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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.
- 1 Signs and symptoms
- 2 Causes
- 3 Toxic effects
- 4 Treatment
- 5 Prevention
- 6 Occurrences of mercury poisoning
- 7 See also
- 8 References
- 9 Further reading
- 10 External links
Signs and symptoms[edit | edit source]
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).
Causes[edit | edit source]
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[edit | edit source]
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.
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[edit | edit source]
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[edit | edit source]
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[edit | edit source]
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.
Treatment[edit | edit source]
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[edit | edit source]
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[edit | edit source]
- 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[edit | edit source]
- 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[edit | edit source]
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[edit | edit source]
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[edit | edit source]
- 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[edit | edit source]
- 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[edit | edit source]
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[edit | edit source]
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[edit | edit source]
- Heavy metal poisoning
- Lead poisoning
- Minamata disease, industrial mercury pollution
- Niigata Minamata disease, industrial mercury pollution
References[edit | edit source]
- Sweet LI, Zelikoff JT (2001). Toxicology and immunotoxicology of mercury: a comparative review in fish and humans. J Toxicol Environ Health B Crit Rev 4 (2): 161–205.
- Horowitz Y, Greenberg D, Ling G, Lifshitz M. Acrodynia: a case report of two siblings. Arch Dis Child 2002; 86: 453. PMID 12023189
- United States Environmental Protection Agency (December 1997) (PDF), Mercury Study Report to Congress, 3, Washington, D.C.: United States Environmental Protection Agency, http://www.epa.gov/ttn/oarpg/t3/reports/volume3.pdf
- ToxFAQs: Mercury. Agency for Toxic Substances and Disease Registry. URL accessed on 2007-07-25.
- Goldman, Lynn R., Michael W. Shannon and the Committee on Environmental Health (2001-07). Mercury in the Environment: Implications for Pediatricians. Pediatrics 108 (1): 197-205.
- Pacyna EG, Pacyna JM, Steenhuisen F, Wilson S (2006). Global anthropogenic mercury emission inventory for 2000. Atmos Environ 40 (22): 4048–63.
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- Hendry WF, A'Hern FPA, Cole PJ. Was Young's syndrome caused by mercury exposure in childhood? BMJ 1993;307:1579-82. PMID 8292944
- Bernard, S., A. Enayati, L. Redwood, H. Roger, T. Binstock (April 2001). Autism: a novel form of mercury poisoning. Medical Hypotheses 56 (4): 462-471.
- Mutter J, Naumann J, Schneider R, Walach H, Haley B (2005). Mercury and autism: accelerating evidence?. Neuro Endocrinol Lett 26 (5): 439–46.
- Freitag CM (2007). The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry 12 (1): 2–22.
- Rutter M (2005). Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatr 94 (1): 2–15.
- Francis Weston Sears and Mark W Zemanski (1955). University Physics, 2nd ed., Addison Wesley.
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- Langford, N.J., R.E. Ferner (October 1999). Toxicity of mercury. Journal of Human Hypertension 13 (10): 651-656.
- The Karen Wetterhahn story - University of Bristol web page documenting her death, retrieved December 9th 2006
- OSHA update following Karen Wetterhahn's death
- Emily Oken, Robert O. Wright, Ken P. Kleinman, David Bellinger, Chitra J. Amarasiriwardena, Howard Hu, Janet W. Rich-Edwards, and Matthew W. Gillman (2005). Maternal Fish Consumption, Hair Mercury, and Infant Cognition in a U.S. Cohort. Environmental Health Perspectives 113 (10): 1376-80. PMID 16203250.
- D. Gonzalez-Ramirez, M. Zuniga-Charles, A. Narro-Juarez, Y. Molina-Recio, K. M. Hurlbut, R. C. Dart and H. V. Aposhian (1998). DMPS (2,3-Dimercaptopropane-1-sulfonate, Dimaval) Decreases the Body Burden of Mercury in Humans Exposed to Mercurous Chloride. Journal of Pharmacology and Experimental Therapy 287 (1): 8-12.
- Duhr EF, Pendergrass JC, Slevin JT, & Haley BE. HgEDTA complex inhibits GTP interactions with the E-site of brain beta-tubulin. Toxicol Appl Pharmacol. 1993 Oct;122(2):273-80. PMID 8212009
- ATSDR - Mercury - Regulations and Advisories
- Waldron HA (1983). Did the Mad Hatter have mercury poisoning?. Br Med J (Clin Res Ed) 287 (6409): 1961.
- Stock, Alfred (1926). Die Gefaehrlichkeit des Quecksilberdampfes. Zeitschrift für angewandte Chemie 39: 461-466.
- Hunter, D, Bomford, R R, and Russell, D S (1940). Poisoning by methylmercury compounds. Quart. J. Med. 9: 193-213.
- Engler, Robert (April 27 1985). Technology out of Control. The Nation 240.
- includeonly>Jose Antonio Vargas. "'Mad Scientist': On Court TV, Fatal Chemistry", The Washington Post, 2007-01-26. Retrieved on 2007-01-28.
- Ann Dally (1997). The Rise and Fall of Pink Disease. Social History of Medicine 10 (2): 291-304.
- (2003-10-30)The Toxicology of Mercury — Current Exposures and Clinical Manifestations. The New England Journal of Medicine 349 (18): 1731-1737.
- Mercury and vaccines (thimerosal). Centers for Disease Control and Prevention. URL accessed on 2007-12-25.
- Clifton JC 2nd (2007). Mercury exposure and public health. Pediatr Clin North Am 54 (2): 237–69, viii.
- Counter, S. Allen (Dec 16, 2003), Whitening skin can be deadly, The Boston Globe, http://www.boston.com/news/globe/health_science/articles/2003/12/16/whitening_skin_can_be_deadly/
- Mercury in Cosmetic Skin Whitening Creams, http://www.hgtech.com/Data/Other/Hg%20Cream.htm
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Further reading[edit | edit source]
- 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.
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- 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
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