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Lead Poisoning
Presentor : Dr.Anurag Fursule
Moderator : Dr. Malini
www.dnbpediatrics.com

Introduction
• Lead has no essential role in the human body.
• Lead poisoning accounts for about 0.6% of the
global burden of disease. (WHO, 2009).
• entirely preventable.
• one of the most common and best-recognized
childhood diseases of toxic environmental origin.
• Lead exposure is estimated to contribute to
6,00,000 new cases of children with intellectual
disabilities every year, it says
• Overall, 99 per cent of the affected children live in
low and middle income countries.(BLL 10x-20x)

Public Health History
• Blood Lead Level (BLL): CDC,AAP, and
numerous other national and international
Organizations consider a BLL of 10 μg/dL or
greater as a level of concern for public health
purposes.
• BLL is the gold standard for determining health
effects.
• However, lead toxicity occurs below this
threshold, and no safe level has been identified

• Between 1976 and 1980, more than 85% of
preschool children in the USA had BLLs of 10
μg/dL or higher; 98% of African-American
preschoolers fulfilled this criterion.
• So govt took following measure
:(1) the elimination of the use of tetraethyl leaded
gasoline
(2) the banning of lead-containing solder to seal
food- and beverage-containing cans
(3) the application of a federal rule that limited
the amount of lead allowed in paint intended for
household use to less than 0.06% by weight.

• Surveillance by the CDC has shown that the
prevalence of elevated BLLs (≥ 10 ?g/dL) has
declined markedly, and by 2004 it was below
1.5% in all preschoolers.
• Risk factors:
-preschool age
-low socioeconomic status
-living in older housing(built primarily before
1960; urban location)
-African-American race
-recent immigrants from less wealthy countries,
including adoptees.

Metabolism
Hand to mouth activity of children
Gut..good absorption if small particle size , in empty
stomach , iron and calcium deficient diet
Poor absorption if large paint chips, presence of iron
and calcium
After absorption:
1)Bones,teeth,hair : may reside for years
2)Blood: (a)RBC:97%
(b) Serum: negligible but may enter cell &
induce toxicity

• Lead binds to enzymes, particularly those with
available sulfhydryl groups, changing the
contour and diminishing function.
•Inhibition of
ferrochelatase
•Accumalation
of
protoporhyrin
•Hb synthesis
inhibition
•Competition with
calcium
•CBP have higher
affinity for lead
•Abnormal
inter/intracellular
signalling(e.g.
Neurotransmittor
release
•Prevention of
development of
normal tertiary
brain
structure,normal
neuronal pruning
process
•Permanent
neuronal
disability:ADHD

Clinical Symptoms
• Fatal dose: lead acetate – 20gms
lead carbonate – 30 gms
• Fatal period: 1-2 days.
• Acute lead poisoning:
-rare
-GI: metallic taste,diarrhea,constipation,intestinal
colic
-CNS: formication,convulsion,insomnia,coma
-CVS: circulatory collapse
-blood level > 150mg/dl

Chronic lead poisoning(plumbism)
• Clinical features:
• A. CNS (BLL>100mcg/dL)
-worsening cerebral edema
-raised ICP
-headache
-abnormal mentation
-encephalopathy : mimics tuberculous meningitis
-lethargy
-CN palsy
-papilledema
-seizure
-coma
-Sudden death : RLN palsy, phrenic nerve palsy

• Neuromuscular effects and peripheral
neuropathy :
-Calf muscle pain
-Easy fatigue ability
-Paralysis of extensor muscle forearm and
hand(dominant hand)(d/t interference with
resynthesis of phosphocreatinine)
-Wrist drop, rarely foot drop
• Developmental dysfunction:
-regression of milestone in children after 12-18
months of normal development
-ADHD blood levels- 30-50 mg/dL
-poor IQ

• Hematological :
-initially polychromasia, polycythemia,
reticulocytosis, basophilic stippling
-hypochromic microcytic anemia
-decreased osmotic fragility RBC
• Renal
-oligouria
-hematuria
-hyperuricemia
-fanconi syndrome
-cast in urine

• GI disturbance :
-nausea , vomiting , anorexia
-metallic taste
-lead line on gum : burtonian line
-abdominal colics.

Diagnosis
• In emergency diagnosis of lead poisoning may be
considered in presence of 2 or more of following:
1)Hypochromic : microcytic anemia
2)Abdominal x rays: radio opaque forign bodies in
gut, bone x rays:broad dense bands at metaphyses.
3)glycosuria,aminoaciduria,hypophosphatemia
4)Coproprphyrinuria : 60-280mg/24hrs
5)Urinary ALA estimation: several fold increased
2mg/24 hrs
6)Raised ICP,CSF protein increased with mild
pleocytosis.
7)Urine lead content: normally < 0.08mg/litre(lead
mobilization test)

•Experimentally, the method of x-ray fluorescence
(XRF) allows direct and noninvasive assessment of
bone lead stores(measurable after years of exposure
when blood level may still be low).
•XRF methodology is not available for clinical use in
children.

• Screening
• Interpretation of Blood Lead Levels:
-A screening value at or above 2 mcg/dL is
consistent with exposure and requires a second
round of testing for a diagnosis and to determine
the appropriate intervention.
• A confirmed venous BLL of 45 mcg/dL or higher
requires prompt chelation therapy.

Erythrocyte Protoporphyrin
• Because BLLs reflect recent ingestion or redistribution
from other tissues but do not necessarily correlate with
the body burden of lead or lead toxicity in an individual
child, tests of lead effects also may be useful.
• After several weeks of lead accumulation and a
BLL higher than 20 mcg/dL, increases in EP values to
more than 35 mcg/dL may occur.
• An elevated EP value that cannot be attributed to iron
deficiency or recent inflammatory illness is both an
indicator of lead effect and a useful means of assessing
the success of the treatment; the EP level will begin to
fall a few weeks after successful interventions that
reduce lead ingestion and increase lead excretion.
• Because EP is light sensitive, whole blood samples
should be covered in aluminum foil (or equivalent) until
analyzed.

Treatment www.dnbpediatrics.com

• Bone stores cannot be depleted easily
• cognitive/behavioral effects of lead may be
irreversible
• So mainstay in treatment it is to prevent
exposure.
• The main components in the effort to eliminate
lead poisoning are :
1. identification and elimination of environmental
sources of lead exposure
2. behavioral modification to reduce nonnutritive
hand-to-mouth activity
3. dietary counseling to ensure sufficient intake of
the essential elements calcium and iron

Preventing Lead Poisoning
• The Centers for Disease Control suggest the
following guidelines:
• Parents should ask a doctor to test their child, if there
is concern about children being exposed to lead.
• If you live in a house or apartment built before 1978,
talk to your state or local health department about
testing paint and dust from your home for lead. This is
especially important if young children live with you or
visit you.
• Wash your children's hands after they play outside,
before eating and going to bed.
• Restrict where your children play. Don't let them play
near major roadways or bridges
• Prepare meals that are high in iron and calcium. A
nutritious diet helps prevent lead absorption in your
children's bodies.

• Damp-mop floors, damp-wipe surfaces, and frequently
wash a child’s hands, pacifiers and toys to reduce
exposure to lead.
• Use only cold water from the tap for drinking, cooking
and for making baby formula. Hot water is more likely
to contain higher levels of lead. Most of the lead found
in household water usually comes from the plumbing
in a house, not from the local water supply.
• Avoid using home remedies (such as azarcon, greta,
pay-loo-ah) and cosmetics (such as kohl, alkohl) that
contain lead.
• Take basic steps to decrease your exposure to lead (for
example, by showering and changing clothes after
finishing the task), if you remodel buildings built
before 1978, or if your work or hobbies involve
working with lead-based products.

Chelation Therapy
• Indications:
1. lead encephalopathy
2. nonencephalopathic children, it prevents
symptom progression and further toxicity
3. A child with a venous BLL 45 mcg/dL or higher
should be treated.

• Principles of treatment:
1. Children with BLLs of 44-70 mcg/dL may be treated
with a single drug, preferably DMSA
2. BLLs of 70 mcg/dL or greater require two-drug
treatment
a. with encephalopathy: Edetate + BAL
b. without encephalopathy : edetate + DMSA/BAL
3. These drugs also may increase lead absorption from the
gut and should be administered to children in lead-free
environments.
4. Repeat chelation is indicated if the BLL rebounds to
45 mcg/dL or higher.
5. Children with initial BLLs higher than 70 mcg/dL are
likely to require more than one course
6. A minimum of 3 days between courses is recommended
to prevent treatment-related toxicities, especially in
the kidney.

• With successful intervention, BLLs decline, with the
greatest fall in BLL occurring in the first 2 mo after
therapy is initiated.
• Subsequently the rate of change in BLL declines
slowly so that by 6-12 mo after identification, the
BLL of the average child with moderate lead
poisoning (BLL >20 mcg/dL) will be 50% lower.
• Children with more markedly elevated BLLs may
take years to reach the CDC threshold of concern,
10 mcg/dL, even if all sources of lead exposure have
been eliminated, behavior has been modified, and
nutrition has been maximized.
• Early screening remains the best way of avoiding
and therefore obviating the need for the treatment
of lead poisoning

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