There are three forms of mercury, ie, elemental (or metallic) mercury, inorganic mercury (mercuric salts) , and organic mercury compounds (eg methy mercury).
Elemental mercury is a shiny, silver-white metal, historically referred to as quicksilver, and is liquid at room temperature.
It can be found in older thermometers, barometers, fluorescent light bulbs among other industrial products.
How do people get exposed?
Elemental mercury has a high vapour pressure, and at room temperature (or when heated) vapourizes a dense, odorless irritant gas.
As a result of high volatility, the route of poisoning is predominantly pulmonary.
People often get exposed to toxic mercury vapours when metallic mercury is spilled, or when products that contain mercury break (eg fluorescent lamps).
Another way people get exposed to metallic mercury is in the artisanal gold mining.
Liquid mercury forms a stable amalgam with gold; thus mercury is used to extract pure gold from ores. Miners get exposed when they inhale mercury during the heating process required to remove mercury from the amalgam.
Metallic mercury widely used in amalgam dental filling may also cause elemental mercury exposure to patients, dental practitioners, or both.
Skin and gastrointestinal tract is a minor route of elemental mercury intoxication. However, skin or mucus membranes that are not intact may cause significant absorption of the metal.
How does mercury cause toxicity?
After oxidation in the brain, elemental mercury is bound to sulfhydryl groups and selenoproteins in the process irreversibly inhibit selenoenzymes such as example glutathione peroxidases, and thioredoxin reductases that are involved in combating oxidative stress.
The inhibition of selenoenzymes leads to oxidative stress particularly in organs that experience high oxygen demands including the brain. Such organs are most affected by mercury poisoning.
Symptoms of acute (within 24 hrs) mercury poisoning
Respiratory symptoms are the predominant symptoms, and include cough, inflammation of the lungs (chemical pneumonitis), difficulty breathing or shortness of breath (dyspnea), and chest pain. Respiratory effects may worsen leading to increased fibrous tissue in the lung (pulmonary fibrosis), fluid accumulation in the lungs (pulmonary edema), respiratory failure, and death by hypoxia.
The CNS effects are also common (elemental mercury easily crosses the blood-brain barrier) and they include and headache, muscular pain and weakness as well as disturbances of vision.
Gastrointestinal effects of elemental mercury include metallic taste, salivation, nausea, vomiting, diarrhoea, difficulty swallowing (dysphagia), abdominal cramps, and diarrhea.
Subcutaneous or intramuscular injection of a solution containing metallic mercury may cause local abscess and granuloma formations.
In contrast, Intravenous injection of mercury causes acute pulmonary embolism and respiratory failure.
Acute toxicity of elemental mercury has also been associated kidney injury, rapid heart rate (tachycardia), and high blood pressure (hypertension).
Symptoms of chronic or repeated exposure
With chronic exposure to mercury vapor, the notable target organs of toxicity are the central nervous system and the kidneys.
Thus, the classic toxic effects of long term mercury exposure are neuropsychiatric effects, loss of kidney function, and inflammation of the upper airway.
Neuropsychiatric effects include tremor, anxiety, frequently changing emotions (emotional lability), forgetfulness, insomnia, loss of appetite (anorexia), fatigue, and disturbances of thought and movement.
Proteinuria is the most common sign of the kidney injury due to tubular damage, and nephrotic syndrome can also occur in severe cases.
Gingivitis, stomatitis, and excessive salivation are also associated with prolonged occupational exposure.
Perform xray of sites of exposure eg an abdominal xray post ingestion show scattered radiopaque material throughout the small bowel, large bowel, and the lung
A blood mercury is a useful biomarker after short-term and high-level exposure.
On the hand, urine mercury is ideal for long-term exposure, and also as a good indicator of body burden.
Treatment of mercury toxication
Treatment is based on the patient’s symptoms, blood and urine mercury concentrations.
In case of a spillage, remove clothing, and wash the skin with copious amounts of water.
Manage hypertension with appropriate antihypertensives as per available treatment protocols.
Use thiol based chelators If the patient is symptomatic; systemic absorption is anticipated; increased blood or urinary mercury levels are present.
The chelator DMSA, also called succimer (orally active) has few side effects and is the chelator of choice in cases of chronic or mild toxicity.
Dimercaprol (British anti-Lewisite) is preferred in the presence of severe kidney dysfunction.
Since mercury binds to the body’s ubiquitous cellular sulfhydryl groups, chelating agents should be given early in the treatment.
In the presence of radiopague materials in the gastrointestinal tract, whole bowel irrigation with polyethylene glycol is indicated to enhance fecal expulsion of the poorly absorbable mercury.
Provide N-acetyl cystein (NAC) and glutathione. NAC, is serve as a donor pool of cysteine for rapid formation of antioxidant selenoproteins and glutathione, the major antioxidant in the body.
Glutathione is also involved in the excretion of mercury by binding mercury in the final transport process. In chronic mercury exposure, more and more glutathione is lost, resulting in their depletion.
If glutathione isn’t replaced, glutathione deficiency occurs and the body is less able to remove mercury and deal with harmful free radicals.
Selenium and zinc have been shown to exert a protective effect against free radical and oxidants likely by induction of metal binding proteins, such as metallothionein and selenoprotein. Chronic mercury toxicity ultimately causes zinc and selenium deficiency.
Selenium supplementation has been shown to reduce oxidative stress than chelators in animal experiments.
Surgery may be used to remove radiopague mercury lodged in the gastrointestinal tract and other anatomic sites.
The ability of regular hemodialysis to filter out mercury is limited because of mercury’s mode of distribution among erythrocytes and plasma. However, hemodialysis with L-cysteine compound as a chelator has been successful.
Because mercury-chelating agent complexes are large molecules, they may fail to be filtered out by standard hemodialysis membranes; exchange transfusion may need to be attempted.
Alpha lipoic acid (ALA) is a powerful antioxidant and a mercury chelator that is also lost when removing mercury. Supplementing it is an essential component of a mercury detoxification program.
Vitamin C (ascorbic acid) is also a powerful antioxidant believed to enhance the body’s ability to remove mercury from the blood. Consider supplementing in chronic mercury exposure.
Of significance is that a patient having suspected occupational exposure to mercury is responding well to NAC treatment and mineral supplements. DMSA could not be found locally.