Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

Childhood Lead Toxicity Janet Serwint MD

OBJECTIVES 1. Know the common sources of lead exposure

2. Recognize the manifestations and effects of lead toxicity

3. Understand the epidemiology and risk factors for lead toxicity

4. Be able to implement current recommendations for lead testing

5. Understand the management of elevated blood lead levels

6. Know the distinction between primary and secondary prevention of lead toxicity

Pretest Questions

1. Which of the following patients would not require lead testing?

a. 2 year old patient who receives Medicaid

b. 3 year old with pica

c. 4 year old with sibling with documented lead toxicity

d. 5 year old with ADHD

2. A 2 year old is noted to have a lead level of 30 ug/dL. In addition to repeating the

lead level, which of the following interventions is most appropriate?

a. Treatment with succimer, an oral lead chelating agent.

b. Increasing vitamin D intake

c. Conducting an environmental investigation

d. Obtain radiographs of the long bones

3. A child is found to have a lead level of 72 ug/dL on routine screening at 24 months of

age. The child has no symptoms. Which of the following actions would you take?

a. Assume that it is a lab error since a child with a lead level of 72 ug/dL should

have symptoms.

b. Repeat the lead level within 7 days

c. Hospitalize immediately, repeat the lead level and begin chelation

Lead toxicity

Sometimes silent, sometimes not

No level is safe

PGY 2, Univ. of Texas, San Antonio

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d. Send hair sample for lead and send a toxicology screen

4. Which of the following exposures could potentially put patients at risk for lead

toxicity?

a. Computers in land fills

b. Blood transfusion

c. Lead dust not visibly apparent in the home

d. All of the above

5. Which of the following groups of children are at highest risk of health effects related

to lead exposure and why?

a. Children under 5 are at higher risk because their developing central nervous

systems are more likely to be affected by lead

b. Children who are obese are at at higher risk because lead is stored in adipose

tissue

c. Infants who are bottle fed because there is a high level of lead in most water

systems in the U.S.

d. Children living in cold climates because they spend more time indoors

6. Which of the following is an example of primary prevention of lead toxicity?

a. Screening a child at 1 and 2 years of age

b. Evaluating the lead dust samples of the floor of an urban home.

c. Repeating a lead level after a 1 year old is found to have a lead level of 18

ug/dL.

d. Performing lead testing on a pregnant woman

Answers 1)d 2)c 3)c 4)d 5)a 6)b

I. SOURCES OF LEAD EXPOSURE

Case 1. Dasia is a one year old who you are seeing for a health maintenance visit.

Her mother read a story in a popular magazine about a child affected by lead

poisoning and asks whether her child is at risk. Which of the following would NOT

be a risk factor for potential lead exposure?

a. Dasia’s home, built in 1980, is undergoing internal renovations.

b. Attendance at day care in a building built in 1948.

c. Dasia’s father works at a factory that makes batteries.

d. Dasia was recently adopted and had lived in Nairobi, Kenya

Answer: a. Lead paint was banned for residential purposes in the United States in 1978.

Knowledge of the age of a child’s home and other dwellings where the child spends large

amounts of time are necessary. Renovations of homes, even those in good repair,

involving sanding or knocking down walls will generate lead dust and create risk if built

prior to 1978While her home would not contribute to her risk, her attendance at day care

at an older home would. Batteries contain lead so factory work can result in lead on the

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father’s clothes. People living in developing countries often have large environmental

exposures to leaded paint and leaded gasoline since these products are still used.

Lead toxicity in adults was recognized by Hippocrates as early as 370 BC. (Gracia

2007). Childhood lead toxicity was first diagnosed a century ago in Australia in 1904.

(Chisolm 2001) Lead is a heavy metal found commonly in the environment of

industrialized nations. Lead enters the body through ingestion or inhalation. The most

common sources of current lead exposure are listed below. (AAP 2005, Laraque 2005)

1. LEAD-DUST FROM LEAD PAINT:

Lead is commonly ingested in the form of lead-contaminated dust or paint chips. Young

children are at highest risk because of increased hand to mouth activity. While lead

poisoning can occur from eating paint chips, ingestion of the very fine lead dust, which

may not be visible but can be produced by paint abrasion from opening and closing

windows, normal wear of walls and floors, or home renovations, also leads to lead

toxicity. The most common source of current lead toxicity is from lead dust. National

legislation has banned lead paint for interior or exterior residential purposes since 1978.

However, any house built before 1950, which includes 27% of U.S. housing, or 16.4

million homes in the US where children 1 year of age or older reside may still have

significant amounts of lead in the paint, dust, or soil.

2. RENOVATIONS:

Renovations in older homes that involve scraping paint and disrupting walls will create

lead dust. This risk applies to all older homes, not just those in poor repair or in

economically disadvantaged areas. A 2006-7 analysis in New York state revealed that

the reason for 14% of children with blood lead levels > 20 ug/dL was related to home

renovation and repair activities. (Franko, 2009). Parents need to be educated about the

need for proper approaches to renovations and remodeling.

3. LEADED GASOLINE:

Leaded gasoline resulted in deposits of lead in air, soil, and house dust which was then

inhaled or ingested. At one time, auto emissions accounted for 86% of lead in the

atmosphere. The introduction of unleaded gasoline in the U.S. in 1973 dramatically

decreased continued lead deposition. Many developing countries still use leaded

gasoline, reinforcing why lead screening is needed for emigrants and for children who are

internationally adopted.

4. SOIL:

Sources of soil contamination include deteriorating lead-based paint from outside walls,

exhaust from burning leaded gasoline, and refinery waste or emissions deposited in the

ground. Lead in the soil does not decay and serves as a long-term source of exposure.

5. DRINKING WATER:

Lead can be leached into water from lead pipes or solder. Older homes may have lead

soldered pipes; modern homes with copper pipes may have lead-soldered joints or brass

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fixtures that contain lead. Acidic water of low mineral content, water standing in pipes

for extended periods and hot water are of particular concern for increased lead content.

For more information, see the EPA website, www.epa.gov/safewater/lead/index.html.

6. FOOD:

Root vegetables may take up soil lead, and airborne lead can fall on leafy vegetables.

Lead soldered cans used for food storage may contaminate food with lead, especially if

the contents are acidic or the cans are refrigerated once opened. Since 1991, lead is no

longer used in the production of food cans in the United States, but imported foods may

still be stored in lead soldered cans. Food also may be contaminated by lead-glazed

pottery or utensils used in cooking.

7. OCCUPATIONAL SOURCES AND HOBBIES:

Lead dust can be brought into the home on the clothing of workers with occupational

lead exposure from lead smelters, brass foundries, copper manufacturing, battery and

aircraft manufacturing, automotive repairs, bridge repairs, painting, plumbing, and

chemical manufacturing. Hobbies involving stained glass, pottery, lead collectible

figurines, lead ammunition and painting are all sources of lead exposure.

8. MEDICATIONS/COSMETICS:

Some foreign medications, as well as herbal remedies may contain significant amounts

of lead.

Herbal Preparation Cultural Origin Use

Greta Hispanic Intestinal ailments

Azarcon Hispanic Intestinal ailments

Pay-loo-ah Southeast Asian Fever and rash

Farouk Middle East Teething

Bint al zahab Middle East Colic

Kohl Middle East / Moslem Eye cosmetic

Surma Middle East / (Hindu) Eye cosmetic

9. OTHER PRODUCTS/TOYS:

Vinyl window blinds and crayons imported from China may include lead in addition to

toys imported from other countries. Old personal computers (PCs) are a concern since a

standard display monitor contains from 4-8 pounds of lead. Safe methods of disposal

will need to be determined so as not to contribute even more to the environmental lead

issue.

10. TRANSFUSED BLOOD: Lead concentrations are not routinely measured in donated blood (AAP 2001). While there are no large studies evaluating the impact of lead in transfused blood, Bearer et al, reported that one third of the blood samples they measured had levels above their recommended cut off for VLBW infants.

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11. MOTHER TO INFANT TRANSFER:

Since lead crosses the placenta, a mother with an elevated lead level risks transmitting

lead to her child. Pregnancy may be a particularly vulnerable time for increased maternal

lead levels because the increased maternal calcium requirements are maintained through

increased bone resorption. Studies have examined prenatal lead exposure in the fetus and

demonstrated later impact on cognitive development (Ronchetti 2006, Jedrychowski

2009, Foltinova 2010, Patel AB, 2009). More research is needed in this area but there are

currently no national organizations that recommend screening US pregnant women for

elevated lead levels (Rischitelli 2006). The strongest current recommendation for

pregnant women is preventing exposure to renovations in homes with lead paint.

Another interesting area of study involves breast feeding and potential lead exposure.

Some studies have shown that while lead may be present in breast milk of mothers, little

is transferred (AAP 2005). Lozoff et al examined children’s lead levels and duration of

breastfeeding in healthy infants in Cost Rica, Chile and Detroit, USA. Higher infant lead

concentrations were found with longer duration of breastfeeding. The authors’

suggestion was that monitoring of lead concentrations in breastfed infants be considered,

(Lozoff B 2009) but no specific recommendations are in place at the present time.

Examining effects of prenatal lead exposure is an area of active research.

12. EMIGRATION FROM OTHER COUNTRIES AND/OR INTERNATIONAL

ADOPTEES:

These patients may be at risk for lead toxicity due to exposure to leaded paint, lead

gasoline, lead in water, and lead soldered cans for storage in countries where laws have

not been put into place (Red Book, 2009). Lead testing is indicated in these patients.

Multiple low-level exposures to lead from several of the above sources may result in

significant aggregate exposure.

The following table provides an overview of sources of lead exposure and prevention

strategies from the 2005 AAP guidelines.

TABLE . Sources of Lead Exposure and Prevention Strategies

Source Prevention Strategy

Environmental

Paint Identify and abate/cover

Dust Wet mop (assuming abatement)

Soil Restrict play in area, plant ground cover,

wash hands frequently

Drinking water Flush cold water pipes (see recs above),

use cold water for cooking and drinking

Folk remedies (examples above) Avoid use

Cosmetics with kohl or surma Avoid use

Old ceramic or pewter cookware Avoid use

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Some imported toys, crayons, cosmetics Avoid use

Parental occupations Remove work clothing at work, wash

separately

Hobbies Proper use, storage and ventilation

Home renovation Proper containment, ventilation

Buying or renting a new home Inquire about lead hazards

Lead dust in carpet Cover or discard

Host

Hand to mouth activity Frequent hand washing, minimize food on

floor

Inadequate nutrition Adequate intake of calcium, iron, Vit C

Developmental disabilities Enrichment programs

Key Points:

*Lead enters the body through inhalation and ingestion

* Lead paint is the most common source

* Renovation of lead paint by scraping or knocking down walls is an important risk

* Mother to infant transfer of lead is an area of ongoing study

* Lead risk assessment must also consider potential sources of soil, water, folk remedies,

cosmetics, hobbies, occupations

* Multiple low level exposures of lead may result in larger aggregate exposure

II. MANIFESTATIONS AND EFFECTS OF LEAD

Case 2. Joshua is a 2 year old with a lead level of 25 ug/dL on a routine screening

test. He had a lead level of 8 ug/dL when tested at 1 year of age. You perform a

complete developmental assessment and find his language and motor development

to be right on target. Which of the following statements is correct?

a. You can reassure his mother that this level is unlikely to cause problems because he

has no evidence of lead toxicity.

b. He has acute lead exposure.

c. The impact of lead toxicity may not become apparent until he nears school age, when

more sensitive cognitive testing is available.

d. Testing the lead level in a sample of his hair is the best method to confirm chronic

exposure.

Answer: c. Children are often asymptomatic when initially diagnosed with lead toxicity,

highlighting why lead testing is necessary. Reassurance would not be appropriate

because the impact of the lead exposure may not become apparent until an older age (4-6

years) when more sensitive cognitive testing is available or the child’s developmental

knowledge is challenged during school. Since you have only two measurements spaced

over a year, so it is difficult to know whether this is long term accumulation of lead or a

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more acute exposure. Hair, teeth or fingernail testing does not provide any extra

evidence of the chronicity of lead toxicity. A repeat lead level within 1-4 weeks will

document whether the level has stabilized or is continuing to rise.

Manifestations and Effects of Lead

Childhood lead poisoning remains a major environmental public health problem. Over

the last few decades, the presentation of lead poisoning has changed significantly. In

earlier years, children commonly presented to their physicians with classic GI and CNS

symptoms. Lead poisoning is now a disease process characterized by subclinical and

biochemical findings in largely asymptomatic children (CDC, 1997, Laraque, 2005).

However, many studies have provided evidence that lead exposure in early childhood,

even when initially asymptomatic, is associated with later adverse cognitive and

behavioral outcomes (AAP, 2005) Therefore, pediatricians have a critical role in the

prevention, identification, and treatment of lead toxicity.

In 2012, the CDC adopted a significant change in its approach to the definition of

elevated blood lead level, eliminating the term “level of concern” and replacing it with

the reference value of >5 ug/dL as the level to prompt further evaluation (CDC 2012).

CDC Guidelines for Lead "Level of Concern"*:

1960- >= 60 ug/dL

1985 >= 25ug/dL

1991 >= 10 ug/dL

2012 "Reference value of lead level" > 5 ug/dL*

*With this most recent change, the CDC rejects the language of "level of concern"

emphasizing that there is no level below which lead is not a concern. No lead level is

considered safe for children. Establishing 5 ug/dL as the level to prompt further

evaluation reflects the 97.5th percentile of blood lead levels in children ages 1 - 5 years in

the United States, based on NHANES data. The CDC, in concurrence with

recommendations from the Advisory Committee on Childhood Lead Poisoning

Prevention, adopted this reference standard to identify children with elevated blood lead

levels and to move the focus toward primary prevention of all lead exposure for children.

The 97.5th percentile will be recalculated every 4 years with new NHANES survey data

to assure population changes are adequately assessed.

(www.cdc.gov/nceh/lead/ACCLPP/Final_Document_030712.pdf)The toxic effects of

lead depend on multiple variables including acute versus chronic exposure, blood lead

level, total body burden of lead, age and other host factors. The observed blood lead

level is influenced by a number of factors including recent exposure, excretion and

equilibrium with other tissues, bone in particular. Blood lead levels may reflect lead

exposure as recently as the last 30 days, while bone lead levels reflect lead exposure for

the past 19 years (Gracia, 2007).

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Lead toxicity can affect almost every organ system including the renal (kidney function

and vitamin D metabolism), endocrine, hematopoietic, reproductive and central and

peripheral nervous systems. The blood lead level at which symptoms occur varies from

child to child. Acute symptoms are usually not present until a child has blood levels of

>50 ug/dL. Some children show no initial signs of acute toxicity even at levels >100

ug/dL. (Davoli, 1996) However, these children will eventually show symptoms over

time and demonstrate long term effects. New studies examining the epigenetic

mechanisms of early lead exposure and the influence on brain and other organ

development are ongoing. (http://www.cdc.gov.nceh/lead/ACCLPP/Final Document

030712.pdf)

Manifestations of Lead Toxicity

Subclinical disease (asymptomatic children with increased body burden of lead: lead

levels < 45 ug/dL.).

Most lead poisoning is clinically not apparent at the time of diagnosis. The detrimental

effects on cognitive function have been the driving force behind public health initiatives.

The data from numerous studies of children from varying socioeconomic groups,

supports the conclusion that low levels of lead have a negative impact on IQ. Studies

show that as lead concentrations increase by 10 ug/dL, the IQ at 5 years and older

decreased by 2 to 3 points. Associations between elevated blood lead levels and

language delay, inattention and decreased ability to follow directions have also been

noted. Elevations in bone lead concentrations have been linked to ADHD, aggression,

school failure, reading disabilities, delinquency and adult criminality. Research has

shown that neuro-cognitive morbidity in children is better overcome for children

who are raised in nurturing and stimulating environments.

Recent evidence shows that blood lead levels lower than 10 ug/dL result in neuro-

cognitive effects of lower IQ and language delay, along with problems with academic

skills such as reading, arithmetic, and fine and gross motor skills. (Canfield 2003,

Bellinger 2003, Lanphear 2005, CDC 2005). While earlier studies had suggested a

threshold of risk with lead toxicity, several more recent studies have suggested that the

rate of decline in IQ scores may be more prominent with blood lead levels less than 10

ug/dL than above 10 ug/dL : a decline of 6.2 points in IQ at lead levels less than 10

ug/dL, 1.9 point decline between 10-19.9 ug/dL and 1.1 point decline between 20-30

ug/dL. The mechanism of this relationship is not certain, but some have hypothesized

that there is a “lead sensitive pathway” that is saturated more quickly at lower levels of

lead exposure (Bellinger 2008). These findings suggest that more children in the United

States may be affected by lead toxicity than previously thought and helped to prompt the

CDC to change its approach from a "level of concern" stance to the reference value

of the 97.5th percentile of blood lead as an upper limit. The take home message is that

no lead exposure is safe and our focus should be on primary prevention of lead

exposure in children.

The precise mechanism by which lead affects the CNS function is not yet clear, (AAP

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statement, 2005) but some possibilities include interference with neurotransmissions and

effects on mitochondrial dysfunction, brain inflammation, and disruption of cell

migration during critical periods of brain development. (Bellinger 2009, Lidsky 2003,

Chandran 2010).

Recall that lead levels measure the burden currently in the body. Lead levels will

decrease over time if a child is not continually exposed. Thus, when a child enters school

and the cognitive impairments are most apparent, the current measurement of the child’s

lead level will not reflect earlier exposure. An elevated level identifies current exposure,

but does not yield any information about exposure during a younger age. A normal lead

level is similarly unhelpful in that it does not rule out earlier exposure.

Symptomatic lead poisoning without encephalopathy (threshold lead level of 45 ug/dL or

higher) Characterized by lethargy, anorexia, decreased activity, sporadic vomiting,

intermittent abdominal pain and constipation. These symptoms may be attributable to

decreased preganglionic acetylcholine release and inhibition of intestinal Na+,

K+ATPase (Gracia 2007). Since all symptomatic children may have neurotoxic effects,

treatment with chelation should be instituted on an urgent basis (AAP 2005). (See

Section V for management)

Acute lead encephalopathy (associated with blood lead concentrations of greater than 70

ug/dL.) Characterized by coma, seizures, bizarre behavior, ataxia, apathy, incoordination,

vomiting, altered state of consciousness and loss of recently-acquired skills. Acute lead

encephalopathy is a medical emergency and inpatient treatment with chelation should

begin immediately. Patients can progress to coma and death. Lead can accumulate in the

brain in children with compromised blood brain barriers. Encephalopathy symptoms are

thought to occur from lead interference with protein kinase C and neurotransmitters

resulting in the opening of ion channels, excessive ion flux, microvascular permeability

and cerebral edema. Note that it is possible for children to have lead levels > 100 ug/dL

acutely and be initially asymptomatic. (Davoli 1996.) Elevated lead levels should never

be ignored or discounted because of lack of symptoms. Chelation should be initiated

immediately in these patients. See section 5 for management.

**Addendum concerning lead toxicity and anemia. Microcytic anemia has been

considered an effect of lead toxicity for a long time. More recent studies have suggested

that the microcytic anemia may be more likely caused by coexisting iron deficiency and

that lead toxicity can exist without microcytosis or anemia ( Cohen 1981, Clark 1988,

Gawarammana IB 2006).

Key Points:

There is no level below which exposure to lead is safe for children.

The new CDC reference value of elevated lead level is > 5 ug/dL. dL

Lead levels < 10 ug/dL. have been found to be associated with cognitive deficits

and affect IQ.

Lead levels <-44 ug/dL are associated with language delay and inattention

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Lead levels > =45 ug/dL without encephalopathy are associated with

gastrointestinal symptoms such as vomiting, abdominal pain and constipation

Lead levels >= 70 ug/dL can lead to coma, seizures and encephalopathy which is

life-threatening and immediate chelation is indicated.

Children with elevated lead levels may initially be asymptomatic at the time of

the blood test results. Elevated lead levels should never be ignored.

The microcytic anemia associated with lead toxicity is most commonly due to

coexisting iron deficiency.

III. EPIDEMIOLOGY and RISK FACTORS

Case 3. Your State Legislature asks you to speak on lead toxicity as part of the

hearings on a new bill that is being proposed. The legislature is interested in better

understanding risk factors of lead toxicity. Which of the following statements are

true?

a. Children are at most risk during the winter months because they are indoors

where exposure is the greatest

b. Children 9 months and younger are at highest risk because of maternal transfer of

lead

c. Children 1-5 years are at highest risk because of increased hand to mouth activity

and a developing central nervous system

d. Children who have private insurance are at highest risk because they are least

likely to be screened routinely.

Answer: c. Children from 1-5 years are at highest risk. The summer and early fall

season are times when lead toxicity is found to be more apparent. The age group of

younger than 9 months has not been identified as a high risk group, although future

research will more adequately examine the effect of maternal to infant transfer of lead.

Children 1-5 years remain at highest risk for lead toxicity. Young children in this age

range are more susceptible to lead toxicity because of:

1) increased mobility, exploration, and hand to mouth activity;

2) a developing CNS that is more susceptible to the neurotoxic effects of lead;

3) average fractional absorption of lead through the gastrointestinal and

respiratory tracts is greater in children compared to adults;

4) slower clearance of lead from their bodies;

5) nutritional deficiencies (iron and calcium) in children, which may enhance

lead absorption and exacerbate toxicity.

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Lead poisoning varies with season, with the peak incidence occurring during the summer

and early fall. This may be related to an increased environmental lead burden created by

the opening and closing of windows in the warm summer months, as well as the amount

of time that children spend outdoors in contact with contaminated soil and other

environmental sources.

Fortunately, the prevalence of lead toxicity has decreased over the years, mostly due to

environmental interventions of lead removal from paint and gasoline. Healthy People

2010 established a target of eliminating childhood lead poisoning as a public health

problem. A recent examination of the NHANES data comparing the prevalence of lead

levels >= 10 ug/dL in children 1-5 years of age between 1991-1994 and 1999-2004 is

presented below: Blood lead levels in children continue to be highest among non-

Hispanic black children compared to Hispanic and non-Hispanic white children. Children

(1-5 years of age) enrolled in Medicaid have a prevalence 3 times higher than children

not enrolled. Medicaid enrollees accounted for 60% of children 1-5 years who had lead

levels > 10 ug/dL. (Jones, 2009)

Characteristic % of children, ages 1-5, with BLLs > 10 ug/dL

1991-1994 1999 – 2004

Race/ Ethnicity

Black, non-Hispanic 11.2% 3.4%

Mexican-American 4.0% 1.2%

White-non Hispanic 2.3% 1.2%

Income

Low 8.0% 1.8%

Middle or High 1.5 % 0.8%

Insurance

Medicaid 1.9%

No Medicaid 1.1%

All children 4.4% 1.4%

State wide screening in Rhode Island examined geomapping and the burden of lead

toxicity in neighborhoods. This study found that those children in the highest quintile

for poverty had higher rates of blood lead levels >= 10 ug/dL.,demonstrating continued

health disparities with lead toxcity. (Vivier 2011)

Despite important gains, children continue to have elevated lead levels, suggesting the

need to consider multiple sources of lead exposure and raising the importance of public

health interventions to reduce or eliminate environmental lead so that children have no

exposure. This further emphasizes the importance of primary prevention in order to meet

the Healthy People 2020 goals. The CDC has identified the following steps as necessary

to try to achieve the Healthy People 2020 goals (Brown 2008):

1. Continue intensive screening/testing to identify affected children while

expanding programs for primary prevention

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2. Identify areas (communities, zip codes) where lead exposure risk is

disproportionately high

3. Provide resources to those areas where children are at higher risk for lead

exposure

4. Identify higher risk populations, such as recent immigrants from developing

countries and provide education

5. Develop and test strategies to ensure that the risk of lead exposure remains

low to children, even after national studies document that blood lead levels

have decreased

Key Points:

The CDC has progressively decreased the lead level defined as toxicity

Lead can affect every organ in the body

Children at highest risk include those who are Non-Hispanic black, have low

income and on Medicaid

Important to continue testing while also finding more precise ways to identify

children at risk.

Primary prevention is needed for next steps to eliminate lead toxicity

IV. SCREENING/ TESTING

Case 4. In an attempt to streamline clinic flow and ensure appropriate screening for

preventable disease, you are developing nursing triage guidelines for routine lead

testing. You have just reviewed the 2005 AAP guidelines on lead exposure in

children. Which of the following children should have blood lead testing

performed?

a. A 4 year old with previously normal lead levels at 1 and 2 years of age with

newly diagnosed anemia.

b. A 32 week gestational age premature infant, parent’s first child, who is now 6

months old

c. A 3 year old who you are seeing for the second time who had a lead level of 15

ug/dL. 3 months earlier.

d. A 6 year old with normal levels at ages 1 and 2, now with a newly identified

speech delay.

Answer: c. A child with a lead level of 15-19 ug/dL should have a follow up level done

within 3 months of age. Prematurity would not influence your decision making for lead

testing and 6 month olds are not routinely screened unless there were other siblings with

elevations or other known risk factors. Anemia and speech delay are not, by themselves,

indications for lead testing.

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The CDC and AAP currently recommend that universal testing of children should

be performed at 1 and 2 years of age for any child who is Medicaid eligible.

Routine testing at 1 year will identify those at increased risk and allow earlier

intervention, screening at 2 years will address the age when the lead levels tend to

peak.(Rischitelli, 2006, Laraque 2005). Children 36 to 72 months of age who previously

had not been tested and meet these criteria, should have blood lead testing. A recent

study in Pediatrics has demonstrated that greater continuity of care was associated with

increased likelihood of receiving screening for lead (Flores, 2008).

For children not eligible for Medicaid, individual state recommendations exist for

targeted screening. While the CDC has suggested that health departments develop

screening strategies based on zip code, a recent study has suggested census block groups

may be better at identifying high risk children and guide testing for those children most at

risk. (Kaplowitz 2010, Vivier 2011). Contact with your local health department may

also help you to determine the areas in your community at highest risk and guide lead

testing. The website http://www.aoec.org/pehsu.htm lists pediatric environmental health

specialty units that may be helpful to clinicians and families.

The 1997-98 lead risk assessment questionnaire proposed by the CDC is listed below.

Any child whose caretaker answers “yes” or doesn’t know the answers to any of the 5

questions should have a lead test performed.

Does your child-

1) Live in or regularly visit a house with peeling or chipping pain built before

1960? This could include a day care center, preschool, the home of a babysitter

or a relative.

2) Live in or regularly visit a house built before 1960 with recent, ongoing, or

planned renovation or remodeling?

3) Have a sibling or playmate being followed or treated for lead poisoning?

4) Live with an adult whose job or hobby involves exposure to lead?

5) Live near an active lead smelter, battery recycling plant, or other industry likely

to release lead?

This questionnaire has not been found to be well validated and has been found to be

particularly ineffective in areas with higher prevalence of lead toxicity. A recent

systematic review of lead assessment questionnaires (including the CDC questionnaire)

reported low sensitvity and specificity for the screen (Ossiander 2012).

The 2005 AAP policy statement doesn’t mention the above questionnaire.

Lead testing should be considered for:

* Siblings of children known to have elevated lead levels

* Children with enhanced pica activity

* Children with known exposures to other risk factors in addition to lead paint

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* Recent immigrants, refugees, or international adoptees when they arrive in the US (Red

Book, 2006)

The following table includes the 2005 AAP Clinical Evaluation for Lead Exposure.

Medical history: ask about:

Symptoms

Developmental history

Mouthing activities

Pica

Previous blood lead concentration measurements

Family history of lead poisoning

Environmental history Paint and soil exposure

What is the age and general condition of the residence or other structure in which

the child spends time?

Is there evidence of chewed or peeling paint on woodwork, furniture or toys?

How long has the family lived at that residence?

Have there been recent renovations or repairs to the house?

Are the windows new?

Are there other sites at which the child spends significant amounts of time?

What is the condition/make-up of indoor play areas?

Do outdoor play areas contain bare soil that may be contaminated?

How does the family attempt to control dust and dirt?

Relevant behavioral characteristics of the child

To what degree does the child exhibit hand-to-mouth activity?

Does the child exhibit pica?

Are the child’s hands washed before meals and snacks?

Exposure to and behaviors of household members

What are the occupations of adult household members? What are the hobbies of household members? (Fishing, working with ceramics or

stained glass, hunting)

Are painted materials or unusual materials burned in household fireplaces?

Miscellaneous

Does the home contain vinyl mini-blinds made overseas and purchased before 1997?

Does the child receive or have access to imported food, cosmetics, or folk

remedies?

Is food prepared or stored in imported pottery or metal vessels?

Does the family use importuned pottery or metal vessels?

Does the family use imported foods in soldered cans?

Nutritional history

Take a dietary history

Evaluate the child’s iron status by using the appropriate laboratory tests

Ask about history of food stamps or participation in the Special Supplemental

Nutrition Program for Women, Infants and Children (WIC)

Physical examination

Pay particular attention to the neurologic examination and the child’s psychosocial

and language development

LABORATORY TESTS:

Blood lead levels (BLL) are the gold standard for identification of lead toxicity. Venous

lead levels are more cost effective in high prevalence regions since capillary samples can

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

be contaminated by lead on the skin resulting in potential false positives.. Blood samples

from capillary specimens may also underestimate the true BLL if the finger is squeezed

to obtain the sample (lead content may be diluted with tissue fluids). Lead does not

remain in blood for long periods (half life about 30 days) and therefore a BLL is a

“snapshot” in time. Low BLLs do not exclude the possibility of bone lead stores. Recent

data has demonstrated that patients with high lead peaks may take years to reach a normal

venous lead level because of equilibrium between bone and blood stores.

Key Points:

Both CDC and AAP suggest testing children who receive Medicaid at 1 and 2

years of age.

Children 36-72 months on Medicaid who were not previously tested should be

tested

Check with your public health departments for local recommendations for lead

testing based on environmental lead burden for children who are not on

Medicaid.

The CDC lead risk assessment has poor specificity for children who live in

older homes built before 1960, ie those in urban environments.

Consider lead testing for siblings of children with elevated lead levels, children

with continued pica behavior, and those exposed to sources of lead, other than

from lead paint

Venous blood lead levels are the gold standard for testing.

V. MANAGEMENT AND FOLLOW-UP

Case 5. Peter is a 5 year old child with a history of mild speech delay. You order a

blood lead level as part of his school entrance physical because you cannot

document any previous lead testing results. His blood lead level is 35 ug/dL today.

Which of the following is true concerning management of elevated blood lead in this

setting?

a. Chelation has been shown to improve cognitive outcomes in children with

levels above 30 ug/dL.

b. Although chelation does not improve cognitive outcomes, it is recommended

in this setting as the best means to return blood lead to normal levels

c. Immediate remediation of the child’s home is required by law and the child

and family should be housed in temporary quarters pending completion of the

remediation

d. Environmental investigation of the home and repeat testing within one week

are indicated.

Answer: d. Environmental investigation of the home by the health department and repeat

lead testing is indicated to ensure that the level is not rapidly increasing. A landmark

randomized controlled trial (Rogan, NEJM, 2001) demonstrated that chelation made no

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difference in cognitive outcomes in children ages 12-33 months of age with lead levels of

20-44 ug/dl when examined 36 months later or at 7years of age (Dietrich 2004).

Although remediation of a child’s home would be preferred, few federal funds have been

available to do so at this lead level although future advocacy efforts may address this

intervention. This also demonstrates why primary preventions are needed, prior to the

child being exposed. Note that the fact that this child had a language delay was not the

reason for lead testing, but rather lack of evidence of a previous lead level.

The most important intervention is identification of a child at risk for lead toxicity and

removal from the lead source. The following tables indicate the most recent

recommended actions for a confirmatory level once an elevated level is identified and

ongoing schedule for follow up.

(http://www.cdc.gov/nceh/lead/ACCLPP/blood_lead_levels.htm

9

Actions Based on Blood Lead Levels

<Reference Value ≥Reference Value ≤45 ug/dL

≥45 and ≤69 ug/dL ≥70 ug/dL

In addition to actions for levels less than reference:

In addition to actions for levels less than 45:

Lead education

Dietary

Environmental

Environmental assessment* for pre -1978 housing Lab work:

Follow up blood

lead monitoring

Complete history and physical exam Lab work:

Iron status

Consider

hemoglobin or

hematocrit

Environmental investigation

Lead hazard

reduction

Neurodevelopmental monitoring Abdominal X-ray (if particulate lead ingestion is suspected) with bowel

Lab work:

Add free

erythrocyte

protoporphyrin

to labs

Oral chelation therapy

Consider

hospitalization if

lead-safe

environment

cannot be

assured

Lab work:

Confirm with

venous blood

lead test

Hospitalize and commence chelation

in

consultation

with medical

toxicologist

or a pediatric

environment

al health

specialty unit

Proceed with actions for blood lead level 45 – 69

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decontamination if indicated

ug/dL

*The scope of an “environmental assessment” will vary based on local resources and site conditions. However, this would include at a minimum a visual assessment and housing conditions, but may also include testing of paint, soil, dust, and water and other lead sources discussed previously. This may also include looking for exposure from imported cosmetics, folk remedies, pottery, food, toys, etc. which may be more important with low level lead exposure.

Schedule for Follow-up Testing after Elevated Levels Identified

Venous Blood Lead Level μ/dL

Early Follow up Testing (2-4 tests after identification)

Later Follow-up Testing After Blood Lead Level Declining

≥ Reference Value -9 3 months* 6-9 months

10-19 1-3 months* 3-6 months

20-24 1-3 months* 1-3 months

25-44 2 weeks – 1 month 1 month

≥45 As soon as possible As soon as possible

a Seasonal variation of BLLs exists and may be more apparent in colder climate areas. Greater exposure in the summer

months may necessitate more frequent follow ups.

*Some case managers or PCPs may choose to repeat blood lead tests on all new patients within a month to ensure that

their BLL level is not rising more quickly than anticipated.

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

While testing can identify children with lead toxicity, follow up of elevated levels is

critical. In a retrospective cohort study of children aged 6 years or younger with a blood

lead level >= to 10 ug/dL, follow up testing was received by only 54% of the children.

Of those who did not have follow up testing, 59% had at least one medical encounter in

the 6 month period after the elevation (Kemper, 2005).The CDC emphasizes the need for

primary care providers to notify families of children with lead level elevations in a timely

and appropriate manner to ensure continued follow up.

(www.cdc.gov/nceh/lead/ACCLP/blood_lead_levels.htm)

Not Recommended at Any Blood

Lead Concentration

Searching for gingival lead lines

Evaluation of renal function (except during

chelation with EDTA)

Testing of hair, teeth, or fingernails for lead

Radiographic imaging of long bones

X-ray fluorescence of long bones

Picture of lead lines in long bones

(www.learningradiology.com/notes/bonenotes/leadpoisonpage.htm.)

Management includes medical interventions by chelation, nutritional and environmental

strategies.

Chelation

Specific medical treatment with chelation should be instituted for children whose lead

levels are > 45 ug/dL. This therapy promotes the mobilization and excretion of lead

mostly from blood and soft tissues (Chisolm 2001), The acute symptoms of lead toxicity

of abdominal pain, renal injury and encephalopathy are related to lead concentration in

the blood and soft tissue, which is only about 5% of the total body burden. No chelating

agents acutely remove lead from the bone.

Chelation agents used in children include dimercaprol, (BAL), calcium disodium

ethylenediaminetettra acetic acid (CaNa2EDTA) and Succimer@, DMSA (2,3

dimercapto-succinic acid or). The table below serves as a brief overview (Laraque 2005,

Gracia 2007, Harriet Lane Handbook). More complete details are beyond the scope of

this module. Remember that chelation for lead toxicity should be done in conjunction

with a toxicology specialist. Please refer to the complete resources if contemplating

chelation therapy in patients.

Agent Recommended

Dosage

Indication Contraindications

Dimercaprol

(BAL)

75 mg/m2 IM every

4 hours for 5 days

BLL>=70 ug/dL

Encephalopathy

Severe symptoms

Hepatic Disease

Peanut Allergy

G6PD deficiency-

hemolysis

Calcium

Disodium

1000-1500

mg/m2/day as

BLL>=45 ug/dL Anuric Patients

Monitor

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

Ethylene-

diaminetetra

Acetic Acid

(EDTA)

Should not be

used as sole

therapy, use

4 hours after

BAL

continuous IV

infusion for 5 days

electrolytes

Succimer

(DMSA)

350mg/m2 every 8

hours po daily for 5

days, then decrease

to every 12 hours

for14 days

or:

10 mg/kg/dose po

every 8 hours for 5

days followed by 10

mg/kg/dose every12

hours for 14 days

Preferred agent for

patients with BLL >

45 ug/dL who are

asymptomatic at

presentation

Monitor LFTs,

CBC

CHELATION SHOULD ALWAYS BE PERFORMED IN CONSULTATION WITH A

PEDIATRICIAN OR TOXICOLOGIST WITH EXPERTISE IN MANAGING LEAD

TOXICITY. CHILDREN NEED TO BE IN A LEAD FREE ENVIRONMENT WHEN

BEING CHELATED.

Several adverse effects are associated with these therapies and a few examples are listed

here, but these are not exhaustive and complete details can be found in the references.

Adverse effects associated with Dimercaprol (BAL) include hemolysis in G6PD deficient

patients, nausea, vomiting, and hypertension. While an effective chelating agent,

Calcium EDTA can increase lead distribution to the central nervous system UNLESS

dimercaprol (BAL) therapy is used 4 hours prior. Hence, Calcium EDTA should NOT be

used as a sole agent. Adverse effects in EDTA include proteinuria, hematuria, fever,

chills and hypokalemia. Succimer is the only oral agent and adverse effects include

nausea, vomiting, diarrhea, appetite loss, rash,elevation of liver function tests, anemia,

and neutropenia. Every effort needs to be made to have children return to live in a lead

free environment both during and fter chelation, otherwise continued exposure will occur.

The take home message is that these chelating agents have toxicity, and should be used

prudently by clinicians who have expertise with their use.

The equilibrium of lead deposition between blood and bone is important to consider. The

blood lead level will often dramatically decrease after a first course of chelation is

completed only to increase 1-3 weeks later as re-equilibration between bone and blood

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

levels occurs. Consequently, multiple courses of chelation are often necessary for

children with highly elevated levels. (Roberts, 2001, Gracia 2007)

Currently there is no indication to chelate children with lead levels < 45 ug/dL as

chelation does not improve cognitive outcomes. The “Toxicity of Lead-Exposed

Children Study” sponsored by the National Institute of Environmental Health Sciences

(NIEHS) examined the impact of oral succimer in children 11-33 months of age with lead

levels of 20-44 ug/dL. This randomized trial of patients receiving either succimer or

placebo showed no statistically significant difference between groups in scores on tests of

cognition, behavior, or neuropsychological function 36 months later ( Rogan 2001) or in

a follow-up study of the same cohort at 7 years of age. (Dietrich 2004). Although the

lead levels of the children in the succimer treated group were initially decreased, the lead

levels were comparable at later time periods in the study. This suggests that permanent

neurocognitive effects occur after lead exposure.

Nutritional Strategies

The current recommendations (AAP 2005) include increasing iron, calcium and vitamin

C in the diet of children with elevated lead levels. While there are no randomized trial

data to support nutritional interventions, laboratory and clinical data suggest that

adequate iron and calcium stores may decrease lead absorption and adequate vitamin C

may increase renal excretion. Recommending a multi vitamin supplement and frequent

handwashing to reduce ingestion of lead dust is warranted. An additional suggestion is to

measure iron status to ensure iron replete.

Environmental Strategies

The environmental investigation of a child identified with an elevated lead level should

include the following: See table from 2005 AAP guidelines:

1) An environmental history (See link)

2) Environmental inspection of home and any other residence where the child

spends a substantial amount of time.

3) Lead measurement of paint, dust, soil or water as is appropriate based on age

of dwelling and zip code prevalence data

4) Attention to and control of any hazards

5) Remediation of the home

6) Relocation depending on the degree of elevation of the lead level and

available lead free housing.

Abatement also remains an important strategy but is difficult to implement widely.

Abatement needs to be done by specialized teams trained in the techniques. Total

abatement of an entire home may cost approximately $15-20,000. Studies done through

the Repair and Maintenance Study in Baltimore looked at different abatement

approaches; 1) cleaning and removal of peeling paint 2) addition of floor sealants,

window and door treatments, and 3) the above plus window replacements, encapsulation

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

of windows and doors and floor coverings. In homes that were in modest repair, these

less intensive levels of abatement led to decreased lead dust, and decreased lead levels in

children 24 months later. Abatement remains an important strategy since a lead toxic

environment remains a risk to other children/families who may move to that property.

While intense professional cleaning in one study demonstrated effectiveness in

decreasing children’s lead levels (Charney, 1983), no study thus far has demonstrated the

benefit of providing families with instructions and cleaning supplies. A recent Cochrane

review of 14 studies of randomized and quasi-randomized controlled trials showed that

household educational and dust control interventions were ineffective in reducing blood

lead levels in an population based measure (Yeoh 2012). This confirmed an earlier

Cochrane review of household intervention trials from 1996-2006 found that “there is no

evidence of effectiveness for household interventions for education or dust control

measures” and “insufficient evidence for soil abatement or combination interventions.”

(Yeoh 2008). However, no changes have yet been made to the AAP recommendations.

Health departments are offering more assistance with testing of lead paint, identifying

environmental lead hazards, remediation and resources concerning lead free housing so

contacting them with lead level elevations is important if not automatically done.

Additional practical interventions include putting a barrier such as furniture or locked

door between the child and areas thought to have increased lead such as a window wells,

or temporarily covering the surface with duct tape or contact paper until remediation can

occur. (http://www.cdc.gov/nceh/lead/tips.htm.

Key points:

Children with elevated lead levels require follow up

Dietary interventions include increasing iron, calcium and vitamin C intake, in

addition to frequent hand washing.

Chelation is only indicated for lead levels >= 45 ug/dL.

Chelation should be conducted in consultation with a pediatrician or

toxicologist with expertise in lead toxicity.

City health departments can be an important resource for testing of lead paint in

the home and recommendations for remediation and other environmental lead

hazards.

VI. PREVENTION: Primary vs. Secondary Prevention

Case 6. You are asked to participate in a city-wide summit on reduction of lead

toxicity. The summit seeks to develop potential interventions to meet the Healthy

People 2020 goal of elimination of lead toxicity. Although the number of lead

exposed children has decreased in the past 2 decades, true elimination will require

primary prevention. Which of the following interventions would you advocate for

in the spirit of primary prevention?

a. Universal lead testing of 2 year old children.

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

b. Lead testing of paint in homes and remediation accordingly.

c. Professional cleaning in homes where a child has an elevated lead level.

d. Facilitating a move to a lead free home when a child is discharged from the hospital

following chelation.

Answer: b. Evaluation and remediation of homes without prior knowledge of whether a

resident has been exposed to lead is an example of primary prevention. The other

answers are all secondary prevention.

Most of what we currently do are examples of secondary prevention; blood lead testing

to identify children at risk, follow-up of elevated levels, and cleaning, nutritional

interventions, abatement of the home or moving once the child has been identified as

having lead toxicity in order to minimize continued exposure. However, as the data

show that the neurocognitive changes from lead toxicity are irreversible, primary

prevention is critical. This is a key area of advocacy for our patients.

Primary prevention is targeted at preventing children from ever being exposed to lead,

rather than intervening after the exposure. Studies have shown that the cost of

hospitalizing a child for treatment of lead toxicity is greater to or equal to what it would

cost to repair the home to make it lead safe (Chisolm 2001). The most effective way to

accomplish primary prevention is to reduce residential lead hazards before the child

moves into the home. Healthy People 2020, has proposed elimination of childhood lead

poisoning; the recommendations are outlined in the attached link:

(www.healthypeople.gov/2020/. This is the first time a strategy of primary prevention,

targeted at housing, has been nationally disseminated. Projects sponsored by the Housing

and Urban Development (HUD) and the Environmental Protection Agency (EPA) have

identified lead hazards in homes (Lanphear 2005).

Reducing blood lead levels to less than 1 ug/dL in US children < 6 years would result in

enhanced high school graduation, crime reductions and improved workforce capability

leading to overall savings of $1.2 trillion. (However, the cost of attaining this goal of lead

reduction wasn’t included in the estimate). The conclusions of the authors support that

more intensive national programs need to be developed to reduce childhood lead

exposure before it ever happens, again reinforcing PRIMARY PREVENTION (Muennig

2009). The new CDC reference value of concern for lead levels > 5 ug/dL reinforces the

need to concentrate on primary prevention.

Federal Laws

Families should be informed about federal laws involving lead-based paint in rental

properties and their legal rights. The main federal laws are mentioned below, with

further information available through the noted web sites.

1. Title X- Federal Residential Lead-based Paint Hazard Reduction Act of 1992.

Sellers and leasers of residential housing built before 1978 must disclose the

presence of known lead-based paint and or lead based paint hazards in the

property. This law went into effect on Dec 6, 1996.

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

2. Federal HUD Lead-Based Regulations 1012/1013. This law is to protect young

children from lead-based paint hazards in housing assisted by the federal

government. This includes stabilization of deteriorated paint, including correction

of moisture leaks or obvious causes of paint deterioration and ongoing

maintenance of the paint in housing built before January 1, 1978. This law went

into effect Sept 15, 2000.

3. Federal Lead-Based Paint Pre-Renovation Education Rule (Lead PRE rule). This

law addresses contractors and property managers who perform renovations for

compensation in residential housing that may contain lead paint. The work is

done in pre-1978 houses or apartments, and an educational pamphlet must be

distributed prior to renovations and confirmation of receipt of the pamphlet.

4. Fair Housing Law Act This prohibits discrimination in housing because of race,

color, religion, familial status or handicap. It also prevents refusal to rent or sell

to a family who has a child who is lead poisoned.

Additional information can be obtained from:

http://www.leadsafe.org/content/homes_and_lead/index.cfm?pageID=146 or the HUD

(http://www.hud.gov/offices/lead ) or EPA (http://www.epa.gov/lead) websites.

Families with young children should understand the lead risks of a home or apartment

they are about to inhabit. Important resources and websites are linked below.

Resources/ websites for Providers and Parents

U.S Department of Health and Human Services, CDC, Lead Poisoning Prevention

Branch. Information about lead screening plans by states. Website:

http://www.cdc.gov/nceh/lead, Last accessed 5/28/2010.

U.S. Department of Housing and Urban Development, Office of Healthy Home and Lead

Hazard Control. Website: http://www.hud.gov/offices/lead. Last accessed 5/28/2010.

U.S. Environmental Protection Agency, Office of Pollution Prevention and Toxics.

Website: http://www.epa.gov/lead, Last accessed 5/28/2010.

U.S. Consumer Product Safety Commission. Website: http://www.cpsc.gov. Last

accessed 5/28/2010.

Key Points of the Module:

1) Lead dust is the most common etiology of lead toxicity

2) Renovation of homes/apartments that have lead paint puts children and pregnant

women at risk

3) The prevalence of lead toxicity is highest in the following populations: low

socioeconomic status, African Americans and children who receive Medicaid.

4) The prevalence of lead toxicity of children with lead levels >= 10 ug/dL has

continuously decreased in the US, most likely secondary to legislature to remove lead

from paint, gasoline and soldered cans.

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

5) New research has shown neurcognitive effects of lead at levels < 10 ug/dL.

6) A new CDC reference value of lead level >= 5 ug/dL. Has been noted with new

follow up strategies. There is no safe lead level.

7) Lead testing at 1 and 2 years of age is required for children who receive Medicaid.

8) The neuro-cognitive effects of lead toxicity appear to be irreversible.

9) Children identified with lead levels >= 45 ug/dL should receive chelation.

10) Chelation will ameliorate acute symptoms associated with lead deposition in blood

and soft tissues, but has not been shown to reverse neurocognitive effects.

11) Continued testing of children with risk factors is needed to identify those with lead

levels that warrant chelation, but also to identify those children for whom an

environmental exploration is needed.

12) Primary prevention is essential in order to PREVENT children from lead exposure.

We as health care providers need to advocate for public health policy to eliminate

lead toxicity and health care disparities.

Post Test:

1. Which of the following exposures is NOT found to be a risk factor associated with lead

toxicity?

a. Father works in a battery plant

b. Recent immigration from Egypt

c. Frequent eating of tuna and salmon

d. Renovation of home built in 1948

2. You receive the results of lead screening for your 2 year old patient and his blood lead

level is 50 ug/dL. He has been asymptomatic thus far. Which of the following responses is

correct?

a. Reassure the parents that chelation will reverse any neurocognitive effects

b. Repeat the lead level and consult with a toxicologist to begin chelation.

c. If an oral chelating agent is warranted, chelation therapy could occur at home.

d. One course of a chelating agent will be sufficient since chelation affects both

blood and bone lead concentration.

3. According to the most recent NHANES data on blood lead levels in US children ages 1-5

years, which of these statements concerning lead toxicity rates is NOT CORRECT?

a. Black, Non-Hispanic children have higher rates of lead toxicity than other

groups

b. Children with Medicaid have higher rates than those with other forms of

insurance

c. Rates have declined in all demographic groups since the 1991-94 NHANES

survey

Johns Hopkins Harriet Lane Continuity Clinic Curriculum 2013

d. Children in middle income families have higher rates of toxicity than those in

either low or high income families

4. You are involved with a quality improvement project in your continuity practice and

performing chart reviews. Which of the following children did not require lead

testing?

a. 2 year old who receives Medicaid, whose lead level at 1 year of age was < 2

ug/dL.

b. 3 year old with microcytic anemia

c. 18 month old whose lead level 3 months ago was 15 ug/dL.

d. 4 year old whose 2 year old sibling was found to have a lead level of 18

ug/dL.

5. Your 2 year old patient is found to have a lead level of 40 ug/dL. Which of the

following is warranted?

a. Perform X ray fluorescence of long bones

b. Enhance intake of vitamin B 12.

c. Initiate chelation since it is bound to increase.

d. Recheck lead level in 1 week and ensure follow up with patient.

6. The mother of a 17 month old patient tells you they have recently moved into an

apartment and that they have noticed peeling paint on one of the walls. The building

is “quite old” according to the mother. Which of the interventions would be

recommended?

a. Place a barrier such as furniture in front of the area as a temporary measure

b. Withhold rent until the landlord completes remediation of the lead problem

c. Scrape away the paint

d. Set up a fan to blow any dust away from the rest of the apartment

Post test answers:

1. c, 2. b, 3. d, 4. b, 5. d 6.a

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American Academy of Pediatrics. Committee on Environmental Health. Screening for

elevated blood lead levels. Pediatrics.1998; 101(6):1072-1078.

Bellinger DC, Needleman HL. Intellectual impairment and blood lead levels. N Engl J

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Bellinger DC. Very low lead exposure and children’s neurodevelopment. Current

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Bernard S, McGeehin MA. Prevalence of blood lead levels>= 5 mcg/dL among US

children 1 to 5 years of age and socioeconomic and demographic factors associated with

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Brown MJ. Childhood lead poisoning prevention: Getting the job done by 2010. J

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Gollenberg AL, Hediger ML, Lee PA, Himes JH, Louis GMB. Association between lead

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