water. Children exposed
to lead paint enough to produce a toxic blood lead (> 15 pg/dL) number ca. 2 million. Dust and
soil Pb exposures were estimated to be more than 10 million. Tap water potential exposure affects
© ca. 4 million children, 240,000 with Pb-B >15 pg/dL.
Toxicity of Pb to the developing human CNS has been shown to be persistent in several studies.
Persistence is also seen in exposed animals. Lead’s effects are pervasive and occur at low
exposures. Since the report’s release, additional studies have appeared. The report articulates
those sources for which abatement would reduce toxicity in U.S. children. The remedies are
legislative and administrative and differ in their likelihood of effectiveness. Exposure reduction
in America is basically a post-hoc process, since the large reservoirs of lead are already in place,
and apt to remain in place indefinitely in some cases.
79 250
INTRODUCTION
The last 20 years has witnessed an explosion of scientific and public health data on lead
contamination and its adverse effects. Such knowledge has not arisen in a vacuum, but represents
a closed-loop interplay between research and policy activities, as seen in Fig. 1. First, the
regulatory, legislative and public health sectors attempt to interpret and act upon new scientific
knowledge. In turn, their conclusions and actions trigger support for further research, closing the
loop. One mechanism by which science interacts with the policy area is the scientific consensus
document. Described below are some elements of the interaction.
Science and
Technology
Research
Policy:
- Legislative
| Regulatory
Public Health
FIGURE LEGEND
Fig. 1. The interplay of science and the policy sectors
In the 1970s, Congress enacted the Clean Air Act (1970) and the Lead-Based Paint Poisoning
Prevention Act (LBPPPA, 1971), two early major legislative anchors for regulatory initiatives
against Pb sources. The newly-created U.S. Environmental Protection Agency (USEPA) also
became involved with lead, both as a gasoline additive and as a criteria air pollutant. It produced
its first comprehensive criteria document for lead, the 1977 "Air Quality Criteria for Lead" report
(USEPA, 1977).
The Federal public health apparatus became involved in the lead problem, beginning with the
Surgeon General's statement (1971). It set a blood lead guideline of 40 pg/dL and recommended
screening for lead poisoning in high-risk children. The U.S. Centers for Disease Control (CDC)
issued two Statements on childhood lead poisoning in the 1970s (CDC, 1975: CDC, 197%).
CDC's statements are intended to reflect the sense of the nation’s pediatric community. Both
Statements used blood lead (Pb-B) and erythrocyte protoporphyrin (EP) levels to classify risk.
The National Academy of Sciences (1972) produced the first of its reports on the lead problem,
focused on airborne lead and gasoline lead combustion. This report included a set of
recommendations for further research. Internationally, the World Health Organization produced
its first health criteria report on lead (WHO, 1977). It covered sources of exposure, toxicology,
environmental epidemiology of lead and an early attempt at risk assessment.
w 25)
The first of a new series of assessments of asymptomatic childhood lead poisoning was published
by Needleman and coworkers (1979). This study attempted to disentangle the effects of lead from
confounding and interactive factors and also addressed the question of an appropriate biological
marker of remote exposure, i.e., times when these children were most vulnerable.
In the 1980s, further Congressional actions were taken. These included the Comprehensive
Environmental Remediation, Compensation and Liability Act (CERCLA/Superfund 1980), the
Superfund Amendments and Reauthorization Act (SARA, 1986), 1986 amendments to the Safe
Drinking Water Act and the Lead Contamination Control Act {1988). The USEPA issued its
second lead criteria document as four comprehensive volumes (USEPA, 1986a) and the Agency
for Toxic Substances and Disease Registry (ATSDR, 1988) released its report to Congress on
childhood lead poisoning. The ATSDR report is the subject of this paper. Internationally, a royal
commission in England issued its report on lead pollution, with emphasis on lead in air from
leaded gasoline combustion (Royal Commission, 1983).
More recently, USEPA issued an update of the 1986 lead criteria document and its addendum
material (USEPA, 1990). Two significant reports from the CDC have appeared in 1991. The
first (CDC, 1991a) was a strategic plan for eliminating childhood lead poisoning. It placed heavy
emphasis on paint-based childhood poisoning due to lead paint and included a cost-benefit analysis
for lead paint abatement. The second report (CDC, 1991b), a revised Statement on childhood lead
poisoning prevention, reduces the Pb-B action level to 10 pg/dL and stratifies intervention into
preventive and conventional forms.
Legislative Genesis of the Report to Congress
One reaction from Congress to the new data on lead was Section 118 (f) of the 1986 SARA.
Section 118 (f) consisted of four subsections that attempted to quantify the scope and depth of the
childhood lead problem in America.
ATSDR was directed to quantitatively evaluate four aspects of the lead problem:
- the number of American children exposed to toxic levels of lead by geographic
unit;
- the number of children exposed to lead ranked by source and source type;
- the nature of childhood lead poisoning and persistence of toxic effects; and
- methods and alternatives for reducing lead exposure in children.
This article summarizes some of the key methodologies and findings in the resulting 1988 report
to Congress and provides an update of material, 1988 to the present. For details, the reader 1s
directed to the report itself (ATSDR, 1988) or publications in the literature based on the report
(Mushak and Crocetti, 1989, 1990; Mushak et al., 1989; Crocetti et al., 1990a, b).
81 FE
ORGANIZATION OF THE REPORT
General Approach
The report posed a number of challenges. First, there was no similar report in the lead literature,
qualitatively or quantitatively. Second, source data were scattered in various places and contained
in different disciplines. Finally, the report’s structure and findings required an extensive analysis
and interpretation in a form understood by a broad readership.
A further complication was the non-specific nature of the mandate’s directives. An adequate
scientific response to the mandate required going beyond the language of the mandate in some
cases, as in the inclusion of numbers of women of childbearing age and pregnant women, so as
to address the full spectrum of lead’s impact on development.
Report Authorship and Peer Review
The report’s principal authors were provided additional data by Federal lead specialists and
produced six interim drafts and a final version. The drafts were critically evaluated through rather
exhaustive peer review, including input from a Federal ad-hoc group of lead experts meeting with
the co-authors in four workshops, review by 19 outside lead experts and over 100 other Federal
reviewers.
NUMBERS OF AMERICAN CHILDREN EXPOSED TO TOXIC LEAD LEVELS BY AREA
Data sets available for this portion of the report included: (1) enumeration information lodged in
the user data tapes of the U.S. Bureau of the Census’s 1980 Census, including residents in U.S.
Standard Metropolitan Statistical Areas (SMSAs) stratified by socioeconomic and demographic
categories, (2) post-Census vital statistics data for updating to 1984, the most recent year for the
childhood age band selected, (3) data in the Second National Health and Nutrition Examination
Survey (NHANES II; Annest and Mahaffey, 1984), which contained aggregated blood lead levels
in socioeconomic and demographic strata for the entire U.S. population, (4) lead screening
programs supported of, first, the CDC categorical program from 1973 to 1981 and then the block
grant program for states since then, and (5) age-stratified housing data for young children in the
American Housing Survey of the 1980 Census.
These data sets allowed three estimation and enumeration exercises for numbers of lead-exposed
children at potential or actual poisoning risk arrayed by geographical unit:
- numbers of children <6 years old estimated to have blood lead (Pb-B) levels above
selected values as a function of 30 national socioeconomic and demographic strata
in 1984
- numbers of total children enumerated in lead screening programs around the nation
and numbers enumerated as having confirmed toxicity risk
82 257%
- numbers of children <6 years old enumerated as living in housing around the
nation built before 1950
Numbers of Children in Various National Strata Having Pb-B Levels Above Selected Values
Estimation of numbers of children with elevated Pb-B in strata involved combining a prevalence
for a selected Pb-B with a base population. This gave the numbers of children above a Pb-B level.
A base population was obtained by enumeration of the total base population for the national
metropolitan strata. The NHANES II survey data required statistical adjustments to 1984, owing
to a continuing decline in population Pb-B levels in response to source Pb reductions. These
adjustments entailed use of linear and logistic regression analysis techniques, described in detail
in an appendix in the report.
Three blood lead ceilings were selected for the report, representing the thresholds selected by
various public agencies for onset of adverse effects or a maximum ceiling to safe level: 25 ug/dL
(CDC, 1985); 20 ug/dL (WHO, 1987) and 15 ug/dL (USEPA, 19863).
Detailed tabulations are in the report to Congress and published material (Crocetti et al., 1990a).
Table 1 presents prevalences > 15 ug/dL for strata at highest risk for lead exposure and toxicity,
1.e., children in inner-city areas of major metropolitan areas. Low-income, inner-city Black
children have the highest rates, over 50%, followed by Black children in higher family income
categories. Differences across income strata for Black children are lower than for Whites. The
most population-dense areas had higher prevalences than smaller cities.
We estimated that 2.4 million metropolitan Black and White children <6 years old had a Pb-B
> 15 pg/dL in 1984. We also estimated that the total number of all U.S. children would be 3 to
4 million children above this value. Elements of overestimation and underestimation are present
in the prevalence modelling and these are described in the report.
Updated Material on Elevated Pb-B in Children by Area
The lowest level of Pb-B selected for prevalence projection modelling in the report to Congress
was 15 pg/dL. Since then, recommendations of the US EPA’s Science Advisory Board (CASAC,
1990) and the guidelines of the newly released CDC 1991 Statement (CDC, 1991b) identify a Pb-
B level of 10ug/dL as the new value of concern. Prevalences were calculated for this Pb-B level
and 5 pug/dL as well. Prevalences of Pb-B above 5 pg/dL in children in most of the high-risk
strata described in the report to Congress are virtually 100% for 1984 (Table 2). Corresponding
prevalences for > 10 pg/dL in Black children are also very high, exceeding 90% in the inner-city
segment of large and smaller U.S. cities (Table 2). Even strata representing minimal Pb exposure
show quite high percentages (Table 3). Table 3 shows the affluent segment of White children
living in smaller areas were still projected to have about 80% >5 pg/dL. The corresponding
figure for 10 pg/dL was 22.1%.
The total numbers of metropolitan Black and White young children projected as having Pb-Bs > 5
pg/dL in 1984 amounted to 12.5 million, or 91% (Table 4). The total number of children with
Fr 25h
Pb-B >5 ug/dL outside the inner—city areas of SMSAs was higher than those inside, due to larger
base populations in the latter.
It has been claimed in at least one USEPA source (USEPA, 1989) that the current Pb-B level as
a U.S. population geometric mean has declined to about 5 wug/dL, determined from crude
projections to account for exposure reduction. It is difficult to compare such estimates to the 1984
projection prevalences at the 5 ug/dL and 10 pg/dL levels. Results of the Third National Health
and Nutritional Survey, NHANES III, should be available in several years.
Numbers of Metropolitan Pregnant Women and Women of Childbearing Age
A full description of the scope of developmental lead toxicity in populations requires an estimate
of in-utero exposures. The methodology for this is detailed in the report and published material
(Crocetti et al., 1990b). Four age bands were selected and it was necessary to estimate both the
number of pregnant women in the reference year, 1984, as well as numbers of women of
childbearing age, since any member of this group can become pregnant at any time.
Results are summarized in Table 5. As seen in Table 5, over 400,000 pregnant women were
projected to have a Pb-B level >10 pg/dL, a level linked to fetal effects. The corresponding
number for women of childbearing age was about 4.5 million.
E rable 1.
hed
Projected % of Children, 0.5-5 y old To Exceed Pb B Values (pg/dl) Who Live
grinside Central City" of SMSAs, 1984*
ii Bi Zi
a
3 | Family Income/Race > 15 pg/dl >20 pg/dl >25 pg/dl
i. <i M. 21M <1 21M < 1M 21M
= < $6,000
white 25.7 136.0 7.6: 511.2 2.3 3.0
Black 56.8 67.8 22.8 30.8 7:7 10.6
$6,000-14,999
white 15.2 22.9 4.0 6.3 1.1 1.5
Black 41.1 53.6 14.1 19.9 "Te 5.9
z $15,000
white 7.1 13.9 1.5 2.5 0.4 0.5
Black 26.6 35.2 6.8. 10.4 1.5 2.2
*+ By family income,
Table 2.
"Inside Central City" of SMSAs,
Projected t of Children,
race and urban status; 1
1984
M = 1 Million
0.5-5 y. 01d To Exceed Pb-B Values (pg/dl)* Who Live
Family Income/ > 5 pg/dl > 10 pg/dl
Race
< 1M 21M < 3M >> 1 M
< $6,000
White 95.0 99.9 670 80.4
Black 09.9 99.9 91.6 96.5
$6,000-14,999
White 96.0 99.0 49.8 65.1
Black 99.9 99.9 83.5 92.0
2 $15,000
White 89.0 96.6 31.9 47.2
Black 99.7 99.9 72.7 85.5
* By family income, race and urban status
85
2.54
Table 3.
woutside Central City" of SMSAs, 1984*
projected % of children 0.5-5 y. 01d To Exceed Pb-B values (pg/dl) Who Live
Family Income/ Race > 5 png/dal > 10 pg/dl fey
x. 1. M < 1M
< $6,000
Yn
White
97.0
55.7 3
Black
99.0
85.2 Ee)
$6,000- 14,999
i
White
90.4
38.3 ie
Black 99.4 74.2 ui
> $15,000
i
White
77.3 22.1 or]
Black 98.5 60.4
* For SMSAs less than 1 Million
Table 4. Numbers of Children in U.S.
Race, Income and Urbanization, 1984°
SMSAs 0.5-5 y. Old Exceeding a Pb-B of 5 pg/dl By
Grand Total: 12,526,000
32 Total SMSA: 91%
Stratum In Central City outside Central City
< $6,000 <. 3 M > 3M <3 M > 1M
White 129,600 256,800 138,700 254,600
Black 142,100 346,100 92,000 76,600
$6,000- 14,999
White 275,800 488,400 387,100 487,200
Black 337,500 341,600 53,700 114,200
> $15,000
White 646,600 1,015,400 3,013,000 2,703,500
Black 156,500 394,900 72,600 212,300
TOTALS 1,488,000 2,843,200 3,757,100 3,848,400
_
«+ Does not include smaller SMSAs; estimates of these total 2.59 million > 5 pg/dl.
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TABLE 5
Estimated Numbers of SMSA Women of Childbearing Age and Pregnant Women
and Projected Numbers Above 10 pg/dL, 1984
Childbearing Age Pregnant Women
Race /Age Number > 10 pg/dl Race /Age iiumber > 10 pg/dl
White 15-19 5,478,000 504,000 white 15-19 433,000 39,800
20-44 29,740,000 2,884,800 20-44 2,380,000 230,900
Black 15-19 1,090,000 90,000 Black 15-19 187,000 15,300
20-44 4,984,000 981,000 20- 595,000 117,200
TOTAL 41,300,000 4,460,600 TOTAL 3,595,000 403,200
Numbers of Young Children Identified in U.S. Lead Screening Programs
Criteria for selection of toxic exposures were the risk classification guidelines in either the 1978
or 1985 CDC Statements (CDC, 1978, 1985). That is, either a Pb-B of 25 pg/dL or higher
confirmed in children with an EP level of 35 pug/dL or higher, or a Pb-B of 30 ug/dL/above and
an EP of 50 pg/dl/above. The methods for data gathering and the results are described in the
report and published material (Crocetti et al., 1990a).
Using screening data obtained from U.S. programs operating in the 1985-1986 period by ATSDR
staff, a total annual screening tally for the interval was enumerated at 785,285, of whom 11,739,
or 1.5%, met CDC criteria for confirmed lead toxicity. This number cannot be related to earlier
screening activity very easily.
Update on Numbers of Pb-Exposed Children Identified in Screening Programs
Preliminary summary lead screening statistics for FY 1989 have been provided to this author
(Public Health Foundation, 1991). Table 6 summarizes the total number screened, total number
of confirmed toxicity cases and toxicity % in states reporting both results. The ten largest
reporting programs are also tabulated. The total preliminary number screened in the 30 reporting
states was 1,228,798, ranging from a low of 34 (Mississippi) to 357,129 (New York). Of these
states, 25 reported both a screening count and the number of confirmed toxicity cases. For these
states, the total number of toxicity cases was 9,305 out of a total screening tally of 1,129,948, or
0.8%. The range of toxicity cases was I (Mississippi) to 2,510 (New York).
87
2%
Numbers of Children Exposed to Paint Lead in Housing
Details as to enumeration methodology and the resulting SMSA-based enumerations are in the
report and the paper of Crocetti et al. (1990a). The total number of children <6 years old living
in pre-1950 housing in the 318 SMSAs documented in 1980 Census tapes was 4,374,600, which
1s 30.6% of the total count of 14,278,000 SMSA children. Size of the SMSA does not necessarily
correlate with size of child population living in pre-1950 housing. The older sections of the nation
contained the largest fractions of young children in the oldest housing. The newest housing stock
1s to be found in the West and Southwest. Thirty-three SMSAs had 50% or more of young
children in pre-1950 housing, while 14% had 70% or more in the oldest dwellings.
Numbers of Children Exposed to Lead by Source or Source Type
Little in the way of specifics was provided to the authors in Section 118 (f) (1) (B) of SARA.
Available data required a multi-tiered response to permit the broadest policy use of such
information. Data sets available for quantifying this response to the mandate included numbers
of children in age- and condition-stratified U.S. housing. Estimates of children potentially exposed
to lead via household plumbing were available, as were estimates of tap water lead levels
exceeding safe limits. One analysis was available showing the number of children having a toxic
Pb-B level due solely to water Pb exposure. EPA estimates were available showing projected
reductions in numbers of exposed children due to leaded gasoline phase-down action. Also
available were estimates of children exposed to lead from smelters and battery plants, the major
stationary sources.
Lead in soil and dust is generally due to contamination via paint and/or atmospheric fallout.
Atmospheric lead arises from leaded gasoline combustion and lead emissions from stationary
sources. No information is available showing numbers of children at risk due only to dust/soil
lead. One must employ summed estimates from the pathway inputs: paint lead, gasoline lead and
emissions from stationary operations.
Available dietary lead data showed percentile distribution of childhood lead intake from
measurements obtained in the 1970s.
Methodologies and strategies in responding to this directive involved exposure numbers for
children at three levels of precision: potential exposures to lead in a given source or pathway,
exposures to lead in different media sufficient to induce elevation in Pb-B, and, finally, numbers
of children exposed in source-specific and pathway-specific ways sufficient to induce blood lead
levels associated with toxic effects.
Numbers of Children Exposed to Lead in Paint
Any young child in a home with lead paint accessible through ingestion of peeling paint chips or
the chewing and gnawing of accessible paint surfaces is potentially at risk for lead paint toxicity.
It was estimated that 12 million children <7 years old lived in the approximately 42 million
residential units build during the period when lead paint was used, i.e., pre-1977.
* 259
In; =
The highest risk for lead paint poisoning occurs in the most deteriorated housing, where paint lead
is relatively available as chips or powdered/weathered particles. The number of children in the
approximately 6.2 million deteriorated, pre-1940 units was estimated to be 1.8 million. We also
found that an estimated 1.2 million children <7 years old had Pb-B > 15 pg/dL due principally
to lead paint.
Numbers of Children Exposed to Lead from Leaded Gasoline
All communities with heavy traffic density have been impacted by leaded gasoline over the years,
especially in past years when lead additive levels were highest. The number of potentially exposed
children in the case of leaded gasoline was chosen to be the number of children <7 years old in
the nation’s 50 largest metropolitan areas. This figure was 5.6 million. Children actually exposed
to lead exhausts at toxic levels were estimated by EPA for children up to 13 years of age
(USEPA, 1985). In EPA’s approach, we cannot identify actual Pb-B levels in children but only
that reduction in Pb-B is sufficient to fall below selected Pb-B levels. Using a toxic Pb-B criterion
value of 15 pg/dL, the corresponding reductions for the six years employed were:
# Children Year
0.7 million 1985
¥.7 ' 1986
1.6 3 1987
1.5 . 1988
1.4 : 1989
1.3 1990
These declines continue past the phase-down year due to the residual effect of past leaded gasoline
fallout onto soils and as dusts.
Numbers of Children Exposed to Lead From Stationary Sources
Several estimates of children potentially exposed to stationary source lead were available and these
base numbers were combined with prevalence of elevated Pb-Bs at stationary source sites to yield
numbers of children with elevated Pb-B. Prevalences ranged widely, producing a range in total
numbers. EPA found that the total number of children <7 years old living around primary and
secondary smelters and battery plants is 230,000. Of this base population, the number of children
with Pb-B above 20 pg/dL was estimated to be 7,500 for those living around secondary smelters.
The corresponding estimate of total numbers for primary smelter exposures with Pb-B >25 pg/dL
is a broad range, 210 to 5500 children.
Numbers of Children Exposed to Lead in Dusts and Soils
Estimates of children exposed to lead in dust and soil are derived from exposures to paint, gasoline
and stationary source lead. Owing to simultaneous exposures, simple summing across sources
gives an over-estimate because of double counting. Summing yields an upper bound to the overall
estimate (because of overlap) of 11.7 million children.
"ILD
Numbers of Children Exposed to Lead in Drinking Water
Lead enters the drinking water of children both at home and away from home, e.g., at
kindergartens, elementary schools, day care centers, etc. Lead contamination in household or
building plumbing is the source rather than from the water source or distribution (USEPA, 1986b).
Potential exposure of children <5 years old in old housing stock with a significant fraction of lead
lines or connectors amounts to 5.2 million subjects. The corresponding number for children 5-13
years old is 8.7 million. Estimates of children in dwelling units built before 1920 total 2.7 million
children, while 0.84 million lived in those built in the past several years before the analysis.
It has been estimated that 42 million U.S. residents consume tapwater lead at a level >20 pg/dL
(USEPA, 1986b). Of these individuals, 3.8 million are children <6 years of age. This level of
contamination will elevate Pb-B by a minimum of several units. In its cost-benefit analysis for
control measures associated with water lead, EPA has estimated (USEPA, 1986b; Levin, 1987)
that about 240,000 children <6 years old will have a Pb-B > 15 ug/dL. Of this figure, 230,000
have a Pb-B level between 15 and 30 ug/dL.
Numbers of Children Exposed to Lead in Food
The report to Congress quantified toxicity risk for dietary lead among children by (1) determining
the level of Pb intake at the 95th percentile in children 2 to 5 years old, adjusted for decline in
contaminant level from the period 1973-1978 to time of the study and (2) translating this
percentage to a total number. The 95th percentile of lead intake was 130 pg diet Pb/day. Use
of a 50% reduction to account for reduced Pb content in foods over recent time yielded a 95th
percentile level of 65 pg/day. This percentile intake translates to a Pb-B of about 10 ug/dL
(Mushak and Crocetti, 1989). This level is linked to early toxicity (CDC, 1991b). As a portion
of American children under six years old, 5 percent, or about 1 million children, are therefore
above the 95th percentile.
Quantitative Ranking of Pb Exposure Sources for American Children
It is not possible to provide a precise, rigid ranking of lead sources and pathways, as requested
in the Congressional directive. First, the level of precision in generating the numbers of exposed
children is variable across sources and pathways, ranging from potential exposures to estimation
of numbers with toxic body lead burdens. Second, there is some degree of unavoidable overlap,
given the multimedia nature of lead exposure in human populations.
It is more useful to rank these sources and pathways by relative magnitude of impact on children’s
lead exposures. We confine ranking to what would be the most pervasive sources. We also
recognized that a myriad of miscellaneous sources existed for ethno-specific or other settings.
These are not trivial sources of exposure, per se. Quantification of their impact is not feasible
given available data.
90
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At present, lead paint ranks first. It is the most pervasive source for exposure of children and
affects those who are also at risk for health problems because of poverty, nutritional deficiencies
and more likely contact with this source. Paint lead may be ingested directly or after its transfer
as particulate matter to dusts and soils (e.g., Charney et al., 1983; Clark et al., 1985; Bornschein
et al., 1987). The report estimated that over 3 million tons of lead remain distributed among the
millions of housing units with lead paint. Lead in dust and soil can be ranked second. Dust/soil
lead intake is a pervasive exposure pathway for children in both urban and certain non-urban
settings (USEPA, 1986a).
Lead in tapwater is a pervasive, potentially troublesome source for childhood exposures, and this
occurs both in the home and away from home, e.g., lead in water fountains at schools.
Lead in gasoline is a declining source of lead relative to other current sources, and should be in
the second rank of sources. Since the 1920s, however, there was a cumulative input through
fallout from leaded gasoline combustion of 4 to 5 million tons. Similarly, lead in children’s diet
‘is presently a low-level source. Lead loadings in diets are highly variable, however, and the
above discussion only refers to a typical dietary profile. Many idiosyncratic sources for lead entry
into food still exist. For example, there remains a problem with canned foods which are imported
from countries which have no controls on lead-seamed cans. Acidic fruit juices and beverages can
still leach sizeable quantities of lead from poorly glazed vessels serving as storage and preparation
containers. ‘The extent to which these sources remain troublesome depends on changes in control
of entry into the market.
Update of Source-Specific Material in the Report to Congress
The magnitude of lead paint as a source has not diminished since the release of the report given
the huge, dispersed inventory of lead paint-impacted housing units. Since the report’s release, a
subsequent appraisal by the Department of Housing and Urban Development in its report to
Congress (HUD, 1990) noted that there were more units in deterioration than identified in the
ATSDR report, i.e., 14 million units nationwide are in unsound condition and 3.8 million of these
were occupied by young children. HUD’s report to Congress expanded ATSDR’s figure of 4
million unit: having some amount of lead paint to 58 million units, representing about 74% of all
housing stock. Studies show the potential for additional paint lead exposure in the course of paint
lead abatement, discussed in Chapter 3 of CDC’s 1991 Statement (CDC, 1991). The Statement
also makes it clear that even partial abatement is effective in reducing children’s body lead
burdens.
Lead in dust and soil remains a pervasive, lingering exposure pathway for children. While the
dust component can be affected by household variables such as cleaning practices (Yankel et al.,
1977), the refractory nature of dust/soil lead is obvious, because the major inputs, particularly lead
paint, remain (CDC, 1991a; HUD, 1990).
Leaded gasoline combustion since the report to Congress continues to make less of a real-time
input to childhood lead exposure. The 1990 Amendments to the Clean Air Act prohibit any lead
in gasoline beginning in 1992, concluding the phaseout by the end of 1995 (CDC, 1991b).
9) ih
Diet as a source of lead continues to decline for the typical American child. It is estimated that
by 1988 the daily dietary lead intake was on the order of 5 pg/day (CDC, 1991b). This decline
reflects reduced food contamination during production and preparation than in earlier years. This
is due to lowered atmospheric fallout and the continued decline of domestic lead-seamed can
production, estimated to be 1.4% of all can production by 1989.
LEAD TOXICITY AND ITS POTENTIAL FOR PERSISTENCE IN
AMERICAN CHILDREN
Lead exposure over a broad range induces a large variety of acute, subacute and chronic toxic
effects in young children. This topic was discussed and analyzed at length in the full report and
in the open literature (Mushak et al., 1989). The topic and an update with illustrative studies are
briefly reviewed here.
The concern in childhood lead exposure is the long-term, persisting impact of low-level lead
exposures on the developing CNS, due to the grave nature of such effects and the reality that
injury to the CNS is apt to be irreversible (American Academy of Pediatrics, 1987).
Prospective Assessments of Developmental Toxicity in American Children
The most persuasive evidence supporting neurotoxicity at low lead exposures in children is to be
found in results from a group of international prospective (longitudinal) studies. These studies
followed development of neurotoxicity and other effects in child cohorts, from gestation through
at least the first four to five years of life. While studies are not identical, they generally evaluated
common toxic endpoints and exposure assessment instruments. These studies are based in Boston,
Cincinnati, Cleveland and Port Pirie, Australia. Other studies are either not as far along or their
results are difficult to evaluate relative to the above-mentioned studies.
Infants in the above studies showed decrements in the Bayley Mental Development Index (MDI)
as a variable function of prenatal (Cincinnati study), cord (Boston and Cleveland studies) or early
postnatal (Australian and Boston studies) Pb-B levels. The MDI is commonly used as an early
measure of neurobehavioral development in infants. The magnitude of the deficit varied from 2-8
MDI points in studies where reported. The public health implications of this level of MDI
decrements have been examined by Grant and Davis (1989) and Davis and Svendsgaard (1987).
Average decrements do not reflect the full impact across the full distribution of decrements, i.e.,
those infants at the lower tail and the higher tail of the distributions sustain proportionately greater
impacts.
There were also reported from the Boston Study results showing that child Pb-B at two years of
age was statistically associated with decrements in McCarthy scales at almost five years (57 mo.)
of age (Bellinger et al., 1987).
These prospective studies also identified effects of prenatal lead exposure on perinatal indicators
of development in the newborn. Effects on gestational age and birth weight were noted in the
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Cincinnati study (Dietrich et al., 1986) while the Australian study indicated that preterm delivery
was significantly associated with maternal blood Pb at delivery (McMichael et al., 1986).
Cross-Sectional Studies of Lead’s Developmental Toxicity in American Children
Cross-sectional studies point, in the aggregate, to a causal role for lead in the identified effects.
Such studies began in earnest with the pioneering general-population report of Needleman et al.
(Needleman et al., 1979). Using secondary dentine lead levels as the exposure marker in a group
of Boston-area children, they reported that verbal IQ and classroom behavior were significantly
affected by lead. As lead level increased, IQ decrement increased and classroom behavior was
more disturbed. Four years later, grade retention of the high-dentine lead children was
significantly greater than in the low-dentine group (Bellinger et al., 1984).
A number of subsequent, well-done cross-sectional studies confirmed neurobehavioral effects of
lead exposure. For example, Fulton et al. (1987) and Hatzakis et al. (1987) reported that there
were significant IQ or IQ-related effects with increases in blood lead levels below 25 ug/dL for
Scottish and Greek children, respectively.
Cross-sectional studies of other neurotoxic outcomes of lead exposure have been described in the
report. Schwartz and Otto (1987) described the inverse association of Pb-B in the NHANES II
survey with decrements In hearing acuity, while Otto et al. (1985) described diverse
neuroelectrophysiological effects in children with relatively low lead exposures.
Other cross-sectional studies of lead were noted. Schwartz et al. (1986) reported that analysis of
NHANES II data showed an inverse relationship between Pb-B and anthropometric measures, j.el,
chest circumference and height. Lauwers et al. (1986) reported the inverse relationship of Pb-B
and growth in children up to about eight years of age. Effects on heme biosynthesis and
calcium/vitamin D functions were also described.
Dose-Effect and Dose-Response Relationships for Lead’s Effects in Children
The various prospective and cross-sectional studies report neurotoxic and other effects which are
associated with a blood lead of 10 and in some cases even < 10 ug/dL. As Pb-B levels rise above
10-15 pg/dL, both the severity of an effect and the multiplicity of adverse effects increase. At
Pb-B levels above 100 pg/dL a fatal outcome becomes more probable.
Persistence of Lead’s Effects in Young Children
In the Boston prospective study, blood lead levels at two years of age produced effects that
persisted at five years of age in the form of impaired performance on the McCarthy Scales
(Bellinger et al., 1987). Bellinger et al. (1984) reported marginally significant inverse
relationships of dentine lead in the Needleman et al. (1979) study with teacher’s ratings and
student 1Qs in schools. Effect persistence has a biological or intrinsic definition and one that 1s
extrinsically or exposure-driven. Effects that are biologically reversible would still require that
204
03
exposures be removed or reduced for reversibility to occur. If exposure persists for years, then
so will the effects.
Update of Lead’s Low-Level Neurotoxicity in Children
Since the release of the report to Congress, a large amount of published material has appeared
providing further support of results noted therein. New material includes statistical ways of
examining validity of studies, the cumulative statistical impact of otherwise limited studies via
meta-analysis, and appearance of new studies. Evidence for lead as a potent, pervasive health
threat to children is supported by a spate of recent studies describing animal models of lead’s
developmental neurotoxicology. Space limits discussion to a few illustrative studies.
Prospective Studies Update
The above-described prospective studies are ongoing. Recent studies have been published,
including updates from the Boston and Cincinnati groups.
Bellinger et al. (1989a) examined the role of lead, IQ and social class (SC) in their study cohort
in the form of Pb-IQ, Pb-SC and IQ-SC relationships. These workers also reported that early
postnatal Pb-B levels > 10 ug/dL were associated with MDI scores, but only among children in
lower socioeconomic strata (Bellinger et al., 1989b). The Boston cohort was also examined with
regard to cord blood and fetal growth (Bellinger et al., 1991). Cord blood was found to be
inversely related to fetal dysmaturity and weight gain at Pb-B levels of 15 pg/dL and above.
In the Cincinnati cohort, Shukla et al. (1989) found that postnatal growth was related to the Pb-B
increment, 3 to 15 mo., but only in infants whose mothers had a prenatal median Pb-B of 7.7
pg/dL. Dietrich (1990) noted a significant inverse association between maternal Pb-B (mean =
8.1 ug/dL) and speech/language abilities in three-year-olds. Four-year-olds were subsequently
found to show an inverse relationship between neonatal Pb-B and all subscales of the Kaufman-
Assessment Battery for Children, but this was for the poorest subset of children (Dietrich et al.,
1991). A weak association was noted between postnatal Pb-B and the SIM subscale, i.e., the one
that measures visual-motor integration and visual-spatial skills. This subscale is analogous to the
portion of the McCarthy Scales found to be linked to postnatal Pb-B in the Australian and Boston
cohorts. Neurotoxicity other than impaired cognitive performance was reported for this cohort
by Bhattacharya et al. (1990). These workers noted that maximum postnatal Pb-B at two years
of age in a group of 63 children (mean age = 5.74 y) was significantly associated with impaired
postural balance. This suggests that lead impairs interconnections of the vestibular and/or
proprioception systems.
Update of Cross-Sectional Studies
A considerable number of new cross-sectional studies were published after the ATSDR report.
Several of the most rigorously controlled studies or study groups are noted below. Also presented
1s a meta-analysis of a number of individual studies.
9
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1 3 3 Winneke et al. (1990) have summarized results of the European Multicenter Study on Lead
{ #5 Neurotoxicity in Children, a cross-sectional multi-group set of neurobehavioral studies under the
i #2 aegis of the World Health Organization and the Commission of the European Communities.
2: Jointly, the studies involved 1879 school-age children and four measures of neurobehavior.
i: Psychometric intelligence was affected, but the consistency across studies was poor. Other, more
consistent findings were affects of lead on visual-motor integration and reaction performance.
© Hansen and co-workers (1989) reported that Danish children with circumpulpal dentine levels
> 18.7 ug/g in shed teeth showed a significant decrease, after controlling for confounding
variables, in the verbal and full-scale IQ components of the Wechsler Intelligence Scale for
Children (WISC). Impairments were also noted in a behavior rating scale and a measure of
visual-motor integration.
Needleman and Gatsonis (1990) carried out a meta-analysis of 12 of the more recently published
. studies exploring the relationship of childhood lead exposure to IQ via multi-regression analysis
. with controlling for covariates and using two forms of such analysis. The joint P values for the
studies using Pb-B (N=7) were 0.0001 for both approaches within the meta-analysis, while for
those studies using dentine lead as the exposure index (N=5), the two subanalyses gave P values
of 0.0005 and 0.004. The approach of meta-analysis in environmental epidemiology theoretically
gets around the chronic problem of single studies that have poor statistical power to isolate an
association with an endpoint affected by covariates.
Update in Persistence of Lead’s Neurotoxicity
Needleman et al. (1990) reported that a subset of subjects in the earlier investigation who showed
behavioral problems and lowered IQ as a function of secondary dentine lead were subsequently
found (mean age = 18.3 y) to have a seven-fold higher risk of failure to graduate from high
school and a six-fold higher risk of having reading problems. These Pb neurotoxic effects
therefore persist at least 11 years.
METHODS AND ALTERNATIVES FOR REDUCING LEAD EXPOSURE IN CHILDREN
The history of efforts to reduce lead exposure in children is one that records few successful results
in terms of actual prevention or reduction of childhood lead poisoning. Our detailed evidence for
this is contained in the full report and the paper of Mushak and Crocetti (1990).
Basic Approaches in Response to the Directive
The language of the relevant subsection in Section 118 (f) of SARA gives little specific direction
as to what Congress meant with respect to the level of lead exposure to be prevented. Does it
mean reducing exposures that would simply lower body lead burdens below some toxicity
threshold? Alternatively, is there implicit in Congress’ intent the notion that reductions in
95
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exposure be such as to also produce some margin of safety? To what level is toxicity risk to be
reduced? Answers to these questions lie to some extent in the differing forms of lead exposure
prevention or reduction that are applicable.
It is common practice in epidemiology to classify exposure prevention methodologies into primary,
secondary and tertiary forms. These distinctions are linked in part to preventing the incidence of
a disease and avoiding subsequent complications of that disease. In the case of lead exposure
prevention, we considered primary and secondary approaches as specifically defined below.
Primary and Secondary Lead Exposure Prevention Classifications
Under the classification of primary prevention, we noted two subcategories: environmental or
source control strategies and a mixture of environmental and biological, i.e., nutritional
augmentation. The first was source-driven: lead in paint, ambient air, dust and soil, drinking
water and food. The second included consideration of calcium and iron supplementation
programs.
We employed three subcategories under secondary prevention: environmental, environmental plus
biological, and extra-environmental. The first of these included case finding, screening programs,
environmental follow-up and event-specific exposure abatement. Nutritional augmentation also
appears in the second one, but implemented on a case-specific basis. Legal actions and strictures
comprise the final subcategory.
Primary prevention strategies range from controls on the entry of a potentially toxic substance such
as lead into commercial channels to removal of the substance from human exposure pathways.
With lead paint, this includes banning sale of lead paint and removal of paint from the child’s
environment. Secondary prevention approaches to lead paint are basically reactive in nature, i.e.,
are responses to existing and identified problems. S~reening programs, although often considered
a mechanism for primary prevention, e.g., reducing the incidence of lead poisoning, are also
ranked here as secondary. That is, it was often required that areas at high risk for lead poisoning
first be identified before screening programs were introduced.
Primary Prevention of Lead Exposure
Lead in Paint
Control of lead paint exposure in young children has largely been a dismal failure. Lead paint was
introduced into commercial use in the United States with little concern for any hazard to the health
of children in homes with lead paint. Few controls were imposed long after lead paint was known
to be a poisoning source. The time between the lead poisoning review of McKhann et al. (1926)
and passage of the LBPPPA was almost half a century. Since Congress enacted the LBPPPA in
1971;
- The Consumer Product Safety Commission in 1977 banned sale of leaded paint
having leaded content > 0.06% in interstate commerce. This act did nothing for
96 24
the approximately 3+ million tons of lead sequestered in dispersed paint in the 58
million living units noted above. It did not affect intrastate production and sale of
lead paint, nor did it ban paint already in the national marketing pipeline.
, Housing and Urban Development, in 1973 and 1976, took several steps that were
generally reactive in nature. It provided a warning to purchasers and tenants of
pre-1950 housing about lead paint and it banned lead in paint at >0.5% (5,000
ppm). In response to court action (Ashton vs. Pierce, 1983), HUD issued a set of
interim guidelines for public and Indian housing. These were described in detail
in the report and in Mushak and Crocetti (1990).
- Municipal and state actions against lead paint exposure have entailed both sale of
leaded paint within jurisdictions and diverse laws and ordinances to ameliorate such
exposures, with little overall success. Some cities were active quite early, e.g.,
Baltimore, but the magnitude of the problem remains relatively undiminished.
Among states, Massachusetts was identified in the report as representing a typical
case study of the complex interplay of opposition from. vested interests which
render seemingly comprehensive regulatory language ineffective in practice.
Lead in Ambient Air
Control of lead in ambient air entails regulation of lead in gasoline and lead emissions from such
stationary sources as lead smelters and battery manufacturing plants. Unlike the abysmal record
for lead paint, there has been a relatively successful effort to reduce lead emissions to air from
leaded gasoline combustion. The USEPA has had regulatory authority over leaded gasoline since
1974. In 1975, EPA classified Pb as a criteria pollutant. This classification required that an
enforceable ambient air standard be issued. The growing use of lead-sensitive pollution control
equipment in new automobiles of the 1970s also produced a practical, compelling reason for
removing lead from gasoline. Effective January 1, 1986, lead in gasoline was reduced to a level
of 0.1 g/gal.
Under rovisions of Section 108 of the 1970 Clean Air Act and 1977 amendments, EPA reduced
the ambient air lead standard to 1.5 micrograms/cubic meter air, averaged quarterly.
~ Lead in Soils and Dusts
At present there are no specific legislative or regulatory actions directed towards dust and soil
lead. Regulatory control is indirectly through the primary input sources, lead paint and
stationary/mobile sources of air lead emissions.
Lead in Drinking Water
USEPA is required by the 1974 Safe Drinking Water Act to set primary and secondary drinking
97 768
water standards for lead and other pollutants. For human health, this was done via the Maximum
Contaminant Level (MCL), which for lead was an enforceable level of 50 ug/L.
Lead in Food
Control of lead in the U.S. food supply has rarely taken the form of specific promulgation of food
lead standards. The U.S. Food and Drug Administration (FDA) has had control over lead in food
dating to use of lead-based pesticides for food crops. There are a number of steps at which lead
can enter the food supply for children. These steps have involved FDA in the form of action goals
to reduce lead intakes in children below certain levels. Lead contamination reduction from lead-
seamed cans entailed non-regulatory cooperative efforts between FDA and the can manufacturers.
FDA does control, albeit with mixed results, the import of poorly glazed food containers which
are known to be hazardous in typical use.
Through various cooperative measures, the lead in daily diet of children has been declining. In
the report to Congress, we noted that major reductions had occurred, when comparing 1982-1984
numbers with 1984-1986 data (Table 6).
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Primary Prevention Measures Using Environmental and Biological Approaches
In theory, biological control methodologies can suppress lead entry into the bodies of exposed
children and assist in reducing the level of toxicity risk. As part of primary prevention, this
entails community-wide nutritional intervention actions. Given the available information on likely
effective nutritional modalities, use of iron and calcium supplements would be particularly helpful.
Such adjuncts are no substitute for effective environmental lead abatement.
Secondary Prevention Measures
The nationwide lead screening programs that were set up in response to the 1971 LBPPPA under
the aegis of CDC, and lasting until 1981, screened approximately 4 million children. Of these,
250,000 children had been identified as lead-toxic cases. About 30% of high-risk children were
estimated to have been screened in this time.
There is considerable support for the argument that lead screening has been very effective at
present levels of case-finding. It will be even more effective as medical intervention costs
continue to rise. The report actually estimated a ratio of >50 for the benefit of averted health
costs to unit screening cost.
Legal sanctions as an adjunct to secondary prevention have been grossly ineffective. The report
described a case study in which it was shown that in one municipality with a large lead paint
poisoning problem, legal measures consisted of minor fines and were largely ineffective.
Update of Alternatives and Methods for Reducing Childhood Lead Exposure
A number of encouraging developments toward reducing childhood exposure have been occurring
on the legislative, regulatory and public health policy fronts.
Recently, CDC (1991 a, b) issued two major documents that directly address the issue of exposure
abatement and responses to unabated exposures. CDC's strategic plan (1991a) makes it clear that
lead paint abatement is cost-effective and the plan offers a schedule for abatement of the worst
housing. The 1991 CDC Statement on preventing childhood lead poisoning is a major departure
from past statements, in that environmental control and interventions are explicitly recommended
on a community as well as individual case basis. The new action level of 10 pg/dL will result in
a large number of new children at risk, requiring more wide-spread abatement measures.
HUD has produced a report to Congress. It has also issued a set of interim (September, 1990)
and revised (May, 1991) guidelines for lead-based paint hazard identification and abatement for
public and Indian housing (HUD, 1991). These guidelines, legislatively mandated by the 1989
HUD-Independent Agencies Appropriations Act and the Housing and Community Development
Act of 1987 and the Stewart B. McKinney Homeless Amendments Act of 1989, deal with testing,
abatement, clean-up and disposal of lead-based paint in public and Indian housing.
99 120
Topics in the HUD guideline document include risk reduction for lead-based paint poisoning (Ch.
2), responsibilities in testing (Ch. 3), abatement considerations and methodologies (Ch. 5-7, 9),
worker protection (Ch. 8) and waste disposal (Ch. 11).
The USEPA has released a lead exposure reduction plan similar to that of CDC, "Strategy to
Reduce Lead Exposures,” issued February 21, 1991. In June, 1991, EPA issued its final rule on
lead in drinking water [56(110) FR 26480-26564; June 7, 1991]. Lead in drinking water has
enforceable regulation at a level of 5 ppb at the water source. Tap levels in homes are to be
covered under action level procedures, depending on the outcome of community tapwater
sampling. Further steps entail corrosion control followed by removal of lead lines, if necessary,
with a 21-year total grace period. The long period for lead plumbing line removal means chronic
Pb exposures of infants and toddlers in communities with such systems.
EPA is also proposing rulemaking [ANPR; 56(92) FR 22098-22098; May 13, 1991] with reference
to regulating uses of lead under Section 6 of the Toxic Substances Control Act (TSCA). Notable
topics for special attention include consideration of the phase-out of current uses of lead posing
unreasonable risks and assessment of overall Pb production and use.
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Grant, L.D. and Davis, J.M. 1989. Effects of low-level lead exposure on paediatric neurobehavioral
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analysis of modern studies. JAMA 263: 673-678.
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in psychologic and classroom performance of children with elevated dentine lead levels. N. Engl. J. Med.
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Abatement of Lead-Based Paint in Privately Owned Housing: Report to Congress. Washington. D.C.
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Lead: Assessment of Scientific and Technical Information. March, Office of Air Quality Planning and
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World Health Organization. 1987. Air Quality Guidelines for Europe. Lead. European Series No. 23,
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767.
| DECL. OF J. ROUTT REIGART
DECLARATION OF J. ROUTT REIGART, M.D.
I, J. Routt Reigart, M.D., declare as follows:
1. The matters stated herein are true of my own personal knowledge. If called
as a witness, I would competently and truthfully testify consistent with the following.
2. I am an Associate Professor of Pediatrics at the Medical University of South
Carolina in Charleston, South Carolina.
3. Since July 1991, I have served as the Chairman of the American Academy of
Pediatrics’ Committee on Environmental Health ("Committee"). This Committee is
reviewing the Academy’s policy on lead testing and treatment, which is currently contained
in a five-year-old document entitled Statement of Childhood Lead Poisoning. We are
currently reviewing this document because recent information about lead toxicity in children
requires revised recommendations to pediatricians. I also serve as Chairman of the
Childhood Lead Poisoning Prevention Advisory Committee of the Centers for Disease
Control ("CDC").
PROFESSIONAL BACKGROUND
4. As a pediatrician I have devoted much of my professional career to the study,
screening and treatment of pediatric lead poisoning. For over 20 years I have been
researching, writing, teaching and lecturing on lead poisoning issues. In my medical
practice I have also screened and treated several thousand children who have been lead
poisoned.
3. I have authored and co-authored numerous articles and papers dealing
specifically with pediatric lead poisoning issues, including: Chisolm, Currant, Finbert
Hopkins, Lin-Fu, Piomelli, Reigart, Houk, "Increased Lead Absorption and Lead Poisoning
234
in Young Children. A Statement by the Centers for Disease Control," J. Pediatrics, 87:824
(1975); Penny, Reigart, Loadhold, Taylor, "Variability in Response to Lead Exposure:
Demonstration of a Genetic Influence," (Abstract), Pediatric Research, 11:438 (1977);
Whitlock, Reigart, Priester, "Lead Poisoning in South Carolina," SCMA Journal, 73:378
(1977); Reigart, "Lead Poisoning," Hospital Medicine, 17:161 16J, 16N, 16P: August, 1981;
Reigart, "Future Directions," Childhood Lead Poisoning — Current Perspectives (1988) and
Reigart, "Recommendations of the American Academy of Pediatrics on Lead Screening in
Children," Proceedings of the First National Conference on Laboratory Issues in Childhood
Lead Poisoning Prevention, October 31 - November 2, 1991.
6. Last month I addressed members of the Annual Academy of Pediatrics at its
annual conference in San Francisco on the issue of "Childhood Lead Poisoning." This
month I lectured at the University of Medicine & Dentistry of New Jersey, School of
Osteopathic Medicine, in Atlantic City, New Jersey, on the topic of "Pediatric Lead Poison
Prevention Continuing Education for Physicians," and in December Iwill facilitate a panel
at the National Childhood Lead Poisoning Prevention Conference discussing "Medical
Management Issues."
3 I serve on numerous committees dedicated to pediatric environmental health
issues, including: Chairman, Committee on Environmental Health, American Academy of
Pediatrics; Member, Lead Poisoning Education Task Force, Presidents Council on
Environmental Quality; Chairman, Centers for Disease Control Childhood Lead-Based
Paint Poisoning Advisory Committee; and as a Member of the Pew Charitable Trust’s
Advisory Committee on Lead Poisoning. In the past I have served on the Centers for
Disease Control Childhood Lead-Based Paint Poisoning ad hoc Advisory Committee and
worked with the Environmental Protection Agency as a Medical Consultant for Acute
Pesticide Poisoning.
LEAD POISONING AND MEDICAID ELIGIBLE CHILDREN
8. Speaking as a pediatrician, I am someone who has actually worked for many
years in lead poisoning prevention out in the field. The situation in my city, Charleston,
South Carolina, illustrates the enormity of the lead poisoning problem in young children.
In 1972, when we began screening in Charleston, we were detecting that somewhere in the
neighborhood of 39% of our children had blood lead levels greater than 40 pg/dL. By
1975, I was following over 1,250 children with lead levels greater than 30 pg/dL. Today the
Centers for Disease Control has decreased the level of concern to 10 pg/dL, so that there
are many more children out there who are potentially injured by dangerous blood lead
levels.
9. Although the American Academy of Pediatrics’ revised report is not yet
completed, one recommendation that will certainly come from the Committee is that there
is a need for more testing. Lead poisoning cannot be detected absent a blood test; a series
of questions cannot verify blood lead levels. Nor will a series of questions guarantee that
a child will be appropriately classified as low risk. In other words, a child can answer all
risk-identifying questions in the negative and still be poisoned.
10. Pediatricians obviously want to test for lead using a test that will accurately
measure blood lead at the levels of concern announced by the CDC (= 10 pg/dL.) The
erythrocyte protoporphyrin or "EP" test (which really does not measure blood lead levels
3
Yi
4 »
at all) is simply incapable of accurately predicting lead levels below 40 pg/dL.
11. In my opinion, as a pediatrician with extensive experience in lead poisoning
prevention, Medicaid eligible children represent a high risk group since the environment
of low-income children often contains numerous sources of lead exposure.
12. As noted in the CDC’s October 1991 statement, "[a]lthough all children are
at risk for lead toxicity, poor and minority children are disproportionately affected. Lead
exposure is at once a by-product of poverty and a contributor to the cycle that perpetuates
and deepens the state of being poor." U.S. Dep’t of Health & Human Services ("HHS"),
Public Health Service, Centers for Disease Control, Preventing I.ead Poisoning in Young
Children, 12 (Oct. 1991) ("CDC Statement").
13. The CDC Statement concludes, and I concur, that accurate measurement of
blood lead levels can only be determined through the use of blood lead tests. Id. at 41.
Accordingly, if the lead testing program is to be effective and if children are to be saved
from lead poisoning’s devastating effects, it is essential that HHS immediately mandate that
States replace the EP test with the blood lead test as the primary lead screening method.
5 Sous Reigart, M.D.
2%
DECL. OF BILL LANNN LEE
DECLARATION OF BILL LANN LEE
[, BILL LANN LEE, declare and say:
3 [ am one of the counsel for the amici curiae and the proposed plaintift-
intervenors People United for a Better Oakland, et al.
2. Attached hereto as Exhibit A is a true and accurate copy of McElvaine, M.D.,
Orbach, H.G., Binder, S., Blanksma, L.A., Maes, E.F., & Krieg, R.M., Evaluation of the
Erythrocyte Protoporphyrin Test as a Screen for Elevated Blood Lead Levels, 119 J. of
Pediatrics 548 (1991).
3. Attached hereto as Exhibit B is a true and accurate copy of Report of the
House Budget Comm. on H.R. 3299, 101 Cong., 1st Sess. (September 20, 1989), reprinted in
Medicare and Medicaid Guide (CCH), Extra Edition No. 596 (October 5, 1989) ( pp. 398 - 410.
I declare under penalty of perjury that the foregoing is true and correct.
Executed the 23rd day of November, 1992, at Los Angeles, California.
7 Lafin Lee
280
CADOC\THOMPSON\PLEADINGAMICIMEM
LEE
EXHIBIT A
2%
Evaluation of the erythrocyte
protoporphyrin test as a screen for
elevated blood lead levels
Michael D. McElvaine, bvM, MPH, Hyman G. Orbach, phD, Sue Binder, MD,
Lorry A. Blanksma, PhD, Edmond F. Maes, PhD. and Richard M. Krieg. PhD
From the Division of Environmental Hazards and Health Effects, Center for Environmental Health
and Injury Control, Centers for Disease Control, Atlanta, Georgia, and the City of Chicago De-
partment of Health, Chicago, Illinois
To study the effect of lowering the definition of an elevated blood lead level on
the performance of the erythrocyte protoporphyrin screening test and the num-
ber of children who would require follow-up, we collected laboratory data from
a screening program. The estimated sensitivity of an erythrocyte protoporphy-
rin level >35 ug/dl for identifying children with elevated blood lead levels was
73% when we used 1985 Centers for Disease Control guidelines (elevated blood
lead level >25 ng/dl). Eight percent of the tests showed positive results. When
we redefined an elevated blood lead level as =15 ug/dl, the sensitivity estimate
was reduced to 37% and the number of positive test results increased fourfold.
(J PEDIATR 1994;119:548-50)
The most recent statement of the Centers for Disease Con-
trol (CDC), published in 1985,! defined an elevated blood
lead level in children as =25 pg/dl (1.21 pmol/L), a
threshold exceeded by an estimated 250,000 children in
1984.2 The 1985 CDC statement recommended screening
for elevated BPD levels by measuring erythrocyte protopor-
phyrin levels and considering an EP level of =35 pg/dl
(0.62 umol/L) as a positive screening test result. EP is a
precursor of heme that accumulates when lead interferes
with normal heme synthesis.
Few data are available on how well the EP test, with a
positive test result defined as =35 ug/dl, would perform in
identifying children with BPb levels of =25 ug/dl in ac-
tual clinic screenings. Among children tested in the Sec-
Presented in part at the 1990 Epidemic Intelligence Service Con-
ference, April 23-27, 1990, Atlanta, Ga.
The authors of this article are solely responsible for all analysis and
interpretation of the data presented here.
Submitted for publication April 3, 1991; accepted June 20, 1991.
Reprint requests: Michael D. McElvaine, DVM, MPH, Division of
Environmental Hazards and Health Effects, Center for Environ-
mental Health and Injury Control, Centers for Disease Control,
Mail Stop F-28, 1600 Clifton Rd. NE, Atlanta, GA 30333.
9/20/31947
ond National Health and Nutrition Examination Survey,
the sensitivity of the EP test in detecting elevated BPb lev-
els was 26% (unpublished data). For low-income black
children in NHANES II who lived in the central city (i.e,
were at high risk for lead poisoning), the sensitivity estimate
was 42%. A more recent survey of urban children in a com-
munity with characteristics associated with high rates of
lead poisoning, Oakland, Calif., yielded a sensitivity esti-
mate of 50%.3
BPb Blood lead
EP Erythrocyte protoporphyrin
NHANES II Second National Health and
Nutrition Examination Survey
Recent research has shown that significant adverse
effects result from BPb levels of 10 to 15 ug/dl or even
lower,2 4 and the CDC is reconsidering its definition of an
elevated BPb level. There is poor correlation between BPb
and EP when BPb levels are less than 18 to 20 ug/dl.>®
Accordingly, to assess how lowering the definition of an el-
evated BPb level would affect EP test performance and the
numbers of children needing follow-up care, we analyzed
laboratory data from a childhood lead poisoning prevention
verse
even
of an
BPb
dis-¢
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Performance of i screening test for lead poisoning 549
Table I. Population blood lead and erythrocyte protoporphyrin values by age group, Chicago, Ill., 1988-1989
Children with
Age group Mean BPb (range) Mean EP (range) BPb >25 ng/di
(yn n (ug/dl) (vg/dl) (%)
<2 231 12.1 (3-83) 29.8 (2-146) 4
2-3 219 14.8 (2-49) 31.8 (1-234) 12
4-5 147 13.4 (3-50) 28.1 (4-214) 8
ToraL 577 13.4 (2-83) 30.1 (1-234) 8
program that screens children at high risk for lead poison-
Ing.
METHODS
The City of Chicago Department of Health Division of
Laboratories measures EP and BPb levels in about 50,000
venous blood samples each year. The EP level is measured
Table Il. Performance of the erythrocyte protoporphyrin
test to identify samples with elevated blood lead levels,
with an EP level >35 ug/dl used as a screening cutoff
point, Chicago, Ill., 1988-1989
by hematofluorometry.” The BPb level is measured by
atomic absorption spectrophotometry® or by anodic strip-
ping voltammetry. This laboratory is one of six reference
laboratories used by the proficiency testing program run
jointly by the CDC, the Health Resources and Services
Children with
Definition of elevated BPb Sensitivity Specificity
elevated BPb (n = 577) (%) (%)
(ng/dl) (%) (95% CI) (95% CI)
Z23 8 73 (60-86) 81 (78-85)
=>20 1S 49 (39-60) 82 (78-85)
=15 32 37 (30-44) 84 (80-87)
>10 66 26 (21-30) 82 (77-88)
Administration, and the University of Wisconsin to estab-
lish target values for BPb testing and is also a regular par-
ticipant in the proficiency testing program for EP.
The population that we studied consisted of children who
visited city-run clinics that operate in low-income neigh-
borhoods. Every child received lead screening as part of the
routine health program. In addition, the city also provided
mobile screening services to underserved areas.
Laboratory and demographic data were abstracted from
a2%systematicsample of laboratory test records (n = 1057)
for the period of Sept. 1, 1988, through Aug. 31, 1989. A
two-digit random number was used as a starting point; then
every fiftieth record was selected. From this sample, we in-
cluded all children from 6 months through 5 years of age
who were tested at the city’s screening centers. For the four
children who appeared twice in the sample, only the first set
of results was used. A total of 577 records met these crite-
ria and were included for analysis.
RESULTS
The study population was 53% male. The ethnic distri-
bution was 68% black, 29% Hispanic, and 3% other. The
highest mean BPb and EP levels were in the 2- and 3-year-
old age group (Table 1).
Performance of the EP test to identify various levels of
BPb elevation is shown in Table I1. Twenty-three percent of
the EP tests were =>35 ug/dl. Using the 1985 CDC defini-
tion of an elevated BPb level, we estimated the sensitivity
t0 be 73%. If an elevated BPb level was redefined as >15
C1, 95% Confidence intervals for estimated values.
ng/dl, the proportion of samples with elevated BPb levels
increased four times and the sensitivity of the EP screen was
reduced by half to 37%. When a definition of > 10 ug/dl was
used, the proportion with elevated BPb levels increased to
66% and the sensitivity decreased further. For this sample
population, the EP test (at >35 wg/dl) identified all
subjects with BPb levels of 35 ug/dl or greater.
DISCUSSION
The results show that the sensitivity of the EP test in this
high-risk population (73%) is higher than that found from
NHANES II overall (26%), from a high-risk subset of
NHANES II (42%) and in Oakland, Calif. (50%).3 The
higher sensitivity estimates seen in the Chicago data may be
the result of several factors. Among subjects with elevated
BPD levels, those levels were relatively higher in Chicago
than in the other populations. In NHANES I1, 55% of the
children with elevated BPb levels had levels in the 25 to 29
ug/dl range. In Chicago, of the tests showing elevated BPb
levels 67% showed levels of >30 ug/dl. Because EP
increases exponentially with increasing BPb values, sensi-
tivity is greater for children with higher BPb levels.5:
Iron deficiency also can cause an increase in the EP level
in children. '0 The apparent sensitivity of the EP test for
identifying elevated BPb levels should be greater in a pop-
ulation in which iron deficiency is more prevalent. Iron de-
ficiency and lead poisoning often coexist.? The prevalence
2.94%
7
550 McElvaine et @
of iron deficiency in the Chicago children (a largely minor-
ity, inner-city population) may have been higher than in the
NHANES Il children (a representative sample of U.S.
children); unfortunately, in this study, no data were avail-
able to assess the iron status of the Chicago children.
These data indicate that the EP test performed accept-
ably as a screening test for BPb levels =25 pg/dl in the
high-risk Chicago population but that when the definition
of an elevated BPb level was lowered to =15 ug/dl, the
sensitivity of the EP test decreased to 37%. This decrease
makes it a less useful screening test for BPb levels in the 10
to 24 ug/dl range. a
The EP test has several practical advantages: it is inex-
pensive and easy to perform, and it can identify iron defi-
ciency in children.’ The sensitivity of the EP test is also good
for identifying children with very high BPb levels, those who
most urgently need follow-up. For identification of the chil-
dren with BPb levels of 10 to 24 ug/dl, another screening
method, probably BPb measurement, will be needed. Such
screening would be facilitated by the development of
cheaper, easier-to-use, portable instruments for measuring
BPb lead levels accurately at the new, lower levels of con-
cern.
Information on the Childhood Lead Screening Program was
provided by Charles R. Catania, City of Chicago Department of
Health. Thomas D. Matte, MD, and Jeffrey J. Sacks, MD, of the
Centers for Disease Control, provided valuable editorial assistance
in the preparation of this manuscript. The NHANES II data tapes
were supplied by the National Center for Health Statistics. Data
management was assisted by Mary Boyd, of CDC, and Nance Du-
laj, of the City of Chicago Department of Health Laboratory.
I'he Journal of Pediatrics
October 199]
REFERENCES
|. Centers for Disease Control. Preventing lead poisoning in
young children: a statement by the Centers for Disease Con-
trol. CDC Report No. 99-2230. Atlanta, Ga.: U.S. Department
of Health and Human Services, 1985.
. Agency for Toxic Substances and Discase Registry. The nature
and extent of lead poisoning in children in the United States:
a report to Congress. Atlanta, Ga.: U.S. Department of Health
and Human Services, 1988.
. California Department of Health Services. Childhood lead
poisoning in California, extent, causes and prevention: report
to the California State Legislature. Sacramento, Calif.: State
of California Health and Welfare Agency, 1991.
. Mushak P, Davis JM, Crocetti AF, Grant LD. Prenatal and
~ postnatal effects of low-level lead exposure: integrated sum-
mary of a report to the U.S. Congress on childhood lead poi-
soning. Environ Res 1989:50:11-36.
. Piomelli S, Seaman C, Zullow D, Curran A, Davidow B.
Threshold for lead damage to heme synthesis in urban children.
Proc Natl Acad Sci USA 1982:79:3335-9.
. Hammond PB, Bornschein RL, Succop P. Dose-effect and
dose-response relationships of blood lead to erythrocytic pro-
toporphyrin in young children. Environ Res 1985;38:187-96.
. Lamola AA, Joselow M, Yamane T. Zinc protoporphyrin
(ZPP): a simple, sensitive, fluorometric screening test for lead
poisoning. Clin Chem 1975:21:93-7.
. Blanksma L. Lead: atomic absorption method. In: Levinson
SA, MacFate RP, eds. Clinical laboratory diagnosis. Philadel-
phia: Lea & Febiger 1969:461-4.
. Mahaffey KR, Annest JL. Association of erythrocyte proto-
porphyrin with blood lead level and iron status in the Second
National Health and Nutrition Examination Survey, 1976-
1980. Environ Res 1986;41:327-38.
. Marcus AH, Schwartz J. Dose-response curves for erythrocyte
protoporphyrin vs blood lead: effects of iron status. Environ
Res 1987;44:221-7.
LEE
EXHIBIT B
|<. MEDICARE and MEDICAID
NUMBER 596 OCTOBER 5, 1989
| —EXTRA EDITION—
; ~~ Omnibus
Budget Reconciliation Act
of 1989 -
H.R 3299
Report of the
House Budget Committee
September 20, 1989
A
G
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R
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ON
7)
T
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e
Explanation of the Energy and Commerce 3
and Ways and Means Committees
Affecting Medicare-Medicaid Programs
CCH Special 1
1 Extra copies of this Extra Edition are available from Commerce Clearing House, Inc., 4025 W. Peterson Ave., Chicago, Illinois 60646. Price: 1-4 copies, $5.00 each: $.9 copies, $4.75 each; 10-24 copies, $4.50 each; 25-49 copies, $4.00 each.
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398
cient time for a mother to make the transition from welfare to a
job that offers health insurance coverage for her and her children.
To further encourage welfare families to work. the Committee
bill would allow the States. at their option, to extend the current
‘2. month transitional coverage period for 2n additional 12 months
or 3. 6. or 9 months, as the re elects). Thus, a State could offer
a working welfare family a total of 24 months of transitional Med-
icaid coverage (12 mandatory. 12 optional). Under the bill, the
structure of the current mandatory benefit would remain un-
changed. Thus, States could. at their option. impose the same
income-related premium during this optional 12-month period that
they are allowed to impose during the 2nd mandatory 6-month
period. The Committee bill would also repeal the sunset.
The Committee bill would also make some technical corrections
to current law. It clarifies that Medicaid transition coverage termi-
nates at the close of the first month in which thé {amily ceases to
include a child. whether or not the child is a dependent child under
part A of Title IV, or would be if needy. The Committee bill also
clarifies that families who. prior to April 1, 1990, are receiving
Medicaid extension coverage under the current law 9-month provi-
sion are entitled to continue receiving this extension coverage after
that date until their 9-month coverage period expires.
Section 4213—Early and periodic screening,” diagnostic, and treat-
ment services
(a) In general. —Under current law, States are required to offer
early and periodic screening, diagnostic, and treatment (EPSDT)
services to children under age 21. States are required to inform all
Medicaid-eligible children of the availability of EPSDT services, to
provide (or arrange for the provision of) screening services in all
cases when they are requested, and, to arrange for (directly or
through referral to appropriate agencies or providers) corrective
treatment for which the child health screening indicates a need.
The EPSDT benefit is, in effect, the nation’s largest preventive
health program for children. Each State must provide, at a mini-
mum, the following EPSDT services: assessments of health, devel-
opmental, and nutritional status: unclothed physical examinations:
immunizations appropriate for age and health history; appropriate
vision, hearing, and laboratory tests; dental screening furnished by
direct referrals to dentists, beginning at age 3: and treatment for
vision. hearing, and dental services found necessary by the screen-
ing. These services are available to children under EPSDT even if
they are not available to other Medicaid beneficiaries under the
State's plan.
The EPSDT benefit is not currently defined in statute. In the
view of the Committee, as Medicaid coverage of poor children ex-
pands, both under current law and under the Committee bill, the
EPSDT benefit will become even more important to the health
status of children in this country. The Committee bill would there-
fore define the EPSDT benefit in statute to include four distinct
elements: (1) screening services, (2) vision services, (3) dental serv-
ices, and (4) hearing services. Each of these service elements would
have its own periodicity schedule that meets reasonable practice
standards. These items and services must be covered for children
SUZ
fare to a
children.
mmittee
current
! months
1.¢ offer
134 Med-
bill. the
ain un-
@ same
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b-month
“rections
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‘eases to
'd under
bill also
eceiving
h provi-
ge after
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to offer
PSD)
orm all
ices. to
5 in all
-ctly or
“rective
ced.
ventive
1 mini-
. devel-
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ypriate
ned by
‘nt for
.creen-
‘ven if
2r the
in the
en ex-
11. the
health
there-
1IStinct
i serv.
would
-actice
tldren
399
even if. under the S:ate Medicaid plan, they are not offered to other groups of program beneficiaries. ‘'nder the Committee bill. screening services must. at a mini- mum. include (1) a comprehensive health and developmental histo. ry including assessment of both physical and mental health deve]. opment. 2! a comprehensive unclothed physical exam. (3) appro- priate immunizations according to age and health history, (4) labo- ratory tess (including blood lead level assessment appropriate for age and risk factors). and (3) health education ‘including anticipato- rv guidance. The Committee emphasizes that anticipatory guid- ance to the child (or the child's parent or guardian) is a mandatory element of any adequate EPSDT assessment. Anticipatory guidance includes health education and counselling to both parents and chijl- dren.
Under the Committee bill, vision services must, at a minimum, include diagnosis and treatment for defects in vision, jSodiny eye- glasses. Dental services must. at a-minimum, includesrelief o and infections, restoration of teeth, and maintenance of dental
necessary, these controls must be consistent with the preventive thrust of the EPSDT benefit. For example, States may not limit
care in the “Guidelines for Health Supervision” (1981) of the Amer- ican Academy of Pediatrics. The Committee is informed that some
tions. The Committee intends that, among older children, dental examinations occur with greater frequency than is the case with
or treatment. These interperiodic screening examinations may occur even in the case of children whose physical, mental, or devel. opmental illnesses or conditions have already been diagnosed. if there are indications that the illness or condition may have become more severe or has changed sufficiently, so that further examina-
essary may be made by a health, developmental, or educational
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400
health care system (eg., State early intervention or special educa-
tion programs, Head Start and day care programs. WIC and other
nutritional assistance programs). As long as the child is referred to
an EPSDT provider, the child would be entitled to an interperiodic
health assessment (or dental. vision, or hearing assessment) or
treatment services covered under the State plan.
These same considerations apply with respect to vision, dental.
and hearing services. all of which must be provided when indicated
as medically necessary to determine the existence of suspected ill-
nesses or conditions. For example, assume that a child is screened
at age 5 according to a State's periodicity schedule and is found to
have no abnormalities. At age six, the child is referred to the
school nurse by a teacher who suspects the child of having a vision
problem. Under the Committee bill, the child can—and should—be
referred at that point to a qualified provider of vision care for full
diagnostic and treatment services,"and the State must make pay-
ment for those services, even eps the next regular vision exam
under the State's periodicity schedule does not occur until age 7.
While States may, at their option, impose prior authorization re-
quirements on treatment services, the Committee intends that, con-
sistent with the preventive thrust of the EPSDT benefit. both the
regular periodic screening services and the interperiodic screening
services be provided without prior authorization.
The Committee notes that Medicaid-eligible children are entitled
to EPSDT benefits even if they are enrolled in a health mainte-
nance organization. prepaid health plan, or other managed care
provider. The Committee expects that States will not contract with
a managed care provider unless the provider demonstrates that it
has the capacity (whether through its own employees or by con-
tract) to deliver the full array of items and services contained in
the EPSDT benefit. The Committee further expects that. in setting
payment rates for managed care providers, the States will make
available the resources necessary to conduct the required periodic
and interperiodic screenings and to provide the required diagnostic
and screening services.
The Committee bill clarifies that States are without authority to
restrict the classes of qualified providers that may participate in
the EPSDT program. Providers that meet the professional qualifi-
cations required under State law to provide an EPSDT screening,
diagnostic, or treatment service must be permitted to participate in
the program even if they deliver services in school settings, and
even if they are qualified to deliver only one of the items or serv-
ices in the EPSDT benefit.
(b) Report on the provision of EPSDT.—In order to assess the ef-
fectiveness of State EPSDT programs in reaching eligible chiidren.
the Committee bill would require the States to report annuaily to
the Secretary, in a uniform form and manner established by the
Secretary, the following information. broken down by age group
and by basis of eligibility for Medicaid: (1) the number of children
receiving child health screening services; (2! the number of chil-
dren referred for corrective treatment (the need for which is dis-
closed by the screening); and (3) the number of children receiving
dental services. These reports would be due April 1 of each year
(beginning with April 1, 1991) and would apply to services provided
af -
° -
-—
2
or special educa-
s. WIC anc other
h:ld 1s referred to
> an interper:odic
assessment’ or J
to vision, dental.
d when indicated
> of suspected ill-
child 1s screened
e and is found to
referred to the
f having a vision
—and should —be
sion care for full
must make pay-
ular vision exam
cur until age 7.
authorization re-
.ntends that. con-
benefit, both the
2riodic screening
iren are entitled
+ health mainte-
T managed care
ot contract with
strates thao: it
>yees or by con-
les contained in
: that. in setting
rates wil; make
aquired periodic
dired diagnostic -
Jut authority to
¥ participate in
2ssional qualifi-
'SDT screening,
0 participate in
Jt settings. and
> "lems or serv-
"9 assess the ef.
ble chiidren.
2riannuiiiy to
32iisned by the
. OV age zZroup
Cer of children
umber of chil-
-r which is dis.
idren receiving
+ of each vear
rvices provided
Po | 2
[1 wd vd,
Ea §
. > 2 ors b& Dia e 1) Eman EE Joos SWC Ha eI 00 1 MA
101
during the Federal fiscal year ending the previous Se tember 30 (beginning with FY 1990).
EE
/ Section 301. ~Ertension of payment provisions for medica. !- neces- sary services tn disproportionate share hospitals :
duration, and scope of covered services. However, effective July 1, 1989, States are prohibited from Imposing any fixed durational limit on Medicaid coverage of medically necessary inpatient hospi- tal services provided to infants under age 1 by disproportionate share hospitals. As of January, 1989, according to the National As. sociation of Childrens’ Hospitals and Related Institutions, 1» States imposed durational limits on inpatient hospital services tor chil- dren (Alabama. Alaska. Arkansas, Florida, Kentucky, Louisiana, Mississippi, Missouri, Oregon, Tennessee, Texas, and West Virgin- 1a). Sus x .. The purpose of the current law exception to fixed durational limits is to prohibit States from using arbitrary length of stay limi- tations (e.g., 20 days per year) to reduce payments for medically necessary services provided by hospitals, including many public and childrens’ hospitals, that serve a disproportionate number of low-income patients. The Committee bill would extend this current law prohibition to any fixed durationa] limits on payment for inpa- tient services provided to ¢hildren under age 18 by disproportionate share hospitals. The requirement is effective for inpatient hospital services furnished on or after July 1, 1990.
(b) Assuring adequaie payment for inpatient hospital seri ices for children in disproportionate share hospitals.—Under current law, States may reimburse hospitals for inpatient services on a prospec- tive basis. If they choose to do so, States must, effective July 1, 1989, provide for an outlier adjustment in payment amounts for medically necessary inpatient services provided by disproportionate share hospitals involving exceptionally high costs or exceptionally
’
The Committee bill would extend this current law requirement to cases involving children from age 1 up to age 18. States that pay for inpatient hospital services on a prospective basis would be re- quired to submit to the Secretary, no later than April 1, 1990, a State plan amendment that provides for an outlier adjustment in payment amounts for medically necessary inpatient services pro- vided by disproportionate share hospitals after July 1, 1990. involy- ing exceptionally high costs or exceptionally long lengths of stay for children age 1 up to age 18.
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