Lead Poisoning

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Lead accumulates slowly in the body and even low doses can eventually lead to poisoning. 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]

Steroid production is also impaired.

Acute poisoning is mainly related to occupational inhalation and foreign body ingestion. Chronic poisoning may be either environmental or occupational.

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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.The effect of long-term elevated lead levels on children is of particular concern and can lead to a reduction of IQ and to disruptive behaviour. A survey by the Health Protection Agency is underway to gather data about the incidence of clinically diagnosed blood lead concentrations ≥10 μg/dL in children aged 0-15 years in the UK and Republic of Ireland. The study is due to be completed by 2013.[3]

Children under the age of three are particularly at risk because ingestion of foreign material is more likely at this age.[4]

In adults, lead poisoning is mostly occupation-related. The occupations mainly involved are the smelting, refining, alloying and casting industry (19.1%), the lead battery industry (18.2%) and the scrap industry (7.4%).[5]

Risk factors

  • Occupations involving contact with lead.
  • 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 condition.[6]
  • Use of various imported tonics, alternative medication[7] and cosmetics containing lead.
  • Associated iron deficiency - increases lead absorption from the gastrointestinal (GI) tract.
  • Poor/old housing (lead paint or pipes).
  • Use of lead-containing folk remedies.[8]
  • 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 system.[9]

Symptoms

Acute poisoning
The severity of symptoms often correlates with blood levels and at high levels the following may be seen:

  • Abdominal pain - moderate-to-severe, usually diffuse but may be colicky.
  • Vomiting.
  • Encephalopathy - more common in children, characterised by seizures, mania, delirium and coma, death.
  • Jaundice (due to hepatitis).
  • Lethargy (due to haemolytic anaemia).

Chronic poisoning

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 co-ordination or subtle visual-spatial impairment.
  • Chronic distal motor neuropathy with decreased reflexes and weakness of extensor muscles in adults.

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.

Other conditions which may need to be considered include:

Laboratory tests

  • Whole blood lead levels:
    • <10 μg/dL - normal.
    • >10 μg/dL - may cause impaired cognitive development in children.
    • >45 μg/dL - GI symptoms in adults and children.
    • >70 μg/dL - high risk of acute CNS symptoms.
    • >100 μg/dL - may be life-threatening.
  • It has been considered for many years that levels of 10 μg/dL have the potential to affect physical and mental development in children. Studies suggest that levels even lower than this can be unsafe.
  • FBC - basophilic stippling of erythrocytes may be seen and features of a microcytic hypochromic anaemia such as a low MCV may be present. Sideroblasts may be seen.
  • Renal function tests to detect renal complications and uric acid levels to detect gout may also be advisable.
  • Nerve conduction tests should be considered if neuropathy is suspected.
  • Psychometric testing should be considered if clinically indicated.

Radio-imaging[10]

  • Plain X-ray may show transverse lines in tubular bones. These are actually areas of arrested bone growth and may persist 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 (eg 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.
  • In the case of foreign body ingestion (eg a child who has swallowed a fishing weight too large to exit the stomach), approximately three days should be allowed to see if the object will pass through. If not, it will need to be removed by endoscopy, surgical means or whole bowel irrigation.
  • Severe lead poisoning (levels >60 μg/dL) due to acute ingestion may require:
    • Airway maintenance.
    • Management of coma and seizures.
    • Intravenous (IV) drip of normal saline.
    • Orogastric or nasogastric catheter and irrigation with polyethylene glycol.
  • Parenteral chelators such as calcium disodium edetate given intramuscularly (IM) or IV. There is a growing trend to administer it by slow IV drip.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 45-60 μg/dL.
  • For mild lead poisoning (<45 μg/dL) it may be sufficient to detect the source of the exposure, remove the patient from it and monitor the clinical status.[4]
  • Oral chelation therapy is an option sometimes used for mild-to-moderate poisoning.
  • Dimercaptosuccinic acid (DMSA, or succimer) is an alternative oral agent. There is some evidence that it can affect growth rate in children.[15]
  • D-penicillamine is occasionally used but it is an unlicensed medication with adverse effects such as white cell and platelet count suppression.[16]
  • Chelation therapy should be withdrawn gradually to avoid the metal leaking out of the bones and causing a rebound rise in blood levels.
  • 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.[10]
  • The prognosis has improved considerably with aggressive treatment and there have been no reported deaths from lead encephalopathy in children 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.[11]
  • The removal of paint from lead and the replacement of old lead pipes have 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 10 μg/dL. However, ongoing research suggests that neurotoxicity can develop at levels below this figure and the effect of chronic low-dose exposure (eg due to flakes of old paint) is currently being investigated.
  • If appropriate, the family or co-workers of the patient should be screened.
  • The Control of Lead at Work (CLAW) Regulations 2002 require all employers to minimise the exposure of their employees to lead and to take measures to reduce such exposure (eg encouraging personal hygiene, regular monitoring, suspension of employees with raised blood levels, training and education).[17]
  • 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.[18]
  • Educating patients to be cautious in the use of folk remedies is, however, still an issue.[8]
  • Further work needs to be done to reduce occupational exposure, particularly in the demolition and tank cleaning industries.[19]
  • In Uruguay, a wide range of measures has been instigated, including reduction of industrial and non-industrial exposure (eg 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).[20]

Further reading & references

  • Cecil KM, Dietrich KN, Altaye M, et al; Proton magnetic resonance spectroscopy in adults with childhood lead exposure. Environ Health Perspect. 2011 Mar;119(3):403-8. Epub 2010 Oct 13.
  • Rosin A; The long-term consequences of exposure to lead. Isr Med Assoc J. 2009 Nov;11(11):689-94.
  • Abelsohn AR, Sanborn M; Lead and children: clinical management for family physicians. Can Fam Physician. 2010 Jun;56(6):531-5.
  • Murray L et al Toxicology Handbook 2nd Ed, Churchill Livingstone,2011. ISBN: 9780 7295 39395
  • Toxicological Profile for Lead, US Department of Health and Human Services, 2007
  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.
  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.
  3. Surveillance of Lead in Children study, Health Protection Agency, 2011
  4. Marcus S, Toxicity, Lead, Medscape, Aug 2010
  5. Exposure to lead, Health and Safety Executive, 2011
  6. 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.
  7. Giampreti A, Bonetti C, Lonati D, et al; A young Indian male with abdominal pain. Clin Toxicol (Phila). 2011 Mar;49(3):191-2.
  8. Ernst E; Heavy metals in traditional Indian remedies. Eur J Clin Pharmacol. 2002 Feb;57(12):891-6.
  9. 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.
  10. Khan A et al, Lead Poisoning, Medscape, May 2011
  11. Lead; New York State Department of Health, April 2010; Links to various resources about lead
  12. 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.
  13. X-ray Fluorescence Spectroscopy, Amptek.com
  14. Payne M, Egden L, Behinaein S, et al; Bone lead measurement. Can Fam Physician. 2010 Nov;56(11):1110-1; author reply 1112.
  15. 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.
  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. Control of Lead at Work Regulations, Health and Safety Executive, 2002
  18. 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.
  19. Gidlow DA; Lead toxicity. Occup Med (Lond). 2004 Mar;54(2):76-81.
  20. 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.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1710 (v22)
Last Checked:
19/08/2011
Next Review:
17/08/2016