- Email: [email protected]
Mercury
Poisonous substances
Mercury
Elemental mercury may occasionally be injected intravascularly. This may lead to mercury embolism and systemic features of mercury poisoning. Soft tissue deposits of metallic mercury initiate a ‘foreign-body’ granulomatous reaction.
Sally Bradberry
Inorganic mercury salts Inorganic mercuric salts such as mercuric chloride cause an irritant gastroenteritis with corrosive ulceration, bloody diarrhoea, and abdominal cramps which may lead to circulatory collapse and shock. Renal tubular damage predominates in those who survive this initial phase.3 Mercurous compounds are less soluble, less corrosive, and less toxic than mercuric salts. Ingestion of mercurous chloride in teething powder has led to ‘pink disease’ or acrodynia in infants. This is characterized by a desquamating erythematous rash of the extremities, irritability, profuse sweating, tachycardia and hypertension. The characteristic neurological features of mercury poisoning may follow chronic exposure.
Abstract Mercury exists in three oxidation states, elemental, mercuric and mercurous and can form both organic and inorganic compounds. The central nervous system is the most susceptible target organ, though mercury is also a potent renal toxin. Chelation therapy with DMPS can enhance mercury elimination and there are case reports demonstrating that chelation therapy can reverse mercury-induced neurological damage.
Organic mercury salts
Keywords dimercaptopropane-1-sulfonate; DMPS; elemental; mercuric;
Methylmercury compounds have been used as fungicides, and poisoning has usually followed ingestion of contaminated foods.4 The characteristic neurological features of mercury poisoning typically occur after a latent period of several weeks.
mercurous; vapour
Mercury is the only metal that is liquid at room temperature. It exists in three oxidation states, (elemental/metallic Hg0, mercurous Hg22+ and mercuric Hg2+) and can form inorganic (e.g. mercuric chloride) and organic (e.g. methylmercury) compounds.
Management Urine mercury excretion is the most appropriate way to assess medium- to long-term mercury exposures while blood mercury concentrations are more appropriate to assess acute exposures. Although there are no controlled clinical data to show that chelation therapy improves outcome in patients with neurological features of mercury poisoning, dimercaptopropane-1-sulfonate (DMPS; 30 mg/kg/day orally) increases urinary mercury elimination and reduces blood mercury concentrations. Case reports suggest benefit.5 Where extracorporeal renal support is required for the management of renal failure, there is some evidence that continuous veno-venous haemofiltration is more effective than haemodialysis at removing DMPS-mercury complexes.3 ◆
Features Mercury is primarily a CNS toxin. The clinical presentation of mercury poisoning is influenced by the chemical form, the amount involved, the route of exposure, and whether the exposure was a single acute episode or repeated.
Metallic/elemental mercury Elemental mercury vapour is the most important form toxicologically because it is absorbed rapidly following inhalation and can cross the blood–brain barrier before oxidation to Hg2+, which accumulates in the brain. Acute mercury vapour inhalation causes headache, conjunctivitis, cough, nausea and vomiting, a metallic taste, dyspnoea and chest pain. Chemical pneumonitis may ensue and, in severe cases, renal and/or liver failure may occur.1 Repeated exposure to low mercury vapour concentrations presents typically with characteristic neurological features including fine tremor, lethargy, memory loss, insomnia, personality changes and ataxia. Other features include stomatitis, gingivitis, hypersalivation and renal tubular damage. Mixed motor and sensory peripheral neuropathy may develop.1 Ingestion of metallic mercury is not usually a significant toxicological hazard because less than 1% is absorbed, though mercury may become sequestered in the appendix.2
References 1 Clarkson TW, Magos L. The toxicology of mercury and its chemical compounds. Crit Rev Toxicol 2006; 36: 609–62. 2 McKinney P. Elemental mercury in the appendix: an unusual complication of a Mexican-American folk remedy. J Toxicol Clin Toxicol 1999; 37: 103–7. 3 Pai P, Thomas S, Hoenich N, et al. Treatment of a case of severe mercuric salt overdose with DMPS (dimercapto-1-propane sulphonate) and continuous haemofiltration. Nephrol Dial Transplant 2000; 15: 1889–90. 4 Hachiya N. The history and the present of Minamata disease entering the second half a century. Jpn Med Assoc J 2006; 49: 112–18. 5 Campbell JR, Clarkson TW, Omar MD. The therapeutic use of 2,3dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning. JAMA 1986; 256: 3127–30.
Sally Bradberry BSc MRCP is Assistant Director of the National Poisons Information Service (Birmingham Unit) and West Midlands Poisons Unit at City Hospital, Birmingham, UK. Competing interests: none declared.
MEDICINE 35:12
632
© 2007 Published by Elsevier Ltd.
Mercury
Elemental mercury may occasionally be injected intravascularly. This may lead to mercury embolism and systemic features of mercury poisoning. Soft tissue deposits of metallic mercury initiate a ‘foreign-body’ granulomatous reaction.
Sally Bradberry
Inorganic mercury salts Inorganic mercuric salts such as mercuric chloride cause an irritant gastroenteritis with corrosive ulceration, bloody diarrhoea, and abdominal cramps which may lead to circulatory collapse and shock. Renal tubular damage predominates in those who survive this initial phase.3 Mercurous compounds are less soluble, less corrosive, and less toxic than mercuric salts. Ingestion of mercurous chloride in teething powder has led to ‘pink disease’ or acrodynia in infants. This is characterized by a desquamating erythematous rash of the extremities, irritability, profuse sweating, tachycardia and hypertension. The characteristic neurological features of mercury poisoning may follow chronic exposure.
Abstract Mercury exists in three oxidation states, elemental, mercuric and mercurous and can form both organic and inorganic compounds. The central nervous system is the most susceptible target organ, though mercury is also a potent renal toxin. Chelation therapy with DMPS can enhance mercury elimination and there are case reports demonstrating that chelation therapy can reverse mercury-induced neurological damage.
Organic mercury salts
Keywords dimercaptopropane-1-sulfonate; DMPS; elemental; mercuric;
Methylmercury compounds have been used as fungicides, and poisoning has usually followed ingestion of contaminated foods.4 The characteristic neurological features of mercury poisoning typically occur after a latent period of several weeks.
mercurous; vapour
Mercury is the only metal that is liquid at room temperature. It exists in three oxidation states, (elemental/metallic Hg0, mercurous Hg22+ and mercuric Hg2+) and can form inorganic (e.g. mercuric chloride) and organic (e.g. methylmercury) compounds.
Management Urine mercury excretion is the most appropriate way to assess medium- to long-term mercury exposures while blood mercury concentrations are more appropriate to assess acute exposures. Although there are no controlled clinical data to show that chelation therapy improves outcome in patients with neurological features of mercury poisoning, dimercaptopropane-1-sulfonate (DMPS; 30 mg/kg/day orally) increases urinary mercury elimination and reduces blood mercury concentrations. Case reports suggest benefit.5 Where extracorporeal renal support is required for the management of renal failure, there is some evidence that continuous veno-venous haemofiltration is more effective than haemodialysis at removing DMPS-mercury complexes.3 ◆
Features Mercury is primarily a CNS toxin. The clinical presentation of mercury poisoning is influenced by the chemical form, the amount involved, the route of exposure, and whether the exposure was a single acute episode or repeated.
Metallic/elemental mercury Elemental mercury vapour is the most important form toxicologically because it is absorbed rapidly following inhalation and can cross the blood–brain barrier before oxidation to Hg2+, which accumulates in the brain. Acute mercury vapour inhalation causes headache, conjunctivitis, cough, nausea and vomiting, a metallic taste, dyspnoea and chest pain. Chemical pneumonitis may ensue and, in severe cases, renal and/or liver failure may occur.1 Repeated exposure to low mercury vapour concentrations presents typically with characteristic neurological features including fine tremor, lethargy, memory loss, insomnia, personality changes and ataxia. Other features include stomatitis, gingivitis, hypersalivation and renal tubular damage. Mixed motor and sensory peripheral neuropathy may develop.1 Ingestion of metallic mercury is not usually a significant toxicological hazard because less than 1% is absorbed, though mercury may become sequestered in the appendix.2
References 1 Clarkson TW, Magos L. The toxicology of mercury and its chemical compounds. Crit Rev Toxicol 2006; 36: 609–62. 2 McKinney P. Elemental mercury in the appendix: an unusual complication of a Mexican-American folk remedy. J Toxicol Clin Toxicol 1999; 37: 103–7. 3 Pai P, Thomas S, Hoenich N, et al. Treatment of a case of severe mercuric salt overdose with DMPS (dimercapto-1-propane sulphonate) and continuous haemofiltration. Nephrol Dial Transplant 2000; 15: 1889–90. 4 Hachiya N. The history and the present of Minamata disease entering the second half a century. Jpn Med Assoc J 2006; 49: 112–18. 5 Campbell JR, Clarkson TW, Omar MD. The therapeutic use of 2,3dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning. JAMA 1986; 256: 3127–30.
Sally Bradberry BSc MRCP is Assistant Director of the National Poisons Information Service (Birmingham Unit) and West Midlands Poisons Unit at City Hospital, Birmingham, UK. Competing interests: none declared.
MEDICINE 35:12
632
© 2007 Published by Elsevier Ltd.