Dr. Robert B. Johnson, DMD, ND, MT, states "Pregnancy, Yeast and Mercury" also deals with how babies can absorb toxins from their mothers before birth. He mentions that mercury is 500 times more toxic than lead."
How many prospective parents paint the nursery just before the baby arrives, unaware that they may be exposing their newborns to dangerous mercury vapors?
AMALGAM MERCURY IN MOTHERS' MILK RISK TO INFANTS!
A newly published study has firmly established the presence of mercury from dental amalgam in the milk of nursing females! [Vimy, MJ; et al, 1997] Since this is a matter of the utmost importance, BioProbe has reviewed the existing literature on the subject, with the pertinent studies abstracted below in the Science section.
Several studies have already established the transfer of dental amalgam mercury into the tissues of unborn babies, in both animals and humans. [Vimy, MJ; 1990; Drasch, G; et al, 1994] The study on humans by Drasch and associates concluded: “Future discussion on the pros and cons of dental amalgam should not be limited to adults or children with their own amalgam fillings, but also include fetal exposure. The unrestricted application of amalgam for dental restorations in women before and during the child bearing age should be reconsidered.” The publication of these studies has already resulted in the issuing of government advisories against the use of mercury amalgam dental fillings in pregnant females (Germany, Sweden and Canada). In Germany, public opinion is encouraging a ban on the use of dental amalgam in all fertile women. The current research on amalgam mercury in breast milk adds further evidence to the wisdom of such an action.
The ability of metal ions to concentrate in mothers' milk has been scientifically established for years, as has the ability for methyl mercury to transfer to breast milk and cause neurologic damage to infants. [AminZaki, L; et al, 1981] The investigation of the possible transfer of mercury specifically from amalgam dental fillings to mothers' milk began in 1990. A study by Vimy and associates implanted amalgam fillings, seeded with radioactively labeled mercury, into pregnant ewes. [Vimy, MJ; et al, 1990] Since radioactively labeled mercury does not occur naturally, it was possible to detect mercury in tissues that was specifically derived from the amalgam dental fillings. The amalgam mercury was found to quickly accumulate in tissues of mothers and fetuses. In the lactating ewes, the levels of labeled mercury in milk were as much as six times higher than the levels of labeled mercury in their blood.
The current study [Vimy, MJ; et al, 1997] evaluated mercury related to amalgam dental fillings transferring to breast milk in both animals and humans. In the animal study, lactating ewes with amalgam fillings nursed foster lambs from ewes without amalgam fillings. The amalgam fillings contained a portion of radioactively labeled mercury, which was found in the tissues of the foster lambs. This confirmed the transfer of mercury from the amalgam fillings of the mothers, into the breast milk, then into the tissues of the foster lambs. The human study examined mercury levels in breast milk of 33 lactating women. The mercury levels correlated with the number of amalgam fillings or mercury vapor concentration levels in mouth air. The infant exposure levels were compared to the United States Public Health Service Minimal Risk Level (MRL) standard for adults, and caution was urged. The combination of prenatal mercury exposure and lactating exposure to maternal amalgam mercury was addressed. Other important factors addressed were mercury exposures related to the differences in body mass between infants and adults and the particular sensitivity of infants to heavy metal toxic effects. This latter concern has also been pointed out by other authors. [Schümann, 1990]
By 1995, the comparison of activity of different forms of mercury had been investigated. [Schümann, K, 1990; Yoshida, M; et al, 1994; Oskarsson, A; et al, 1995] It has been found that any form of mercury can transfer to breast milk and, from there, into the tissues of infants, although the fat soluble forms of mercury (methyl mercury and mercury vapor) will concentrate more in brain tissue of infants. The Schümann study pointed out that milk increases the bioavailability of Hg++ as the ionic mercury is bound to a greater extent in the red blood cells of the suckling infants. In an evaluation of lactating human females, the study by Oskarsson and associates found that dental amalgam mercury transferred to mothers' milk, but that methyl mercury from consumption of fish correlated to mercury levels in blood but not to levels in milk. In the portion of the study on rats and mice, the mercury was found to cause pathologic effects in the offspring, including alteration of the thymocytes, increased lymphocyte activities, and effects on noradrenaline and nerve growth factor in the developing brains. These effects occurred in the animals exposed to methyl mercury.
It has been well established scientifically that mercury vapor, being lipid soluble, functions very similar to methyl mercury pathologically. There have been other studies confirming the harmful effect of mercury vapor on unborn babies and developing infants. [Danielsson, BR; et al, 1993; Warfinge, K; et al, 1994; Fredriksson, A; et al, 1996] It should be emphasized that the studies cited herein clearly show that mercury damage to unborn babies and infants is not readily observable early on. The neurologic damage is developmental in nature, primarily effecting learning, behavior and neurologic function. These effects can dramatically alter the functioning of the individual throughout life. Early exposure to inorganic or organic mercury can even result in mental retardation. [Schümann, K, 1990]
In a subsequent study, Oskarsson and colleagues confirmed the accumulation of dental amalgam mercury in mothers' milk. [Oskarsson, A; et al, 1996] This study found that amalgam mercury dental fillings were the main source of mercury in the milk of lactating humans, related the exposure to the World Health Organization standard for daily intake for adults, and concluded it to be significant enough to be a risk to infants.
At this point, the scientific evidence clearly establishes that mercury transfers from amalgam dental fillings to the tissues of unborn babies and to mothers' milk, from the milk to body tissues of infants, and, according to existing standards, presents a health risk to the infants. The combination of prenatal exposure and neonatal exposure from nursing presents an undeniable concern. Oskarsson and associates [1996] stated: "We concluded that efforts should be made to decrease mercury burden in fertile women." Since amalgam dental fillings have now been identified as a significant, if not the major, contributor of mercury in mothers' milk, the formal regulatory limitation of amalgam fillings in fertile women is clearly indicated! BioProbe now calls upon all responsible public officials to immediately initiate action to protect unborn babies and infants from the scientifically proven health risk of mercury exposure from the amalgam fillings of their mothers. The use of mercury amalgam fillings in all fertile women should be banned forthwith!
Reprinted from Whole Life Times Magazine January/February 1989
by Stephen R. Goldberg, DDS
Several years ago I realized that as a result of routine, accepted, establishment type of dentistry, many human beings are becoming transformed into walking time bombs. Throughout their lives certain metals have been placed quite permanently in their bodies by dentists. What other health provider is repeatedly placing foreign, inorganic materials like metals, year after year into their patient's bodies? I don't know of any.
Because the mass media has been exposing the lay public to the newly discovered and newly proven problem of mercury vapors coming out of silver amalgam fillings in our mouths, several questions have arisen in the minds of many people. How toxic to the body is the mercury coming out of each person's individual fillings? How can the standards be established to decide on "safe" levels of mercury from fillings? Is there a safe level? What are some of the signs and symptoms of systemic mercury toxicity? Can we be gradually poisoned over many years cumulatively without ever experiencing any negative symptoms? What measures can one take to prevent insidious disease processes from occurring if we already have a confirmed mercury toxicity problem from mercury silver fillings? Should I have all my mercury silver fillings removed? What measures can be taken to avoid further body contamination while the amalgam fillings are being removed? And finally, why doesn't the Food and Drug Administration (FDA) do something to stop the use of this poisonous metal in dental patients?
A machine was invented about 20 years ago to measure the mercury vapors emanating from mercury silver fillings (see figure 1). It is called the Jerome Gold Film Mercury Vapor Analyzer. It registers the number of micrograms of mercury per cubic meter of air. Our method consists of an initial baseline mercury reading on each tooth containing a metal filling or crown. This is followed by a second set of readings after the patient chews gum for fifteen minutes. Chewing gum simulates the normal function of mastication, and if the second readings are appreciably higher than the first, mercury is definitely being released from the fillings when eating. If this happens, mercury combines with the food which is consumed. Then the elemental mercury vapor is converted in the stomach to the much more toxic methyl mercury. This form is more readily absorbed into the bloodstream. This mercury form is subsequently transported to every organ and is spread to every cell in the body.
A few years ago, one of my patients told me that I saved her marriage. She related to me that she used to be very irritable, dizzy and extremely weak with headaches upon awakening. As soon as all the mercury fillings were removed from her mouth, her attitude and personality changed dramatically for the better. According to her, she had an extremely severe case of candidiasis which was virtually cured after this dental procedure was completed. It is important to note that many of the symptoms resulting from mercury toxicity sound very similar to those of hypoglycemia, hidden food allergies (food intolerances), Temporomandibular Joint disease (TMJ) and also to candidiasis.
Another patient felt that because of changing her fillings, she was able to start and pursue a successful acting career. I didn't know initially that she used to work for a dentist twenty years ago and that she handled mercury fillings without any precautions when assisting that dentist. I was unaware that her asthma had been so severe that she was hospitalized frequently in the past. At age forty, after I had removed all her mercury silver fillings, she no longer had any problem breathing on cold, wintry days. She used to have trouble walking outside more that a block at a time during the winter. Her sinus congestion completely disappeared and her friends wondered why she wasn't sneezing and congested anymore, and why she wasn't holding her telltale handkerchief.
The most dramatic success story of all is about a patient who came to me for testing after attending one of my lectures. She had about twenty fillings with the highest readings of mercury I had ever recorded. After ten years and thousands of dollars spent on hospital and laboratory tests, she finally knew why she was so sick even though her blood test results were virtually normal. She had so little energy she couldn't sit up in my dental chair for more than ten minutes at a time. When most of her fillings had already been removed, she was able to sit upright in the chair for over an hour and a half. As she was leaving after that last visit she got off the chair and walked out of the room without my help and without her cane. Before treatment, she was highly allergic and could tolerate only two or three foods. Afterwards she was allergic to fewer and fewer foods. Three months later she told me that she had already gained back about ten pounds. She was still about thirty pounds under weight. She also told me that a sore on her leg healed for the first time in ten years.
It may seem baffling to many of you why dentists are still permitted to use mercury in fillings. Many clinicians and patients who have seen the overt benefits of removing their mercury silver fillings are frustrated because of the political and economic impediments in this whole affair. The American Dental Association (ADA) is not ready to take a stand to abolish the use of mercury since they feel that when they do eventually prohibit the use of mercury fillings, those dentists that are still using them will be sued by their patients. The ADA seems to evade the question. They also keep responding with allusions to the very few people who exhibit an "allergic" reaction to the mercury or metal alloy in these mercury silver fillings. Allergy does not come into this picture at all. We are talking about heavy metal "toxicity".
One major breakthrough in this heated controversy occurred in Sweden on May 19, 1987. In an historic about-face, an expert commission formed by the Swedish Social Welfare and Health Administration announced that they had been wrong in maintaining that mercury fillings were safe. "We now realize that we made a mistake, "acknowledged Division Chief Viking Falk at Socialstyrelsen. "This has caused people to suffer unnecessarily," he said.
The last consideration related to mercury toxicity is perhaps the most horrible and devastating of all. It concerns women of child-bearing age. Since it has been proven that methyl mercury passes readily through the placental barrier, some very serious questions are raised concerning its possible influences in cases of still births, miscarriages, birth defects and other profound and far reaching ramifications. On May 20, 1987, the Swedish newspaper Svenska Dagbladet reported that amalgam is, from a toxicological view, an unacceptable dental filling. The article stated that a first step in the process to eliminate the use of amalgam in dental fillings, comprehensive amalgam work on pregnant women shall be stopped in order to prevent mercury damage to the fetus.
TITLE: Methylmercury transport across the placenta via neutral amino acid carrier.
Kajiwara Y; Yasutake A; Adachi T; Hirayama K
Pathology Section, National Institute for Minamata Disease, Minamata City, Japan.
Arch Toxicol, 1996, 70:5, 310-4
ABSTRACT: Methylmercury (MeHg) penetrates the placental barrier to affect developing fetuses in the uterus. However, the mechanism of placental MeHg transport is not well defined. To clarify the MeHg transport system that functions in the placenta, pregnant rats were intravenously administered MeHg on day 18 of gestation. The fetal blood was collected from the umbilical cord at 30 and 60 min after the administration, and its mercury concentration was measured. MeHg was found to be rapidly transported to the fetal blood in a time- and dose-dependent manner, and predominantly distributed in the blood cells there. MeHg transport was effectively suppressed by the co-injection of neutral amino acids, i.e., L-methionine and L-phenylalanine, suggesting that MeHg is actively transported as its cysteine conjugate via the neutral amino acid carrier system. The suppression by methionine was not so marked as by phenylalanine. Since methionine administration caused a rapid increase of the cysteine, which functioned as a predominant carrier in MeHg transport, in the maternal plasma, newly synthesized cysteine seemed to accelerate the mercury uptake. Accordingly, the acceleration by the extra cysteine would compensate partly the competitive effect of methionine as a neutral amino acid.
TITLE: Mercury From Maternal "Silver" Tooth Fillings in Sheep and Human Breast Milk: A Source of Neonatal Exposure.
Vimy, MJ; Hooper, DE; King, WW; Lorscheider, FL.
Biological Trace Element Res., 56:14352, 1997.
ABSTRACT: Neonatal uptake of Hg from milk was examined in a pregnant sheep model, where radioactive mercury (Hg203)/silver tooth fillings (amalgam) were newly placed. A crossover experimental design was used in which lactating ewes nursed foster lambs. In a parallel study, the relationship between dental history and breast milk was also examined.
Results from the animal studies showed that, during pregnancy, a primary fetal site of amalgam Hg concentration is the liver, and, after delivery, the neonatal lamb kidney receives additional amalgam Hg from mother's milk. In lactating women with aged amalgam fillings, increased Hg excretion in breast milk and urine correlated with the number of fillings or Hg vapor concentration levels in mouth air.
It was concluded that Hg originating from maternal amalgam tooth fillings transfers across the placenta to the fetus, across the mammary gland into milk ingested by the newborn, and ultimately into neonatal body tissues. Comparisons are made to the U.S. minimal risk level recently established for adult Hg exposure. These findings suggest that placement and removal of "silver" tooth fillings in pregnant and lactating humans will subject the fetus and neonate to unnecessary risk of Hg exposure.
TITLE: Total and Inorganic Mercury in Breast Milk in Relation to Fish Consumption and Amalgam in Lactating Women.
ABSTRACT: Total mercury concentrations (mean ±standard deviation) in breast milk, blood, and hair samples collected 6 wk after delivery from 30 women who lived in the north of Sweden were 0.6 ± 0.4 ng/g (3.0 ± 2.0 nmol/kg), 2.3 ±1.0 ng/g (11.5 ±5.0 nmol/kg), and 0.28 ± 0.16 microg/g (1.40 ± 0.80 micromol/kg) respectively. In milk, an average of 51% of total mercury was in the form of inorganic mercury, whereas in blood an average of only 26% was present in the inorganic form.
Total and inorganic mercury levels in blood (r = .55, p = .003; and r = .46, p = .016; respectively) and milk (r = .55, p = .01; and r = .45, p = .018; respectively) were correlated with the number of amalgam fillings. The concentrations of total mercury and organic mercury (calculated by subtraction of inorganic mercury from total Mercury) in blood (r = .59, p = .0006, and r = .56, p = .001; respectively) and total mercury in hair (r = .52, p = .006) were correlated with the estimated recent exposure to methyl mercury via intake of fish.
There was no significant correlation between the milk levels of mercury in any chemical form and the estimated methyl mercury intake. A significant correlation was found between levels of total mercury in blood and in milk (r = .66, p = .0001), with milk levels being an average of 27% of the blood levels. There was an association between inorganic mercury in blood and milk (r = .96, p .0001); the average level of inorganic mercury in milk was 55% of the level of inorganic mercury in blood. No significant correlations were found between the levels of any form of mercury in milk and the levels of organic mercury in blood.
The results indicated that there was an efficient transfer of inorganic mercury from blood to milk and that, in this population, mercury from amalgam fillings was the main source of mercury in milk. Exposure of the infant to mercury from breast milk was calculated to range up to 0.3 microg/kg x d, of which approximately onehalf was inorganic mercury. This exposure, however, corresponds to approximately onehalf the tolerable daily intake for adults recommended by the World Health Organization. We concluded that efforts should be made to decrease mercury burden in fertile women.
TITLE: Exposure to Toxic Elements Via Breast Milk.
Oskarsson, A; Palminger Hallaen, I; Sundberg, J.
Analyst, 120(3):76570, 1995.
ABSTRACT: Breast milk is the ideal nutrient for the newborn, but unfortunately also a route of excretion for some toxic substances. Very little attention has been paid to breast milk as a source of exposure to toxic elements. The dosedependent excretion in breast milk and the uptake in the neonate of inorganic mercury, methyl mercury and lead were studied in an experimental model for rats and mice.
The transfer of mercury from plasma to milk was found to be higher in dams exposed to inorganic mercury than to methyl mercury. In contrast, the uptake of mercury from milk was higher in the sucklings of dams exposed to methyl mercury than to inorganic mercury. Pre and postnatal exposure to methyl mercury resulted in increased numbers and altered proportions of the thymocyte subpopulation and increased lymphocyte activities in the offspring of mice and also effects on the levels of noradrenaline and nerve growth factor in the developing brain of rats.
Mercury in blood and breast milk in lactating women in Sweden was studied in relation to the exposure to mercury from fish and amalgam. Low levels were found; the mean levels were 0.6 ng/g1 in milk and 2.3 ng/g1 in blood. There was a statistically significant correlation between mercury levels in blood and milk, showing that milk levels were approximately 30% of the levels in blood. Inorganic mercury exposure from amalgam was reflected in blood and milk mercury levels. Recent exposure to methyl mercury from consumption of fish was reflected in mercury levels in the blood but not in milk. (Abstract truncated at 250 words.)
TITLE: Maternal Fetal Distribution of Mercury (203Hg) Released From Dental Amalgam Fillings.
Vimy, MJ; Takahashi, Y; Lorscheider, FL.
Amer J Physiol., 258(RICP 27):R93945, 1990.
ABSTRACT: In humans, the continuous release of Hg vapor from dental amalgam tooth restorations is markedly increased for prolonged periods after chewing. The present study establishes a timecourse distribution for amalgam Hg in body tissues of adult and fetal sheep.
Under general anesthesia, five pregnant ewes had twelve occlusal amalgam fillings containing radioactive 203Hg placed in teeth at 112 days gestation. Blood, amniotic fluid, feces, and urine specimens were collected at 1 to 3 day intervals for 16 days. From days 16-140 after amalgam placement (16-41 days for fetal lambs), tissue specimens were analyzed for radioactivity, and total Hg concentrations were calculated.
Results demonstrate that Hg from dental amalgam will appear in maternal and fetal blood and amniotic fluid within 2 days after placement of amalgam tooth restorations. Excretion of some of this Hg will also commence within 2 days. All tissues examined displayed Hg accumulation. Highest concentrations of Hg from amalgam in the adult occurred in kidney and liver, whereas in the fetus the highest amalgam Hg concentrations appeared in liver and pituitary gland. The placenta progressively concentrated Hg as gestation advanced to term, and milk concentration of amalgam Hg postpartum provides a potential source of Hg exposure to newborn.
It is concluded that accumulation of amalgam Hg progresses in maternal and fetal tissues to a steady state with advancing gestation and is maintained. Dental amalgam usage as a tooth restorative material in pregnant women and children should be reconsidered.
TITLE: Mercury Burden of Human Fetal and Infant Tissues.
Drasch, G; Schupp, I; Hofl, H; Reinke, R; Roider, G.
Pediatrics, 153(8):60710, 1994.
ABSTRACT: The total mercury concentrations in the liver (HgL), the kidney cortex (HgK) and the cerebral cortex (HgC) of 108 children aged 1 day to 5 years, and the HgK and HgL of 46 fetuses were determined. As far as possible, the mothers were interviewed and their dental status was recorded. The results were compared to mercury concentrations in the tissues of adults from the same geographical area.
The HgK (n= 38) and HgL (n= 40) of fetuses and HgK (n= 35) of older infants (11-50 weeks of life) correlated significantly with the number of dental amalgam fillings of the mother. The toxicological relevance of the unexpected high HgK of
older infants from mothers with higher numbers of dental amalgam fillings is discussed.
CONCLUSION: Future discussion on the pros and cons of dental amalgam should not be limited to adults or children with their own amalgam fillings, but also include fetal exposure. The unrestricted application of amalgam for dental restorations in women before and during the child bearing age should be reconsidered.
TITLE: Milk Transfer and Tissue Uptake of Mercury in Suckling Offspring After Exposure of Lactating Maternal Guinea Pigs to Inorganic or Methyl mercury.
Yoshida, M; Watanabe, C; Satoh, H; Kishimoto, Y.
Arch Toxicol, 68(3):1748, 1994.
ABSTRACT: Maternal guinea pigs were injected with mercuric chloride (HgCl2; 1 mg Hg/Kg body weight) or methyl mercury (MeHg; 1 mg Hg/kg) 12 h after parturition, and exposure of the offspring to mercury (Hg) via breast milk were studied on days 3, 5 and 10 postpartum. Milk Hg concentrations were lower than maternal plasma Hg concentrations regardless of the form of Hg given to the dams.
Milk Hg was higher in HgCl2 treated dams than in MeHg treated dams. In MeHg treated dams, MeHg was separately determined. While the ratio of MeHg to THg decreased in the dams' plasma, it did not in the milk. There was a strong correlation between milk and plasma THg concentrations in HgCl2 treated dams. In the milk of MeHg treated dams, the plasma MeHg concentrations correlated better than did the plasma THg concentrations.
In the offspring, regardless of the chemical forms of Hg given to the dams, the highest Hg concentrations were found in the kidney, followed by the liver and the brain. Brain Hg concentrations were, however, significantly higher in the offspring of MeHg treated dams than in those of HgCl2 treated dams. In addition, Hg levels in the major organs of the offspring of HgCl2 treated peaked on day 5 postpartum, while those of MeHg treated dams did not show a significant decrease up to day 10 postpartum.
These facts indicate that the two chemical forms of Hg were transferred to the offspring via the breast milk and were distributed differently, depending on the chemical form, to the offspring's tissues.
TITLE: Methyl mercury Poisoning in the Iraqi Suckling Infant: A Longitudinal Study Over Five Years.
ABSTRACT: In a five year longitudinal study of mothers and infants exposed to methyl mercury during the Iraq epidemic of 1972, the frequencies of signs and symptoms exhibited by the mothers were typical of methyl mercury poisoning. When blood concentrations of mercury are corrected to 1 March 1972, mothers with the most severe signs and symptoms had an average blood mercury concentration significantly higher (p less than 0.01) than either the milder or asymptomatic groups.
Analytical data indicate that the predominant route of exposure for the infant was through breast milk in which approximately 60% of total mercury was determined, by cold vapor atomic absorption, to be organic mercury. Abnormal neurological signs in these infants became more obvious with time: hyperreflexia was observed in 8 of 22 infants at first examination, and in 17 of 22 at second examination. Delayed motor development became evident at the second and third examinations. The frequency of pathological reflexes and delayed motor developmental milestones was so high as to be considered significant even the absence of a controlled study. There was no increase in mortality as compared to a control group.
TITLE: The Toxicological Estimation of the Heavy Metal Content (Cd, Hg, Pb) in Food for Infants and Small Children.
Schümann, K.
Z Ernahrungswiss, 29(1):5473, 1990.
ABSTRACT: There are differences between young and adult organisms regarding toxokinetic aspects and clinical manifestations of heavy metal intoxications. Chronically, toxic Cd intake causes a microcytotic hypochromic anemia in young rats at lower exposure levels and after shorter exposure periods than in adult animals. Cd absorption is increased by coadministration of milk and in conjunction with iron deficiency. After long exposure periods toxic Cd concentrations accumulate in the kidney cortex; this process starts very early in life. In 3 year old children Cd concentrations in the kidney can reach up to onethird of those found in adults.
Hg++ and methyl Hg can cause Hg encephalopathia, and frequently cause mental retardation in adults. Correspondingly, Hg++ accumulation in the brains of suckling rats is approx. 10 times higher than in grown animals. Milk increases the bioavailability of Hg++. In suckling rats Hg is bound to a greater extent to ligands in the erythrocytes. Methyl Hg concentrations in breast milk reach 5% of those in maternal plasma and that is a severe hazard for breastfed children of exposed mothers.
Toxic Pb concentrations can lead to Pb encephalopathia. A high percentage of surviving children have seizures and show signs of mental retardation. Anemia and reduced intelligence scores were recently observed in children after exposure to very low levels of Pb. Pb absorption is increased in children and after coadministration of Milk.
The average heavy metal uptake from such diets [infant formulas or breast milk] exceeds the provisional tolerable weekly intake levels set by the WHO for adults, calculated on the basis of an average food intake and a down scaled body weight. These considerations do not even provide for differences in absorption and distribution or for the increased sensitivity of children to heavy metal exposure. [Abstract truncated.]
TITLE: Behavioral Effects of Prenatal Metallic Mercury Inhalation Exposure in Rats.
ABSTRACT: The effects of administration by inhalation of metallic mercury vapour (Hg0) to pregnant rats, approximately corresponding to doses of 0.2 mg Hg0/kg/day (high dose) or 0.07 mg Hg0/kg/day (low dose), on the developmental and behavioral repertoire of the offspring were studied. Exposure occurred during days 11-14 plus 17-20 of gestation. The dose levels were selected so as not to induce maternal toxicity.
Maturation variables such as surface righting, negative geotaxis, pinna unfolding, and tooth eruption revealed no difference between Hg0treated offspring and controls. Tests of spontaneous motor activity showed that the Hg0treated offspring were hypoactive at 3 months of age, but hyperactive at 14 months. In spatial learning tasks the prenatally exposed offspring showed retarded acquisition in the radial arm maze but no differences in circular swim maze. A simple test of learning, habituation to a novel environment (activity chambers), indicated a reduced ability to adapt.
These data suggest that prenatal exposure to Hg0 vapour results in similar behavior changes in the offspring as reported for methyl mercury.
TITLE: The Effect on Pregnancy Outcome and Fetal Brain Development of Prenatal Exposure to Mercury Vapour.
Warfinge, K; Berlin, M; Logdberg, B.
Neurotoxicology, 15(4), 1994.
ABSTRACT: Fourteen pregnant female squirrel monkeys were exposed to mercury vapour (Hg0) 5 days/week from 57 weeks of gestation until delivery in an exposure chamber. Hg0 exposure varied from 1 mg/m3 for 22 hr/d (1 monkey), 7 hr/d or 4 hr/d to 0.5 mg/m3 for 7 hr/d or 4 hr/d. Hg concentration in maternal blood ranged 0.05-0.09 mcg/g.
There was a dose related increase in abortion rate and perinatal mortality in the exposed monkeys compared to unexposed controls. The morphology of perinatally sacrificed or succumbed offspring brains showed signs of migration disturbances such as increased cell density in the cerebral subcortical white matter, abnormal cell collections near the cerebral lateral ventricles. Autometallographically, Hg was preferentially localized in the heterotopic cells and in the verticular aspects of the pseudostratified neuroepithelium. Hg concentration in the brain of exposed offspring ranged 0.01-0.70 mcg/g.
Autometallography of the maternal brains revealed that the pyramidal neurons of neocortical layer V contained more visualized Hg than the other neurons. In the offspring brains, Hg was visualized throughout the whole neocortex and no laminar distribution pattern was found. In the fiber systems, the offspring brains contained more Hg than the adult brains. In the cerebellum, the Purkinje cells, the Bergmann glial cells, the astrocytes of the medullary layer and the deep cerebellar nuclei were the main targets, for Hg accumulation in both maternal and offspring brains.
Title: The effect of mercury vapour on cholinergic neurons in the fetal brain: studies on the expression of nerve growth factor and its low- and high-affinity receptors.
Soederstroem S, Fredriksson A, Dencker L & Ebendal T
Developmental Brain Research 85(1):96-108 (1995)
Abstract: "The effects of mercury vapour on the production of nerve growth factor during development have been examined. Pregnant rats were exposed to two different concentrations of mercury vapour during either embryonic days E6-E11 (early) or E13-E18 (late) in pregnancy, increasing the postnatal concentration of mercury in the brain from 1 ng/g tissue to 4 ng/g tissue (low-dose group) or 11 ng/g (high-dose group). The effect of this exposure in offspring was determined by looking at the NGF concentration at postnatal days 21 and 60 and comparing these levels to age-matched controls from sham-treated mothers. Changes in the expression of mRNA encoding NGF, the low- and hogh-affinity receptors for NGF (p75 and p140 trk, respectively) and choline acetyltransferase (ChAT) were also determined. When rats were exposed to high levels of mercury vapour during early embryonic development there was a significant (62%) increase in hippocampal NGF levels at P21 accompanied by a 50% decrease of NGF in the basal forebrain. The expression of NGF mRNA was found to be unaltered in the dentate gyrus. The expression of p75 mRNA was significantly decreased to 39% of control levels in the diagonal band of Broca (DB) and to 50% in the medial septal nucleus (MS) whereas no alterations in the level of trk mRNA expression were detectable in the basal forebrain. ChAT mRNA was slightly decreased in the DB and MS, significantly in the striatum. These findings suggest that low levels of prenatal mercury vapour exposure can alter the levels of NGF and its receptors, indicating neuronal damage distributed trophic regulations during development."
Amalgam Mercury in Mothers' Milk Risk to Infants! BioProbe Newsletter by Sam Ziff