Module 3: Toxicology - Section 10: Other Heavy Metals

TOX 10.2: Mercury

MERCURY:

Uses and high risk exposures:

• inorganic mercury is mined primarily as cinnabar (HgS) and in very rich ores as metallic mercury → heated by roasting to produce mercury vapour; secondary production from dental amalgams, scrap batteries, discarded instruments and electrical devices;

• inorganic mercury mainly used for electrical apparatus, chemical industry(chlorine and caustic soda production), catalysts (polyurethane foams), dentistry, industrial and control instruments (thermometers, barometers, manometers), dry batteries, soldering;

• organic mercury produced in chemical industry: aryls (eg. phenylmercury acetate - PMA), alkyls (eg. methyl/ethyl mercury) and alkoxyalkyls;

• inorganic mercury mainly used for medical purposes eg. antiseptics and in pesticides and as catalysts/alkylating agents.

Physical and chemical properties:

• only metal that is a liquid at room temperature mercury vapour (high vapour pressure);

• when heated → mercuric oxide (HgO);

• HgO and other mercuric salts eg. mercuric chloride, mercuric acetate are water soluble.

Metabolism:

a) Absorption:

• metallic mercury: mainly by inhalation (80%), but also via skin;
• inorganic mercuric salts are readily absorbed by inhalation (as aerosols) and ingestion;
• organic mercury: inhalation, ingestion and dermal contact.

b) Distribution:

• mercury vapour is rapidly absorbed by alveoli and redistributed via RBCs and plasma to rest of body (t_½ in blood = 2-3 days) and accumulates in kidneys and brain;
• inorganic mercury compounds are rapidly redistributed via RBCs and plasma to rest of body (t_½ in blood = 2-3 days) and accumulates in kidneys;
• organic mercury compounds are rapidly redistributed mainly via RBCs (90%) to rest of body (t_½ in blood = 2-3 days).

c) Excretion:

• renal (and biliary) route is the major means of elimination;
• the t_½ for excretion from the body is 60 days and from the brain is many years.

Health effects:

• toxic effects are due to oxidation of metallic Hg to mercuric ion (Hg²⁺) which results in precipitating protein and inhibiting sulfhydryl groups;
• preferential CNS toxicity of metallic Hg is due to initial uptake by brain prior to it being metabolised, whereas mercuric salts do not cross the blood brain barrier;
• mercurous (Hg⁺) compounds are more toxic than mercuric compounds;
• inhibition of enzymes by Hg are reversible upon removal from mercury exposure (forms the basis for chelation therapy).

a) Acute effects:

• inhalation of high concentrations of vapour or dust resulting in acute interstitial pneumonitis, bronchitis and bronchiolitis, metallic taste in mouth, GIT symptoms, coma, death;
• ingestion of corrosive mercury salts are due to inflammation of the bowel presenting with abdominal pain, diarrhoea and bleeding which may lead to kidney failure, coma, fits and death.

b) Subacute and chronic effects:

1. Classical syndrome: inflammation of the mouth; muscle tremors and psychic irritability.

• mouth inflammation: gingivitis, loosening of teeth, salivary gland swelling, excess salivation, stomatitis, blue-grey line along gum margins (individuals with poor oral hygiene);

• muscle tremors: initially affects the eyelids, tongue, fingers ® difficulty in writing (jerky appearance); progress to arms and legs ® difficulty in walking; absent during sleep (similar to Parkinson’s disease); disappears on removal from exposure;

• psychic irritability (erethism): workers become timid and anxious, lose self confidence, easily embarrassed, fearful of criticism and job loss, irritable, anger outbursts, insomnia, nightmares and excessive drowsiness (during waking hours).

2. Peripheral Nerves:

• peripheral sensory neuropathy of distal extremities, around tongue and lips;
• symptoms: paresthesia and hypothesia.

3. Skin:

a) Eczematous dermatitis:

• red, itchy and painful swelling of the skin;
• usually irritant in nature;
• commonly associated with organic mercurials (mercury fulminate) than inorganic compounds.

b) Skin ulcers:

• may result from penetration of skin lesions.

4. Kidney:

• not well characterised;
• proteinuria;
• nephrosis, anuria and renal failure after ingestion of mercury bichloride (HgCl₂).

5. Enzymes:

• elevated lactate dehydrogenase (LDH): indicative of renal and liver dysfunction.

Risk Management:

a) Limiting exposure:

• engineering controls;
• administrative controls;
• personal protective equipment;
• personal hygiene;
• education and training.

b) Industrial hygiene monitoring:

The occupational exposure limit (OEL) according to the Regulations for Hazardous Chemical Substances (HCS):

• Mercury alkyls: (also skin absorption)
      TWA - 0.01 mg/m³ (recommended limit)
      TWA - 0.03 mg/m³ (STEL);

• Mercury and compounds: (except alkyls)
      TWA - 0.05 mg/m³ (recommended limit)
      TWA - 0.15 mg/m³ (STEL).

ACGIH:

• Mercury alkyls:
      TWA - 0.01 mg/m³     TWA - 0.03 mg/m³ (STEL).

• Mercury aryls:
      TWA - 0.1 mg/m³ (recommended limit).

• Inorganic and metallic mercury:
      TWA - 0.025 mg/m³.

c) Biological monitoring:

• blood mercury is a useful indicator of exposure and correlates better with exposure than urine mercury; levels reflect methyl mercury as well as inorganic and organic forms and is therefore affected by dietary fish intake; airborne inorganic mercury of 50 µg/m³ corresponds to 3-3.5 µg/100 ml; proteinuria associated with levels > 3 µg/100ml; persons with no occupational exposures have levels <2 µg/100ml; for alkyl mercury clinical signs of intoxication occur >20 µg/100ml;

• urine mercury is a good indicator of recent exposure to inorganic Hg and aryl/alkyl Hg compounds (not methyl mercury); clinical signs of poisoning usually occur with urine levels >300 µg/g creatinine; persons with no occupational exposures have urine levels <5 µg/g creatinine; dietary fish intake (methyl mercury) does not appreciably influence levels;

• hair determination not useful in industry since there is no way to differentiate between adsorbed and endogenous mercury;

• biological exposure indices (BEI) for total inorganic mercury according to the Regulations for Hazardous Chemical Substances (HCS) and ACGIH:

  • preshift urine levels not exceeding 35 µg/g creatinine (includes background levels);
  • end of shift end of workweek blood levels not exceeding 15 µg/L (includes background levels).

d) Medical surveillance:

• Urine examination : ? proteinuria eg. N acetyl-B-D-glucosaminidase (NAG).
• Neurobehavioral tests.
• Nerve conduction tests.

e) Treatment:

• Dimercaprol (IM) is treatment of choice in acute poisoning.
• D-penicillamine is treatment of choice for chronic poisoning.
• in acute poisoning: effect diuresis during chelation treatment to protect kidney from high concentrations.
• haemodialysis may be necessary in extreme cases.

f) Compensation:

Any disease or pathological manifestation due to mercury is compensable under COIDA as it is listed as one of the substances in schedule 3 of the Act.

g) Notify the case to the Chief Inspector in DOL:

• medical practitioners are required by the OHSA to notify all cases of suspected occupational disease to the Chief Inspector, Department of Labour .
• form WCl 22 (First Medical Report in respect of an Occupational Disease).

Postgraduate Diploma in Occupational Health (DOH) - Modules 3: Occupational Medicine & Toxicology (Basic) by Profs Mohamed Jeebhay and Rodney Ehrlich, Health Sciences UCT is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 2.5 South Africa License. Major contributors: Mohamed Jeebhay, Rodney Ehrlich, Jonny Myers, Leslie London, Sophie Kisting, Rajen Naidoo, Saloshni Naidoo. Source available from here. For any updates to the material, or more permissions beyond the scope of this license, please email healthoer@uct.ac.za or visit www.healthedu.uct.ac.za. Last updated Jan 2007.
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