INFERTILITY, BIRTH DEFECTS, AND
FETAL DEVELOPMENTAL EFFECTS
RELATED TO MERCURY FROM AMALGAM DENTAL
FILLINGS & other toxins
B. Windham (Ed.)
I.
Introduction
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
organochlorine chemicals, 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). Autism 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/M3)[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/M3[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 lactational
organic (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 in
IQ[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/M3 [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.
References
1. ATSDR/EPA Priority List
for 1999: Top 20 Hazardous Substances, Agency for Toxic Substances and Disease
Registry, U.S. Department of Health and Human Services,
http://www.atsdr.cdc.gov/99list.html; & U.S. CDC, National Center for Environmental Health , National Report on
Human Exposure to Environmental Chemicals, 2001 www.cdc.gov/nceh/dls/report/Highlights.htm
2. Agency for Toxic Substances and Disease Registry, U.S. Department
of Health and Human Services, Public
Health Service, Toxicological Profile for Mercury, March 1999.
3. Electric Power Research
Institute. Mercury in
the Environment. Electric EPRI Journal 1990; April, p5.
4. Florida Department of Health, Bureau of
Environmental Toxicology,
Health Advisories for Mercury in Florida Fish 1997;
10-15; & United States
Environmental Protection
Agency, Office of Water, November
2000, The National Listing of Fish and Wildlife Advisories: Summary of 1999 Data, EPA‑823‑F‑00‑20,
http://www.epa.gov/ost/fish/advisories/general.html ; & U.S. EPA, Office of
Water, Mercury Update: Impact on Fish Advisories-Fact Sheet,
http://www.epa.gov/ost/fish/mercury.html
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 Biophys Acta 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:R939‑945.
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. Neuroendocrinology Letters, 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) ) www.xs4all.nl/~stgvisie/AMALGAM/EN/SCIENCE/tubingen.html
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://
www.niwl.se/ah/1998-02.html)
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 www.doctorsdata.com/repository.asp?id=43
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;& www.flcv.com/damspr1.html
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;
http://www.atsdr.cdc.gov/mrls.html
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, Ostrea
E, 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):e289-95.
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,
www.dn.se/DNet/jsp/polopoly.jsp?d=597&a=134259&previousRenderType=6
www.tv4.se/nyheterna/lopsedel.html
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 Quecksilberintoxikation. Intensivmed
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 Wyl, Urbach 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; & Khera KS, 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;
68(6):440‑4.
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), www.flcv.com/epilepsy.html
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; www.safeminds.org/
; & Dr. A Holmes,
Autism Treatment Center,Baton Rouge, La, http://healing‑arts.org/children/holmes.htm
; & www.flcv.com/autismc.html
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 Endocrinol Lett. 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; http://www.safekidsinfo.org ;
& & Dr. Fionta Stanley,
Department of Paediatrics, the University of Western
Australia “Before the bough breaks” National Library of
Australia , July 24, 2003 http://www.nla.gov.au/events/seminars/kmyer03.html
(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, www.flcv.com/kidshg.html
(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, www.flcv.com/tmlbn.html
(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. www.flcv.com/amalg6.html
(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), 2007, www.flcv.com/hgsynerg.html
(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 http://www.generationrescue.org/pdf/seed.pdf & Mercury
pollution from power plants, NWF, http://www.nwf.org/wildlife/pdfs/MercuryMythsFacts.pdf
& (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, http://www.melisa.org/abstracts.php#1
(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 & www.flcv.com/damspr2f.html
(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. Epub 2007 Jul 16.
(161) Developmental
Effects of estrogenic chemicals-Review, B. Windham (Ed.), www.flcv.com/endocrin.html; & 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, www.flcv.com/endohg.html;
Definitions
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
************