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The Dangers of Mercury in the H1N1 Vaccine

Posted Oct 26 2009 11:00pm

Last night I attended a SAD 75 (a Maine school district) public meeting on the H1N1 response and school vaccine clinics. It was a strange experience for me, as I feel like I had stepped back in time to a day ten years ago when giving mercury to children was no big deal, perfectly safe, just like candy really.

I pointed out a number of problems with doing so, which I assumed were common knowledge, that proved at the very least that mercury containing vaccines were not desirable and I will list some of those here for those of you who watched the meeting on TV and wanted references to my points.

As I want every parent and individual to have the informed consent that I was not given in vaccinating my child, I will also list several other references.

I am compiling this tonight and will add as I go, so check back this weekend for the full list.

First, a reminder of what mercury does in the brain:






CDC's toxicology division, ATSDR, says that this is what mercury can do to children:

How does mercury affect children?

Very young children are more sensitive to mercury than adults. Mercury in the mother's body passes to the fetus and may accumulate there. It can also can pass to a nursing infant through breast milk. However, the benefits of breast feeding may be greater than the possible adverse effects of mercury in breast milk.

Mercury's harmful effects that may be passed from the mother to the fetus include brain damage, mental retardation, incoordination, blindness, seizures, and inability to speak. Children poisoned by mercury may develop problems of their nervous and digestive systems, and kidney damage.

And they have set up a new web site to warn children of the dangers of mercury complete with scary video:

Don't Mess With Mercury


A reminder of the damage that mercury does in the body:

Mercury impairs the immune system at a tiny fraction of the dose that is in vaccines:

Uncoupling of ATP-mediated Calcium Signaling and Dysregulated IL-6 Secretion in Dendritic Cells by Nanomolar Thimerosal

Environmental Health Perspectives, July 2006.

Samuel R. Goth, Ruth A. Chu Jeffrey P. Gregg

This study demonstrates that very low-levels of Thimerosal can contribute to immune system disregulation.

Excerpt: "Our findings that DCs primarily express the RyR1 channel complex and that this complex is uncoupled by very low levels of THI with dysregulated IL-6 secretion raise intriguing questions about a molecular basis for immune dyregulation and the possible role of the RyR1 complex in genetic susceptibility of the immune system to mercury."

The type of mercury in vaccines becomes trapped in the brain at higher rates than ingested mercury from fish:

Comparison of Blood and Brain Mercury Levels in Infant Monkeys Exposed to Methylmercury or Vaccines Containing Thimerosal

Environmental Health Perspectives, Aug 2005.

Thomas Burbacher, PhD [University of Washington].

Thimerosal is a preservative that has been used in manufacturing vaccines since the 1930s. Reports have indicated that infants can receive ethylmercury (in the form of thimerosal) at or above the Environmental Protection Agency (EPA) guidelines for methylmercury (MeHg) exposure, depending on the exact vaccinations, schedule, and size of the infant. This study compared the systemic disposition and brain distribution of total and inorganic mercury in infant monkeys following thimerosal exposure with infants exposed to MeHg. Monkeys were exposed to MeHg (via oral gavage) or vaccines containing thimerosal (via i.m. injection) at birth and 1, 2, and 3 weeks of age. Total blood mercury (Hg) levels were determined 2, 4 and 7 days after each exposure. Total and inorganic brain Hg levels were assessed 2, 4, 7 or 28 days after the last exposure.

The initial and terminal half-life of Hg in blood following thimerosal exposure was 2.1 and 8.6 days, which are significantly shorter than the elimination half-life of Hg following MeHg exposure at 21.5 days. Brain concentrations of total Hg were significantly lower by ~3-fold for the thimerosal-exposed infants when compared to the MeHg infants, while the average brain-to-blood concentration ratio was slightly higher for the thimerosal-exposed infants (3.5±1.0 vs. 2.5±0.6). A higher percentage of the total Hg in the brain was in the form of inorganic mercury for the thimerosal-exposed infants (34% vs 7%). The current study indicates that MeHg is not a suitable reference for risk assessment from exposure to thimerosal derived Hg. Knowledge of the toxicokinetics and developmental toxicity of thimerosal is needed to afford a meaningful assessment of the developmental effects of thimerosal-containing vaccines.

It causes neuro-inflammation (ie, rapid brain growth) by activating "glial" cells in the brain:

Increases in the number of reactive glia in the visual cortex of Macaca fascicularis following subclinical long-term methyl mercury exposure.

Toxicology and Applied Pharmacology, 1994

Charleston JS, Bolender RP, Mottet NK, Body RL, Vahter ME, Burbacher TM., Department of Pathology, School of Medicine, University of Washington

The number of neurons, astrocytes, reactive glia, oligodendrocytes, endothelia, and pericytes in the cortex of the calcarine sulcus of adult female Macaca fascicularis following long-term subclinical exposure to methyl mercury (MeHg) and mercuric chloride (inorganic mercury; IHg) has been estimated by use of the optical volume fractionator stereology technique. Four groups of monkeys were exposed to MeHg (50 micrograms Hg/kg body wt/day) by mouth for 6, 12, 18, and 12 months followed by 6 months without exposure (clearance group). A fifth group of monkeys was administered IHg (as HgCl2; 200 micrograms Hg/kg body wt/day) by constant rate intravenous infusion via an indwelling catheter for 3 months. Reactive glia showed a significant increase in number for every treatment group, increasing 72% in the 6-month, 152% in the 12-month, and 120% in the 18-month MeHg exposed groups, and the number of reactive glia in the clearance group remained elevated (89%). The IHg exposed group showed a 165% increase in the number of reactive glia. The IHg exposed group and the clearance group had low levels of MeHg present within the tissue; however, the level of IHg was elevated in both groups. These results suggest that the IHg may be responsible for the increase in reactive glia. All other cell types, including the neurons, showed no significant change in number at the prescribed exposure level and durations. The identities of the reactive glial cells and the implications for the long-term function and survivability of the neurons due to changes in the glial population following subclinical long-term exposure to mercury are discussed.

It impairs methylation, a biological process that creates the compound gluthatione, that allows the body to process out toxic substances:
Activation of Methionine Synthase by Insulin-like Growth Factor-1 and Dopamine: a Target for Neurodevelopmental Toxins and Thimerosal

Molecular Psychiatry, July 2004.

Richard C. Deth, PhD [Northeastern University].

This study demonstrates how Thimerosal inhibits methylation, a central driver of cellular communication and development. Excerpt:

"The potent inhibition of this pathway [methylation] by ethanol, lead, mercury, aluminum, and thimerosal suggests it may be an important target of neurodevelopmental toxins."

Thimerosal, at a fraction of the dose found in vaccines, causes motochondrial damage so severe, that it causes the cell actually self-destruct:

Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria.

International Journal of Molecular Medicine, 2006

Yel L, Brown LE, Su K, Gollapudi S, Gupta S.Department of Medicine, University of California, Irvine, CA 92697, USA. lyel@uci.edu

There is a worldwide increasing concern over the neurological risks of thimerosal (ethylmercury thiosalicylate) which is an organic mercury compound that is commonly used as an antimicrobial preservative. In this study, we show that thimerosal, at nanomolar concentrations, induces neuronal cell death through the mitochondrial pathway. Thimerosal, in a concentration- and time-dependent manner, decreased cell viability as assessed by calcein-ethidium staining and caused apoptosis detected by Hoechst 33258 dye. Thimerosal-induced apoptosis was associated with depolarization of mitochondrial membrane, generation of reactive oxygen species, and release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria to cytosol. Although thimerosal did not affect cellular expression of Bax at the protein level, we observed translocation of Bax from cytosol to mitochondria. Finally, caspase-9 and caspase-3 were activated in the absence of caspase-8 activation. Our data suggest that thimerosal causes apoptosis in neuroblastoma cells by changing the mitochondrial microenvironment.

Mitochondrial mediated thimerosal-induced apoptosis in a human neuroblastoma cell line (SK-N-SH).

Neurotoxicology. 2005

Humphrey ML, Cole MP, Pendergrass JC, Kiningham KK. Department of Pharmacology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV 25704-9388, USA.
Environmental exposure to mercurials continues to be a public health issue due to their deleterious effects on immune, renal and neurological function. Recently the safety of thimerosal, an ethyl mercury-containing preservative used in vaccines, has been questioned due to exposure of infants during immunization. Mercurials have been reported to cause apoptosis in cultured neurons; however, the signaling pathways resulting in cell death have not been well characterized. Therefore, the objective of this study was to identify the mode of cell death in an in vitro model of thimerosal-induced neurotoxicity, and more specifically, to elucidate signaling pathways which might serve as pharmacological targets. Within 2 h of thimerosal exposure (5 microM) to the human neuroblastoma cell line, SK-N-SH, morphological changes, including membrane alterations and cell shrinkage, were observed. Cell viability, assessed by measurement of lactate dehydrogenase (LDH) activity in the medium, as well as the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay, showed a time- and concentration-dependent decrease in cell survival upon thimerosal exposure. In cells treated for 24 h with thimerosal, fluorescence microscopy indicated cells undergoing both apoptosis and oncosis/necrosis. To identify the apoptotic pathway associated with thimerosal-mediated cell death, we first evaluated the mitochondrial cascade, as both inorganic and organic mercurials have been reported to accumulate in the organelle. Cytochrome c was shown to leak from the mitochondria, followed by caspase 9 cleavage within 8 h of treatment. In addition, poly(ADP-ribose) polymerase (PARP) was cleaved to form a 85 kDa fragment following maximal caspase 3 activation at 24 h. Taken together these findings suggest deleterious effects on the cytoarchitecture by thimerosal and initiation of mitochondrial-mediated apoptosis.

And mercury leads to heart disease:

Mercury Activates Vascular Endothelial Cell Phospholipase D through Thiols and Oxidative Stress

Thomas J. Hagele, Jessica N. Mazerik, Anita Gregory, Bruce Kaufman, Ulysses Magalang, M. Lakshmi Kuppusamy, Clay B. Marsh, Periannan Kuppusamy, Narasimham L. Parinandi,

Lipidomics and Lipid Signaling Laboratory, Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, Ohio, United States

Correspondence: Address correspondence to Narasimham L. Parinandi, PhD, Room 611-A, Division of Pulmonary, Critical Care, and Sleep Medicine, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, 473 W. 12th Avenue, Columbus, OH 43210, USA. E-mail:narasimham.parinandi@osumc.edu

Currently, mercury has been identified as a risk factor of cardiovascular diseases among humans. Here, the authors tested the hypothesis that mercury modulates the activity of the endothelial lipid signaling enzyme, phospholipase D (PLD), which is an important player in the endothelial cell (EC) barrier functions. Monolayers of bovine pulmonary artery ECs (BPAECs) in culture, following labeling of membrane phospholipids with [32P]orthophosphate, were exposed to mercuric chloride (inorganic form), methylmercury chloride (environmental form), and thimerosal (pharmaceutical form), and the formation of phosphatidylbutanol as an index of PLD activity was determined by thin-layer chromatography and liquid scintillation counting. All three forms of mercury significantly activated PLD in BPAECs in a dose-dependent (0 to 50 µM) and time-dependent (0 to 60 min) fashion. Metal chelators significantly attenuated mercury-induced PLD activation, suggesting that cellular mercury-ligand interaction(s) is required for the enzyme activation and that chelators are suitable blockers for mercury-induced PLD activation. Sulfhydryl (thiol-protective) agents and antioxidants also significantly attenuated the mercury-induced PLD activation in BPAECs. Enhanced reactive oxygen species generation, as an index of oxidative stress, was observed in BPAECs treated with methylmercury that was attenuated by antioxidants. All the three different forms of mercury significantly induced the decrease of levels of total cellular thiols. For the first time, this study revealed that mercury induced the activation of PLD in the vascular ECs wherein cellular thiols and oxidative stress acted as signal mediators for the enzyme activation. The results underscore the importance of PLD signaling in mercury-induced endothelial dysfunctions ultimately leading to cardiovascular diseases.

( More studies on the damage that vaccination and their components are known to do)

CDC reports that approximately 100 children die of the flu every year.

It was reported by the panel that 40-50 children die of flu per year, and that the 86 that have died from H1N1 this far had vastly exceeded that number. I told the panel that my understanding was that the number was 100 per year, and that we had not yet exceeded that. I had gotten that number from this CDC video that was posted a year ago on their You Tube Channel (50 seconds in Dr. Jeanne Santoli states that about 100 children die of influenza every year).






They have either doubled the real number, or cut it in half, presumably to encourage vaccination.

So my question is... was CDC inflating the number of children who die per year from the flu last year to scare parents into getting the seasonal flu vaccine OR are they deflating number of children who die per year from the flu this year to scare parents into getting the H1N1 vaccine?


Thimerosal Containing Vaccines are legally classified as Hazardous Materials

Because of the mercury content in these vaccines, they cannot be thrown away, or even disposed of according to medical waste guidelines. To do so would be illegal.

They must be disposed of according to HazMat rules. From the Wisconsin guidelines:

Some vaccines are preserved with 1:10,000 or 0.01 percent Thimerosal (see the vaccines in the table titled "Thimerosal Content in Some U.S. Licensed Vaccines" at www.vaccinesafety.edu/thi-table.htm that have .01% in the Thimerosal Concentration column). Thimerosal contains about 50 percent mercury by weight. Vaccines with 1:10,000 or 0.01 percent Thimerosal have about 50 mg/L mercury, which exceeds the 0.2 mg/L hazardous waste toxicity characteristic regulatory level for mercury. According to state and federal hazardous waste management requirements, discarded Thimerosal-preserved vaccines may need to be managed as hazardous waste, using the waste code D009 (mercury).

It is illegal to manage Thimerosal-preserved vaccines as infectious waste or regular trash.

A (just in case) correction on my statement on mercury concentrations in vaccines. I may have said "parts per million" when I meant "parts per billion", but I can't remember.

None the less, the mercury concentration in the H1N1 and seasonal flu shots is exponentially larger than what is considered hazmat material. A comparison of mercury concentrations from Pediatrics:

0.5 parts per billion (ppb) mercury = Kills human neuroblastoma cells (Parran et al., Toxicol Sci 2005; 86: 132-140).

2 ppb mercury = U.S. EPA limit for drinking water http://www.epa.gov/safewater/contaminants/index.html#mcls

20 ppb mercury = Neurite membrane structure destroyed (Leong et al., Neuroreport 2001; 12: 733-37).

200 ppb mercury = level in liquid the EPA classifies as hazardous waste. http://www.epa.gov/epaoswer/hazwaste/mercury/regs.htm#hazwaste

25,000 ppb mercury = Concentration of mercury in the Hepatitis B vaccine, administered at birth in the U.S., from 1990-2001.

50,000 ppb Mercury = Concentration of mercury in multi-dose DTaP and Haemophilus B vaccine vials, administered 4 times each in the 1990's to children at 2, 4, 6, 12 and 18 months of age. Current "preservative" level mercury in multi-dose flu (94% of supply), meningococcal and tetanus (7 and older) vaccines. This can be confirmed by simply analyzing the multi- dose vials.


EPA says you must weigh 550 lbs. to safely process the mercury in a flu vaccine

Thimerosal containing flu shots have 25 mcg of mercury in them.

EPA daily limits on mercury intake are .1 mcg per kilogram of weight.  1 kilo = 2.20462262 pounds  My 55 pound 7 year old therefore weighs 25 kelograms.

25 x .1 =  2.5

The EPA says that my son should receive no more than 2.5 mcg of mercury in a day.  The vaccine he will be offered at school contains ten times that amount.

I weigh 255 lbs or 116 kelos.  116 x .1 = 11.6

The vaccine is still more than twice what a big girl like me should be exposed to.

Further these EPA standards are based on ingested methyl mercury, the kind found in fish, (only about a tenth of which is absorbed through the GI tract into the blood stream).  We have already seen from the Burbacher study above, that injected thimerosal becomes trapped in the brain at a much higher rate than ingested mercury.  So the EPA standards I am using are probably should be upped by ten fold when being applied to vaccination.

EPA/FDA/CDC will not set safety limits for injected methyl mercury, despite the demand from parents for them to do so for many years.

No one has died from mercury

One of the panelists, a physician, suggested that no one has died from mercury in vaccines. This is a disingenuous statement as vaccine deaths are attributed to the vaccine as a whole, not to the components of the vaccine. And of course Death is a known outcome of vaccination and is covered under the HHS Vaccine Injury Compensation Program.

And yes... peoplehavediedfrommercury.

Government agencies and states are trying to eliminate mercury in daily life, but it is still in vaccines.


Bills and laws limiting and eliminating mercury are ubiquitous now. It is the height of cognitive dissonance to say that mercury should be eliminated from the environment, but injected into babies as young as 6 months.


And all this is true BEFORE you even begin the discussion on whether or not mercury containing vaccines can cause autism.  Note that this paragraph is the first time the word "autism" is even appears in this piece.  And the last.

There is a saying in our community....

Giving Mercury to Children on Purpose is Stupid
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