Pediatrics (October 2005)  [Printer-friendly version]


Committee on Environmental Health

Abstract: Fatal lead encephalopathy has disappeared and blood lead
concentrations have decreased in US children, but approximately 25%
still live in housing with deteriorated lead-based paint and are at
risk of lead exposure with resulting cognitive impairment and other
sequelae. Evidence continues to accrue that commonly encountered blood
lead concentrations, even those less than 10 micrograms/deciliter, may
impair cognition, and there is no threshold yet identified for this
effect. Most US children are at sufficient risk that they should have
their blood lead concentration measured at least once. There is now
evidence-based guidance available for managing children with increased
lead exposure. Housing stabilization and repair can interrupt exposure
in most cases. The focus in childhood lead-poisoning policy, however,
should shift from case identification and management to primary
prevention, with a goal of safe housing for all children.


CDC, Centers for Disease Control and Prevention
AAP, American Academy of Pediatrics
EPA, Environmental Protection Agency
CNS, central nervous system
EP, erythrocyte protoporphyrin
EDTA, ethylenediaminetetraacetic acid
TLC, Treatment of Lead-Exposed Children
HUD, Department of Housing and Urban Development

In 1991, when 1 in 11 US children had a blood lead concentration
greater than 10 micrograms/deciliter, both the Centers for Disease
Control and Prevention (CDC) and the American Academy of Pediatrics
(AAP) recommended that all US children have their blood lead
concentration measured at around 1 and 2 years of age, when
concentrations increase and then peak. By 1997, the median blood lead
concentration in the United States had decreased, and screening in
some areas with newer housing turned up few cases of elevated blood
lead concentration. The CDC and AAP then began to recommend screening
only those children with a greater chance of having an elevated blood
lead concentration -- those in older housing, those who had a sibling
or playmate with an elevated blood lead concentration, or those who
had lived in or visited a structure that might contain deteriorated,
damaged, or recently remodeled lead-painted surfaces. Screening of all
children eligible for Medicaid, among whom were found 80% of those
with increased blood lead concentration,[1] continued to be
recommended and had been required by Health Care Financing
Administration (now the Centers for Medicare and Medicaid Services)
regulation since 1989.

This new policy statement replaces the 1998 statement and includes
discussion of new data, including:

** Reliable estimates of the percentage of the US homes containing
lead hazards[22;

** Results from a large clinical trial showing that chelation in
children with moderately elevated blood lead concentrations does not
improve cognitive or neuropsychologic test scores[3];

** Documentation of unacceptably low screening rates among Medicaid-
eligible children[4];

** Further confirmation of the link between lead exposure in early
childhood and delinquent behavior during adolescence[5,6]; and

** New data showing inverse associations between blood lead
concentrations less than 10 micrograms/deciliter and IQ.[7,8]

The best approach to lead poisoning is to prevent exposure in the
first place, but it will be years before that goal is realized. In the
meantime, case finding, case management, and prevention of additional
exposure will still be required. This document considers relevant
aspects of the epidemiology, clinical toxicology, prevention, and
treatment of lead exposure in young children and provides
recommendations for pediatricians as well as public health

Sources of Lead Exposure

Lead is an element and occurs naturally, but blood lead concentrations
are quite low in the absence of industrial activities.9 In the United
States, there were historically 2 major sources of industrially
derived lead for children: airborne lead, mostly from the combustion
of gasoline containing tetraethyl lead; and leaded chips and dust,
mostly from deteriorating lead paint. Both contribute to soil lead. A
steep decrease in exposure to airborne lead in the United States has
occurred since 1980. Federal legislation in the 1970s removed lead
from gasoline and decreased smokestack emissions from smelters and
other sources, causing blood lead concentrations in children to

From 1976 to 1980, before the regulations had their full effect, US
children 1 to 5 years of age had a median blood lead concentration of
15 micrograms/deciliter.10 In 1988-1991, the median was 3.6
micrograms/deciliter[11]; in 1999, the median was 1.9
micrograms/deciliter.[12] Although concentrations have decreased in
all children, black children and poor children continue to have higher
blood lead concentrations. Airborne lead should no longer be a source
of community exposure in the United States, but individual counties
sometimes still exceed airborne lead regulations, and continued
vigilance is warranted. Individual children may still be exposed to
airborne lead in fumes or respirable dust resulting from sanding or
heating old paint, burning or melting automobile batteries, or melting
lead for use in a hobby or craft.

Lead Paint, Dust, and Soil

The source of most lead poisoning in children now is dust and chips
from deteriorating lead paint on interior surfaces.[13] Children who
developed lead encephalopathy with blood lead concentrations more than
100 micrograms/deciliter often had chips of lead paint visible on
abdominal plain films. Children who live in homes with deteriorating
lead paint, however, can achieve blood lead concentrations of 20
micrograms/deciliter or greater without frank pica.[14] The use of
leaded paint on interior surfaces ceased in the United States by the
mid-1970s. However, in 1998, of the 16.4 million US homes with 1 child
younger than 6 years, 25% still had significant amounts of lead-
contaminated deteriorated paint, dust, or adjacent bare soil ("lead
hazard").[2] Dust and soil are also a final resting place for airborne
lead from gasoline and dust from paint. Lead in dust and soil can
recontaminate cleaned houses[15] and contribute to elevating blood
lead concentrations in children who play on bare, contaminated

Transplacental Exposure and Lead in Human Milk

Lead crosses the placenta, and the blood lead concentration of the
infant is similar to that of the mother.[17] The source of lead in the
infant's blood seems to be a mixture of approximately two thirds
dietary and one third skeletal lead, as shown by studies that
exploited the differences in lead isotopes stored in the bones of
women migrating from Europe to Australia.[18] Although lead appears in
human milk, the concentration is closer to plasma lead and much lower
than blood lead, so little is transferred. Because infant formula and
other foods for infants also contain lead, women with commonly
encountered blood lead concentrations who breastfeed their infants
expose them to slightly less lead than if they do not breastfeed.19 In
Mexico, giving women supplemental calcium during lactation resulted in
a small (less than 2 micrograms/deciliter) decrease in the mother's
blood lead concentration, presumably by decreasing skeletal
resorption.[20] Theoretically, this could diminish transfer of lead
through breast milk even further. In the United States, however, where
calcium intake may be higher, calcium supplementation does not prevent
bone loss during lactation[21] and, thus, might not affect lead
transfer at all.

Other Sources

Lead plumbing (in Latin, "plumbus" = lead) has contaminated drinking
water for centuries, and lead in water can contribute to elevated
blood lead concentrations in children.[13] In 2003-2004, some tap
water in Washington, DC, was found to exceed Environmental Protection
Agency (EPA) regulations. This was thought to be caused by a change in
water disinfection procedures, which increased the water's ability to
leach lead from connector pipes between the water mains and interior
plumbing in old houses. The extent of this problem in Washington and
other cities is not yet known. Affected families are drinking filtered
or bottled water until the pipes can be replaced. (Most bottled water
is not fluoridated; its consumption may lead to marginal fluoride
intakes in children.) Much more about lead in drinking water is
available on the EPA Web site.

Table 1 includes questions about less common sources of lead exposure,
which include hobbies, contaminated work clothes, ceramics, cosmetics,
imported canned foods, etc. Such questions may be useful if a child
has an elevated blood lead concentration but no exposure to leaded
dust or soil. They have not been validated for the purpose of deciding
whether to screen.

TABLE 1. [Available on the web.]

The lead concentration of blood for transfusion is not routinely
measured. After exchange transfusion in the extremely low birth weight
infant, 90% of the infant's blood is donor blood. Bearer et al[22]
recommended that only units with lead concentrations of less than 0.09
micro mol/L be used in these patients, on the basis of their
adaptation of the World Health Organization tolerable weekly intake
from ingestion to intravenous injection. Approximately one third of
the units of blood that they measured were above this concentration.
The effect of lead in transfused blood used in older children has not
been considered.

Toxicity of lead

Subclinical Effects

At the levels of lead exposure now seen in the United States,
subclinical effects on the central nervous system (CNS) are the most
common effects. The best-studied effect is cognitive impairment,
measured by IQ tests. The strength of this association and its time
course have been observed to be similar in multiple studies in several
countries.[23] In most countries, including the United States, blood
lead concentrations peak at approximately 2 years of age and then
decrease without intervention. Blood lead concentration is associated
with lower IQ scores as IQ becomes testable reliably, which is at
approximately 5 years of age.[23] The strength of the association is
similar from study to study; as blood lead concentrations increase by
10 micrograms/deciliter, the IQ at 5 years of age and later decreases
by 2 to 3 points. Canfield et al[7] recently extended the relationship
between blood lead concentration and IQ to blood lead concentrations
less than 10 micrograms/deciliter. They observed a decrease in IQ of
more than 7 points over the first 10 micrograms/deciliter of lifetime
average blood lead concentration. Bellinger and Needleman[8]
subsequently reported a similarly steep slope in a reanalysis of data
from their study of children with blood lead concentrations similar to
those in the Canfield et al study. To confirm the adverse effects of
lead on IQ at these concentrations, however, more children whose blood
lead concentration has never been more than 10 micrograms/deciliter
should be studied. A reanalysis of the primary data from several of
the prospective studies is underway to help resolve this issue. At the
moment, however, these data have not yet been incorporated into
policy, and the CDC[16] and AAP[24] both currently use 10
micrograms/deciliter (Table 2) as the blood lead concentration of

TABLE 2. Summary of Recommendations for Children With Confirmed
(Venous) Elevated Blood Lead Concentrations[16]

Other aspects of brain or nerve function, especially behavior, also
may be affected. Teachers reported that students with elevated tooth
lead concentrations were more inattentive, hyperactive, disorganized,
and less able to follow directions.[25,26] Additional follow-up of
some of those children[25] showed higher rates of failure to graduate
from high school, reading disabilities, and greater absenteeism in the
final year of high school.[27] Elevated bone lead concentrations are
associated with increased attentional dysfunction, aggression, and
delinquency.[28] In children followed from infancy with blood lead
measurements, self-reported delinquent behavior at 15 to 17 years of
age increased with both prenatal and postnatal lead exposure,5 and
bone lead, thought to represent cumulative dose, is higher in
adjudicated delinquents.[6] These data imply that the effects of lead
exposure are long lasting and perhaps permanent. Subclinical effects
on both hearing[29] and balance[30] may occur at commonly encountered
blood lead concentrations.

Although there are reasonable animal models of low-dose lead exposure
and cognition and behavior,[31] the mechanisms by which lead affects
CNS function are not known. Lead alters very basic nervous system
functions, such as calcium-modulated signaling, at very low
concentrations in vitro,[32] but it is not yet clear whether this
process or some other one yet to be examined is the crucial one. Lead
interferes detectably with heme synthesis beginning at blood lead
concentrations of approximately 25 micrograms/deciliter.[33] Both
aminolevulinate dehydratase, an early step enzyme, and ferrochelatase,
which completes the heme ring, are inhibited. Ferrochelatase
inhibition is the basis of an erstwhile screening test for lead
poisoning that measures erythrocyte protoporphyrin (EP), the immediate
heme precursor. Because it is insensitive to the lower concentrations
of blood lead that are of concern now, the test is obsolete for that
use; however, EP measurement is still used clinically in managing
children with higher blood lead concentrations.

Clinical Effects

Children with blood lead concentrations greater than 60
micrograms/deciliter may complain of headaches, abdominal pain, loss
of appetite, and constipation and display clumsiness, agitation,
and/or decreased activity and somnolence. These are premonitory
symptoms of CNS involvement and may rapidly proceed to vomiting,
stupor, and convulsions.[34] Symptomatic lead toxicity should be
treated as an emergency. Although lead can cause clinically important
colic, peripheral neuropathy, and chronic renal disease in adults with
occupational exposures, these symptoms are rare in children.


In an influential 1994 study, 154 children who were 13 to 87 months
old and had blood lead concentrations between 25 and 55
micrograms/deciliter were given chelation with
ethylenediaminetetraacetic acid (EDTA) and therapeutic iron when
clinically indicated and then followed for 6 months. Those whose blood
lead concentrations decreased the most had improved cognitive test
scores independent of whether they had been given iron or chelation
therapy.[35] An Australian study[36] of 375 children with longer
follow-up, however, found only small and inconsistent improvement in
the IQs of children whose blood lead concentrations decreased the
most. A large (780-children) randomized trial of the use of succimer
in children with blood lead concentrations of 20 to 44
micrograms/deciliter, the Treatment of Lead-Exposed Children (TLC)[3]
Trial, showed no benefit on cognitive or neuropsychologic testing
despite an abrupt but transient decrease in the treated children's
blood lead concentrations. The children were randomly assigned at
approximately 2 years of age and followed with cognitive,
neuropsychologic, and behavioral tests until they were approximately 5
years of age. The large size of the trial permits confident exclusion
of a drug-related improvement of 2 IQ points or more. Additional
follow-up at 7 years of age with more sophisticated testing still
showed no advantage for the succimer-treated children.[37]

Because blood lead concentrations decreased as the children in the TLC
Trial got older regardless of whether they had chelation, Liu et
al[38] used the TLC data to attempt to replicate the reported
relationship between decreasing blood lead concentrations and improved
cognitive test scores. Test scores were unrelated to decreasing blood
lead concentrations at 6 months' follow-up, but results from following
the children for 36 months, when they were approximately 5 years of
age, showed improved test scores with greater decreases in blood lead
concentration but only in the placebo group. Additional research on
whether some effective intervention can be isolated to account for
this phenomenon is needed. There remains no evidence that chelation
will reverse cognitive impairment, and the predominance of data is
consistent with a noncausal association between decreasing blood lead
concentrations and improved cognitive test scores.

Costs Of Childhood Lead Poisoning And Benefits Of Prevention

Cost-Benefit Analyses

The removal of lead from gasoline cost money, and it will cost more
money to remove lead from housing. If childhood lead exposure,
however, affects cognitive function and its consequences, such as
graduating from high school, then it is plausible that it will affect
social function, employment, and earnings. Several groups have
estimated the long-term dollar costs of childhood lead exposure,
assuming that the effect of lead on IQ is linear and permanent; they
also assume a specific economic value of increased IQs. Grosse et
al[39] estimated the economic benefit of the 25-year secular downward
trend in childhood lead exposure in the cohort of children 2 years of
age in 2000. The estimated increase in earnings for the 3.8 million
children would be between $110 billion and $319 billion over their
lifetimes, compared with what they would have earned if they had been
exposed to 1975 lead levels. Landrigan et al[40] estimated the
lifetime costs for each year's cohort of children currently exposed to
lead to be $43 billion. On the cost side, Needleman[41] estimated a
$10 billion cost for deleading the estimated 2 million lead-
contaminated houses that existed in 1990. In 2002, a more reliable
estimate is that there are 4 million such lead-contaminated houses,[2]
and when adjusting for inflation (with the Consumer Price Index
inflation calculator), Needleman's estimate becomes approximately $28
billion in 2002. Combining these estimates leads to the conclusion
that removing lead paint is cost-effective if it prevents even two
thirds of lead exposure for any single year's cohort of 2-year-olds.

Similarly, a presidential task force estimated that the net nationwide
benefit of interim control of lead hazards in the nation's pre-1960
housing would be $1 billion to $9 billion over 10 years. The benefit
of abating the hazards permanently would be $21 billion to $38
billion. Such quantitation allows planning and setting priorities to
be done more transparently and allows comparisons to estimates of the
cost for lead-abatement programs and other preventive activities.
Although these are exemplary numbers in simplified analyses, all parts
of which could be challenged, they illustrate the rationale for
viewing lead exposure as a problem that should be solved, even on
economic grounds.

Federal Strategy to Prevent Lead Poisoning

The President's Task Force on Environmental Health Risks and Safety
Risks to Children was formed in 1997 by executive order. It consists
of government officials from the EPA, the Department of Health and
Human Services, the Consumer Product Safety Commission, the Department
of Housing and Urban Development (HUD), and others. One of its first
projects was to formulate a plan to eliminate childhood lead
poisoning,[42] a goal that was incorporated into the Healthy People
2010 goals for the nation. For the first time, the strategy
concentrated on primary prevention and was directed at housing. It did
not require that a lead-poisoned child first be identified before a
house was considered eligible for participation (the principle of
primary prevention). The core of the strategy is a grant-based program
administered by the HUD that would accelerate the pace at which in-
place management of lead hazards would occur in US homes. The strategy
projected that more than 20 million houses could be remediated in the
decade from 2000-2010, making lead-safe housing available to a large
majority of US children. The strategy also included continued
screening, especially among Medicaid-eligible children, enforcement of
existing statutes and regulations, and research, especially on the
effectiveness of in-place management of lead hazards. The HUD plans
periodic evaluations and progress reports, which can be tracked on
its Web site.

Diagnostic Measures

The diagnosis of lead poisoning or increased lead absorption depends
on the measurement of blood lead concentration. This is best performed
by using a venous sample, but a carefully collected finger-stick
sample can be used. Most blood lead measurements are now performed
because the child meets some general eligibility criteria (screening)
and not because they are at especially high risk of exposure or have
symptoms suggestive of lead poisoning (diagnosis).


Between 1991 and 1997, both the AAP and CDC recommended universal
screening, that is, that all children have their blood lead
concentration measured, preferably when they are 1 and 2 years of age.
Because the prevalence of elevated blood lead concentrations has
decreased so much, a shift toward targeted screening has begun,[43]
and the criteria for and implementation of targeted screening
continues to develop. As of early 2005, the situation is as follows.
All Medicaid- eligible children must be screened.[4] Medicaid will
reimburse 2 screenings, one at 1 year of age and one at 2 years of
age. Most children with elevated blood lead concentrations are
Medicaid eligible, and most Medicaid-eligible children have not been
screened.[4] The Advisory Committee on Childhood Lead Poisoning
Prevention has proposed criteria by which a state could acquire an
exemption from this requirement, and the proposal is under
consideration in the Secretary of Health and Human Services' office.
Until such exemptions are granted, both the CDC[4] and AAP support
universal screening of Medicaid-eligible children. The thinking behind
the availability of exemptions is not primarily to decrease the number
of screenings performed but rather to increase it among groups in
which increased lead absorption will be found. Children whose families
participate in any assistance program but who, for whatever reason,
are not eligible for Medicaid should also be screened.

For children not eligible for Medicaid, several states and some
municipalities have developed targeted screening recommendations or
policies using suggestions made by the CDC,[43] their own data, or
some combination of the two. All practitioners should determine if
such recommendations are in place where they practice. Appropriate
contacts at state and city health departments with CDC-funded programs
are listed on the CDC Web site.

The approach to screening children who are not eligible for Medicaid
and who live in areas in which health authorities have not made
locale-specific recommendations is less clear. Although targeted
screening may be desirable, well-validated tools with which to achieve
it are not yet in place.[44] In the absence of policy, current
recommendations support screening all children who are not enrolled in
Medicaid and who live in areas in which local authorities have not
issued specific guidance.

There are now many case reports of children who are recent immigrants,
refugees, or international adoptees who have elevated (sometimes very
elevated) blood lead concentrations.[45] Such children should be
screened on arrival in the United States.

Diagnostic Testing

Some experienced clinicians measure the blood lead concentration in
children with growth retardation, speech or language dysfunction,
anemia, and attentional or behavioral disorders, especially if the
parents have a specific interest in lead or in health effects from
environmental chemicals. However, a persistent elevation of blood lead
concentration into school age is unusual, even if peak blood lead
concentration at 2 years of age was high and the child's housing has
not been abated. This is probably because hand-to-mouth activity
decreases and the child's body mass increases. Thus, a low blood lead
concentration in a school-aged child does not rule out earlier lead
poisoning. If the question of current lead poisoning arises, however,
the only reliable way to make a diagnosis is with a blood lead
measurement. Hair lead concentration gives no useful information and
should not be performed.[46] Radiograph fluorescence measurement of
lead in bone is available in a few research centers and has been used
in children as young as 11 years with acceptable validity for research
purposes,[47] but it has no clinical utility as yet.

Management Of Children With Elevated Blood Lead Concentrations

In 2002, the national Advisory Committee on Childhood Lead Poisoning
Prevention published a monograph, "Managing Elevated Blood Lead Levels
Among Young Children."[16] The goal of the monograph was to provide an
evidence-based, standard approach to management usable throughout the
United States. Anyone involved with the management of children with
elevated blood lead concentrations needs access to it. This section is
consistent with the monograph.

The management of children with elevated blood lead concentrations is
determined primarily by how high the concentration is (Table 2).
Children with concentrations less than 10 micrograms/deciliter are not
currently considered to have excess lead exposure. Children with
concentrations 10 micrograms/deciliter or greater should have their
concentrations rechecked; if many children in a community have
concentrations greater than 10 micrograms/deciliter, the situation
requires investigation for some controllable source of lead exposure.
Children who ever have a concentration greater than 20
micrograms/deciliter or persistently (for more than 3 months) have a
concentration greater than 15 micrograms/deciliter require
environmental and medical evaluation.

Residential Lead Exposure

Most children with elevated blood lead concentrations live in or
regularly visit a home with deteriorating lead paint on interior
surfaces. Some children eat paint chips, but pica is not necessary to
achieve blood lead concentrations of 20 micrograms/deciliter or
greater.[14] Children can ingest lead-laden dust through normal
mouthing behaviors by simply placing their hand or an object in their
mouth. This also happens when children handle food during
eating.[48,49,50] There is increasing evidence that professional
cleaning, paint stabilization, and removal and replacement of building
components can interrupt exposure. Cooperation with the health
department in investigating and decreasing the source is necessary.
Although some authorities insist that moving children to unleaded
housing or removal of all lead paint from their current housing is the
only acceptable solution,[51] alternative housing is rarely available
and extensive on-site removal of leaded paint can raise the
concentration in house dust and resident children.[52]

Lead in soil is higher around houses with exterior lead paint and in
places where there has been a smokestack or other point source or
heavy traffic. Soil concentrations are related to blood lead
concentrations but not as closely as are interior dust lead
concentrations.[13] Soil can be tested for lead content, and the EPA
has guidelines for testing on its Web site.

Lead should no longer be a problem in municipal water supplies, but
wells, old pipes from the municipal supply to the house (as has been
the case in Washington, DC), or soldered joints may add lead to

Other Sources

Some children will have persistently elevated blood lead
concentrations without access to lead paint, bare soil, or lead in
their drinking water. Their exposure may come from any of the sources
listed in Table 3. Blood lead concentrations should decrease as the
child passes approximately 2 years of age, and a stable or increasing
blood lead concentration beyond that age is likely to be caused by
ongoing exposure.

TABLE 3. Sources of Lead Exposure and Prevention Strategies[59]

The recommended approach to environmental investigation of a child
with an elevated blood lead concentration consists of (1) an
environmental history, such as the one shown in Table 1, (2) an
inspection of the child's primary residence and any building in which
they spend time regularly, (3) measurement of lead in deteriorated
paint, dust, bare soil, or water as appropriate, (4) control of any
immediate hazard, and (5) remediation of the house, which may require
temporary relocation of the child. If new or lead-safe housing is an
option for the family, it offers a simple and permanent solution.

These situations can be frightening for the families. Involving the
family and providing them with information as it is obtained is the
right thing to do and may help lessen anxiety.

Although intense regimens of professional cleaning decrease children's
blood lead concentrations, providing families with instructions and
cleaning materials does not. Washing children's hands has intuitive
appeal, but no data support its role in decreasing exposure. Suggested
prevention strategies are listed in Table 3.

Medical Management

If the blood lead concentration is greater than 45
micrograms/deciliter and the exposure has been controlled, treatment
with succimer should begin. A pediatrician experienced in managing
children with lead poisoning should be consulted; these pediatricians
can be found through state health department lead programs, through
pediatric environmental health specialty units, at hospitals that
participated in the largest clinical trial of succimer,[3] or by
calling the local poison control center or the AAP Committee on
Environmental Health. The most common adverse effects of succimer
listed on the label are abdominal distress, transient rash, elevated
hepatocellular enzyme concentrations, and neutropenia. The drug is
unpleasant to administer because of a strong "rotten-egg" odor, and
40% of the families on active drug compared with 26% on placebo found
the drug difficult to administer.[53] The succimer label provides
dosages calculated both by body surface area and by weight, but the
equivalent dose by both methods would occur in a child approximately 5
years of age. For the younger children typically given the drug, body
surface area calculations give higher doses, which are those that are

Although chelation therapy for children with blood lead concentrations
of 20 to 44 micrograms/deciliter can be expected to lower blood lead
concentrations, it does not reverse or diminish cognitive impairment
or other behavioral or neuropsychologic effects of lead.[3] There are
no data supporting the use of succimer in children whose blood lead
concentrations are less than 45 micrograms/deciliter if the goal is to
improve cognitive test scores.

Children with symptoms of lead poisoning, with blood lead
concentrations higher than 70 micrograms/deciliter, or who are
allergic or react to succimer will need parenteral therapy with EDTA
and hospitalization. Guidelines for these circumstances are beyond the
scope of this statement, but the same consultation as described above
is recommended. There are academic centers that use D-penicillamine,
another oral chelator used in Wilson disease, for lead poisoning. Its
safety and efficacy, however, have not been established,[55] and the
AAP Committee on Drugs considers it to be a third-line drug for lead

Dietary Intervention

The Advisory Committee on Childhood Lead Poisoning Prevention reviewed
the evidence for dietary intervention in lead-exposed children.[16]
They concluded that there are no trial data supporting dietary
interventions aimed specifically at preventing lead absorption or
modulating the effects of lead. However, there are laboratory and
clinical data suggesting that adequate intake of iron, calcium, and
vitamin C are especially important for these children. Adequate iron
and calcium stores may decrease lead absorption, and vitamin C may
increase renal excretion. Although there is epidemiologic evidence
that diets higher in fat and total calories are associated with higher
blood lead concentrations at 1 year of age,[57] the absence of trial
data showing benefits and the caloric requirements of children at this
age preclude recommending low-fat diets for them.

Psychological Assessment

The Advisory Committee on Childhood Lead Poisoning Prevention reviewed
the evidence for psychological assessment and intervention in lead-
exposed children.[16] Despite data from several large epidemiologic
studies suggesting that moderate exposure to lead produces specific
deficits in attention or executive functions, visual-spatial skills,
fine-motor coordination, balance, and social-behavioral modulation,58
there is no specific "signature" syndrome yet identified. In addition,
although 2-year-olds tend to have the highest blood lead
concentrations, they will usually not have detectable cognitive
damage, which can be expected to become more apparent at 4 years of
age and later. It seems reasonable to manage children whose blood lead
concentration is 20 micrograms/deciliter or greater at its peak as
having a higher risk of developmental delay and behavior
abnormalities.[16] Because the effects emerge later, after the child's
blood lead concentration will have decreased, the child's record must
be kept open even after the blood lead concentration has decreased.

Although there is not specific literature supporting the use of
enrichment programs in lead-poisoned children, programs aimed at
children with delay from another cause should be effective in lead-
poisoned children.

Recommendations For Pediatricians

Provide anticipatory guidance to parents of all infants and toddlers
about preventing lead poisoning in their children. In particular,
parents of children 6 months to 3 years of age should be made aware of
normal mouthing behavior and should ascertain whether their homes,
work, or hobbies present a lead hazard to their toddler. Inform
parents that lead can be invisibly present in dust and can be ingested
by children when they put hands and toys in their mouths.

Inquire about lead hazards in housing and child care settings, as is
done for fire and safety hazards or allergens. If suspicion arises
about the existence of a lead hazard, the child's home should be
inspected. Generally, health departments are capable of inspecting
housing for lead hazards. Expert training is needed for safe repair of
lead hazards, and pediatricians should discourage families from
undertaking repairs on their own. Children should be kept away from
remediation activities, and the house should be tested for lead
content before the child returns.

Know state Medicaid regulations and measure blood lead concentration
in Medicaid-eligible children. If Medicaid-eligible children are a
significant part of a pediatrician's practice or if a pediatrician has
an interest in lead poisoning, he or she should consider participating
in any deliberations at the state and local levels concerning an
exemption from the universal screening requirement.

Find out if there is relevant guidance from the city or state health
department about screening children not eligible for Medicaid. If
there is none, consider screening all children. Children should be
tested at least once when they are 2 years of age or, ideally, twice,
at 1 and 2 years of age, unless lead exposure can be confidently
excluded. Pediatricians should recognize that measuring blood lead
concentration only at 2 years of age, when blood lead concentration
usually peaks, may be too late to prevent peak exposure. Earlier
screening, usually at 1 year of age, should be considered where
exposure is likely. A low blood concentration in a 1-year-old,
however, does not preclude elevation later, so the test should be
repeated at 2 years of age. Managed health care organizations and
third-party payers should fully cover the costs of screening and
follow-up. Local practitioners should work with state, county, or
local health authorities to develop sensitive, customized questions
appropriate to the housing and hazards encountered locally.

Be aware of any special risk groups that are prevalent locally, such
as immigrants, foreign-born adoptees, refugees, or children whose
parents work with lead or lead dust in their occupation or hobby and,
of course, those who live in, visit, or work on old houses.

In areas with old housing and lead hazards, encourage application for
HUD or other moneys available for remediation.

Keep current with the work of the national Advisory Committee on
Childhood Lead Poisoning Prevention and any relevant local committees.
Although there is now evidence that even lower blood lead
concentrations may pose adverse effects to children, there is little
experience in the management of excess lead exposure in these
children. Although most of the recommendations concerning case
management of children with blood lead concentrations of 15
micrograms/deciliter should be appropriate for children with lower
concentrations, tactics that decrease blood lead concentrations might
be expected to be less and less effective as they are applied to
children with lower and lower blood lead concentrations.

Recommendations For Government

Identify all children with excess lead exposure, and prevent further
exposure to them. The AAP supports the efforts of individual states to
design targeted screening programs, even for Medicaid children.
However, the goal must be to find all children with excess exposure
and interrupt that exposure, not simply to screen less. To do this,
state and local government activities must focus on the children who
are most at risk, which requires more and better data about the
prevalence of elevated blood lead concentrations in specific
communities. Prevalence estimates based on convenience samples or
clinic attendees are not reliable and should not be used as the basis
of policy.

Realize that case-finding per se will not decrease the risk of lead
poisoning. It must be coupled with public health programs including
environmental investigation, transitional lead-safe housing
assistance, and follow-up for individual cases. Lead-screening
programs in high-risk areas should be integrated with other housing
and public health activities and with facilities for medical
management and treatment.

Continue commitment to the Healthy People 2010 goal of eliminating
lead poisoning by 2010. The AAP supports the current plan with
emphasis on lead-safe housing. Continued monitoring and commitment
will be necessary. Research findings on low-cost methods of
remediating housing have become controversial. The federal government
should support impartial scientific and ethical inquiry into the best
way to carry out the needed research.

Minimize the further entry of lead into the environment. Regulations
concerning airborne lead should be enforced, use of lead in consumer
products should be minimized, and consideration should always be given
to whether a child might come into contact with such a product.

Encourage scientific testing of the many simple, low-cost strategies
that might decrease lead exposure. Examples include hand-washing and
use of high chairs. Exploration of innovative, low-technology tactics
should be encouraged, perhaps through the use of special study
sections or review groups. Educational resources for parents and
landlords need to be developed and tested.

Require coverage of lead testing for at-risk children by all third-
party payers by statute or regulation.

Fund studies to confirm or refute the finding that blood lead
concentrations of less than 10 micrograms/deciliter are associated
with lower IQ. The next important step in lead research is conducting
of studies in which confounding by socioeconomic factors is not so
strong. Funding of studies in this area needs to be given high
priority, as was done in the early 1980s when the question of effects
of blood lead concentrations less than 20 micrograms/deciliter was

Gather the nationally representative data necessary for a rational
public health response to the problem of childhood lead poisoning. The
federal government should continue measuring children's blood lead
concentrations in the National Health and Nutrition Surveys to allow
national estimates of exposure and should periodically resurvey
housing to measure progress in the reduction of lead-paint hazards. In
addition, state governments can improve monitoring of trends among
screened children by supporting electronic reporting of blood lead
test results to the CDC.

Committee on Environmental Health, 2004-2005

Michael W. Shannon, MD, MPH, Chairperson Dana Best, MD, MPH Helen Jane
Binns, MD, MPH Janice Joy Kim, MD, MPH, PhD Lynnette Joan Mazur, MD,
MPH William B. Weil, Jr, MD Christine Leigh Johnson, MD David W.
Reynolds, MD James R. Roberts, MD, MPH

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Copyright 2005 by the American Academy of Pediatrics
PEDIATRICS Vol. 116 No. 4 October 2005, pp. 1036-1046