Mercury
Mercury is found naturally in the environment in several forms. In its elemental form, mercury is a shiny, silver-white, liquid metal. It can be combined with other chemicals to form inorganic compounds. Mercury can evaporate to form colorless, odorless mercury vapors. Mercury can combine with organic substances to form organic compounds such as methyl mercury.
Use of mercury
Mercury is used as electrode in industrial production of chlorine, manufacture of fungicides, anti-fouling paints, laboratory apparatus, thermometers, detonators, dental amalgams and batteries.
Absorption, metabolism and excretion
Elementary mercury is absorbed after the inhalation of mercury vapour. Ingested elemental mercury is poorly absorbed from the gastrointestinal tract. Soluble mercurial salts and aryl mercury compounds are also absorbed after inhalation and to a limited extent after ingestion. Mercury compounds may also be absorbed through the skin.
Mercury inhibits the action of enzymes containing -SH groups. Inorganic mercury is distributed almost equally between the red blood cells and the plasma, but alkyl compounds are concentrated in the red cells. The mercury absorbed into the body is distributed to many tissues, primarily the CNS and the kidney. Both organic and elemental mercury compounds readily cross the blood-brain barrier and the placenta and are excreted in breast milk. Mercury compounds are eliminated gradually in the urine, faeces, saliva and sweat. The average half-life in human is about 60 days for inorganic mercury and around 70 days for organic mercury compounds.
Signs and symptoms of mercury poisoning
Acute poisoning commonly results from inhalation of elemental mercury vapor, or from deliberate or accidental ingestion of mercury or its salts. Owing to their corrosive nature, ingestion of mercury and its compounds can cause pain, inflammation and necrosis of the oropharyngeal mucosa, nausea, vomiting, abdominal pain, and renal damage with lesions of the proximal tubule and glomerulus. Severe cases may have acute papillary necrosis or chemical colitis with shock, edema, tremor, and ataxia. Chemical pneumonitis with cough, dyspnoea, retrosternal pain, basal late inspiratory crackles and patchy shadowing on CXR may follow copious inhalation. There may be pulmonary edema and blood stained sputum.
Chronic exposure to mercury salts can result in central nervous system toxicity, including personality changes, nervousness, irritability, fatigue, deterioration in memory, difficulty in concentration, insomnia, hearing loss, constriction of visual field, and a metallic taste. Tremors often have an intentional component which may impair fine and complex movements. Peripheral neuropathy (predominantly sensory) is more common in those with organic mercury poisoning. Gingivitis, stomatitis and excessive salivation may be early signs. The most common renal effect is tubular damage, with necrosis being more common in inorganic than organic poisoning. Glomerular damage may lead to albumunuria. Inorganic poisoning may occasionally result in nephrotic syndrome.
In children, mercury poisoning can result in the syndrome of acrodynia, which is characterized by severe leg cramps, irritability, paresthesia, excessive perspiration, pruritus, and painful redness and peeling of the palms of the hands and soles of the feet.
Laboratory diagnosis
Laboratory evaluation of mercury poisoning should include a complete blood count, serum electrolytes, liver and renal function tests, and urinalysis. Urine and blood mercury levels are used to detect exposure. For organic mercury, whole blood is the preferred medium since it is concentrated in the red blood cells. For inorganic mercury, blood is considered useful if samples are taken following recent exposure owing to its short half-life (2-4 days). In contrast, urinary mercury peaks approximately 2-3 weeks after exposure to inorganic mercury and decreases at a much slower rate with half-life of 40-60 days for short-term exposures and 90 days for long-term exposures. Therefore, urine is a more appropriate indicator for longer exposures than blood samples. Urinary mercury is normally less than 10 ug/l (50 nmol/l). Signs and symptoms of mercury poisoning may develop above 20 ug/l (100 nmol/l).
Treatment
Acute mercury poisoning by ingestion of mercuric salts can be treated by induced emesis or gastric lavage. Effective chelating agents for mercury include dimercaprol (e.g., 24 mg/kg per day in divided dose, given in 5-day courses separated by several days of rest) and N-acetyl penicillamine (e.g., 30mg/kg per day in divided doses). However, use of dimercaprol is contraindicated in acute poisoning with organic mercury compounds because this may enhance passage of mercury across the blood-brain barrier. Newer agents include DMPS and DMSA which have a lower side effect profile. DMSA is administered in doses of 10mg/kg 3 times daily for 5 days, then twice daily for another 14 days. Monitoring of clinical status and blood and urine mercury excretion is used to guide repeat dosing.
Therapy for chronic mercury poisoning depends on the severity of the symptoms, and whether evidence of neurologic or renal toxicity is present.