As with other metals, mercury exists in multiple oxidative states, as inorganic salts, and as organic complexes. The oxidative states include elemental mercury (Hg0), mercurous (Hg+1), or mercuric (Hg+2). Inorganic mercury compounds are generally in solid states as mercurous or mercuric salts and mercury compounds with chlorine, sulfur, or oxygen. Methylmercury and ethylmercury are common organic forms of mercury combined with carbon. Organic mercury compounds are formed when mercury combines with carbon. Microscopic organisms in water and soil can convert elemental
and inorganic mercury into an organic mercury compound, methylmercury, which accumulates in the food chain. Mercury in any form is toxic.
Mercury is one of the most toxic elements on our planet and exhibits varying levels of toxicity in each form, caused in part by varying routes of exposure, doses, and sites of deposition. Toxicity aside, Hg has many chemical properties that have made it useful to humans. There is evidence that Hg has been utilized throughout antiquity. Prehistoric cave drawings were made using cinnabar, the red ore containing mercuric sulfide. The Romans mined cinnabar to extract mercury and operated a Hg mine in Spain with prisoner and slave labor. They used Hg as a pigment in their paint; mercury-containing paint has been found in Roman homes buried by the volcanic ash of Mount Vesuvius in 79CE. The use of Hg in paint has continued into the modern area, although in recent history, mercury was added as a fungicide rather than for its chromatic properties. It was not until 1991 that the use of Hg in paint was phased out in the United States.
Thomas Edison’s incandescent lamp contained Hg (to this day compact fluorescent lightbulbs have Hg added to them). In 1894, H.Y. Castner discovered that Hg could be used in the chlor-alkali process to produce chlorine and caustic soda. And during WWII, the Ruben-Mallory battery (mercury dry-cell battery) was invented and widely used. By the 1960s, the production of electrical apparati, caustic soda, and chlorine accounted for over 50% of mercury uses. Caustic soda is largely associated with the paper industry; it is used to achieve whiter paper. Except for manufactures in China, chlor-alkali production has now shifted to a non-mercury method. However, the chlor-alkali industry still accounts for 1% of total Hg emissions into the atmosphere and potentially a much larger contribution to water and land releases.
The historical use of Hg has set the stage for many of the modern products and processes that utilize mercury. It is estimated that, over the last 4000 years, historical and continued use of mercury have released 350,000 tons of Hg from the depths of the earth into air, surface land, and water, where its toxicity becomes problematic for human health and Earth’s sensitive biosphere.
Early human interest in Hg was raised by its unique physical appearance: a liquid metal must have magical, and therefore, curative properties, and in this capacity, it was used as a germicide before the discovery of germs. Besides its germicidal effects, liquid mercury is a good electrical conductor, has high density and surface tension, and responds uniformly to changes in temperature and pressure.
Over the last three decades, numerous articles
have appeared on the toxic effect of mercury on humans. This growing interest in mercury toxicity
is due to increased exposure of mercury from environmental sources as well as from dental mercury amalgams. Mercury contamination of the oceans eventually finds its way into food resources, and fish are becoming another primary source of this corruption. Over 20,000 tons of mercury are released into the environment each year by human activities, including byproducts from the combustion of fossil fuels and regular dumping of industrial waste.
Atomic mass: 200.59
Sources of Exposure
The following are all potential Hg sources: mercury amalgam dental fillings, air pollution - especially in dental offices and near crematoriums that incinerate mercury amalgam fillings, mercury batteries, cosmetics, diuretics (mercurial), vaccines (see thimerosal below) electrical devices and relays, explosives, foods (grains), fungicides, fluorescent lights, freshwater fish (especially large bass, pike, and trout), saltwater fish (especially large halibut, shrimp, snapper, and swordfish), shellfish, and tap water, mining, paints manufactured outside the United States.
Mercuric chloride is used for many applications including wood preservative, photographic intensifier, dry battery depolarizer, tanning agent for leather, catalyst in the manufacture of chemicals such as vinyl chloride and disinfectants, separating lead from gold, and others.
Mercuric nitrate, commonly used in the felting industry, is the source of the neurological changes observed in felters in the 1800s that led to the term “mad as a hatter”. Inorganic mercury, found mostly in the mercuric salt form (eg, batteries), is both toxic and corrosive.
Elemental mercury is found as a liquid and is extremely volatile. Since mercury easily vaporizes at room temperature, the route of absorption is often through the lungs. In humans, approximately 70-85% of a dose is absorbed in this manner - whereas less than 3% of a dose will be absorbed dermally. If elemental mercury is ingested orally, less than 0.1% is absorbed from the gastrointestinal (GI) tract and, therefore, when orally ingested is only mildly toxic.
Elemental mercury (Hg0) is highly lipid soluble - a characteristic that facilitates its diffusion across the alveoli into the circulation, as well as its distribution throughout the lipophilic compartments of the body - including passage across the blood-brain barrier into the central nervous system (CNS) and across the placenta. In the circulation, elemental mercury binds to numerous tissues, proteins, and erythrocytes. In erythrocytes, catalase can oxidize elemental mercury to an inorganic metabolite. If elemental mercury penetrates the blood-brain barrier, it is ionized and becomes trapped in the compartment where it is available to exert its neurotoxicity. Elemental mercury has the longest retention in the brain with detectable levels present for years following exposure. The half-life of elemental mercury in adults is approximately 60 days (range: 35 to 90 days).
Inorganic mercury salts are found in 2 oxidation states: mercurous (Hg+1), or mercuric (Hg+2). Common routes of inorganic mercury exposure include the GI tract (following oral ingestion) and the skin. Studies using volunteers have shown that about 7% to 15% of an ingested dose of mercuric chloride is absorbed from the GI tract. Absorption is, in part, related to the water solubility of this compound. It has a non-uniform mode of distribution secondary to poor lipid solubility.
The highest accumulation of inorganic mercury is in the kidneys. Animal studies suggest that mercuric forms have a high affinity for metallothionein in renal cells. In contrast, methylmercury has low affinity for metallothionein. Excretion of inorganic mercury, as with organic mercury, is mostly through feces.
The organic mercury compounds are of great interest today because they are often found in the food chain and have been used to inhibit bacterial growth in medications. Organic mercury is also found in fungicides and industrial run-off. As a result, exposure to these materials is common. Organic mercurials are absorbed more completely from the GI tract than inorganic salts in part because they are more lipid soluble and because they bind to sulfhydryl groups. More often, organic mercurials are absorbed from the GI tract by forming a complex with L-cysteine and crossing cell membranes on the large neutral amino acid carrier. They are also corrosive, although less corrosive than inorganic forms.
Organic mercurials also cross the blood-brain barrier and placenta and penetrate erythrocytes, attributing to neurological symptoms, and teratogenic effects. Methylmercury has a high affinity for sulfhydryl groups, which explains its effect on enzyme dysfunction. One enzyme that is inhibited is choline acetyl transferase, which is involved in the final step of acetylcholine production. This inhibition may lead to acetylcholine deficiency, contributing to the signs and symptoms of motor dysfunction, like Parkinson’s disease. Excretion of alkyl mercury occurs mostly in the form of feces (90%), secondary to significant enterohepatic circulation. The biological half-life of methyl mercury is approximately 65 days.
Dental Mercury Amalgam
In the 1830′s, a revolutionary new dental restorative material called “amalgam” was introduced to the United States. This amalgam was developed in England and France and contained silver, tin, copper, zinc and mercury (as much as 50% mercury). The amalgam fillings were not openly embraced by organized dentistry in America: in 1840, members of the American Society of Dental Surgeons were required to sign pledges not to use mercury fillings. In fact, several New York City dentists were suspended from this organization in 1848 for “malpractice for using mercury fillings”. In 1859, a new organization was formed as a result of the internal strife over the use of mercury in dentistry: the American Dental Association.
In 1988, the Environmental Protection Agency declared dental mercury amalgam a toxic material to be deposed of in toxic waste sites. In 1990, the World Health Organization stated that there is zero tolerance to mercury in humans. They further stated that the greatest source of mercury contamination in all populations was dental amalgam. Mercury comprises approximately 50% of an amalgam filling. When chewing or eating hot or acidic foods, mercury vapors are given off and small particles of mercury are released into the body. In addition, mercury vapors are inhaled, while particles are absorbed by tooth-roots, the mucous membranes of the mouth and gums. The esophagus and stomach lining directly absorb mercury into the lymphatic system and/or bloodstream. The output of mercury can be intensified by the number of fillings and other activities, such as chewing, teeth-grinding, and the consumption of hot liquids. Mercury is also known to be released during the placement, replacement, and removal of dental mercury amalgam fillings.
In people with mercury amalgam fillings, measurements of the mercury level in the mouth ranges between 20 and 400 mcg/m3. Keep in mind that this is continuous exposure. The National Institute of Occupation Safety and Health places the safe limit of environmental exposure to mercury at 20 mcg/m3, but this assumes a weekly exposure of 40 hours (the work week) and that the mercury involved is outside the body. The Environmental Protection Agency's allowable limit for continuous mercury exposure is 1 mcg/m3 but, again, this is based on mercury sources outside the body. Neither figure addresses 24-hour-a-day exposure from mercury in one's mouth.
In 1984, the American Dental Association (ADA), without providing scientific evidence, claimed that only 5% of the U.S. population is reactive to mercury exposure, and that this figure is “insignificant”. Meanwhile, the ADA mandates that dentists alert all dental personnel to the potential hazards of inhaling mercury vapors. The Environmental Protection Agency (EPA) goes further, instructing dentists to treat mercury amalgam as a toxic material while handling before insertion, and as toxic waste after removal.
Ever since dentists first started installing amalgams in their patients' teeth, there has been an issue as to whether mercury would be released and cause health (pathophysiologic) problems. In 1984, a group of conscientious dentists formed the International Academy of Oral Medicine and Toxicology (IAOMT). One of their objectives was to scientifically explore the safety of amalgam restorations. Members of the IAOMT have inspired many renowned medical scientists at universities around the world to research possible pathophysiologic effects associated with mercury leaking from amalgam restorations. To their credit is a growing number of scientific studies that document pathophysiologic effects associated with amalgam mercury.
The IAOMT has developed extensive safety recommendations for the removal of existing dental mercury amalgam fillings. The IAOMT protocol recommendations were officially renamed the Safe Mercury Amalgam Removal Technique (SMART), and training courses for IAOMT dentists to become certified in SMART is now available. The IAOMT has published a position statement against dental mercury amalgam fillings for medical and dental practitioners, dental students, dental patients, and policymakers.
Another source of mercury exists in the form of thimerosal (ethylmercury-thiosalicylate) which is 49.6% ethylmercury by weight. Developed by the pharmaceutical company Eli Lilly in 1928, over the years thimerosal has been used in a variety of medical products, including topical antiseptics, nasal sprays, eye drops, immune globulin products, and vaccines. The Eli Lilly Material Safety Data Sheet (MSDS) for thimerosal acknowledges that exposure to thimerosal in utero and in children can cause “mild to severe mental retardation and mild to severe gross motor impairment.” The Sigma Aldrich MSDS lists abortion and fetal death as possible outcomes of in utero exposure.
After increased concern and protest by numerous toxicologists that the amount of mercury in the childhood vaccination schedule recommended by the CDC exceeded all national and global maximum safety limits, the American Academy of Pediatrics and the United States Public Health Service called for the immediate removal of thimerosal from all vaccines on July 7, 1999. Today, however, several vaccines still contain thimerosal - the most notable being the seasonal influenza (flu) vaccine. Most, but not all, influenza vaccines still contain thimerosal. Also, many vaccines used in third world countries still contain mercury exceeding US safety guidelines. Because of its application as a vaccine preservative, almost every human and animal (domestic and farmed) that has been immunized with thimerosal-containing vaccines has been exposed to ethylmercury.
Depending on the vaccines administered, at six months of age, infants born today to mothers who received flu vaccines during pregnancy could receive up to 71 mcg of ethylmercury compared to 187.5 mcg prior to efforts to decrease the amount of thimerosal in infant vaccines. Moreover, the new CDC guidelines recommend that all children from 2 to 5 years of age receive an annual influenza vaccine. As a result, the total amount of thimerosal given to children under 5 years of age is almost what it was prior to 2000.
The following data includes levels of mercury in parts per billion:
0.5 parts per billion (ppb) mercury = Kills human neuroblastoma cells (Parran et al., Toxicol Sci 2005; 86: 132-140).
2 ppb mercury = U.S. EPA limit for drinking water.
20 ppb mercury = Neurite membrane structure destroyed (Leong et al., Neuroreport 2001; 12: 733-37).
200 ppb mercury = level in liquid the EPA classifies as hazardous waste.
25,000 ppb mercury = Concentration of mercury in the Hepatitis B vaccine, administered at birth in the U.S., from 1990-2001.
50,000 ppb Mercury = Concentration of mercury in multi-dose DTaP and Haemophilus B vaccine vials, administered 4 times each in the 1990's to children at 2, 4, 6, 12 and 18 months of age.
50,000 ppb Mercury = Current "preservative" level mercury in multi-dose flu (94% of supply), meningococcal and tetanus (7 and older) vaccines. This can be confirmed by simply analyzing the multi-dose vials.
Further information on vaccines that contain significant amounts of thimerosal can also be found on the Food and Drug Administration's website and Johns Hopkins Bloomberg School of Public Health's Institute for Vaccine Safety website.
For children, thimerosal is 50 times more toxic than methylmercury (MeHg). The reasons for this include:
Injected mercury is more toxic than ingested mercury.
The blood-brain barrier in infants is far more permeable than adults. Without a complete blood-brain barrier, an infant's brain and spinal cord are vulnerable to exposure.
Mercury accumulates in brain cell and nervous tissue. Once in the nerve cells, mercury is changed back to the inorganic form and becomes tightly bound. Mercury can then remain for years, like a time-release capsule, causing permanent degeneration and death of brain cells.
Infants do not produce bile, which is necessary to excrete mercury.
Thimerosal is a poison, neurotoxin, carcinogen, and can interrupt the immune system and the normal development of an unborn baby or a child. Studies show that thimerosal at relatively low doses causes apoptosis (cell death) in neuronal cells via the mitochondrial pathway. Continued efforts are needed to find an anti-microbial and preservative compound to replace thimerosal in vaccines, cosmetics, and ophthalmic solutions.
Basically, mercury can travel anywhere in the body and especially gravitates into the nervous system (central and peripheral), appetite and pain centers in the brain, cell membranes, kidneys, liver, and glandular tissue such as thyroid, breast, prostate and ovaries. Other areas include, but are not limited to, the jawbone, eyes, ears, cranial nerves, connective tissue (extracellular matrix) bone and skin.
Cysteine, an essential amino acid, can be depleted with the chronic stress of metal burden. Cysteine becomes a pivotal factor to support detoxification and the body's attempt to produce more GSH and metallothionein. Interestingly, evidence from animal studies clearly indicates supplementation of cysteine at high doses can increase the transport
of Hg into the brain. Pregnant rats received intravenous infusions of saline, L-cysteine,
L-leucine, or GSH prior to infusion of MeHg. Although total body Hg was similar for all groups
of pups and dams, brain Hg concentrations were significantly increased in dams and pups given cysteine. In contrast, brain Hg levels were lower for the animals receiving intravenous GSH.
In subsequent studies it was clearly demonstrated that the mechanism for transport of MeHg across the blood-brain barrier is the large neutral amino acid (LNAA) transport system, also known as the L (leucine-preferring) system. Based on these studies, it is suggested high doses (e.g. 500 mg three times daily) of cysteine (as L-cysteine or N-acetylcysteine) in a metal-burdened patient can facilitate redistribution of Hg from tissues and organs throughout the body into the brain, where it elicits its insidious neurotoxic effects. It should be noted intravenous administration of GSH had protective effects on brain Hg accumulation, but it cannot be assumed high doses of GSH administered orally would have the same beneficial effect, due to the potential for hydrolysis of GSH in the gastrointestinal tract.
L-leucine inhibits transport of the MeHg-cysteine complex across the blood brain barrier. Therefore, it seems prudent to provide small amounts of cysteine in conjunction with sufficient quantities of leucine and the other amino acids which compete for the L-amino acid transport system, including valine, isoleucine, phenylalanine, tyrosine and tryptophan. Whey protein, derived from milk, contains about 2.53.0% cysteine/cystine and about 22-25% branched-chain amino acids. Therefore, a high quality, partially hydrolyzed whey protein product provides a good source of cysteine/cystine to support intracellular GSH production and metallothionein synthesis, yet adequate leucine to minimize the transport of metals into the CNS. Partial hydrolysis of whey protein yields about 10% di-, tri-, and oligopeptides. Low temperature, enzymatic hydrolysis appears to be the preferred method of production. It is noteworthy that undenatured whey protein has been reported to enhance immune function. An alternative to whey protein might be to provide reasonable amounts of N-acetylcysteine (200-300 mg daily) with a relatively high (quantity and quality) protein diet. The important point here is that pharmacological doses of cysteine/NAC, in the range of 1500 mg daily, have the potential to exacerbate the adverse neurological effects of toxic metals.
Provision of cysteine/cystine in a complete, balanced source of protein will also provide important amino acids that are precursors to neurotransmitters. Cell studies indicate Hg exposure directly affects uptake and release of dopamine, norepinephrine, and serotonin. Indirectly, Hg burden can be associated with depletion or poor assimilation of specific amino acids that are precursors of neurotransmitters. For example, taurine is a neurotransmitter derived from methionine/cysteine. Available pools of these sulfhydryl amino acids can be depleted by the metal-induced high turnover of GSH. Persistent candidiasis/dysbiosis associated with Hg burden can compromise the absorption of aromatic amino acids such as phenylalanine/tyrosine and tryptophan, which are precursors to dopamine/norepinephrine and serotonin, respectively.
Cysteine and Mercury Translocate Across the Blood-Brain Barrier
Mercury is called the “great masquerader” because of its many and varied symptomatic effects, such as: abnormal nervous and physical development (fetal and childhood), anemia, anorexia, anxiety, blood changes, blindness, blue line on gums, cancer, colitis, depression, dermatitis, difficulty chewing and swallowing, dizziness, drowsiness, emotional instability, fatigue, fever, hallucinations, headache, hearing loss, hypertension, inflamed gums, insomnia, kidney damage or failure, loss of appetite and sense of smell, loss of muscle coordination, memory loss, metallic taste in mouth, nerve damage, numbness, psychosis, salivation, stomatitis, tremors, vision impairment, vomiting, weakness, and weight loss.
Mercury most commonly affects the neurologic, gastrointestinal, and renal organ systems. Because it can readily cross the blood-brain barrier, Hg exerts its toxic effects primarily on the central nervous system, but further studies have shown toxic effects on the immune system. Most toxicologists studying the effects of mercury agree upon the following six basic mercury-induced disorder categories:
Emotional manifestations (depression, suicidal impulses, irritability, inability to cope) and motor symptoms (muscle spasms, facial tics, seizures, multiple sclerosis)
Nonspecific chest pain, arrhythmias, and cardiac myopathy
Arthritis, bursitis, autoimmune diseases - scleroderma, and systemic lupus erythematosus
Cancer and compromised immunity
Airborne allergies, food allergies, and "universal" reactors. One of the keys to mercury's effects on health may be its ability to block the functioning of minerals such as selenium, zinc, manganese and iodine.
The endocrine system is also affected by Hg burden. Like cadmium, Hg inhibits the conversion of thyroxine (T4) to active T3. It has been suggested the metal-induced inhibition of the 5'deiodinase enzyme is related to general peroxidative effects; however, the inhibition by Hg may be more specific. Hg is known to irreversibly bind to and "waste" selenium, and 5'deiodinase is a selenium-dependent enzyme. Therefore, Hg may inhibit the conversion of T4 to T3 by interfering with selenium availability.
Hg may also interfere with progesterone metabolism without affecting serum levels of progesterone. In vitro studies indicate Hg binds to a free sulfhydryl group on the progesterone receptor and may thereby diminish progesterone binding and cellular response.
The aforementioned Hg-induced disruptions in hormone metabolism could certainly contribute to chronic fatigue, which is one of the hallmark features of Hg burden. Another possible link of metal toxicity to chronic fatigue is via metal binding to the sulfhydryl-containing antioxidant, lipoic acid, making lipoic acid unavailable for its vital role in the energy-producing tricarboxylic acid (citric acid, Krebs) cycle.
For a long time, the finger-to-nose test was part of the periodic medical examination of mercury-exposed workers, but with decreasing level of exposure there was a need for instrumental tests which give numerical values for tremor, skill, coordination and nerve conduction velocity.
Signs & Symptoms
Nutrients Known to be Protective Against Mercury
Sulfur containing amino acids
(L-cysteine or N-acetylcysteine, IV Glutathione), methylsufonyl methane, L-leucine, glycine, cilantro, certain algae (laminaria, fucus, chlorella), selenium, Vitamin E, and vitamin C all are antagonistic for reuptake and retention of mercury.
Protocols for Mercury Detoxification
There exist numerous opinions as to how to detoxify from (and what to detoxify with) regarding mercury. Some protocols are well thought out, whereas others are not. While the jury is still out on optimal mercury detoxification, the golden rule is to always be cautious!
The following may serve as a basic guideline for detoxification of excess mercury caused by chronic exposure.
Before initiating a detoxification program, a CBC with chemistry, including a thyroid panel with lipids should be performed. In addition, whole blood elements to assess the mineral status and a urine creatinine clearance should be performed every 60 days when using synthetic detoxifying agents.
Administration of glycine and synthetic agents may cause a depletion of essential elements such as zinc, iron, calcium, magnesium, copper and other trace minerals. Of greatest concern is potential kidney toxicity that can occur when the body releases its mercury stores for excretion through the kidneys.
Those with underlying kidney disease may not be able to undergo aggressive mercury detoxification therapy.
1. First, identify the source(s) of mercury in the individual’s environment (mouth) and remove them. Check for dental mercury amalgams and refer patient to a biological dentist that is SMART protocol certified as described by the International Academy of Oral Medicine and Toxicology (IAOMT).
2. Assess whole blood cell element analysis to determine mineral nutrient deficiency and supplement appropriately; repeat every 60 days.
3. Supplement 200 mcg of selenium daily. Do not use selenium concurrently with DMSA. (See DMSA precautions.)
4. Supplement buffered vitamin C (corn free source) at 2000 mg up to 5000 mg daily adjusting to bowel tolerance.
5. Supplement vitamin E at 400 to 800 IU daily.
6. Supplement Alpha Lipoic Acid at 250 mg twice daily.
7. Algal cells have a remarkable ability to take up and accumulate heavy metals from their external environment. The primary ones used for toxic metal excess is Chlorella vulgaris, a green microalga, and Laminaria japonica, a brown alga. Chlorella and Laminaria japonica are both chelators, moving toxic metals out of the body, and transporters, moving metals from deeper stores to more readily removal areas. Both work in unison with each other and can remove toxic metals from the body through urinary excretion. Administer 1000 to 2000 mg of Laminaria japonica concentrate (Modifilan) daily and 1000 to 2000 mg of chlorella. Adjust dosage to bowel tolerance; may be taken for long periods of time.
8. Cilantro works well with alga to chelate, or bind, up toxic metals. The issue with cilantro taken alone is that although it chelates metals, it does not remove them in the urine. This means they can recirculate to deposit elsewhere in the body. Hence, taken with alga, metals are more effectively eliminated in the urine.
9. Shilajit is an ancient traditional medicine (Tibetan and Ayurvedic) and has been ascribed a number of pharmacological activities and has been used for ages as a rejuvenator and for treating a number of disease conditions. It is an effective detoxifier of metals and contains over 60 minerals. Modern scientific research has systematically validated a number of properties of shilajit and has proven that shilajit is truly a panacea. It is important to purchase the highest grade of shilajit.
10. Thiol-containing chelating agents such as 2,3-dimercaptosuccinic acid (DMSA, succimer) or 2,3- dimercapto-1-propane sulfonic acid (DMPS), which compete with endogenous sulfhydryl groups have all been used for treating mercury toxicity. One of the most effective of these detoxifying agents for mercury is DMPS which is usually administered by slow IV push or sometimes intramuscularly – but with some discomfort. Those versed in neural therapy have injected DMPS into mercury-intoxicated ganglia with excellent results. DMPS reaches the saliva, hence is not appropriate for those that still have amalgam fillings, unless used only as a challenge substance for testing. DMPS may be dosed orally as well (see DMPS information). Administer oral reduced L-glutathione at 5 to 10 mg per KG of body weight in divided doses on the day before detoxification with DMPS. Reduced GSH further enhances urinary mercury excretion. Do not administer cysteine, N-acetylcysteine, or glutathione concurrently with DMPS, DMSA or D-Penicillamine. The result will yield disulfide formation with a reduced excretion of mercury. Glutathione is contraindicated in insulin deficiency.
11. Instruct patient to drink adequate amount of pure water (adult’s urine volume should be about 2 liters per day).
Acute mercury poisoning is a medical emergency. For acute exposure, seek immediate medical attention and call Poison Control Services. As with all detoxification protocols, the type, dose and duration of detoxification agents should always be individually assessed and administered by a licensed medical practitioner.
Al-Neamah, Ghusoon AK, Rajiha A. AL Naimiand Eman HY, and Al Taae. Assessment the therapeutic effects of aqueous extracts of Cilantro and Garlic in mercuric chloride poisoning in rats.
Aschner M, Clarkson TW. Distribution of mercury 203 in pregnant rats and their fetuses following systemic infusions with thio-containing amino acids and glutathione during late gestation. Teratol 1988;38:145-155.
Aschner M, Eberle NB, Miller K, Kimelberg HK. Interactions of methylmercury with rat primary astrocyte cultures: inhibition of rubidium and glutamate uptake and induction of swelling. Brain Res 1990; 530:245-250.
Baum CR. Treatment of mercury intoxication. Curr Opin Pediatr 1999 Jun;11(3): 265-8.
Benov LC, Benchev IC, Monovich OH. Thiol antidotes effect on lipid peroxidation in mercury-poisoned rats. Chem Biol Interact 1990;76:321-332.
Belles M, Sanchez DJ, Gomez M, Domingo JL, Jones MM, Singh PK. Assessment of the protective activity of monisoamyl meso-2,3-dimercaptosuccinate against methylmercury-induced maternal and embryo/fetal toxicity in mice. Toxicology 1996; 106(1-3):93-97.
Björkman L, Lind B. Factors influencing mercury evaporation rate from dental amalgam fillings. Scand J Dent Res. 1992; 100(6):354–60.
Brown, L. E., and L. Yel. Thimerosal induces programmed cell death of neuronal cells via changes in the mitochondrial environment. UCI Undergrad. Res. J 6 (2003): 7-14.
Campbell, J. R., Clarkson, T. W., and Omar, M. D. (1986) The therapeutic use of 2,3-dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning. J. Am. Med. Assoc. 256, 3127- 3130.
Clarkson, T. W., Magos, L., and Myers, G. J. (2003). The toxicology of Mercury - Current exposures and clinical manifestations. N. Engl. J. Med. 349, 1731-1737
Gonzalez-Ramizez, D., Maiorino, R. M., Zuniga-Charles, M., Xu, Z., Hurlbut, K. M., Junco-Munoz, P., Aposhian, M. M., Dart, R. C., Diaz Gama, J. H., Echeverra, D., Woods, J. S., and Aposhian, H. V. (1995). Sodium 2,3-dimercaptopropane-1-sulfonate challenge test for mercury in humans: II. Urinary mercury, porphyrins and neurobehavioral changes of dental workers in Monterrey, Mexico. J. Pharmacol. Exp. Ther. 272, 264-274.
Haley BE, Virtue WE. Position statement on dental amalgam from the International Academy of Oral Medicine and Toxicology submitted to the European Commission. IAOMT; October 10, 2012. Available from IAOMT website. Accessed December 22, 2015.
Humphrey, Michelle L., et al. Mitochondrial mediated thimerosal-induced apoptosis in a human neuroblastoma cell line (SK-N-SH). Neurotoxicology 26.3 (2005): 407-416.
Hursh JB, Clarkson TW, Miles EF, et al. Percutaneous absorption of mercury vapor by man. Arch Environ Health. 1989;44:120-127.
Isaac Eliaz, M. D. MINDING Your MERCURY: Solutions to Mercury Toxicity. Alternative Medicine 13 (2013): 44.
Issa, Y., D.C. Watts, A.J. Duxbury, P.A. Brunton, M.B. Watson, and C.M. Waters. Mercuric Chloride: Toxicity and Apoptosis in a Human Oligodendroglial Cell Line MO3.13. Biomaterials 24.6 (2003): 981-987.
Jativa, Liliana. Reducing the Negative Impact of Mercury Exposure Using Native Food Plants as Heavy Metal Scavengers.
Karper LE, Ballatori N, Clarkson TW. Methylmercury transport across the blood-brain barrier by an amino acid carrier. Am J Physiol. 1992; 267:R761-R765.
Kaplan, Drora, Daniel Christiaen, and Shoshana Malis Arad. Chelating properties of extracellular polysaccharides from Chlorella spp. Applied and environmental microbiology 53.12 (1987): 2953-2956.
Keller, Jeffrey N., Keith B. Hanni, and William R. Markesber. 4- Hydroxynonenal Increases Neuronal Susceptibility to Oxidative Stress. Journal of Neuroscience Research 58 (1999): 823-830.
Kerper LE, Ballatori N, Clarkson TW. Methyl-mercury transport across the blood-brain barrier by an amino acid carrier. Am J Physiol 1992;262:R761-R765.
Kershaw TG, Clarkson TW, Dhahir PH. The relationship between blood-brain levels and dose of methylmercury in man. Arch Environ Health. 1980;35:28-36.
Kidd, Robert F. Results of dental amalgam removal and mercury detoxification using DMPS and neural therapy. Alternative therapies in health and medicine 6.4 (2000): 49.
Klinghardt, D., M.D., P.h.D. Migraines, seizures, and mercury toxicity. Alternative Medicine Digest 21 (December-January 1997-98).
Kroemer, G. and J.C. Reed. Mitochondrial Control of Cell Death. Natural Medicine 6 (2000): 513-519.
Leong, Christopher CW, Naweed I. Syed, and Fritz L. Lorscheider. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport 12.4 (2001): 733-737.
Makani, S., S. Gollapudi, L. Yel, S. Chiplunkar, and S. Gupta. Biochemical and Molecular Basis of Thimerosal-induced Apoptosis in T Cells: A Major Role of Mitochondrial Pathway. Genes and Immunity 3 (2002): 270-278.
Miller A. Dimercaptosuccinic acid (DMSA), a non-toxic, water-soluble treatment for heavy metal toxicity. Altern Med Rev 1998;3:199-207.
Moyer TP. In: Burtis and Ashwood, eds, Tietz Textbook of Clinical Chemistry. 3rd ed. 1999; 992- 993.
Nagashima, Kazuo, Yukiko Fujii, Tetsu Tsukamoto, Souichi Nukuzuma, Mami Satoh, Miri Fujita, Yasunori Fujioka, and Hirokatsu Akagi. Apoptotic Process of Cerebellar Degeneration in Experimental Methylmercury Intoxication of Rats. Acta Neuropathologica 91 (1995): 72-77.
Njue, Martin Kivuti. Using Cilantro Leaves and Stems to Remove Lead, Cadmium and Turbidity from Contaminated Water. Diss. Kenyatta University.
Nylander M, Friberg L, Lind B. Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Swed Dent J. 1987; 11(5): 179-187.
Omura Y, Beckman SL. Role of mercury (Hg) in resistant infections & effective treatment of Chlamydia trachomatis and Herpes family viral infections (and potential treatment for cancer) by removing localized Hg deposits with Chinese parsley and delivering effective antibiotics using various drug uptake enhancement methods. Acupunct Electrother Res. 1995 Aug-Dec;20(3-4):195-229.
Parran, Damani K., Angela Barker, and Marion Ehrich. Effects of thimerosal on NGF signal transduction and cell death in neuroblastoma cells. Toxicological Sciences 86.1 (2005): 132-140.
Piyasirisilp, Sucheep and Thiravat Hemachudha. Neurological Adverse Events Associated with Vaccination. Current Opinions in Neurology 15 (2002): 333-338.
Policy Statement of the American Academy of Pediatrics. Thimerosal in Vaccines-An Interim Report to Clinicians. Pediatrics 104.3 (1999): 570-574.
Reinhardt JW. Side-effects: Mercury contribution to body burden from dental amalgam. Adv Dent Res. 1992; 6(1):110-3.
Schiele R, Schaller KH, Welte D: Mobilization of mercury reserves in the organism by means of DMPS. Occup Med Soc Med Prevent Med 1989;24: 249-251.
Shenker, Bruce J., Tai L. Guo, and Irving M. Shapiro. Low-Level Methylmercury Exposure Causes Human T-cells to Undergo Apoptosis: Evidence of Mitochondrial Dysfunction. Environmental Research Section A 77 (1998): 149-159.
Shenker, Bruce J., Tai L. Guo, and Irving M. Shapiro. Mercury-induced Apoptosis in Human Lymphoid Cells: Evidence that the Apoptotic Pathway is Mercurial Species Dependent. Environmental Research Section A 84 (2000): 89-99.
Snapp KR, Svare CW, Peterson LD. Contribution of dental amalgams to blood mercury levels. J Dent Res. 1981; 65(5): 311, Abstract #1276, Special issue.
Stock A. [Zeitschrift für angewandte Chemie, 29. Jahrgang, 15. April 1926, Nr. 15, S. 461-466, Die Gefährlichkeit des Quecksilberdampfes, von Alfred Stock (1926).] The Dangerousness of Mercury Vapor. Translated by Birgit Calhoun.
Thimerosal in Vaccines. Centers for Disease Control National Immunization Program.
Vimy MJ, Lorscheider FL. Intra-oral air mercury released from dental amalgam. J Den Res. 1985; 64(8):1069-71.
Vimy MJ, Lorscheider FL: Serial measurements of intra-oral air mercury; Estimation of daily dose from dental amalgam. J Dent Res. 1985; 64(8):1072-5.
Vimy MJ, Luft AJ, Lorscheider FL. Estimation of mercury body burden from dental amalgam computer simulation of a metabolic compartment model. J. Dent. Res. 1986; 65(12):1415-1419.
Waterhouse, Nigel J. and Douglas R. Green. Mitochondrion and Apoptosis: HQ or High-Security Prison? Journal of Clinical Immunology 19 (1999): 378-387.
Xue H.B., W.Stumm, L.Sigg: The Binding of Heavy Metals to Algal Surfaces, Water Res 1988;22, 917.
Zahir F, Rizwi SJ, Haq SK, Khan RH. Low dose mercury toxicity and human health. Environ Toxicol Pharmacol. 2005; 20(2): 351-360.