1. Mercury poisoning

Poisonous forms of mercury

• Poisonous forms are elemental mercury: alkyl mercuryinorganic mercurial salts Aryl mercury compounds each with a relatively unique pattern of clinical toxicity.

Mercury is mainly mined as

Mercury mainly mined as HeS in cinnabar ore, then converted to various forms. Key industrial and commercial applications are found in: electrolyte production of chlorine

Mercury is used to manufacture

Manufacture of electrical equipments, thermometers, and other instruments, fluerescent lamps, dental amalgam, artisanal gold production.

Pharmaceutical and biocidal manufacture has reduced

Occasional use in antiseptics and folk medicines still occurs.

PK OF MERCURY

Pharmacokinetics of Mercury

1. Absorption

• Inhalation: Most significant route, especially elemental mercury vapor; rapid and efficient absorption.

• Dermal: Alkyl (organic) mercury compounds can be absorbed through intact skin.

• GIT:
  

  • Elemental mercury: Poorly absorbed if ingested.

  • Organic mercury (like methylmercury): Well absorbed through GIT.

2. Distribution

• Mercury distributes widely; highest levels are found in the kidneys.

• Methylmercury readily crosses the blood-brain barrier and placenta—a major concern in pregnancy.

• Binds to sulfhydryl groups in proteins and accumulates in:
  

  • Hair and nails (keratin-rich tissues)

  • CNS, especially for methylmercury

3. Metabolism

• Inorganic and organic forms can interconvert in the body.

• Methylmercury is lipophilic, contributing to its CNS accumulation.

4. Excretion

• Primarily via urine and feces.

• A small fraction remains in the body for years.

• Elemental mercury (inhaled):
  

  • Urinary levels decline with a half-life of 1–3 months.

• Methylmercury:
  

  • Half-life >50 days

  • Undergoes enterohepatic circulation (biliary excretion + reabsorption)

  • Can also be excreted through hair, nails, and breast milk

acute mercury poisoning

Acute Mercury Poisoning

A. Elemental Mercury (Inhalation):

• Seen in occupational exposure (e.g., mining, broken thermometers in enclosed spaces)

• Pulmonary toxicity:
  

  • Chemical pneumonitis

  • Non-cardiogenic pulmonary edema

• Other acute symptoms:
  

  • Acute gingivostomatitis

  • Neurological symptoms (tremors, irritability)

B. Inorganic Mercury Salts (e.g., mercuric chloride – ingestion):

• Severe corrosive GI effects:
  

  • Hemorrhagic gastroenteritis

• Followed by:
  

  • Acute tubular necrosis

  • Oliguric renal failure within hours–days

Chronic mercury poisoning

Most often due to prolonged inhalation of elemental mercury.

Classic Triad:

1. Tremor (starting as fine intention tremor, can progress)

2. Neuropsychiatric symptoms (”erethism mercurialis”):
   

   • Memory loss, irritability, insomnia

   • Social withdrawal, shyness, depression, explosive anger

4. Gingivostomatitis:
   

   • Swollen gums, salivation, tooth loss

Rarely: Peripheral neuropathy (uncommon)

Acrodynia

Acrodynia (Pink Disease):

• Seen in children, idiosyncratic reaction

• Painful erythema of palms and soles

• Associated features: Hypertension, diaphoresis, insomnia, irritability/apathy, anorexia, rash (morbilliform)

Methyl mercury toxicity

• Lipophilic → crosses BBB & placenta

• CNS signs (appear after delay):
  

  • Paresthesia

  • Ataxia

  • Dysarthria

  • Hearing loss

  • Visual field constriction (progressive)

• Reproductive toxicity:
  

  • Yes, you can say it’s teratogenic

  • Prenatal exposure → mental retardation, cerebral palsy-like syndrome

  • Low-dose → subclinical developmental delays (e.g., cognition, coordination)

Dimethylmercury poisoning

Dimethylmercury:

• Highly potent neurotoxin

• Tiny exposures (even through latex gloves) can be lethal

• Delayed-onset severe neurotoxicity, often fatal

Diagnosis of mercury poisoning

Diagnosis of Mercury Poisoning

• Based on:
  

  • History of exposure

  • Physical signs

  • Lab confirmation

Biomarkers:

• Urine mercury → best for chronic elemental/inorganic exposure

• Blood mercury → better for recent or methylmercury exposure

Normal levels:

• Blood: < 5 µg/L

• Urine: < 5 µg/L (some say up to 10 µg/L is acceptable in adults)

Treatment

Treatment of Mercury Poisoning

1. General Measures

• Remove from exposure

• Supportive care:
  

  • Hydration → maintain urine output

  • Dialysis → if acute renal failure

• Chelation therapy → cornerstone of treatment

2. Chelation Agents & Their Uses

Chelator	Route	Used for
Dimercaprol (BAL)	IM	Acute inorganic mercury poisoning only
Unithiol (DMPS)	Oral/IV	Acute or chronic mercury (elemental/inorganic)
Succimer (DMSA)	Oral	Acute/chronic inorganic or organic mercury
NAC	Oral/IV	Methylmercury enhancement (off-label/adjunct)

why is dimercaprol (BAL) contraindicated in chronic mercury poisoning

?

Dimercaprol can actually worsen mercury toxicity in chronic exposure, particularly for these reasons:

1. Redistribution to the CNS:
   

   • Dimercaprol is lipophilic, so when given over time, it can mobilize mercury from peripheral tissues and drive it into the brain, where it causes irreversible damage.

3. Increased neurotoxicity risk:
   

   • In chronic exposure, a large portion of mercury may already be deposited in the brain.

   • Dimercaprol can’t effectively chelate mercury in the CNS, so it might just increase CNS mercury burden.

5. Less effective and more toxic long-term:
   

   • Compared to succimer or unithiol, BAL has more side effects, requires IM injections, and has less favorable kinetics in chronic treatment.