AN EVALUATION OF DENTAL AMALGAM AND IT’S ABILITY TO INJURE HUMAN HEALTH – 02/10/2010
1) I am Professor of Chemistry/Biochemistry in the Department of Chemistry at the University of Kentucky. Throughout my career I have studied the effects of numerous compounds on the changes of the activity of enzymes, proteins and cellular function proteins and the relationship of these changes to disease states. In the past 20 years I have concentrated my research on the effects of mercury toxicity on human health. Specifically, I have researched and evaluated the contributions of dental amalgam, biologics and vaccines on the human body burden of mercury and organic-mercury compounds and the potential effects of these compounds on specific enzymes and cells. It is my opinion that the most critical mistake of modern medicine is the lack of understanding of the synergistic toxic effects associated with mercury and organic mercury toxicity. Synergistic effects drive the toxic level of mercury exposure to levels much lower than expected and can change the toxicity profiles substantially.
2) Mercury exposure to humans comes from various chemical forms such as elemental vapors, inorganic salts and organic-mercurials such as thimerosal and phenylmercury acetate (PMA). All chemical forms of mercury have been proven toxic at relatively low levels. There is no doubt that mercury and mercury compounds represent the most dangerous form of metal toxicity since research shows them to cause adverse effects in animals and humans at very low levels and that a “retention toxicity” where seemingly non-toxic levels, when constantly present as in dental amalgam vapors, can slowly build up in tissues causing severe illnesses. Mercury and mercury containing compounds are listed under the State of California’s Proposition 65 as compounds that need to be evaluated for their level of toxicity to ensure the safety of the citizens. Mercury vapor is one of the most toxic forms of mercury along with some of the organic mercury compounds. It is this vaporous form of mercury that is released from dental amalgams and is the major contributor to human mercury body burden.22
3) It is important to understand two concepts regarding mercury toxicity. The first is the level of exposure and the second is the contribution to human body burden. One can be exposed to mercury in the diet by eating fish, etc. This mercury is effectively excreted and does not appear to lead to a build up of mercury in the body but may cause subtle effects difficult to identify. Much of the mercury in seafood is bound to selenium and render much less toxic to mammals. The studies in the fish eating populations of the Faroe Islands and the Seychelles are examples of this. 36, 37 The citizens of these studies were exposed to high levels of mercury in their diets, but maintained a fairly low level of mercury body burden and urinary mercury levels not dramatically different from the USA population. In my opinion, the blood levels were higher due to excretion of the daily diet intake of bound mercury from sea food. This is most likely due to the fact that dietary mercury in fish has already reacted with protective compounds in the fish and are not as reactive or as capable of being retained on ingestion as would be other forms of mercury that have not been previously exposed to a biological system (e.g. mercury vapor).
4) In contrast to mercury from a fish diet, mercury vapor from amalgams has all of its chemical reactive potential and easily penetrates into the cells of the central nervous system where it is converted to the toxic form (Hg2+), reacts with proteins in the brain, etc. and is retained for much longer periods of time and builds up in these tissues causing a significant toxic effect. Research has determined that about 80% of inhaled mercury vapor is retained by the human body and that the major contributor to human body burden is from dental amalgam. This is the position of the World Health Organization. Recent studies show that released Hg vapor from dental amalgams setting quietly in sealed test tubes is in the range of 4 to 21 μg/cm2/day.55 This surface area is approximately the size of a small, single spill amalgam filling. It has been shown that fecal mercury levels average about 65 μg per day in amalgam bearers. These are exact measurements and agree well with each other. However, many publications “estimate” the amount of mercury released by amalgams based on the blood or urine levels. In one study it was stated that “The integrated daily Hg dose absorbed from amalgam was estimated up to 3 micrograms for an average number of fillings and at 7.4 for a high amalgam load.” 50 The “estimated levels” defy explanation as the numbers would not allow for more than 2 amalgam fillings and would never reach the 65 μg average mercury in fecal material plus the urinary mercury excretion. We also know that abrasion by a toothbrush elevates the daily mercury excretion in sealed amalgams by over 10-fold. This points out the major problem of most reported experiments on dental amalgam, the amount of patient exposure is mostly “estimated” and almost always estimate very low compared to the level measured outside the mouth under rigorously maintained conditions. However, even after amalgam removal, inorganic Hg dropped rapidly in plasma and red cells, stabilizing at 27% of pre-removal levels after 60 days. Concentrations of organic Hg in plasma remained unchanged, indicating no change in dietary uptake of organic Hg.50
The 73% decrease in blood/plasma mercury levels supports the concept that dental amalgams account for the vast majority of inorganic mercury found in the human body of amalgam bearers.50 However, the “estimated” levels of mercury released from amalgams in this study (3μg on average) is refuted by other studies which found oral emission of mercury ranged up to 125 μg Hg/24 h, and urinary excretions ranged from 0.4 to 19 μg Hg/24 h.51 Also, fecal excretions ranged from 1 to 190 μg Hg/24 h, which was 100 times the mean intake of total Hg from a normal Swedish diet. These data, done on the same patients, also point out explicitly that urinary excretions do not reflect amalgam release or exposure of mercury and that the concept of low 3 to 8 micrograms release of mercury per day as an estimate of amalgam contribution to human exposure is not at all accurate, in fact it is absurdly low.50 In an earlier paper from this same group they had stated that “In saliva, there was an exponential decline in the Hg concentration during the first 2 weeks after amalgam removal (t 1/2 = 1.8 days)” and concluded that amalgam fillings were a significant source of mercury in saliva and feces.”52 However, they later stated “The Hg concentrations in saliva remained elevated for at least 1 wk, suggesting that dissolved Hg vapor is not the major source of mercury in mixed saliva.”50 They also reported that fecal levels in amalgam bearers were 11.7 times higher than found in amalgam free subjects (2.7 vs 0.23 mumol Hg/kg dry weight, p < 0.001) and increased 2 days after amalgam removal to a median 280 mumol Hg/kg dry weight, a fecal increase of over 100 fold.52 This is one of the negative effects of placing amalgams, they may have to be removed and repaired and doing so can lead to a bolus exposure to mercury.
4) The exceptional toxicity of mercury vapor is probably due to the efficient partitioning of vaporous mercury into certain body organs (e.g CNS, kidney) and into specific cellular organelles (e.g. the mitochondria) based on mercury vapor’s ability to easily penetrate membranes and the blood brain barrier. In this manner mercury vapor, Hg0, is quite different from ionic Hg2+ and Hg1+. For example, air and oral ingestion of mercury vapor (Hg0) primarily affects the central nervous system whereas the kidney is the major organ affected by the cationic forms of mercury (e.g. Hg1+ and Hg2+). Add to this problem is the fact that prolonged mercury vapor exposure can lead to inhibition of the mercury excretion process itself. Therefore, extended exposure to mercury vapor from amalgams will, by itself, decrease the body’s ability to excrete mercury. The recent data presented in the Children’s Amalgam Trials, published in JAMA, shows that extended exposure to mercury from dental amalgams lead to a marked +40% decrease in the ability to excrete mercury in the urine.27, figure 2, page 1788 from year two to year seven of the study. Even though the children (orphans in a Lisbon, Portugal orphanage) were given additional amalgams from year two to year seven the rate of mercury excretion in their urine dropped dramatically. Therefore, urine mercury levels do not represent in any way an accurate measure of the level of exposure of an individual. Another evaluation of this data, separating the urinary excretion of mercury ability of boys versus girls shows that boys, who are much more likely to have neurological illnesses as found in autism spectrum disorders, were much less capable of excreting mercury than girls38. In fact, the boys with amalgams placed had urinary mercury excretion rates at year 7 similar to boys without amalgams indicating that within the 7 year time frame of the experiment they had lost the ability to excrete the additional mercury from their amalgam exposures.
Since this data in the Children’s amalgam trial only evaluated urine mercury it must be considered with caution as this measure does not accurately reflect what may be happening with regards to total exposure, excretion or retention. For example, research has shown that the oral emission or mercury in amalgam bearers ranged up to 125 micrograms Hg/24 h, and urinary excretions ranged from 0.4 to 19 micrograms Hg/24 h.42 In 10 subjects, urinary and fecal excretions of mercury and silver were also measured. Fecal mercury excretions ranged from 1 to 190 micrograms Hg/24 h. The worst-case individual showed a fecal mercury excretion amounting to 100 times the mean intake of total Hg from a normal Swedish diet.42 These studies also imply that urinary measures are not indicative of the total mercury intake at all and the mercury levels reported are orders of magnitude higher than that speculated by the ADA from “estimations” by dental researchers.34,50
5) The pro-amalgam group in the USA has “estimated” the amount of mercury excreted from amalgams by using urine mercury levels34, which is obviously invalid, since over 90% of mercury is excreted via fecal routes, not through the urine.41 The British Dental Association also uses this same study to infer that amalgams do not contribute significantly to human mercury exposure.35 The pro-amalgam group are also aware of publications showing that over 90% of mercury excreted by the human body leaves through the bilary transport system of the liver and is excreted in the feces—yet they constantly refer to low urine mercury levels as their source of suggesting low exposures from dental amalgams. They make the comment that “the dose make the poison”35 yet avoid determining the actual dose but instead depend on an “estimation” based on the urine excretion rate that represents at best 10% of the total mercury being excreted and even this is not accurate in individuals who are low in glutathione and unable to effectively excrete mercury.
In a recent study the level of mercury in feces and saliva were measured in amalgam free controls and amalgam bearers before and after removal of the amalgams.41 Before removal, the median Hg concentration in feces of amalgam bearers was more than 10 times higher than in samples from an amalgam free reference group consisting of 10 individuals (2.7 vs 0.23 mumol Hg/kg dry weight, p < 0.001). A considerable increase of the Hg concentration in feces 2 days after amalgam removal (median 280 mumol Hg/kg dry weight) was followed by a significant decrease. Sixty days after removal the median Hg concentration was still slightly higher than in samples from the reference group.41
6) It is now well known that the relative toxicity of mercury and organic mercury compounds fluctuate dramatically in humans depending on: (1) delivery route (2) the presence of other synergistic toxic metals such as lead, cadmium, aluminum, etc. (3) different diets (4) antibiotic exposure (5) genetic susceptibility23,24 and allergic reactions (estimated as at least 1% of the human population7 with 8.7 to 13.4% showing sensitivity to a diagnostic patch test 5 & references therein) (6) gender (7) state of health and (8) age of exposure19. Therefore, attempting to determine a generalized, lowest observable affect level (LOAEL) or no observable effect level (NOAEL) regarding mercury vapor exposure is a complicated, if not impossible, procedure as explained by the analysis of published refereed research articles (these are presented below).
7) The end point for measuring toxicity is also critical. That is, if lethality versus loss of neurological function are the end points then different values for a minimum daily acceptable limits of exposure will be arrived at. Also, when lethality is compared to loss of neurological function, or suppression of the immune system, as the end points a different minimum acceptable daily exposure would be expected. In today’s medicine the health of the individuals metabolism and neurological is of prime concern and this has lowered the level of mercury exposure that is considered a NOEL. For example, mercury is a potent immunomodulator and a well known relationship exists between impaired B-cell receptor (BCR) signal strength and autoimmune disease. A group that had previously shown that in mouse B cells, non-cytotoxic concentrations of inorganic mercury interfered with BCR-mediated growth control, suggesting that BCR signal strength was impaired by Hg+2, later showed that the kinetics and magnitude of BCR-mediated activation of ERK-MAPK are markedly attenuated in these same cells and in spleenic B cells that have been exposed to low and nontoxic burdens of Hg+2. 53 It therefore appears plausible that suppression of the immune system can occur at levels of mercury that are not considered toxic by many.
8) It is obvious that lethality requires a higher level of exposure to mercury vapor than does neurological, immunological or developmental damage. For example, adverse immunological effects and autoimmunity induced by dental amalgam and alloy in mice has been demonstrated.25 This has been further supported by observations that the phagocytosis by macrophages, the first step in the innate and acquired immune systems, is inhibited by low nanomolar levels of mercury.30 Neurotoxicity combined with a suppressed immune system in an aged patient would be considered a danger for an amalgam exposed person with a neurological disease, such as a motor neuron disease. Low nanomolar levels of mercury are reached in the blood and urine of individuals with amalgam fillings. For example, in a urine or blood with a low 3 micrograms/liter of mercury the concentration would be about 15 nanomolar or 15 x 10-9 molar (3 x 10-6 grams divided by 201 grams/mole for Hg). One to five nanomolar levels of mercury can have dramatic effects on certain enzymes or neurons or immune system cells in culture. Porphyrin profiles (see below), leading to the synthesis of heme, in dentists show mercury induced aberrancies at urine levels in the 3 microgram/liter range23,24
Hg has been shown to induce autoimmune disease in susceptible animals with effects including overproduction of specific autoantibodies and pathophysiologic signs of lupus-like disease. However, these effects are only observed at high doses of Hg that are above the levels to which humans would be exposed. A study was done to test the hypothesis that Hg does not cause autoimmune disease directly, but that mercury interacts with triggering events, such as genetic predisposition, exposure to antigens, or infection, to exacerbate autoimmune disease.46 They found that treatment of mice not susceptible to Hg-induced autoimmune disease with very low doses and short term exposures of inorganic Hg (20-200 μg/kg) exacerbates disease and accelerates mortality in the graft versus host disease model of chronic lupus. Also, low dose Hg exposure increased the severity and prevalence of experimental autoimmune myocarditis. In a human study involving Amazonian populations exposed to Hg through small-scale gold mining, with and without current or past malaria infection they reported a significantly increased prevalence of antinuclear and antinucleolar antibodies and a positive interaction between Hg and malaria. They proposed that their findings supported a new model for Hg immunotoxicity. Namely, mercury can serve as a co-factor in autoimmune disease, increasing the risks and severity of clinical disease in the presence of other triggering events, either genetic or acquired.46
It is well known that the initiation and severity of systemic autoimmune diseases is influenced by genetic and environmental factors, including bacterial infections. To explore the involvement of innate immunity in mercury-induced autoimmunity in mice a recent study employed bacterial lipopolysaccharide (LPS), which non-specifically activates the immune system.47 Resistant mice were rendered susceptible to mercury-induced autoimmunity by co-administration of LPS. These findings indicate that activation of the innate immune system by bacterial infection plays a key role in both the induction and severity of mercury induced autoimmunity. 47
9) Many individuals may appear normal and have apparently non-toxic levels of blood and urine mercury and still suffer from extreme mercury toxicity. For example, young athletes and others who died from Idiopathic Dilated Cardiomyopathy (IDCM) have been found to have 22,000 times the mercury in their heart tissue when compared to their muscular levels or the mercury in the hearts of individuals who died of other forms of heart disease18. This level, 178,400ng/g, would have definitely have been lethal to the kidney and CNS cells and this level has never, to my knowledge, been observed in a blood, urine or hair sample of a human. In my opinion, the unexplained, abnormal partitioning of huge levels of mercury into specific organs in certain individuals essentially renders it impossible to identify a hair, blood or urine level of mercury that is safe for all, a NOEL. It certainly indicates that a person with an existing motor neuron disease would be at elevated risk if constantly exposed to low level mercury vapors. It is important to note that mercury toxicity is a retention toxicity, where mercury is extracted from the blood and retained in certain tissues, leading to elevated levels that can cause illnesses.
10) For an accurate determination of a LOEL or NOEL for injury causing mercury exposure it is clear that using data from one strain of a genetically inbred rat or mouse strain could result in a very inaccurate answer, going either way.4 However, this has been done. Humans are not genetically inbred and their diets differ dramatically. Some are on antibiotic medications that would enhance the toxicity of all mercury compounds. Further more, it has been established in the literature that different strains of mice and rats give different sensitivities to mercury and that there can be dramatic differences in sensitivity to specific toxicants between species such as rats and humans. Therefore, basing safety on animal data is often very misleading.
11) Recent studies on dentists and dental technicians (selected as they are exposed to mercury vapor) has shown that a specific polymorphism in the CPOX gene leads to enhanced disruption of the porphyrin pathway which leads to the synthesis of heme. About 85% of all dentists had abnormal porphyrin profiles that indicated their ability to make heme was being impeded, and 15% of this 85% displayed a marked inhibition that correlated with their mercury exposure. 23,24 Similar data has been reported for autistic children, where 53% have shown abnormal porphyrin profiles indicative of mercury toxicity.26 Treating a subset of these autistic children with a mercury chelator effected a porphyrin profile change back towards the normal range indicating that the cause of the abnormality was toxicity, not genetics.26 This implies that very low levels of mercury exposure as determined by urinary mercury levels can have an effect on 85% of the population and a dramatic affect on certain susceptible individuals who represent 15% of the population.
Another study showed the irreversible effects of occupational exposure to color blindness. About 3 years after exposure the mercury level had dropped to 1.4 ± 1.4 μg/g creatinine for exposed patients, a level considered non-toxic, compared with 0.5 ± 0.5 μg/g creatinine for controls. However, the findings indicate that following a long-term occupational exposure to Hg vapor, even several years away from the source of intoxication, color vision impairment remains irreversible.43 Such studies point out that mercury damage cannot be evaluated by the current level of mercury in the urine. Another study evaluated the automated visual field perimetry in 35 ex-workers (30 males; 44.20±5.92 years) occupationally exposed to mercury vapor and 34 controls (21 males; 43.29±8.33 years). Compared to controls, visual field sensitivities of the Hg exposed group measured were lower for the fovea as well as for all five eccentricity rings of vision (p<0.05).49
Another study compared neutrophil function in non-exposed and exposed populations (with a mean +/- s.d. urinary mercury concentration of 24.0 +/- 20.1 μg/1 creatinine) in which 44 of the workers urinary mercury levels were below the accepted threshold level (TLV) of 50 μg/1 creatinine.45 The neutrophil functions were significantly reduced in the mercury-exposed workers compared with the controls. In 28 of these workers, neutrophil chemotaxis was re-evaluated 6 months later after the daily exposures were decreased significantly and urinary mercury concentrations showed a significant reduction. However, neutrophil migration did not return to within the normal range in these subjects. These results suggest that a current ‘safe’ level of mercury exposure may lead to impairment of neutrophil function.45
12) It is very important to note the negative contributions secondary to the mercury inhibition of heme synthesis. Heme is required for oxygen carrying capacity of blood, it is also necessary for a critical step in the electron transport system of the mitochondria. Both of these steps, if impeded, will decrease the ability of the body to make energy for physiological functions that are necessary for good health. Also, heme is a needed cofactor for the P450 enzymes that have a primary role in detoxing the body of many organic toxins such as pesticides, PCBs, herbicides, etc. Without adequate heme a human will have an impeded ability to detox many different toxins that they may be exposed to.(ref. Any good biochemistry textbook)
12) Additionally, recent research has shown that the removal of beta-amyloid protein from the brain in a normal fashion requires a specific heme, and that a lack of this heme prevents beta-amyloid excretion and leads to the formation of amyloid plaques (senile plaques) in the brain.32 The amyloid plaque build up is a major pathological, diagnostic hallmark of Alzheimer’s disease.27 Therefore, the mercury inhibition of heme synthesis could lead to a secondary systemic abnormality that contributes to severe neurological illnesses, including the neuronal disease classified as Alzheimer’s disease. The observation of increased amyloid build up due to inadequate forms of the proper heme molecule is also supported by the observed formation of neurofibillary tangles (NFTs) from neurons in culture by the exposure to sub-nanomolare levels of mercury, much lower (by about 1,000 fold) than is found in many human brains.31 NFTs are also a major pathological, diagnostic hallmark of Alzheimer’s disease. This data is consistent with the observations published earlier where mercury, and again, only mercury could cause a major biological abnormality in a major brain protein when added to normal human brain tissues or in rat brain on exposure to mercury vapor.12, 13 Therefore, mercury, and only mercury at very low levels, can generate the two major pathological hallmarks of a major neurological disease as well as mimic the protein level aberrancies. The exposure to mercury and its known effects on neurons may explain the uptake of inorganic mercury by olfactory patways and the entry of low doses of mercury vapor into the nervous system.6, 14 A more recent study states that mercury was elevated in the plasma of Alzheimer’s disease patients when compared to age-matched controls.39
13) Synergistic toxicity of two or more toxic metals has been known for some time. It has been shown that the relative toxicity of mercury containing compounds appears to be dramatically affected by the presence of other compounds and heavy metals that synergistically enhance the toxicity of mercury. For example, mixing of an LD1 dose of mercury with a 1/20 dilution of an LD1 of lead produces a mixture with an LD100, not an LD2 or less that would be expected with additive toxicities1. Since there is considerable concern about the lead levels in the drinking water in our nation’s capital and other major cities it seems the citizens there would be under more toxic stress from dental amalgams than those in locations with little or no lead exposure.
14) Consider also that mercury from different exposures are at the least additive in their toxicity effects and they may come from different types of iatrogenic exposures.15, 16, 17 A report from the National Center for Health Statistics, Center for Disease Control and Health in 2003 stated that approximately 8% to 10% of women of child-bearing age had concentrations of mercury higher than the US EPA’s recommended reference dose, below which exposures are considered to be without adverse effects3. One would expect similar mercury levels, or higher, in the male population and in the population of individuals with motor neuron disease or other neurological illnesses. This blood level in women caused more recent concern with data showing that cord blood was 1.7 times the level of maternal blood indicating that more than 8% of children being born are being exposed to toxic levels of mercury from their mother’s blood. A recent report states “Levels of Hg in the cord blood were significantly associated with the number of maternal amalgam fillings (rho=0.46, P<0.001) and with the number of years since the last filling (rho=-0.37, P<0.001); these associations remained significant after adjustment for maternal age and education. Dental amalgam fillings in girls and women of reproductive age should be used with caution, to avoid increased prenatal Hg exposure.40 All of these individuals would definitely be more at risk during transient mercury exposures than would the general population and are certainly not comparable to animals in a pristine environment being exposed to only one mercury toxicant and fed a chow that is designed to be free of other toxic metals. Therefore, a 10-fold reduction for urinary mercury levels, as is common in converting a LOEL into a NOEL, most likely does not provide the protection factor predicted as it would not account for exposures to materials that synergistically enhance mercury toxicity nor does it account for the reduction of urinary mercury excretion caused by prolonged mercury vapor exposures.
15) It is well known that diet plays a major role in the ability of mammals to excrete mercury2. Studies have shown that three different diets fed to adult female mice (high protein synthetic diet; standard rat chow diet; milk diet) dramatically changed the rate of fecal excretion of mercury. Mercury was introduced orally as methyl-mercury (MeHg) and diet caused differential rates of whole body mercury elimination. The results showed that mice fed a synthetic, high protein diet had the lowest tissues levels of mercury whereas those fed the milk diet retained the highest mercury levels. This was confirmed by the total percentage of mercury excreted in the feces after 6 days of 43%, 29% and 11% in the high protein, rat chow and milk diets, respectively. Therefore, diet plays a major role in the fecal excretion rates of mercury from an organic mercury compound. As expected, diet also affected the excretion rate of mercury from body tissues. The obvious importance of this data is that the retention of mercury in the body of someone on a milk diet would be much higher. Twenty year old studies report that suckling animals absorb about 50% of Hg2+ versus 5% in non-suckling animals11. Since the level of toxicity would likely increase with retention time, especially if the exposure rate to mercury were consistent over any significant period of time, then the diet can have a major affect on a calculated NOELs and minimum acceptable daily levels. Another study examined the effects of inorganic mercury (mercuric chloride) exposure exclusively through maternal milk on the biochemistry related to oxidative stress in the cerebellum of weanling mice.54 Their results showed that with pups, the lactational exposure to mercury increased cerebellar glutathione reductase activity as well as cerebellar lipoperoxidation. However, these changers were not observed in dams. The authors concluded that their results imply that inorganic mercury exposure through maternal milk is capable of inducing motor deficits as well as biochemical changes in the cerebellum of weanling mice.54
16) Gender effects of mercury toxicity appear to be based on both the protective effects of the female hormone28 and the enhancement of mercury and ethylmercury toxicity by testosterone, the male hormone29. Research in our laboratory showed that testosterone dramatically enhanced the toxicity of mercury and ethylmercury whereas estrodiol showed a potent protective effect. A significant quote from another lab states “The estrogenic effects were associated with a reduction of mercury content of the anterior pituitary gland and medial hypothalmus, suggesting a protective estrogenic effect.”28 Further, a study has found that amniotic fluid testosterone levels appear higher in mother who give birth to children with autism spectrum disorders. The conclusions of one paper stated “These finding implicate foetal testosterone in both social development and attentional focus. They may also have implications for understanding the sex ratio in autism.”33 What is of importance here is the fact that gender plays a major role in susceptibility to mercury toxicity with the male gender appearing to be more susceptible. A study confirming this was done on 7 male plus 7 female rats that were exposed to the same level of thimerosal. At doses of 38.4–76.8 mg/kg using 10% DMSO as diluent, seven of seven male mice compared to zero of seven female mice tested succumbed indicating a definite gender effect.44 Since boys are dramatically more susceptible to neurological illnesses, such as autism, than are girls it seems reasonable to consider environmental insults from mercury and organic mercury as the most likely cause.
17) Toxicity is also known to vary with the chemical species of mercury that exists in the body’s tissues. Diets can change this as it was observed that foods ingested played a major role in the mercury chemical species that existed in the mice given oral doses of MeHg. Hg2+ was the species found at the highest level in test animals on a synthetic protein diet (35.3%) and was the lowest in test animals on a milk diet (6.6%). It is reasonable to predict that diet changes the conversion of MeHg to Hg2+ and would likely do so for other organic mercury compounds, such as ethyl-mercury (Et-Hg), which is released from thimerosal. The toxicity of organic mercury compounds (e.g. MeHg versus EtHg), which partition into the body organs similar to mercury vapor, has been suggested to be greater than Hg2+ (inorganic mercury). It is also reasonable to expect the toxicity to be partially determined by the rate that the organic mercury compounds are converted to Hg2+ after the chemical nature of the mercury source has allowed effective partitioning across the blood brain barrier.
18) Other studies confirm that the renal uptake and toxicity of circulating mercury is significantly enhanced in rats by the co-ingestion of the essential amino acid L-cysteine8 and disease marker homocysteine9. Elevated blood homocysteine level is also a major risk factor for cardiovascular disease. Therefore, humans with risk for cardiovascular disease would be more at risk by low level mercury exposure than others due to the more effective mercury uptake stimulated by elevated homocycteine levels.
19) Medical status is of concern when considering mercury compound toxicity, especially when bacterial infections are being treated. Treatment of adult female mice with widely used antibiotics 7 days prior to MeHg exposure dramatically influenced mercury retention of tissues from mice receiving similar organic mercury exposures2. The calculated whole body mercury elimination half-times from day 1 to day 6 varied from 34, 10 and 5 days for mice fed a milk diet, mice chow or high protein diet. A remarkable 6.8 fold increase in retention half-life existed between a milk diet and high protein diet that was caused by antibiotic treatment that also changed the gut microflora. Antibiotic treatment dropped the fecal mercury excretion to near zero in the high protein and milk diets and to less than 8% with the mouse chow diet.2 Therefore, it can be concluded that the relative toxicity of mercury and organic-mercury compounds would be dramatically increased if the test subjects were on certain antibiotics.
20) The toxicity of mercury vapor is dependent on retention and excretion and these vectors are dramatically affected by diet and antibiotic treatment as well as other factors. This makes it nearly impossible to define a safe level of exposure for any individual, but especially individuals with other types of neurological illnesses like motor neuron diseases or impending dementias. Being exposed minute by minute to mercury vapor for years has never been established as safe, but it has been effectively avoided by the dental organizations with the exception of giving their opinions regarding perceived safety. It is incredible that the responsible US government agencies and the organizations and companies using dental amalgam have not felt the need to produce such research. Especially with the obvious severe toxic nature mercury vapor and the ease at which the level of mercury vapor that would escape from a dental amalgam could be measured. The quality data is just not available in the literature to evaluate and determine the level at which mercury vapor is emitted from the various types of dental amalgam. However, it is my opinion that the reason is not because it would be difficult to do, but to do so would place the manufacturers and users of dental amalgam at risk for major lawsuits and they would lose their businesses.
21) One has to ask the simple question “Why are producers of amalgam products not required to produce data in the packages that describe the amount of mercury vapor that escapes daily from their amalgam of known weight and surface area under conditions that mimic the mouth with regards to temperature, pH and brushing?” In my opinion, the reason they don’t is well known since to do so would quickly establish their amalgam products as dangerous to human health.
22) The process of placing or removing dental amalgam’s in a pregnant mother has to increase the exposure of the in utero infant to elevated mercury vapors as it would dramatically increase the mother’s blood mercury levels. It is well known that mercury vapor can cross the placenta, and is even concentrated in the cord blood versus the mother’s blood. Other studies have shown that mercury increases in the birth hair of normal children in response to increasing dental amalgams in the birth mother20. Other similar studies point to aberrant mercury hair levels in children with neurological problems20,21. There can be little doubt that the exposure of a pregnant mother to mercury vapor by aggressive dental amalgam treatment could cause harm to her infant in utero. It also points out that the most effective protection of the body cannot keep mercury from spreading throughout the most susceptible of our population, the very young, the very old and the very ill.
Boyd E. Haley, Ph.D.,
Professor Emeritus, Department of Chemistry,
University of Kentucky,
Lexington, KY 40506
1. Schubert, J., Riley, E.J. and Tyler, S.A., Combined Effects in Toxicology—A Rapid Systemic Testing Procedure: Cadmium, Mercury and Lead. J. of Toxicology and Environmental Health v4;763-776, 1978.
2. Rowland, I.R., Robinson, R.D. and Doherty, R.A. Effects of Diet on Mercury Metabolism and Excretion in Mice Given Methylmercury: Role of Gut Flora Archives of Environmental Health V39, 401-408, 1984.
3. Schober, S.E., Sinks, T.H., Jones, R.L., Bolger, P.M., McDowell, M., Osterland, Garrett, E.S. Canady, R.A., Dillon, C.F., Sun, Y., Joseph, C.B. and Mahaffey, K. Blood Mercury Levels in US Children and Women of Childbearing Age, 1999-2000. JAMA April2;289(13) 1667-74, 2003.
4. Hornig, M., Chian, D. and Lipkin, W.I. Neurotoxic Effects of Postnatal Thimerosal are Mouse Strain Dependent. Molecular Psychiatry p1-13, 2004.
5. Havarinasab, S., Lambertsson, L., Qvarnstrom, J., and Hultman, P. Dose-response Study of Thimerosal-induced Murine Systemic Autoimmunity. Toxicology and Applied Pharmacology V194, 169-179, 2004.
6. Henriksson, J. and Tjalve, H. Uptake of Inorganic Mercury in the Olfactory Bulbs via Olfactory Pathways in Rats. Environmental Research 77, 130-140, 1998.
7. Berlin, M. Mercury in Dental Filling Materials-An Updated Risk Analysis in Environmental Medical Terms. The Dental Material Commission Care and Consideration, September 2003, Sweden URL: http://www.dental material.gov.se/mercury.pdf.
8. Zalups, R.K., Barfuss, D.W. Nephrotoxicity of Inorganic Mercury Co-administered with L-cysteine. Toxicology 109, 15-29, 1996.
9. Zalups, R.K., Barfuss, D.W. Participation of Mercuric Conjugates of Cysteine, Homocysteine, and N-acetylcysteine in Mechanisms Involved in the Renal Tubular Uptake of Inorganic Mercury. J. American Society of Nephrology V9 (4) 551-561, 1998.
10. Schardein, J.L. Chemically Induced Birth Defects, 2nd Edition, Chapter 8, Psychotropic Drugs. Marcel Dekker, Inc. NY, NY
11. Clarkson, T.W., Nordberg, G.F., and Sager, P. Reproductive and Developmental Toxicity of Metals. Scand. J. Work Environ. Health 11, 145-154, 1985.
12. Pendergrass, J.C. and Haley, B.E. Inhibition of Brain Tubulin-Guanosine 5′-Triphosphate Interactions by Mercury: Similarity to Observations in Alzheimer’s Diseased Brain. In Metal Ions in Biological Systems V34, pp 461-478. Mercury and Its Effects on Environment and Biology, Chapter 16. Edited by H. Sigel and A. Sigel. Marcel Dekker, Inc. 270 Madison Ave., N.Y., N.Y. 10016 (1996).
13. Pendergrass, J. C., Haley, B.E., Vimy, M. J., Winfield, S.A. and Lorscheider, F.L. Mercury Vapor Inhalation Inhibits Binding of GTP to Tubulin in Rat Brain: Similarity to a Molecular Lesion in Alzheimer’s Disease Brain. Neurotoxicology 18(2), 315-324 (1997).
14. Pamphlett, R. and Coote, P. Entry of Low Doses of Mercury Vapor into the Nervous System. NeuroToxicology 19(1), 39-48, 1998.
15. Gasset, A.R. Motokazu, I. Ishij, Y and Ramer, R.M. Teratogenicities of Opthalmic Drugs. Arch. Ophthalomol. V93, 52-55, 1975.
16. Lowell, J.A., Burgess, S., Shenoy, S., Curci, J.A., Peters, M., and Howard, T.K. Mercury Poisoning Associated with High-Dose Hepatitis-B Immune Globulin Administration after Liver Transplantation for Chronic Hepatitis-B. Liver Transplantation and Surgery V2(6) 475-478, November 1996.
17. Quadir, M., Zia, H., and Needham, T.E. Toxicological Implications of Nasal Formulations. Drug Delivery V6, 227-242, 1999.
18. Frustaci, A., Magnavita, N., Chimenti, C., Cladarulo, M., Sabbioni, E., Pietra, R., Cellini, C., Possati, G.F. and Maseri, A. J. American College of Cardiology V33(6), 1578-1583, 1999.
19. Kostial, K., Kello, D., Jugo, S., Rabar, I. and Maljkovic, T. Influence of Age on Metal Metabolism and Toxicity. Environmental Health Perspectives V25, 81-86, 1978.
20. Holmes, A.S., Blaxill, M.F. and Haley, B. Reduced Levels of Mercury in First Baby Haircuts of Autistic Children. International J. of Toxicology, 22:1-9, 2003
21. L-W. Hu, J. A. Bernard and J. Che, “Neutron Activation Analysis of Hair Samples for the Identification of Autism”, Transactions of the American Nuclear Society; 2003;89:681-2.
22. Kingman et al. J. Dental Research 77(3) 461, 1998. In a study of 1,127 military personnel by NIH the level of mercury in the urine of amalgam bearers was 4.5 times that of amalgam free controls. Some with extensive amalgams had levels 8 times or high than the amalgam free controls.
23. Echeverria, D., Woods, JS et al. Chronic low-level mercury exposure, BDNF (brain derived neurotrophic factor) polymorphism, and associations with cognitive and motor function. Neurotoxicol. Teratol, 2005 Nov-Dec; 27(6) 781-96.
24. Echeverria, D. Woods, JS, et al. The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans. Neurotoxicol. Teratol. 2005 Dec 8.
25. Hultman, P. et al. Adverse immunological effects and autoimmunity induced by dental amalgam and alloy in mice. The FASEB Journal 8 Nov 1183-1190, 1994.
26. Nataf, Robert. Porphyrinuria in Childhood Autistic Disorder. Conference on Autism in Edinburgh, Scotland December 2005. Also, Nataf et al. J. Toxicology and Applied Pharmacology 2006 (in press).
27. DeRouen et al. JAMA 295, 1784-92, 2006
28. Oliveria et al. Estradiol Reduces Cumulative Mercury and Associated Disturbances in the ypothalamus-Pituitary Axis of Ovariectomized Rats. Ecotoxicol. Environ. Safety Jan.10, 2006.
29. Haley, B. Medical Veritas
30. Rampersad et al., Transfusion 45(3):384-93,2005).
31. Leong, CCW, Syed, N.I., and Lorscheider, F.L. Retrograde Degeneration of Neurite Membrane Structural Integrity and Formation of Neruofibillary Tangles at Nerve Growth Cones Following In Vitro Exposure to Mercury. NeuroReports 12 (4):733-737, 2001
32. Atamna, H. and Frey, W.H. A Role for Heme in Alzheimer’s Disease: Heme Binds Amyloid-ß and has Altered Metabolism. Proc. Natl. Acad. Sci. 101(30) 11153-11158, 2004.
33. Knickmeyer, R., Baron-Cohen, S. Raggatt, P. and Taylor, K. Foetal Testosterone, Social Relationships, and Restricted Interests in Children. J. Child Psychology and Psychiatry 46:2 198-210, 2005.
34. Mackert, J.R. and Berglund, A. Mercyr Expposures from Dental Amalgam Fillings: Absorbed Dose and the Potential for Adverse Effects. Crit. Rev. Oral Biol. 8: 410-436, 1997.
35. British Dental Association website http;//www.bda-dentistry.org.uk/advice/factfile.cfm 2006
36. Murata, K., Weihe, P., Budtz-Jorgensen, E., Granjean, P. and Grandjean, P. Delayed Brainsteam Auditory Evoked Potential Latencies in 14 year old Children Exposed to Methylmercury. J. Pediatrics 44:177-183, 2004.
37. Huang, L.S., Cox, C Wilding, G.E., Meyers, G.J. Davidson, P.W. et al. Using measurement Error Models to Assess Effects of Prenatal and Postnatal Methylmercury Exposure in the Seychelles Child Development Study. Environ. Res. 93:115-122, 2003.
38. J. Woods, et al., Environmental Health Perspectives (2007) 115;10, 1527-1531.
39. Gerhardsson L, Lundh T, Minthon L, Londos E. Alzheimer’s Metal Concentrations in Plasma and Cerebrospinal Fluid in Patients with Disease. Dement Geriatr Cogn Disord. 2008 May 5;25(6):508-515..
40. Palkovicova L, Ursinyova M, Masanova V, Yu Z, Hertz-Picciotto I. Maternal amalgam dental fillings as the source of mercury exposure in developing fetus and newborn. J Expo Sci Environ Epidemiol. 2007 Sep 12.
41. Bjorkman, L. et al. Mercury in saliva and feces after removal of amalgam fillings. Toxicol. Appl. Pharmacol. 1997 May :144(1) :156-62. Department of Basic Oral Sciences, Karolinska Institutet, Stockholm, Sweden.
42. Skare, I and Engqvist, A. Human exposure to mercury and silver released from dental amalgam restorations. Arch Environ Health. 1994 Sep-Oct;49(5):384-94. National Institute of Occupational Health Stockholm, Sweden.
43. Feitosa-Santana et al. Irreversible color vision losses in patients with chronic mercury vapor intoxication. Visual Neuroscience (2008), 25:487-491
44. Donald R. Branch. Gender-selective toxicity of thimerosal. Departments of Medicine and Laboratory Medicine and Pathobiology, University of Toronto, 67 College St., Toronto, Ontario, Canada M5G 2M1 Experimental and Toxicologic Pathology (accepted 22 July 2008)
45. Perlingeiro RC, Queiroz ML. Measurement of the respiratory burst and chemotaxis in polymorphonuclear leukocytes from mercury-exposed workers. Hum Exp Toxicol. 1995 Mar;14(3):281-6.
46. Silbergeld EK, Silva IA, Nyland JF. Mercury and autoimmunity: implications for occupational and environmental health. Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):282-92. Department of Environmental Health Sciences, The Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA.
47. Abedi-Valugerdi M, Nilsson C, Zargari A, Gharibdoost F, DePierre JW, Hassan M. Bacterial lipopolysaccharide both renders resistant mice susceptible to mercury-induced autoimmunity and exacerbates such autoimmunity in susceptible mice. Clinical and Experimental Immunology 141: 238–247.
48. Rothwell JA, Boyd PJ. Amalgam dental fillings and hearing loss. Int J Audiol. 2008 Dec;47(12):770-6.
49. Mirella Telles Salgueiro Barbonia, b, , , et al. Visual field losses in workers exposed to mercury vapor. Environmental Research Volume 107, Issue 1, May 2008, Pages 124-131
50. Halbach S, Vogt S, Köhler W, Felgenhauer N, Welzl G, Kremers L, Zilker T, Melchart D. Blood and urine mercury levels in adult amalgam patients of a randomized controlled trial: interaction of Hg species in erythrocytes. Environ Res. 2008 May;107(1):69-78. Epub 2007 Sep 4. Institute of Toxicology, GSF Research Center for Environment and Health, Munich, Germany.
51. Skare, I. and Engqvist, A. Human exposure to mercury and silver released from dental amalgam restorations A. Arch Environ Health. 1994 Sep-Oct;49(5):384-94. National Institute of Occupational Health Stockholm, Sweden.
52. Björkman L, Sandborgh-Englund G, Ekstrand J. Mercury in saliva and feces after removal of amalgam fillings. Toxicol Appl Pharmacol. 1997 May;144(1):156-62. Department of Basic Oral Sciences, Karolinska Institutet, Stockholm, Sweden.
53. Michael J. McCabe, Jr*, Michael D. Laiosa*, Li Li, Sherri L. Menard, Raymond R. Mattingly and Allen J. Rosenspire. Low and Nontoxic Inorganic Mercury Burdens Attenuate BCR-Mediated Signal Transduction. Toxicological Sciences 2007 99(2):512-521.
54. Franco et al. Lactational Exposure to Inorganic Mercury: Evidence of Neurotoxic Effects. Neurotoxicol Teratol. 2007 May-Jun;29(3):360-7.
55. Haley, B. The relationship of the toxic effects of mercury to exacerbation of the medical condition classified as Alzheimer’s disease. Medical Veritas 4 (2007) 1510–1524.
56. Transport of thiol-conjugates of inorganic mercury in human retinal pigment epithelial cells.
Christy C. Bridges , a, , Jamie R. Battlea and Rudolfs K. Zalupsa data suggest that Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy are taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly systems B0, + and ASC. These amino acid transporters may play a role in the retinal toxicity observed following exposure to mercury.
57. Amalgam dental fillings and hearing loss.
Rothwell JA, Boyd PJ. Int J Audiol. 2008 Dec;47(12):770-6. In this study we investigated the effects of amalgam dental fillings on auditory thresholds. The results suggest an association between more amalgam fillings and poorer thresholds at higher frequencies, which could contribute to presbyacusis in developed countries.
58. Enhanced toxicity for mice of pertussis vaccines when preserved with Merthiolate.
Nelson, E.A. Gottshall, R.Y. Appl Microbiol. 1967 May;15(3):590-3. Pertussis vaccines preserved with 0.01% Merthiolate are more toxic for mice than unpreserved vaccines prepared from the same parent concentrate and containing the same number of organisms. An increase in mortality was observed when Merthiolate was injected separately, before or after an unpreserved saline suspension of pertussis vaccine.
59. Fish from 291 streams test positive for mercury in USGS survey”Data on Mercury in Water, Bed Sediment, and Fish from Streams Across the United States, 1998–2005,” the United States Geological Survey (USGS), a division of the Department of the Interior (DOI) More than two-thirds of the fish exceeded the U.S. EPA level of concern for fish-eating mammals.
60. HEPATITIS B VACCINATION OF MALE NEONATES AND AUTISM
CM Gallagher, MS Goodman, Graduate Program in Public Health, Stony Brook University Medical Center, Stony Brook, NY Annals of Epidemiology Vol. 19, No. 9 ABSTRACTS (ACE) September 2009: 651–680 p. 659 P24Boys who received the hepatitis B vaccine during the first month of life had 2.94 greater odds for ASD (Nz31 of 7,486; OR Z 2.94; p Z 0.03; 95% CI Z 1.10, 7.90) compared to later- or unvaccinated boys. Non-Hispanic white boys were 61% less likely to have ASD (ORZ0.39; pZ0.04; 95% CIZ0.16, 0.94) relative to non-white boys.CONCLUSION: Findings suggest that U.S. male neonates vaccinated with hepatitis B vaccine had a 3-fold greater risk of ASD; risk was greatest for non-white
61. Gender-selective toxicity of thimerosal
Donald R. Branch Departments of Medicine and Laboratory Medicine and Pathobiology, University of Toronto, 67 College St., Toronto, Ontario, Canada M5G 2M1 Experimental and Toxicologic Pathology (accepted 22 July 2008) At doses of 38.4–76.8 mg/kg using 10% DMSO as diluent, seven of seven male mice compared to zero of seven female mice tested succumbed to thimerosal. it was completely unexpected to observe a difference of the MTD between male and female mice. Thus, our studies, although not directly addressing the controversy surrounding thimerosal and autism, and still preliminary due to small numbers of mice examined, provide, nevertheless, the first report of gender-selective toxicity of thimerosal and indicate that any future studies of thimerosal toxicity should take into consideration gender-specific differences.
62. Mercury in saliva and feces after removal of amalgam fillings.
Björkman L, et al. Toxicol Appl Pharmacol. 1997 May;144(1):156-62. Department of Basic Oral Sciences, Karolinska Institutet, Stockholm, Sweden. The purpose of this study was to obtain data on Hg concentrations in saliva and feces before and after removal of dental amalgam fillings. Before removal, the median Hg concentration in feces was more than 10 times higher than in samples from an amalgam free reference group consisting of 10 individuals (2.7 vs 0.23 mumol Hg/kg dry weight, p < 0.001). Sixty days after removal the median Hg concentration was still slightly higher than in samples from the reference group. In saliva, there was an exponential decline in the Hg concentration during the first 2 weeks after amalgam removal (t 1/2 = 1.8 days). It was concluded that amalgam fillings are a significant source of Hg in saliva and feces.
63. Human exposure to mercury and silver released from dental amalgam restorations.
Skare, I and Engqvist, A. Arch Environ Health. 1994 Sep-Oct;49(5):384-94. National Institute of Occupational Health Stockholm, Sweden. In 35 healthy individuals, the number of amalgam surfaces was related to the emission rate of mercury into the oral cavity and to the excretion rate of mercury by urine. Oral emission ranged up to 125 micrograms Hg/24 h, and urinary excretions ranged from 0.4 to 19 micrograms Hg/24 h. In 10 cases, urinary and fecal excretions of mercury and silver were also measured. Fecal excretions ranged from 1 to 190 micrograms Hg/24 h and from 4 to 97 micrograms Ag/24 h. Except for urinary silver excretion, a high interplay between the variables was exhibited. The worst-case individual showed a fecal mercury excretion amounting to 100 times the mean intake of total Hg from a normal Swedish diet. With regard to a Swedish middle-age individual, the systemic uptake of mercury from amalgam was, on average, predicted to be 12 micrograms Hg/24 h.
64. Maternal amalgam dental fillings as the source of mercury exposure in developing fetus and newborn. Journal of Exposure Science and Environmental Epidemiology (2008) 18, 326–331.
Lubica Palkovicovaa, Monika Ursinyovaa, Vlasta Masanovaa, Zhiwei Yub and Irva Hertz-Picciottob”. The main aim of this analysis was to assess the relationship between maternal dental amalgam fillings and exposure of the developing fetus to HgThe median values of Hg concentrations were 0.63 mcg/l (range 0.14–2.9 g/l) and 0.80 mcg/l (range 0.15–2.54 mcg/l) for maternal and cord blood, respectively. Levels of Hg in the cord blood were significantly associated with the number of maternal amalgam fillings (=0.46, P<0.001) and with the number of years since the last filling (=- 0.37, P<0.001); these associations remained significant after adjustment for maternal age and education. Dental amalgam fillings in girls and women of reproductive age should be used with caution, to avoid increased prenatal Hg exposure. None of the cord blood Hg concentrations reached the level considered to be hazardous for neurodevelopmental effects in children exposed to Hg in utero (EPA reference dose for Hg of 5.8 mcg/l in cord blood).
65. Irreversible color vision losses in patients with chronic mercury vapor intoxication
66. CLÁUDIA FEITOSA-SANTANAa1a2 c1, MIRELLA T.S. BARBONIa1a2, NESTOR N. OIWAa1a2, GALINA V. PARAMEIa3, ANA LUISA A.C. SIMÕESa2, MARCELO F. DA COSTAa1a2, LUIZ CARLOS L. SILVEIRAa4a5 and DORA F. VENTURAa1a2 Visual Neuroscience (2008), 25:487-491. This longitudinal study addresses the reversibility of color vision losses in subjects who had been occupationally exposed to mercury vapor. These findings indicate that following a long-term occupational exposure to Hg vapor, even several years away from the source of intoxication, color vision impairment remains irreversible.
67. Alzheimer’s Metal Concentrations in Plasma and Cerebrospinal Fluid in Patients with Disease. Dement Geriatr Cogn Disord. 2008 May 5;25(6):508-515. Gerhardsson L, Lundh T, Minthon L, Londos E. The plasma concentrations of manganese and total mercury were significantly higher in subjects with AD (p < 0.001) and AD + vasc (p
68. Blood mercury levels rising among U.S. women. Dr. Dan Laks, UCLA August 09. Using data from the U.S. Centers for Disease Control and Prevention’s National Health and Nutrition Examination Survey (NHANES), a researcher from the University of California, Los Angeles, found that while inorganic mercury was detected in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006. “My study found compelling evidence that inorganic mercury deposition within the human body is a cumulative process, increasing with age and overall in the population over time,” study author and neuroscience researcher Dan R. Laks said in an UCLA news release. “My findings also suggest a rise in risks for disease associated with mercury over time.” Laks also found a connection between levels of the pituitary hormone lutropin and chronic mercury exposure, which he said might help explain mercury’s link to neurodegenerative disease. “these results suggest that chronic mercury exposure has reached a critical level where inorganic mercury deposition within the human body is accumulating over time,” Laks said. “It is logical to assume that the risks of associated neurodevelopmental and neurodegenerative diseases will rise as well.”