SUPERStudy: Lead Poisoning (Plumbism) 

By usmlevideoss

SUPERStudy: Lead Poisoning (Plumbism) 

Introduction

Lead poisoning (plumbism) is a condition resulting from the toxic accumulation of lead in the body, affecting multiple organ systems, particularly the nervous system, hematopoietic system, and kidneys. It is a major concern in children due to their increased susceptibility to its neurotoxic effects.

Etiology

  • Sources of exposure:
    • Lead-based paints (common in older homes built before 1978)
    • Contaminated soil and dust
    • Drinking water from lead pipes
    • Occupational exposure: Battery manufacturing, welding, or construction
    • Traditional remedies or cosmetics containing lead

Epidemiology

  • More common in children aged 1–5 years due to hand-to-mouth activity.
  • Increased risk in populations living in older, poorly maintained housing.
  • Also common in developing countries where environmental regulations may be less strict.
  • Adults are mainly affected through occupational exposure.

Absorption 

   Once absorbed from the respiratory or gastrointestinal tract, lead enters the bloodstream, where approximately 99% is bound to erythrocytes and 1% is present in the plasma. Lead is subsequently distributed to soft tissues such as the bone marrow, brain, kidney, liver, muscle, and gonads; then to the subperiosteal surface of bone; and later to bone matrix. Lead also crosses the placenta and poses a potential hazard to the fetus. 

Pathophysiology

  • Lead interferes with enzymes involved in heme synthesis, particularly δ-aminolevulinic acid dehydratase (ALAD) and ferrochelatase.
    • This results in accumulation of protoporphyrin and δ-aminolevulinic acid (ALA).
    • Microcytic, hypochromic anemia occurs due to impaired heme production.
  • Lead disrupts calcium-dependent processes, contributing to neurotoxicity by interfering with neurotransmitter release and neuronal development.
  • Deposits of lead in bones lead to chronic toxicity, with slow release over time.

Clinical Manifestations

1.Neurological symptoms:

  • Children: Developmental delay, intellectual disability, behavioral problems (e.g., irritability, hyperactivity)
  • Adults: Peripheral neuropathy (wrist drop, foot drop), headache, memory impairment, encephalopathy

2.Gastrointestinal symptoms:

  • Abdominal pain (lead colic), constipation, nausea

3.Hematologic effects:

  • Microcytic, hypochromic anemia with basophilic stippling of red blood cells
  • Fatigue, pallor

4.Musculoskeletal symptoms:

  • Bone pain, “lead lines” on X-ray (dense metaphyseal lines)

5.Renal damage:

  • Chronic interstitial nephritis with proteinuria

6.Cardiovascular: hypertension,  prolongation of the QTc interval on the electrocardiogram

7.Other signs: Lead lines on gums (Burton’s lines): Bluish-black discoloration of the gingiva due to lead deposition

Diagnosis

  1. History of exposure: Environmental history, occupation, and housing
  2. Blood lead level (BLL): The diagnostic test of choice. Levels >5 µg/dL are concerning in children.
  3. Complete blood count (CBC): Shows microcytic, hypochromic anemia with basophilic stippling.
  4. Free erythrocyte protoporphyrin (FEP) or zinc protoporphyrin: Elevated in lead poisoning due to impaired heme synthesis.
  5. X-rays: Metaphyseal “lead lines” in children; may be seen in long bones.

Treatment

  1. Immediate removal from lead source
  2. Chelation therapy (based on BLL):
    • 2,3 Dimercaprol (British Anti-Lewisite/BAL) or EDTA for severe cases (>70 µg/dL)
    • DMSA (succimer): The oral lead chelator succimer is approved for outpatient treatment of asymptomatic children with blood lead levels higher than 45 mcg/dL.
  3. Supportive care: Manage anemia, hydration, and symptom relief.
  4. Environmental interventions: Identify and eliminate lead sources in the home.
  5. Nutritional support: Adequate intake of calcium, iron, and vitamin C can reduce lead absorption.

Prognosis

  • Early detection and intervention improve outcomes, especially in children.
  • Severe, prolonged exposure can cause irreversible neurological damage, particularly in children with developmental delays or cognitive deficits.
  • Chronic renal damage and hypertension may persist in adults with long-term exposure.

Memory Aid or Mnemonic:

“LEAD TOXIC” 

L: Lead lines on gums and long bones

E: Encephalopathy and neurodevelopmental delay

A: Abdominal pain (lead colic), anemia with basophilic stipling 

D: Drops (wrist/foot drop), developmental delay

T – Teeth: Burton’s line (blue-black gingival line) is a classic sign. 

        Treatment starts with Terminating exposure

O – Occupational exposure: Adults at risk include painters, battery workers, and construction workers.

X – X-ray findings: Lead lines (dense metaphyseal bands) on X-rays of long bones in children.

I – Iron deficiency: Increases lead absorption; screen for and treat iron deficiency.

C – Chelation therapy: Indicated for:

  • Symptomatic patients.
  • BLL ≥45 µg/dL in children.
  • Agents: Dimercaprol (BAL), succimer, or Ca-EDTA.

SUPERPoint:

Lead poisoning primarily affects the nervous system and hematopoietic system, leading to developmental delays, microcytic anemia with basophilic stippling, abdominal pain, and neuropathy. Diagnosis is confirmed by elevated blood lead levels, and treatment involves chelation therapy and removal from the lead source.

SUPERFormula:

Child presents with colicky abdominal pain +  developmental delay + lines on gums (Burton’s lines) +  neuropathy + lived or lives in a old house + impaired heme synthesis (basophilic stippling, anemia) + chelation therapy = Lead Poisoning

References: 

Smollin C. Lead Poisoning. In: Papadakis MA, Rabow MW, McQuaid KR, Gandhi M. eds. Current Medical Diagnosis & Treatment 2025. McGraw-Hill Education; 2025. 

Disorders of the Nervous System Caused by Alcohol, Drugs, Toxins, and Chemical Agents. In: Ropper AH, Samuels MA, Klein JP, Prasad S. eds. Adams and Victor’s Principles of Neurology, 12e. McGraw-Hill Education; 2023.