Pediatric Mercury Toxicity 

  • Author: David K Tan, MD, EMT-T, FAAEM; Chief Editor: Timothy E Corden, MD   more...
 
Updated: Jun 30, 2010
 

Background

Mercury has various forms and thousands of industrial uses; however, it is probably best known as the silver liquid in thermometers. Mercury is ubiquitous in nature, occurring as mercuric sulfide or cinnabar.

Mercury has 3 forms: (1) elemental mercury, (2) inorganic salts, and (3) organic compounds. Perhaps the most deadly form of mercury is methyl mercury. Only 2-10% of the ingested mercury is absorbed from the gut, and ingested elemental mercury is not absorbed at all; however, 90% of any methyl mercury ingested is absorbed into the bloodstream from the GI tract.

Organic mercury compounds, specifically methyl mercury, are concentrated in the food chain. Fish from contaminated waters are the most common culprits. Industrial mercury pollution is often in the inorganic form, but aquatic organisms and vegetation in waterways such as rivers, lakes, and bays convert it to deadly methyl mercury. Fish eat contaminated vegetation, and the mercury becomes biomagnified in the fish. Fish protein binds more than 90% of the consumed methyl mercury so tightly that even the most vigorous cooking methods (eg, deep-frying, boiling, baking, pan-frying) cannot remove it.

Methyl mercury poisoning, better known as Minamata disease, is one of the most devastating forms of mercury exposure. It is named for Minamata Bay, a body of water in Japan where, in the early 1950s, the fish contained high concentrations of methyl mercury from the polluted waste of a nearby industrial plant.[1] Local villagers ate the fish and began to exhibit signs of neurologic damage such as visual loss, extremity numbness, hearing loss, and ataxia. Babies exposed to the methyl mercury in utero were the most severely affected members of the village. Furthermore, because mercury was also discovered in the breast milk of the mothers, the babies' exposure continued after birth.

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Pathophysiology

Organic forms, specifically methyl mercury, are the most toxic of the 3 classes of mercurials. The GI tract absorbs more than 90% of the methyl mercury ingested, which then enters the bloodstream. Because mercury binds to the body's ubiquitous sulfhydryl groups, toxicity involves multiple organ systems. Structural proteins, membranes, and enzymes are all disrupted.

Methyl mercury exerts its most devastating effect on the CNS by causing psychiatric disturbances, ataxia, visual loss, hearing loss, and neuropathy. Methyl mercury is lipophilic and readily crosses the blood-brain and placentofetal barriers. Neurologic damage in the form of diffuse and widespread neuronal atrophy is most severe in patients exposed in utero.

Necrosis of the proximal tubules is a common direct renal toxic effect. Unexplained renal abnormalities with neuropsychiatric disturbances should prompt the physician to consider Minamata disease or other forms of mercury poisoning.

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Epidemiology

Frequency

United States

Mercury poisoning is episodic and usually involves the inhalation of elemental mercury vapor or an exposure to inorganic mercuric salts; methyl mercury intoxication has been reported in the United States.

International

Worldwide, outbreaks of methyl mercury intoxication are sporadic. Minamata Bay in Japan was involved in the first and most famous epidemic but not the largest. In the early 1970s, one of the most severe mass poisonings in history occurred in Iraq when nearly 95,000 tons of seed grains treated with a methyl mercury–based fungicide were accidentally baked into bread for human consumption.[2] More than 6000 individuals were hospitalized, and hundreds died. Many were hospitalized for weeks before methyl mercury intoxication was correctly diagnosed.

Mercury mining areas in China have also contributed to cases of methyl mercury poisoning through the ingestion of rice grown in contaminated soil.[3]

Mortality/Morbidity

Of the original 121 individuals from Minamata Bay who were affected, nearly one third died shortly after their initial presentation.

Subsequent investigations over the last 3 decades resulted in the identification of more than 2000 additional patients who were affected by chronic sequelae of Minamata disease.

Of the more than 6000 Iraqi patients, 459 died.[2]

Sex

Both sexes can be affected.

Age

Although Minamata disease can affect children of all ages, babies exposed in utero are most severely affected.

  • Autopsy evidence reveals that brain atrophy is significantly worse in children than in adults.
  • Exposure to mercury has been suggested to contribute to the development of autism in children.
    • Although the mechanism for this disorder has many hypotheses, no evidence has confirmed or disproved a causal relationship between mercury exposure and the development of autism. In fact, in one recent study, the discontinuation of thimerosal-containing vaccines in Denmark seemed to be followed by an increase in incidence of autism.[4]
    • Further studies are needed to elucidate a link, if any, between mercury exposure and autism development.
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Contributor Information and Disclosures
Author

David K Tan, MD, EMT-T, FAAEM  Assistant Professor and Chief, EMS Section, Division of Emergency Medicine, Medical Director, Washington University EMS, Washington University in St Louis School of Medicine

David K Tan, MD, EMT-T, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine and National Association of EMS Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Michael E Mullins, MD  Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine

Michael E Mullins, MD is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Emergency Physicians

Disclosure: Johnson & Johnson stock ownership None; Savient Pharmaceuticals stock ownership None

Specialty Editor Board

William T Zempsky, MD  Associate Director, Assistant Professor, Department of Pediatrics, Division of Pediatric Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center

William T Zempsky, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, eMedicine

Disclosure: Nothing to disclose.

Jeffrey R Tucker, MD  Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center

Disclosure: Merck Salary Employment

Daniel Rauch, MD, FAAP  Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

Timothy E Corden, MD  Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin

Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society

Disclosure: Nothing to disclose.

References
  1. Harada M. Minamata disease: methylmercury poisoning in Japan caused by environmental pollution. Crit Rev Toxicol. 1995;25(1):1-24. [Medline].

  2. Amin-zaki L, Majeed MA, Clarkson TW, Greenwood MR. Methylmercury poisoning in Iraqi children: clinical observations over two years. Br Med J. Mar 11 1978;1(6113):613-6. [Medline].

  3. Feng X, Li P, Qiu G, Wang S, Li G, Shang L, et al. Human exposure to methylmercury through rice intake in mercury mining areas, Guizhou province, China. Environ Sci Technol. Jan 1 2008;42(1):326-32. [Medline].

  4. Madsen KM, Lauritsen MB, Pedersen CB, et al. Thimerosal and the occurrence of autism: negative ecological evidence from Danish population-based data. Pediatrics. Sep 2003;112(3 Pt 1):604-6. [Medline]. [Full Text].

  5. Andersen AH. Experimental studies on the pharmacology of activated charcoal; III. Acta Pharmacol. 1948;4:275-84.

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  7. Davis LE, Kornfeld M, Mooney HS, et al. Methylmercury poisoning: long-term clinical, radiological, toxicological, and pathological studies of an affected family. Ann Neurol. Jun 1994;35(6):680-8. [Medline].

  8. Eisler R. Mercury hazards from gold mining to humans, plants, and animals. Rev Environ Contam Toxicol. 2004;181:139-98. [Medline].

  9. Grandjean P, Weihe P, White RF, Debes F. Cognitive performance of children prenatally exposed to "safe" levels of methylmercury. Environ Res. May 1998;77(2):165-72. [Medline].

  10. Isik S, Güler M, Oztürk S, Selmanpakoglu N. Subcutaneous metallic mercury injection: early, massive excision. Ann Plast Surg. Jun 1997;38(6):645-8. [Medline].

  11. Knobeloch LM, Ziarnik M, Anderson HA, Dodson VN. Imported seabass as a source of mercury exposure: a Wisconsin case study. Environ Health Perspect. Jun 1995;103(6):604-6. [Medline].

  12. Magos L. Three cases of methylmercury intoxication which eluded correct diagnosis. Arch Toxicol. Nov 1998;72(11):701-5. [Medline].

  13. Malm O. Gold mining as a source of mercury exposure in the Brazilian Amazon. Environ Res. May 1998;77(2):73-8. [Medline].

  14. Mayo Clinic Health Letter. Mercury in fish: concerns shouldn't dampen your appetite. 1996 Apr.

  15. Morgan JN, Berry MR, Graves RL. Effects of commonly used cooking practices on total mercury concentration in fish and their impact on exposure assessments. J Expo Anal Environ Epidemiol. Jan-Mar 1997;7(1):119-33. [Medline].

  16. Nuttall KL. Interpreting hair mercury levels in individual patients. Ann Clin Lab Sci. 2006;36(3):248-61. [Medline].

  17. Pierce PE, Thompson JF, Likosky WH, Nickey LN, Barthel WF, Hinman AR. Alkyl mercury poisoning in humans. Report of an outbreak. JAMA. Jun 12 1972;220(11):1439-42. [Medline].

  18. Sue, Young-Jin. Mercury. In: Goldfrank LR, Flomenbaum NE, Lewin NA, eds. Goldfrank's Toxicologic Emergencies. 1319-29.

  19. Uchino M, Tanaka Y, Ando Y, Yonehara T, Hara A, Mishima I, et al. Neurologic features of chronic minamata disease (organic mercury poisoning) and incidence of complications with aging. J Environ Sci Health B. Sep 1995;30(5):699-715. [Medline].

  20. Yotsuyanagi T, Yokoi K, Sawada Y. Facial injury by mercury from a broken thermometer. J Trauma. May 1996;40(5):847-9. [Medline].

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