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Lead Poisoning

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PatientPlus 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.[1] 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 lifespan of erythrocytes, causing a hypochromic microcytic anaemia. One study showed altered hippocampal volume and brain metabolites in workers occupationally exposed to lead.[2] Another showed a significant increase in the frequency of chromosomal aberrations in workers exposed to lead compared to the controls.[3] 

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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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 Public Health England's Health Protection Agency of lead levels in children was concluded in 2012 but the results have yet to be published. In the interim, a study of the incidence of high lead levels in a cohort of children with global developmental delay and moderate-to-severe learning difficulty living in Leeds and Wakefield has been published.[4] Of 104 children, only 1 had a high blood lead level (BLL). However, this result was obtained when the cut-off level used by the British Paediatric Surveillance Unit - of 0.483 μmol/L (10 μg/dL) was used. The USA organisation, Centers for Disease Control and Prevention (CDC), recommends a BLL of 0.24 μmol/L (5 μg/dL). When this was used the prevalence was nine times higher. The authors recommended the lower cut-off level of 0.24 μmol/L should be used to trigger environmental investigations.

Younger children are particularly at risk because of ingestion of foreign material, increased gastrointestinal (GI) absorption and because their nervous systems are still developing.[5] 

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%).[6]

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.[7]
  • Use of various imported tonics, alternative medication and cosmetics containing lead.[8] 
  • Associated iron deficiency - increases lead absorption from the GI tract.
  • Poor/old housing (lead paint or pipes).
  • Use of lead-containing folk remedies.[9] 
  • 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.[10]


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).
  • Black diarrhoea.

Chronic poisoning

  • Mild abdominal pain.
  • Constipation.
  • Weight loss.
  • Aggression.
  • Antisocial behaviour.
  • Headaches.
  • Hearing loss.
  • Subfertility.
  • Foot drop - due to motor peripheral neuropathy.
  • Wrist drop - this is a late sign.
  • Carpal tunnel syndrome.
  • Gout.
  • Autonomic dysfunction.[13]


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 in adults, no lower limit 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.[4] However, there is considerable confusion about the interpretation of the adoption of the USA's CDC Reference Value for a blood level of lead in children aged 1-5 of 5 μg/dL The CDC does not equate its Reference Value with lead poisoning. The Reference Value is intended to help 'identify high-risk childhood populations and geographic areas most in need of primary prevention' so steps can be taken to avoid further lead exposure. The level at which medical intervention is recommended remains at greater than or equal to 45 μg/dL.[17] 
  • 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.


  • Plain X-ray may show transverse lines in tubular bones. These are actually areas of arrested bone growth and may persist for 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.[19]
  • 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), the received wisdom is that approximately three days should be allowed to see if the object will pass through. However, in children the absorption of lead through the gut is considerably greater than it is for adults and toxic levels can be achieved very quickly. If gastroscopic or colonoscopic removal is possible, this should be performed sooner rather than later.[21] 
  • Severe lead poisoning (levels >60 μg/dL) due to acute ingestion may require:[22] 
    • Airway maintenance.
    • Management of coma and seizures.
    • Intravenous (IV) drip of normal saline.
    • Orogastric or nasogastric catheter and irrigation.
  • 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.
  • 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.
  • D-penicillamine is occasionally used but it is an unlicensed medication with adverse effects such as white cell and platelet count suppression.
  • 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 acute kidney injury from the chelated lead compound.[20] 
  • Lead exposure is estimated to account for 143,000 deaths per year, with the highest burden in developing regions.
  • Cases of acute lead encephalopathy in children still occur and can result in severe neurological damage, seizure disorders, depressed school function and learning disabilities.
  • It is now acknowledged that, due to its cumulative effects, there is no known level of lead exposure that is considered safe.
  • 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.
  • It is now well established that neurotoxicity can develop below the level of 10 μg/dL and the Global Alliance to Eliminate Lead Paint has been formed by the World Health Organization and other bodies to minimise this risk.
  • 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).[15] 
  • 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.[25]
  • Educating patients to be cautious in the use of folk remedies is, however, still an issue.[14] 
  • Further work needs to be done to reduce occupational exposure, particularly in the demolition and tank cleaning industries.[26]
  • 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).[27]

Further reading & references

  • Ozkan OV, Muderris V, Altintoprak F, et al; An Unusual Cause of Abdominal Pain: Three Lead Pellets within the Appendix Vermiformis. Case Rep Surg. 2015;2015:496372. doi: 10.1155/2015/496372. Epub 2015 May 28.
  • 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.
  • Toxicological Profile for Lead; US Department of Health and Human Services, 2007
  1. Subroto D et al; Effect of lead on the health of silver jewellery workers: A case study of Ajmer City, Rajasthan, India
  2. 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.
  3. 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.
  4. Ghosh P et al; Prevalence of high lead levels in children with global developmental delay and moderate to severe learning difficulty in Leeds and Wakefield: A cohort study, Arch Dis Child 2014;99:A133-A134.
  5. Schwartz M; The Five MInute Pediatric Consult, 2012.
  6. Exposure to lead; Health and Safety Executive
  7. 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.
  8. Giampreti A, Bonetti C, Lonati D, et al; A young Indian male with abdominal pain. Clin Toxicol (Phila). 2011 Mar;49(3):191-2.
  9. Gorospe EC, Gerstenberger SL; Atypical sources of childhood lead poisoning in the United States: a systematic review from 1966-2006. Clin Toxicol (Phila). 2008 Sep;46(8):728-37. doi: 10.1080/15563650701481862.
  10. 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.
  11. Lead Poisoning Prevention; New York State Department of Health
  12. D'souza HS, Dsouza SA, Menezes G, et al; Diagnosis, evaluation, and treatment of lead poisoning in general population. Indian J Clin Biochem. 2011 Apr;26(2):197-201. doi: 10.1007/s12291-011-0122-6. Epub 2011 Feb 18.
  13. 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.
  14. Childhood Lead Poisoning; World Health Organization, 2010
  15. Lead, General Information; Public Health England (formerly Health Protection Agency), 2011
  16. Updated protocols and research on Clinical Metal Toxicology; Micro Trace Minerals Laboratory, 2013
  17. Understanding the US CDC’s ‘Reference Value’ for Blood Lead Levels in Children; International Lead Association, 2013
  18. Lead Poisoning; Learning Radiology, 2015
  19. Payne M, Egden L, Behinaein S, et al; Bone lead measurement. Can Fam Physician. 2010 Nov;56(11):1110-1; author reply 1112.
  20. Flora SJ, Pachauri V; Chelation in metal intoxication. Int J Environ Res Public Health. 2010 Jul;7(7):2745-88. doi: 10.3390/ijerph7072745. Epub 2010 Jun 28.
  21. Gustavsson P, Gerhardsson L; Intoxication from an accidentally ingested lead shot retained in the gastrointestinal tract. Environ Health Perspect. 2005 Apr;113(4):491-3.
  22. Schaider J et al; Rosen & Barkin's 5-Minute Emergency Medicine Consult, 2012.
  23. Flora G, Gupta D, Tiwari A; Toxicity of lead: A review with recent updates. Interdiscip Toxicol. 2012 Jun;5(2):47-58. doi: 10.2478/v10102-012-0009-2.
  24. Lead poisoning and health; World Health Organization, 2015
  25. 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.
  26. Gidlow DA; Lead toxicity. Occup Med (Lond). 2004 Mar;54(2):76-81.
  27. 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 (v23)
Last Checked:
Next Review:
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