Mercury poisoning

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·

---

This article needs rewriting to enhance its relevance to psychologists..
Please help to improve this page yourself if you can..

Hg_Mercury.jpg|

Mercury poisoning

ICD-10	T561
ICD-9	985.0
OMIM	[1]
DiseasesDB	8057
MedlinePlus	002476
eMedicine	emerg/813
MeSH	{{{MeshNumber}}}

Template:Toxicology

Mercury poisoning (also known as mercurialism, hydrargyria, Hunter-Russell syndrome, or acrodynia when affecting children) is a disease caused by exposure to mercury or its toxic compounds. Mercury is a cumulative heavy metal poison which occurs in its elemental form, inorganically as salts, or organically as organomercury compounds; the three groups vary in effects due to differences in their absorption and metabolism, among other factors. However, with sufficient exposure all mercury-based toxins damage the central nervous system and other organs or organ systems such as the liver or gastrointestinal tract.

Symptoms typically include sensory impairment (vision, hearing, speech), disturbed sensation and a lack of coordination. The type and degree of symptoms exhibited depend upon the individual toxin, the dose, and the method and duration of exposure.

Due to its toxicity, there have been campaigns in many countries to ban mercury altogether.

Signs and symptoms

Common symptoms include peripheral neuropathy (presenting as paresthesia or itching, burning or pain), skin discoloration (pink cheeks, fingertips and toes), edema (swelling), and desquamation (dead skin peels off in layers).

Because mercury blocks the degradation pathway of catecholamines, epinephrine excess causes hyperhidrosis (profuse sweating), tachycardia (persistently faster-than-normal heart beat), mercurial ptyalism (hypersalivation) and hypertension (high blood pressure). Mercury is thought to inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-o-methyl transferase.

Affected children may show red cheeks and nose, erythematous lips (red lips), loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and photophobia. Other symptoms may include kidney disfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms (emotional lability, memory impairment, insomnia).

Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease.

An example of desquamation of the hand of a child with severe mercury poisoning acquired by handling elemental mercury is this photograph in Horowitz, et al (2002).

Causes

Mercury poisoning is caused by sufficient exposure to elemental mercury or mercury compounds. The consumption of fish is by far the most significant source of ingestion-related mercury exposure in humans, although plants and livestock also contain mercury due to bioaccumulation of mercury from soil, water and atmosphere, and due to biomagnification by ingesting other mercury-containing organisms. Exposure to mercury can occur from breathing contaminated air, or from improper use or disposal of mercury and mercury-containing objects, for example, after spills of elemental mercury or improper disposal of fluorescent light bulbs.

Human-generated sources such as coal plants emit approximately half of atmospheric mercury, with natural sources such as volcanoes responsible for the remainder. An estimated two-thirds of human-generated mercury comes from stationary combustion, mostly of coal. Other important human-generated sources include gold production, non-ferrous metal production, cement production, waste disposal, crematoria, caustic soda production, pig iron and steel production, mercury production (mostly for batteries), and biomass burning.

Mercury and many of its chemical compounds, especially organomercury compounds, can also be readily absorbed through direct contact with bare, or in some cases (such as dimethyl mercury) insufficiently protected, skin. Mercury and its compounds are commonly used in chemical laboratories, hospitals, dental clinics, and facilities involved in the production of items such as fluorescent light bulbs, batteries, and explosives.

Toxic effects

Mercury damages the central nervous system, endocrine system, kidneys, and other organs, and adversely affects the mouth, gums, and teeth. Exposure over long periods of time or heavy exposure to mercury vapor can result in brain damage and ultimately death. Mercury and its compounds are particularly toxic to fetuses and infants. Women who have been exposed to mercury in pregnancy have sometimes given birth to children with serious birth defects (see Minamata disease).

Mercury exposure in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. Mercury inhibits the formation of myelin, the building block protein that forms these sheaths.

There is some evidence that mercury poisoning may predispose to Young's syndrome (men with bronchiectasis and low sperm count).

Mercury poisoning in the young has been hypothesized as a cause of autistic behaviors. This hypothesis is controversial, as much evidence suggests that about 90% of autism is explained by genetics. The hypothesis has not been confirmed by reliable studies.

Mercury poisoning's effects partially depend on whether it has been caused by exposure to elemental mercury, inorganic mercury compounds (as salts), or organomercury compounds.

Elemental mercury

Elemental mercury (pure mercury) is readily absorbed through the skin. However, because mercury has a very high surface tension at room temperature, it does not wet the skin (as water would) and the contact area is therefore limited (reducing absorption rates). Materials with high surface tensions tend to form near spherical droplets which do not conform fully to topologically complex surfaces like skin (the mercury touches the papillary ridges, not the grooves). Nonetheless, handling mercury with unprotected hands has resulted in cases of severe mercury poisoning.

Mercury vapour is rapidly absorbed into the body through the respiratory tract during inhalation. Chronic exposure, even at low concentrations in the range 0.7–42 μg/m³, has been shown in case control studies to cause effects such as tremors, impaired cognitive skills, and sleep disturbance in workers. Mercury is only poorly absorbed through the gastrointestinal tract.

Inorganic mercury compounds

Mercury occurs inorganically as salts such as mercury(II) chloride. Mercury salts primarily affect the gastro-intestinal tract and the kidneys, and can cause severe kidney damage; however, as they can not cross the blood-brain barrier easily, mercury salts inflict little neurological damage without continuous or heavy exposure. As two oxidation states of mercury form salts (Hg⁺¹ and Hg⁺²), mercury salts occur in both mercury(I) (or mercurous) and mercury(II) (mercuric) forms. Mercury(II) salts are usually more toxic than their mercury(I) counterparts because their solubility in water is greater; thus, they are more readily absorbed from the gastrointestinal tract.

Organic mercury compounds

Compounds of mercury tend to be much more toxic than the element itself, and organic compounds of mercury are often extremely toxic and have been implicated in causing brain and liver damage. The most dangerous mercury compound, dimethyl mercury, is so toxic that even a few microliters spilled on the skin, or even a latex glove, can cause death. Dimethylmercury can be fatal within hours or less.^{[How to reference and link to summary or text]} One of the chief targets of the toxin is the enzyme pyruvate dehydrogenase (PDH). The enzyme is irreversibly inhibited by several mercury compounds, the lipoic acid component of the multienzyme complex binds mercury compounds tightly (mercury binds to the sulfur atoms in lipoic acid) and thus inhibits PDH.

Through bioaccumulation in the environment, methyl mercury works its way up the food chain, reaching high concentrations among populations of some species. Larger species of fish, such as tuna or swordfish, are usually of greater concern than smaller species. The U.S. Food and Drug Administration (FDA) advises women of child-bearing age and children to completely avoid swordfish, shark, king mackerel and tilefish and to limit consumption of king crab, snow crab, albacore tuna and tuna steaks to 6 oz. or less per week. However, there is no evidence that moderate consumption of fish in the U.S. poses a significant health hazard. One recent Harvard Medical School study of mothers and their infants suggests that the nutritional benefits of eating fish outweighs the potential drawbacks of methylmercury. In the study, each additional weekly serving of fish consumed by the mother during pregnancy was associated with an increase in infant cognition.

Ethylmercury is a breakdown product of the antibacteriological agent thimerosal which has effects similar but not identical to methyl mercury.

Treatment

The standard of care for mercury poisoning is chelation therapy using DMSA (in U.S.), DMPS and ALA (in Europe, Russia and former Soviet republics). A study of workers involved in the production of mercurous chloride, showed that the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS) was effective in lowering the body burden of mercury and in decreasing the urinary mercury concentration to normal levels.

Alternative medicine makes use of these same substances along with others, such as vitamin C (ascorbic acid), EDTA and "high sulfur foods". However, it has been shown that inorganic mercury (Hg²⁺) bound to EDTA (a necessary step in EDTA-induced mercury chelation) forms a complex (HgEDTA) that is "potentially injurious to the neuronal cytoskeleton".

Some of the toxic effects of mercury are in some cases partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. However, heavy or prolonged exposure can do irreversible damage, particularly in fetuses, infants, and young children.

Prevention

Mercury poisoning can be prevented (or minimized) by eliminating or reducing exposure to mercury and mercury compounds. To that end, many governments and private groups have made efforts to avoid common hazards or to ban mercury altogether.

Regulations

• There have been growing efforts to limit exposure from all sources. For children, these efforts have centered on reducing mercury exposure in its organic form by limiting consumption of contaminated fish such as tuna and swordfish, and fish caught from mercury-contaminated waters. (AAP advocacy)
• As a precautionary measure, thimerosal, a mercury-containing preservative, is being eliminated from vaccines as quickly as manufacturers can alter their production processes and obtain FDA approval. (AAP advocacy)
• AAP recommends that pediatricians stop using all mercury-containing devices, including thermometers, and encourage parents to do the same. (AAP advocacy)

The variability among regulations and advisories are at times confusing for the lay person as well as scientists.

Country	Regulating Agency	Regulated activity	Medium	Type of mercury compound	Type of limit	Limit
US	OSHA	occupational exposure	air	elemental mercury	Ceiling (not to exceed)	0.1 mg/m³
US	OSHA	occupational exposure	air	organic mercury	Ceiling (not to exceed)	0.05 mg/m³
US	FDA	drinking	water	inorganic mercury	Maximum allowable concentration	2 ppb (0.002mg/L)
US	FDA	eating	sea food	methyl mercury	Maximum allowable concentration	1 ppm
US	EPA	drinking	water	inorganic mercury	Maximum Contaminant Level	2 ppb (0.002mg/L)

Occurrences of mercury poisoning

• The phrase mad as a hatter is likely a reference to mercury poisoning, as mercury-based compounds were once used in the manufacture of felt hats in the 18th and 19th century. (The Mad Hatter character of Alice in Wonderland was almost certainly inspired by an eccentric furniture dealer, not by a victim of mercury poisoning.)
• An early scientific study of mercury poisoning was in 1923-6 by the German inorganic chemist, Alfred Stock, who himself became poisoned, together with his colleagues, by breathing mercury vapour that was being released by his laboratory equipment — diffusion pumps, float valves, and manometers — all of which contained mercury, and also from mercury that had been accidentally spilt and remained in cracks in the linoleum floor covering. He published a number of papers on mercury poisoning, founded a committee in Berlin to study cases of possible mercury poisoning, and introduced the term micromercurialism.
• The term Hunter-Russell syndrome derives from a study of mercury poisoning among workers in a seed packing factory in England in the late 1930s who breathed methylmercury that was being used as a seed disinfectant and preservative.
• From 1932 to 1968 methyl mercury was released into the sea around the city of Minamata in Kumamoto prefecture, Japan. The toxin bioaccumulated in fish, which when eaten by the local population caused the largest case of mercury poisoning known. Minamata disease caused the deaths of over 1000 people and permanently disabled a great many more.
• Widespread mercury poisoning occurred in rural Iraq in 1971-1972, when grain treated with a methyl mercury-based fungicide that was intended for planting only was used by the rural population to make bread, causing at least 6530 cases of mercury poisoning and at least 459 deaths (see Basra poison grain disaster).
• On August 14, 1996, Karen Wetterhahn, a chemistry professor working at Dartmouth College, spilled a small amount of dimethylmercury on her latex glove. She began experiencing the symptoms of mercury poisoning five months later and, despite aggressive chelation therapy, died a few months later from brain malfunction due to mercury intoxication.
• In April of 2000, Alan Chmurny attempted to kill a former employee, Marta Bradley, by pouring mercury into the ventilation system of her car.
• The first emperor of unified China, Qin Shi Huang Di, was driven insane and killed by mercury pills intended to give him eternal life.

Acrodynia epidemic

Acrodynia is a type of mercury poisoning in children characterized by pain and pink discoloration of the hands and feet. The word is derived from the Greek, where ακρος means high (as in:in an extremity) and οδυνη means pain. As such, it might be (erroneously) used to indicate that a patient has pain in the hands or feet. However, acrodynia is a disease rather than a symptom. Also known as pink disease, erythredema, Selter's disease, or Swift-Feer disease, acrodynia was relatively commonplace amongst children in the first half of the 20th century. Initially, the cause of the acrodynia epidemic among infants and young children was unknown; however, mercury poisoning, primarily from calomel in teething powders, began to be widely accepted as its cause in the 1950s and 60s. The prevalence of acrodynia decreased greatly after calomel was excluded from most teething powders in 1954.

Medical procedures

Because elemental mercury often passes through the GI tract without being absorbed, it was used medically for various purposes until the dangers of mercury poisoning became known. For example, elemental mercury was used to mechanically clear intestinal obstructions (due to its great weight and fluidity), and it was a key ingredient in various medicines throughout history, such as blue mass. The toxic effects often were either not noticed at all, or so subtle or generic that they were attributed to other causes and were not recognized as poisoning caused by mercury. While the usage of mercury in medicine has declined, mercury-containing compounds are still used medically in vaccines and dental amalgam, both of which have been the subject of controversy regarding their potential for mercury poisoning.

Thimerosal

For more details on this topic, see Thimerosal controversy.

Thimerosal, a preservative that contains mercury, has been added to vaccines to prevent their deterioration since the 1930s. No adverse effects of thimerosal have ever been proven, although some allergic reactions have been noted.^{[How to reference and link to summary or text]} However, organizations such as the American Academy of Pediatrics have recommended that the use of thimerosal be reduced as a precautionary measure. With the exception of some flu vaccines, it is no longer used as a preservative in routinely recommended childhood vaccines in the United States; it is still in limited use as a preservative in multi-dose flu and tetanus vaccines and a few other non-childhood vaccines.

Dental amalgam

For more details on this topic, see Dental amalgam controversy.

Dental amalgam, an alloy of about 50% elemental mercury, has been used to fill decayed teeth since 1830 in the U.S. Although this amalgam is a source of low-level exposure to mercury, no scientific evidence links it as a cause of clinically significant toxic effects, except for the rare local hypersensitivity reaction. The National Institutes of Health has stated that amalgam fillings pose no personal health risk, and that replacement by non-amalgam fillings is not indicated.

Cosmetics

Some skin whitening products contain the toxic chemical mercury(II) chloride as the active ingredient. When applied, the chemical readily absorbs through the skin into bloodstream. The use of mercury in cosmetics is illegal in the United States. However, cosmetics containing mercury are often illegally imported. Following a certified case of mercury poisoning resulting from the use of an imported skin whitening product, the FDA warned against the use of such products. Symptoms of mercury poisoning have resulted from the use of various mercury-containing cosmetic products. The use of skin whitening products is especially popular amongst Asian women. In Hong Kong in 2002, two products were discovered to contain between 9,000 to 60,000 times the recommended dose.

Fluorescent lamps

Fluorescent lamps contain mercury vapor, and if broken, they can contaminate the surrounding environment and poison its inhabitants. A 1987 report described a 23-month-old toddler who suffered anorexia, weight loss, irritability, profuse sweating, and peeling and redness of fingers and toes. This case of acrodynia was traced to exposure of mercury from a carton of 8-foot fluorescent light bulbs that had broken in a potting shed adjacent to the main nursery. The glass was cleaned up and discarded, but the child often used the area for play.

See also

• Quicksilver
• Heavy metal poisoning
• Lead poisoning
• Minamata disease, industrial mercury pollution
• Niigata Minamata disease, industrial mercury pollution

Further reading

• Adams, P. M., Hanlon, R. T., & Forsythe, J. W. (1988). Toxic exposure to ethylene dibromide and mercuric chloride: Effects on laboratory-reared octopuses: Neurotoxicology and Teratology Vol 10(6) Nov-Dec 1988, 519-523.
• Aschner, M., Aschner, J. L., & Kimelberg, H. K. (1992). Methylmercury neurotoxicity and its uptake across the blood-brain barrier. New York, NY: Plenum Press.
• Aschner, M., & Walker, S. J. (2002). The neuropathogenesis of mercury toxicity: Molecular Psychiatry Vol 7(Suppl 2) Aug 2002, S40-S41.
• Bagedahl-Strindlund, M., Ilie, M., Furhoff, A. K., Tomson, Y., Larsson, K. S., Sandborgh-Englund, G., et al. (1997). A multidisciplinary clinical study of patients suffering from illness associated with mercury release from dental restorations: Psychiatric aspects: Acta Psychiatrica Scandinavica Vol 96(6) Dec 1997, 475-482.
• Bailer, J., Rist, F., Rudolf, A., Staehle, H. J., Eickholz, P., Triebig, G., et al. (2001). Adverse health effects related to mercury exposure fron dental amalgam fillings: Toxicological or psychological causes? : Psychological Medicine Vol 31(2) Feb 2001, 255-263.
• Bernard, S., Enayati, A., Roger, H., Binstock, T., & Redwood, L. (2002). The role of mercury in the pathogenesis of autism: Molecular Psychiatry Vol 7(Suppl 2) Aug 2002, S42-S43.
• Beuter, A., Edwards, R., & Lamoureux, D. (2000). Neuromotor profiles: What are they and what can we learn from them? : Brain and Cognition Vol 43(1-3) Jun-Aug 2000, 39-44.
• Bornhausen, M., & Hagen, U. (1984). Operant behaviour performance changes in rats after prenatal and postnatal exposure to heavy metals: IRCS Medical Science: Psychology & Psychiatry Vol 12(9-10) Sep-Oct 1984, 805-806.
• Cuomo, V., & et al. (1984). Behavioural and neurochemical changes in offspring of rats exposed to methyl mercury during gestation: Neurobehavioral Toxicology & Teratology Vol 6(3) May-Jun 1984, 249-254.
• Dahl, R., White, R. F., Weihe, P., & Sorensen, N. (1996). Feasibility and validity of three computer-assisted neurobehavioral tests in 7-year-old children: Neurotoxicology and Teratology Vol 18(4) Jul-Aug 1996, 413-419.
• Davis, L. E., Kornfeld, M., Mooney, H. S., Fiedler, K. J., & et al. (1994). Methylmercury poisoning: Long-term clinical, radiological, toxicological, and pathological studies of an affected family: Annals of Neurology Vol 35(6) Jun 1994, 680-688.
• DeRouen, T. A., Martin, M. D., Leroux, B. G., Townes, B. D., Woods, J. S., Leitao, J., et al. (2006). Neurobehavioral Effects of Dental Amalgam in Children: A Randomized Clinical Trial: JAMA: Journal of the American Medical Association Vol 295(15) Apr 2006, 1784-1792.
• Diamond, R., White, R. F., Gerr, F., & Feldman, R. G. (1995). A case of developmental exposure to inorganic mercury: Child Neuropsychology Vol 1(2) Oct 1995, 140-149.
• Donlin, W. D. (2005). The percentile IRT schedule: High rate behavior as a tool for examining the toxic motor effects of methylmercury exposure. Dissertation Abstracts International: Section B: The Sciences and Engineering.
• Echeverria, D., Woods, J. S., Heyer, N. J., Rohlman, D. S., Farin, F. M., Bittner, A. C., Jr., et al. (2005). Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function: Neurotoxicology and Teratology Vol 27(6) Nov-Dec 2005, 781-796.
• Elsner, J., Hodel, B., Suter, K. E., Oelke, D., & et al. (1988). Detection limits of different approaches in behavioral teratology, and correlation of effects with neurochemical parameters: Neurotoxicology and Teratology Vol 10(2) Mar-Apr 1988, 155-167.
• Evans, H. L., Laties, V. G., & Weiss, B. (1975). Behavioral effects of mercury and methylmercury: Federation Proceedings Vol 34(9) Aug 1975, 1858-1867.
• Fagala, G. E., & Wigg, C. L. (1992). Psychiatric manifestations of mercury poisoning: Journal of the American Academy of Child & Adolescent Psychiatry Vol 31(2) Mar 1992, 306-311.
• Feldman, R. G. (1982). Neurological manifestations of mercury intoxication: Acta Neurologica Scandinavica Vol 66(Suppl 92) 1982, 201-209.
• Flaherty, C. M., Sass, G. G., & Stiles, K. E. (2003). Human Mercury Toxicity and Ice Angler Fish Consumption: Are People Eating Enough to Cause Health Problems? : Risk Analysis Vol 23(3) Jun 2003, 497-504.
• Gilbert, S. G., Rice, D. C., & Burbacher, T. M. (1996). Fixed interval/fixed ratio performance in adult monkeys exposed in utero to methylmercury: Neurotoxicology and Teratology Vol 18(5) Sep-Oct 1996, 539-546.
• Giombetti, R. J., Rosen, D. H., Kuczmierczyk, A. R., & Marsh, D. O. (1988). Repeated suicide attempts by the intravenous injection of elemental mercury: International Journal of Psychiatry in Medicine Vol 18(2) 1988, 153-167.
• Godfrey, M. E. (1990). Diagnosis of intra-oral metal toxicity and management protocol: International Journal of Biosocial & Medical Research Vol 12(2) 1990, 155-171.
• Godfrey, M. E., Wojcik, D. P., & Krone, C. A. (2003). Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity: Journal of Alzheimer's Disease Vol 5(3) 2003, 189-195.
• Gottwald, B., Kupfer, J., Traenckner, I., Ganss, C., & Gieler, U. (2002). Psychological, allergic, and toxicological aspects of patients with amalgam-related complaints: Psychotherapy and Psychosomatics Vol 71(4) Jul-Aug 2002, 223-232.
• Goulet, S., Dore, F. Y., & Mirault, M. E. (2003). Neurobehavioral changes in mice chronically exposed to methylmercury during fetal and early postnatal development: Neurotoxicology and Teratology Vol 25(3) May-Jun 2003, 335-347.
• Grandjean, P., Weihe, P., White, R. F., Debes, F., & et al. (1997). Cognitive deficit in 7-yr-old children with prenatal exposure to methylmercury: Neurotoxicology and Teratology Vol 19(6) Nov-Dec 1997, 417-428.
• Hanninen, H. (1982). Behavioral effects of occupational exposure to mercury and lead: Acta Neurologica Scandinavica Vol 66(Suppl 92) 1982, 167-175.
• Hanson, M. (1983). Amalgam--hazards in your teeth: Journal of Orthomolecular Psychiatry Vol 12(3) 1983, 194-201.
• Hellberg, J., & Nystrom, M. (1972). The influence of methyl mercury exposure on learning-set behavior of squirrel monkeys (Saimiri sciureus): Psychological Research Bulletin Vol 12(8) 1972.
• Hua, M. S., Huang, C. C., & Yang, Y. J. (1996). Chronic elemental mercury intoxication: Neuropsychological follow-up case study: Brain Injury Vol 10(5) Jul 1996, 377-384.
• Huggins, H. A. (1982). Mercury: A factor in mental disease? : Journal of Orthomolecular Psychiatry Vol 11(1) 1982, 3-16.
• Hughes, J. A. (1973). Developmental and behavioral effects of methyl mercury in mice: Dissertation Abstracts International.
• Hughes, J. A., & Annau, Z. (1976). Postnatal behavioral effects in mice after prenatal exposure to methylmercury: Pharmacology, Biochemistry and Behavior Vol 4(4) Apr 1976, 385-391.
• Hughes, J. A., Rosenthal, E., & Sparber, S. B. (1976). Time dependent effects produced in chicks after prenatal injection of methylmercury: Pharmacology, Biochemistry and Behavior Vol 4(5) May 1976, 507-513.
• Hughes, J. A., & Sparber, S. B. (1978). d-Amphetamine unmasks postnatal consequences of exposure to methylmercury in utero: Methods for studying behavioral teratogenesis: Pharmacology, Biochemistry and Behavior Vol 8(4) Apr 1978, 365-375.
• Hupp, E. W., & Day, H. D. (1980). Methylmercuric chloride poisoning in the pigtailed macaque monkey (Macaca nemestrina): Psychological Reports Vol 46(3, Pt 2) Jun 1980, 1023-1029.
• Istoc-Bobis, M., & Gabor, S. (1987). Psychic troubles caused by professional intoxications with lead and mercury: Revista de Psihologie Vol 33(1) 1987, 31-40.
• Istoc-Bobis, M., & Gabor, S. (1987). Psychological disfunctions in lead- and mercury-occupational exposure: Revue Roumaine des Sciences Sociales - Serie de Psychologie Vol 31(2) Jul-Dec 1987, 183-191.
• Junior, Q. C., Faria, M. D. A. M., & Fraguas Junior, R. (2003). Depression, Insomnia, and Memory Loss in a Patient With Chronic Intoxication by Inorganic Mercury: Journal of Neuropsychiatry & Clinical Neurosciences Vol 15(4) Fal 2003, 457-458.
• Kelkar, S. A. (1975). Psychomotor skill changes in workers exposed to mercury: Indian Journal of Psychology Vol 50(1) Mar 1975, 17-24.
• Klein, S. B., & Atkinson, E. J. (1973). Mercuric chloride influence on active-avoidance acquisition in rats: Bulletin of the Psychonomic Society Vol 1(6-B) Jun 1973, 437-438.
• Landis, T., Graves, R., Benson, D. F., & Hebben, N. (1982). Visual recognition through kinaesthetic mediation: Psychological Medicine Vol 12(3) Aug 1982, 515-531.
• Laties, V. G., & Evans, H. L. (1980). Research strategies for assessing the effects of methylmercury on behavior: Revista Mexicana de Analisis de la Conducta Vol 6(1) Jun 1980, 27-37.
• Laties, V. G., & Evans, H. L. (1982). Effects of methylmercury on operant behavior: Neurobehavioral Toxicology & Teratology Vol 4(6) Nov-Dec 1982, 683-688.
• Levine, T. E. (1978). Conditioned aversion following ingestion of methylmercury in rats and mice: Behavioral & Neural Biology Vol 22(4) Apr 1978, 489-496.
• Maghazaji, H. I. (1974). Psychiatric aspects of methylmercury poisoning: Journal of Neurology, Neurosurgery & Psychiatry Vol 37(8) Aug 1974, 954-958.
• Magos, L. (1982). Neurotoxicity, anorexia and the preferential choice of antidote in methylmercury intoxicated rats: Neurobehavioral Toxicology & Teratology Vol 4(6) Nov-Dec 1982, 643-646.
• Marlowe, M., Errera, J., Stellern, J., & Beck, D. (1983). Lead and mercury levels in emotionally disturbed children: Journal of Orthomolecular Psychiatry 12(4) 1983, 260-267.
• Marlowe, M., Moon, C. E., Errera, J., Jacobs, J., & et al. (1986). Low mercury levels and childhood intelligence: Journal of Orthomolecular Medicine Vol 1(1) 1986, 43-49.
• Merigan, W. H., & et al. (1983). Neurotoxic actions of methylmercury on the primate visual system: Neurobehavioral Toxicology & Teratology Vol 5(6) Nov-Dec 1983, 649-658.
• Moon, C., Marlowe, M., Stellern, J., & Errera, J. (1985). Main and interaction effects of metallic pollutants on cognitive functioning: Journal of Learning Disabilities Vol 18(4) Apr 1985, 217-221.
• Murata, K., Weihe, P., Renzoni, A., Debes, F., Vasconcelos, R., Zino, F., et al. (1999). Delayed evoked potentials in children exposed to methylmercury from seafood: Neurotoxicology and Teratology Vol 21(4) Jul-Aug 1999, 343-348.
• Mutter, J., & Naumann, J. (2005). Blood Mercury Levels and Neurobehavior: JAMA: Journal of the American Medical Association Vol 294(6) Aug 2005, 679-680.
• Nerdrum, P. (1989). Amalgam and psychosomatic disorders: Nordisk Psykiatrisk Tidsskrift Vol 43(5) 1989, 453-458.
• Nierenberg, D. W., Nordgren, R. E., Chang, M. B., Siegler, R. W., Blayney, M. B., Hochberg, F., et al. (1998). Delayed cerebellar disease and death after accidental exposure to dimethylmercury: New England Journal of Medicine Vol 338(23) Jun 1998, 1672-1676.
• Ninomiya, T., Imamura, K., Kuwahata, M., Kindaichi, M., Susa, M., & Ekino, S. (2005). Reappraisal of somatosensory disorders in methylmercury poisoning: Neurotoxicology and Teratology Vol 27(4) Jul-Aug 2005, 643-653.
• Null, G., & Feldman, M. (2002). Mercury dental amalgams: The controversy continues: Journal of Orthomolecular Medicine Vol 17(2) 2002, 85-110.
• O'Carroll, R. E., Masterton, G., Dougall, N., Ebmeier, K. P., & et al. (1995). The neuropsychiatric sequelae of mercury poisoning: The Mad Hatter's disease revisited: British Journal of Psychiatry Vol 167(1) Jul 1995, 95-98.
• O'Kusky, J. R. (1992). The neurotoxicity of methylmercury in the developing nervous system. New York, NY: Plenum Press.
• O'Kusky, J. R., & McGeer, E. G. (1985). Methylmercury poisoning of the developing nervous system in the rat: Decreased activity of glutamic acid decarboxylase in cerebral cortex and neostriatum: Developmental Brain Research Vol 21(2) Aug 1985, 299-306.
• O'Kusky, J. R., Radke, J. M., & Vincent, S. R. (1988). Methylmercury-induced movement and postural disorders in developing rat: Loss of somatostatin-immunoreactive interneurons in the striatum: Developmental Brain Research Vol 40(1) May 1988, 11-23.
• Ozuah, P. O. (2001). Folk use of elemental mercury: A potential hazard for children? : Journal of the National Medical Association Vol 93(9) Sep 2001, 320-322.
• Piikivi, L. (1989). Health effects of low level, long-term exposure to mercury (Hg) vapour: Acta Universitatis Ouluensis: Series D Medica Vol 183 1989, 98.
• Piikivi, L., & Hanninen, H. (1989). Subjective symptoms and psychological performance of chlorine-alkali workers: Scandinavian Journal of Work, Environment & Health Vol 15(1) Feb 1989, 69-74.
• Pleva, J. (1983). Mercury poisoning from dental amalgam: Journal of Orthomolecular Psychiatry Vol 12(3) 1983, 184-193.
• Powell, T. J. (2000). Chronic neurobehavioural effects of mercury poisoning on a group of Zulu chemical workers: Brain Injury Vol 14(9) Sep 2000, 797-814.
• Pryor, G. T., Uyeno, E. T., Tilson, H. A., & Mitchell, C. L. (1983). Assessment of chemicals using a battery of neurobehavioral tests: A comparative study: Neurobehavioral Toxicology & Teratology Vol 5(1) Jan-Feb 1983, 91-117.
• Rohling, M. L., & Demakis, G. J. (2006). A meta-analysis of the neuropsychological effects of occupational exposure to mercury: Clinical Neuropsychologist Vol 20(1) Feb 2006, 108-132.
• Rosenthal, E., & Sparber, S. B. (1972). Methylmercury dicyandiamide: Retardation of detour learning in chicks hatched from injected eggs: Life Sciences Vol 11(18, Pt 1) Sep 1972, 883-892.
• Ross, W. D., Gechman, A. S., Sholiton, M. C., & Paul, H. S. (1977). Need for alertness to neuropsychiatric manifestations of inorganic mercury poisoning: Comprehensive Psychiatry Vol 18(6) Nov-Dec 1977, 595-598.
• Rossini, S. R. G., Reimao, R., Lefevre, B. H., & Medrado-Faria, M. A. (2000). Chronic insomnia in workers poisoned by inorganic mercury: Psychological and adaptive aspects: Arquivos de Neuro-Psiquiatria Vol 58(1) Mar 2000, 32-38.
• Sandulescu, G., & et al. (1982). Aspects of occupational toxic encephalopathy following intoxication with mercury-ethyl chloride: Revista de Medicina Interna, Neurologie, Psihiatrie, Neurochirurgie, Dermato-Venerologie Vol 27(4) Oct-Dec 1982, 271-276.
• Schalock, R. L., Brown, W. J., Kark, R. A., & Menon, N. K. (1981). Perinatal methylmercury intoxication: Behavioral effects in rats: Developmental Psychobiology Vol 14(3) May 1981, 213-219.
• Schmid, C., & Rotenberg, J. S. (2005). Neurodevelopmental Toxicology: Neurologic Clinics Vol 23(2) May 2005, 321-336.
• Siblerud, R. L. (1989). The relationship between mercury from dental amalgam and mental health: American Journal of Psychotherapy Vol 43(4) Oct 1989, 575-587.
• Sine, L. F. (1984). The relationship of mercury to cognitive, affective and perceptual motor functioning in a normal sample in Hawaii: Dissertation Abstracts International.
• Smith, P. J. (1979). Short-term memory scanning is related to memory span and mercury exposure: Dissertation Abstracts International.
• Smith, P. J., & Langolf, G. D. (1981). The use of Sternberg's memory-scanning paradigm in assessing effects of chemical exposure: Human Factors Vol 23(6) Dec 1981, 701-708.
• Spyker, J. M. (1975). Assessing the impact of low level chemicals on development: Behavioral and latent effects: Federation Proceedings Vol 34(9) Aug 1975, 1835-1844.
• Spyker, J. M., Sparber, S. B., & Goldberg, A. M. (1972). Subtle consequences of methylmercury exposure: Behavioral deviations in offspring of treated mothers: Science Vol 177(4049) Aug 1972, 621-623.
• Stenman, S., & Grans, L. (1997). Symptoms and differential diagnosis of patients fearing mercury toxicity from amalgam fillings: Scandinavian Journal of Work, Environment & Health Vol 23(Suppl 3) 1997, 59-63.
• Stock, A., & Jaensch, E. (1983). Nothing new under the sun: Experiences with mercury poisoning: Journal of Orthomolecular Psychiatry Vol 12(3) 1983, 202-207.
• Tachibana, T. (1989). Behavioral teratogenic insult of methylmercury assessed by using sets of measures: Reanalysis of data from the Collaborative Behavioral Teratology Study of National Center for Toxicological Research: Physiology & Behavior Vol 45(6) Jun 1989, 1243-1247.
• Tanan, C. L., Ventura, D. F., de Souza, J. M., Grotzner, S. R., Mela, M., Gouveia, A., Jr., et al. (2006). Effects of mercury intoxication on the response of horizontal cells of the retina of thraira fish (Hoplias malabaricus): Brazilian Journal of Medical and Biological Research Vol 39(7) Jul 2006, 987-995.
• Tang, N., & Li, Y. M. (2006). Neurotoxic effects in workers of the clinical thermometer manufacture plant: International Journal of Occupational Medicine & Environmental Health Vol 19(3) 2006, 198-201.
• Triebig, G., & Schaller, K.-H. (1982). Neurotoxic effects in mercury-exposed workers: Neurobehavioral Toxicology & Teratology Vol 4(6) Nov-Dec 1982, 717-720.
• Uzzell, B. P., & Oler, J. (1986). Chronic low-level mercury exposure and neuropsychological functioning: Journal of Clinical and Experimental Neuropsychology Vol 8(5) Oct 1986, 581-593.
• Ventura, D. F., Costa, M. T. V., Costa, M. F., Berezovsky, A., Salomao, S. R., Simoes, A. L., et al. (2004). Multifocal and full-field electroretinogram changes associated with color-vision loss in mercury vapor exposure: Visual Neuroscience Vol 21(3) May-Jun 2004, 421-429.
• Watanabe, C., Yin, K., Kasanuma, Y., & Satoh, H. (1999). In utero exposure to methylmercury and Se deficiency converge on the neurobehavioral outcome in mice: Neurotoxicology and Teratology Vol 21(1) Jan-Feb 1999, 83-88.
• Weil, M., Bressler, J., Parsons, P., Bolla, K., Glass, T., & Schwartz, B. (2005). Blood Mercury Levels and Neurobehavioral Function: JAMA: Journal of the American Medical Association Vol 293(15) Apr 2005, 1875-1882.
• Yeates, K. O., & Mortensen, M. E. (1994). Acute and chronic neuropsychological consequences of mercury vapor poisoning in two early adolescents: Journal of Clinical and Experimental Neuropsychology Vol 16(2) Apr 1994, 209-222.
• Zelman, M., Camfield, P. R., Moss, M., Camfield, C., & et al. (1991). Toxicity from vacuumed mercury: A household hazard: Clinical Pediatrics Vol 30(2) Feb 1991, 121-123.
• Zenick, H. (1974). Behavioral and biochemical consequences in methylmercury chloride toxicity: Pharmacology, Biochemistry and Behavior Vol 2(6) Nov-Dec 1974, 709-713.
• Zenick, H. (1974). The behavioral, biochemical, and electrophysiological consequences of methylmercury chloride toxicity: Dissertation Abstracts International.
• Zenick, H. (1976). Evoked potential alterations in methylmercury chloride toxicity: Pharmacology, Biochemistry and Behavior Vol 5(3) Sep 1976, 253-255.

External links

• ATSDR - Toxicological Profile: Mercury at CDC
• National Pollutant Inventory - Mercury and compounds Fact Sheet at Department of the Environment and Water Resources
• Overview at NIH
• Mercury activity at National Internet Science Educational Resource