eMedicine Specialties > Neurology > Neurotoxicology

Mercury

Author: David A Olson, MD, Clinical Neurologist, Dekalb Neurology Associates, Decatur, Georgia
Contributor Information and Disclosures

Updated: Sep 21, 2009

Introduction

Background

At least some of the toxic effects of mercury have been well known since the 18th century. In 1889, Charcot's Clinical Lectures on Diseases of the Nervous System attributed some rapid oscillatory tremors to mercury exposure.1 In Wilson's classic textbook of neurology, published in 1940, Wilson concurred with Charcot's attribution of tremors to mercury poisoning. Wilson also identified mercury-induced cognitive impairments, such as inattention, excitement, and hallucinosis.2 In 1961, researchers in Japan correlated elevated urine mercury levels with the features of the previously mysterious Minamata disease. Before the etiology of Minamata disease was discovered, it plagued the residents around Minamata Bay in Japan with tremors, sensory loss, ataxia, and visual field constriction.3

Toxicity from mercury exposure occurs with both organic and inorganic forms. Minamata disease is an example of organic toxicity. In Minamata Bay, a factory discharged inorganic mercury into the water. The mercury was methylated by bacteria and subsequently ingested by fishes and then by humans.

Inorganic mercury toxicity occurs in several forms: metallic mercury (Hg), mercurous mercury (Hg1+), or mercuric mercury (Hg2+). Toxicity from inorganic mercury can result from direct contact through the skin or gastrointestinal tract or from inhalation of mercury vapors. Vaporous mercury diffuses through the alveoli, becomes ionized in the blood, and ultimately deposits in the CNS.

Pathophysiology

Organic methylmercury toxicity and inorganic mercury toxicity show different pathologic effects. Organic methylmercury toxicity causes prominent neuronal loss and gliosis in the calcarine and parietal cortices and cerebellar folia, as seen in cases of classic Minamata disease. Inorganic mercury causes cerebral infarctions as well as systemic features, such as pneumonia, renal cortical necrosis, and disseminated intravascular coagulopathy. A more diffuse direct neuronal toxicity may also exist with organic mercury, as the brain weights of patients with Minamata disease are substantially lower than those of controls.4

Nevertheless, both types of exposure may blur. In monkey models of methylmercury intoxication, demethylation resulted in inorganic mercury deposition in brain cells.5

Mercury damages the nervous system through several potential mechanisms. Mercury binds to sulfhydryl groups and incapacitates key enzymes involved in the cellular stress response, protein repair, and oxidative damage prevention.6 Methylmercury disrupts the muscarinic cholinergic systems in the brainstem and occipital cortices in mink as well.7 Methylmercury also inactivates the Na+/K+-ATPase, which leads to membrane depolarization, calcium entry, and eventual cell death.8

Researchers have also identified excessive excitotoxins and dysregulation of the nitric oxide system in rodents exposed to methylmercury.9 Methylmercury also induces brain edema, and this produces sulcal artery compression and consequent ischemia, which may account, at least in part, for the calcarine and parietal cell loss and gliosis.

Frequency

United States

Despite the serious, even fatal, consequences of toxicity, prevalence and incidence rates are not readily available, partly because some sequelae of low-level exposure are controversial.

Mortality/Morbidity

  • Mercury toxicity is a function of the frequency and intensity of exposure as well as the chemical form of mercury involved. Acute fulminant intoxication with methylmercury resulted in coma and death in the Minamata catastrophe. In a recent case, death resulted several months following absorption of dimethylmercury through the skin.10 Mercury vapors also can result in both acute neurological and generalized symptoms.
  • Morbidity manifesting as peripheral neuropathy and tremulousness can persist for several decades after toxic exposure to mercury vapors.11

Race

No racial predisposition has been clearly identified.

Sex

No sex predisposition has been clearly identified.

Age

Toxicity probably affects developing fetuses and children preferentially compared to other age groups, but even on this point, the data are incomplete. Prenatal exposure through maternal consumption of predominantly whale meat has been shown to impair development among children in the Faroe Islands, while maternal mercury exposure from fish consumption in the Seychelles did not result in significant developmental problems among children prenatally exposed12,13 In one family exposed to methylmercury through the ingestion of contaminated pork, the more severe clinical manifestations were found in the younger children.14

Clinical

History

The symptoms of mercury intoxication are manifold. Patients can present with complaints of numbness, tingling, hearing loss, visual difficulties, gait unsteadiness, and tremulousness, as well as emotional and cognitive difficulties. Obviously, assessing the risk of exposure, which can be acute or long term, is paramount to making a diagnosis.

  • Some unique features of mercury poisoning have generated their own nomenclature.
    • Metal fume fever occurs in the acute phase of mercury vapor toxicity and is manifested by fatigue, weakness, fever, chills, dizziness, headache, abdominal cramping, dyspnea, dysuria, and ejaculatory pain.
    • Acrodynia also occurs acutely and predominates in children. A pink peeling rash, along with generalized pain, sweating, and tachycardia are characteristic.15
    • Erethism is the constellation of irritability, excitability, anxiety, insomnia, and social withdrawal. Erethism traditionally is seen in the chronic phase of the toxicity.

Physical

Although no physical findings are pathognomonic for mercury toxicity, the constellation of gait ataxia, tremulousness, hearing loss, visual field constriction, dysarthria, and distal limb sensory loss, coupled with cognitive and emotional dysfunction, is suggestive.

  • Hearing loss and visual field impairments more often occur with organic poisoning, as in Minamata disease.
  • Distal sensory loss, uncoordinated limb movements, resting tremors, gait ataxia, and a positive Romberg sign have been described after exposure to both organic and inorganic mercury. A 2004-2005 study of 197 Minimata Bay residents who were exposed to methylmercury before 1968 found 90% with sensory impairments on the bedside neurologic examination.16
  • Emotional instability and cognitive impairments can be present in both types of exposure; however, these deficits are more characteristic of acute inorganic mercury toxicity. Neuropsychological testing in these cases has revealed pronounced impairments in traditional frontal lobe domains.17
    • Low-level organic mercury exposures have been controversial. A study of 129 residents of fishing villages in Brazil reported that higher hair mercury levels were associated in a dose-dependent manner with reduced response inhibition and manual dexterity.18
    • More recently, elevated blood mercury levels were associated with significantly reduced visual recall but improved manual dexterity in 474 elderly people in Baltimore, Md. Multiple other tested domains were unaffected, and because of the disparate results, these researchers concluded that study provided no "compelling evidence" that blood mercury levels influenced the neurobehavioral status of their subjects.19
    • In 240 adults living near an abandoned chloralkali factory in Taiwan, those with the higher blood methylmercury levels had significantly worse memory and mental manipulation abilities than those with lower methylmercury levels.20
    • Finally, the interaction between mercury exposure and a genetic polymorphism in heme biosynthesis (coproporphyrinogen oxidase) yielded additive impairments on a test of visual-motor skills in dental workers.21 Such interactions between specific genetic systems and environmental exposures supply rich terrain for future exploratory studies.
  • Non-neurologic findings include skin changes with contact dermatitis predominating, although cutaneous hyperpigmentation and stomatitis also occur.22 Erythematous papules and papulovesicles, primarily on palms, have been recently reported to be associated with mercury toxicity attributed to seafood ingestion.23

Causes

  • One major risk factor is industrial contamination.
    • Workers, particularly those employed in the manufacturing of mirrors, thermometers, incandescent lights, and x-ray machines, are at risk for inorganic mercury toxicity.
    • Organic mercury poisoning can occur among exposed workers in the paper and pulp industries.
  • In the United States, exposure to organic mercury is primarily through ingestion of contaminated fish. Those who consume large amounts of seafood from contaminated waters have an increased risk of toxicity. Surveys indicate that public awareness of the risks of mercury-contaminated fish is limited.
  • Exposure to contaminated grains, on which mercury was used as a fungicide, resulted in mercury toxicity in Iraq.
  • More unusual sources of exposure have included numerous pools of standing and vaporizing liquid mercury in a renovated building in New Jersey. Several residents of this building exhibited urinary mercury levels in the neurotoxic range (Centers for Disease Control and Prevention, 1995).
  • The Centers for Disease Control and Prevention identified at least 3 residents of the southwestern United States who developed toxic effects from a Mexican beauty cream that contained 6-8% mercurous chloride (Centers for Disease Control and Prevention, 1996). Others have identified renal disease secondary to mercury toxicity from such putative beautifying topicals.24
  • Traditional religious and healing practices are risk factors for mercury exposure. Mercury has been identified as a contaminant of Chinese herbal balls,25 and it has been used deliberately for its supernatural attributes in the Santeria religion as well as in Tibetan medicine.26 Indeed, spectrophotometric measurements of mercury vapor concentrations were elevated in New Jersey buildings located near "botanicas" in a primarily Latino community compared to a control community.27 Furthermore, of herbal Ayurvedic preparations, 20% were recently found to contain high levels of mercury.28
  • Even the mercury vapors from dental amalgam have been implicated as a possible, though controversial, source of exposure among dental workers and the general population. A study of 1663 veterans used a wide battery of noncognitive tests and found no clinically evident deficits associated with amalgam exposure. However, a subclinical decrement in vibration as measured by an automated device correlated with amalgam exposure and accounted for 15% of the variance in a multiple regression model.29 Two recent randomized studies of a total of 1041 children aged 6-10 years whose dental caries were treated with either amalgam or resin composite fillings showed no group differences on extensive batteries of neuropsychological tests after 5-7 years of follow up.30,31
  • Intentional self-poisoning with oral or injected inorganic mercury has been described with outcomes varying from coma and death despite heroic efforts32 to surprisingly scant clinical sequelae in the setting of persistently elevated blood mercury levels 5 years after the attempt.33
  • Finally, concerns about the mercury content of childhood vaccines that used mercury derivatives for their antimicrobial and preservative qualities have led to the increased availability of mercury-free vaccines.34

More on Mercury

Overview: Mercury
Differential Diagnoses & Workup: Mercury
Treatment & Medication: Mercury
Follow-up: Mercury
References
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References

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Further Reading

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Keywords

mad hatter's syndrome, metal fume fever, erethism, Minamata disease, methylmercury, methyl mercury, mercury poisoning, mercury toxicity, mercury-induced cognitive impairments, mercury intoxication, mercury exposure, prenatal mercury exposure

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Contributor Information and Disclosures

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David A Olson, MD, Clinical Neurologist, Dekalb Neurology Associates, Decatur, Georgia
David A Olson, MD is a member of the following medical societies: American Academy of Neurology
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Joseph Quinn, MD is a member of the following medical societies: American Academy of Neurology, Society for Neuroscience, and Society for Pediatric Radiology
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Richard J Caselli, MD, Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale
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Chief Editor

Tarakad S Ramachandran, MBBS, FRCP(C), FACP, Professor of Neurology, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Chair, Department of Neurology, Crouse Irving Memorial Hospital
Tarakad S Ramachandran, MBBS, FRCP(C), FACP is a member of the following medical societies: American Academy of Neurology, American Academy of Pain Medicine, American College of Forensic Examiners, American College of International Physicians, American College of Managed Care Medicine, American College of Physicians, American Heart Association, American Stroke Association, Royal College of Physicians, Royal College of Physicians and Surgeons of Canada, Royal College of Surgeons of England, and Royal Society of Medicine
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