Heavy Metal Toxicity


The term heavy metal refers to any
metallic chemical element that has a
relatively high density and is toxic or
poisonous at low concentrations.
Examples of heavy metals include
mercury (Hg), cadmium (Cd), arsenic
(As), chromium (Cr), thallium (TI), and
lead (Pb).
Points to note:

  • Heavy metals are not entirely
  • Some heavy metals like copper, selenium, or zinc are essential trace elements. They functions in various biological processes also driving the entire human metabolism

General characteristics of Heavy Metal Toxicity

  • Most common toxic heavy metals include: lead (pb), mercury (Hg), cadmium (Cd), and Arsenic (As).
  • They are mainly produced by industrial
    activities and deposit slowly in the surrounding water and soil
  • Their toxicity may occur through ingestion, inhalation or dermal exposure
  • Toxicity is either acute or chronic
  • They give metallic taste if ingested except arsenic which is tasteless
  • They can cause both local & systemic effect
  • Most metals cause diarrhea except
    lead which cause constipation
  • The antidotes for heavy metals are
    called CHELATORS.

1. Lead (Pb) Toxicity

  • Lead is the most common metallic poison
  • Occurs in organic and inorganic forms
  • -After ingestion, absorption in children
    is higher than in adults (50% in children, 10% in adults)
  • In children, no organ system is immune to the effects of lead poisoning
  • Developing brain is the most risky organ to be affected

Methods of exposures

  1. Occupational: Over 900 occupations
    linked, parents may bring home lead dust.
  2. Water and food contamination: lead
    pipes or storage tanks, andb contaminated food
  3. Foreign body ingestion: Childhood lead poisoning resulting from the ingestion of lead based foreign bodies.
  4. Retained bullet and illegally manufactured alcohols
  5. Inhalation of lead from motor vehicles 

Pathophysiology of Lead Toxicity

  • Lead has high affinity for sulfhydryl groups.
  • Particularly toxic to a variety of enzyme system
  • Many lead’s toxic effects also result from its inhibition of cellular function requiring calcium
  • Lead binds to calcium activated proteins 105 times than Ca2+
  • Pb²+ and Ca²+ competes at the plasma membrane for transport systems, which affect the entry or exit (i.e. Ca2+ channels and Ca²+ pump).
  • Intracellular Ca2+ is buffered by proteins in endoplasmic reticulum, and mitochondria, Pb2+ disturb intracellular ca24 homeostasis
  • Pb²+ interact with a number of Ca²+ dependent effectors mechanisms such as calmodulin Ca2+ binding protein, which couple to several enzymes e.g phoshodiestrase and protein kinase).

Haematological Effects of Lead Toxicity

  • Lead induced anemia
  • Hypochromic microcytic anemia
  • This is more in children

Renal Effects of Lead Toxicity

  • Acute toxicity may cause renal colic
  • Acute toxicity may cause direct tubular damage
  • Chronic toxicity may cause chronic interstitial nephritis
  • Alters uric acid excretion resulting in hyperuricemia and gout

CNS Effect of Lead Toxicity

  • It can lead to encephalopathy especially in children
  • It can lead to Permanent leaning disability. Here, children below 3years are most at risk as their brain are rapidly developing
  • D-ALA thought to be neurotoxic by interfering with GABA
  • Affect peripheral nerves mainly motor nerve

Reproductive System Effects

  • Abortion
  • Stillbirth
  • Neurodevelopmental problems
  • May cause decreased sperm count
  • Increased number of abnormal sperm

Bone Effects

  • Triggers hypermineralization
  • They reflect bone growth arrest and not deposition.
  • Lead inhibits the conversion of vitamin D into its active form.

Treatment of Lead Toxicity

a. 2,3-Dimercaprol (a.k.a British Anti

  • It removes intracellular and extracellular lead
  • It is lipid-soluble drug and must be administered IM only as IV cause fat embolism

b. Calcium disodium edentate
(CaNa²+ EDTA)

  • This allows extracellular lead to be renally eliminated
  • Once started, CaNa₂EDTA should be
    given in full 5 days course.
  • Dimercaprol should be given first to avoid redistribution of lead mobilized CaNa₂EDTA to CNS.

c. D-penicillamine

  • This is taken orally and has few adverse effects
  • It can chelate lead even in low blood
  • It is effective in children with levels 20 40Hg/100ml

2. Mercury Toxicity

  • Mercury is the only metal that is liquid at room temperature
  • It is found in 3 form but they’re all are toxic. These forms include elemental (metallic) mercury, Inorganic and Organic.

Methods of Exposure


  • Barometers
  • Batteries
  • Dental amalgams
  • Electroplating
  • Finger print product
  • Fuorescent and mercury lamps
  • Infrared detectors
  • Jewelry industry
  • Manometer
  • Neon lamps
  • Paints
  • Photography
  • Silver and gold product
  • Thermometers.
  • Thimerosal: It is used in vaccine preservation to prevent bacterial contamination. Common vaccines containing thimerosal are DTP, haemophilus influenza, and hepatitis B.
  • Toxicity is by inhalation
  • It is poorly absorbed from GIT (e.g thermometer)
  • Once inhaled it in mostly converted to the inorganic form
  • Chronic exposure result in;
    Neurologic, dermatologic and renal effects
Acute Toxicity of Elemental Mercury 
  • Might result in fever fatigue and clinical signs of pneumonitis.
  • Dyspnea and pleuritic chest pain
  • Lethargy, confusion
  • Fatal acute respiratory disease has been reported following elemental mercury inhalation.

Other Sign & symptoms include.

  • Neuropsychiatric disturbance (e.g
    memory loss)
  • Tremor
  • Hypertension
  • Flushing, discoloration and desquamation of the hand and feet.


  • Ingestion is the main route of exposure of this.
  • Largest outbreaks are related to organic are related to organicmercury (fungicides, seed dressing,
    contaminated fish)
  • Marine animal convert elemental to organic mercury in their tissue. 
  • Minamata (1940) Japan 
  • Iraq (1974) – Grain disaster 
Acute Ingestion of Organic Mercury
  • This is usually via contaminated foods
  • Organic mercury target specific sites in the brain including the cerebral cortex, motor and sensory centers, auditory center, etc
  • Onset of symptoms usually is delayed (days to week).
  • Depletion of enzymes must occur before the onset of symptoms
  • Symptoms are typically neurological such as visual ataxia, hearing loss, mental deterioration, muscle tremor, and movement disorder


  • Main route of inorganic mercury exposure is via ingestion and skin.
  • It can be corrosive to mucosal membrane
  • Poor liquid solubility
  • Causes a non-uniform distribution with kidney accumulation, causing renal damage
  • Limited CNS penetration, but chronic exposure allow for CNS accumulation/toxicity.
Acute ingestion of inorganic

Mercury and mercuric salt toxicity presentation

  • Gray mucous membranes
  • Vomiting
  • Severe abdominal pain
  • Hematemesis, and
  • Hypovolemic shock.

Systemic effects usually begin several hours post ingestion and may last several days.

Chronic toxicity
  • The traid: Tremor, Gingivities, Erethism
  • GIT: metallic taste, hypersalivation
  • Neurologic: Neurasthenia and Erethism.

Management of Mercury Toxicity

  • Removal of contaminated clothing and
    skin irrigation
  • Do not induce emesis if the compound ingested is caustic inorganic form.
  • Gastric lavage is recommended for organic ingestion,
  • Whole bowel irrigation may be used until rectal effluent is clear.
  • Use chelating agents if the patient is symptomatic

Metallic Mercury in Acute or
Chronic Poisoning

  • D-Penicillamine is an alternative
    oral treatment

Inorganic mercury salts:

  • BAL if begun within minutes to a few hours after ingestion may reduce severe renal injury

Organic Mercury

  • Oral 2,3-Dimercaptosuccinic Acid
    (DMSA) may be effective in decreasing
    Hg in tissues, including brain
  • BAL is contraindicated in metallic and organic mercury as it redistributes mercury to brain
  • Also Ca Na₂ EDTA is contraindicated because it makes Hg a nephrotoxic complex.

3. Arsenic Toxicity

  • Arsenic is referred to as king of poisons.
  • It is used as homicidal agents
  • Sign and symptoms is similar to natural disease
  • Ease of ingestion as it is odorless, tasteless

Sources of Contaminations

  1. Foods: Daily human intake of arsenic
    contained in food 0.5 -Img with the greatest mainly from fish in seafood. Arsenic in mainly found in its less toxic organic form.
  2. Water: Over 137 million people in more
    than 70 countries are probably affected by arsenic poisoning from drink of water
  3. Industry: herbicide, fungicide, wood preservative.

Forms of Arsenic

  1. Inorganic (Arsenite)
  2. Organic (Arsine)
  3. Elemental form.

Pathophysiology of Arsenic Poisoning

  • Arsenic distributes rapidly to
    erythmocytes and binds to the globin portion of haemoglobin
  • Redistribution occur within 24hrs to the liver, spleen, kidney and GIT
  • Arsenic impairs cellular respiration by inhibiting mitochondrial enzyme and oxidative phosphorylation.
  • Blocks pyruvate dehydrogenase in kreb’s cycle
  • Over a period of weeks, deposits may be found in skin, hair, nails and bone 

Arsenic produce cellular damage by:

  • Binding to enzyme SH groups
  • It blocks the conversion of pyruvate to acetylcoenzyme A and inhibit gluconeogenesis.
  • Long term exposure results in nerve
    damage and may lead to lung, skin and liver cancer
  • Once inhaled, arsine gas combines with haemoglobin resulting in severe hemolysis and anemia.

Acute severe arsenic poisoning

  • Vital signs of Acute severe arsenic poisoning: tachycardia and hypotension, even shock
  • CNS: altered mental status, delirium, coma, and seizures
  • Patients exposed to arsenic have a garlic smell to their breath and tissue fluid
  • Acute exposure generally manifest with the cholera-like GIT symptoms of vomiting (most times bloody) and severe diarrhea
  • These patients will experience acute distress, dehydration and hypovolemic shock.

Chronic toxicity

  • Peripheral neuropathy: affects sensory
    neurons more than motor neurons
  • Black foot disease: peripheral vascular disease
  • Dermatologic effects: Alopecia, hypo or hyper pigmentation
  • Contact dematitis may also be induced in ocupational arsenic poisoning.

Arsenic dust coming into contact with the skin produces four main types of reaction

  1. Toxic reaction
  2. eczemation
  3. combined toxic and eczematous reaction
  4. reactions characterized by
    follicular lesions. 


  • BAL (British Antilewisite)
    Lewisite in arsenic containing vesicant
  • DMSA (2,3 dimercaptosuccinic acid)


  1. Kalia, K.; Flora, S.J.S. Strategies for Safe and Effective Treatment for Chronic Arsenic and Lead Poisoning. J. Occup. Hlth. 2005, 47, 1-21. 
  2. Andersen, O. Chemical and biological considerations in the treatment of metal intoxications by chelating agents. Mini Rev. Med. Chem. 2004, 4, 11-21
  3. Llobet, J.M.; Domingo, J.L.; Corbella, J. Comparison of the effectiveness of several chelators after single administration on the toxicity, excretion and distribution of cobalt. Arch. Toxicol. 1986, 58, 278-281
  4. Andersen, O. Principles and recent developments in chelation treatment of metal intoxication. Chem. Rev. 1999, 99, 2683-2710.

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