Childhood Lead Poisoning: Is It Still a Problem

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Childhood Lead Poisoning Is It
Still a Problem?

• John Pardalos, M.D.
• Assistant Professor, Neonatology
• Department of Child Health

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EPSDT Screening

• Comprehensive Health and Developmental History
• Unclothed Physical Exam
• Health Education (including anticipatory
  guidance)
• Hearing, Vision and Dental Screens
• Immunization Status
• Lead Screening
• Appropriate Laboratory Tests
• Referrals for Follow-up Care or Evaluation
• EPSDT 72 Level 3 visit 33.50

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Infants Screened for Lead
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What is the public health problem?

• Childhood lead poisoning major preventable
  environmental health problem
• Lead poisoning causes
• Low levels Learning disabilities, behavior
  problems
• High levels seizures, coma, death
• CDC goal Eliminate lead poisoning by 2010

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So What is Lead?

• Lead (Pb) is a metallic element
• Atomic Number 82
• Atomic Weight 207
• First smelted around 4000 B.C.
• By-product of silver processing
• Contributed to the fall of Roman Empire

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Childhood Lead Poisoning

• Lead poisoning Recognized disorder in 1917
• Added lead to gasoline in 1920s
• Continued use of lead paint into 1970s
• After leaded gas and paint were stopped, average
  BLL dropped from 16 to 10 mcg/dL
• Lead remains in environment -- not degraded
• Developing world still uses lead gas and paint

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Toxic Blood Lead Levels
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Prevalence of Lead Toxicity

• Prevalence has decreased over last 30 years
• Preschool screening programs
• Increased public awareness
• Removal of lead from gasoline and paint
• Prevalence of BLL gt 10 mcg/dL
• 1976 88 1994 4.4
• Currently 1 million kids lt 6 yrs old
• Inner city African Americans 36
• Suburban non-poor White 4

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Prevalence of Lead Toxicity

• Highest rate Inner-city children in
  deteriorating houses built pre-1970s
• Urban gt Rural
• Low income gt Middle income
• Higher risk
• Older housing
• Refugee children
• Foster care children

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Prevalence of Lead Toxicity

• Children lt 6 years old (12-36 months) more
  susceptible to lead than adults
• Incomplete blood-brain barrier gt Lead enters CNS
• Due to greater tendency of Fe deficiency gt
  increased GI absorption of lead
• Greater exposure risk due to crawling and
  hand-to-mouth behavior

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Sources of Lead Exposure
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Exposure to Lead

• Normal development places kids at risk if live in
  lead-containing environment
• On floor crawling gt walking
• Hands in contact with lead dust or soil
• Normal hand-to-mouth and mouthing behavior
  (teething 6-24 months)

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Exposure to Lead

• Before 1955, lead content in white house paint
  was 50
• Eliminated in 1978 Consumer Product Safety
  Commission limited lead content of paint to lt
  0.06 (residential surfaces, toys, or furniture)
• Window sills highest conc. of lead dust
• 1990-DHUD 3 M. tons of lead in 57 M. homes
• Screen kids in homes built before 1950

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Exposure to Lead

• Soil Lead in top 2-5 cm
• Water
• Lead absorbed from water gt food
• 50 of lead ingested by children from H2O
• Municipal water tested but not in homes
• House water Lead solder in copper pipes,
  storage cisterns, Non-city water, aging coolers,
  water heaters, H2O acidity, higher H2O
  temperature, standing in pipes

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Exposure to Lead

• Food contaminated during production, processing
  or packaging
• Grown in leaded soil
• Exposed to car exhaust (lead fuel)
• Food cans Used lead soldergt oxidation when
  opened (worse with acidic food)
• Other sources Lead-glazed pottery, lead
  crystal, lead cooking vessels, plastic bags with
  yellow or red lead pigment

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Exposure to Lead

• Inhaled lead from leaded gas
• Leaded gasoline outlawed in 1978
• From 1976 to 1989
• Use of leaded gasoline dropped 50
• BLL dropped 37
• Other sources Industry using lead, smelting or
  mining lead,
• Leaded gasoline Other countries
• European Union Banned in 2000
• World Bank and UN Commission on Sustainable
  Development global ban

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Exposure to Lead

• Hobbies
• Stained-glass windows
• Glazed pottery
• Lead shot
• Home remodeling

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Toxicology Absorption

• Route of exposure
• Inhaled 100
• Age and nutritional status
• GI tract
• Kids and pregnant women 70 vs Adults 20
• Increased absorption Fasting, Fe or Ca
  deficiency

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Toxicology

• Half-life depends on location
• Blood 28-36 days
• Soft tissue 40 days
• Mineralized tissue gt 25 years
• Excretion-Kidneys, Biliary tree
• Retention-Kids (lt 2 yrs) 1/3, Adults 1
• gt 70 of total body lead in mineralized tissue
• BLL not good reflection of total body lead burden

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Toxicology

• Mineralized tissue
• Labile compartment exchanges with blood
• Inert pool mobilized during stress
• Pregnancy, lactation, fractures, chronic disease
• Represents endogenous lead source gt may cause
  lead toxicity

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Toxicology Molecular

• Toxic substance with no threshold
• Interferes with interaction of divalent cations
  and sulfhydryl groups
• In vitro, lead acts as competitive inhibitor and
  is reversible
• In vivo, downstream events cause cell death and
  irreversible damage (CNS)

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Toxicology Molecular

• Disrupts signal transduction cascades
• Activates protein kinase C
• Competes with Mg
• Inhibits cyclic nucleotide hydrolysis by
  phosphodiesterases
• Inhibits N-methyl-D-aspartate-type glutamate
  receptor
• Uncouples mitochondrial oxidative phosphorylation
• Competes with Ca in synaptosomes
• Interacts with numerous receptor-activated and
  voltage-gated cation channels
• Increases infidelity of DNA and RNA polymerase
  gt somatic and germline mutations.

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Toxicology Molecular

• Inhibits aminolevulinic acid synthetase and
  aminolevulinic acid dehydratase heme
  biosynthesis
• Inhibits ferrochelatase
• Inhibits 5 pyrimidine nucleotidase gt basophilic
  stippling of RBC

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Peripheral Blood Smear
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Clinical Manifestations CNS

• Development delay to loss of milestones to
  encephalopathy
• Population-based studies show BLL gt10 mcg/dL
  affect cognitive and behavioral development.
  Also seen in lower BLL
• Symptoms persist despite decreasing BLL
• Other symptoms
• Hearing loss higher frequencies
• Peripheral neuropathy-rare except with SC anemia
• Decrease nerve conduction velocity BLL gt20
  mcg/dL

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Clinical Manifestations CNS

• Acute encephalopathy BLL gt100-150 mcg/dL
• Persistent vomiting
• Altered or fluctuating state of consciousness
• Ataxia
• Seizures
• Coma
• Cerebral edema Younger gt Older children
• Develop SIADH, partial heart block, decreased
  renal function

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Clinical Manifestations Hematology

• Rarely causes anemia
• Decreased Hgb synthesis BLL gt40 mcg/dL
• Blocks heme pathway enzymes
• Increased hemolysis BLL gt70 mcg/dL
• Actually due to Fe deficiency
• Lead mild, hemolytic and normocytic anemia
• Fe deficiency hypochromic, microcytic,
  reticulocytopenic

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Diagnosis

• Definition of lead poisoning
• BLL gt10 mcg/dL
• Most children with mild lead toxicity are
  asymptomatic and can only be diagnosed through a
  lead screening program

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Diagnosis

• Acute encephalopathy of unknown cause
• Clinical findings consistent with lead
• Strongly positive qualitative urine
  coproporphyrin
• Basophilic stippling of RBC or erythroblasts in
  marrow
• Hypophosphatemia
• Glycosuria
• Lead flecks on abdominal x-ray
• Lead lines on long-bone x-ray
• Elevated free erythrocyte protoporphyrin levels
  gt35 mcg/dL
• Aminolevulinic acid in urine

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Evaluation
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Evaluation History

• Onset and severity of symptoms
• Nutritional history Fe and Ca intake
• History of Pica
• Family history of lead poisoning
• Potential sources of lead parents work history,
  hobbies, age of home, history of renovations,
  water supply, location and condition of play
  area, imported or glazed ceramics, proximity to
  industrial facilities or hazardous waste sites

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Evaluation Physical Exam

• Assess for neurologic deficits
• Language development
• Neurobehavioral function
• Lethargy May indicate encephalopathy

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Evaluation Laboratory

• 1st obtain venous blood lead level (gold
  standard)
• Patient, siblings, housemates and/or playmates
• Capillary blood lead level Ideal for screen but
  may have false result
• Phlebotomist was not wearing gloves
• Used EtOH wipes contaminated with lead ink
• Inadequate cleansing of finger
• Failure to wipe off 1st drop of blood

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Evaluation Laboratory

• Free erythrocyte protoporphyrin gt35 mcg/dL
• Fe def, lead toxicity, inherited porphyrias
• Rule out Fe def CBC, retic count, serum Fe,
  Total IBC, and ferritin
• Prior to chelation therapy Serum lytes, BUN,
  Cr, Ca, Mg, LFTs and UA. May need to rule out
  G6PD def (pre succimer or dimercaprol)
• X-ray Abdominal, Long bones (gt45 mcg/dL)

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Treatment

• Cognitive and behavioral effects of lead toxicity
  are not reversible.
• Goal of treatment
• Reduce further lead exposure
• Skeletal system serves as endogenous reservoir
• Chelating agents
• Reduce immediate toxicity of acute ingestion
• Limited effect on reversing neurocognitive
  symptoms

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Treatment

• Management depends on lead level
• All children with level gt 10 mcg/dL
• Complete History and Physical Exam
• Identify source of lead exposure
• Symptoms of lead toxicity
• Identify others at risk
• Lab studies CBC, Reticulocyte count, serum Fe,
  TIBC and ferritin levels
• Notify the public health department to evaluate
  the environment for exposure (especially if gt15)
• Follow-up lead levels according to CDC schedule

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Chelation Therapy

• Dimercaprol (BAL)
• Increases urinary excretion of heavy metals by
  forming stable, nontoxic soluble chelates.
• Dissolve in peanut oil and give IM
• Contraindicated hepatic insufficiency/peanut
  allergy
• Use cautiously in renal impairment or HTN
• May induce hemolysis with G6PD deficiency
• Dose 75 mg/m2 every 4 hours
• Pretreat Diphenhydramine
• Encephalopathy 5 days Severe Toxicity 3-5
  days
• Goal 300-350 cc/m2 urine output (may need IVFs)

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Chelation Therapy

• CaNa2EDTA
• Increases urinary excretion of lead by forming
  non-ionizing soluble chelates.
• May increase lead conc. in CNS
• use it 4 hours after BAL given and urine output
  improves
• Route IV or IM (IM for acute encephalopathy)
• Dose
• IV 1000-1500 mg/m2 per day continuous or
  divided into 2-4 doses for 5 days
• IM 250 mg/m2 per dose every 4 hours for 5 days
• Discontinue CaNa2EDTA if anuric but continue BAL

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Chelation Therapy

• Agents remove lead from blood and soft tissues
  including brain reverse effects of acute
  encephalopathy
• Mortality decreased from 66 to 1-2 when both
  agents used
• Chelation therapy does not affect the neurologic
  sequelae of chronic lead toxicity
• Repeat lead level 2 days after treatment. Repeat
  therapy until level below 45 mcg/dL.
• If asymptomatic and BLL is 45-70 mcg/dL, may use
  DMSA (succimer) for 2nd etc. chelation course.

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Moderate Lead Poisoning

• Definition BLL is 45-70 mcg/dL and asymptomatic
• Chelation Therapy Oral vs IV
• Compliance with oral regimen
• Duration of lead toxicity
• Likelihood of renal or hepatic toxicity
• Allergy Sulfa or penicillin drugs
• Indications for hospitalization
• Close monitoring of patient during chelation
  therapy
• Removes child from source of lead exposure
• BLL gt 50 mcg/dL

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Chelation Therapy

• CaNa2EDTA
• Dose 1000-1500 mg/m2/day continuous drip IV for
  5 days.
• BAL not used
• Succimer (DMSA) Oral
• Increases urinary excretion of lead.
• Dose 10 mg/kg/dose or 350 mg/m2/dose TID for 5
  days then BID for 14 days
• Check level 10-14 days later. If rebounds to 80
  of original level repeat succimer course.

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Follow Up Recommendations

• Do not discharge until environmental
  investigation is complete and corrective actions
  taken. Discharge to lead-safe environment.
• Monitor BLL Every 2 weeks x 3, then every 1
  month x 3-4 and then every 3-4 months for 1 year.
  Follow until levels remain lt 30 mcg/dL

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Treatment

• Mild toxicity
• Venous BLL 25-44 mcg/dl
• Venous BLL 15-24 mcg/dl
• Venous BLL 10-14 mcg/dl

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Treatment
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Treatment
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Treatment
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Prevention

• Primary prevention Remove lead hazards from the
  environment
• Secondary prevention
• Early detection of lead-poisoned children
• Minimize further exposure and absorption

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Prevention

• Lead dust remains major source of lead exposure
  for children in US
• Lead paint abatement
• Difficult to assess due to release of lead from
  endogenous stores and/or increased exposure to
  dust during the abatement process
• EPA (1998) studied effectiveness
• Interventions reduce BLL in kids and lead dust in
  homes
• Magnitude of decline in BLL is directly related
  to preintervention BLL
• None of the interventions resulted in BLL lt 10
  mcg/dL
• CDC 10 Prevention (10-20 mcg/dL) Educate
  families to reduce lead exposure

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Prevention
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Prevention
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Prevention
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Screening

• Universal screening
• Inadequate data on the prevalence of elevated BLL
• gt 27 of houses built before 1950 (gt22 in MO)
• gt 12 of 1-2 year olds with BLL gt 10 mcg/dL
• Screen at 9-12 mon. of age and again at 24 mon.
• Targeted screening
• lt 12 of 1-2 year olds with BLL gt 10 mcg/dL
• lt 27 of houses build before 1950(lt22 in MO)
• Assess risk periodically from 6-72 mon. Draw BLL
  if risk factor present.

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Screening

• CDC screening questions
• Does child live in or regularly visit a house or
  child care facility built before 1950?
• Does your child live in or regularly visit a
  house or child care facility built before 1978
  that is being or has recently been renovated or
  remodeled (lt 6 mon)?
• Does your child have a sibling or playmate who
  has or did have lead poisoning?

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Screening

• Other risk factors
• Home renovation
• Folk remedies
• Old ceramic or pewter cookware
• Some parental occupations (smelting, soldering,
  auto body repair) or hobbies
• Inadequate nutrition
• Frequent hand-mouth activity
• Developmental disabilities
• Abused or neglected children

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Lead in Missouri

• Lead first found in Missouri in the 1700s along
  the Meramac River by French explorers
• In 1907 Missouri 1 lead producing state
• 2000 Census
• 24 of Missouri houses built before 1950
• 80 of Missouri houses built before 1978
• 6 of Missouri children (lt 6 year olds) had BLL
  gt10 mcg/dL

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Missouri Statutes

• Prior recommendations
• A risk assessment should be done on every child
  6-72 months when they present for a WCC.
• All Medicaid eligible children should have a
  blood lead level at 12 and 24 months as a minimum

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Missouri Statutes Senate Bill 266 (7/31/03)

• High risk
• Any lt 6 yr old who lives in or visits for gt 10
  hrs/wk a high risk community BLL annually
• All day care facilities in high risk areas will
  require a proof of lead testing signed by the
  healthcare provider within 30 days of the childs
  enrollment. Parents may sign note stating reason
  declined test. Otherwise the day care provider
  will need to offer assistance in scheduling lead
  test.
• Risk assessment form still needs to be done from
  6-72 mon. It may indicate need for earlier
  and/or more frequent testing.
• If child lives in residence built before 1978
  that is undergoing renovation, test child for
  lead every 6 mon. and once renovation is
  complete.

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Missouri Statutes Senate Bill 266 (7/31/03)

• Low risk
• Any lt 6 yr old who does not reside in high-risk
  community or visit a high-risk community for gt 10
  hrs/wk is in low risk category.
• If Medicaid eligible, must have BLL at 12 and 24
  mon. Its recommended that all children be
  tested at 12 and 24 mon. (Not in law but
  recommended by CMS and DHSS policies.)
• Risk assessment form still needs to be done at
  every WCC from 6-72 mon. It may indicate need for
  earlier and/or more frequent testing.

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Housing Built Prior to 1950
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Prevalence Rates--2002
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Issues

• My patients are not at risk!
• But 12 of 18 counties are High Risk per CDC
• A venous blood sample takes 7 cc of blood and we
  cant get that much out of a 12 mon old.
• Capillary-sample
• Filter paper
• Didnt know it was federal mandate that all
  Medicaid patients have a verbal risk assessment
  done at each WCC from 6-72 mon. and BLL drawn at
  12 and 24 mon.

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QA Plan

• All PCPs get a list of Mo Care patients each
  month who will turn 12 or 24 mon. old in the next
  month
• Letter is sent to each member with copy to PCP
  stating that they are due for BLL and if they
  need assistance setting up appointment, call
  member services.
• WCC reminder cards sent to each member. The 6-72
  mon. cards remind the patient about the verbal
  risk assessment and/or BLL requirements.

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Can Lead Poisoning be Prevented?

• Lead poisoning is entirely preventable.
• Stop kids from being exposed to lead
• Screen kids so elevated BLL are caught at lower
  level so further neurologic damage can be
  prevented.
• Train the public and healthcare providers about
  lead poisoning,how to prevent our kids from being
  exposed, and how to treat them if they do.