AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 (Charcot, 1994). 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 (Wilson, 1994). 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 (Harada, 1995).

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 (Takeuchi, 1996).

Nevertheless, both types of exposure may blur. In monkey models of methylmercury intoxication, demethylation resulted in inorganic mercury deposition in brain cells (Vahter, 1995).

The mechanism by which mercury ultimately causes disruption of the central and peripheral nervous systems is not clear. Multiple processes seem to be affected. Mercury binds to reduced sulfhydryl groups and potentially depletes free radical scavengers. Inorganic mercury impairs adenosine 5'diphosphate (ADP)–dependent protein genesis in rat neurons (Palkiewicz, 1994).

Researchers have also identified excessive excitotoxins and dysregulation of the nitric oxide system in rodents exposed to methylmercury (Yamashita, 1997).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. Others have discovered alterations of nerve growth factor in the basal forebrain of the offspring of rats that were exposed to methylmercury during pregnancy and nursing (Larkfors, 1991).

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 (Nierenberg, 1998). 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 (Albers, 1999).

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 exposed (Myers, 1996; Stern, 2004) In one family exposed to methylmercury through the ingestion of contaminated pork, the more severe clinical manifestations were found in the younger children (Davis, 1994).

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 (Jao-Tan, 2003).
  • 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.
• 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 (Haut, Morrow, and Pool, 1999).
• • 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 (Yokoo, 2003).
  • 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 (Weil, 2005).
  • 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 (Echeverria, 2006). 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 (Boyd, 2000). Erythematous papules and papulovesicles, primarily on palms, have been recently reported to be associated with mercury toxicity attributed to seafood ingestion (Danzig, 2003).

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 (Tang, 2006).
• Traditional religious and healing practices are risk factors for mercury exposure. Mercury has been identified as a contaminant of Chinese herbal balls (Espinoza, 1998), and it has been used deliberately for its supernatural attributes in the Santeria religion as well as in Tibetan medicine (Sallon, 2006). Of herbal Ayurvedic preparations, 20% were recently found to contain high levels of mercury (Saper, 2004).
• 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 (Kingman, 2005). 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 (Bellinger, 2006; DeRouen, 2006).
• Finally, recent 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 (Bigham, 2005).

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Paraproteinemic neuropathy

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Laboratory studies are imperative, although exact toxicity levels remain undefined.
• • In the United States, based on the 2003 National Health and Nutrition Examination Survey (NHANES) data, urine mercury levels of 5 mcg/L and blood mercury levels of 7.1 mcg/L encompassed 95% of the sample and have recently been recommended as medically "credible comparison" levels (Risher, 2005). While blood levels are useful for more acute exposures, long-term exposures are best reflected in hair mercury measurements, and a mercury value of 1.2 mcg/g encompassed 90% of the NHANES sample (Risher, 2005).
  • Toenail mercury has also been used as a measure of long-term mercury exposure, with mean levels of 0.25-0.45 mcg/g among Western samples. Toenail mercury has been correlated with fish and shellfish consumption (Guallar, 2002; Yoshizawa, 2002; Rees, 2006).
  • Correlations have been found between signs, symptoms, and electrophysiological studies of subjects exposed to mercury with various statistical extrapolations of measures of exposure, such as duration of exposure, peak urinary mercury levels, and estimated cumulative mercury dose.
  • Interestingly, investigators of Minamata disease identified chronic forms of the disease in which hair mercury levels were not elevated. A delayed neurotoxic effect, with symptoms emerging after age-induced neuronal loss, was hypothesized (Harada, 1995). Similarly, some researchers have been unable to correlate the fluctuations of mercury blood levels with signs and symptoms of toxicity in mercury vapor exposure (Urban, 1996).

Imaging Studies

• Neuroimaging is probably more helpful in excluding other diagnoses than in ruling in mercury toxicity.
• MRI imaging in cases of Minamata disease, nevertheless, confirms the clinical and pathologic findings. Marked atrophy of the calcarine and parietal cortices as well as the cerebellar folia has been visualized (Korogi, 1997).
• MRI findings in one patient with inorganic mercury toxicity revealed mild cortical atrophy and T2 hyperintensities in frontal and subcortical regions (White, 1993).
• Single-photon emission computed tomography (SPECT) demonstrated right cingulate hypermetabolism in a 38-year-old man with emotional lability and inattention following exposure to inorganic mercury (O'Carroll, 1995).

Other Tests

• Electrophysiological studies have demonstrated a sensorimotor neuropathy, typically axonal, in some workers exposed to elemental mercury or mercury vapors. Abnormalities have been documented in visual-evoked potential studies among workers exposed to mercury vapors as well (Urban, 1996).
• In the Faroe Islands, intrauterine methylmercury exposure (as determined by maternal hair and cord blood measures) was positively correlated with prolonged brainstem evoked potentials (III and V latency peaks) 14 years after initial exposure (Murata, 2004).

Histologic Findings

Occasional sural nerve biopsies have been performed on patients with mercury toxicity. Two cases of inorganic mercury poisoning revealed a combination of axonal and demyelinating changes (Chu, 1998). Organic mercury toxicity in Minamata disease resulted in the preferential loss of large myelinated nerve fibers (Miyakawa, 1976).

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

• Treatment of mercury toxicity consists of removal from the source of exposure, supportive care, and chelation therapy. Although laboratory studies are important, acute treatment in critical situations should be based on the history and clinical presentation without waiting for laboratory confirmation.
• Chelating agents contain thiol groups, which bind to mercury. For acute, inorganic toxicity, dimercaprol (British antilewisite [BAL]) has been recommended traditionally, but oral agents are gaining prominence. Chelation with 2,3-dimercaptosuccinic acid (DMSA or succimer) has been shown to result in increased mercury excretion compared to N-acetyl-D,L-penicillamine in adults with acute mercury vapor exposure. DMSA is generally well tolerated and has recently demonstrated efficacy in children exposed to mercury (Forman, 2000).
• Exchange transfusion has been used as a treatment of last resort.
• Despite the increased excretion of mercury with chelating agents, chelation removes only a small portion of the body's mercury stores. Furthermore, the efficacy of chelating agents in treating neurological complications has not been established; however. Among patients with amalgam fillings, placebo responses to chelation treatment have been reported (Grandjean, 1997).

Surgical Care

Surgery occasionally has been employed to remove ingested mercury that has become lodged in the intestine or colon (Cantor, 1951).

Consultations

Consultation with a toxicologist or poison control center, especially in the acute phases of the illness, is important.

Diet

Seafood rich in organic mercury should of course be avoided. Predators such as sharks and tuna typically have increased mercury concentrations compared with herbivorous fishes.

Activity

Employment and driving should be restricted if patients have significant emotional or cognitive problems.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

As discussed in the treatment section, both 2,3-dimercaptosuccinic acid and N-acetyl-D,L-penicillamine have been used in the treatment of mercury toxicity.

Drug Category: Chelating agents

These agents are used to help remove a portion of the body's mercury stores.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• Determine follow-up care on a case-by-case basis. Obtain laboratory measurements of toxicity in patients with possible continued sources of exposure.

In/Out Patient Meds

• Chelation treatment may be administered in the outpatient setting with an oral chelator, such as DMSA.
• Little information is available about the treatment of mercury-induced tremulousness, but initiation of empiric treatment for patients who are functionally impaired with this complication would be reasonable.
• Patients with cognitive and emotional sequelae may require psychotropic medications.

Transfer

• Serious clinical manifestations due to exposure should be managed in a tertiary care facility by physicians experienced with toxicological emergencies.

Deterrence/Prevention

• Unfortunately, a clinician can do little to prevent mercury toxicity. Public education can raise awareness about the risks associated with easily preventable sources of toxicity, such as contaminated herbal preparations or mercury thermometers.
• Workplace hygiene and careful monitoring and disposal of industrial waste are equally important.
• Publicizing the amount of mercury contained in frequently eaten fish can help reduce toxicity on a local level.

Prognosis

• Recovery from mercury poisoning is variable. While the cognitive and emotional sequelae, at least in adults, may diminish with time, tremors and neuropathic changes have been reported to persist for decades after inorganic mercury exposure. For example, among 104 workers examined 30 years following inorganic mercury exposure, the presence of resting tremors correlated significantly with prior cumulative mercury exposure (Letz, 2000).

Patient Education

• See Deterrence/Prevention.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• The American Dental Association has reported that 34 of 38 lawsuits alleging amalgam-induced mercury toxicity have been dismissed since 2002.
• The recent book Evidence of Harm outlines the litigious efforts of parents of autistic children who claim that thimerosal-containing vaccines caused their children's neurologic dysfunction. At least one described lawsuit alleged that the vaccinating pediatrician was liable (Kirby, 2005).
• Because of the potential for extensive litigation, exercise extreme care in documenting the route and circumstances of the exposure along with the presenting symptoms and physical findings.
• Supportive documentation with carefully processed laboratory measures of exposure is also essential.
• Reserve neuroimaging and electrophysiological testing for selected cases.

Special Concerns

• Notify state and local health officials to clarify the mechanism of exposure and to institute appropriate decontamination measures should these be necessary.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

• Albers JW, Kallenbach LR, Fine LJ, et al. Neurological abnormalities associated with remote occupational elemental mercury exposure. Ann Neurol. Nov 1988;24(5):651-9. [Medline].
• Andersen A, Ellingsen DG, Morland T, Kjuus H. A neurological and neurophysiological study of chloralkali workers previously exposed to mercury vapour. Acta Neurol Scand. Dec 1993;88(6):427-33. [Medline].
• Ballatori N. Transport of toxic metals by molecular mimicry. Environ Health Perspect. Oct 2002;110 Suppl 5:689-94. [Medline].
• Bellanger TM, Caesar EM, Trachtman L. Blood mercury levels and fish consumption in Louisiana. J La State Med Soc. Feb 2000;152(2):64-73. [Medline].
• Bellinger DC, Trachtenberg F, Barregard L, et al. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. JAMA. Apr 19 2006;295(15):1775-83. [Medline].
• Bender MT, Williams JM. A real plan of action on mercury. Public Health Rep. Sep-Oct 1999;114(5):416-20. [Medline].
• Bigham M, Copes R. Thiomersal in vaccines: balancing the risk of adverse effects with the risk of vaccine-preventable disease. Drug Saf. 2005;28(2):89-101. [Medline].
• Bluhm RE, Bobbitt RG, Welch LW, 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. May 1992;11(3):201-10. [Medline].
• Boyd AS, Seger D, Vannucci S, et al. Mercury exposure and cutaneous disease. J Am Acad Dermatol. Jul 2000;43(1 Pt 1):81-90. [Medline].
• Cantor MO. Mercury lost in the gastrointestinal tract; report of an unusual case. J Am Med Assoc. Jun 9 1951;146(6):560-1. [Medline].
• Centers for Disease Control and Prevention. Mercury exposure among residents of a building formerly used for industrial purposes--New Jersey, 1995. MMWR Morb Mortal Wkly Rep. May 24 1996;45(20):422-4. [Medline].
• Centers for Disease Control and Prevention. Mercury poisoning associated with beauty cream--Texas, New Mexico, and California, 1995-1996. MMWR Morb Mortal Wkly Rep. May 17 1996;45(19):400-3. [Medline].
• Centers for Disease Control and Prevention. Update: expanded availability of thimerosal preservative-free hepatitis B vaccine. MMWR Morb Mortal Wkly Rep. Jul 21 2000;49(28):642, 651. [Medline].
• Cernichiari E, Myers GM, Clarkson TW, Weiss B. Did Andrew Jackson have mercury poisoning?. JAMA. Jan 12 2000;283(2):200-1. [Medline].
• Charcot JM. Clinical lectures of diseases of the nervous system. The Landmark Library of Neurology and Neurosurgery. 1994;186.
• Chu CC, Huang CC, Ryu SJ, Wu TN. Chronic inorganic mercury induced peripheral neuropathy. Acta Neurol Scand. Dec 1998;98(6):461-5. [Medline].
• Dantzig PI. A new cutaneous sign of mercury poisoning?. J Am Acad Dermatol. Dec 2003;49(6):1109-11. [Medline].
• 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].
• DeRouen TA, Martin MD, Leroux BG, et al. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. JAMA. Apr 19 2006;295(15):1784-92. [Medline].
• Deleu D, Hanssens Y, al-Salmy HS, Hastie I. Peripheral polyneuropathy due to chronic use of topical ammoniated mercury. J Toxicol Clin Toxicol. 1998;36(3):233-7. [Medline].
• Dodes JE. The amalgam controversy. An evidence-based analysis. J Am Dent Assoc. Mar 2001;132(3):348-56. [Medline].
• Echeverria D, Aposhian HV, Woods JS, et al. Neurobehavioral effects from exposure to dental amalgam Hg(o): new distinctions between recent exposure and Hg body burden. FASEB J. Aug 1998;12(11):971-80. [Medline].
• Echeverria D, Woods JS, Heyer NJ, et al. The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans. Neurotoxicol Teratol. Jan-Feb 2006;28(1):39-48. [Medline].
• Espinoza EO, Mann MJ, Bleasdell B. Arsenic and mercury in traditional Chinese herbal balls. N Engl J Med. Sep 21 1995;333(12):803-4. [Medline].
• Eto K, Takizawa Y, Akagi H, et al. Differential diagnosis between organic and inorganic mercury poisoning in human cases--the pathologic point of view. Toxicol Pathol. Nov-Dec 1999;27(6):664-71. [Medline].
• Eto K, Yasutake A, Kuwana T, et al. Methylmercury poisoning in common marmosets--a study of selective vulnerability within the cerebral cortex. Toxicol Pathol. Sep-Oct 2001;29(5):565-73. [Medline].
• Fonfria E, Vilaro MT, Babot Z, et al. Mercury compounds disrupt neuronal glutamate transport in cultured mouse cerebellar granule cells. J Neurosci Res. Feb 15 2005;79(4):545-53. [Medline].
• Forman J, Moline J, Cernichiari E, et al. A cluster of pediatric metallic mercury exposure cases treated with meso-2,3-dimercaptosuccinic acid (DMSA). Environ Health Perspect. Jun 2000;108(6):575-7. [Medline].
• Grandjean P, Guldager B, Larsen IB, et al. Placebo response in environmental disease. Chelation therapy of patients with symptoms attributed to amalgam fillings. J Occup Environ Med. Aug 1997;39(8):707-14. [Medline].
• Guallar E, Sanz-Gallardo MI, van't Veer P, et al. Mercury, fish oils, and the risk of myocardial infarction. N Engl J Med. Nov 28 2002;347(22):1747-54. [Medline].
• Harada M. Minamata disease: methylmercury poisoning in Japan caused by environmental pollution. Crit Rev Toxicol. 1995;25(1):1-24. [Medline].
• Haut MW, Morrow LA, Pool D, et al. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999;6(4):193-200. [Medline].
• Hursh JB, Cherian MG, Clarkson TW, et al. Clearance of mercury (HG-197, HG-203) vapor inhaled by human subjects. Arch Environ Health. Nov-Dec 1976;31(6):302-9. [Medline].
• Jao-Tan C, Pope E. Cutaneous poisoning syndromes in children: a review. Curr Opin Pediatr. Aug 2006;18(4):410-6. [Medline].
• Juárez BI, Martínez ML, Montante M, et al. Methylmercury increases glutamate extracellular levels in frontal cortex of awake rats. Neurotoxicol Teratol. Nov-Dec 2002;24(6):767-71. [Medline].
• Juarez BI, Portillo-Salazar H, Gonzalez-Amaro R, et al. Participation of N-methyl-D-aspartate receptors on methylmercury-induced DNA damage in rat frontal cortex. Toxicology. Feb 14 2005;207(2):223-9. [Medline].
• Kingman A, Albers JW, Arezzo JC, et al. Amalgam exposure and neurological function. Neurotoxicology. Mar 2005;26(2):241-55. [Medline].
• Kirby D. Evidence of Harm. Mercury in Vaccine and the Autism Epidemic: A Medical Controversy. New York: Saint Martin's Press;2005.
• Korogi Y, Takahashi M, Shinzato J, et al. MR findings in seven patients with organic mercury poisoning (Minamata disease). Am J Neuroradiol. Sep 1994;15(8):1575-8. [Medline].
• Korogi Y, Takahashi M, Hirai T, et al. Representation of the visual field in the striate cortex: comparison of MR findings with visual field deficits in organic mercury poisoning (Minamata disease). AJNR Am J Neuroradiol. Jun-Jul 1997;18(6):1127-30. [Medline].
• Langworth S, Sallsten G, Barregard L, et al. Exposure to mercury vapor and impact on health in the dental profession in Sweden. J Dent Res. Jul 1997;76(7):1397-404. [Medline].
• Larkfors L, Oskarsson A, Sundberg J, Ebendal T. Methylmercury induced alterations in the nerve growth factor level in the developing brain. Brain Res Dev Brain Res. Oct 21 1991;62(2):287-91. [Medline].
• Letz R, Gerr F, Cragle D, et al. Residual neurologic deficits 30 years after occupational exposure to elemental mercury. Neurotoxicology. Aug 2000;21(4):459-74. [Medline].
• Mahaffey KR. Recent advances in recognition of low-level methylmercury poisoning. Curr Opin Neurol. Dec 2000;13(6):699-707. [Medline].
• Miyakawa T, Murayama E, Sumiyoshi S, et al. Late changes in human sural nerves in Minamata disease and in nerves of rats with experimental organic mercury poisoning. Acta Neuropathol (Berl). Jun 15 1976;35(2):131-8. [Medline].
• Murata K, Weihe P, Budtz-Jorgensen E, et al. Delayed brainstem auditory evoked potential latencies in 14-year-old children exposed to methylmercury. J Pediatr. Feb 2004;144(2):177-83. [Medline].
• Myers GJ, Davidson PW. Prenatal methylmercury exposure and children: neurologic, developmental, and behavioral research. Environ Health Perspect. Jun 1998;106 Suppl 3:841-7. [Medline].
• Nierenberg DW, Nordgren RE, Chang MB, et al. Delayed cerebellar disease and death after accidental exposure to dimethylmercury. N Engl J Med. Jun 4 1998;338(23):1672-6. [Medline].
• O''Carroll RE, Masterton G, Dougall N. The neuropsychiatric sequelae of mercury poisoning. The Mad Hatter''s disease revisited. Br J Psychiatry. Jul 1995;167(1):95-8. [Medline].
• Ozuah PO. Mercury poisoning. Curr Probl Pediatr. Mar 2000;30(3):91-9. [Medline].
• Palkiewicz P, Zwiers H, Lorscheider FL. ADP-ribosylation of brain neuronal proteins is altered by in vitro and in vivo exposure to inorganic mercury. J Neurochem. May 1994;62(5):2049-52. [Medline].
• Palmer C. House committee hears testimony on medical mercury use. American Dental Association News. Apr 30 2001.
• Pamphlett R, Waley P. Mercury in human spinal motor neurons. Acta Neuropathol (Berl). Nov 1998;96(5):515-9. [Medline].
• Rees JR, Sturup S, Chen C, et al. Toenail mercury and dietary fish consumption. J Expo Sci Environ Epidemiol. Aug 16 2006;[Medline].
• 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. Aug 2005;26(4):691-9. [Medline].
• Sallon S, Namdul T, Dolma S, et al. Mercury in traditional Tibetan medicine - panacea or problem?. Hum Exp Toxicol. Jul 2006;25(7):405-12. [Medline].
• Saper RB, Kales SN, Paquin J, et al. Heavy metal content of ayurvedic herbal medicine products. JAMA. Dec 15 2004;292(23):2868-73. [Medline].
• Stern AH, Jacobson JL, Ryan L. Do recent data from the Seychelles Islands alter the conclusions of the NRC Report on the toxicological effects of methylmercury?. Environ Health. Jan 30 2004;3(1):2. [Medline].
• Takeuchi T, Eto K, Kinjo Y, Tokunaga H. Human brain disturbance by methylmercury poisoning, focusing on the long-term effect on brain weight. Neurotoxicology. 1996;17(1):187-90. [Medline].
• Tang HL, Chu KH, Mak YF, et al. Minimal change disease following exposure to mercury-containing skin lightening cream. Hong Kong Med J. 2006;12:316-8.
• Tokuomi H, Okajima T, Kanai J, et al. Minamata disease. World Neurol. Jun 1961;2:536-45. [Medline].
• Urban P, Lukas E, Benicky L, Moscovicova E. Neurological and electrophysiological examination on workers exposed to mercury vapors. Neurotoxicology. 1996;17(1):191-6. [Medline].
• Vahter ME, Mottet NK, Friberg LT, et al. Demethylation of methyl mercury in different brain sites of Macaca fascicularis monkeys during long-term subclinical methyl mercury exposure. Toxicol Appl Pharmacol. Oct 1995;134(2):273-84. [Medline].
• Weil M, Bressler J, Parsons P, et al. Blood mercury levels and neurobehavioral function. JAMA. Apr 20 2005;293(15):1875-82. [Medline].
• White RF, Feldman RG, Moss MB, Proctor SP. Magnetic resonance imaging (MRI), neurobehavioral testing, and toxic encephalopathy: two cases. Environ Res. Apr 1993;61(1):117-23. [Medline].
• Wilson SAK. Neurology. The Landmark Library of Neurology and Neurosurgery. 1994;739-740.
• Yamashita T, Ando Y, Sakashita N, et al. Role of nitric oxide in the cerebellar degeneration during methylmercury intoxication. Biochim Biophys Acta. Mar 15 1997;1334(2-3):303-11. [Medline].
• Yokoo EM, Valente JG, Grattan L, et al. Low level methylmercury exposure affects neuropsychological function in adults. Environ Health. Jun 4 2003;2(1):8. [Medline].
• Yoshizawa K, Rimm EB, Morris JS, et al. Mercury and the risk of coronary heart disease in men. N Engl J Med. Nov 28 2002;347(22):1755-60. [Medline].

Article Last Updated: Sep 19, 2006