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This is a PatientPlus article. PatientPlus articles are written for doctors and so the language can be technical. However, some people find that they add depth to the articles found in the other sections of this website which are written for non-medical people.

Heavy Metal Poisoning

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Heavy metals are commonly defined as those elements with a high (>5.0) relative density. There is however, an ongoing debate regarding the exact definition and in terms of health it is better to think of these as metals or semi-metal compounds which have the potential to cause environmental or human toxicity. Heavy metal poisoning can be acute or chronic and may be caused by the following:

  • Lead
  • Mercury
  • Iron
  • Cadmium
  • Thallium
  • Bismuth
  • Arsenic (technically not a true metal but a semi-metal i.e. non-metal with some metallic properties)

The metals may enter the body by:

  • Ingestion
  • Inhalation
  • Absorption through the skin or mucous membranes

They are then stored in the soft tissues of the body. The heavy metals once absorbed, compete with other ions and bind to proteins resulting in impaired enzymatic activity resulting in damage to many organs throughout the body.

Epidemiology

Heavy metal poisoning is rare in the UK, even in industries where there is an increased risk.1

  • The most common cause of heavy metal poisoning is lead. The incidence of lead poisoning has been falling steadily in affluent countries due to removal of lead from paint, petrol and food cans.2
  • Lead poisoning remains a problem though in older housing where lead water pipes and lead paint may still be present. In housing such as this there is a particular risk to children and the American Centre for Disease Control and Prevention has recognised this and recommended screening of children in areas considered to pose a threat from this hazard, in order to prevent the children from developing neurological damage.3
  • Other sources of lead poisoning are occupations (e.g. smelting, battery manufacture), traditional remedies, or occasionally foreign bodies (lead weights).
  • Mercury can be found in the elemental state (dental amalgam, thermometers), inorganic (industrial processes) and organic compounds (pesticides, wood preservatives, some medicines, and contaminated fish).
  • Poisoning from other heavy metals most often occurs in individuals regularly exposed to the metals in their work environment.
  • Criminal poisoning with lead has been reported.
Presentation

The presentation will depend on the age of the individual, the metal absorbed, and whether this was the result of acute exposure e.g. vapour inhalation, or exposure over a more prolonged period of time.

Lead poisoning

Also see article on Lead Poisoning.

Acute poisoning presentation:

  • A metallic taste in mouth
  • Severe abdominal pain with vomiting
  • Diarrhoea ± black stool
  • There may be lethargy, muscle cramps and weakness
  • Patients may develop abnormal LFTs or renal complications (acute interstitial nephritis)
  • In children there may be an encephalopathy with cerebral oedema (headache, drowsiness, confusion, seizures and coma)
  • It is rare in adults

Chronic poisoning presentation:

  • Anorexia
  • Abdominal pain and constipation
  • Rarely toxic megacolon
  • Headaches, irritability, malaise, insomnia and depression also occurs
  • There may be a primarily motor peripheral neuropathy (e.g. wrist drop)
  • Mental retardation occurs in children
  • Encephalopathy is rare in adults

Mercury poisoning

The toxic dose for mercury compounds is about 10-50mg/kg. Mercury is poorly absorbed from the gut and ingestion is usually harmless (unless aspiration occurs). A single dose (e.g. broken thermometer) usually causes no problems. It is only slowly absorbed through the skin but can cause a contact dermatitis.

In the mid 1950 - 1968 the people of Minamata, Japan suffered chronic mercury poisoning from pollution from a local factory (Minamata disease). "Mad as a Hatter" is derived from poisoning among hatmakers who used mercuric nitrate to soften the hair of animal hides.

Acute poisoning:


Chronic poisoning:

  • Irritability
  • Personality changes
  • Headache
  • Peripheral neuropathy
  • Memory problems
  • Ataxia
  • Coma
  • Respiratory problems (pneumonitis and ARDS)
  • Gastrointestinal upset (abdominal pain, gingivitis and stomatitis, nausea, vomiting)
  • Renal problems include acute renal failure, nephrotic syndrome and acute tubular necrosis

Iron poisoning

Iron overdose can present with:

  • Nausea ±vomiting
  • Abdominal pain and diarrhoea
  • There may be GI bleeds
  • Serious overdose causes hepatocellular necrosis (jaundice, hepatic failure)
  • Gastric outflow obstruction may be a late complication

Cadmium poisoning

Toxic by inhalation and ingestion but rarely absorption through the skin.
Symptoms develop 12-36 hours after inhalation: (cadmium fume fever is an occupational illness due to exposure to fumes during welding).

Presents with:

  • Metallic taste and increased salivation
  • Nausea, vomiting and diarrhoea
  • Impaired sensation
  • Difficulty breathing, cough, chest pain

Complications include pneumonitis and pulmonary oedema.

Chronic exposure may cause anaemia, emphysema or renal failure, and cadmium may be a risk factor in the development of prostate or lung cancer.

Thallium poisoning

Also see article on Thallium Poisoning.

Acute poisoning tends to produce gastro-intestinal effects whilst chronic poisoning tends to produce neurological manifestations. The classical triad of acute poisoning that should suggest the diagnosis of acute thallium toxicity is:

  • Nausea and vomiting
  • Followed by painful peripheral neuropathy
  • Then alopecia

History is of abdominal pain, nausea and vomiting occurring within a few hours of an acute exposure. Painful sensory neuropathy occurs especially on the soles and palms. It may take 48 hours to develop. It may be followed by weakness of the lower leg, ataxia, confusion, hallucinations, convulsions and coma.

Other reported problems include:

  • Diplopia, abnormal colour vision and reduced visual acuity.
  • Hair loss, rashes and palmar erythema take 2 to 4 weeks to appear.
  • Cardiac arrhythmias.
  • Urine may be green.

Chronic cases may lead to dementia, depression and psychosis.

Bismuth poisoning

Has a few industrial uses in pigments, ceramics and low-melting alloys.
Can cause:

  • Kidney damage and the development of a nephrotic syndrome
  • May also cause the development of a reversible encephalopathy

Arsenic poisoning

Also see article on Arsenic Poisoning.

  • Take a work history where painful peripheral neuropathy presents.
  • Exposure to arsine gas is usually the result of an industrial accident and the worker presents rapidly.
  • Within 30 minutes of exposure there is a metallic taste in the mouth and slight odour of garlic in the breath along with dry mouth and dysphagia.
  • This is quickly followed by severe nausea and vomiting, colicky abdominal pain and profuse diarrhoea, sometimes bloody with rice water stools.

Large quantities will cause:

  • Cyanosis
  • Cold clammy extremities
  • Hypoxic encephalopathy
  • Convulsions
  • Acute tubular necrosis may occur following shock
  • Hyperpyrexia, pulmonary oedema and acute haemolysis may also occur

If death does not occur in the first few hours from shock, the patient may die a few days later from acute hepatic or renal failure.

Differential diagnosis

The differential diagnosis will depend on the symptoms and signs displayed, but may include causes of encephalopathy, dementia, substance abuse and causes of vomiting and diarrhoea.

Investigations

Investigation of any person in whom a diagnosis of heavy metal poisoning is a possibility may include:

  • Full history - including occupational history, age of house and water supply if known
  • Examination
  • FBC and film - basophilic stippling with lead and arsenic poisoning, normochromic or microcytic anaemia with lead toxicity
  • Blood levels for lead and mercury
  • 24 hour urine collection - mercury and arsenic levels
  • Long bone X-ray in children - horizontal metaphyseal lines ("lead bands" caused by failure of the bones to remodel, not seen in adults)
  • CXR - may show radiodense pulmonary emboli following injection of mercury
Management

Current advice on the management of any form of heavy metal poisoning may be obtained from the UK National Poisons Information Service or TOXBASE.

Lead poisoning

  • The treatment for lead poisoning begins with removing the source of lead e.g. renewing lead pipes. Lead should then be removed from the body using chelation therapy such as calcium edetate (EDTA), d-penicillamine or dimercaprol. Chelation therapy should be accompanied by active hydration, and should be continued until the lead excreted in the urine drops below a level of 500 micrograms per day.

Mercury poisoning

  • Inhalation of mercury should be treated with IV hydrocortisone to minimise pulmonary complications. Acute intakes of inorganic mercury should be treated with chelating agents such as dimercaprol or d-penicillamine. Organic mercury poisoning should not be treated with dimercaprol as this may result in higher mercury levels in the brain.

Iron poisoning

  • This needs urgent treatment - patient needs urgent admission and desferrioxamine (iv) as an antidote. Chronic iron excess is dealt with in Iron Overload article.

Cadmium poisoning

  • At present there is no effective therapy for cadmium poisoning, and treatment is supportive and symptomatic. It is hoped that some of the newer chelating agents may help in reducing cadmium levels in the body.

Thallium poisoning

  • Remove source of exposure if possible and any contaminated clothing.
  • If ingestion has occurred in the last ½ hour induce vomiting. With ingestion, activated charcoal and Prussian blue (potassium ferric hexacyanoferrate) are recommended.
  • Measure thallium levels in blood and urine 3 times per week to confirm a decreasing trend.
  • Physiotherapy may reduce or prevent muscle contractures.

Bismuth poisoning

  • A chelating agent can be used, but treatment is not always necessary.

Arsenic poisoning

  • The main treatment for arsenic intoxication is using the chelating agent dimercaprol. Penicillamine is also used but is less effective at promoting excretion.
  • Dimercapto-1-sulphonate (DMPS, Unithiol) has been successfully tried in some cases.
  • Patients may also need supportive treatment if they develop liver or renal failure, or to correct electrolyte and fluid imbalance.


Document references
  1. Baldwin DR, Marshall WJ; Heavy metal poisoning and its laboratory investigation. Ann Clin Biochem. 1999 May;36 ( Pt 3):267-300.
  2. Pirkle JL, Brody DJ, Gunter EW, et al; The decline in blood lead levels in the United States. The National Health and Nutrition Examination Surveys (NHANES) JAMA. 1994 Jul 27;272(4):284-91. [abstract]
  3. No authors listed; Screening for elevated blood lead levels. American Academy of Pediatrics Committee on Environmental Health. Pediatrics. 1998 Jun;101(6):1072-8. [abstract]

Internet and further reading Acknowledgements EMIS is grateful to Dr Gurvinder Rull for writing this article and to Dr Cathy Jackson for earlier versions. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2009.
Document ID: 2245
Document Version: 22
Document Reference: bgp1401
Last Updated: 14 May 2009
Planned Review: 14 May 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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