Mercury toxicity

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Background

Common Exposures

  • Industrial
    • Batteries, fungicide
  • Seafood consumption
    • Mostly methylmercury

Exists as three major forms

  • All disrupt sulfhydryl ezymes leading to impaired cellular function

Elemental

  • Liquid metal at room temperature (Think of the Terminator recongealing)
  • 14x more dense than water
  • Volatile and lipid soluble, therefore rapidly absorbed through lungs (approximately 70-80%)
  • Oxidized rapidly to inorganic form
  • Poorly absorbed from GI tract
    • Therefor most ingestions are non-toxic

Organic

  • Exists in three major forms:
  1. Long chain
  2. Short chain
  3. Aryl
  • Long chain and Aryl forms are rapidly converted to inorganic forms
  • Short chain forms are highly lipophilic and cross the blood-brain barrier and placenta
    • Metabolized in the liver to N-acetyl-homocysteine-methylmercury which undergoes enterohepatic recirculation

Inorganic

  • Exists as monovalent and divalent
  • Corrosive
  • Chronic exposures lead to accumulation in brain and CNS
  • Found in many batteries, little risk of toxicity from the mercury components s/p ingestion
    • Other dangers exist though!!!
  • The California Department of Public Health issued a health alert on May, 2014 noting mercury poisoning linked to use of skin-lightening or acne Creams from Mexico[1]

Historical Exposures

Atomic symbol of Hg from latin name hydrargyros which means silver water

  • Hat felters (Elemental)
    • "Mad as a hatter"
  • Anti-syphilitic agents (Inorganic)
    • "A night in the arms of venus lead to a lifetime on mercury"
  • Calomel (Inorganic)
    • Mercurous Chloride sold as a teething powder
    • Causes "pink disease"
      • pain and erythema of the palms and soles, irritability, insomnia, anorexia, diaphoresis, photophobia, and skin rash
  • Minamata Bay, Japan (Organic)
    • Massive exposure to methylmercury from contaminated seafood secondary to industrial dumping of mercury containing compounds
  • Iraq 1971 (Organic)
    • 95,000 tons of methylmercury coated grain sold for human consumption
  • Miners and smelters (Elemental)
    • Mostly secondary to exposure to Cinnabar (HgS)
  • Dental workers through amalgams (Elemental)
    • Clinical effects secondary to exposure to mercury through amalgams is controversial

Clinical Features

  • Clinical presentation highly dependent on form, concentration and duration of exposure
    • Inhalation of elemental mercury and ingestion of inorganic can cause acute or subacute toxicity
    • Organic mercury more likely causes chronic toxicity

Elemental Mercury

Acute Exposure

Chronic Exposure

  • Classic Triad:
  1. Tremor
  2. Gingivitis/stomatitis
  3. Hyperexcitable state/emotional lability

Inorganic Mercury

Acute Exposure

  • Primarily toxic through oral route
  • Causes caustic burns
    • Severity dependent on type [Hg(2)Cl vs Hg(1)Cl] and concentration of mercurial salts
      • Mercuric forms [Hg(2)] more toxic
    • Other symptoms include pain, nausea, hematemesis, hypovolemia, acute tubular necrosis
    • Sequelae include renal failure

Chronic Exposure

  • Chronic exposures usually secondary to inhalation exposure
  • Symptoms include renal failure, dementia, acrodynia
  • Neuropsychiatric disturbances

Organic Mercury

  • Acute and chronic exposures present similarly
    • Acute presentations usually show signs days to weeks after exposure
  • Neuro symptoms predominate
  • May also cause thrombocytopenia and agranulocytosis
  • Highly fetotoxic
    • Easily crosses placenta
    • May lead to severe intellectual disability (like those with Minamata disease), developmental delay, ataxia and seizures in offspring
    • Controversy exists over exposure from regular diet
      • Albacore tuna may contain up to 0.34ppm of organic mercury
      • Please see Faroe Island and Seychelles studies
    • Thimerosal (mercury containing preservative found in many vaccines) has NOT been linked to developmental delays or autism

Differential Diagnosis

Background

Heavy metal toxicity results from exposure to metals like lead, mercury, arsenic, or cadmium, which interfere with cellular function. Exposure may occur occupationally, environmentally, through ingestion, or from alternative medicines. Chronic toxicity can present insidiously, while acute toxicity may mimic sepsis or encephalopathy. Diagnosis is often delayed due to nonspecific symptoms.

Clinical Features

Symptoms depend on the metal and exposure duration but may include:

Neurologic: Peripheral neuropathy, confusion, tremor, encephalopathy

GI: Abdominal pain, nausea, vomiting, diarrhea, anorexia

Heme: Anemia (especially microcytic or hemolytic), basophilic stippling (lead)

Renal: Tubular dysfunction, proteinuria, Fanconi syndrome

Dermatologic: Mees’ lines (arsenic), hyperpigmentation, hair loss

Others: Fatigue, weight loss, hypertension (cadmium), immunosuppression

Differential Diagnosis

Sepsis or systemic inflammatory response

Drug toxicity or overdose

Metabolic disorders (e.g., porphyria, uremia)

Psychiatric illness (if symptoms are vague or bizarre)

Neurologic diseases (e.g., Guillain-Barré, MS, Parkinson’s)

Vitamin deficiencies (e.g., B12, thiamine)

Evaluation

Workup

History: Occupational exposures, home remedies, hobbies (e.g., jewelry making, battery recycling), diet, water source, imported goods

Labs:

  • CBC, CMP, urinalysis
  • Blood lead level, serum/urine arsenic, mercury, or cadmium (based on suspicion)
  • Urine heavy metal screen (note: spot testing may require creatinine correction)

Imaging: Abdominal X-ray (radiopaque material in GI tract, especially with lead)

EKG: Evaluate for QT prolongation or arrhythmias in severe cases

Diagnosis

Confirmed by elevated blood or urine levels of the specific metal in the context of clinical findings. Hair and nail testing are unreliable for acute toxicity. Interpret results with toxicologist input if possible.

Management

Remove the source of exposure (e.g., occupational control, GI decontamination if recent ingestion)

Supportive care: IV fluids, seizure control, electrolyte repletion

Chelation therapy (in consultation with toxicology or Poison Control):

Lead: EDTA, dimercaprol (BAL), succimer

Mercury/arsenic: Dimercaprol or DMSA

Cadmium: No effective chelation—focus on supportive care

Notify local public health authorities if exposure source is environmental or occupational

Disposition

Admit if symptomatic, unstable, or requiring chelation

Discharge may be appropriate for asymptomatic patients with low-level exposure and outpatient follow-up

Arrange toxicology or environmental medicine follow-up for source control and serial testing

See Also

Evaluation

Work-Up

  • Urine and blood mercury levels
  • CBC
  • Chem 7
  • Type and screen
  • Radiographs

Evaluation

  • Urine mercury levels (>25μg/L is elevated) for elemental and organic mercury
    • Levels >300μg/L usually symptomatic
    • Organic mercury poorly excreted
  • Blood levels for organic mercury
  • Hair analysis is not sufficient

Management

  • ABC's
  • Decontaminate
    • Of note, mercury can penetrate through latex and nitrile gloves

Inhalation injuries

Caustic injuries

  • May consider milk or egg whites
    • Thought to bind mercury
  • WBI

Chelation therapy

The choice of chelating agent is dependent of the type of mercury poisoning.

  • Penicillamine 250mg PO QID x 1-2wks
    • Avoid in renal failure
  • Dimercaprol (BAL) 2.5-5mg IM Q6-12hr
    • Contraindicated in organic mercury poisoning as can paradoxically increase mercury levels
  • DMSA (succimer) 10mg/kg TID x 5days then 10mg/kg BID x 14days

Disposition

See Also

External Links

References

  1. ↑ http://www.ehib.org/papers/Health_Alert%20_Mercury_Poisonings_from_Mexican_creams_5_2014.pdf
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