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What is lead poisoning?
The biological effects of lead are dependent on the level and duration of exposure. Lead inhibits 3 enzymes of haem biosynthesis (δ amino levulinic acid dehydratase (ALAD), coproporphyrin oxidase, and ferrochelatase). This effects erythrocyte formation by impairing haem synthesis and also depresses the serum level of erythropoietin. Lead exposure also affects calcium metabolism.
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.
Another showed a significant increase in the frequency of chromosomal aberrations in workers exposed to lead compared to the controls.
Steroid production is also impaired.
Acute lead poisoning is mainly related to occupational inhalation and foreign body ingestion. Chronic lead poisoning may be either environmental or occupational.
Lead poisoning 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.
Blood lead levels of less than 5 µg per dL are associated with impairments in neurocognitive and behavioral development that are irreversible.
Younger children are particularly at risk because of ingestion of foreign material, increased gastrointestinal (GI) absorption and because their nervous systems are still developing.
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%).
Risk factors for lead poisoning
- Occupations involving contact with lead-containing products are radiation shields, ammunition, certain surgical equipment, developing dental X-ray films prior to digital X-rays, fetal monitors, plumbing, circuit boards, jet engines, and ceramic glazes. The risk of toxicity increases with increasing exposure.
- 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.
- Use of various imported tonics, alternative medication and cosmetics containing lead.
- Associated iron deficiency - increases lead absorption from the GI tract.
- Older houses (lead-based paint or pipes).
- Use of lead-containing folk remedies.
- Age - compared to an adult, a child can absorb twice as much lead from the GI tract. Children aged under 5 years are at increased risk of lead poisoning.
Lead poisoning symptoms
Acute lead poisoning
The severity of lead poisoning 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.
- 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 lead poisoning
- Mild abdominal pain.
- Weight loss.
- Antisocial behaviour.
- Hearing loss.
- Foot drop - due to motor peripheral neuropathy.
- Wrist drop - this is a late sign.
- Carpal tunnel syndrome.
- Autonomic dysfunction.
Signs of lead poisoning
There are no pathognomonic signs of lead poisoning 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. Lead poisoning 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:
- Acute confusional states.
- Acute memory loss.
- Frontal lobe syndromes.
- Attention deficit hyperactivity disorder.
- General learning disability (includes learning disorder, developmental delay, language disorder).
- Autism or pervasive developmental disorder.
- Organic solvent poisoning.
- Other heavy metal poisoning.
- Radial mononeuropathy and other peripheral neuropathies.
- Diabetic neuropathy.
- Anaemias, acute and chronic.
- Guillain-Barré syndrome.
- 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.
- 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.
- 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.
- CT or MRI scan of the brain may be contributory in patients with symptoms suggestive of encephalopathy.
Lead poisoning treatment and management
Acute poisoning, especially with encephalopathy, requires immediate treatment in hospital. Chelation therapy is recommended if blood lead level is 45 μg/dL or higher. For blood levels between 20 and 45 μg/dL, treatment is indicated if the child is symptomatic. Asymptomatic children with blood levels below 20 μg/dL require long-term neurodevelopmental follow-up, and counselling is required. In all cases, immediate removal of the source of lead exposure is essential.
- 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.
- 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.
- 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 therapy itself can cause problems and treated patients can develop hypertension, raised intracranial pressure and acute kidney injury from the chelated lead compound.
Lead poisoning prognosis
- 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.
- Evidence suggests that childhood lead exposure may raise the risk of adult neurodegenerative disease, particularly dementia.
- 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).
- 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.
- Educating patients to be cautious in the use of folk remedies is, however, still an issue.
- Further work needs to be done to reduce occupational exposure, particularly in the demolition and tank-cleaning industries.
- 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).
Further reading and references
Mazumdar I, Goswami K, Ali MS; Status of Serum Calcium, Vitamin D and Parathyroid Hormone and Hematological Indices Among Lead Exposed Jewelry Workers in Dhaka, Bangladesh. Indian J Clin Biochem. 2017 Mar32(1):110-116. doi: 10.1007/s12291-016-0582-9. Epub 2016 May 25.
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 26181(2):118-25. Epub 2008 Jul 23.
Madhavi D, Devi KR, Sowjanya BL; Increased frequency of chromosomal aberrations in industrial painters exposed to lead-based paints. J Environ Pathol Toxicol Oncol. 200827(1):53-9.
Mayans L; Lead Poisoning in Children. Am Fam Physician. 2019 Jul 1100(1):24-30.
Schwartz M; The Five MInute Pediatric Consult, 2012.
Exposure to lead; Health and Safety Executive
Wani AL, Ara A, Usmani JA; Lead toxicity: a review. Interdiscip Toxicol. 2015 Jun8(2):55-64. doi: 10.1515/intox-2015-0009.
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 Mar46(3):267-9.
Giampreti A, Bonetti C, Lonati D, et al; A young Indian male with abdominal pain. Clin Toxicol (Phila). 2011 Mar49(3):191-2.
Gorospe EC, Gerstenberger SL; Atypical sources of childhood lead poisoning in the United States: a systematic review from 1966-2006. Clin Toxicol (Phila). 2008 Sep46(8):728-37. doi: 10.1080/15563650701481862.
D'souza HS, Dsouza SA, Menezes G, et al; Diagnosis, evaluation, and treatment of lead poisoning in general population. Indian J Clin Biochem. 2011 Apr26(2):197-201. doi: 10.1007/s12291-011-0122-6. Epub 2011 Feb 18.
Madan K, Sharma PK, Makharia G, et al; Autonomic dysfunction due to lead poisoning. Auton Neurosci. 2007 Mar 30132(1-2):103-6. Epub 2006 Nov 21.
Lead Poisoning; World Health Organization, October 2021
Lead, General Information; Public Health England (formerly Health Protection Agency), October 2016
Updated protocols and research on Clinical Metal Toxicology; Micro Trace Minerals Laboratory, 2013
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 201499:A133-A134.
Childhood Lead Poisoning Prevention; Centers for Disease Control and Prevention (CDC)
Lead Poisoning; Learning Radiology, 2015
Payne M, Egden L, Behinaein S, et al; Bone lead measurement. Can Fam Physician. 2010 Nov56(11):1110-1
Flora SJ, Pachauri V; Chelation in metal intoxication. Int J Environ Res Public Health. 2010 Jul7(7):2745-88. doi: 10.3390/ijerph7072745. Epub 2010 Jun 28.
Hon KL, Fung CK, Leung AK; Childhood lead poisoning: an overview. Hong Kong Med J. 2017 Dec23(6):616-21. doi: 10.12809/hkmj176214. Epub 2017 Oct 13.
Gustavsson P, Gerhardsson L; Intoxication from an accidentally ingested lead shot retained in the gastrointestinal tract. Environ Health Perspect. 2005 Apr113(4):491-3.
Schaider J et al; Rosen & Barkin's 5-Minute Emergency Medicine Consult, 2012.
Flora G, Gupta D, Tiwari A; Toxicity of lead: A review with recent updates. Interdiscip Toxicol. 2012 Jun5(2):47-58. doi: 10.2478/v10102-012-0009-2.
Reuben A; Childhood Lead Exposure and Adult Neurodegenerative Disease. J Alzheimers Dis. 201864(1):17-42. doi: 10.3233/JAD-180267.
Lead poisoning and health; World Health Organization, 2015
Meyer PA, Brown MJ, Falk H; Global approach to reducing lead exposure and poisoning. Mutat Res. 2008 Jul-Aug659(1-2):166-75. Epub 2008 Mar 20.
Gidlow DA; Lead toxicity. Occup Med (Lond). 2004 Mar54(2):76-81.
Manay N, Cousillas AZ, Alvarez C, et al; Lead contamination in Uruguay: the "La Teja" neighborhood case. Rev Environ Contam Toxicol. 2008195:93-115.