23.  Screening for Elevated Lead Levels in Childhood and Pregnancy

RECOMMENDATION

Screening for elevated lead levels by measuring blood lead at least once at

age 12 months is recommended for all children at increased risk of lead

exposure. All children with identifiable risk factors should be screened,

as should all children living in communities in which the prevalence of

blood lead levels requiring individual intervention, including residential

lead hazard control or chelation therapy, is high or is undefined (see

Clinical Intervention). Evidence is currently insufficient to recommend an

exact community prevalence below which targeted screening can be

substituted for universal screening. Clinicians can seek guidance from

their local or state health department. There is insufficient evidence to

recommend for or against routine screening for lead exposure in

asymptomatic pregnant women, but recommendations against such

screening may be made on other grounds. There is also insufficient

evidence to recommend for or against counseling families about the

primary prevention of lead exposure, but recommendations may be made on

other grounds. Recommendations regarding the primary prevention of lead

poisoning by population-wide environmental interventions are beyond the

scope of this chapter. 

Burden of Suffering

Prevalence.  The prevalence of elevated blood lead levels in the U.S.

population has declined 78% in the past decade,1 due primarily to marked

declines in lead in gasoline, soldered cans, and air.1-6 In a 1988-1991

national survey of children aged 1-5 years, 9% and 0.5% had blood lead

levels 10 mg/dL and 25 mg/dL, respectively, down from 88% and 9% a

decade before.7 (The units mg/dL will be used throughout this chapter; to

convert to mmol/L, divide by 20.72.) Prevalence varies widely among

different communities and populations, however, with studies reporting

2-41% of children having blood lead levels 10 mg/dL, 0-3% 25 mg/dL,

and 0-0.5% 40 mg/dL.8-19 Current national data for pregnant women have

not been published, but only 0.5% of U.S. women aged 12-49 years of age

have blood lead levels 10 mg/dL.7 Two large surveys of low-income

pregnant women found 0%20 and 6%21 with blood lead levels >15 mg/dL.

Risk Factors for Elevated Lead Levels.  The highest mean blood lead levels

in the U.S. occur in children aged 1-2 years (mean 4.1 mg/dL) and in adults

50 years of age (4.0 mg/dL), with the lowest in adolescents (1.6 mg/dL).7

Among adults, geometric mean levels are significantly higher in males

than in females. Correlates of higher blood lead levels at all ages include

minority race/ethnicity, central city residence, low income, low

educational attainment, and residence in the Northeast region of the

U.S.7,22 These factors are associated with increased exposure to

important lead sources, including dilapidated, pre-1950 housing with

lead-based paint, lead-soldered pipes and household lead dust; and lead in

dust and soil from heavy traffic and industry.22-27 Other potential

sources of household lead exposure include clothing or waste material

brought home by workers in lead-based industries or hobbies, lead-based

paint and dust contamination in pre-1950 housing that is undergoing

remodeling or renovation, dietary intake from lead-soldered cans and

lead-based pottery, and traditional ethnic remedies.23,24,28

Neurotoxic Effects of Lead Exposure in Children.  Very high levels of

inorganic lead exposure can produce serious neurologic complications,

which may result in death or long-term sequelae.23 A growing number of

studies have reported associations between neurotoxic effects and blood

lead levels once thought to be harmless. Adequately designed and

conducted prospective cohort studies from a broad range of child

populations have reported that a rise in blood lead from 10 to 20 mg/dL is

associated with a likely decrement of about 2 points (reported range -6 to

+1) in intelligence test scores (IQ).29-35 In these studies, the mean blood

lead levels at age 1-2 years (7.7-35.4 mg/dL) were higher than the current

U.S. mean for this age group (4 mg/dL), but most levels were below 35

mg/dL. A meta-analysis36 that included the five oldest of these cohort

studies concluded that a doubling of blood lead levels from 10 to 20 mg/dL

measured at age 2 years was associated with a statistically significant

mean reduction of 1-2 IQ points; evidence was inconclusive regarding an

association of IQ with mean postnatal blood lead levels. Although most

cross-sectional studies evaluating the association of tooth and blood lead

with IQ suffer from methodologic problems such as selection bias and

limited adjustment for covariates, they have been generally consistent in

reporting small negative effects of elevated lead levels on IQ.e.g., in 36,37

A meta-analysis that included studies of whole tooth lead published since

1979 reported a statistically significant 1 point reduction in IQ

associated with a doubling of tooth lead from 5 to 10 mg/g.36 Evidence is

not sufficient to quantify the exact nature of the relationship between IQ

and higher blood lead levels (i.e., 40-100 mg/dL). Cross-sectional

studies38-42 have consistently reported small, inverse associations

between blood or tooth lead and reaction (attentional) performance, but

studies evaluating the effect of mildly elevated lead levels on other

measures of neurodevelopmental function (.g., behavior, learning

disorders, auditory function) have produced inconclusive results. These

have been less thoroughly evaluated than IQ, however.

In most studies, the size of the estimates of lead effects on IQ are

reduced when adjusted for potentially confounding variables,36

suggesting that some of the observed association may be due to

imperfectly measured or unmeasured covariates. Studies in rodents and

primates, however, which can avoid most of the methodologic weaknesses

of observational studies in humans, report cognitive, attentional, and

behavioral deficits, as well as auditory and visual dysfunction, with

mildly elevated blood lead levels,43-45 supporting a causal relationship

between low-level lead exposure and neurotoxic effects in children.

Studies demonstrating laboratory abnormalities (e.g., impaired vitamin D

metabolism) in persons with blood lead levels as low as 10-15

mg/dL23,46-48 also support a causal relationship.

Adverse Effects of Lead Exposure on Pregnancy Outcomes.  The effects of

very high blood lead levels during pregnancy on reproductive outcomes

such as abortion and stillbirth have been recognized for many years.23

Observational studies in pregnant women with blood lead levels <30 mg/dL

have reported associations between elevated levels and birth weight,

length of gestation (including preterm delivery), and neonatal head

circumference.49-56 The associations have been small, variable in

direction of effect, and not statistically significant in most studies.

These studies failed to detect important effects on other reproductive

outcomes. Inconsistent results may be due in part to imprecise measures

of fetal lead exposure.55-59 All but one34 of six previously cited cohort

studies,29-34 as well as the meta-analysis described above,36 reported

no association between antenatal or perinatal maternal blood lead levels

and full-scale IQ measured at preschool or school age. Although very high

lead levels in pregnancy are clearly hazardous, the adverse effects on the

fetus of antepartum lead levels in the range typically found in the U.S. are

not established.

Other Adverse Effects of Lead Exposure.  Lead exposure affects many organ

systems, including cardiovascular, renal, and hepatic, but most clinically

apparent (i.e., symptomatic) effects occur with blood lead levels 50

mg/dL.23,60-63 Small increases in systolic blood pressure have been

asso-ciated with mildly elevated blood lead levels (i.e., 1-3 mm Hg for a

rise in blood lead from 10 to 20 mg/dL) in most large, population-based,

cross-sectional studies evaluating nonpregnant adults and pregnant

women.64-70 In children, evidence of blood pressure effects is more

limited: one cross-

sectional study found no association between elevated blood lead levels

(range 7-70 mg/dL) and elevated blood pressure.71 Adverse effects on

height from lead levels well below 40 mg/dL have been suggested by

analyses of national cross-sectional data,72,73 but cohort studies with

more extensive covariate adjustment report either transient or no effect

of elevated lead levels (peak sample means 11-17 mg/dL) on

growth.35,74,75

Accuracy of Screening Tests

Screening tests considered for detecting lead exposure include blood lead

and free erythrocyte (or zinc) protoporphyrin levels. Blood lead

concentration is the more sensitive of the two for detecting modest lead

exposure, but its accuracy, precision and reliability can be affected by

environmental lead contamination during blood collection, day-to-day

biologic variability, and laboratory analytic variation. Lead contamination

of collecting equipment, and skin contamination during capillary sampling,

may each positively bias blood lead levels by up to 1.0 mg/dL, on average,

although individual effects of skin contamination may be much greater.76-

80 Studies defining abnormal results as blood lead levels above 10 or 20

mg/dL have reported false-positive rates of 3-9% for capillary sampling

compared to simultaneously collected venous blood lead.77-78 Day-to-day

biologic variability and trends over time contribute to higher false-

positive rates for initial capillary samples when compared to results

from venous testing done at a later date.77,81 False-negative rates with

capillary sampling appear to be lower, reported in one study as 1-8%

compared to venous blood.78 In published surveys,76,82 80-90% of

clinical laboratories participating in proficiency testing programs met

performance criteria for blood lead (within 4 mg/dL of target values, for

values <40 mg/dL82); unpublished national data show >95% of

participating laboratories meeting these criteria and >80% achieving

accuracy to within 2 mg/dL of target values (unpublished data, Centers

for Disease Control and Prevention, November 1993). Nonparticipating

laboratories are likely to be less proficient. Reported blood lead values

may differ by as much as 5 mg/dL from true values due to these sources of

variability and bias, which may affect the predictive value of a positive

test. Results from capillary samples may vary even more, although recent

studies suggest the positive bias can be reduced with increased attention

to reducing skin lead contamination.77,78

The erythrocyte protoporphyrin (EP) test, an indirect measure of lead

exposure based on lead's effects on the hematopoietic system, is

unaffected by contamination with environmental lead and is easily

performed on capillary blood specimens, making it more acceptable for

use with young patients. Erythrocyte (or zinc) protoporphyrin is

insensitive, however, to modest elevations in blood lead levels.21,83-89

The test also lacks specificity,21,83,84,86,87,90 thus limiting its

predictive value. In one study, EP measurements were taken on 47,230

suburban and rural children; although 4.7% of the children had an elevated

erythrocyte protoporphyrin level, only 0.6% had elevated blood lead

levels.91 

In communities where there is a low prevalence of lead levels requiring

individual intervention with chelation or residential lead hazard control,

blood lead screening will have a low yield, and many unaffected children

will be tested at potentially high cost and inconvenience. A questionnaire

that can predict those at high risk for elevated lead levels would allow

targeted screening in low prevalence areas, increasing the yield of blood

testing by increasing the pretest probability of elevated lead levels in

those who are tested. Cross-sectional studies13-15,92-93a in urban and

suburban, mostly midwestern, populations have shown that one or more

positive responses to five questions (about exposures to deteriorated

paint from older or renovated housing, to other lead-poisoned children, or

to lead-related hobbies or industry)128 detects 64-87% of children with

blood lead levels 10 mg/dL. Three studies reported higher sensitivities

(81-100%) for blood lead levels 15-20 mg/dL.15,92,93a None of these

studies evaluated the ability of questionnaires to detect levels above 20

mg/dL, in part because so few patients had levels so high. Specificity

among the studies ranged from 32% to 75%. In the samples with a lower

prevalence (2-7%) of levels 10 mg/dL, the proportion of those with a

negative questionnaire who had elevated blood lead levels was predictably

low (0.2-3.5%), but increased to 19% when the population prevalence of

elevated lead levels was higher (17-28%).

Effectiveness of Early Detection

Detection of lead exposure before the development of potentially

irreversible complications permits the clinician to recommend

environmental interventions to limit further exposure and, when

necessary, to begin medical treatment with chelating agents. Early

detection may also result in interventions that prevent exposure of other

children to lead (the child with elevated blood lead level acting as a

sentinel for a hazardous environment). There is relatively little

convincing evidence that these interventions improve health, however. One

issue is that most available studies in asymptomatic children evaluate

the effects of various interventions on blood lead levels rather than on

clinical outcomes. Second, blood lead levels typically decline with the

passage of time. On average, blood lead levels in childhood decrease with

age after peaking at about 2 years of age, even without intervention.7

Longitudinal studies of asymptomatic children with elevated lead levels

have shown reductions in blood lead levels after short- and long-term

follow-up in the absence of any intervention,94,95 a result attributable at

least in part to regression to the mean, random variation, and laboratory

error. To evaluate adequately the effects of interventions on blood lead

levels, studies must take into account these changes over time, preferably

by the use of controls who do not receive the intervention.

Effect of Screening on Clinical Outcomes.  Evidence is not available to

demonstrate that universal screening for blood lead results in better

clinical outcomes than either screening targeted to high-risk persons or

individualized testing in response to clinical suspicion. Several older

studies reported that, compared to historical results from individualized

testing, intensive screening programs targeted to children in high-risk

neighborhoods reduced case fatality rates, mortality rates, and

proportions of children detected with very high blood lead levels or who

developed symptomatic lead poisoning.96-98 In the absence of concurrent

controls, it is not clear whether the reported reductions in mortality and

case fatality rates were due to screening, or to improvements in medical

care over time. Reductions in mean lead levels may also have been due to

secular trends, changes in screening tests, and to screening greater

numbers of children, including many at low risk for severe lead poisoning.

Thus, the available evidence regarding the efficacy of screening programs

is weak.

Effect of Interventions to Lower Blood Lead Levels on Clinical Outcomes. 

In contrast to substantial evidence that chelating agents benefit children

with symptomatic lead poisoning, few studies have compared potential

clinical benefits of chelation therapy with its adverse effects in

asymptomatic children. Ethical considerations preclude such trials for

children with blood lead levels above 45 mg/dL. A large randomized

controlled trial assessing the effect of chelation therapy on IQ in young

children with venous blood lead concentrations of 20-45 mg/dL is

currently under way (G. Rhoads, personal communication, Environmental

and Occupational Health Sciences Institute, Piscataway, NJ, January

1994). An observational study99,100 compared children with blood lead

levels between 13 and 46 mg/dL (median 30 mg/dL), who did and did not

receive EDTA chelation therapy depending on the results of a lead

mobilization test. There was no effect of chelation on IQ at either 7

weeks or 6 months follow-up after controlling for age and initial IQ.

Changes in concentrations of blood lead, bone lead, and EP also did not

differ significantly between chelated and unchelated children. The

greatest reductions in blood lead were associated with the highest initial

lead levels, independent of chelation. The method of treatment assignment

(i.e., based on a positive mobilization test) was most likely to have biased

the study toward finding an effect of chelation, yet no effect was

observed. There is thus little evidence presently available to confirm a

clinical benefit from chelation therapy for children with lead levels <45

mg/dL. A comprehensive literature review found no studies evaluating

clinical effects of residential lead hazard control. Their effects on blood

lead levels are reviewed below.

Effects of Chelation Therapy on Blood Lead Levels.  In uncontrolled

experiments and case series in asymptomatic children with initial blood

lead levels ranging from 40 to 471 mg/dL, chelating agents reduced blood

lead levels substantially, to levels <40-70 mg/dL (varying with initial

levels); these reductions were maintained for weeks to years after

therapy was discontinued.101-105 Most of these children were also

returned to homes that had undergone lead hazard reduction, and the effect

of this additional intervention was not specifically evaluated. Chelating

agents have caused short-term reductions in blood lead levels in children

whose pretreatment values ranged from 20 to 49 mg/dL in nonrandomized

comparative trials, cohort studies, and uncontrolled experiments; these

reductions have not been sustained over longer periods in the absence of

repeated or continuing chelation therapy or environmental

interventions.104,106-109 Most of these studies did not report whether

chelation therapy was combined with environmental interventions. With

such weak evidence, including the previously cited cohort study reporting

no effects of chelation on IQ,99 it is difficult to make a convincing

argument that chelation therapy to lower moderately elevated blood lead

levels has a long-term benefit.

Effect of Residential Lead Hazard Control on Blood Lead Levels.  For most

asymptomatic children with elevated lead levels, the primary goal of

intervention is to reduce exposure to lead-contaminated paint, dust, and

soil in the child's home environment, since these sources account for most

excessive lead exposure. Residential lead-based paint hazard control

methods have become increasingly effective for reducing exposure to lead

paint and lead-contaminated dust.25,110,111 These new techniques are

now replacing the older strategies, which often created lead dust during

the intervention process, but there are currently few published studies of

their effect on blood lead levels. 

Because most published studies used older, less effective techniques, the

effects of residential interventions on blood lead reported in the

literature, and outlined below, probably indicate the minimum possible

benefit of residential lead-paint and lead-contaminated dust hazard

control. In an early cohort study112 of 184 children with initial blood lead

levels 50 mg/dL, children discharged after chelation therapy to lead-free

(i.e., new or completely gutted and renovated) housing had significantly

lower mean blood lead levels when compared to children exposed to

"legally abated" or to inadequately abated housing (28.8 mg/dL vs. 38.5 and

57 mg/dL, respectively). Children in lead-free housing also had fewer

recurrences of levels 50 mg/dL at 12 and 24-30 months follow-up. A

nonrandomized trial113 of households with children having initial blood

lead levels >29 mg/dL compared more intensive experimental lead-

reduction procedures with the lead-reduction procedures commonly in use

in the study community. Neither intervention had any effect on mean dust

or blood lead levels as tested 6 months after abatement, but an untreated

control group was not included. Published114 and unpublished115

retrospective cohort studies suggest that residential lead paint hazard

control is associated with modest declines (4-10 mg/dL) in mean blood

lead levels in children with initial blood lead levels  25 mg/dL, although

in one study114 those with initial blood lead levels <35 mg/dL benefitted

little from intervention. Case series and uncontrolled experiments, both

weak study designs, have also evaluated lead-paint hazard control efforts

in children with initial blood lead levels of 25-55 mg/dL;100,116-119

several were published only as abstracts or summaries.115,120 These

studies reported statistically significant declines in mean blood lead

levels, ranging from 2.5 to 10.2 mg/dL, 6-12 months after residential

lead-based paint hazard control. All of the studies cited suffer from

important design flaws, such as substantial drop-out rats and inadequate

control for confounding variables such as season and age. Despite their

flaws, the consistency of the results from these studies suggests a small,

beneficial effect of lead-based paint hazard control on blood lead levels.

As noted, there are as yet no published studies evaluating the effects on

blood lead levels of newer residential lead hazard control techniques.

There are important problems with using one-time residential lead-paint

hazard control as the sole method to reduce lead exposure in children.121

Poor, inner-city families tend to move frequently, so that treating the

current residence may have limited long-term benefit to the child,

although benefit may accrue to other children moving in to that residence

(see below). Residential lead-paint hazard control is costly and labor-

intensive, resulting in low rates of intervention, especially in poor

communities.24,122 Lead dust is ubiquitous and highly mobile, so that

recontamination by nearby lead sources, including soil lead, may occur

after lead-paint hazard control efforts take place in a

dwelling.110,123,124 These problems indicate a need for additional

individual interventions, as well as more comprehensive community-based

interventions, to reduce household lead exposure.

The small effect noted in studies evaluating lead-paint hazard control

methods may be attributable in part to recontamination of the dwelling by

nearby lead sources and from subsequent deterioration of painted

surfaces.110,123,124 Several studies have evaluated measures designed

to reduce ongoing lead-dust contamination from lead-contaminated paint

and soil. In a nonrandomized controlled trial among children with blood

lead levels of 30-49 mg/dL, having a research team wet-mop all lead-

contaminated interior surfaces twice a month with a high-phosphate

detergent cleanser resulted in significantly greater adjusted declines in

mean blood lead levels  of children in intervention households compared to

children in control households (6.9 vs. 0.7 mg/dL) at 1-year follow-up.125

There have been no controlled studies to evaluate whether counseling

families to perform similar cleaning would be equally effective in

reducing blood lead levels. In one uncontrolled experiment, the families of

78 children with blood lead levels of 10-35 mg/dL, who were living in the

vicinity of a defunct lead smelter, received intensive (30-45 minutes) in-

home education and literature on prevention of lead exposure.126 The

mean blood lead levels in the 51 (65%) children who had follow-up blood

lead levels at 4 months declined from 15.0 to 7.8 mg/dL (and maximum

levels from 35.0 to 12.7 mg/dL). Without concurrent controls, it is not

possible to determine how much regression to the mean and seasonal and

age variations contributed to these reductions in blood lead levels. There

is also evidence that clinician counseling at the worksite to reduce lead

dust ingestion by workers (e.g., through personal hygiene practices) can

significantly reduce mean blood lead levels at 1-year follow-up,127 but

this study also lacked controls and may not be generalizable to the

residential setting.

A third focus of residential lead hazard control is exposure to soil lead. In

a randomized controlled trial123 of young children with initial blood lead

levels of 7-24 mg/dL, extensive soil abatement, one-time dust abatement,

and removal of loose interior paint resulted in a statistically significant

reduction in mean blood lead levels of 1.2-1.3 mg/dL compared to loose

paint removal alone. This clinically insignificant decline was associated

with a substantial reduction in soil lead from a median 2,000 to 105 ppm.

Preliminary results of the U.S. Environmental Protection Agency's Three

City Urban Soil Lead Abatement Demonstration Project similarly suggest

that substantial declines in soil lead cause only modest reductions in

mildly elevated blood lead concentrations.124 The small effect was due at

least in part to rapid recontamination with dust lead in households

undergoing soil abatement. Among children living near a closed lead

smelter, only 3% of the variance in blood lead levels was attributable to

soil lead.127a

An important potential benefit of residential lead hazard control is its

effect on the lead levels or clinical outcomes of other children who live in

the same household as a child identified with elevated lead levels, or who

subsequently move into the remediated residence. The literature review

revealed no published evidence evaluating the effect of residential lead

hazard control measures on such children. Based on the biokinetics of

lead,23 it is reasonable to believe that environmental interventions

conducted before children are exposed are likely to prevent increases in

blood lead levels more effectively than the same interventions in children

who have already been exposed.

Effect of Nutritional Interventions on Blood Lead Levels.  In most settings,

neither residential lead-based paint or dust hazard control nor chelation

therapy is routinely offered to children with blood lead levels <20 mg/dL,

but some experts have recommended offering these children dietary

counseling to reduce their blood lead levels.128 Diets deficient in

calories, calcium, and zinc have been associated with increased

gastrointestinal absorption of lead,129,130 but there is only limited

evidence that counseling to correct such nutritional inadequacies will

reduce blood lead levels or prevent further increases. Results of

experimental studies of the effects of iron deficiency on lead absorption

and retention in adult humans have been equivocal.129,131 In a cohort

study of children with initial blood lead levels of 13-46 mg/dL,99 all

children who were iron deficient or depleted were prescribed iron

supplementation. Although most children were still iron deficient at the

end of the study, there were improvements in ferritin level that were not

associated with either declines in blood lead or improvements in cognitive

function. Cross-sectional and cohort studies have failed to establish a

clear association between mean blood lead levels and measures of iron

status in women at midpregnancy or delivery, in newborns (cord blood), or

in children.57,99,131-134

Adverse Effects of Screening and Intervention.  The most common adverse

effects of screening for elevated lead levels are false-positive

fingerstick results, and the anxiety, inconvenience, work or school

absenteeism, and financial costs associated with return visits and repeat

tests. An EDTA lead mobilization test, used for some children with blood

lead levels of 30-44 mg/dL,135 requires intramuscular or intravenous

infusion, a stay at the clinical center for at least 8 hours, and for young

children, application of urine collection bags.136 Residential lead-based

paint and dust hazard control, when improperly done,25 may produce acute

increases in blood lead levels in resident children and abatement workers,

occasionally necessitating hospitalization and chelation

therapy.113,116,137-139 Currently recommended techniques for lead

hazard reduction are likely to reduce these adverse effects.25 Chelating

agents for asymptomatic lead poisoning have also been associated with

important adverse effects. EDTA and dimercaprol (BAL) have transient

renal, hepatic, and other toxicity, require intravenous or intramuscular

injection, and generally require hospitalization for

administration.128,140,141 Common adverse effects of d-penicillamine

are penicillin-like sensitivity reactions and transient nephrotoxicity;

there are rare life-threatening reactions.96,105,107,128 Succimer

(meso-2,3-dimercaptosuccinic acid, or DMSA) causes mild

gastrointestinal and systemic symptoms, rashes, and transient elevations

in liver function tests, in up to 10% of cases.104,106,108,142

Recommendations of Other Groups

Several states mandate either universal screening for lead exposure or

selective screening of populations at high risk for lead exposure.143

Periodic screening of children with blood lead measurement is also

required for Medicaid's Early and Periodic Screening, Diagnostic, and

Treatment Program.144 The American Academy of Pediatrics145 and the

Bright Futures guidelines146 recommend: (a) screen all children for lead

exposure at about 12 months of age, and possibly again at about 24 months

of age; (b) take a history of lead exposure (using questionnaires provided

with the guidelines) between the ages of 6 months and 6 years to identify

high-risk children who should be screened earlier or more frequently; and

(c) provide education to parents on safe environmental, occupational,

nutritional and hygiene practices to protect their children from lead

exposure. Follow-up screening intervals should be based on risk

assessment and previous blood lead levels. The Centers for Disease

Control and Prevention (CDC) recommends screening all children at 12

months of age using a blood lead test, except in communities where no

childhood lead poisoning problem exists; high-risk children require earlier

and more frequent screening.128 The American Academy of Family

Physicians (AAFP)147 and the Canadian Task Force on the Periodic Health

Examination148 recommend screening all children who are at high risk of

lead exposure (e.g., due to exposure to heavy traffic and industry, or to

dilapidated older housing). The recommendations of the AAFP are currently

under review. The American Medical Association recommends regularly

screening all children under the age of 6 years for lead exposure through

history-taking and, when appropriate, blood lead testing.149 They

recommend that the decision to employ universal or targeted screening be

made based on prevalence studies of blood lead levels in the local

pediatric population.

No major organizations currently recommend screening pregnant women

for elevated lead levels.

Discussion

There is fair evidence that screening for elevated lead levels in

asymptomatic children at increased risk for lead exposure will improve

clinical outcomes. Because there have been no controlled trials directly

evaluating screening for elevated lead levels, this conclusion is based on a

chain of evidence constructed from studies of weaker design. First, in

young asymptomatic children, blood lead levels as low as 10 mg/dL are

associated with measurable neurodevelopmental dysfunction. Second,

although the national prevalence of elevated lead levels has declined

substantially in the past decade, a high prevalence persists in some

communities, particularly poor urban communities in the northeastern U.S.

Third, measurement of venous blood lead concentration is a convenient,

reliable, precise and reasonably valid screening test for assessing lead

exposure. Fourth, current interventions, including residential lead hazard

control and chelation therapy, can reduce blood lead levels in children

identified with levels 25 mg/dL, although the quality of evidence

supporting their effectiveness is weak and a beneficial effect on IQ or

other clinical outcomes has not yet been demonstrated. There is also weak

evidence that screening high-risk children for elevated lead levels results

in improved clinical outcome compared to historical controls identified by

case-finding. Based on this evidence of the current burden of suffering and

the effectiveness of early detection, the Task Force recommends

screening children at increased risk for lead exposure.

While no studies have evaluated a specific age at which to screen, the

natural history of blood lead levels in children, which increase most

rapidly between 6 and 12 months and peak at age 18-24 months, suggests

that screening at about 12 months of age is likely to be most effective for

the early detection of elevated lead levels.

For those children who are screened and found to have initial blood lead

levels <25 mg/dL, there is as yet little evidence regarding the

effectiveness of early detection and intervention, or of repeated screening

to detect further increases in blood lead. Longitudinal and cross-sectional

studies suggest that in children 2 years, most such levels will decline

naturally with time, but elevated levels may persist in children who are

chronically exposed.101

There is no direct evidence comparing the outcomes of universal screening

with the outcomes from targeted screening for elevated lead levels.

Recent studies indicate that the prevalence of elevated blood levels in the

U.S. has declined dramatically in the past decade, but that local prevalence

is highly variable, with more than 10-fold differences between

communities. In a community with a low prevalence of elevated blood lead

levels, universal screening may result in disproportionate risks and costs

relative to benefits. The prevalence level at which targeted screening can

replace universal screening is a public health policy decision requiring

consideration of factors in addition to the scientific evidence for

effectiveness of early detection, such as available resources, competing

public health needs, and costs and availability of alternative approaches

to reducing lead exposure. Good quality analyses are needed to determine

the population prevalence below which universal lead screening is not

cost-effective. Clinicians can consult with their local or state health

department regarding appropriate screening policy for the local child

population.

In communities where data suggest that universal screening is not

indicated, there may nevertheless be some children who are at increased

risk of blood lead levels in the range for which individual intervention by

chelation therapy or residential lead hazard control has been

demonstrated to be effective. These children may have had exposure to

lead sources such as lead-based hobbies or industries, traditional ethnic

remedies, or lead-based pottery. Selective blood lead screening of such

high-risk children is appropriate even in low prevalence communities.

There is fair evidence that a validated questionnaire of known and

acceptable sensitivity and specificity can identify those at high risk. In

several studies, the CDC128 and similar questionnaires correctly

identified 64% to 87% of urban and suburban children who had blood lead

levels 10 mg/dL. These questionnaires have not been adequately

evaluated as a screening tool to detect higher blood lead levels (e.g., 20-

25 mg/dL), or to detect exposure in other populations (e.g., migrant

workers, rural communities). Locale-specific questionnaires that inquire

about likely local sources of lead exposure may lead to improved

prediction.

As is the case in children, there are no controlled trials evaluating

screening for elevated lead levels in pregnant women, nor are there

sufficient data to construct an adequate chain of evidence demonstrating

benefit. The prevalence of levels >15 mg/dL appears to be quite low in

pregnant women. There is fair evidence that mildly elevated lead levels

during pregnancy are associated with small increases in antepartum blood

pressure, but limited evidence that these levels have important adverse

effects on reproductive or other outcomes, including intelligence of

offspring. An extensive literature search failed to identify studies

evaluating screening or intervention for lead exposure in pregnant women.

There are potentially important adverse effects of chelation therapy on

the fetus, and of residential lead hazard control on both the pregnant

woman and fetus if they are not performed according to established

standards. Removal to a lead-free environment would theoretically be

effective in reducing lead exposure but has not been specifically evaluated

in pregnancy. There is thus insufficient evidence to recommend for or

against screening pregnant women for the detection of elevated lead

levels.

Population-based interventions for the primary prevention of lead

exposure are likely to be more effective, and may be more cost-effective,

than office-based screening, treatment and counseling. Community,

regional, and national environmental lead hazard reduction efforts, such

as reducing lead in industrial emissions, gasoline, and cans, have proven

highly effective in reducing population blood lead levels.1-6,150,151

Remaining important sources of lead (e.g., lead paint and pipes in older

homes, lead-contaminated soil) are, however, more difficult to address on

a population-wide basis. Studies of community-based efforts to reduce

lead exposure from these and other sources in order to prevent the

occurrence of elevated lead levels are ongoing.25,110,152 Evaluation of

the effectiveness of community-based interventions, and

recommendations regarding their use, are beyond the scope of this

document.

CLINICAL INTERVENTION

Screening for elevated lead levels by measuring blood lead at least once at

age 12 months is recommended for all children at increased risk of lead

exposure ("B" recommendation). All children with identifiable risk factors

should be screened, as should children living in communities in which the

prevalence of blood lead levels requiring individual intervention, including

chelation therapy or residential lead hazard control, is high or is

undefined. If capillary blood is used, elevated lead levels should be

confirmed by measurement of venous blood lead. The optimal frequency of

screening for lead exposure in children, or for repeated testing of children

previously found to have elevated blood lead levels, is unknown and is left

to clinical discretion; consideration should be given to the degree of

elevation, the interventions provided, and the natural history of lead

exposure, including the typical peak in lead levels at 18-24 months of age.

In communities where the prevalence of blood lead levels requiring

individual intervention is low, a strategy of targeted screening, possibly

using locale-specific questionnaires of known and acceptable sensitivity

and specificity, can be used to identify high-risk children who should have

blood lead testing. Examples of individual risk factors include: (a) living in

or frequently visiting an older home (built before 1950) with dilapidated

paint or with recent or ongoing renovation or remodeling, (b) having close

contact with a person who has an elevated lead level, (c) living near lead

industry or heavy traffic, (d) living with someone whose job or hobby

involves lead exposure, (e) using lead-based pottery, or (f) taking

traditional ethnic remedies that contain lead.128 There is currently

insufficient evidence to recommend an exact population prevalence below

which targeted screening can be substituted for universal screening. The

results of cost-benefit analyses, available resources and public health

priorities are among the determinants of the prevalence below which

targeted screening is recommended for a community. Clinicians can seek

guidance from their local or state health department.

There is insufficient evidence to recommend for or against routine

screening for lead exposure in asymptomatic pregnant women ("C"

recommendation). Recommendations against such screening may be made

on the grounds of limited and conflicting evidence regarding the current

burden of suffering, high costs, and the potential for adverse effects from

intervention.

There is insufficient evidence to recommend for or against trying to

prevent lead exposure by counseling families to control lead dust by

repeated household cleaning, or to optimize caloric, iron, and calcium

intake specifically to reduce lead absorption ("C" recommendation). For

high-risk individuals or those living in high-prevalence communities, such

recommendations may be made on other grounds, including minimal risk of

adverse effects from the cleaning or the dietary advice, and the

additional, unrelated benefits from optimizing nutrition (see Chapter 22,

Screening for Iron Deficiency Anemia, and Chapter 56, Counseling to

Promote a Healthy Diet).

Recommendations regarding community- or population-based

interventions for the primary prevention of lead poisoning, assessment of

community lead contamination, or the setting of community priorities for

lead hazard reduction, are beyond the scope of this document.

The draft update of this chapter was prepared for the U.S. Preventive

Services Task Force by Carolyn DiGuiseppi, MD, MPH.

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