Mercury, with its unique properties, was discovered in antiquity as far back as 3500 years ago (Royal Society of Chemistry, 2017). Originally, it was called Hydrargyrum which is a Latin-based word meaning “water silver” or “liquid silver” (Harper, 2017). Mercury, as Figure 1 depicts, remains as Hydrargyrum (Hg) in the periodic with its atomic weight and corresponding atomic number. Mercury directly follows the 79-element gold (Au). It is the only metal that is in a liquid state at room temperature (Han et al., 2014). Mercury can readily be found in one of three forms, that of elemental mercury (Hg) usually in vapor or liquid form, inorganic mercury (iHg) usually in combination with another compound such as sulfur, and organic mercury (oHg) as methyl-mercury (MeHg) and ethyl-mercury (EtHg) (Crowe et al., 2017).
Toxic Properties of Mercury
Mercury inhalation, ingestion, and/or absorption have been attributed to a plethora of diseases. It has been associated with neurological disease, kidney disease, cardiovascular disease, autoimmune disease, endocrine disease, and muscular dysfunction. It has also been controversially associated with causing behavioral disorders and even Parkinson’s and Alzheimer’s disease (Bernhoft, 2012; Crowe et al., 2017; Hornsted-Bindslev, 2004; Houston, 2007). Tissue and organ damage is the main concern with exposure to Hg and it appears that it is chronic exposure to the specific form of methyl-mercury that is of greatest concern to living organisms. It is proposed that the accumulation of Hg in the tissues results in Hg poisoning rather than a single exposure. When chronic exposure to any form of Hg ceases, there is an estimated half-life in the brain of the exposed organism of one year with a range up to 18 years (Mutter et al., 2004). The mechanisms of action that produce toxic effects appear to be multifaceted. One known effect of Hg intoxication is from a dramatic increase in systolic and diastolic blood pressure of higher organisms. This rise in blood pressure is directly related to a MeHg mediated response of a loss of endothelium-dependent vasorelaxation (Omanwar et al., 2013; Houston, 2007). Methyl-mercury has also been shown to interfere with DNA transcription and protein synthesis. This includes protein synthesis in the developing brain and therefore is of great concern in pregnancy (Bernhoft, 2012). Other studies have shown that MeHg produces actual cellular death of mononuclear cells in blood at a lower concentration than inorganic mercury (Crowe et al., 2017).
Testing for Mercury exposure
Several tests are available to indicate whether an exposure to Hg has occurred along with the degree of the exposure. Urine samples are the easiest to test, however, such a test only indicates an exposure to elemental or inorganic mercury. Urine samples reflect the cumulative exposure of inorganic Hg in the kidneys and have a weak correlation to levels in other organs (Mutter et al., 2004; McKelvey et al., 2007). Blood tests can be obtained which indicate an exposure to the more toxic form of Hg that is methyl-mercury (Ucar and Brantley, 2011). However, the half-life of mercury in blood is approximately three days. Therefore, blood tests are usually not a reliable indicator of chronic exposure. Blood tests must therefore be performed as soon as possible post-exposure to indicate the degree of exposure to Hg (Mutter et al., 2004).
However, urine and blood concentrations of Hg do not necessarily relate to the amount of Hg contained in the tissues of an organism (Mutter et al., 2004; Melchart et al., 2008). It is this fact that can make the exposure to mercury a confusing and controversial topic.
Ancient Historical Uses
In is natural occurring state, mercury can be found in the element cinnabar commonly known as vermilion, a mercury sulfide (HgS). It was used as a pigment by Paleolithic painters approximately 30,000 years ago to produce a bright red hue that decorated caves in Spain and France (Royal Society of Chemistry, 2017).
In its elemental form, mercury is not found commonly in nature, however, as early as at least 1500 BCE, it was discovered that cinnabar could be heated in a crucible to release the mercury contained therein. At room temperature, cinnabar is a solid red mass. As the cinnabar is heated, the vapors produced can be distilled to form mercury in its common liquid form. Mercury’s true value was soon discovered for its capacity to dissolve gold out of sediment and form an amalgam of metals. Thus, the ancients used this 80th element in the periodic table labeled Hg as a gold scavenger. Upon distillation of the mercury, the gold can then be recovered and refined. The reclaimed mercury in liquid form could then be used again to obtain more gold from various deposits and ores (Shakhashiri, 2017).
Another common use of cinnabar is in Chinese medicine. It is estimated that approximately 5 percent of all patented Chinese medicines contain cinnabar. Mercury intoxication from this source is rare but inadequate use and/or overuse can result in damage to renal organs. This appears to be one of the primary accumulation sites of HgS, an inorganic form of mercury in the body, which has a low water solubility (Wang et al., 2015; Shi et al., 2011).
Pre-Current Day Historical Uses
Historically, mercury was used in many applications with a few of those industries being noteworthy. Fur hat production tends to be the most well know industry for the use of mercury. In the early 18th Century, probably between 1720 and 1740, English hat makers developed a technique for felting rabbit fur termed “mercury carroting.” The process entailed treating the pelt with a solution of mercury salts diluted in nitric acid. Such treatment would dissolve the keratin in the hair fibers allowing them to interlock with the felt more readily. However, such a process would turn the fur orange thus giving it the name of “carroting.” To resolve this undesired side effect, steam would be applied to the fur releasing the mercury vapors into the air. The workers performing the carroting procedure were unfortunately exposed to these fumes through inhalation. Figure 2 reveals an image of how intimately a hat maker would be to mercury; gloves or masks were never provided. Without any protective measures in place, a type of neurological damage often resulted. The term “mad hatter” was apparently derived from the neurological disorders presented through the strange behaviors exhibited by those who engaged in the carroting process of hat making (Crean, 1962; Feinstein, 2006).
Another field that enlisted the usage of mercury was that of alchemy. The well-known father of physics, Sir Isaac Newton, regularly performed experiments with mercury in an attempt to produce the illusive and fabled philosopher’s stone. He believed that if such an element existed, it could turn common metals into gold. Mercury was thought to be the catalyst to producing this magical material. It is now believed, because of his experiments with mercury, Newton went through a phase of near madness and depression. Since his death, researchers have examined Newton’s hair samples and have found high levels of mercury (Lesney, 2003). It is believed that it was not until he gave up the quest to create the mystical element that he regained his sanity. This return to sanity for Newton can serve to illustrate the fact that, upon cessation of exposure to Hg, the half-life of one year in the brain has validity.
Current Day Uses
Mercury is now known to be very toxic in two main forms, 1) elemental vapor, and 2) the organic species of methyl-mercury. Thus, mercury is the source of much debate as to its safety and usefulness in society today (Bernhoft, 2012).
Environmental mercury is mostly produced from natural and anthropogenic (man-made) sources. Natural sources of mercury arise from volcanic activity, natural erosion of mineral deposits, degassing from the earth’s crust, as well as from soil turnover and vegetation growth. It is estimated that 2700 to 6000 tons of elemental mercury is released into the environment annually from these sources (Horsted-Bindslev, 2004). It is also estimated that ocean emissions of mercury into the atmosphere account for approximately 39 percent of the total load of mercury in the environment (Bates, 2006; Han et al., 2014).
Anthropogenic sources include industrial waste byproducts, medical waste, biomass burning, and fuel consumption. The latter two account for 36 percent and 33 percent of the total amount of mercury released into the atmosphere from man-made sources respectively (Zhou et al., 2016). It is estimated that waste from industrial sources and the burning of fossil fuels contributes 2000 to 3000 tons of mercury into the environment annually (Hornsted-Bindslev, 2004). Thus, almost 70 percent of the anthropogenic source of mercury in the atmosphere is from the burning of fuels and biomass.
Mercury has limited application in society today. However, some uses persist and have been the source of much controversy, especially in the latter part of the last century.
Some of the modern day uses include mercury vapor lamps, (most commonly used in street lights and gymnasiums), thermometers and barometers, (although they have mostly been phased out), and in some paints, fungicides, and insecticides, (again, most of which have been removed or eliminated). In the industrial realm, mercury has been traditionally used in battery manufacturing and electrolysis of aqueous sodium chloride to sodium hydroxide in chlorine production (Shakhashiri, 2017).
Controversially, mercury is also a key component in some vaccines as a preservative otherwise known as ethyl-mercury (EtHg), an organic form from thimerosal (Crowe et al., 2017). However, some studies have concluded the greatest forms of elemental mercury exposure to humans is that of dental amalgam fillings and industrial fuel emissions (Mackey et al., 2014; Bernhoft, 2012; Crowe et al., 2017).
Since a large part of mercury in the environment tends to be anthropogenic and thus already present, the focus of this study is to identify blood levels of safety for the exposure of humans to mercury from the bio-available form of mercury often found in aquatic species of animals known as methyl-mercury (MeHg) and the elemental form of mercury (Hg) found in dental fillings both as a solid amalgam and as a byproduct of wear and erosion of those fillings in the form of mercury vapor.
Methyl-mercury (MeHg) is an organic species of mercury and can also be combined with two methyl groups to produce a dimethyl-mercury molecule as figure 3 depicts. This molecule is produced by sulfate reducing bacteria in an anaerobic environment, usually found in muddy river beds, lakes, and the ocean floor. Elemental mercury in the environment readily bonds to sulfur forming an inorganic compound, mercury sulfate (HgS). Anaerobic bacteria utilize the HgS for cellular respiration by stripping off the sulfur. The remaining mercury is then combined with a methyl group producing methyl-mercury or dimethyl-mercury. Therefore, the higher the level of HgS in the aquatic environment, the more methyl-mercury is produced. The newly formed MeHg is absorbed or taken up by zooplankton, phytoplankton, and/or other microbes. These organisms are then consumed by other aquatic invertebrate and vertebrate species which are then consumed by other animals in the food chain (Shakhashiri, 2017). Figure 4 illustrates this process. Bio-magnification, which is the build-up of MeHg from the continued consumption of contaminated food sources up the food chain, creates a highly toxic food source for the end species that consumes that marine life. Often, that end species is human beings. Thus, the top predatory aquatic organisms of fish and shellfish can have a high concentration of
MeHg which has prompted many organizations to warn communities that subsist upon a various diet of seafood against consuming large quantities of those marine food sources (EPA and FDA, 2004).
Methyl-mercury has been identified as an environmental toxin by the World Health Organization (WHO), the International Labor Organization, and the United States Environmental Protection Agency (EPA) (Mackey et al., 2014). An example of the detrimental effects of the bio-magnification of mercury (Figure 4) and the negative effects it can have on end consuming organisms is prevalent in the 1956 mercury poisoning in Minimata, Japan. During this public health crisis, thousands of individuals died from eating seafood that had been contaminated by industrial waste water containing high levels of mercury. Bio-magnification occurred in the local marine life at such a high level that many residents of Minimata became seriously ill simply by consuming fish and shellfish in that region (Mackey et al., 2014). It is well established science that the aquatic food chain tends to be the main source of human exposure to this most toxic form of mercury (Hornsted-Bindslev, 2004). The World Health Organization has now reported that eating seafood once a week from any region can raise Hg levels in the urine to as high as 20ug/L (Ucar and Brantley, 2011). The fish of concern that possess the highest level of methyl-mercury are the top predatory fish such as King mackerel, Tilefish, Tuna, Shark, and Swordfish (Silbernagel, 2011). One study performed in 2007 found that 25 percent of adults in New York City had blood mercury levels above 5ug/L and 50 percent of Asian New Yorkers had levels that exceeded that amount as well (McKelvey et al., 2007).
Methylation of mercury can occur in any area that is exposed to a form of mercury. Unfortunately, the area affected by an exposure to mercury released into the environment does not have to be in close proximity to the source of mercury release. Mercury is a highly volatile metal that can be transmitted to other areas globally through various physical, chemical, and other interactional means (Bates, 2006). Atmospheric dispersion can cause mercury emissions to be transported worldwide in the form of gaseous elemental mercury (GEM). Of the total atmospheric mercury in the ambient air, GEM can account for 98 percent of that mercury and can easily be spread by air currents. It is now known that GEM can have a lifespan of up to two years which gives it plenty of time to be dispersed worldwide (Zhou et al., 2016). Thus, there is no such thing as a “local” mercury emissions exposure event. All mercury emissions can be globally effective.
Tooth decay is one of the most common diseases in the population at large. It was estimated in 2001 to 2004 that 181 million Americans had 1.46 billion dental fillings, the majority of which were amalgam (Richardson et al., 2011).
Amalgam restorations have been used as a satisfactory dental filling material globally for almost 200 years (Bates, 2006; Craig and Powers, 2002; Jamil et al., 2016). Amalgam is a mixture of metal elements that begins as a malleable combination placed into a cavity prepared by a dentist and subsequently solidifies where decay or dental caries once resided. The proportion of solid metals in the form of powder contained in most amalgams consists of 40 to 70 percent silver, 12 to 30 percent tin, 12 to 30 percent copper, and trace amounts of indium, palladium, and zinc (Bates, 2006; Richarson et al., 2011). The liquid that mixes the concoction together and binds all the elements is elemental mercury. The amount of mercury in dental amalgam usually consists of 43 to 50 percent of the total mix (Richarson et al., 2011). Mercury is the key ingredient that provides the malleability and ease of placement of the filling. Mercury also initiates the bonding of all the other metals to allow the filling to solidify. Figure 5 depicts a capsule of dental amalgam (left) with its corresponding contents of powdered metals and a mercury packet (middle) above the powder. The mercury is encapsulated in a spill pouch that punctures upon mixing. The pellet (left) is ready for condensation into a prepared tooth cavity. The qualities of malleability, durability, ease of use, and cost effectiveness have made amalgam the filling of choice in the United States especially for children (Roulet, 1997; Xibiao, 2008).
The wear and attrition of dental amalgams through chewing and brushing has been reported to release small amounts of elemental Hg in the form of vapor that is subsequently breathed into the lungs of the individual possessing the filling(s) (Ucar and Brantley, 2011). Elemental Hg vapor can also be released from dental amalgam during the steps of placement of the filling. It has also been reported that Hg vapor can be released from fillings in the consumption of hot beverages (Patterson et al., 1985). However, most of the literature regarding the release of mercury vapor from dental amalgam in situ reports a negligible mercury exposure to those who possess such dental fillings. Mackert and Berglund (1997) report the amount of mercury vapor released from dental amalgams as significantly lower than the standard level which produces the least effects in the most susceptible individual established by the WHO of 30ug/g of creatinine in urine. According to their assessment, it would take 450 to 530 surfaces of teeth restored with amalgam to reach that established threshold. It is interesting to note that there are only 160 surfaces in which an amalgam can be placed in an adult human mouth with all 32 teeth present. The complexity of measuring actual vapor release of mercury from dental amalgams was addressed in this study. However, direct measurement of Hg vapor can produce an overestimating effect of exposure if flow rate and collection volume of inhaled and exhaled air are not considered separately.
Levels of Hg can also be influenced by recent consumption of seafood, environmental exposure, aggressive chewing or bruxism, and longevity of the amalgams. Thus, true Hg levels from dental amalgam can be difficult to determine. Vapor of Hg inhaled from any source is absorbed into the lungs at a rate of 80 percent (Richarson et al., 2011). Absorption of ingested mercury occurs at 7 to 10 percent and absorption through skin contact with mercury occurs at only a 1 percent rate (Bernhoft, 2012). The high solubility of Hg vapor allows it to cross into the alveolar membranes and subsequently enters the blood stream of the individual exposed (Xibiao et al., 2008). As the Hg enters the erythrocytes, it binds with a sulfhydryl group which allows the Hg to be circulated throughout the tissues. When mercury enters the cells, it is oxidized by a catalase and becomes one of the various forms of inorganic Hg (Crowe et al., 2017). Other potential exposure routes of human beings to mercury reported from dental amalgam in its less soluble inorganic form have be identified as a corrosion product that can be released from the normal wear of dental amalgams (Patterson et al., 1985; Ucar and Brantley, 2011). It has been noted, however, that some of the mercury released from dental amalgam reacts with unreacted particles in the alloy mix resulting in a very little amount of Hg that escapes into the oral environment. Thus, it appears that elemental mercury exposure can occur in the actual placement of the filling material prior to the final set rather than upon the mere existence of a dental amalgam. Ingestion of small particles of amalgam can also take place as well and absorption of the Hg can also occur when the soft tissue comes into contact with the amalgam. A major route of elimination of absorbed Hg is through the urine and feces. It is estimated that approximately 40 percent of the absorbed Hg is eliminated via this route within 30 days of a vapor exposure (Ucar and Brantley, 2011).
Measured Rates of Mercury Toxicity in Urine
It is well established that chronic exposure to large doses of mercury vapor can produce neurological dysfunction in the form of tremors, severe behavior and personality changes, emotional excitability, depression, fatigue, loss of memory, even hallucinations and delirium, permanent brain damage and death (Berglund et al., 1988; Bernhoft, 2012). The average rate of mercury in the urine contributed to the presence of amalgam restorations in the mouth has been established at 1 to 5 ug/L (Craig and Powers, 2002). The WHO has determined that the consumption of seafood every week can raise the Hg level of urine to 5-20ug/L (Ucar and Brantley, 2011). Ucar and Brantley (2011) report that neurological changes can be seen when urine mercury levels are >500ug/L. They also report that this level of Hg in urine is 170 times greater than the levels observed when a dental amalgam restoration is placed. The established rate set by the Occupational Safety and Health Administration (OSHA) of the United States as an acceptable amount of work place exposure to mercury vapor is 0.05mg/cu.m. This rate, established by OSHA, is equivalent to 100 times the amount of mercury vapor that is released in a person with nine dental amalgams (Patterson et al., 1985; Ucar and Brantley, 2011).
Measured Rates of Mercury Toxicity in Blood
Safe blood levels of Hg have been set by a joint effort of the Food and Drug Administration (FDA) and the Environmental Protections Agency (EPA) of the United States at 5ug/L (EPA, FDA, 2004). Some reports place the level of medically acceptable to 3ug/L (Craig and Powers, 2002). The Mayo Medical Laboratories have set three blood levels of mercury detection according to exposure and the resultant effects. Those levels are 0-9ug/L as normal, 10-15ug/L as mild exposure, and 15-50ug/L as high exposure (Jamil et al., 2016). The Centers for Disease Control and Prevention have placed blood levels for excessive exposure to mercury at >10ug/L (CDC, 2006).
When it comes to exposure to MeHg, markers of urine mercury of <10ug/L with corresponding blood levels of >5ug/L usually points to a positive methyl-mercury exposure. Elementary or inorganic mercury exposure to amalgam fillings in the blood is not as readily established and measurable due to the variable number of amalgams present in each individual tested and the smaller amount of elemental mercury released (Silbernagel, 2011).
Although mercury in large doses is highly toxic, (i.e. blood levels of mercury >50ug/L), it appears through research and the literature currently available that certain levels of exposure to Hg are relatively safe. Much of the mercury controversy has been spurred on by the internet and other social media avenues exaggerating the toxic properties of mercury in seafood and dental amalgams. Multiple studies have been performed measuring those blood levels of mercury in individuals who consume seafood regularly and the corresponding blood level of mercury from those who have amalgam dental restorations. It is therefore a worthwhile endeavor to discuss mercury level from both sources, seafood and dental amalgam.
Mercury Levels from Consumption of Seafood
An exhaustive study was performed in 2011-2012 regarding dietary intake and subsequent biomarkers for levels of metal, including mercury, in food sources among different racial and ethnic populations in the United States. Almost 6100 participants were utilized in this study. The authors found that the estimated consumption of dietary Hg was 0.09ug/kg/day for Asians and 0.05 to 0.07ug/kg/day for all others. It was determined that fish and shellfish were the main source of this ingestion of Hg in the higher rate (Awata et al., 2017). Unfortunately, no blood levels of Hg were taken of the participants prior to the study thus the absorption rates are undetermined. This appears to be a major downfall of the study as there is no reference point for blood levels and consumption. There is also no mention of mercury toxicity symptoms at certain consumption rates.
Another study regarding maternal blood level of Hg from the consumption of fish was performed using a base line of 3.5 to 5.8 μg/L as a predetermined level of concern. It is interesting to point out that this study concluded that an attempt to describe patterns of MeHg exposure was a major challenge as the MeHg concentrations among different fish species can vary by more than 10-fold. The study revealed that the national average percentage that was ≥ 3.5 μg/L was 10.4; for those who had levels ≥ 5.8 μg/L it was 4.7 (Mahaffey et al., 2009). However, no symptoms of mercury toxicity were analyzed in this report regardless of elevated blood levels. Had the researchers performed an analysis of mercury toxicity symptoms with corresponding blood levels, a possible safe level of Hg in blood may have been determined. Elevated blood mercury levels do not necessarily point to mercury toxicity.
Mercury Levels from Amalgam Fillings
One study performed in May of 2004 in five elementary schools in Shanghai, China found that out of 205 children who had never receive a dental amalgam versus 198 who had received an average of two amalgam restorations, neither group displayed any significant changes in IQ or school performance as well as no significant changes in neurological behaviors or personality, even though the amalgam group had urine Hg levels 15% higher than the non-amalgam group. It is important to note that all students within the study had mercury levels below general background levels of <5ug/g Cr (Xibiao et al., 2008); however, these reported levels were from urine samples and used Creatine as a biomarker which is a more accurate test for current mercury exposure rather than chronic exposure. However, there is no evidence in this study that either group had other potential mercury exposures accounted for such as seafood intake.
Another study performed in New England and reported in 2006 in the Journal of the American Medical Association reveals that 534 children were followed from age 6 to 10, half of which had amalgam restorations and the other half had composite (non-amalgam) restorations. The authors of the study reported no statistical significance in IQ scores, renal glomerular function, general memory deficiencies, visual motor skills and neuropsychological dysfunction (Bellinger et al., 2006).
The measurement of acceptable levels of Hg in the blood is still controversial (Ucar and Brantley, 2011). One case study of 24 individuals who had symptoms of MeHg poisoning from an industrial source had blood levels ranging from 7ug/L to 125ug/L with most of those tested having levels in the 40ug/L (Silbernagel et al., 2011). This wide range of Hg blood levels illustrates the differing susceptibility of individuals to mercury, which also complicates the establishment of safe guidelines.
Although levels of mercury were found to be elevated in one study of 18 cadavers who had dental amalgam fillings, Ucar and Brantley (2011) point out that an increase in mercury levels does not necessary equate to a decrease in biological functioning. It is worthwhile to note that in all the studies reviewed, establishing a control group that has no mercury exposure and no detectible blood levels of mercury seems to be lacking. An appropriate study to determine safe levels of mercury in blood would have to account for all sources of potential mercury exposures and symptoms of mercury toxicity against those control groups who are asymptomatic and have no exposure to mercury. With seafood as a common food source, as well as the vast extent of amalgam restorations in the population at large combined with environmental mercury, such a study could be quite difficult to obtain and could become quite costly.
There is no doubt in the scientific community that mercury exposure in large doses is highly toxic. The question remains as to how much mercury will produce a toxic symptom? The multiple tests used to determine an effective dose from the research prompts a recommendation for a universal standard of measurement for levels of mercury in the population at large. Such a universal standard would allow all mercury exposures to be considered in a national or international database similar to the National Cancer Registry. If such a database was created, it could serve to establish a possible determination of the toxic effects of mercury and at what level those effects begin. Until such is determined, it is difficult to recommend a ban or even a reliable control on the use of dental amalgams and/or the consumption of seafood. Although research has been performed to recommend such restrictions, until that research can be unified by a universal standard of measurement with associated effective doses, mercury exposure to human beings, and the environment is still a controversial topic.
Some individuals advocate for a complete ban on all mercury dental fillings. Although such a ban would be possible, the feasibility of such a ban could be detrimental to lower income families and communities that might not be able to obtain the pricier non-amalgam fillings.
A ban on seafood is not possible and would serve to cause a food and even a possible economic crisis on those communities that depend upon the seafood industry. Industrial sources of potential mercury exposures should be responsibly disposed of and not readily released into the environment, especially into waters that contribute to food sources. It appears from the literature that the majority of mercury poisonings that have occurred have been the result of contaminated seafood with high levels of methylmercury from industrial sources.
Although elemental mercury is released through normal masticatory processes and care of the oral cavity of those who have amalgam restorations, the amounts released appear to be well below the threshold of toxicity. With amalgam being the restorative material of choice for almost 200 years, it would appear that a direct causative factor for a particular disease would have already been identified. Two hundred years of use of any substance will reveal large amount of evidence of untoward affects. Ucar and Brantly (2011) report the following:
Although mercury vapor is released from amalgam restorations, research over the past decades has failed to identify deleterious health outcomes. This can be attributed to insufficient mercury being released from dental amalgam restorations to cause a medical problem. (p. 3).
Therefore, it is proposed that dental amalgams are an acceptable form of restorations for decayed teeth as the amount of vaporized elemental mercury from regular wear is within an acceptable margin of safety. The American Dental Association (ADA) has issued a statement in 1998 affirming the safety of dental amalgam as a restorative material for decayed teeth and as recently as 2009, the ADA reaffirmed that statement (Ucar and Brantley, 2011). The United States FDA issued a statement in 2002 claiming that there is no real scientific evidence proving that mercury amalgams are a source of harm to dental patients (FDA, 2002)
However, exposure to the more toxic form of mercury, methyl-mercury, by consuming MeHg bio-magnified seafood can increase the total Hg content in tissues resulting in severe neurotoxicity and in some cases death. Therefore, dietary habits and possible further exposure to Hg should be taking into consideration when selecting an appropriate dental restorative material. Other filling materials are available to restore decayed teeth; however, those materials have not been time tested as long as amalgam and there are concerns regarding their placement, toxicity, and durability. The discussion and validity of these materials are not a part of this work, nor is the discussion of whether or not to consume seafood a consideration of this study.
It is recommended that each individual consider their own dietary seafood intake as well as their choice for restorative dental materials. The fact that these sources do contain mercury and has been shown to be neurologically toxic at very high exposure rates should be taken into account as well. It is proposed that individuals who may be concerned with high levels of Hg should take the necessary steps to have their blood tested for Hg levels with the goal of keeping that level below the 10ug/L threshold. It is also recommended that each individual make informed, educated, and evidence based decisions regarding their exposure to mercury in any of its forms.
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Ronald is the Dental Director of the Fourth Street Homeless Clinic here in Salt Lake, and became involved in this research because he gets asked about the safety of dental amalgam with mercury on a constant daily basis. Ronald found a lot of misinformation about dental mercury in fillings, and thus conducted his own research. For his second paper, he became interested in the topic through an ethics class at Westminster. It is a very politically charged topic and so it was challenging for him to find unbiased information.