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Lead Poisoning

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Description

Lead accumulates slowly in the body and even low doses can eventually lead to poisoning. Serum level of lead at which treatment is indicated in young children is 100 mcg/L. 95% of lead in body is deposited in the bones and teeth while 99% of lead in blood is associated with erythrocytes. Lead poisoning can cause nervous system toxicity and renal tubular dysfunction leading to irreversible interstitial nephrosis with progressive renal impairment and hypertension. Lead also depresses haem synthesis and shortens the life span of erythrocytes causing a hypochromic microcytic anaemia. One study showed altered hippocampal volume and brain metabolites in workers occupationally exposed to lead.1 Another showed a significant increase in the frequency of chromosomal aberrations in workers exposed to lead compared to the controls.2

Epidemiology

Incidence

Lead poisoning is a lot less common than it used to be with less use in petrol, paints or cosmetics and generally improved housing. One English review which looked at hospital admissions over 15 years, 3 years' worth of mortality statistics and reports to the Health and Safety Executive found one death and 83 hospital admissions. The authors concluded that lead poisoning was rare, but when it did occur, it was associated with considerable morbidity.3

Risk factors

  • Reclamation of lead from scrap metal, battery manufacture and other industries where lead is involved
  • Children chewing lead painted items or ingesting fishing weights, bullets or contaminated soil
  • Deliberate ingestion (pica) is occasionally seen in adults as part of a psychiatric condition4
  • Use of various imported tonics, alternative medication5 and cosmetics containing lead
  • Associated iron deficiency - increases lead absorption from gastro-intestinal (GI) tract
  • Poor/old housing (lead paint or pipes)
  • Use of lead-containing folk remedies6
  • Age - compared to an adult, a child can absorb twice as much lead from the GI tract
  • One study reports the emergence of lead poisoning in a pregnant woman years after exposure - presumably due to increased reabsorption of lead from the skeletal system7
Presentation8,9

Symptoms

Signs

There are no pathognomonic signs, but the following may be seen:

  • A blue discoloration of gum margins
  • Mild anaemia
  • Behavioural abnormalities (more marked in children) - irritability, restlessness, sleeplessness
  • Cognitive dysfunction
  • Impaired fine-motor coordination or subtle visual-spatial impairment
  • Chronic distal motor neuropathy with decreased reflexes and weakness of extensor muscles in adults
Differential diagnosis8

This depends on the presentation. Diagnosis may be difficult in the UK where lead poisoning is a relative rarity, but the condition should be on the list in patients presenting with diffuse abdominal pain.10

Other conditions which may need to be considered include:

Investigations8

Laboratory tests

  • Serum lead levels
    • <100 mcg/L - normal
    • >100 mcg/L - may cause impaired cognitive development in children
    • >450 mcg/L - GI symptoms in adults and children
    • >700 mcg/L - high risk of acute CNS symptoms
    • >1000 mcg/L - may be life threatening
  • One study suggests that levels less than 100 mcg/L can affect physical and mental development in children12
  • Full blood count - basophilic stippling of erythrocytes may be seen

Radio-imaging8

  • Plain X-ray may show transverse lines in tubular bones. These are actually areas of arrested bone growth and may persists a long time after exposure ends. They are not seen in the early phase of exposure.
  • Plain abdominal X-rays may show radio-opaque flecks in cases of suspected lead foreign body ingestion (e.g. pica in children).
  • X-ray fluorescence works by detecting specific emissions from tissues when bombarded with X-rays. It is a sensitive method of detecting low levels of lead in the body.13,14
  • CT or MRI scan of the brain may be contributory in patients with symptoms suggestive of encephalopathy.
Management15
  • For mild lead poisoning (<450 mcg/L) it may be sufficient to detect the source of the exposure, remove the patient from it and monitor the clinical status.15
  • Oral chelation therapy is an option sometimes used for mild to moderate poisoning. The word chelator is derived from the Greek for claw and chelators work by forming a tight chemical bond with heavy metals, enabling them to be excreted. Opinions vary as to when chelation therapy should be used, but it is often employed at levels of 450-600 mcg/L.
  • D-Penicillamine is a commonly used but unlicensed medication. Lower dose ranges (15 mg/kg/day) are to be preferred due to the adverse effects (mainly white cell and platelet count suppression).16
  • Dimercaptosuccinic Acid (DMSA, Succimer) is an alternative oral agent. There is some evidence that it can affect growth rate in children.17
  • Severe lead poisoning (levels > 600 mcg/L) due to acute ingestion may require:
    • Airway maintenance
    • Management of coma and seizures
    • Intravenous drip of normal saline
    • Orogastric or nasogastric catheter and irrigation with polyethylene glycol
  • Parenteral chelators should be given.
  • Dimercaprol (British Anti-Lewisite, BAL) - this is given intramuscularly (IM) but often results in a bad taste which patients find hard to tolerate.
  • Calcium disodium edetate is another option, which is sometimes given as an adjunct in cases of encephalopathy.18 It may be used IM or intravenously (IV). There is a growing trend to administer it by slow IV drip.
  • Chelation therapy should be withdrawn gradually to avoid the metal leaking out of the bones and causing a rebound rise in blood levels.
Complications
  • Lead poisoning, with or without encephalopathy, can affect all the systems of the body.
  • Hepatic, renal and neurological damage can occur.
  • Chelation itself can cause problems and treated patients can develop hypertension, raised intracranial pressure and renal failure from the chelated lead compound.8
Prognosis
  • The prognosis has improved considerably with aggressive treatment and there have been no reported deaths in children from lead encephalopathy in recent years.
  • Cases of acute lead encephalopathy in children still occur and can result in severe neurological damage, seizure disorders, depressed school function and learning disabilities.
  • Adults tend to fare better, but long term effects can include distal motor neuropathies, depressive disorders, aggressive behaviour, defects in sexual performance and fertility problems.9
Prevention
  • The removal of paint from lead and the replacement of old lead pipes has done much to reduce the burden of lead poisoning, particularly on children. The aim has been to reduce lead levels in children to less than 100 mcg/L. However, ongoing research suggests that neurotoxicity can develop at levels below this figure and the effect of chronic low-dose exposure (e.g. due to flakes of old paint) is currently being investigated.19
  • Global reduction in the use of lead-containing petrol has resulted in a significant reduction in exposure. However, new sources continue to emerge, including improper disposal of electronics and children's toys contaminated with lead.20
  • Educating patients to be cautious in the use of folk remedies is however still an issue.6
  • Further work needs to be done to reduce occupational exposure, particularly in the demolition and tank cleaning industries.21
  • In Uruguay, a wide range of measures have been instigated including reduction of industrial and non-industrial exposure (e.g. metallurgical industries, lead-acid battery processing, lead wire and pipe factories, metal foundries, metal recyclers, leaded gasoline,lead water pipes in old houses, and scrap and smelter solid wastes).22


Document references
  1. Jiang YM, Long LL, Zhu XY, et al; Evidence for altered hippocampal volume and brain metabolites in workers occupationally exposed to lead: a study by magnetic resonance imaging and (1)H magnetic resonance spectroscopy. Toxicol Lett. 2008 Sep 26;181(2):118-25. Epub 2008 Jul 23. [abstract]
  2. Madhavi D, Devi KR, Sowjanya BL; Increased frequency of chromosomal aberrations in industrial painters exposed to lead-based paints. J Environ Pathol Toxicol Oncol. 2008;27(1):53-9. [abstract]
  3. Elliott P, Arnold R, Barltrop D, et al; Clinical lead poisoning in England: an analysis of routine sources of data. Occup Environ Med. 1999 Dec;56(12):820-4.; Occup Environ Med. 1999 Dec;56(12):820-4. [abstract]
  4. Sabouraud S, Testud F, Descotes J, et al; Lead poisoning following ingestion of pieces of lead roofing plates: pica-like behavior in an adult. Clin Toxicol (Phila). 2008 Mar;46(3):267-9. [abstract]
  5. Creemers L, Van den Driessche M, Moens M, et al; Safety of alternative medicines reconsidered: lead-induced anaemia caused by an indian ayurvedic formulation. Acta Clin Belg. 2008 Jan-Feb;63(1):42-5. [abstract]
  6. Ernst E; Heavy metals in traditional Indian remedies. Eur J Clin Pharmacol. 2002 Feb;57(12):891-6. [abstract]
  7. Riess ML, Halm JK; Lead poisoning in an adult: lead mobilization by pregnancy? J Gen Intern Med. 2007 Aug;22(8):1212-5. Epub 2007 Jun 12. [abstract]
  8. Khan A, Munir U; Lead Poisoning. eMedicine, May 2007.
  9. Lead; New York State Department of Health December 2008.; Links to various resources about lead
  10. Sood A, Midha V, Sood N; Pain in abdomen--do not forget lead poisoning. Indian J Gastroenterol. 2002 Nov-Dec;21(6):225-6.; Indian J Gastroenterol. 2002 Nov-Dec;21(6):225-6. [abstract]
  11. Madan K, Sharma PK, Makharia G, et al; Autonomic dysfunction due to lead poisoning. Auton Neurosci. 2007 Mar 30;132(1-2):103-6. Epub 2006 Nov 21. [abstract]
  12. Binns HJ, Campbell C, Brown MJ; 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 Nov;120(5):e1285-98. [abstract]
  13. Amptek.com; X-ray Fluorescence Spectroscopy
  14. Hu H, Milder FL, Burger DE; X-ray fluorescence measurements of lead burden in subjects with low-level community lead exposure. Arch Environ Health. 1990 Nov-Dec;45(6):335-41. [abstract]
  15. Marcus S; Toxicity, Lead. eMedicine, Dec 2007.
  16. Shannon MW, Townsend MK; Adverse effects of reduced-dose d-penicillamine in children with mild-to-moderate lead poisoning. Ann Pharmacother. 2000 Jan;34(1):15-8.
  17. Peterson KE, Salganik M, Campbell C, et al; Effect of succimer on growth of preschool children with moderate blood lead levels. Environ Health Perspect. 2004 Feb;112(2):233-7.
  18. Gordon JN, Taylor A, Bennett PN; Lead poisoning: case studies. Br J Clin Pharmacol. 2002 May;53(5):451-8. [abstract]
  19. Health Protection Agency; Press Release 2004
  20. Meyer PA, Brown MJ, Falk H; Global approach to reducing lead exposure and poisoning. Mutat Res. 2008 Jul-Aug;659(1-2):166-75. Epub 2008 Mar 20. [abstract]
  21. Gidlow DA; Lead toxicity. Occup Med (Lond). 2004 Mar;54(2):76-81. [abstract]
  22. Manay N, Cousillas AZ, Alvarez C, et al; Lead contamination in Uruguay: the "La Teja" neighborhood case. Rev Environ Contam Toxicol. 2008;195:93-115. [abstract]

Internet and further reading
  • DEFRA; Advice on lead in old paint - Advice sheet 1. Department for Environment, Food and Rural Affairs. August 2005.
Acknowledgements EMIS is grateful to Dr Laurence Knott for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
DocID: 1710
Document Version: 21
DocRef: bgp375
Last Updated: 22 Jan 2009
Review Date: 22 Jan 2011

The authors and editors of this article are employed to create accurate and up to date content reflecting reliable research evidence, guidance and best clinical practice. They are free from any commercial conflicts of interest. Find out more about updating.

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