> Table of Contents > Lead Poisoning
Lead Poisoning
Jason Chao, MD, MS
image BASICS
DESCRIPTION
  • Consequence of a high body burden of lead (Pb), an element with no known physiologic value
  • Synonym(s): lead poisoning, inorganic
EPIDEMIOLOGY
  • Predominant age: 1 to 5 years, adult workers
  • Predominant sex: male > female (1:1 in childhood)
Prevalence
  • 2007 to 2010: Centers for Disease Control and Prevention (CDC) estimated that 2.6% of U.S. children aged 1 to 5 years had blood Pb levels >5 &mgr;g/dL, but levels are variable among communities and populations.
  • Sporadic cases in adults
ETIOLOGY AND PATHOPHYSIOLOGY
  • Inhalation of Pb dust or fumes, or ingestion of Pb
  • Pb replaces calcium in bones. Pb interferes with heme synthesis, causes interstitial nephritis, and interferes with neurotransmitters, especially glutamine; high levels affect blood-brain barrier and lead to encephalopathy, seizures, and coma.
  • Early life Pb exposure causes methylation changes leading to epigenetic alterations that may lead to brain dysfunction.
RISK FACTORS
  • Children with pica or with iron-deficiency anemia
  • Residence in or frequent visitor to deteriorating pre-1960 housing with lead-painted surfaces or recent renovation
  • Soil/dust exposure near older homes, Pb industries, or urban roads
  • Sibling or playmate with current or past Pb poisoning
  • Dust from clothing of Pb worker or hobbyist
  • Pb dissolved in water from Pb or Pb-soldered plumbing
  • Pb-glazed ceramics especially with acidic food or drink
  • Recent refugee
  • Folk remedies and cosmetics
    • Mexico: Azarcon, Greta
    • Dominican Republic: Litargirio, a topical agent
    • Asia and Middle East: Chuifong tokuwan, paylooah, ghasard, bali goli, kandu, ayurvedic herbal medicine from South Asia, kohl (alkohl, ceruse), surma, saoott, cebagin
  • Hobbies: glazed pottery making, target shooting, Pb soldering, preparing Pb shot or fishing sinkers, stained-glass making, car or boat repair, home remodeling
  • Occupational exposure: plumbers, pipe fitters, Pb miners, auto repairers, glass manufacturers, shipbuilders, printer operators, plastic manufacturers, Pb smelters and refiners, steel welders or cutters, construction workers, rubber product manufacturers, battery manufacturers, bridge reconstruction workers
  • Dietary: zinc or calcium deficiency
  • Imported toys with Pb
Pediatric Considerations
  • Children are at increased risk because of incomplete development of the blood-brain barrier at <3 years of age, allowing more Pb into the CNS; ingested Pb has 40% bioavailability in children compared with 10% in adults.
  • Common childhood behaviors such as frequent hand-to-mouth activity and pica (repeated ingestion of nonfood products), greatly increase the risk of ingesting Pb.
GENERAL PREVENTION
  • Family should receive counseling on potential sources of Pb and methods to decrease Pb exposure. Children at high risk should receive blood Pb screening (1)[C].
  • Warn parents about the dangers posed by unsafe renovation methods.
  • Wet mopping and dusting with a high-phosphate solution (e.g., powdered automatic dishwasher detergent with 1/4 cup/gallon of water) will help to control Pb-bearing dust. But high-phosphate detergent is no longer available in some states.
  • Pregnant women with community-specific or any individual risk factor for Pb poisoning should be screened for Pb toxicity (2)[C].
COMMONLY ASSOCIATED CONDITIONS
Iron-deficiency anemia
image DIAGNOSIS
PHYSICAL EXAM
Often normal, but abdominal tenderness may be severe. Neurologic exam may reveal neuropathy or encephalopathy.
DIFFERENTIAL DIAGNOSIS
  • Alimentary type may be confused with acute abdomen.
  • Neuromuscular type may be confused with other polyneuropathies.
  • Cerebral type may be confused with ADD, mental retardation, autism, dementia, and other causes of seizures.
  • Elevated erythrocyte protoporphyrin may be caused by iron-deficiency anemia or, less commonly, hemolytic anemia.
  • Erythropoietic protoporphyria produces a very high erythrocyte protoporphyrin level.
DIAGNOSTIC TESTS & INTERPRETATION
  • Blood Pb >5 &mgr;g/dL (0.24 &mgr;mol/L) collected with Pb-free container
  • Use a laboratory that can achieve routine performance within 2 &mgr;g/dL.
  • In 2012, CDC recommended using a reference value as the basis for management, currently >5 &mgr;g/dL
  • Screening capillary Pb levels >5 &mgr;g/dL (0.24 &mgr;mol/L) should be confirmed with a venous sample.
  • Hemoglobin and hematocrit slightly low; eosinophilia or basophilic stippling on peripheral smear may be seen but is not diagnostic of Pb toxicity.
  • Renal function is decreased in late stages.
  • Abdominal radiograph for Pb particles in gut if recent ingestion is suspected.
  • Radiograph of long bones may show lines of increased density in the metaphyseal plate resulting from growth arrest but does not usually alter management and is not routinely recommended.
  • X-ray fluorescence for the total body burden of Pb is experimental.
image TREATMENT

Blood level (&mgr;g/dL)

Time to confirmation testing

≥ref value-9

1-3 months

10-44

1 week-1 month

45-59

48 hours

60-69

24 hours

≥70

Urgently as emergency test

MEDICATION
  • Consider oral chelation for asymptomatic and Pb >45 and <70; chelation (preferably parenteral) for Pb >70 or symptomatic Pb <70 (5)[C].
  • Do not begin chelation until Pb particles present in gut are cleared (5)[C].
P.595

First Line
  • Oral chelation: Succimer (Chemet), dimercaptosuccinic acid (DMSA) 10 mg/kg q8h for 5 days; then 10 mg/kg q12h for 2 weeks. This may be repeated after 2 weeks off if Pb levels are not stabilized at <15 &mgr;g/dL (<0.72 &mgr;mol/L) (5)[C].
  • Parenteral chelation (begin after establishment of adequate urine output):
    • Dimercaprol (British anti-Lewisite [BAL]) 75 mg/m2 given deep IM; then BAL 450 mg/m2/day divided q4h for 5 days plus Ca edetate calcium disodium (EDTA) 1,500 mg/m2/day continuous IV infusion for 5 days. If rebound Pb level ≥45 &mgr;g/dL (≥2.17 &mgr;mol/L), chelation may be repeated after 2-day interval if symptomatic or after 5-day interval if asymptomatic.
    • Ca EDTA 1,000 mg/m2/day for 5 days; may be repeated after 5 to 7 days
  • Diazepam for initial control of seizures; further control maintained with paraldehyde
  • Contraindications: BAL should not be given to patients allergic to peanuts (the drug solution contains peanut oil).
  • Precautions
    • Succimer: GI upset, rash, nasal congestion, muscle pains, elevated liver function tests
    • Ca EDTA: renal failure, increased excretion of zinc, copper, and iron
    • BAL: nausea, vomiting, fever, headache, transient hypertension, hepatocellular damage
  • Significant possible interactions
    • Vitamins should not be given concurrently with oral chelation.
    • BAL may precipitate hemolytic crisis in a patient with glucose-6-phosphate dehydrogenase deficiency.
Second Line
Oral chelation with penicillamine (D-penicillamine, Depen, Cuprimine) (5)[C]
  • Penicillin-allergic patient should not receive penicillamine (cross-sensitivity is common).
  • 10 to 15 mg/kg/day given BID mixed in apple juice/sauce on empty stomach (not approved by the FDA)
  • Penicillamine may cause GI upset, renal failure, granulocytopenia, liver dysfunction, iron deficiency, and drug-induced lupus-like syndrome.
ISSUES FOR REFERRAL
Consider consultation if parenteral chelation is required.
ADDITIONAL THERAPIES
Remove patient from potential source of Pb or Pb level >45 until complete home inspection is performed.
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
  • Blood Pb level >70 &mgr;g/dL
  • If symptomatic, blood Pb level >35 &mgr;g/dL
  • Outpatient care unless parenteral chelation is required or immediate removal from contaminated environment.
Discharge Criteria
  • If Pb source is in the home, the patient must reside elsewhere until the abatement process is completed.
  • Avoid visit to any site of potential contamination.
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
  • After chelation, check for rebound Pb level in 7 to 10 days. Follow with regular monitoring, initially biweekly or monthly.
  • Correct iron deficiency or any other nutritional deficiencies present.
  • Once Pb <35 &mgr;g/dL, repeat testing every 1 to 3 months until level <25 &mgr;g/dL is achieved. Then monitor every 3 to 6 months until level <10 &mgr;g/dL. Once <9 &mgr;g/dL, test every 6 to 9 months (4)[C].
DIET
  • If symptomatic, avoid excessive fluids.
  • Avoid pica.
  • Adequate calcium, iron, zinc, and vitamin C to reduce absorption and retention of Pb (6)[B]
PATIENT EDUCATION
  • Needleman HL, Landrigan PJ. Raising Children Toxic Free: How to Keep Your Child Safe From Lead, Asbestos, Pesticides, and Other Environmental Hazards. New York, NY: Farrar, Straus and Giroux; 1995.
  • National Lead Information Center, 422 South Clinton Avenue, Rochester, NY 14620; 800-424-5323; www.epa.gov/lead/
  • National Safety Council, 1121 Spring Lake Drive, Itasca, IL 60143-3201; 800-621-7615; http://www.nsc.org/learn/safety-knowledge/Pages/Lead-Poisoning-Prevention.aspx
PROGNOSIS
  • Symptomatic Pb poisoning without encephalopathy generally improves with chelation, but subtle CNS toxicity may be long lasting or permanent.
  • If encephalopathy occurs, permanent sequelae (e.g., mental retardation, seizure disorder, blindness, and hemiparesis) occurs in 25-50%.
REFERENCES
1. Wengrovitz AM, Brown MJ. Recommendations for blood lead screening of Medicaid-eligible children aged 1-5 years: an updated approach to targeting a group at high risk. MMWR Recomm Rep. 2009;58(RR-9):1-11.
2. Centers for Disease Control and Prevention. Guidelines for the Identification and Management of Lead Exposure in Pregnant and Lactating Women. Atlanta, GA: Centers for Disease Control and Prevention; 2010.
3. Binns HJ, Campbell C, Brown MJ, et al. Interpreting and managing blood lead levels of less than 10 microg/dL in children and reducing childhood exposure to lead: recommendations of the Centers for Disease Control and Prevention Advisory Committee on Childhood Lead Poisoning Prevention. Pediatrics. 2007;120(5):e1285-e1298.
4. Centers for Disease Control and Prevention. Low Level Lead Exposure Harms Children: A Renewed Call for Primary Prevention. Atlanta, GA: Centers for Disease Control and Prevention; 2012.
5. American Academy of Pediatrics Committee on Drugs. Treatment guidelines for lead exposure in children. Pediatrics. 1995;96(1, Pt 1):155-160.
6. Woolf AD, Goldman R, Bellinger DC. Update on the clinical management of childhood lead poisoning. Pediatr Clin North Am. 2007;54(2):271-294, viii.
Additional Reading
&NA;
  • American Academy of Pediatrics Committee on Environmental Health. Lead exposure in children: prevention, detection, and management. Pediatrics. 2005;116(4):1036-1046.
  • Chandramouli K, Steer CD, Ellis M, et al. Effects of early childhood lead exposure on academic performance and behaviour of school age children. Arch Dis Child. 2009;94(11):844-848.
  • Senut MC, Cingolani P, Sen A, et al. Epigenetics of early-life lead exposure and effects on brain development. Epigenomics. 2012;4(6):665-674.
See Also
&NA;
Anemia, Iron Deficiency
Codes
&NA;
ICD10
  • T56.0X4A Toxic effect of lead and its compounds, undetermined, init
  • T56.0X1A Toxic effect of lead and its compounds, accidental, init
Clinical Pearls
&NA;
  • The following children should have Pb screening:
    • 6 to 11 months of age with ≥1 risk factors:
      • Live in or visit a house built before 1960 with peeling paint or recent renovation
      • Sibling/playmate with elevated Pb
      • Live with adult with job or hobby involving Pb
      • Live near industry likely to release Pb
    • Children living in high-risk communities (>12% elevated Pb) should be tested yearly from ages 1 to 5.
    • Newly arrived refugees
    • Children in low-risk areas should be screened by a questionnaire containing the above risk factors.
  • There is no clear safe Pb level. Many experts consider Pb levels >4 &mgr;g/dL as elevated.
  • There are no studies that show benefit of chelation for asymptomatic children with Pb <45. Removal of sources of Pb is paramount.