Many of the elements that can be considered heavy metals have no known benefit for human physiology. Lead, mercury, and cadmium are prime examples of such “toxic metals.” Yet, other metals are essential to human biochemical processes. For example, zinc is an important cofactor for several enzymatic reactions in the human body, vitamin B-12 has a cobalt atom at its core, and haemoglobin contains iron. Likewise, copper, manganese, selenium, chromium, and molybdenum are all trace elements that are important in the human diet. Another subset of metals includes those used therapeutically in medicine; aluminium, bismuth, gold, gallium, lithium, and silver are all part of the medical armamentarium. Any of these elements may have pernicious effects if taken in quantity or if the usual mechanisms of elimination are impaired.
The toxicity of heavy metals depends on a number of factors. Specific symptomatology varies according to the metal in question, the total dose absorbed, and whether the exposure was acute or chronic. The age of the person can also influence toxicity. For example, young children are more susceptible to the effects of lead exposure because they absorb several times the percent ingested compared with adults and because their brains are more plastic and even brief exposures may influence developmental processes. The route of exposure is also important. Elemental mercury is relatively inert in the gastrointestinal tract and also poorly absorbed through intact skin, yet inhaled or injected elemental mercury may have disastrous effects.
Some elements may have very different toxic profiles depending on their chemical form. For example, barium sulfate is basically nontoxic, whereas barium salts are rapidly absorbed and cause profound, potentially fatal hypokalemia. The toxicity of radioactive metals like polonium, which was discovered by Marie Curie but only recently brought to public attention after the 2006 murder of Russian dissident Alexander Litvinenko, relates more to their ability to emit particles than to their ability to bind cell proteins.
Exposure to metals may occur through the diet, from medications, from the environment, or in the course of work or play. Where heavy metal toxicity is suspected, time taken to perform a thorough dietary, occupational, and recreational history is time well spent, since identification and removal of the source of exposure is frequently the only therapy required.
A full dietary and lifestyle history may reveal hidden sources of metal exposure. Metals may be contaminants in dietary supplements, or they may leech into food and drink stores in metal containers like lead decanters. Persons intentionally taking colloidal metals for their purported health benefits may ultimately develop toxicity. Metal toxicity may complicate some forms of drug abuse. Beer drinker’s cardiomyopathy was diagnosed in alcoholics in Quebec, and later Minnesota, during a brief period in the 1970s when cobalt was added to beer on tap to stabilize the head. More recently, a parkinsonian syndrome among Latvian injection drug users of methcathinone has been linked to manganese toxicity.
Currently, millions of people living in and around Bangladesh are at risk for organ dysfunction and cancer from chronic arsenic poisoning from the water supply. In an effort to bypass ground water sources rife with bacterial contamination, tube wells were sunk throughout that area, deep into the water table. Bedrock rich in arsenic gives these deeper water stores—and the crops they irrigate—a high concentration of arsenic, and toxicity is epidemic throughout the area. Childhood lead poisoning linked to the ingestion of old paint chips in the North American setting is another good example of environmental contamination.
Metals have been used as instruments of murder. Arsenic is perhaps more rightly classified as a metalloid, but it is consistently the single substance most commonly thought of as a poison. Metals have also been used in warfare as chemical weapons. Again, arsenic was the primary component of the spray known as Lewisite that was used by the British during trench warfare in World War I. Exposure produced severe edema of the eyelids, gastrointestinal irritation, and both central and peripheral neuropathies.
This article provides a brief overview of general principles in the diagnosis and management of metal toxicity. The Table below reviews the typical presentation of the most commonly encountered metals and their treatment in summary form. It is not intended to guide clinical decision in practice or for self-diagnosis***
Typical Presentation of the Most Commonly Encountered Metals and Their Treatment
|Diabetes, hypo pigmentation/ hyperkeratosis
cancer: lung, bladder, skin, encephalopathy
|24-h urine: para,
≥50 µg/L urine,
100 µg/g creatinine
|BAL (acute, symptomatic)
|Bismuth||Renal failure; acute tubular necrosis||Diffuse myoclonic encephalopathy||No clear reference standard||**|
|Cadmium||Pneumonitis (oxide fumes)||Proteinuria, lung cancer, osteomalacia||Proteinuria and/or ≥15 µg/ g creatinine||**|
|Chromium||GI hemorrhage, hemolysis, acute renal failure (Cr6+ ingestion)||Pulmonary fibrosis, lung cancer (inhalation)||No clear reference standard||NAC (experimental)|
|Cobalt||Beer drinker’s (dilated) cardiomyopathy||Pneumoconiosis (inhaled); goiter||Normal excretion:
0.1-1.2 µg/L (serum)
0.1-2.2 µg/L (urine)
|NAC , CaNa2 , EDTA|
|Copper||Blue vomitus, GI irritation/ haemorrhage, hemolysis, MODS (ingested); MFF (inhaled)||vineyard sprayer’s lung (inhaled); Wilson disease (hepatic and basal ganglia degeneration)||Normal excretion:
25 µg/24 h (urine)
|BAL, D-Penicillamine, Succimer|
|Iron||Vomiting, GI haemorrhage, cardiac depression, metabolic acidosis||Hepatic cirrhosis||Nontoxic: < 300 µg/dL
Severe: >500 µg/dL
|Lead||Nausea, vomiting, encephalopathy (headache, seizures, ataxia, obtundation)||Encephalopathy, anaemia, abdominal pain, nephropathy, foot-drop/ wrist-drop||Pediatric: symptoms or [Pb] ≥45 µ/dL (blood); Adult: symptoms or [Pb] ≥70 µ/dL||BAL, CaNa2 , EDTA, Succimer|
|Manganese||MFF (inhaled)||Parkinson-like syndrome, respiratory, neuropsychiatric||No clear reference standard||**|
|Mercury||Elemental (inhaled): fever, vomiting, diarrhea, Inorganic salts (ingestion): caustic gastroenteritis||Nausea, metallic taste, gingivo-stomatitis, tremor, neurasthenia, nephrotic syndrome; hypersensitivity (Pink disease)||Background exposure “normal” limits: 10 µg/L (whole blood); 20 µg/L (24-h urine)||BAL, Succimer DMPS (Europe)|
|Nickel||Dermatitis; nickel carbonyl: myocarditis, ALI, encephalopathy||Occupational (inhaled): pulmonary fibrosis, reduced sperm count, nasopharyngeal tumors||Excessive exposure: ≥8 µg/L (blood)
≥500 µg/L (8-h urine)
|Selenium||Caustic burns, pneumonitis, hypotension||Brittle hair and nails, red skin, paresthesia, hemiplegia||Mild toxicity: [Se] >1 mg/L (serum); Serious: >2 mg/L||**|
|Silver||Very high doses: hemorrhage, bone marrow suppression, pulmonary edema, hepatorenal necrosis||Argyria: blue-grey discoloration of skin, nails, mucosae||Asymptomatic workers have mean [Ag] of 11 µg/L (serum) and 2.6 µg/L (spot urine)||Selenium, vitamin E (experimental)|
|Thallium||Early: Vomiting, diarrhea, painful neuropathy, coma, autonomic instability, MODS||Late findings: Alopecia, Mees lines, residual neurologic symptoms||Toxic: >3 µg/L (blood)||MDAC , Prussian blue|
|Zinc||MFF (oxide fumes); vomiting, diarrhea, abdominal pain (ingestion)||Copper deficiency: anemia, neurologic degeneration, osteoporosis||Normal range:
0.6-1.1 mg/L (plasma)
10-14 mg/L (red cells)
** No accepted Chelation regimen; Contact toxicologist regarding treatment plan.
For more information regarding toxicity of metals, metal detox, sources of metals or treatment, click on the following links
And please be sure to check the number for your local poisoning hotline in case of emergency.