💊 Chemical information

Hydrarg.; Hydrargyrum; Hydrargyrum Depuratum; Mercure; Mercurio; Quecksilber; Quicksilver; Rtęć. Hg = 200.59.
CAS — 7439-97-6.
ATC — D08AK05.


Mercury is a shining, silvery white, very mobile liquid, easily divisible into globules, which readily volatilises on heating.

💊 Adverse Effects

Poisoning with liquid mercury or inorganic mercury salts has arisen from sources such as batteries, cosmetics, dental materials, medical equipment, and jewellery manufacture. Barometers, sphygmomanometers, and thermometers are still sources of liquid mercury. Trace amounts of organic and inorganic mercury may also be ingested in the diet. The effects of acute exposure depend on the nature of the compound.
Elemental (liquid) mercury if ingested is poorly absorbed and, unless there is aspiration or pre-existing gastrointestinal disorders, is not considered to be a severe toxicological hazard. The greatest dangers from elemental mercury arise from the inhalation of mercury vapour, which can cause gastrointestinal effects including nausea, vomiting, and diarrhoea; more importantly it is toxic to the respiratory system and this effect can be fatal. Some CNS involvement has also been reported. Adverse effects have also been reported after accidental or intentional parenteral dosage.
Inorganic salts such as mercuric chloride are corrosive when ingested causing severe nausea, vomiting, pain, bloody diarrhoea, and necrosis. The kidney is also involved and tubular necrosis may develop. Mercurous salts are considered to be less hazardous, but the mercurous form can be converted to the mercuric.
Organic mercurial compounds produce similar toxic effects to inorganic compounds, but they have a more selective action on the CNS that has proved difficult to treat. The degree of toxicity varies; those used as preservatives or disinfectants are less toxic than the ethyl or methyl compounds that are not used pharmaceutically or clinically. Methylmercury is notorious for its toxicity; there have been cases of fetal neurotoxicity during outbreaks of methylmercury poisoning. Chronic mercury poisoning may result from inhalation of mercury vapour, skin contact with mercury or mercury compounds, or ingestion of mercury salts over prolonged periods. It is characterised by many symptoms including tremor, motor and sensory disturbances, mental deterioration, gastrointestinal symptoms, dermatitis, kidney damage, salivation, and gingivitis. A blue line may be present on the gums. There is little difference between acute and chronic poisoning with organic mercurials. The syndrome of acrodynia (pink disease), with symptoms of sweat, rash, erythema of the extremities, photophobia, wasting, weakness, hypertension, tachycardia, and diminished reflexes, occurred in children given mercury in teething powders or in ointments or dusting powders. Such preparations have long since been withdrawn from use. However, the syndrome is still a feature of mercury poisoning from other sources. Hypersensitivity to mercury and mercurial compounds has been reported. Mercurialentis has been reported in patients treated with eye drops containing an organomercurial preservative.

Chronic exposure.

Acute occupational exposure to mercury vapour in 53 men resulted in an initial phase described as metal fume fever, an intermediate phase of severe symptoms with CNS, gastrointestinal, respiratory, and urological involvement, and a late phase with persistent CNS symptoms, dysuria, and pain on ejaculation.1,2 Although persistent hyperchloraemia was noted in the 11 patients with the highest mercury levels, renal impairment tended to be temporary.2 Long-term follow-up of a patient who had an intravenous injection of mercury 12 years previously also revealed no persistent renal impairment,3 despite the presence of mercury microemboli in lungs, kidneys, liver, and subcutaneous tissues and high concentrations in the urine. At this time, the patient had residual reductions in respiratory function, polyneuropathy, and marked asthenozoospermia. Spermatozoal abnormalities may also have contributed to his wife’s miscarriage. Mercury deposits mimicking gallbladder cancer were found in the gallbladder of a patient 35 years after he had injected himself with elemental mercury.4 Fetal neurotoxicity after maternal exposure to methylmercury is well recognised, and there has been widespread concern about the effect of maternal diets on the developing fetus because of mercury concentrations in freshwater and marine organisms. Results from a study in the Faroe Islands showed an association between delays in neurological development in children and maternal consumption of pilot whale meat.5 Follow-up studies of this population when they reached 14 years of age suggest that the neurotoxic effects of methylmercury might compromise brain development into the teenage years,6 as well as affecting autonomic regulation of heart function.7 However, data from a study conducted in a fish-consuming population in the Seychelles failed to find a similar connection.8 There has been considerable concern over the systemic absorption of mercury from dental amalgam, which typically contains between 40 and 70% of mercury. However, the quantity absorbed from amalgam fillings is reported to be relatively small9,10 and current evidence suggests that the use of dental amalgam for tooth restoration is both safe and effective.11-14 The main risks appear to be occupational exposure of dental staff and environmental pollution. Some patients with hypersensitivity to mercury (manifest most commonly as local lichenoid reactions) may benefit from removal of amalgam fillings.15-17 Ethylmercury is contained in thiomersal, which is used as a preservative in some vaccines for infants and children, thus representing a potential source of mercury exposure. The safety of these vaccines has been a matter of considerable debate worldwide for many years although it is now usually accepted that there is no evidence of neurotoxicity. However, some countries have phased out vaccines containing thiomersal in favour of alternative preservatives. The symptoms of acrodynia have been mistaken for those of phaeochromocytoma.18-21
1. Bluhm RE, et al. Elemental mercury vapour toxicity, treatment, and prognosis after acute, intensive exposure in chloralkali plant workers part I: history, neuropsychological findings and chelator effects. Hum Exp Toxicol 1992; 11: 201–10
2. Bluhm RE, et al. Elemental mercury vapour toxicity, treatment, and prognosis after acute, intensive exposure in chloralkali plant workers part II: hyperchloraemia and genitourinary symptoms. Hum Exp Toxicol 1992; 11: 211–15
3. dell’Omo M, et al. Long-term toxicity of intravenous mercury injection. Lancet 1996; 348: 64
4. Zippel D, et al. Quicksilver cholecystitis. Ann Intern Med 2006; 144: 941
5. Grandjean P, et al. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol 1997; 19: 417–28
6. Murata K, et al. Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury. J Pediatr 2004; 144: 177–83
7. Grandjean P, et al. Cardiac autonomic activity in methylmercury neurotoxicity: 14-year follow-up of a Faroese birth cohort. J Pediatr 2004; 144: 169–76
8. Myers GJ, et al. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Lancet 2003; 361: 1686–92
9. Eley BM. The future of dental amalgam: a review of the literature. Part 3: mercury exposure from amalgam restorations in dental patients. Br Dent J 1997; 182: 333–8
10. Eley BM. The future of dental amalgam: a review of the literature. Part 4: mercury exposure hazards and risk assessment. Br Dent J 1997; 182: 373–81
11. FDI/WHO. Consensus statement on dental amalgam. FDI World 1995; 4 (July/Aug): 9–10
12. Eley BM. The future of dental amalgam: a review of the literature. Part 6: possible harmful effects of mercury from dental amalgam. Br Dent J 1997; 182: 455–9
13. Bellinger DC, et al. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. JAMA 2006; 295: 1775–83
14. DeRouen TA, et al. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. JAMA 2006; 295: 1784–92
15. Ibbotson SH, et al. The relevance and effect of amalgam replacement in subjects with oral lichenoid reactions. Br J Dermatol 1996; 134: 420–3
16. McGivern B, et al. Delayed and immediate hypersensitivity reactions associated with the use of amalgam. Br Dent J 2000; 188: 73–6
17. Laeijendecker R, et al. Oral lichen planus and allergy to dental amalgam restorations. Arch Dermatol 2004; 140: 1434–8
18. Henningsson C, et al. Acute mercury poisoning (acrodynia) mimicking pheochromocytoma in an adolescent. J Pediatr 1993; 122: 252–3
19. Velzeboer SCJM, et al. A hypertensive toddler. Lancet 1997; 349: 1810
20. Wößmann W, et al. Mercury intoxication presenting with hypertension and tachycardia. Arch Dis Child 1999; 80: 556–7
21. Torres AD, et al. Mercury intoxication and arterial hypertension: report of two patients and review of the literature. Abstract: Pediatrics 2000; 105: 627. Full version: (accessed 14/07/06)

Effects on the kidneys.

The kidneys are one of the primary sites for the accumulation of mercury in the body. All forms of mercury (liquid mercury, inorganic mercury, and organic mercury) may be toxic to the kidney although the inorganic forms are the most nephrotoxic.1
1. Zalups RK. Molecular interactions with mercury in the kidney. Pharmacol Rev 2000; 52: 113–43.


Systemic contact dermatitis in a patient apparently sensitised by red, mercury-based tattoo pigments, developed when he ate raw swordfish and alfonsino, both renowned for high mercury levels.1
1. Tsuruta D, et al. A red tattoo and a swordfish supper. Lancet 2004; 364: 730.

💊 Treatment of Adverse Effects

The treatment of acute mercury toxicity depends on the form of mercury, the route of exposure, and the dose. Supportive measures may be needed with all types of toxicity. Ingestion of elemental mercury seldom requires active treatment since it is poorly absorbed by this route, although inhalation or aspiration of elemental mercury vapour is a potentially serious problem. Poisoning due to organic mercury is difficult to treat and supportive measures are the mainstay of treatment. Acute exposure to mercury by injection requires mainly supportive therapy, although excision of the affected area has been recommended after subcutaneous or intramuscular injection. Mercurials on the skin should be removed by copious washing with soap and water; for contamination in the eye, irrigation with water at room-temperature for at least 15 minutes should be performed. Acute oral poisoning due to inorganic mercury salts should be treated if appropriate by activated charcoal or gastric lavage to reduce absorption if within 1 hour of ingestion of a potentially life-threatening dose. Decontamination is not usually necessary after ingestion of small amounts such as elemental mercury from a thermometer. Some inorganic mercury compounds may be corrosive to the gastrointestinal tract when ingested, which can make gastrointestinal decontamination problematic; induction of emesis is not recommended. Gastric decontamination may be tried for organic mercury compounds, although the benefits are uncertain. In severe cases of toxicity with all forms of mercury poisoning, chelation therapy may be required to facilitate the removal of mercury from the body. Unithiol is the chelating agent of choice in the UK and should be considered in symptomatic patients with a blood-mercury concentration of 100 micrograms/litre, and in asymptomatic patients with a blood-mercury concentration of 200 micrograms/litre. Other chelating agents that may be used are succimer, dimercaprol, and penicillamine. The treatment of choice may vary in other countries depending on local policies and availability of the above chelating agents. Penicillamine may be associated with more adverse effects than other chelating agents and should be reserved for use when others are unavailable or not tolerated. Dimercaprol should be avoided in poisoning with metallic mercury or methylmercury because it may exacerbate neurological effects through redistribution of mercury to the brain from other sites. Some centres start haemodialysis early in the course of treatment; others wait until renal failure develops. Giving a thiol resin complex to prevent the reabsorption of mercury from the bile has also been tried. The management of chronic toxicity is generally symptomatic although chelation therapy has been used in some patients if the blood-mercury concentration is raised or the patient is symptomatic.
1. Kostyniak PJ, et al. Extracorporeal regional complexing haemodialysis treatment of acute inorganic mercury intoxication. Hum Exp Toxicol 1990; 9: 137–41
2. Ferguson L, Cantilena LR. Enhanced mercury clearance during hemodialysis with chelating agents. Clin Pharmacol Ther 1991; 49: 131
3. Florentine MJ, Sanfilippo DJ. Elemental mercury poisoning. Clin Pharm 1991; 10: 213–21
4. Bluhm RE, et al. Elemental mercury vapour toxicity, treatment, and prognosis after acute, intensive exposure in chloralkali plant workers part I: history, neuropsychological findings and chelator effects. Hum Exp Toxicol 1992; 11: 201–10
5. Toet AE, et al. Mercury kinetics in a case of severe mercuric chloride poisoning treated with dimercapto-1-propane sulphonate (DMPS). Hum Exp Toxicol 1994; 13: 11–16
6. Houeto P, et al. Elemental mercury vapour toxicity: treatment and levels in plasma and urine. Hum Exp Toxicol 1994; 13: 848–52
7. Aaseth J, et al. Treatment of mercury and lead poisonings with dimercaptosuccinic acid and sodium dimercaptopropanesulfonate: a review. Analyst 1995; 120: 853–4
8. Isik S, et al. Subcutaneous metallic mercury injection: early, massive excision. Ann Plast Surg 1997; 38: 645–8
9. Baum CR. Treatment of mercury intoxication. Curr Opin Pediatr 1999; 11: 265–8
10. Satar S, et al. Intoxication with 100 grams of mercury: a case report and importance of supportive therapy. Eur J Emerg Med 2001; 8: 245–8
11. Risher JF, Amler SN. Mercury exposure: evaluation and intervention — the inappropriate use of chelating agents in the diagnosis and treatment of putative mercury poisoning. Neurotoxicology 2005; 26: 691–9.

💊 Pharmacokinetics

There is little absorption of elemental mercury from globules in the gastrointestinal tract. The main hazard of elemental mercury is from absorption after inhalation of mercury vapour; this mercury is widely distributed before being oxidised to the mercuric form. Concentrations can be detected in the brain. Soluble inorganic mercuric salts are absorbed from the gastrointestinal tract and can also be absorbed through the skin. The mercury is distributed throughout the soft tissues with high concentrations in the kidneys; it is mainly excreted in the urine and faeces with an elimination half-life of about 60 days, although it may take years to eliminate mercury from the brain; elimination from other tissues can take several months. Organic alkyl mercury compounds are more readily absorbed from both the gastrointestinal and the respiratory tracts. They are widely distributed and can produce high concentrations in the brain. Alkyl mercury compounds are excreted in urine and in the faeces with extensive enterohepatic recycling. The biological half-life varies but is longer than that of inorganic mercury. Organic mercury, and to some extent inorganic mercury, diffuse across the placenta and are distributed into breast milk.

💊 Uses and Administration

The hazards associated with mercury generally outweigh any therapeutic benefit and its clinical use has largely been abandoned. The use of mercurial diuretics such as mersalyl has generally been superseded by other diuretics. Ointments containing mercurials, such as ammoniated mercury have also generally been replaced by less toxic preparations. Mercurials were formerly used as spermicides. Some ionisable inorganic mercury salts and certain organic compounds of mercury have been used as disinfectants, and some mercury salts are effective parasiticides and fungicides. Organic mercurials such as phenylmercuric acetate, borate, and nitrate are also used as preservatives. Mercury is a component of dental amalgams. Other mercury salts that have been used for their antibacterial activity include mercuric chloride, yellow mercuric oxide, and mercurous chloride (above).


Mercury and some mercury compounds have been used in homoeopathic medicines under the following names:
Mercury: Hydrargyrum metallicum; Mercurius vivus; Merc. viv.
Mercuric cyanide: Hydrargyrum bicyanatum; Mercurius cyanatus
Mercuric iodide: Mercurius iodatus flavus; Merc. i. f.
Red mercuric iodide: Hydrargyrum biiodatum; Mercurius bijodatus; Mercurius iodatus ruber; Merc. i. r.
Mercuric nitrate: Hydrargyrum nitricum oxydulatum; Mercurius nitricus oxydulatus; Mercurius nitricus; Merc. nit.
Red mercuric sulfide: Hydrargyrum sulfuratum rubrum; Cinnabaris; Cinbar.
Ammoniated mercuric nitrate: Mercurius solubilis; Mere. sol.
Potassium mercuric iodide: Mercurius et kali iodatus; Merc. ki.
See also Ammoniated Mercury, Mercuric Chloride (above), and Mercurous Chloride (above).

💊 Preparations

Proprietary Preparations

Arg.: Lagrimas de Santa Lucia†. Multi-ingredient: Austria: Coldophthal; Belg.: Ocal; Spain: Oftalmol Ocular.
Published May 08, 2019.