B. Windham (Ed.)             


I.              Introduction


The health effects of toxic metals are  synergistic  with other toxic exposures such as  pesticides , herbicides,& other  endocrine disrupting substances like organochlorine compounds , POP s, PAHs , PCBs, etc. There are also synergistic effects with the various types of parasites, bacteria, viruses to which people have common exposures and commonly become infected when the immune system is weakened by toxic exposures. Studies have found considerable genetic variability in  susceptibility  to toxic metals as well. The health effects caused to children by pesticides and herbicides include birth defects, ADHD, seizures, developmental conditions, etc. While there is considerable commonality to the health effects commonly caused by the toxic metals, and effects are cumulative and  synergistic  with other toxic exposures, this paper will concentrate on the health effects of elemental mercury from amalgam fillings and toxic metals. 


 Mercury is one of the most toxic substances commonly encountered, and according to Government agencies causes adverse health effects in large numbers of people in the U.S. [1,2] The extreme toxicity of mercury can be seen from documented effects on wildlife by very low levels of mercury exposure. Because of the extreme toxicity of mercury, only ½ gram is required to contaminate the ecosystem and fish of a 10- acre lake to the extent that a health warning would be issued by the government to not eat the fish [3].  Over half the rivers and lakes in Florida have such health warnings [4] banning or limiting eating of fish, as do approximately 20% of all U.S. lakes, all Great Lakes, 7% of all U.S. river miles, and many bays.  Other countries including Canada have similar experience. 


  Mercury has been documented by studies on animals to be extremely cytotoxic, neurotoxic, immunotoxic , genotoxic, and to be an endocrine disrupter and cause of infertility and fertility problems (153). Humans have significant toxic exposures other than mercury, but mercury and other toxic metals have been documented to have similar synergistic effects on children and adults (151,153). Toxic metals have been documented by the U.S. Department of Health and EPA to cause large numbers of adverse health effects each year, more than any other toxic exposures, with mercury, lead, and arsenic affecting the largest number of people (1).  A study by the National Academy of Sciences and other similar studies have documented that in the 1990s the majority of U.S. pregnancies resulted in birth defects, neurological, or other significant developmental conditions (150). Studies have documented that the majority of these were due to toxic exposures, with toxic metals being the major factor in most (151,152).  Vaccines and other toxic exposures have been documented to be the main cause or a major factor in many chronic developmental children’s conditions including autism, ADHD, learning disabilities, eczema, epilepsy, asthma and chronic lung conditions, diabetes, SIDS, etc. (151,152).   Exposures to mercury along with other toxic metals together have been found by hundreds of thousands of medical tests to be very common, and synergistic toxic effects that are more than 10 fold more dangerous have been  documented( 155).        


That mercury can affect fertility is well known since mercury has been commonly used as a spermicide in birth control products. Potential effects can again be seen from effects on wildlife.  Some Florida panthers that eat birds and animals that eat fish, frogs, and turtles containing very low levels of mercury (about 1 part per million) have died from chronic mercury  poisoning[ 5,6].   Since mercury is an estrogenic chemical and reproductive toxin, the majority of the rest cannot reproduce.  The average male Florida panther  has  estrogen  levels as high as females, due to the estrogenic properties of mercury.  Similar is true of some other animals at the top of the food chain like alligators and wading  birds[ 5,6,7], and marine mammals such as polar bears, seals, beluga and orca whales.      Other estrogenic chemicals such as dioxins, PCBs, organophosphate pesticides, other pesticides, toxic metals, and some  organochlorinechemicals , and Phthalates are also known to cause neurological and other developmental conditions in  children( 161,152)

 Under the Proposition 65 procedures, passed by the state of California in 1986, mercury has been determined to be a reproductive toxin, and to cause birth defects.  Thus, products that use mercury and cause significant mercury exposure must provide warnings to the public of the known health  risk( 156).  Use of dental amalgam by dentists in California requires such a warning.  Several other states have passed similar laws requiring warnings by dentists of the known health risk related to use of dental amalgam.  Dental amalgam has been documented by tests at medical labs to be the largest source of mercury exposure for most people who have several amalgam fillings (31), with exposure levels as much as 10 times the average for those without amalgam fillings. And as later shown mother’s dental amalgam is similarly the largest source of mercury to the fetus and young infants. 

A study of environmental mercury levels in Texas school districts  found a 61 percent increase in autism and a 43 percent increase in special education cases for every 1,000 pounds of mercury released into the environment(157a). A utism prevalence diminished by 2 percent for every 10 miles of distance from a mercury source.    Another similar study found similar results and estimated economic costs due to disability or lower IQ (157b).  Fossil fuel-burning power plants were the largest source of the widespread mercury pollution(157), but dental amalgam was the largest source in most people with several dental amalgams(31) plus the largest source of mercury in sewers and a significant source of environmental mercury in water bodies, fish, and air emissions(158).


      Historically most of the research and concern regarding mercury's toxic effects on humans and in particular on fetal development have focused on methyl mercury rather than mercury vapor or inorganic mercury or the type of mercury in vaccines, ethyl mercury. This has been due to a combination of factors, but basic misunderstandings of the differential nature and effect mechanisms of the different forms of mercury appears to have played a role in this.   There have been highly publicized major acute poisonings affecting many people and infants of those exposed through fish in Japan and food in Iran.  Methylmercury has also been shown to be extremely neurotoxic, much moreso than inorganic forms that do not as readily cross cellular membranes such as the blood‑brain barrier, even though they are also very neurotoxic.  Additionally, doctors and researchers have traditionally tended to use  blood tests  to test for mercury exposure, without the understanding from more recent experience that has found blood tests mainly relevant to methylmercury, not mercury vapor or inorganic mercury body burden and only measure recent exposures. Mercury vapor has been found to have an extremely short half‑life in the  blood[ 8-10] since the vapor form rapidly crosses cellular membranes including the blood‑brain barrier and placenta, where it is rapidly oxidized to inorganic forms. While the half life of vapor in the blood has been found to be about 8 seconds[ 8], the inorganic form does not readily cross cellular membranes resulting in accumulation in the body organs, especially the brain where the half life can be over 20 years[11,12].  The form of mercury found in the blood by blood tests is thus mostly  organic[ 9,13], while most of the mercury in body organs and urine is mostly inorganic.  However, unfortunately there is no simple or commonly accepted test methodology for inorganic mercury body burden, other than post‑mortem autopsies which have verified the accumulation of inorganic mercury in the brain and other organs [12,14,15,127].  In a large U.S.CDC survey more than 16 % of infants had blood levels of mercury above the upper level of mercury exposure recommended by the German Commission on Human Biomonitoring of 10 micrograms per liter in the blood(54), and over 10% of women of childbearing age had blood levels above the WHO standard of 40 ug/L at which infants born would be at significant risk of developmental disabilities(1).   The upper level of mercury exposure recommended by the German Commission on Human Biomonitoring is 10 micrograms per liter in the blood(54), but adverse effects such as  increases in blood pressure and cognitive effects have been documented as low as 1 ug/L, with impacts higher in low birthweight babies(54). Thus the European and U.S. National Academy of Sciences mercury limit was lowered to 5 ug/L(54b). A much higher percentage of child bearing women are thus seen to have mercury levels above the new safety limits.  Studies have found that prenatal mercury exposure commonly results in metal retardation, lowered IQs,  learning disabilities , and  autism (138,148,149,118,119,132-137).

      While urine mercury correlates with inorganic mercury exposure and is a better measure than blood, urine mercury is an unreliable measure for those chronically exposed since mercury excretion through the kidneys deteriorates with cumulative exposure.   It apparently also is not widely understood that mercury commonly changes forms within the body, both from organic mercury to inorganic mercury and from inorganic mercury to organic mercury. It has been demonstrated that bacteria in the mouth and intestines as well as yeast methylate inorganic mercury to organic mercury, and methylation of mercury from  amalgam is the largest source of methyl mercury in most people with amalgam [11,16,31,29].  Some patients who eat no fish but have high levels of inorganic mercury exposure have been tested to have high levels of organic mercury in the body.  


      Also while it has been known that the general public is commonly exposed to methylmercury which is the main form of mercury in fish, it has not been commonly understood that there was significant widespread exposure to inorganic mercury.  Although it has now been well documented that the major exposure to mercury for most people is from amalgam fillings and that likewise maternal amalgam fillings are a major source of exposure for the fetus and infants, this information has not been widely publicized and appears to be unknown to the majority of doctors, dentists, and the public.  This paper clarifies and documents some of these recent findings, and also reviews the fertility and fetal development effects of mercury vapor, which have been documented at even lower levels than for methylmercury in some cases.


II. Mechanisms of Mercury Leakage from Amalgam fillings and Levels of Exposure.


The average amalgam filling weighs more than ½ gram and is 50% mercury.  Mercury is known to have a low vapor pressure and to be continuously vaporized and absorbed by the body.  Amalgam has  also  been  shown to act like a battery, setting up galvanic currents in the mouth, resulting in high levels of mercury being deposited through this action in the oral tissues and mucosa, from which it also spreads to other parts of the body[17-23].   Levels commonly found in the oral tissues of those with amalgam fillings were 100 to 1200 times the FDA/EPA action level for health warnings in food, which is 1 part per million (ppm)  mercury[ 4].


Except for special populations such as occupationally exposed workers and populations with a high level of fish in the diet, the number one source of mercury in most people has been documented to be dental amalgam  fillings[ 13,24-31].  Most of the thousands of people with several amalgam fillings who have been tested were found to have daily exposure levels of mercury vapor exceeding government safety guidelines. The U.S. ATSDR mercury vapor minimum risk  level( MRL) is 0.2 micrograms per cubic meter(ug/M 3 )[32]. Most people with amalgam fillings who have been tested have been found to have much higher levels of mercury in their oral air than this, with some as high as 100 ug/M 3 [24,25,28-31].   


For an adult breathing 0.2 ug/day of mercury and breathing approximately 20 cubic meters per day of  air[ 27], the ATSDR MRL gives a guideline level of exposure of approx. 4 micrograms per day.  Most of the many thousands tested who have 9 or more amalgam fillings were found to have exposure levels above this level and above U.S. government health guidelines for  mercury[ 11,13,24-31].    While most studies such as Richardson’s analysis for Health  Canada[ 27] that are primarily based on urine measurements use conservative estimates of daily mercury exposure from amalgam in the range 3 to 5 ug/day, studies which measure levels of mercury in feces or saliva found considerably higher daily exposure levels.  Two studies found daily excretion in feces  betweeen  30 to 190 ug for subjects with between 18 and 82 amalgam surfaces, with an average of 60 ug/ day[ 25,28].  Another  study[ 29] found daily excretion through feces from 10 to 87 ug.  A medical laboratory,  BIOSPECTRON  SWEDEN AB, that has performed thousands of fecal tests for mercury reports a similar range of daily excretion.  Large studies that measured mercury levels in saliva have found that over 90 % of mercury in saliva typically comes from amalgam fillings, and the level of mercury found in saliva has a similar range as the studies for level in feces previously quoted[ 24,29].  A large study of mercury levels in the U.S. military population found average daily excretion levels in urine for subjects with 20 amalgam surfaces to be  appoximately  6.2 ug, assuming 2 liters of urine excreted per  day[ 13].  Significant levels of mercury have also been found in sweat and appear to often be more than 2 ug per day for subjects with approximately 1200 ml of sweat per day.  Additionally autopsy  studies[ 12] have found that for those with chronic exposure, daily exposure levels are higher than excretion levels so mercury accumulates in the major body organs including the brain, heart, kidneys, liver, etc.  Thus altogether daily exposure levels for those with several fillings appear to often exceed 50 ug/day, with exposure levels of over 100 ug/day not uncommon[ 24,29]. Studies have also found the majority of such exposure to come from vapor rather than particles, with relatively high absorption rates in the  body[ 25].



III. Effects of Mercury Exposure on Fertility and Fetal Development  


Many studies have documented health effects occurring to the neurological, immune, hormonal, and reproductive systems due to the high levels of mercury accumulating from chronic occupational exposure.  But many recent studies have found reproductive effects including infertility (153,154) and developmental effects in the fetus and infants at much lower levels than those having significant effects on adults.  As compared to adults, the fetus and newborns have been found to be much more susceptible to the effects of low levels of mercury exposure due to low body weight with higher food consumption rate per kilogram of body weight, higher gastrointestinal absorption rate, less effective renal excretion, and a less effective blood-brain barrier[33].


Mercury has been found to be a significant cause of seizures and  epilepsy( 147). The effects of chronic, low-dose fetal and  lactationalorganic ( MeHgCl ) and inorganic (HgCl2) mercury intoxication on epilepsy/seizures were investigated and compared in rats and were found to have significant correlations between seizure susceptibility and cortical mercury level(147a) Inorganic mercury exposure facilitated the duration of seizure discharges in younger animals and appeared to be more permanent than methyl mercury exposure.  Another researcher had similar findings for infants(147b) 

The most common source of maternal exposure to mercury vapor, as previously shown, is amalgam fillings, while the most common sources of methyl mercury in people are  amalgam( 31) and fish.  Both have been demonstrated to cause rapid transmittal through the placenta to the fetus [14,15,34-51/52-54].   The fetal mercury content after maternal inhalation of mercury vapor was found to be over 20 times that for maternal exposure to an equivalent dose of inorganic mercury[48-50], and levels of mercury in the brain, heart, and major organs have been found to be higher after equal exposure levels to mercury vapor than for the other mercury forms [8,55].  Some developmental and behavioral effects from mercury vapor have been found at levels considerably below that required for similar effects by methyl mercury [10,38,49,56-58].  The studies reviewed found that mercury vapor and organic mercury have independent and synergistic toxic and developmental effects along with those of other toxic metals such as nickel, palladium, gold, and cadmium, and that additionally conversions occur in the body between the various forms of  mercury[ 16,59].  Extensive immune system tests for populations of patients with chronic autoimmune diseases such as Chronic Fatigue Syndrome or chronic neurological conditions have also demonstrated that a much higher percentage of the patients have autoimmune reactions to inorganic mercury than to organic mercury, and that immune reactivities and symptoms improve in the majority of cases when amalgam fillings are replaced[16,59] 


 Based on animal studies using rats, sheep, and monkeys as well as human studies, mercury from amalgam in the blood of pregnant women crosses the placenta and appears in amniotic fluid and fetal blood, liver, and pituitary gland within 2 days of placement [10,14,15, 34-36,43-47,60,/54].    Studies have  found  a  significant correlation between number of amalgam fillings of the mother and the level of mercury in the fetus, infants, and young children[10,14,15,34-40], and also with the level in mother's milk [10,38-42].   Breast milk has been found to increase the bioavailability of inorganic mercury, which was found to be excreted to milk from blood at a higher level than organic  mercury( 41,44,45,61). The main mechanism of transfer was found to be binding to  albumin( 45).  For non-occupationally exposed populations and populations without high fish consumption, these studies found dental amalgams appear to be the main source of mercury in breast milk and the fetus, but significant levels of methyl mercury are also often found in breast milk [43,44,46,54,61].  U.S. ATSDR  staff[ 62] indicate that under normal circumstances mercury in mother’s milk should be under 1.7 ug/L, and 3.5 ug/L appears to be an adequate screening level for health risk. They indicate that there is evidence that contaminated breast milk is a source of potential risk to infants.  An Italian study indicates that a commonly used mercury tolerance level for human milk is 4  ppb( 43).


      Mercury is often stored in breast milk and the fetus at much higher levels than that in the mother [10,36,38-46,60,61/54].   Milk from mothers with 7 or more fillings was found to have levels of mercury approximately 10 times that of amalgam free mothers. The milk sampled ranged from 0.2 to 57 ug/L.    In a population of German women, the concentration of mercury in early breast milk ranged from 0.2 to 20.3 ug/L.  After 2 months lactation the level had declined and was 0.1 to 11.7 ug/ L[ 64].   A Japanese study found that the average mercury level in samples tested increased 60% between 1980 and 1990[47b].    The study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, but more so in the linguistic pathway(47b).   The level of mercury in umbilical cord blood, meconium, and placenta is usually higher than that in mother's  blood[ 43- 47].  A recent study found hundreds of toxic chemicals in umbilical cords of newborns including mercury(160) and toxic chemicals are known to have  synergistic effects

Meconium( first stool) level appears to be the most reliable indicator of fetal mercury exposure and often has significant levels when there are low levels in mother’s blood and cord blood(46c). The level of maternal blood or hair mercury is significantly correlated with mercury level in meconium and in nursing  infants ,  so maternal tests can be easily used as a screen for developmental dangers[43-47,127]. But fetal levels can be significant when there are low levels in maternal blood(46c). 

The highest levels of mercury are usually found in the pituitary gland of the fetus which affects development of the endocrine, immune, and reproductive systems.    Mercury has been well documented to be an endocrine system disrupting substance in animals and people, preferentially accumulating in and disrupting function of the pituitary gland[10,12,39,65], hypothalamus, and thyroid gland[12,65-67]; along with disrupting or blocking enzyme production processes[57,68-73], glucose transfer[57], and many hormonal functions[74-79] at very low levels of exposure.   The pituitary gland  controls  many  of the body's endocrine system functions and secretes hormones that control most bodily processes, including the immune system and reproductive systems[79].  The hypothalamus regulates body temperature and many metabolic processes. 


Mercury has also been documented to be a reproductive and developmental toxin in humans.  Some  of  mercury’s   documented hormonal effects at very low levels of exposure  include effects on the reproductive system resulting in lowered sperm counts, defective sperm cells, and lowered testosterone levels in males; along with menstrual disturbances,  infertility, spontaneous abortions in women, and birth defects.   Low level lead exposure has been found to have similar  effects( 159).      Studies found that very low levels of exposure to mercury cause genetic/ DNA damage[34,81-88] and inhibits DNA  & RNA  synthesis[81,85/86]; damages sperm, lowers sperm counts and reduces motility [34,81,88-92,5,6/88,93,95]; causes menstrual disturbances [96,97]; reduces blood’s ability to transport oxygen to fetus, and transport of essential amino acids and nutrients including magnesium, zinc and Vit B12 [40,57,71,72,98,99]; depresses enzyme function and  isocitric  dehydrogenase (ICD) in fetus[92-95,99]; causes reduced iodine uptake, inhibited ATP activity, & hypothyroidism[66]; causes  infertility[74-78,89-93,95,100-104,146,/88,106], and causes spontaneous abortions and birth defects[36,40,51,66,75,78,79,100,101,104,107-113/106,113,114].  Pregnant women who suffer from hypothyroidism (under active thyroid) have a four-times greater risk for miscarriage during the second trimester than those who don’t, and women with untreated thyroid deficiency were four-times more likely to have a child with a developmental disabilities and lower I.Q.( 66) 

 Reviews of recent studies have found that the incidence of abnormalities of genitourinary abnormalities in human males has increased during the past 50 years, including cryptorchidism and  hypospadia [ 79,81,115].  The incidence of testicular cancer was found to have increased 3 to 4 fold since the 1940s.  The reviews also found that studies indicate that sperm quality and quantity have decreased significantly during this period,  with  an  average decrease in sperm density of approximately 40 % since 1940 along with increased sperm abnormalities. Mercury and other toxic metals are among the toxics that have been found in animal  studies  to  have such effects  [5-7,40,79,88,95]. 


A large cohort study of occupationally exposed women found an increased risk of spontaneous abortion and other pregnancy  complications[ 101]. Women with hormonal problems seeking help at a gynecological clinic in Germany were found to have higher body burdens of  heavy metals, including mercury[74,75,78], and women with idiopathic menstrual problems had higher levels of mercury[75,77,96,100]. Women with hormonal related  alopecia( hair loss) also had higher mercury levels than controls[78,116,117] and the condition was alleviated by amalgam removal.  Most women with very high levels of mercury were infertile, and after clearance of metals many were fertile  again[ 74-78].


The human brain forms and develops over a long period of time compared to other organs, with neuron proliferation and migration continuing in the postnatal period.  The blood-brain barrier is not fully developed until the middle of the first year of life.   Similarly there is postnatal activity in the development of receptors and transmitter systems as well as in the production of myelin.  Many of the toxic substances such as mercury are known to damage the developing brain by interfering with one of these developmental processes, interfering with structural development depending on what is developing at the time of  exposure[ 118-126].  Mercury and other toxic substances are known to accumulate in endocrine system organs such as the pituitary gland, thyroid, and  hypothallamous  and to alter hormone levels and endocrine system development during crucial periods of development( 10,12,33,41,47-49,79,132).  Such effects are usually permanent and affect the individual throughout their life. Some of the relatively subtle effects that have been found to occur such as small decreases in IQ, attention span, and connections to delinquency and  violence , if they occur in relatively large numbers over a lifetime can have potentially serious consequences for individuals as well as for society[118,119].      Infant head circumference was found to be negatively correlated to infant meconium mercury levels(46c).  


Animal studies of developmental effects of mercury on the brain have found significant effects at extremely low exposure levels, levels commonly seen in those with amalgam fillings or in dental staff working with amalgam.  One  study[ 120] found mercury vapor affected NGF concentration, RNA, and choline  acetyltransferese  in rat’s forebrain at between 4 and 11  parts per billion(ppb) tissue concentration.  Another  study[ 123] found general toxicity effects at 1 micromole( uM ) levels in immature cell cultures, increased immunoreactivity for glial fibrillary protein at 1  nanamole  (0.2 ppb) concentration, and microglial response at even lower levels.  Other animal studies on rodents and monkeys have found brain cellular migration disturbances, behavioral changes, along with reduced learning and adaption capacity after low levels of mercury vapor or methylmercury exposure [49-53,58,128-130/92,124-126].  The exposure levels in some of these studies are seen in the fetus and newborn babies of mother’s with amalgam fillings or who had work involving amalgam during  pregnancy[ 14,15].


Epidemiological studies have found that human embryos are also highly susceptible to brain damage from prenatal exposure to  mercury[ 120,121,124-126,148,149].  Prenatal/early postnatal exposure to mercury affects level of nerve growth  factor( NGF) in the brain and causes imbalances in development of the brain [40,120-123,130, /94,124-126].  Exposure of developing neuroblastoma cells to sub-cytotoxic doses of mercuric oxide resulted in lower levels of neurofilament proteins than unexposed  cells[ 126].  Mercury vapor exposure causes impaired cell proliferation in the brain and organs, resulting in reduced volume for cerebellum and organs and subtle  deficiencies[ 40,120-23].  Neurotoxicity as a result of mercury exposure has also been found to be due to the inducing of reactive oxygen species such as superoxide ion, hydrogen peroxide, and hydroxyl radical causing enhanced lipid peroxidation, DNA damage, and altered calcium and sulfhydryl  homeostasis[ 120,121,131].

Recent studies found that prenatal mercury exposures from mother’s amalgams and other sources along with susceptibility factors such as ability to excrete mercury appear to be major factors in those with chronic neurological conditions like  autism( 148,149).  Infants whose mothers received prenatal Rho D immunoglobulin injections containing mercury thimerosal for RH factor or whose mother’s had high levels of amalgam fillings had a much higher incidence of autism.  While the hair test levels of mercury of infants without chronic health conditions like autism were positively correlated with the number of the mother’s amalgam fillings, vaccination thimerosal exposure, and mercury from fish, the hair test levels of those with chronic neurological conditions such as autism were much lower than the levels of controls and those with the most severe effects had the lowest hair test levels, even though they had high body mercury levels.  This is consistent with past experience of those treating children with autism and other chronic neurological conditions.


Several studies found that mercury along with other toxic metals cause learning disabilities and impairment, and reduction inIQ [ 40,58,129,132-139]. Mercury has an effect on the fetal nervous system at levels far below that considered toxic in adults, and background levels of mercury in mothers correlate significantly with incidence of birth defects and still births [36,40,100-102].  Prenatal exposure to 7 heavy metals was measured in a population of pregnant women at approximately 17 weeks   gestation[ 134].  Follow-up tests on the infants at 3 years of age found that the combined prenatal toxic exposure score was negatively related to performance on the McCarthy Scales of Children’s Abilities and positively related to the number of childhood illnesses reported.  Exposure to mercury and 4 other heavy metals measured by hair tests in a study of school children accounted for 23% of the variation in test scores for reading, spelling and visual motor skills[ 135].    A Canadian study found that blood levels of a similar group of metals were able to predict with a 98% accuracy which children were learning  disabled[ 136]. Another group of students were scored by their classroom  teacher  on  the Walker Problem Behavior Identification Checklist(WPBIC).  A combined hair level score for mercury, lead, arsenic, cadmium and aluminum was found to be significantly related to increased scores on the WPBIC subscales measuring acting-out, disturbed peer relations, immaturity, and the total score[ 133].   Similar tests  in the California juvenile justice system have found significant relations to classroom achievement, juvenile delinquent temperaments, and criminality.


The saliva and feces of children with amalgams have approximately 10 times the level of mercury as children  without[ 140,141], and much higher levels in saliva after chewing. A group of German children with amalgam fillings had urine mercury level 4 times that of a control group without  amalgams[ 142], and in a Norwegian group with average age 12 there was a  significant correlation between urine mercury level and number of amalgam fillings(143).   Since mercury vapor is known to rapidly cross cellular  membranes  and  to bioaccumulate over time with chronic exposure, these relationships get stronger with age, with the most serious health effects occurring more commonly in middle‑aged individuals.


     Studies  have  found  much higher levels of mercury and copper in infants whose mother’s were treated with amalgam during pregnancy[37], as well as children with congenital hearing deficiencies[63].  Most researchers in this field advise that fertile women should not be exposed to vapor levels above government health guidelines or have amalgams placed or removed during pregnancy [10-12,15,16,24,27,39,40,65,74,103,144,145]; the U.S. ATSDR mercury health MRL is 0.2 ug/M 3  [32].  Many governments of developed countries have bans or guidelines restricting use of amalgam by women of child‑bearing age. These include Canada, Sweden, Germany, Norway, Austria, Great Britain, France, Australia, New Zealand, and Japan. 




1. ATSDR/EPA Priority List for 2019: Top 20 Hazardous Substances , Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services; & U.S. CDC, National Center for Environmental Health, National Report on Human Exposure to Environmental Chemicals , 2019

2. Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services,  Toxicological Profile for Mercury , March 2019.   

3. Electric Power Research Institute.   Mercury in the Environment.  Electric EPRI Journal 1990; April, p5.

4. Florida Department of Health, Bureau of Environmental Toxicology, Mercury Fish Advisory , 2020, & FFWGC,  Health Advisories for Mercury in Florida Fish ;  2021; & United States  Environmental Protection Agency,    Office of Water, November 2020, The National Listing of Fish and Wildlife Advisories: Summary of 2020 Data , EPA ; & U.S. EPA, Office of Water, Mercury Update : Impact on Fish Advisories-Fact Sheet,

5.   Facemire  CF, Gross TS,  Guillette , LJ.  Reproductive impairment in the Florida panther. Health  Perspect  1995; 103 (Supp4):79‑86;

6.  Florida Panther Interagency Committee,  Status  Report:Mercury  Contamination in Florida Panthers , Florida Department of Environmental Protection, Dec 1989.  

7.  Maretta  M,  Marettova   E,Skrobanek  P,  Ledec  M.  Effect of mercury on the epithelium of the fowl testis. Vet Hung 1995; 43(1):153‑6; & Rao MV, Sharma PS.  Protective effect of vitamin E against mercuric chloride reproductive toxicity in male mice.    Reprod   Toxicol . 2001 Nov;15(6):705-12; &  Monsees  TK, Franz M, Gebhardt S, Winterstein U, Schill WB, Hayatpour J.  Sertoli cells as a target for reproductive hazards.    Andrologia . 2000 Sep;32(4-5):239-46; &  Orisakwe OE, Afonne OJ,  Low-dose mercury induces testicular damage   in mice that is protected against by zinc.Eur J Obstet Gynecol Reprod Biol. 2001 Mar;95(1):92-6.

8.  Magos  L, Clarkson TW, Hudson AR.  The effects of dose of elemental mercury and first pass circulation time on organ distribution of inorganic mercury in rats.   Biochim   BiophysActa  1989; 991(1):85-9.

9. Nixon, DE,  Mussmann  GV, Moyer TP.  Inorganic, organic, and total mercury in blood and urine.  J Anal Toxicol , 1996; 10(1): 17-22.

10.  Vimy   MJ,TakahashiY Lorscheider  FL.   Maternal ‑Fetal Distribution of Mercury Released  From  Dental Amalgam Fillings.  Amer J  Physiol  1990; 8:R 939‑945.

11.   Pleva  J.  Mercury‑ A Public Health Hazard. Reviews on Environmental Health, 1994; 10:1‑27.

12. Weiner JA, Nylander M.  The relationship between mercury concentration in human organs and predictor variables.  Sci Total Environ 1993; 138(1-3):101-15.

13. Kingman A, Albertini T, Brown L, National Institute of Dental Research, Mercury                 concentrations in urine and blood associated with amalgam exposure in the U.S. military population. Dent Res 1998; 77(3):461-71.

14. Lutz E, Lind B,  Herin  P,  Krakau  I, Bui TH,  Vahter  M.  Concentrations of mercury, cadmium, and lead in brain and kidney of second trimester fetuses and Infants.  Journal of Trace Elements in Medicine and Biology 1996;10: 61‑67.

15. Drasch  G, Schupp I,  Hofl  H, Reinke R,  Roider  G.  Mercury Burden of Human Fetal and Infant Tissues, Eur J Pediatrics 1994; 153:607‑610; &  Drasch  G, The Influence of Amalgam fillings of mothers on the mercury levels in fetal and baby organs, in International Symposium: “Status Quo and

Perspectives of Amalgams and other dental materials” European Academy,  Ostenhausen , Germany, April 29, 1994.

16. Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al,       Metal-specific memory  lymphoctes : biomarkers of sensitivity in man.  NeuroendocrinologyLetters , 1999.

17.  Nogi  N, Electric current around dental metals as a factor producing allergic metal ions in the oral cavity. Nippon  Hifuka  Gakkai  Zasshi  1989; 99(12):1243-54.   

18.  Certosimo  AJ, O’Conner RP, National Naval Dental Center, Oral Electricity. Gen Dent 1996; 44(4):324-6. 

19. Ogletree RH, Marek M.   School of Materials Science, Georgia Institute of Technology, Atlanta. Effect of mercury on corrosion of eta’ Cu-Sn phase in dental amalgams, Dent Mater 1995; 11(5):332-6. 

20.  Willershausen-Zonnchen  B, Zimmermann M,  Defregger  A,  Schramel  P, Hamm G. Mercury in the mouth mucosa of patients with amalgam fillings.  Dtsch  Med  Wochenschr , 1992, 117:46, 1743‑7.

21.Till T, Mercury release from amalgam fillings and oral dysbacteriosis as a cause of    periodontal degeneration.   Zahnarztl  Welt/ Reform( ZWR) 1978; 87:1130‑1134.

22.  Arvidson  K. Corrosion studies of dental gold alloy in contact with amalgam.   Swed  Dent J 1984; 68: 135‑139.

23.  Freden  H,  Hellden  L,  Milleding  P.  Mercury in gingival tissues adjacent to amalgam fillings.  Odontal  Revy 1974; 25(2): 207‑210.

24. Kraub P, Deyhle M, Universitat Tubingen- Institut fur Organische Chemie.   Field  Study  on the Mercury Content of Saliva, 1997.    (20,000 patients tested) )                                     

25.  Engqvist  A,  Colmsjo  A,  Skare  I. Speciation of mercury excreted in feces from individuals with amalgam fillings. Arch Environ Health 1998; 53(3):205-13; & Dept. of  Toxicology & Chemistry, Stockholm Univ., National Institute for Working Life, 1998   http://

26. World Health  Organization( WHO),1991, Environmental Health criteria 118,  Inorganic      Mercury, WHO, Geneva;

27. Richardson GM,  Environmental  Health Directorate, Health Canada, Assessment of Mercury Exposure and Risks from Dental Amalgam,  1995,  Final Report.

28.   Skare  I,  Engqvist  A.  Swedish National Board of Occupational Safety and Health, Human Exposure to Hg and Ag Released from Dental Amalgam Restorations.    Archives of Environmental Health 1994; 49(5):384‑394. 

29. Bjorkman L,  Sandborgh -Englund,  Ekstrand  J.  Mercury in Saliva and Feces after Removal of Amalgam Fillings.   Toxicol  And Applied  Pharmacol  1997; 144:156-162; &   Doctor’s Data Lab

30.    Vimy  MJ,  Lorscheider  FL.  Intra oral Mercury released from dental  amalgams  and  estimation of daily dose.   J Dent Res 1985;64(8):1069‑1075 : &    Jokstad  A.  Dental amalgam and mercury.   Pharmacol   Toxicol 1992; 70(4): 308‑13.

31.  Leistevuo  J et al, Dental amalgam fillings and amount of organic mercury in human saliva.  Caries Res 2001 May‑Jun;35(3):163‑6; &   

32.  U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, Apr 19,1999 Media Advisory,  New Minimum Risk Levels for toxic substances, MRL: elemental mercury vapor/ inhalation/ chronic     & MRL: methyl mercury/oral/acute;

33.  Kostial  K,  Blanusa  M,  Malikovic  T.  Age and sex influence the  metablolism  and toxicity of metals.  In:  Trace Elements in Man and Animals  (Monograph ) ,  1991, Inst Med Res Occup Health, University of Zagreb, Yugoslavia , p11/1-11/5.  

34. Boyd ND,  Benediktsson  H,  Vimy  MJ, Hooper DE,  Lorscheider  FL.    Mercury from dental silver tooth fillings impairs sheep kidney function",  Am.J . Physiol. 261 (Regulatory Integrative  Comp    Physiol  1991: 30: R1010‑R1014.  

35. Hahn LJ, Kloiber R, Leininger RW, Vimy MJ, Lorscheider FL.   Distribution of mercury released from amalgam fillings into monkey tissues.    FASEB  J  1990; 4:5536

36. Kuntz WD, Pitkin RM, Bostrom AW, Hughes MS.  Maternal and chord blood  mercury  background  levels; a longitudinal surveillance. Am J  Obstet  and  Gynecol  1982; 143(4):                 440‑443.

37. Friese KH.  Konnen Amalgamplomben angebornene Innenohrschaden verusachen?”, Therapeutikon 1993; 7(11): 492-496; &  Razagui  IB, Haswell SJ ; . Mercury and selenium concentrations in maternal and neonatal scalp hair: relationship to amalgam-based dental treatment received during pregnancy. Biol Trace Elem Res 2001 Jul;81(1):1-19 

38.Vimy MJ, Hooper DE, King WW,  Lorscheider  FL.   Mercury from maternal silver tooth fillings: a source of neonatal exposure", Biological Trace Element Research, 56: 143‑52,1997.

39.Hanson M. Amalgam hazards in your teeth.  J Orthomolecular Psychiatry 1983; 2(3):194‑201.

40. Ziff S and Ziff M.   Infertility and Birth Defects: is Mercury from Dental Fillings a Hidden Cause ?  , Bio‑Probe, Inc., 1987.  ISBN: 0‑941011‑03‑8.

41.  Oskarsson  A, Schultz A,  Skerfving  S,  Hallen  IP, Ohlin B, Lagerkvist BJ. Mercury in breast milk in relation to fish  consumption  and  amalgam.  Arch Environ Health, 1996,51(3):234‑41.

42. Drasch G, Aigner S, Roider G, Staiger F, Lipowsky G.   Mercury in human colostrum and early breast milk.  J Trace Elem Med Biol 1998; 12:23‑27;

43.  Paccagnella  B,  Riolfatti  M.  Total mercury levels in human milk from Italian mothers. Ann Ig 1989: 1(3-4):661-71;  &   Grandjean  P; Jurgensen PJ,  Weihe  P., Milk as a Source of Methylmercury Exposure in Infants.    Environ Health  Perspect  1994 Jan;102(1):74‑7.

44. Yang J, Jiang  Z,Wang  Y, Qureshi IA, Wu XD. Maternal‑fetal transfer of metallic mercury via placenta and milk. Ann Clin Lab Sci 1997; 27(2):135‑141.

45. Soong YK, Tseng R, Liu C, Lin PW.  J of Formosa Medical Assoc 1991; 90(1): 59‑65; &

Sundberg J,  Ersson  B,  Lonnerdal  B,  Oskarsson  A.   Protein binding of mercury in milk and     plasma from mice and man‑‑a comparison between methylmercury and inorganic mercury.      Toxicology 1999 Oct 1;137(3):169‑84.  

46. Kuhnert PM, Kuhnert BR, Erhard P.  Comparison of mercury levels in maternal blood, fetal blood, fetal cord blood, and placental tissues. Am J  Obstet   Gynecol , 1981, 139(2): 209-13, &  Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M, " Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women , as well as in umbilical cord blood ", Environ Res 2000 Oct;84(2):186-94 ; &   &   G. B. Ramirez,  C. V. Cruz,  C. Dalisay,  The Tagum Study I: Analysis and Clinical Correlates of Mercury in Maternal and Cord Blood, Breast Milk, Meconium, and Infants' Hair ,  PEDIATRICS Vol. 106 No. 4 October 2000, pp. 774-781. 

47. Suzuki T, Takemoto T, Shishido S,  Kani  K.  Mercury in human amniotic fluid.  Scand J Work Environ Health 1977; 3(1):32-5; & (b) Ramirez GB, Cruz MC,  Pagulayan  O,  OstreaE , Dalisay C.  The Tagum study I: analysis and clinical correlates of mercury in maternal and cord blood, breast milk, meconium, and infants' hair.   Pediatrics 2000 Oct;106(4):774‑81; & (c) Ramirez GB,  Pagulayan  O, Akagi H, Francisco Rivera A, Lee LV,  Berroya  A, Vince Cruz MC,  Casintahan  D.  Tagum study II: follow-up study at two years of age after prenatal exposure to mercury.  Pediatrics. 2003 Mar;111(3 ):e 289-95. 

48. Clarkson TW,  Magos  L, Greenwood MR.  Transport of elemental mercury into  fetal  tissues , Biol Neonate 1972; 21:239-244;  &  Greenwood MR, Clarkson TW,  Magos  L.  Transfer of metallic mercury into the fetus.    Experientia  1972; 28:1455-1456.

49. Newland MC,  Warfvinge  K, Berlin M.  Behavioral consequences of in utero exposure to mercury vapor.  Toxicology & Applied Pharmacology 1996; 139: 374-386;  &   Berlin , M; et al.  Prenatal Exposure to Mercury Vapor: Effects on Brain Development. The Toxicologist, 12(1):7(A245), 1992;  &  " Expert Consulted For Amalgam Study Demands Amalgam Ban", Swedish Dental Materials Study  ," Dagens   Nyheter ", April 26 2003,

50.  Warfvinge  K, Hua J,  Logdberg  B.  Mercury distribution in cortical areas and fiber systems of the neonatal and maternal cerebrum after exposure to mercury vapor.  Environmental Research 1994; 67:196-208.

51. Oster O,  Prellwitz  W.  Die  Pathobiochemie , Diagnose und  Therapie  der  Metall - und Metalloidintoxikation-2. Die  QuecksilberintoxikationIntensivmed  1985; 22(3):130-9. 

52. Inouye M, Hoshino K, Murakami U.  Behavioral and neuropathological effects of prenatal methyl mercury exposure in mice.  Neurobehav   Toxicol   Teratol  1985; 7;227‑232.

53.  Annau  Z, Cuomo V, Johns Hopkins Univ., School of Public Health, Mechanisms of  neuro-toxicity and their relationships to behavioral changes. Toxicology, 1988, 49(2): 219‑25.

54.   Mottet  NK, Shaw CM,  Burbacher , TM,  Health Risks from Increases in Methylmercury Exposure, Health  Perspect  1985; 63: 133‑140; & (b)  P.Grandjean  et al, “ MeHg  and neurotoxicity in children”, Am J Epidemiol, 1999; & Sorensen N, et al; Prenatal mercury exposure  rasises  blood pressure, Epidemiology 1999, 10:370-375; &  [Environmental epidemiology research leads to a decrease of the exposure limit for mercury]  [Article in Danish]   Weihe  P,  Debes  F, White RF, Sorensen N,Budtz -Jorgensen E,  Keiding  N,  Grandjean  P. Ugeskr   Laeger . 2003 Jan 6;165(2):107-11. 

& (c) National Research Council, Toxicological Effects of Methylmercury (2000), pp. 304‑332: Risk Characterization and Public Health Implications, Nat'l Academy Press 2000; &  Kate Mahaffey, U.S. EPA, The National Forum on Contaminants in Fish, Jan 2004; and Environ Health Perspectives, 2003, 111: 1465-1470; 

55.  Buchet  JP.  Influence of DMPS on the mobilization of mercury from tissues of rats pretreated with mercuric chloride, phenylmercury acetate, or mercury vapor. Toxicology 1989; 54(3): 323-33.

56. Leonhardt R,  Pekel  M, Platt B, Haas HL,  Busselberg  D.  Voltage‑activated calcium channel currents of rat DRG neurons are reduced by mercuric chloride and methylmercury.   Neurotoxicology 1996 Spring;17(1):85‑92 

57.  Boadi   WylUrbach  J,  Brandes  JM,  Yannai  S, In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Environ Res 1992; 57(1):96-106.

58. Fredriksson A,  Dencker  L, Archer T, Danielsson BR.  Prenatal exposure to metallic mercury  vapour  and methylmercury  produce interactive behavioral changes in adult rats.  Neurotoxicol   Teratol  1996; 18(2): 129-34.

59.  Tibbling  L, Thomas KA,  Lenkei  R, Stejskal  V,   Immunolocial  and brain MRI changes in patients with suspected metal intoxication.  Int J Occup Med Toxicol 1995; 4(2):285-294.

60.  Warfvinge  K, Berlin M,  Logdberg  B.  The effect on pregnancy outcome and fetal brain development of prenatal exposure to mercury  vapour . Neurotoxicology 1994; 15(4).

61. Schumann K.  The toxicological estimation of heavy metal  content( Hg,Cd,Pb ) in food for infants and small children.   Z  Ernahrungswiss  1990; 29(1):54-73. (article in German with English abstract)

62.  Abadin  HG, Hibbs BF, Pohl HR, U.S. Department of Health, Division of Toxicology, Agency for Toxic Substances and Disease Registry.  Breast-feeding exposure of infants to cadmium, lead, and mercury: a public health viewpoint.  Toxicol  Ind Health 1997; 13(4):495-517.

63. Friese KH.  Amalgamvergiftung_moglicher Zusammenhang mit angeborener Schwerhorgkeit.  Der Naturazt 1995; 135(8):13-15.

64. Drexler H, Schaller KH.  The mercury concentration in breast milk resulting from amalgam fillings and dietary habits.  Environ Res 1998; 77(2): 124-9.

65. Nylander M, Friberg L, Eggleston D, Bjorkman L.  Mercury accumulation in tissues from dental staff and controls in relation to exposure.  Swedish Dental Journal 1989. 13:235-243.

66. Kawada J, Nishida M, Yoshimura Y,  Mitani  K.    Effects of inorganic and methyl mercury on thyroidal function.   J  Pharmacobiodyn  1980; 3(3):149‑59; & Allan W.( MD),  Journal of Medical Screening, 2000; & Assoc. for Birth Defect  Children,Birth  Defect News, March 2001.  

67.  Lindqvist B.  Effects of removing amalgam fillings from patients with diseases affecting the immune system.  Med Sci Res 1996; 24(5): 355-356.

68.  Markovich D, James K.M.  Heavy metals ( Hg,Cd ) inhibit the activity of the liver and kidney sulfate transporter Sat‑1.   Toxicol   Appl   Pharmacol  1999; 154(2):181‑7.

69. Berndt WO, Baggett JM, Blacker A, Houser M.  Renal  glutathione  and  mercury uptake.  Fundam   Appl   Toxicol 1985; 5(5):832‑9.

70. Hussain S, Rodgers DA,  Duhart  HM, Ali SF.    Mercuric chloride‑induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain.  Environ Sci Health B 1997 May;32(3):395‑409.

71.  Boadi  WY,  Urbach  J, Branes JM,  Yannai  S.  In vitro exposure to mercury and cadmium alters term human placental membrane fluidity,  Pharmacol  1992; 116(1): 17-23.

72.  Urbach  J,  Boadi  W,  Brandes  JM, Kerner H,  Yannai  S.  Effect of inorganic mercury on in     vitro placental nutrient transfer and oxygen consumption.  Reprod   Toxicol 1992;6(1):69-        75.
73. Karp WB, Robertson AF,    Correlation of human placental enzymatic  activity with trace metal concentration in placenta.  Environ Res 1977; 13:470‑477.

74. Gerhard I,  Moonga  B,  Waldbrenner  A,  Runnebaum  B, Tubingen Univ. Gynecological Clinic, Heidelberg.  Heavy Metals and Fertility.  J of Toxicology and Environmental Health, 1998; Part A, 54(8):593‑611.

75. Gerhard I, Waibel S, Daniel V,  Runnebaum  B.  Impact of heavy metals on hormonal  and  immunological  factors in women with repeated miscarriages. Hum  Reprod  Update 1998; 4(3):301‑9.

76. Gerhard I. Amalgam  aus   gynakologischer  Sicht.  Der  Frauenarzt  1995; 36(6): 627-28.

77. Gerhard I, Runnebaum B, Schdstoffe und Fertillitatsstorungen.  Schwermetalle und Mineralstoffe, Geburtshilfe Frauenheikd, 1992, 52(7):383-396; &  Gerhard I, Waldbrenner P, Thuro H, Runnebaum B, [ Diagnosis of heavy metal loading by the oral DMPS and chewing gum tests ]. Klinisches Labor 38:404-411 (1992)

78. Gerhard I,  Runnebaum . Environmental pollutants and fertility disorders.  Geburtshilfe   Frauenheilkd  1992; 52(7), 383-96;  &  Roller  E et al, J Fert  Reprod , 1995, 3, 31-33: & Gerhard I.  Ganzheitiche Diagnostik un Therapie bie Infertilitat.    Erfahrungsheilkunde,      1993, 42(3): 100-106; &  Gerhard I,  Runnebaum  B,  The limits of hormone substitution in pollutant exposure and fertility disorders.   Zentralbl   Gynakol  1992; 114, 593‑602.

79.  T.Colborn (Ed.), Chemically Induced Alterations in Functional Development ,  Princeton  Scientific Press,1992.  

80.  Ogura H, Takeuchi  T,Morimoto  K.  A comparison of chromosome aberrations and micronucleus techniques for the assessment of the genotoxicity of mercury compounds in human blood lymphocytes.  Mutat  Res 1996 Jun; 340(2‑3):175‑82. 

81.   Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R.  Effect of occupational exposures on male fertility: literature review.  Ind Health. 2003 Apr;41(2):55-62; & Leung TY, Choy CM,  Yim  SF, Lam CW, Haines CJ.  Whole blood mercury concentrations in sub-fertile men in Hong Kong.  Aust N Z J  Obstet   Gynaecol . 2001 Feb;41(1):75-7; &    KheraKS , Teratogenic and genetic effects of mercury  toxicity .   In: The  Biochemistry   of Mercury in the Environment,   Nriagu , J.O.(Ed) Amsterdam ,  Elsevier, 503‑18,1979;  & Prati M, Gornati R, Boracchi P, Biganzoli E, Fortaner S, Pietra R, Sabbioni E, Bernardini G.   A comparative study of the toxicity of mercury dichloride and methylmercury, assayed by the Frog Embryo Teratogenesis Assay--Xenopus (FETAX).  Altern Lab Anim. 2002 Jan-Feb;30(1):23-32.   & John Aitken, Head- Dept. Of Biological Sciences, University of Newcastle in Australia. “Sperm on the wane”, paper for Conference on Male-Mediated Developmental Toxicity. Montreal, June 22, 2001,    The Gazette, June 22, 2001;   

82.  Babich  H. The mediation of mutagenicity  and   clastogenicity  of heavy metals by physiochemical factors.  Environ Res 1985: 37;253‑286.   

83.  Bucio  L, Garcia C, Souza V, Hernandez E, Gonzalez C, Betancourt M, Gutierrez‑Ruiz MC. Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line.   Mutat  Res 1999; Jan 25;423(1‑2):65‑72. 

84.  Pamphlett  R, Slater M, Thomas S.  Oxidative damage to nucleic acids in motor neurons containing Hg.  J Neurol Sci 1998; 159(2):121‑6. (rats  &  primates )   

85. O’Halloran TV.  Transition metals in control of gene expression.  Science 1993; 261(5122):715-25.     

86.  Verschaeve  L, Kirsch‑ Volders  M, Susanne C, Groetenbriel C, Haustermans R, Lecomte A, Roossels D.  Genetic damage induced by occupational low level mercury exposure.      Envir  Res, 12:306‑10,1976.       

87. Ariza ME, Williams MV. Mercury mutagenesis.    Biochem  Mol Toxicol 1999; 13(2):107‑12.  

88.  Lee IP, Dixon RL.  Effects of mercury on spermatogenesis studied by velocity sedimentation cell separation., J  Pharmacol  Exp Thera 1975, 194(1);171‑ 181; & Ben-Ozer EY,  Rosenspire  AJ, et al, Mercuric chloride damages cellular DNA by a non-apoptotic mechanism.   Mutat  Res. 2000 Oct 10;470(1):19-27; & Ogura H, Takeuchi T, Morimoto K,  “ A comparison of chromosome aberrations and micronucleus techniques for the assessment of the genotoxicity of mercury compounds in human blood lymphocytes.  Mutat  Res 1996 Jun;340(2‑3):175‑82

89. Eggert‑Kruse W, Effect of heavy metals on in vitro interaction between human sperm and cervical mucus.  Dtsch  Med  Wochenschr  1992; 117(37): 1383‑9(German). 

90. Ernst E, Lauritsen JG.  Effect of mercury on human sperm motility.   Toxicol 1991;            


91. Dally A, Hendry B, Declining sperm count: evidence that Young's syndrome is associated with mercury, BMJ, 1996, 313(7048): 44; &   de Kretser DM, Huidobro C, Southwick GJ, Temple-Smith PD (1998) The role of the epididymis in human infertility J Reprod Fertil Suppl  53: 271–275

92.  Ng TB, Liu WK.  Toxic effect of heavy metals on cells isolated from the rat adrenal and     

          testis.  In Vitro Cell Dev Biol 1990 Jan;26(1):24‑8. 

93.  Ivanitskaia  NF, Evaluation of combined effect of mercury and ionizing  radition  on reproductive function of animals. Gig  Sanit  1991; 12: 48‑51.   

94. Mohamed MK,  Mottet  NK. " Lazer  Light  Scatering  Study of the Toxic Effects of Methylmercury on sperm motility". J   Androl.,7(1):11‑15.,1986. 

95. Mohamed MK,  Burbacher  TM,  Mottet   NK,  Effects  of methyl mercury on  testicular functions in monkeys. Toxicol 1987; 60(1):29‑36;   

96.Gerhard I, “Reproductive risks of heavy metals in women”, in:  Reproductive Toxicology

          Richardson M(Ed.), VCH Weinheim, 1993,167-83.  

97.  Lorscheider  FL,  Vimy  MJ, Summers AO.  Mercury exposure from silver tooth fillings: emerging evidence questions a paradigm.  FASEB J 1995; 9(7):504‑508; & Yang JM, Chen QY, Jiang XZ.    Effects of metallic mercury on the perimenstrual symptoms and menstrual outcomes of exposed workers.   Am J Ind Med. 2002 Nov;42(5):403-9. 

98.  Iioka  H, Moriyama I, Oku M, Hino K,  Itani  Y, Okamura y,  Ichijo  M. The effect of inorganic   

mercury on placental amino acid transport. Nippon  sanka   Fujinka  Gakkai  Zasshi   1987;    39(2): 202-6.  

99.  Danielsson BR, Dencker L, Khayat A, Orsen  I,  Ferotoxicity  of inorganic mercury in the mouse: distribution and effects on nutrient uptake by placenta and fetus. Biol Res  Preg       Perinatal 1984; 5(3):102-9.  

100.  Schulte-Uebbing C.  Umweltbedingte Frauenkranheiten.  Sonntag-Verlag, Stuttgart, 1996;  &  Umweltmedizin in der Frauenheilkunde.  Arztezeitschr Naturheilkunde 35(2):9-17.

101. Sikorsky R, Women in Dental Surgeries: Reproductive Hazards. Int Arch Occup Environ     Health 1987; 59:551-557;

102. Brodsky JB.  Occupational exposure to mercury in dentistry and pregnancy outcome. JADA 1985; 111(11):779‑780.   

103. Daunderer M, Kostler W.  Die Amalgamvergiftung und ihre medizinische Folgen”, Forum Prakt Allgem Arzt 1991; 30(2): 44-66; &  M.Daunderer , “ Jugendicher   starb  an     Amalgam”, Forum  Prakt   Allgen   Arzt  1990; 29(11): 294.  

104. Neuburger  N,Arend  V, Guzek B.  Kompendium Umweltmedizin. MediVerlagsgesellschaft, Hamburg, 1996.    

105.   Mikhailova  LM. Influence of occupational factors on disease of reproductive organs.  Pediatriya   Akusherstvoi   Ginekologiya  1971; 33(6):56‑ 58;  &   Elghany  NA, Stopford W, Bunn WB, Fleming LE.  Occupational exposure to inorganic mercury  vapour  and reproductive outcomes.     Occup Med ( Lond ). 1997 Aug;47(6):333-6. 

106. Dickman MD, Leung CD, Leong MK.  Hong Kong subfertility links to mercury in human hair and fish. Sci Total Environ 1998; 214:165‑74;  &  Choy  CM, Lam CW, Cheung LT, Briton-Jones CM, Cheung LP, Haines CJ.  Infertility, blood mercury concentrations and dietary seafood consumption: a case-control study. BJOG. 2002 Oct;109(10):1121-5. 

107.  Cordier S;  Deplan  F;  Mandereau  L;  Hemon  D.   Paternal exposure to mercury and  spontaneous  abortions .  Br J Ind Med 1991 Jun;48(6):375‑81

 108.   Savitz  DA; Sonnenfeld NL; Olshan AF.   Review of epidemiologic studies of paternal       occupational exposure and spontaneous abortion.  Am J Ind Med 1994, Mar;25(3):361‑83; & (b) Anttila   A,  Finnish Inst.  Of  Occupational  Health, Effects of paternal occupation

 exposure on spontaneous abortion.  J of Occup & Environ Med 1995; 37(8):915‑21.

109.   Occupational exposure in dentistry and miscarriage.    Lindbohm ML,  Ylostalo P,  et al,    Occup  Environ Med. 2007 Feb;64(2):127-33.  Epub  2006 Oct 19.

110.  Wiksztrajtis  M, Baranski B.  Epidemiological survey of  Lithunia  dental office s. Med Pr 111 1973; 24:248; & Baranski B.  Effect of mercury on the sexual cycle and prenatal and     postnatal development of progeny.  Med Pr 1981; 32(4): 271-6.      

111. Bjorklund G. Risk evaluation of the occupational environment in dental care.  Tidsski  Nor  Laegeforen  1991; 111(8): 948-50.    

112.  Schoeny  R, U.S. Environmental Protection Agency. Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study. Environ Health  Perspect , 1996; 104, Supp 3: 663-73.    

113. Lee CH Lin RH, Liu SH, Lin- Shiau  SY. Genotoxicity of  phenylHg  acetate in humans as compared to other mercury compounds. 392(3):269-76.  

114.  Marsh DO, Clarkson TW, Cox C, Myers GJ, Amin- Zaki  L, Al-Tikriti S.  Fetal              Methylmercury Poisoning.  Ann Neurol 1980; 7:348-355.  

115.  Giwercman  A, Carlsen E,  Keiding  N, Skakkebaek N.E.  Evidence for increasing  abnormaties  of the human testis: a review.  Environ Health  Perspect  1993; 101(Supp2): 65-71.

116.  Klobusch  J, Rabe T, Gerhard I,   Runnebaum  B. Alopecia and environmental pollution. 

Klinisches  Labor 1992, 38:469‑ 476; 

117.   Klobusch , J, Gerhard I; Schwermetallbelastungen bei Patientinnen mit Alopezie.  Arch       Gynecol Obstet 1993; 254(1-4):278-80.

118.  Rodier  P.M.  Developing brain as a target of toxicity.  Environ Health  Perspect  1995; 103(Supp 6): 73-76

119. Rice, D.C., Issues in developmental neurotoxicology: interpretation and implications of the data.  Can J Public Health 1998; 89(Supp1): S31-40.

120.   Soderstrom  S, Fredriksson A,  Dencker  L,  Ebendal  T.  The effect of mercury vapor on  cholinergic  neurons  in  the fetal brain.  Developmental Brain Research, 1995; 85(1): 96‑108.

121. Atchison WD.  Effects of neurotoxicants on synaptic transmission.  Neuroltoxicol   Teratol 1998; 10(5):393-416.

122.  Ronnback  L, Hansson E.  Chronic encephalopathies induced by low doses of mercury or lead. Br J Ind Med 49:233‑240, 1992.

123. F. Monnet- Tschudi  et al, “Comparison of the developmental effects of 2 mercury compounds on glial cells and neurons in the rat telencephalon”, Brain Research, 1996, 741:52-59.

124. Larkfors L, Oskarsson A, Sundberg J, Ebendal T.  Methylmercury induced alterations in the nerve growth factor level in the developing brain.  Res Dev Res 1991;62(2):287‑ 94; &     Choi BH, Lapham LW, Amin- Zaki  L, Saleem T.  Abnormal neuronal migration of human fetal brain.   Journal of  Neurophalogy  1978; 37:719-733.

125.  Rice DC, Evidence of delayed neurotoxicity produced by methylmercury developmental exposure. Neurotoxicology 1996; 17(3‑4): 583‑96.

126. Abdulla EM,  Calaminici  M, Campbell IC.  Comparison of neurite outgrowth with            neurofilament protein levels in neuroblastoma cells following mercuric oxide exposure.        Clin Exp Pharmocol  Physiol  1995, 22(5): 362-3.

127.  Cernichiari  E, Brewer R, Myers GJ, Marsh DO,  Berlin  M, Clarkson TW;                    Monitoring methylmercury during pregnancy: maternal hair predicts  fetal brain              exposure.  Neurotoxicology 1995 Winter;16(4):705‑10.

128. Danielsson BR,  Fredricksson  A, Dahlgren L,  Gardlund  AT, Olsson L,  Dencker  L, Archer T.  Behavioral effects of prenatal metallic mercury inhalation exposure in rats. Neurotoxicol   Teratol  1993; 15(6): 391-6.

129. Fredriksson A.  Behavioral effects of neonatal metallic mercury exposure in rats. Toxicology, 1992, 74(2-3):151‑160.

130.  C. K.Mittal  et al, "Interaction of heavy metals with the nitric  oxide  synthase", Mol Cell  Biochem,149‑150:263‑5, Aug 1995.

131.  Stohs  SJ,  Bagchi  D.  Oxidative mechanisms in the toxicity of metal ions.  Free  radic  Biol Med 1995; 18(2): 321-36.

132. Needleman HL,  Behaviorial  Toxicology. Environ Health  Perspect  1995; 103(Supp6): 77-9.

133. Marlowe M,  Cossairt  A, Moon C,  Errera  J,  MacNeel  A, Peak R, Ray J, Schroeder C.          Main and interactive effects of metallic toxins on classroom behavior.  Journal of          Abnormal Child Psychology 1985; 13(2):185‑98.

134. Lewis M,  Worobey  J, Ramsay DS, McCormack MK.  Prenatal exposure to heavy metals: effect on childhood cognitive skills and health status. Pediatrics 1992;89(6 Pt 1): 1010-5.

135. Moon C, Marlowe M,  Stellern  J,  Errera  J.  Main and interaction effects of metallic pollutants on cognitive functioning. Learn  Disabil  1985 Apr;18(4):217-21.

136. Pihl RO,  Rarkes  M. Hair element content in Learning Disabled Children.  Science 1977; 198: 204‑6.

137.  Gowdy  JM, Demers FX.  Whole blood mercury in mental hospital patients. Am J Psychiatry 1978; 135(1):115‑7.

138.  Roeleveld  N,  Zielhuis  GA,  Gabreels  F.  Mental retardation and parental occupation.          Br J Ind Med 1993; 50(10):  945‑954; & (b)  Trasande  L, Schechter CB, Haynes KA,  Landrigan  PJ.  Mental retardation and prenatal methylmercury toxicity.  Am J Ind Med. 2006 Mar;49(3):153-8

139. Smith PJ,  Langolf  GD, Goldberg J. Effect of exposure to elemental mercury on short term memory.  Br J Ind Med 1983; 40(4):413-9.

140. Engin‑Deniz B.  Die queckssilberkonzentration im spichel zehnjariger kinder in korrelation zur anzahl und Grobe iher  amalgamfullungen”  Zeitschrift  fur Stomatologie, 1992, 89:471‑179.

141. Malmstrom C.  Amalgam derived mercury in feces”, Journal of Trace Elements in Experimental Medicine 1992; 5 (Abs 122).

142. Schulte A, Stoll R,  Wittich  M, Pieper K,  Stachniss  V.    Mercury Concentrations in                 Children with and without Amalgam Restorations.  Schweiz Monatsschr  Zahnmed,         1994,104(11):1336‑40(German).  &  J .Dent Res 73(4): 980 A‑334; & Childhood urine    mercury excretion: dental amalgam and fish consumption as exposure    factors.  M. Levy et al, Arch Environ Health. 1994 Sep-Oct; 49(5):    384-94

143. Olmsted ML, Holland RI,  Wandel  N,  Petterson  AH.  Correlation between amalgam         restorations and mercury in urine.  J Dent Res 1987, 66(6): 1179‑1182

144. Drasch G, Roider G.  Zahnamalgam und Schwangerschaft. Geburtshilfe Frauenheikd                     1995;       55(6): M63-M65

145.  Kistner  A.   Quecksilbervergiftung   durch  Amalgam: Diagnose und  Therapie .  ZWR, 1995;

146. Choy CM, Lam CW, et al, 2002, Infertility, blood mercury concentrations, and dietary seafood consumption: a case control study, BJOG: An International Journal of Obstetrics and  Gynaecology , 109: 1121-1125.

147. (a) Effects of continuous low-dose exposure to organic and inorganic mercury 

during development on epileptogenicity in rats.  Szasz A,  Barna  B, et al,

Neurotoxicology. 2002 Jul;23(2):197-206; & (b)  D.Klinghardt (MD), “Migraines, Seizures, and Mercury Toxicity”, Future  Medicine Publishing, 1997; &© Mechanisms by which mercury causes epilepsy and seizures, B. Windham(Ed),2020,

148.  A.S. Holmes, M.F.  Blaxill  and B.E. Haley,  Reduced Levels of Mercury in First Baby Haircuts of Autistic Children;  International Journal of Toxicology, 2003;  ; & Dr. A Holmes, Autism Treatment  Center,Baton  Rouge, La,  http://healing‑  ; &

149.  Waly M,  Olteanu  H,  Deth  R C, et al; Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal. Mol Psychiatry. 2004 Jan 27; & (b)  Mercury and autism: accelerating evidence? Mutter J, Naumann J, Schneider R,  Walach  H, Haley B.  Neuro  EndocrinolLett . 2005 Oct;26(5):439-46; &  © Hornig M,  Chian  D, Lipkin WI., Neurotoxic effects of postnatal thimerosal are mouse strain dependent. Mol Psychiatry. 2004 Jun 8;

(150)  National Academy of Sciences, National Research Council, Committee on Developmental Toxicology,  Scientific      Frontiers       in Developmental Toxicology and Risk Assessment,  June 1, 2000,   313 pages; &  Evaluating Chemical and     Other Agent Exposures for  Reproductive and Developmental Toxicity Subcommittee on Reproductive and Developmental Toxicity,    Committee on Toxicology, Board on Environmental Studies and Toxicology, National Research Council National Academy Press,   262 pages, 6 x 9, 2001; &  National Environmental Trust (NET),  Physicians for Social  Responsibility and the Learning      Disabilities Association of America,   "Polluting Our Future: Chemical Pollution in the U.S. that Affects Child Development and Learning" Sept 2000; ; &  &  Dr.  Fionta  Stanley, Department of  Paediatrics , the University of Western Australia  “Before the bough breaks”     National Library of Australia ,  July 24, 200 3

(151)  Mechanisms by which autism spectrum disorders(ASD) and childrens developmental conditions have been caused by vaccines and other toxic prenatal and neonatal exposures, Review;  B. Windham (Ed), over 150 peer-reviewed studies and Government agency documentation cited,

(152) Neurological and behavioral effects of mercury and toxic metals on children, Review; B. Windham (Ed.), over 150 peer-reviewed studies and Government agency documentation cited,

(153) Cytotoxic, neurotoxic,  immunotoxic , and endocrine disrupting effects of mercury, Review; B. Windham (Ed), cites over 3000 peer-reviewed medical studies and Government agency documentation.

(154 ) Sensitization to inorganic mercury could be a risk factor for infertility. Podzimek S, Prochazkova J, Bultasova L, Bartova J, Ulcova-Gallova Z, Mrklas L, Stejskal VD., The Institute of Dental Research, 1st MF and GUH, Charles University, Prague, Czech Republic. Neuro Endocrinol Lett. 2005 Aug;26(4):277-82.

(155) Synergistic Effects of Mercury with other toxic metals can multiply toxic effects more than 10 fold, Review, B Windham (Ed), 2017,

(156) Laws of the State of California, Proposition 65, Safe Drinking Water and Toxic Enforcement Act of 1986. 

(157)  Environmental mercury release, special education rates, and autism disorder: an ecological study of Texas,   Health and Place,  R.F. Palmer et al, March 2005       &   Mercury pollution from power plants, NWF,

& (b) Mental retardation and prenatal methylmercury toxicity.,  Trasande  L, Schechter CB, Haynes KA,  Landrigan  PJ., Department of Community and Preventive Medicine, Center for Children's Health and the Environment, New York, New York. Am J Ind Med. 2006 Mar;49(3):153-8,

(158) Dental amalgam is the largest source of mercury in sewers and a significant source of mercury in water bodies, fish, and the environment,  EPA &

(159) Reproductive toxicity of low-level lead exposure in men. Telisman S, Colak B, Pizent A, Jurasović J, Cvitković P. Environ Res. 2007 Oct;105(2):256-66. Epub2007 Jul 16.

(160) Study finds hundreds of toxic chemicals in umbilical cords of newborns

(161) Developmental Effects of estrogenic chemicals-Review, B. Windham (Ed.), ; &  Prenatal phthalate exposure is associated with childhood behavior and executive functioning.   Engel SM, Miodovnik A, Canfield RL, Zhu C, Silva MJ, Calafat AM, Wolff MS. Environ Health  Perspect .  2010 Apr;118(4):565-71; & endocrine system effects of mercury, ;



ATSDR- United States Department of Health, Agency for Toxic Substances and Disease Registry

MRL - Minimum Risk Level- the estimate of level of daily exposure to a hazardous substance that is likely to be without appreciable risk of non-cancer health effects over a specific period of exposure.

EPA- United States Environmental Protections Agency

ug micrograms; L Liter; M Meter