Mercury Detoxification, Chronic Mercury Poisoning and Amalgam Fillings

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Referenced and Abstracted Articles: Mercury

In my many years of researching mercury detoxification, chronic mercury poisoning, and mercury amalgam fillings, I've accumulated a wealth of information on these subjects. The majority of the information consists of studies and articles obtained from journals and medical reference sites. Each article is referenced and an abstract is provided and, where possible, the PIMD number for PubMed—indexed for MEDLINE—will be included with the referenced article. In some cases I limited the amount of information and in others I included the entire abstract. (You can access the PubMed website to enter the PIMD number by Clicking Here.)

This Referenced Database contains over 1100 referenced articles (175 pages) and to make searching easier I’ve included a Table of Contents that lists key topics in alphabetical order. Some of the topics are further broken down into subtopics. All referenced articles listed are also in alphabetical order; but by the title of the article. While this isn’t the standard format used by medical texts and journals, I’m certain you'll find that it makes your search for a topic/subject significantly easier. (If you are looking for a particular author or topic you can use the Find feature on your computer to search the database.)

The Referenced Database is extremely easy to use and search. Each subject listed in the Table of Contents will be linked to the articles about that topic and you only have to click on the topic to go to that section in database. Because there nearly 150 pages of referenced articles I've made it simple to maneuver throughout the database by adding Return to Table of Contents links throughout the site. Clicking on it will take you back to the Table of Contents. From there you can click on another subject of interest and move quickly around the site.

Sample References

In order to give you an idea of what you will be getting by purchasing this database, I chose referenced articles and abstracts from the topic, Fetus, Nursing Baby and Child, as an example of how the Referenced Database works. I selected this topic because I consider the poisoning of the fetus, nursing baby and child by mercury to be one of the most important health issues of the 21st century.

Every child born to a mother who has mercury amalgam fillings will, from conception and all during fetal development and nursing, be exposed to potentially toxic levels of mercury. I also believe that every mother-to-be, health professional and dentist should be aware of this critical health issue and take the necessary actions to deal with it. My book, The Poison in Your Teeth: Mercury Amalgam (Silver) Fillings . . . Hazardous to Your Health has a chapter that every mother should read. Get more information about the relationship of Mercury from Amalgam Fillings and Autism. For those of you who are interested in removing mercury from the body, I recommend by book, Mercury Detoxification: The Natural Way to Remove Mercury from Your Body.

To see how easy it is to use the Table of Contents database scroll down the Table of Contents until you get to Fetus, Nursing Baby and Child and click on the link. Keep in mind that the referenced articles and abstracts I’ve included as an example is but 3 of the over 175 pages available to you when you purchase the Referenced Database. Researching, reviewing and compliling these articles took thousands of hours. Accessing them will save you that time and the purchase price is only $225.00.

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Table of Contents


Amount from Amalgam Fillings-vs-Other Sources 
Antioxidants: General  Antioxidants: Specific                                          
       Alpha Lipoic Acid                                          



Blood and Body Fluids                                           
Breast Milk                                                


       DMSA & DMPS                                           
Cellular Damage

Chewing and Grinding                                                 
Composite Fillings and Bis-GMA                                


Dentists and Dental Office

Diseases and Symptoms
Amyotrophic lateral sclerosis (ALS)                      
Chronic Fatigue Syndrome (CFS)                       
Multiple Sclerosis (MS)                               
Parkinson’s Disease                                           

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Environmental Release                                           


Factors Affecting Release of Mercury from Amalgam Fillings          
      Tooth Grinding                                           
      Hot Drinks                                              
      Tooth Brushing                                           
      Acid conditions in Mouth                                    
Fecal Metals                                                   
Fetus, Baby, and Child                                            
Fish and Food                                                 
Free Radicals                                               


Galvanic and Corrosion Effects                                  

General Health                                                 
Genetic/ Mutations                                          

Hair Analysis                                                 


Immune System, Autoimmune, and Allergy                            
     Relationship to Amalgam Fillings                              
Infertility and Birth Defects                                        


Legal and Political     

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Methylation of Mercury                                               





Regulatory Agencies                                             
Release and Absorption                                          
Removal Protocol                                               
Resistance to Antibiotics                                        


Symptoms Improvement after Amalgam Removal                     


Types of Amalgam fillings                                         


WHO: No Safe level of Hg

Fetus, Nursing Baby and Child: Sample of Referenced and Abstracted Articles

Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Grandjean P, Weihe P, White RF, Debes F, Araki S, Yokoyama K, Murata K, Sorensen N, Dahl R, Jorgensen PJ. Neurotoxicol Teratol. 1997 Nov-Dec; 19(6):417-28. 9392777 PubMed. However, mercury-related neuropsychological dysfunctions were most pronounced in the domains of language, attention, and memory, and to a lesser extent in visuospatial and motor functions. The effects on brain function associated with prenatal methylmercury exposure therefore appear widespread, and early dysfunction is detectable at exposure levels currently considered safe.

Comparison of mercury levels in maternal blood, fetal cord blood, and placental tissues. Kuhnert PM, Kuhnert BR, Erhard P. Am J Obstet Gynecol. 1981 Jan 15; 139(2):209-13. 7457537 PubMed. From our data it is clear that methyl mercury accumulates in cord erythrocytes: A total of 30% more methyl mercury was found in fetal erythrocytes than in maternal erythrocytes. Also correlation analysis of the methyl mercury levels in maternal and fetal erythrocytes showed a strong correlation (r = 0.87). In regard to inorganic mercury, the highest concentration was found in the placenta, suggesting a barrier role, but a significant correlation (r = 0.62) was also found between the maternal and fetal plasma levels of inorganic mercury. Moreover, the inorganic mercury concentration per gram of plasma was higher in fetal cord plasma than in maternal plasma.

Concentrations of heavy metals in maternal and umbilical cord blood. Ong CN, Chia SE, Foo SC, Ong HY, Tsakok M, Liouw P. Biometals. 1993 Spring; 6(1):61-6. 8471826 PubMed. These results suggest that, like essential metals, most heavy metals can move rather freely across the human placenta. The potential health effects of heavy metal transfer from mothers to young infants cannot be discounted.

Disposition of inhaled mercury vapor in pregnant rats: maternal toxicity and effects on developmental outcome. Morgan DL, Chanda SM, Price HC, Fernando R, Liu J, Brambila E, O'Connor RW, Beliles RP, Barone S Jr. Toxicol Sci. 2002 Apr;66(2):261-73. 11896293 PubMed. Total Hg concentrations in maternal tissues increased with increasing number of exposure days and concentration. In general, approximately 70% of Hg was eliminated from maternal tissues during the week following the last exposure (GD 15 to PND 1). Elimination of Hg from maternal brain and kidney was slower than in other tissues, possibly due to higher levels of metallothionein. Total Hg concentrations in fetal tissues increased with increasing number of exposure days and concentration, demonstrating that a significant amount of Hg crossed the placenta. One week after the last exposure, significant amounts of Hg were still present in brain, liver, and kidney of PND 1 neonates. The total amount of Hg in neonatal brain (ng/brain) continued to increase after termination of inhalation exposure, suggesting a redistribution of Hg from the dam to neonatal brain. These data demonstrate that inhaled Hg0 vapor is distributed to all maternal and fetal tissues in a dose-dependent manner. Adverse effects of Hg on developmental outcome occurred only at a concentration that caused maternal toxicity.

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Distribution and transfer pathways of antioxidant molecules inside the first trimester human gestational sac. Jauniaux E, Cindrova-Davies T, Johns J, Dunster C, Hempstock J, Kelly FJ, Burton GJ. J Clin Endocrinol Metab. 2004 Mar;89(3):1452-8. 15001647 PubMed. The first-trimester human placenta has limited antioxidant enzyme capacity. We investigated the distribution and transfer pathways of antioxidant molecules inside the first trimester gestational sac. The coelomic fluid of the exocoelomic cavity, which borders the inside of the first-trimester placenta, contained a very low level of reduced glutathione. Glutathione disulfide was undetectable in most coelomic samples, suggesting that the role of glutathione-related detoxification system is limited in fetal fluid compartments. The coelomic fluid contained similar concentrations of ascorbic and uric acid to maternal plasma. The levels of alpha- and gamma-tocopherol were lower in coelomic fluid, compared with maternal plasma. The presence of these molecules inside the early gestational sac suggests that they may play an essential role in the fetal tissues' antioxidant capacity at a time when the fetus is most vulnerable to oxidative stress. We also demonstrated by immunostaining the presence of alpha-tocopherol transfer protein in the cytoplasm of trophoblastic cells, glandular epithelium of the decidua, and mesothelial layer of the secondary yolk sac. This finding indicates that the uterine glands and the secondary yolk sac play key roles in supplying this essential vitamin to the developing fetus before the placental circulations are established.

Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Urbach J, Boadi W, Brandes JM, Kerner H, Yannai S. Reprod Toxicol. 1992; 6(1):69-75. 1562801 PubMed. The effect of mercury (HgCl2) on placental amino acid and glucose transfer as determined by the use of their nonmetabolizable radioactive analogues, aminoisobutyric acid (AIB) and 3-o-methyl glucose (3MG), respectively, was studied in an in vitro perfusion model of a term human placenta. Hg2+ was found to decrease the transfer and accumulation of AIB without affecting 3MG transfer. It was also found to decrease the placental oxygen consumption rate. Placental circulation and tissue morphology remained intact, as demonstrated by the antipyrine transfer rate, and by electron microscopy, respectively. The mechanism by which Hg2+ may interfere with placental amino acid transfer and accumulation is discussed. Although much higher concentrations than those found in the ordinary polluted environment were used, this is the first report showing that Hg2+ interferes with an essential human placental function in a system employing a whole human placental cotyledon. This finding may indicate the possible involvement of Hg2+ in impaired organogenesis in early pregnancy or deranged fetal growth during the last trimester.

Environmental factors associated with a spectrum of neurodevelopmental deficits. Mendola P, Selevan SG, Gutter S, Rice D. Ment Retard Dev Disabil Res Rev. 2002; 8(3):188-97. 12216063 PubMed. At high levels of prenatal exposure, methylmercury produces mental retardation, cerebral palsy and visual and auditory deficits in children of exposed mothers. Exposure to environmental agents with neurotoxic effects can result in a spectrum of adverse outcomes from severe mental retardation and disability to more subtle changes in function depending on the timing and dose of the chemical agent.

Evolution of our understanding of methylmercury as a health threat. Watanabe C, Satoh H. Environ Health Perspect. 1996 Apr; 104 Suppl 2:367-79. 9182044 PubMed. After repeated occurrences of MeHg poisoning, it gradually became clear that the fetus is much more susceptible to the toxicity of this compound than the adult. The results of these studies revealed that the effects encompass a wide range of behavioral categories without clear identification of the functional categories distinctively susceptible to MeHg.

Influence of prenatal mercury exposure upon scholastic and psychological test performance: benchmark analysis of a New Zealand cohort. Crump KS, Kjellstrom T, Shipp AM, Silvers A, Stewart A. Risk Anal. 1998 Dec; 18(6):701-13. 9972579 PubMed. The original analyses of five test scores found an association between high prenatal mercury exposure and decreased test performance, using category variables for mercury exposure. Our regression analyses, which utilized the actual hair mercury level, did not find significant associations between mercury and children's test scores. However, this finding was highly influenced by a single child whose mother's mercury hair level (86 mg/kg) was more than four times that of any other mother. When that child was omitted, results were more indicative of a mercury effect and scores on six tests were significantly associated with the mothers' hair mercury level. BMDs calculated from five tests ranged from 32 to 73 mg/kg hair mercury, and corresponding BMDLs (95% lower limits on BMDs) ranged from 17 to 24 mg/kg.

Intrauterine methylmercury intoxication. Consequence of the inherent brain lesions and cognitive dysfunction in maturity. Kakita A, Wakabayashi K, Su M, Yoneoka Y, Sakamoto M, Ikuta F, Takahashi H. Brain Res. 2000 Sep 22; 877(2):322-30. 10986347 PubMed. Morphometric analysis of the amygdala and hippocampus revealed significantly fewer neurons in both areas in the MeHg-exposed rats. Thus, chronic intrauterine exposure to low-dose MeHg induces a decrease in neuron population in the limbic system, and the offspring have impaired higher brain function. 

Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood.
Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M. Environ Res. 2000 Oct ;84(2):186-94. 11068932 PubMed. We have investigated exposure to methylmercury (MeHg) and mercury vapor (Hg0) in pregnant women and their newborns in Stockholm. The women were followed for 15 months post delivery. MeHg, inorganic Hg (I-Hg), and total Hg (T-Hg) in maternal and cord blood were determined by automated alkaline solubilization/reduction and cold vapor atomic fluorescence spectrometry. T-Hg in urine was determined by inductively coupled plasma mass spectrometry. About 72% of the Hg in blood (n = 148) in early pregnancy was MeHg (median 0.94 microg/L, maximum 6.8 microg/L). Blood MeHg decreased during pregnancy, partly due to decreased intake of fish in accordance with recommendations to not eat certain predatory fish during pregnancy. Cord blood MeHg (median 1.4 microg/L, maximum 4.8 microg/L) was almost twice that in maternal blood in late pregnancy and was probably influenced by maternal MeHg exposure earlier and before pregnancy. Blood I-Hg (median 0.37 microg/L, maximum 4.2 microg/L) and urine T-Hg (median 1.6 microg/L, maximum 12 microg/L) in early pregnancy were highly correlated, and both were associated with the number of amalgam fillings. The concentrations decreased during lactation, probably due to excretion in milk. Cord blood I-Hg was correlated with that in maternal blood. The results show the importance of speciation of Hg in blood for evaluation of exposure and health risks.

Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vimy MJ, Takahashi Y, Lorscheider FL. Am J Physiol. 1990 Apr; 258(4 Pt 2):R939-45. 2331037 PubMed. In humans, the continuous release of Hg vapor from dental amalgam tooth restorations is markedly increased for prolonged periods after chewing. The present study establishes a time-course distribution for amalgam Hg in body tissues of adult and fetal sheep. Under general anesthesia, five pregnant ewes had twelve occlusal amalgam fillings containing radioactive 203Hg placed in teeth at 112 days gestation. Blood, amniotic fluid, feces, and urine specimens were collected at 1- to 3-day intervals for 16 days. From days 16-140 after amalgam placement (16-41 days for fetal lambs), tissue specimens were analyzed for radioactivity, and total Hg concentrations were calculated. Results demonstrate that Hg from dental amalgam will appear in maternal and fetal blood and amniotic fluid within 2 days after placement of amalgam tooth restorations. Excretion of some of this Hg will also commence within 2 days. All tissues examined displayed Hg accumulation. Highest concentrations of Hg from amalgam in the adult occurred in kidney and liver, whereas in the fetus the highest amalgam Hg concentrations appeared in liver and pituitary gland. The placenta progressively concentrated Hg as gestation advanced to term, and milk concentration of amalgam Hg postpartum provides a potential source of Hg exposure to the newborn. It is concluded that accumulation of amalgam Hg progresses in maternal and fetal tissues to a steady state with advancing gestation and is maintained. Dental amalgam usage as a tooth restorative material in pregnant women and children should be reconsidered.

Maternal-fetal transfer of metallic mercury via the placenta and milk. Yang J, Jiang Z, Wang Y, Qureshi IA, Wu XD. Ann Clin Lab Sci. 1997 Mar-Apr; 27(2):135-41. 9098513 PubMed. Therefore, this study concluded that the metallic mercury can be transferred to the fetus via the placenta and secreted to a newborn via milk.

Mercury burden of human fetal and infant tissues. Drasch G, Schupp I, Hofl H, Reinke R, Roider G. Eur J Pediatr. 1994 Aug; 153(8):607-10. 7957411 PubMed. The toxicological relevance of the unexpected high Hg-K of older infants from mothers with higher numbers of dental amalgam fillings is discussed. CONCLUSION: Future discussion on the pros and cons of dental amalgam should not be limited to adults or children with their own amalgam fillings, but also include fetal exposure. The unrestricted application of amalgam for dental restorations in women before and during the child-bearing age should be reconsidered.

Mercury in human colostrum and early breast milk. Its dependence on dental amalgam and other factors. Drasch G, Aigner S, Roider G, Staiger F, Lipowsky G. J Trace Elem Med Biol. 1998 Mar; 12(1):23-7. 9638609 PubMed. The Hg-M in the breast milk samples correlates positively with the number of maternal teeth with dental amalgam. The mean Hg-M of amalgam-free mothers was < 0.2 microgram/L, while milk from mothers with 1-4 amalgam fillings contained 0.57 microgram/L, with 5-7 fillings 0.50 microgram/L and with more than 7 fillings 2.11 micrograms/L. 

Placental to fetal transfer of mercury and fetotoxicity. Yoshida M. Tohoku J Exp Med. 2002 Feb; 196(2):79-88. 12498319 PubMed. Mercury vapor is known penetrate the placental barrier more easily than inorganic mercury. A relative amount of mercury accumulates in the fetus after exposure of pregnant animals to mercury vapor. Mercury concentration in fetal organs is much lower than that in maternal organs except the liver, and fetal liver shows significantly higher mercury concentrations than maternal liver. In fetal liver, a substantial portion of mercury is bound to metallothionein (MT), which plays an important role as a reservoir of mercury during the prenatal period. The mercury retained in fetal liver is redistributed to other organs, such as the brain and kidney, with diminishing MT levels during postnatal development. Consequently, an increase in mercury concentration in the brain and kidney of the neonate is observed. In studies on animal offspring in utero exposed to mercury vapor, behavioral changes, such as radial arm maze, morris maze and lever-press durations, are observed when the levels of mercury vapor exceed the threshold limit value (TLV).

Placental transfer of mercury in pregnant rats which received dental amalgam restorations. Takahashi Y, Tsuruta S, Arimoto M, Tanaka H, Yoshida M. Toxicology. 2003 Mar 14; 185(1-2):23-33. 12505442 PubMed. The results of the present study demonstrated that mercury vapor released from the amalgam fillings in pregnant rats was distributed to maternal and fetal organs in dose-dependent amounts of the amalgam fillings.

Technical report: mercury in the environment: implications for pediatricians. Goldman LR, Shannon MW. American Academy of Pediatrics: Committee on Environmental Health. Pediatrics. 2001 Jul; 108(1):197-205. 11433078 PubMed. Mercury is a ubiquitous environmental toxin that causes a wide range of adverse health effects in humans. Three forms of mercury (elemental, inorganic, and organic) exist, and each has its own profile of toxicity. Exposure to mercury typically occurs by inhalation or ingestion. Readily absorbed after its inhalation, mercury can be an indoor air pollutant, for example, after spills of elemental mercury in the home; however, industry emissions with resulting ambient air pollution remain the most important source of inhaled mercury. Because fresh-water and ocean fish may contain large amounts of mercury, children and pregnant women can have significant exposure if they consume excessive amounts of fish. The developing fetus and young children are thought to be disproportionately affected by mercury exposure, because many aspects of development, particularly brain maturation, can be disturbed by the presence of mercury. Minimizing mercury exposure is, therefore, essential to optimal child health. This review provides pediatricians with current information on mercury, including environmental sources, toxicity, and treatment and prevention of mercury exposure.

The effect of mercury vapour on cholinergic neurons in the fetal brain: studies on the expression of nerve growth factor and its low- and high-affinity receptors. Soderstrom S, Fredriksson A, Dencker L, Ebendal T. Brain Res Dev Brain Res. 1995 Mar 16;85(1):96-108. 7781173 PubMed. These findings suggest that low levels of prenatal mercury vapour exposure can alter the levels of the NGF and its receptors, indicating neuronal damage and disturbed trophic regulations during development. 

The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Drexler H, Schaller KH. Environ Res. 1998 May;77(2):124-9. 9600805 PubMed. The concentration of mercury in the breast milk collected immediately after birth showed a significant association with the number of amalgam fillings as well as with the frequency of meals. Urine mercury concentrations correlated with the number of amalgam fillings and amalgam surfaces.

Total and inorganic mercury in breast milk in relation to fish consumption and amalgam in lactating women. Oskarsson A, Schultz A, Skerfving S, Hallen IP, Ohlin B, Lagerkvist BJ. Arch Environ Health. 1996 May-Jun;51(3):234-41. 8687245 PubMed. The concentrations of total mercury and organic mercury (calculated by subtraction of inorganic mercury from total mercury) in blood (r = .59, p = .0006, and r = .56, p = .001; respectively) and total mercury in hair (r = .52, p = .006) were correlated with the estimated recent exposure to methylmercury via intake of fish. A significant correlation was found between levels of total mercury in blood and in milk (r = .66, p = .0001), with milk levels being an average of 27% of the blood levels. There was an association between inorganic mercury in blood and milk (r = .96, p < .0001); the average level of inorganic mercury in milk was 55% of the level of inorganic mercury in blood. The results indicated that there was an efficient transfer of inorganic mercury from blood to milk and that, in this population, mercury from amalgam fillings was the main source of mercury in milk. Exposure of the infant to mercury from breast milk was calculated to range up to 0.3 microg/kg x d, of which approximately one-half was inorganic mercury. This exposure, however, corresponds to approximately one-half the tolerable daily intake for adults recommended by the World Health Organization. We concluded that efforts should be made to decrease mercury burden in fertile women.

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