Interpreting and Managing Blood Lead Levels <10 µg/dL in Children and Reducing Childhood Exposures to Lead






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Recommendations of CDC’s Advisory Committee on Childhood
Lead Poisoning Prevention


Please note:

An erratum has been published for this article. To view
the erratum, please click here.


Prepared by


Advisory Committee on Childhood Lead Poisoning Prevention*

The material in this report originated in the National Center for Environmental Health/Agency for Toxic Substances and Disease Registry,
Howard Frumkin, MD, DrPH, Director; and the Division of Environmental and Emergency Health Services, Sharrunda Buchanan, PhD, Director.

Corresponding preparer: Mary Jean Brown, ScD, Division of Environmental and Emergency Health Services, National Center for Environmental
Health/Agency for Toxic Substances and Disease Registry, CDC. Telephone: 770-488-7492; Fax: 770-488-3635; E-mail:
MBrown6@cdc.gov.

Abstract


Lead is a common environmental contaminant, and exposure to lead is a preventable risk that exists in all areas of
the United States. Lead is associated with negative outcomes in children, including impaired cognitive, motor, behavioral,
and physical abilities. In 1991, CDC defined the blood lead level (BLL) that should prompt public health actions as 10
µg/dL. Concurrently, CDC also recognized that a BLL of 10
µg/dL did not define a threshold for the harmful effects of
lead. Research conducted since 1991 has strengthened the evidence that children’s physical and mental development can
be affected at BLLs <10
µg/dL.

This report summarizes the findings of a review of clinical interpretation and management of BLLs <10
µg/dL conducted by CDC’s Advisory Committee on Childhood Lead Poisoning Prevention. This report provides information
to help clinicians understand BLLs <10
µg/dL, identifies gaps in knowledge concerning lead levels in this range,
and outlines strategies to reduce childhood exposures to lead. In addition, this report summarizes scientific data relevant
to counseling, blood lead screening, and lead exposure risk assessment.

To aid in the interpretation of BLLs, clinicians should understand the laboratory error range for blood lead values
and, if possible, select a laboratory that achieves routine performance within ±2
µg/dL. Clinicians should obtain an environmental history on all children they examine, provide families with lead prevention counseling, and follow
blood lead screening recommendations established for their areas. As local and patient circumstances permit, clinicians
should consider early referral to developmental programs for children at high risk for exposure to lead and consider more
frequent rescreening of children with BLLs approaching 10
µg/dL, depending on the potential for exposure to lead, child age,
and season of testing. In addition, clinicians should direct parents to agencies and sources of information that will help
them establish a lead-safe environment for their children. For these preventive strategies to succeed, partnerships between
health-care providers, families, and local public health and housing programs should be strengthened.


Introduction

Lead is a common environmental contaminant, and exposure to lead is a preventable risk in all areas of the
United States. Lead is associated with negative outcomes in children, including impaired cognitive, motor, behavioral,
and physical abilities (1–4). In 1991, CDC defined the blood lead level (BLL) that should prompt public health actions
as 10 µg/dL. Concurrently, CDC also recognized that a BLL of 10
µg/dL did not define a threshold for the harmful
effects of lead (5). Research conducted since 1991 has strengthened the evidence that children’s physical and
mental development can be affected at BLLs <10
µg/dL (1,3).

During 2002–2004, a workgroup of CDC’s Advisory Committee on Childhood Lead Poisoning Prevention
(ACCLPP) reviewed the scientific literature regarding adverse health
effects associated with BLLs <10 µg/dL, including
23 published reports that analyzed 16 separate populations with
Intelligence Quotient (IQ) or general cognitive
index outcomes and 12 publications related to other health outcomes. In its 2005 report, the workgroup concluded that
an inverse association exists between BLLs and cognitive function, with no evidence of a weaker association in
populations

with lower BLLs (1). The direct evidence for this inverse association was strongest in a study conducted in
Rochester, New York, that included children born in 1994 and1995, enrolled at age 6 months, and followed for 5 years
(6). The majority of children studied had BLLs <10
µg/dL throughout the study period. The IQ and blood lead level
relationship was most accurately described by a nonlinear negative association, with a decrease in IQ of more than seven points
over the first 10 µg/dL increase in lifetime average blood lead concentration. On the basis of the evidence, the
workgroup concluded that a causal association between lead exposure and impaired cognitive functioning was most likely.
However, the potential for residual confounding, particularly by social factors, made the strength and shape (i.e., linear
or nonlinear) of this association across BLLs uncertain. In addition, the workgroup concluded that children with BLLs
<10 µg/dL should not be classified as “lead poisoned.” The report noted that no safe level for blood lead in children has
been identified (1).

Two studies published subsequently have reported negative effects of BLLs <10
µg/dL on developmental outcomes
(7,8). One study, which included participants from the Rochester cohort
(6) and from six other past prospective
studies of children with peak BLLs across a range of values, reaffirmed an inverse association between lead at low levels and
IQ (7). In these studies, key potential confounders were accounted for, including maternal IQ, the Home Observation
for Measurement of the Environment Inventory (HOMEI) score (which is a measure of the quality and quantity
of stimulation and support available to a child in the home environment),
maternal education, and birth weight.

Although ACCLPP has previously reviewed case management of children with BLLs
>10 µg/dL (2), this is the
first ACCLPP report to summarize scientific information relevant to clinical management of children with BLLs <10
µg/dL. This report also outlines recommendations from ACCLPP to reduce childhood exposure to lead. Information
on assessing an environmental history and prevention strategies to decrease exposures to lead have been published
previously (2,3) and are not included in this report.


Methods

ACCLPP provides advice and guidance to the U.S. Department of Health and Human Services and CDC
regarding new scientific knowledge and technologic developments and their practical implications for preventing childhood
lead poisoning, and recommends improvements, as needed. ACCLPP members are selected on the basis of their expertise
in childhood lead poisoning prevention, blood lead screening, diagnosis, and medical management. ACCLPP
liaisons represent federal agencies and organizations with particular interest and expertise in childhood lead
poisoning prevention.

In October 2003, ACCLPP formed another workgroup comprising three pediatricians and a CDC health scientist
to review the scientific literature regarding clinical management options for BLLs <10
µg/dL and to outline recommendations for clinical care providers. On the basis of its analysis, the workgroup developed
draft recommendations that were reviewed and later adopted by ACCLPP in February 2006.


Results


Historic Trends in Children’s BLLs in the United States

Since 1976, BLLs in U.S. children aged 1–5 years have
decreased substantially (Table 1), primarily as a result
of policies that have reduced the dispersal of lead into the environment
(9–12). However, many U.S. children continue
to be exposed to lead, primarily in their homes
(13). Overt clinical symptoms of lead intoxication are uncommon in
the United States, and lead evaluation and management strategies typically are intended to reduce the negative effects of
lead on central nervous system development in children who are clinically asymptomatic. Because no safe BLL has
been defined (1),small reductions in population-level exposures to lead will likely affect substantial numbers of children,
and can be expected to reduce the number of children affected by adverse health outcomes associated with lead
exposure (14).


Blood Lead Measurements

As with any biologic test, blood lead measurements entail inherent uncertainties as a result of imprecise
analytic techniques and preanalytic variables (e.g., the specimen collection process). However, the ratio of imprecision
to measurement value, particularly at BLLs <10
µg/dL, is relatively high. The degree of inherent error in blood lead
analysis varies by analytic methodology used, but whichever method is used, laboratory performance depends on the
procedures and skills of the laboratory team
(15,16). Federal regulations allow laboratories that perform blood lead testing
to operate with a total allowable error of ±4
µg/dL or ±10%, whichever is greater. Consequently, at BLLs
<10 µg/dL, a laboratory might operate within an error range of 8
µg/dL and still meet federal proficiency standards. For example,
an actual value of blood lead at 7 µg/dL could be reported as being any value ranging from 3
µg/dL to 11 µg/dL and
still remain within the allowable error limit. A study of duplicate testing of identical blood samples (all with a mean
blood lead value <10 µg/dL) at eight laboratories reported all results as <10
µg/dL and within 3 µg/dL of the overall mean
for that specimen value (17). A study conducted in 2006 indicated that the majority of blood lead laboratories can
achieve routine performance of ±2
µg/dL at concentrations of <10
µg/dL without difficulty (18).

Blood lead test reliability also depends on adhering to blood collection techniques that reduce sample
contamination. Collection of capillary blood from a fingerstick into a lead-free collection device is an accepted method for obtaining
a screening test (19–23) and contamination by lead from the skin surface can be minimized if a protocol for
proper capillary specimen collection is followed
(24).† However, because lead levels from a capillary blood sample will vary
from those of a simultaneously drawn venous sample, elevated capillary
results should be confirmed with blood drawn by venipuncture. Multiple studies have reported on the uncertainty introduced by collecting capillary blood rather
than venipuncture at thresholds of 10
µg/dL or 15 µg/dL
(19–23), but none has examined the sensitivity or specificity
of capillary methods at thresholds <10
µg/dL.


Children’s BLL Patterns

BLLs increase quickly after an acute exposure, then gradually (over weeks) reach equilibrium with body stores of
lead. Lead is distributed unevenly within the human body; in children, approximately 70% is stored in the
bone compartment (25–27). The residence time of lead in bone can be decades
(28). Thus, an elevated BLL will decline within a few weeks to months after an acute exposure. However, for those children with chronic lead exposure
and, presumably higher bone lead stores, the decline in BLL can take much longer
(29). Although bone lead levels can provide information regarding past absorption of lead, measurements of lead in bone using X-ray
fluorescence instruments are available for research
purposes only.

A newborn infant’s BLL closely reflects that of the mother
(30). During 1999–2002, the geometric mean BLL
for U.S. women aged 20–59 years was 1.2
µg/dL, with 0.3% having a BLL
>10 µg/dL (12). Typically, as infants
become more active and increase their environmental exposures, BLLs increase. Longitudinal studies of lead-exposed
children have confirmed an increase in BLLs beginning in late infancy, with a peak level reached at age 18–36 months
(6,31–33). No studies have examined blood lead patterns specifically for children with peak levels <10
µg/dL, although certain studies have included children with levels this low. A study of children born during 1994–1995 in which >50% of
the children had peak BLLs <10 µg/dL reported an expected pattern in mean BLLs of
3.4 µg/dL at age 6 months, 9.7
µg/dL at age 24 months, and 5.8
µg/dL at age 61 months (6). A study of children born in
Boston during 1979–1981 identified mean BLLs of 7.2
µg/dL at birth, and subsequent BLLs in these children remained relatively constant (6.2
µg/dL at age 6 months, 6.8
µg/dL at age 24 months, and 6.4
µg/dL at age 57 months) (34–36). In both studies,
higher levels of lead in home environmental samples were associated directly with higher BLLs in children
(35,37). In addition, the Boston study demonstrated an association between the occurrence of home renovation and
increased BLLs (35). The blood lead pattern for individual children with BLLs <10
µg/dL varies depending on their environmental
exposures (29). More research is needed to better understand age-related patterns for BLLs that remain
<10 µg/dL. However, in

clinical practice, even should additional research data become available, laboratory uncertainty might interfere with
a clinician’s ability to detect patterns for individual children.

Once a high BLL has been established in a child, the time required for the BLL to decline to <10
µg/dL can range from months to years, depending on the duration and dose of
exposure. For example, for a group of children starting at
a BLL of 10–14 µg/dL and receiving case management services, the mean time required for 50% to achieve a BLL <10
µg/dL was 9 months (38). How much time is needed for BLLs
<10 µg/dL to decline in response to interventions
is unknown.

Multiple studies have confirmed that blood lead measurements vary seasonally. For example, a study conducted
in Boston reported that BLLs were highest in late June and lowest in March
(39). A Milwaukee study indicated that BLLs were higher in the summer than in the winter
(40). Some of the variability (higher blood lead in summer) might
result from increased exposure to lead in dust and soil in summer months
(41). Blood lead values for urban children
are predicted to be 1–2 mg/dL higher in the summer than winter months
(42).


Association of BLL Patterns with Developmental Outcomes

Although BLLs peak in early childhood, when young children are especially vulnerable to lead, negative effects
are associated with lead exposure at any age. Multiple studies have examined the effects of lead on children’s
development outcomes; in these studies, the ages at which BLLs were measured varied, as did the range of ages over which BLLs
were averaged (1–4). Statistically significant associations have been identified between average BLLs over a specific
period (e.g., 0–5 years) and various adverse health outcomes
(6,43–45); other studies have reported statistically
significant associations with a single lead measurement at a specific age (e.g., prenatal, 24 months, and 6.5 years) or with a
peak measurement (6,31,46). Concurrent BLLs (i.e., those measured close to the time of neurodevelopmental testing)
might demonstrate stronger associations with neurodevelopmental abilities than other blood lead measures
(6–8,32,47).

Lead has a continuing negative association with IQ as children reach elementary school age. For children
who participated in a trial of chelation therapy, a subsequent data analysis indicated that BLLs measured concurrently
with developmental testing were associated more closely with children’s cognitive abilities than was a peak level
at approximately age 2 years (48). This association was stronger when children were tested at age 7 years than at age
5 years, which underscores the continuing need to reduce lead exposures after age 5 years.


Strategies to Enhance Children’s Positive Developmental Outcomes

Although lead is a risk factor for developmental and behavior problems, its presence does not indicate that
these problems will necessarily occur. No characteristic developmental pattern is attributable solely to the effects of lead,
and measures of the effects of lead on children are imperfect. Thus, for an individual child, neurobehavioral test
performance might indicate clinically-significant impairments related to lead
exposures but might not fully capture the array of negative outcomes caused by lead
(14). The effects of lead at levels approaching 10
µg/dL might not be recognizable to either the child’s family or clinician or be identified through neurobehavioral testing. However, lead exposure
might assume greater importance for children with other environmental,
genetic, biologic, social, or demographic developmental risks factors. Effects of exposures to lead at lower levels might not be evident in testing of
individual children but are best evaluated on a communitywide basis
(14).

Multiple factors influence a child’s development, including how the child is treated by parents or other
adult caregivers. The child’s family and personal psychosocial experiences are strongly associated with performance
on neurodevelopment measures and account for a greater proportion of the explained variance in these measures than
BLLs <10 mg/dL(2,43,45,49). A child’s blood lead measurement is estimated to account for 2%–4% of variance
in neurodevelopment measures (approximately 4%–8% of the explained variance)
(2,43,50).

All children benefit from parental nurturing, regardless of their BLL. For example, a child’s language skills
are enhanced by the amount of language addressed to the child (more is better), combined with a predominant pattern
of positive feedback (51). This pattern of parenting of children under age 3 years has been associated with
enhanced language and cognitive skills when children were tested in the third grade
(52). Thus, parents might help counteract
the negative effects of lead by providing a nurturing and enriched environment during development. Studies to
examine

effects of lead have attempted to control for this psychosocial factor by including measures such as the HOMEI
score (7). Although no studies have specifically evaluated the effects of early intervention programs on cognitive or
behavioral outcomes in relationship to children’s BLLs, several laboratory studies that applied a nurturing environment to
very young animals during lead acquisition demonstrated the beneficial effect of the social environment on ameliorating
lead-related negative developmental outcomes
(53,54).

Early enrichment programs, although not tested specifically in relation to BLLs, have been effective in
improving cognitive development and social competence of young children, particularly infants from families with low levels
of social or economic resources (55). Research demonstrates that children whose development has been delayed or who
are at high risk for delay benefit most from interventions applied at an early age
(56–58).


Strategies to Prevent and Reduce Exposure to Lead

CDC and the American Academy of Pediatrics (AAP) recommend that preventive care for every child should
include obtaining an environmental history and identifying occupational lead exposure of household members
(2,3,5). The major sources of lead exposure among U.S. children are lead-contaminated dust, deteriorated lead-based paint, and
lead-contaminated soil (37,59). Typically, lead contamination of water contributes less to a child’s lead burden than
home and soil sources (59); however, if additives to water (e.g., those used in disinfection processes), are changed,
the contribution of lead contamination might be greater
(60). The extent of lead paint hazards (i.e., the presence of lead
in an accessible condition, such as deteriorated lead-based paint or
lead-contaminated dust or soil) on interior and
exterior surfaces and in soil is associated with increased BLLs in children
(59). Children also are exposed to nonhousing
lead sources (e.g., lead in foods, cosmetics, pottery, folk remedies, and toys)
(2,3,61).


Home-Related Lead Exposure

An estimated 4.1 million homes in the United States (25% of U.S. homes with children aged <6 years) have a
lead-based paint hazard (13). An estimated 68% of U.S. homes built before 1940 have lead hazards, as do 43% of
those built during 1940–1959 and 8% of those built during 1960–1977; estimates are higher for homes in the
Northeast and Midwest and for homes in which young children reside
(13). Despite considerable attention and resources
from federal, state, and local agencies and advocacy groups, publicly available funding has not been able to provide
sufficient resources to eliminate all lead paint hazards from U.S. homes. Publicly funded home inspections are most often
limited to homes of children with elevated BLLs; the blood lead threshold value that prompts an inspection varies by state
or municipality (62). In addition, even when a child’s elevated BLL triggers an inspection, public funding for repairs
to reduce or eliminate identified lead hazards typically is not available.

Since 1991, lead-hazard–control grant programs through the U.S. Department of Housing and Urban
Development’s (HUD) Office of Healthy Homes and Lead Hazard Control (OHHLHC) have provided funding for local and
state agencies to reduce lead and other environmental hazards in privately owned low-income housing. In 2005,
OHHLHC allocated $139 million for this purpose, administered through seven different grant types. Other federal
programs provide funding to eliminate lead-based paint hazards in federally
assisted housing. Typically, the focus of these programs is on housing rehabilitation and activities that remediate lead hazards after children are identified
with elevated BLLs, but HUD-funded local programs also now include primary prevention interventions that control
or eliminate lead before children are exposed.

CDC is working with HUD, the U.S. Environmental Protection Agency (EPA), state and local health department
lead poisoning prevention grantees, and child health and environmental justice advocates to promote primary
prevention strategies to reduce exposure to lead
(1,63,64). In addition to their traditional role of providing services to children
with elevated BLLs, CDC-funded state and local lead poisoning prevention programs have been charged with
implementation of housing-based primary prevention strategies in their jurisdictions. This moves beyond their traditional role
of providing services to children with elevated BLLs and involves developing responses to local risks and a focus
on identifying and remediating housing-based lead hazards. ACCLPP recommendations for essential elements for state
and local primary prevention plans have been published previously
(63), and strategies that have been implemented at
the state and local levels to address the problem also have been outlined previously
(64). As ACCLPP noted, implementation of state and local primary prevention plans will require 1) targeting the highest risk areas, populations, and activities;
2)

fostering political will for jurisdictions to provide an adequate level of funding; 3) expanding resources for
housing remediation; identification and correction of lead hazards; and 4) establishing a regulatory infrastructure to create
and maintain lead-safe housing and to support the use of lead-safe construction work practices
(63,65). Links to state and local health department web sites, which include their primary prevention plans, are available at
http://www.cdc.gov/nceh/lead/grants/contracts/CLPPP%20map.htm.

Certain state and local health departments initiate case management services and home inspections when BLLs
reach 10 mg/dL. As more primary prevention strategies are implemented, the number of health departments pursuing
home inspections when BLLs reach 10 µg/dL will likely increase. Certain communities have developed online registries to
help parents identify homes that are lead-safe or that have lead
hazards (66).


Steps to Identify and Safely Reduce Lead-Based Paint Hazards in Homes

Lead-based paint hazards in homes are important sources of lead exposure. Preventive actions can be implemented
to identify and address these hazards. Tenants can request a copy of all lead testing reports for housing sites from
landlords at any time. Their landlord should have been provided with such information when they purchased the
building; compliance with a tenant request for a copy of all lead testing reports is required by federal law
(67). In addition, federal regulations require sellers and landlords 1) to disclose the possible presence of lead-based paint in any
pre-1978 property and 2) to provide information on known lead-based paint and lead-based paint hazards at the time
final agreements are signed on the purchase or rental of most housing built before 1978 (e.g., by providing results of any
past evaluations of the property for lead)
(67). Prospective buyers or renters have the opportunity to arrange for a
lead inspection or risk assessment by a qualified professional at their own expense; buyers have up to 10 days to check
for lead. Further, the law requires sellers, landlords, and renovators to provide buyers, renters, and those hiring
renovators with an EPA-approved pamphlet, “Protect Your Family from Lead in Your Home”
(68). To protect their children from lead, parents might choose not to buy or rent a property or to negotiate remediation of identified lead hazards.
However, landlords or homeowners might not know whether their property has any lead-based paint or lead
hazards.

Lead-based paint hazards are likely to be present in older homes; all homes built before 1978 should be
presumed either to have a lead hazard present or to contain intact lead-based paint unless a licensed lead inspector has
determined otherwise. Lack of a deteriorated surface decreases the likelihood of lead-contaminated dust being present but does
not ensure its absence. Knowledge of general characteristics of lead-based paint and lead-based paint hazards and
their control might help parents to understand their home better (Box)
(69–73).

Screening for lead dust hazards through dust wipe testing (i.e., standardized collection of dust by wiping surfaces
and measurement of lead collected) can help identify areas of concern. Because lead is not distributed uniformly within
a home, wipe testing neither ensures absence of lead hazards at locations in the home that were not tested, nor does
it ensure future protection from lead dust hazards if lead-painted surfaces subsequently deteriorate or are
disturbed. Potential sources of future contamination include lead-containing paint on areas disturbed by impact/friction
(e.g., windows, doors, and floors) and the interior migration of lead-contaminated exterior dust and soil
(70). However, identifying lead dust hazards in the home is a first step toward protecting children and might help parents lower
lead dust levels in their homes (74). Proper training is recommended for those collecting dust wipes to focus tests on areas
at highest risk (63). Parents or property owners who wish to perform dust wipe sampling may consult their local health
or housing departments for advice regarding sampling procedures, interpretation of
results, and further actions based on results.

For a lead-safe environment to be established in older buildings, repair of lead hazards and careful attention
to maintenance is necessary. However, local ordinances typically do not require action until a child’s BLL is elevated,
and property owners might be unaware of lead hazards or ignore them. Primary prevention is possible only if the focus
on safety in older housing is increased and lead hazards are repaired proactively before a child is exposed. In all
pre-1978 properties, owners should use lead-safe work techniques when implementing routine maintenance to decrease
the likelihood of lead hazards developing in a home.

Home renovation or repair is known to be a risk factor for increasing or elevated BLLs, principally through
exposures to the dust residue generated during the work
(35,75–77). All contractors who perform repair and renovation work
in older housing should be trained in lead-safe work practices and comply with any state and local requirements
governing work with lead paint hazards (78). Property owners doing work themselves should seek expert advice and training
to

protect themselves and their families
(79,80). Lead-safe work practices include 1) relocating families when the
work warrants, 2) minimizing the amount of dust created, 3) containing dust in the work area, 4) cleaning up completely,
5) disposing of waste safely, and 6) performing clearance testing (i.e., testing of dust for lead after site clean up) to
ensure that residual lead levels do not exceed EPA standards
(81). Families with young children should be restricted from
work areas until clearance testing has been performed and the area has been judged safe.

In previous evaluation studies, lead dust clearance standards were not low enough to protect children from
increased exposures to lead-contaminated dust after lead hazard remediation; as a result, after home repairs, BLLs of children
with preremediation BLLs <25 µg/dL increased
(82). In 2001, the EPA’s lead dust clearance standards were lowered to 40
µg/ft2 for floors, 250
µg/ft2 for windowsills, and 400
µg/ft2 for window wells
(81). No studies have evaluated if these
lower clearance levels protect children whose BLLs are <10
µg/dL adequately from ongoing lead exposure. A
cross-sectional study estimated that 20% of children with a current exposure to floor dust-lead at 40
µg/ft2 will have BLLs
>10 µg/dL (83).

A study conducted in 1994–1999 in 14 U.S. cities involving 2,682 pre-1978 homes demonstrated reductions in
lead dust levels and fall in children’s BLLs when lead-safe work practices were used during remediation efforts
(69,84,85). The study applied lead dust clearance standards substantially less stringent than those currently in place,
although clearance floor dust lead levels were generally low (geometric mean:
16 µg/ft2) (86). However, among the 869
children in this study who were tested within 4 months before home lead remediation and approximately 7 weeks
after remediation, 81 (9.3%) had a clinically significant increase
(>5 µg/dL) in BLLs; infants, children of
less-educated mothers, and children from homes with higher numbers of preintervention exterior lead hazards were at highest
risk (87). Dust lead levels at clearance were not associated significantly with an increase in BLLs. The study listed
multiple types of exposures (e.g., other homes, parental job exposures) that might have accounted for increasing BLLs, but
these were not evaluated systematically. Although lead remediation work reduced overall lead dust and BLLs, the finding
that >9% of children had a rise in BLL of
>5 µg/dL underscores the need to maintain a high level of vigilance to ensure
that children are protected when homes or apartments undergo renovation and repair.


Educational Strategies

Lead exposure prevention strategies for children with BLLs <10
µg/dL typically focus on education and promotion
of home cleanliness, without further identifying lead hazards or repairing them. Providing low-income parents with
lead-related education via video in a pediatric office has been demonstrated to be effective in increasing knowledge
and parental report of compliance with lead prevention actions in the home
(88). No studies have evaluated
office-based education with accompanying in-home strategies or used children’s BLLs as the outcome measure for an
office-based education strategy.

Studies of children at high risk that applied intervention strategies in the home or community have demonstrated
the failure of education and nonprofessional cleaning conducted alone (i.e., in the absence of other measures to reduce
lead exposure) in preventing the development of BLLs
>10 µg/dL (2,89–91). Few studies have applied prospective
designs that included control groups. One study indicated that a highly intensive education program starting at birth
and lasting for >3 years (28 sessions) delivered by community members lowered the risk of BLLs >10
µg/dL 34%, but this result was not statistically significant
(92). Repeated in-home lead prevention education, even when accompanied
by complimentary supplies of cleaning materials, was ineffective in lowering the incidence of elevated BLLs
(93,94). A review of four studies
(90) involving caregiver education
(94,95) and professional house cleaning
(96,97) indicated that such low-cost interventions reduced the overall proportion of children with BLLs
>15 µg/dL or >20
µg/dL, but the effect on mean BLLs was not statistically significant (p>0.05).

Intensive cleaning regimens reduce lead levels; in one study, biweekly professional cleaning resulted in a 17%
decrease in mean BLLs after 1 year (96). However, the benefit of such intense and repeated cleaning was limited to
homes without carpets (98). Intense cleaning can be used without subjecting children to a risk for increased lead exposure
from unsafe repair methods (i.e., those not in compliance with lead-safe work practices). A single intensive cleaning alone
does reduce levels of lead in dust by 32% to 93% depending on surface tested and starting lead concentration
(99), but reaccumulation occurs within 3–6 months
(100,101).

A study that involved children with BLLs 15–19
µg/dL compared the effects of nurse home visits (five visits during
1 year) accompanied by lead dust tests with those of usual care (one or two visits by an outreach worker during 1
year)

(74). After 1 year, dust lead levels were significantly lower (p<0.05) in homes where lead dust tests had been
conducted during intervention than in usual care homes. This finding suggests that dust testing might help parents
better understand lead hazards and take action to lower them. However, changes in dust lead were not mirrored by changes
in BLLs in this group of children with elevated BLLs.


Blood Lead Screening Strategies

CDC (102) and AAP (3) have recommended that health-care providers conduct blood lead tests on children
enrolled in Medicaid and those identified as being at risk on the basis of the state or local screening plan or the risk
assessment process. Federal policy requires that all children enrolled in Medicaid receive screening blood lead tests at ages 12
and 24 months and that blood lead screening be performed for children aged 36–72 months who have not been
screened previously (103). Despite this, blood lead screening rates for Medicaid children have been low (<20%)
(104) and in certain areas remain at approximately 20%
(105). In 1997, CDC requested state and local health officials to use
local communitywide data (e.g., BLL prevalence, housing age, and poverty status) to develop plans for blood lead
screening for their jurisdictions and provide them to clinicians
(102). These plans recommend either universal or targeted
blood lead screening. State and local screening plans are available at
http://www.cdc.gov/nceh/lead/grants/contacts/CLPPP%20Map.htm.

Targeted screening strategies enable clinicians to assess risks for individual children and recommend blood lead
testing for a subset of children in the jurisdiction thought to be at
increased risk for lead exposure. CDC recommends that
risk evaluations be conducted on the basis of such factors as residence in a geographic area, membership in a group at
high risk, answers to a personal-risk assessment questionnaire (which might include local factors such as cultural practices
or products, such as herbal remedies, traditional cosmetics or imported spices), or other risk factors relevant to
the jurisdiction (102).

CDC recommends that locally developed targeted risk
assessment and blood lead screening strategies be applied
at ages 1 and 2 years (102). Children aged 36–72 months who have been identified as being at risk and who have
not been screened previously also should receive a blood lead test
(102). For clinicians in areas that lack a state or
local screening plan, CDC recommends that a blood lead test be performed on all children at ages 1 and 2 years and
on children aged 36–72 months who have not been screened previously
(102).

Because lead exposures might change with a child’s developmental progress (e.g., walking or reaching window sills)
or as a result of external factors (e.g., family relocation or home remodeling), two routine screenings are recommended
(at approximately ages 1 and 2 years). Among children in Chicago at high risk with BLLs <10
µg/dL at age 1 year, 21% had a BLL of
>10 µg/dL when tested again at age
>2 years (103). This report does not change current
CDC recommendations in ages for routine blood lead testing. However, certain
local health departments (e.g., those in Chicago, Illinois; New York, New York; and Philadelphia, Pennsylvania) recommend blood lead screening at
younger ages or more frequently (106–108). For example, these departments recommend BLL testing starting at ages
6–9 months in high risk areas, blood lead testing at more frequent intervals (e.g., every 6 months) for children aged <2
years, or the provision of additional education and more rapid follow-up blood lead testing for children aged <12 months
with BLLs 6–9 µg/dL.


Personal Lead Risk Assessment Questionnaires

The effectiveness of personal risk assessment questionnaires in identifying children with elevated BLLs has
been documented in the scientific literature (Table 2)
(109–125). However, no studies have evaluated the performance
of these questionnaires at cut-off levels <10
µg/dL or their effectiveness in directing counseling or in identifying
lead hazards in the home. When applied in consecutive samples of patients in clinical settings, the sensitivity of
such questionnaires to identify children with BLLs
>10 µg/dL varies considerably by population
(109–128). In certain studies, the sensitivity
improved if higher cut-off levels were used in the analysis
(103,115,119,120) or if the questions used were developed
specifically for the population tested
(113,116,117,119,120,122). In general, to
identify approximately 80% of children with BLLs
>10 µg/dL, a blood test had to be performed for more than half of
those

children whose risk factors for lead exposure were assessed using a questionnaire. Multiple studies in populations
with low (109,110,112–114, 127,128) or high
(123,124) prevalence for elevated BLLs concluded that risk
assessment questionnaires were not effective in their clinical settings.


Future Research Needs

Further study is needed to assess the effects of BLLs <10
µg/dL on children. Such research will entail following
large and diverse populations, with careful attention to potential confounders and measurements of social factors.
Additional research also is needed to evaluate the effectiveness of strategies to lower exposures to lead. This should include
research on the effectiveness of strategies applied in the medical office and home and those that provide interventions
through medical, public health, and environmental means.

Blood lead screening strategies should be evaluated to
determine the most appropriate ages for screening and
the utility of screening strategies applied at the community level. Evaluations of lead surveillance strategies should test
ways to identify changing patterns of environmental risks and subpopulations exposed to established and emerging sources
of lead. In addition, better ways should be identified to alert public and clinical health-care professionals of changes
in exposure sources and patterns and to enhance their response to such changes by increased surveillance and blood
lead monitoring of populations identified as being at increased risk for exposure. Additional studies might provide data
that can be used to improve laboratory methods and performance monitoring. This will require developing criteria to
evaluate individual laboratories and mechanisms to provide this information to clinicians.


Summary of Recommendations


For Clinicians

  • Provide anticipatory guidance to parents of all young children regarding sources of lead and help them
    identify sources of lead in their child’s environment. Obtain an environmental and family occupational history and
    educate parents about the most common sources of childhood lead exposure for their child and in their
    community. Encourage parents to identify lead hazards and sources in their homes and reduce their child’s potential
    for exposure to lead, including the safe implementation of control measures before BLLs increase. Warn parents
    about the dangers poised by unsafe renovation methods and to be cognizant of the possibility of new and
    reemerging sources of lead in children’s environments. Direct parents to local, state, and federal agencies and organizations
    for information, particularly concerning methods to identify and safely repair lead hazards (Appendix).
  • Help parents to understand the uncertainty of a blood lead value and potential reasons for its
    fluctuation, including error introduced by the sampling methods and laboratory-, age-, and season-related exposures.
  • Assess all children for developmental and behavior status and seek further evaluation and therapy to
    reduce developmental or behavioral problems, as necessary. Consider the potential influences of lead when
    conducting developmental screening. For children with multiple developmental risk factors, which might include
    lead exposures, consider more frequent developmental surveillance or conduct more extensive developmental evaluations.
  • Discuss with parents the potential impact of lead on child development and promote strategies that foster
    optimum development, including encouraging parents to influence their child’s development positively by
    providing nurturing and enriching experiences. For all children from economically and socially low-resource families living
    in areas where exposure to lead is likely, promote participation in early enrichment programs regardless of the
    child’s BLL.
  • Whenever possible, utilize laboratories that can achieve routine performance of ±2
    µg/dL for blood lead analysis. Evaluate laboratory performance by reviewing the laboratory’s quality control chart or statistical
    quality control summary.
  • Review office procedures and policies to ensure that lead exposure risk assessment or blood lead screening
    is performed on all children as required by state or local health officials or as recommended by CDC. Consider
    the child’s age, season of testing, and exposure history when deciding when to obtain follow-up blood lead tests. For
    a child whose BLL is approaching 10 µg/dL, more frequent blood lead screening (i.e., more than annually) might
    be appropriate, particularly if the child is aged <2 years old, was tested at the start of warm weather when BLLs tend
    to increase, or is at high risk for lead exposures.
  • Perform a diagnostic blood lead test on all children suspected of having lead exposure or an elevated BLL
    and institute the recommended management guidelines if a child’s BLL increases to
    >10 µg/dL.
  • Become informed about lead exposure prevention strategies of local or state health departments and partner
    with public health agencies, community groups, and parents to work toward establishing lead-safe environments
    in homes and schools for all children and the reduction of exposure to lead from all sources. Advocate for
    the expansion of services that foster lead poisoning primary prevention.


For Government Agencies

  • Increase efforts to resolve lead-based paint hazards safely before children are exposed.
  • Expand services that promote lead poisoning primary prevention and develop systems that enable clinicians
    and parents to learn about such services.
  • Develop and implement strategies to encourage the safe elimination of lead hazards in properties using
    trained workers and lead-safe work practices, in compliance with federal, state, and local regulations.
  • Establish jurisdictional policies that mandate ensuring lead safety in housing and enforce these mandates.
  • Develop and apply systematic approaches to prevent
    exposures to even small amounts of lead in food or
    consumer products, particularly when safer alternatives are available.
  • Promote implementation of state and local primary prevention plans that target areas, populations, and activities
    of highest risk; foster political will; expand resources for housing remediation; identify and correct lead hazards;
    and establish a regulatory infrastructure to create and maintain lead-safe housing and support the use of
    lead-safe construction work practices.
  • Expand the availability of and promote the use of early enrichment programs for all children from economically
    and socially low-resource families living in areas where exposure to lead is likely.
  • Promote and fund research that will further evaluate the effects of lead in blood at levels <10
    µg/dL and evaluate strategies to identify and reduce exposure or the potential for exposure to lead, including strategies applied
    in medical offices and in homes.


Acknowledgment

Helpful suggestions were provided by Patrick J. Parsons, PhD, Lead Poisoning/Trace Elements Laboratory, Wadsworth Center, New
York State Department of Health, Albany, New York.

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* A list of members of this committee appears on
page 16 of this issue.

† A complimentary video or DVD entitled, “CDC Guidelines for Collecting and Handling Blood Lead Samples—2004,” may be obtained from the
National Center for Environmental Health, Division of Laboratory Sciences, Lead and Multielement Proficiency Program at e-mail ncehdls@cdc.gov.

Advisory Committee on Childhood Lead Poisoning Prevention

Membership List, October 2004–February 2006

Chairperson: Carla Campbell, MD, Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania.

Executive Secretary: Mary Jean Brown, ScD, Division of Environmental and Emergency Health Services/Agency for Toxic Substances and
Disease Registry, National Center for Environmental Health, CDC, Atlanta, Georgia.

Members: Magaly C. Angeloni, MBA, Rhode Island Department of Public Health, Providence, Rhode Island; Valerie Charlton, MD,
California Department of Health, Richmond, California; Walter S. Handy, Jr., PhD, Cincinnati Health Department, Cincinnati, Ohio; Ing Kang Ho,
PhD, University of Mississippi Medical Center, Jackson, Mississippi; Valarie Johnson, Urban Parent to Parent, Rochester, New York; Linda Kite,
MBA, Healthy Homes Collaborative, Los Angeles, California; Jessica Leighton, PhD, New York City Department of Health and Mental Hygiene, New
York City, New York; Sally Odle, SafeHomes, Inc., Waterbury, Connecticut; George G. Rhoads, MD, University of Medicine and Dentistry of
New Jersey, Piscataway, New Jersey; Catherine M. Slota-Varma, MD, Medical College of Wisconsin, Milwaukee, Wisconsin; Wayne R. Snodgrass,
MD,

PhD, University of Texas Medical Branch, Galveston, Texas; Kevin U. Stephens, Sr., MD, JD, New Orleans Department of Health, New
Orleans, Louisiana; Helen J. Binns,* MD, Feinberg School of Medicine, Northwestern University, Chicago, Illinois; Kimberly M.
Thompson,† ScD, Harvard University, Boston, Massachusetts.

Nonvoting Federal Members: Phyllis Stubbs-Wynn, MD, Maternal and Child Health Bureau, Health Resources and Services
Administration, Washington, DC; Michael Bolger, PhD, U.S. Food and Drug Administration; Washington, DC; John Borrazzo, PhD, U.S. Agency for
International Development, Washington, DC; David
Jacobs,§ PhD, U.S. Department of Housing and Urban Development, Washington, DC; Warren
Friedman, PhD, U.S. Department of Housing and Urban Development, Washington, DC; Jacqueline E. Mosby, MPH, U.S. Environmental Protection
Agency, Washington, DC; Walter Rogan, MD, National Institute of Environmental Health Sciences, Washington, DC; Robert J. Roscoe, MS,
National Institute for Occupational Safety and Health, CDC, Cincinnati, Ohio; Lori E. Saltzman, MS, U.S. Consumer Product Safety
Commission, Washington, DC; Jerry Zelinger, MD, Center for Medicare and Medicaid and Services, Washington, DC.

Nonvoting Liaison Representatives: Steve M, Hays, American Industrial Hygiene Association, Nashville, Tennessee; Ezatollah Keyvan-Larijani,
MD, DrPH, Council of State and Territorial Epidemiologists, Baltimore, Maryland; Pat
McLaine,¶ MPH, National Center for Healthy Housing,
Columbia, Maryland; Jonathan Wilson, MPP, National Center for Healthy Housing, Columbia, Maryland; Benjamin Gitterman, MD, American Public
Health Association, Washington, DC; Routt Reigart II,** MD, American Academy of Pediatrics, Charleston, South Carolina; George C. Rodgers, Jr.,
MD, PhD, American Association of Poison Control Centers, Georgetown, Indiana; Jan Towers, PhD, American Academy of Nurse Practitioners,
Gettysburg, Pennsylvania; Anne M Guthrie, MPH, Alliance for Healthy Homes, Washington, DC; Calvin B. Johnson, MD, American State and Territorial
Health Officials, Harrisburg, Pennsylvania.

* Member 2002–2004.
.

† Member 2002–2005.

§ Member 1996–2004.

¶ Representative 1998–2005.

** Representative 1997–2004.

Table 1Table 1

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Table 2Table 2

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BoxBox 3

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Date last reviewed: 10/10/2007




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