Friday, November 6, 2009

Comprehensive Vaccine Ingredient Information


Vaccination ingredients according to the product insert:

MMR II: Measles, Mumps and Rubella

http://www.merck.com/product/usa/pi_circulars/m/mmr_ii/mmr_ii_pi.pdf

The Ingredients: measles, mumps, rubella virus, neomycin, sorbitol, hydrolized gelatin, chick embryonic fluid, and human diploid cells from aborted fetal tissue.

Infanrix: Dipthetheria, Tetanus and Pertussis

http://us.gsk.com/products/assets/us_infanrix.pdf

The Ingredients: Diphtheria, Tetanus and Pertussis toxoids, 2-Phenoxyethanol, Aluminum hydroxide, and Formaldehyde.

IPOL: Polio

http://www.vaccineshoppe.com/US_PDF/IPOL_942420_11.06.pdf

The Ingredients: 3 types of polio viruses, neomycin, streptomycin, polymyxin B, formaldehyde, 2-phenoxyethenol, and a continuous line of monkey kidney cells.


Act-Hib: Haeomophilus Influenza type B

http://www.novaccine.com/pdffiles/Act_HIB_package_insert.pdf

The Ingredients: Haemophilus influenza Type B, polyribosylribitol phosphate, ammonium sulfate, formalin, and sucrose.


Menactra: Meningococcal

www.fda.gov/CbER/products/menactra.htm

The Ingredients: Neisseria meningitidis A, C, Y and W-135 strains, Mueller Hinton Agar, Watson Scherp Media, polysaccharide antigens, formaldehyde, diphtheria toxoid protein, ammonium sulfate.


Prevnar: Pneumococcal

http://www.wyeth.com/content/showlabeling.asp?id=134

The Ingredients: saccharides from capsular Streptococcus pneumoniae antigens (7 serotypes) individually conjugated to diphtheria CRM 197 protein, aluminum phosphate, ammonium sulfate, soy protein, and yeast.

Varivax: Varicella (chickenpox)

www.merck.com/product/usa/pi_circulars/v/varivax/varivaxpi.pdf

The Ingredients: varicella live virus, neomycin, phosphate, sucrose, and monosodium glutamate (MSG), processed gelatin, fetal bovine serum, guinea pig embryo cells, albumin from human blood, and human diploid cells from aborted fetal tissue.


Rotarix: Rotavirus

http://www.fda.gov/CbER/label/rotarixLB.pdf

The Ingredients: weakened human rotavirus, dextran, sorbitol, xanthan, Dulbecco's Modified Eagle Medium (DMEM), which contains: sodium chloride, potassium chloride, magnesium sulphate, ferric (III) nitrate, sodium phosphate, sodium pyruvate, D-glucose, concentrated vitamin solution, L-cystine, L-tyrosine, amino acids solution, L-glutamine, calcium chloride, sodium hydrogenocarbonate, and phenol red.


Gardasil:HPV
http://www.merck.com/product/usa/pi_circulars/g/gardasil/gardasil_pi.pdf


The Ingredients: HPV types 6, 11, 16 and 18, saccharomyces cerevisiae, "fermentation media", aluminum, sodium chloride, polysorbate 80, sodium borate.


FluZone (or FluShield, same product): Influenza

www.fda.gov/CBER/label/fluzoneLB.pdf

The Ingredients: Trivalent influenza virus, gentamicin sulphate, formaldehyde, thimerosal, polysorbate 80 (Tween 80) and chick embryonic fluid

Havrix: Hepatitis A

http://us.gsk.com/products/assets/us_havrix.pdf

Ingredients: Hepatitis A virus/toxoids, formalin, aluminum hydroxide, 2-phenoxyethanol, polysorbate 20, and residual MRC5 proteins -human diploid cells from aborted fetal tissue.


Energix B: Hepatitis B

http://us.gsk.com/products/assets/us_engerixb.pdf

The Ingredients: genetic sequence of the hepatitis B virus that codes for the surface antigen (HbSAg), cloned into GMO yeast, aluminum hydroxide, and thimerosal.


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The vaccine ingredients effects on the human body, followed by links to substantiating documentation of causation


Aluminum= Neurotoxin


http://informedcitizensagainstvaccination.blogspot.com/2009/11/aluminum-neurotoxic-vaccine-adjuvant.html

Formaldehyde= Carcinogen (cancer causer); linked causally to an assortment of cancers, most recently Leukemia. The International Agency for Research on Cancer (IARC) classified it as a known human carcinogen in 2004.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/formaldehyde-carcinogen-in-vaccinations.html

Thimerosal= Neurotoxin; controversially linked to Autism in the media, but is well known and causally proven to cause many neurological disorders, cell death in the brain, mitochondrial damage, etcetera. Thimerosal is still being used in the Hepatitis B and Influenza vaccines as of 2009, and is also contained within several of the H1N1 vaccinations.

http://informedcitizensagainstvaccination.blogspot.com/2009/11/thimerosal-neurotoxic-in-plethora-of.html


2-Phenoxyethanol aka "Antifreeze" aka "ethylene glycol monomethyl ether"= neurotoxic, CNS toxicant.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/2-phenoxyethanol-antifreeze-neurotoxin.html

Phenol= nephrotoxic; CNS toxin, heart toxin, gastrointestinal, kidney, lung and blood vessel toxin... known to induce coma's and death; by far one of the most toxic of all vaccine ingredients.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/phenol-cns-toxin-causes-comas-and-death.html

Sorbitol= cardiac toxin, causes neuropathy in and exacerbation of diabetes, CNS toxin, our own government states under no uncertain terms that this substance is NOT to be injected... then allows it to be used in childhood vaccinations.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/sorbitol-cardiac-toxin-causes.html

Neomycin, Streptomycin, Polyxmyxin B, Gentamicin Sulfate= Antibiotics. Immune suppressing, lead to the development of more virulent organisms and antibacterial resistance so people cannot combat them.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/antibiotics-in-vaccinations.html


Egg (chick embryonic fluid), soy, yeast, gelatin= Allergens, risk of anaphylaxis and the development of Asthma.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/allergens-in-vaccinations.html


Monosodium Glutamate= Excitotoxin; hazardous to your health in so many ways: read the full length article for further details.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/monosodium-glutmate-creating-dumb-obese.html

Polysorbate 80 or Tween 80= anaphylaxis risk, also permeates the BBB (blood brain barrier) which means vaccine toxins can enter the brain.


http://informedcitizensagainstvaccination.blogspot.com/2009/11/polysorbate-80-aka-tween-80-allows.html


Chick embryonic fluid, fetal bovine serum, guinea pig embryo cells, monkey kidney cells= Animal products in vaccinations that are highly susceptible to contamination. There is a particularly elevated risk with bovine serum (bovine polyomavirus) and monkey kidney cells (SV40 contamination causing cancer).


http://informedcitizensagainstvaccination.blogspot.com/2009/11/animal-products-contaminants-in.html


See also:

The dangerous impurities of vaccines by Janine Roberts

On the toxic ingredients of vaccinations: plays special emphasis to animal by-products and their production process in vaccinations.

http://www.foresight-preconception.org.uk/pdf/dangerous-impurities-of-vaccines.pdf

Thimerosal: Neurotoxic in a plethora of forms, still used in Hep B, Influenza, H1N1 vaccines

Thimerosal: neurotoxicity is not limited to the autism link as many people assume. Thimerosal is causally linked to a plethora of ND's (neurological disorders), cell death, mitochondrial dysfunction, and more.

http://www.iaomt.org/testfoundation/thimtox.htm

This is a very lengthy article on thimerosal toxicity and it's relevance to vaccinations and brain damage. It cannot be copy/pasted because of the file type but is more than worth the read.

Medical studies on thimerosal:

Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds Geier DA, King PG, Geier MR.Toxicological & Environmental Chemistry 2009, 1–15

iFirsthttp://www.informaworld.com/smpp/content~content=a910652305~db=all~order=pubdate

Thimerosal (ethylmercurithiosalicylic acid), an ethylmercury (EtHg)-releasing compound (49.55% mercury (Hg)), was used in a range of medical products for more than 70 years. Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants. This study was undertaken to investigate cellular damage among in vitro human neuronal (SH-SY-5Y neuroblastoma and 1321N1 astrocytoma) and fetal (nontransformed) model systems using cell vitality assays and microscope-based digital image capture techniques to assess potential damage induced by Thimerosal and other metal compounds (aluminum (Al) sulfate, lead (Pb)(II) acetate, methylmercury (MeHg) hydroxide, and mercury (Hg)(II) chloride) where the cation was reported to exert adverse effects on developing cells. Thimerosal-associated cellular damage was also evaluated for similarity to pathophysiological findings observed in patients diagnosed with autistic disorders (ADs). Thimerosal-induced cellular damage as evidenced by concentration- and time-dependent mitochondrial damage, reduced oxidative–reduction activity, cellular degeneration, and cell death in the in vitro human neuronal and fetal model systems studied. Thimerosal at low nanomolar (nM) concentrations induced significant cellular toxicity in human neuronal and fetal cells. Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies. Thimerosal was found to be significantly more toxic than the other metal compounds examined. Future studies need to be conducted to evaluate additional mechanisms underlying Thimerosal-induced cellular damage and assess potential co-exposures to other compounds that may increase or decrease Thimerosal-mediated toxicity.Thimerosal induces DNA breaks, caspase-3 activation, membrane damage, and cell death in cultured human neurons and fibroblasts.

Baskin DS, Ngo H, Didenko VV.Department of Neurosurgery, Baylor College of MedicineToxicol Sci. 2003 Aug;74(2):361-8. {free online}

http://toxsci.oxfordjournals.org/cgi/content/full/74/2/361

Thimerosal is an organic mercurial compound used as a preservative in biomedical preparations. Little is known about the reactions of human neuronal and skin cells to its micro- and nanomolar concentrations, which can occur after using thimerosal-containing products. A useful combination of fluorescent techniques for the assessment of thimerosal toxicity is introduced.
Short-term thimerosal toxicity was investigated in cultured human cerebral cortical neurons and in normal human fibroblasts. Cells were incubated with 125-nM to 250-microM concentrations of thimerosal for 45 min to 24 h. A 4', 6-diamidino-2-phenylindole dihydrochloride (DAPI) dye exclusion test was used to identify nonviable cells and terminal transferase-based nick-end labeling (TUNEL) to label DNA damage. Detection of active caspase-3 was performed in live cell cultures using a cell-permeable fluorescent caspase inhibitor. The morphology of fluorescently labeled nuclei was analyzed. After 6 h of incubation, the thimerosal toxicity was observed at 2 microM based on the manual detection of the fluorescent attached cells and at a 1-microM level with the more sensitive GENios Plus Multi-Detection Microplate Reader with Enhanced Fluorescence. The lower limit did not change after 24 h of incubation. Cortical neurons demonstrated higher sensitivity to thimerosal compared to fibroblasts. The first sign of toxicity was an increase in membrane permeability to DAPI after 2 h of incubation with 250 microM thimerosal. A 6-h incubation resulted in failure to exclude DAPI, generation of DNA breaks, caspase-3 activation, and development of morphological signs of apoptosis. We demonstrate that thimerosal in micromolar concentrations rapidly induce membrane and DNA damage and initiate caspase-3-dependent apoptosis in human neurons and fibroblasts. We conclude that a proposed combination of fluorescent techniques can be useful in analyzing the toxicity of thimerosal.Thimerosal induces micronuclei in the cytochalasin B block micronucleus test with human lymphocytes.

Westphal GA et al.Georg-August-University, Gottingen, Germany.Arch Toxicol. 2003 Jan;77(1):50-5.

Excerpt: Thimerosal is a widely used preservative in health care products, especially in vaccines. Due to possible adverse health effects, investigations on its metabolism and toxicity are urgently needed. An in vivo study on chronic toxicity of thimerosal in rats was inconclusive and reports on genotoxic effects in various in vitro systems were contradictory. Therefore, we reinvestigated thimerosal in the cytochalasin B block micronucleus test. Glutathione S-transferases were proposed to be involved in the detoxification of thimerosal or its decomposition products. Since the outcome of genotoxicity studies can be dependent on the metabolic competence of the cells used, we were additionally interested whether polymorphisms of glutathione S-transferases (GSTM1, GSTT1, or GSTP1) may influence the results of the micronucleus test with primary human lymphocytes. Blood samples of six healthy donors of different glutathione S-transferase genotypes were included in the study. At least two independent experiments were performed for each blood donor. Significant induction of micronuclei was seen at concentrations between 0.05-0.5 micro g/ml in 14 out of 16 experiments. Thus, genotoxic effects were seen even at concentrations which can occur at the injection site. Toxicity and toxicity-related elevation of micronuclei was seen at and above 0.6 micro g/ml thimerosal. Marked individual and intraindividual variations in the in vitro response to thimerosal among the different blood donors occurred. However, there was no association observed with any of the glutathione S-transferase polymorphism investigated. In conclusion, thimerosal is genotoxic in the cytochalasin B block micronucleus test with human lymphocytes. These data raise some concern on the widespread use of thimerosal.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W81-4DF44GF-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1078617709&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7296b93ae240e5babf6f09e485dffb27

Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors

http://www.nature.com/mp/journal/v9/n9/abs/4001529a.html

M. Hornig; Neurotoxic effects of postnatal thimerosal; Molecular Psychiatry (2004) 9, 833–845

The developing brain is uniquely susceptible to the neurotoxic hazard posed by mercurials. Host differences in maturation, metabolism, nutrition, sex, and autoimmunity influence outcomes. How population-based variability affects the safety of the ethylmercury-containing vaccine preservative, thimerosal, is unknown. Reported increases in the prevalence of autism, a highly heritable neuropsychiatric condition, are intensifying public focus on environmental exposures such as thimerosal. Immune profiles and family history in autism are frequently consistent with autoimmunity. We hypothesized that autoimmune propensity influences outcomes in mice following thimerosal challenges that mimic routine childhood immunizations. Autoimmune disease-sensitive SJL/J mice showed growth delay; reduced locomotion; exaggerated response to novelty; and densely packed, hyperchromic hippocampal neurons with altered glutamate receptors and transporters. Strains resistant to autoimmunity, C57BL/6J and BALB/cJ, were not susceptible. These findings implicate genetic influences and provide a model for investigating thimerosal-related neurotoxicity.

http://www.theflucase.com/index.php?option=com_content&view=article&id=819%3Aaluminum-in-vaccines-increases-thimerosals-toxicity&catid=1%3Alatest-news&Itemid=64&lang=en

Boyd E. Haley, Ph.D., is Professor Emeritus of chemistry and has published important studies about mercury (eg, 1-3). One of his team's finding documented that a major phenomenon in Alzheimer's-like pathologies could be induced by physiologically occurring levels of mercury (1). A recent essay is titled "Aluminum in vaccination-associated cognitive decline, motor neuron disease, autism" (4). That essay prompted an insightful comment from Dr. Haley, wherein he reports that vaccine-levels of aluminum exacerbate the pathologic potential of vaccinal thimerosal: Dr. Haley explained, "Note that aluminum alone does not cause the abnormal biochemistry and production of neurofibillary tangles as does mercury (and only mercury) due to the specific interaction of mercury at specific sulfhydryl sites in specific enzymes/proteins known to be affected dramatically in Alzheimer’s disease. However, in our studies on neurons in culture we found that aluminum at levels found in vaccines dramatically enhanced the toxicity of thimerosal and mercury cation thereby decreasing the level of mercury required to have the toxic effects."Importantly, some vaccines including many flu shots still contain thimerosal, and many contain one or another of the aluminum compounds used as adjuvants. Thus we repeat: aluminum at levels present in vaccines increases the toxicity of thimerosal, which is ~49.6% ethylmercury by weight. Thus when an infant, toddler, or pregnant woman is injected with a vaccine or a combination of vaccines containing aluminum compounds and thimerosal, the likelihood of adverse effects is increased.

Perhaps we should ask, Why care?

Many media reports assure us that no evidence links thimerosal with neurologic harm. For instance, Melissa Healy of the Los Angeles Times expresses a popular notion by writing, "Many argue that environmental exposures -- in particular, to preservatives used in certain vaccines -- are a key factor in the development of autism. But a wide range of comprehensive investigations has failed to find such a link." (5) Unfortunately, Melissa Healy's glib statement is misleading. However, at least three major studies have found thimerosal injections to be associated with developmental disabilities including autism. Two researchers at Stony Brook medical school found that male infants injected with thimerosal via hepatitis B vaccinations (a) were nine times as likely to be enrolled in special education services, and (b) were three times as likely to have autism -- when compared with male infants who had not been so vaccinated (6-7). Importantly, these findings are consistent with the original CDC study (Verstraeten et al 1999) wherein early live thimerosal injections were associated with autism, PDD, language problems, sleep disorders, and tics (reviewed in 8).

Furthermore, other peer-reviewed studies have documented some of the mechanisms by which aluminum and mercury induce pathologies seen as neurodeneneration (eg, 10-14, 15-17).

Noteworthy: in a recently published study, researchers dared mention that "The demonstrated neurotoxicity of aluminum hydroxide and its relative ubiquity as an adjuvant suggest that greater scrutiny by the scientific community is warranted." (14)Similarly, "Although Thimerosal has been recently removed from most children's vaccines, it is still present in flu vaccines given to pregnant women, the elderly, and to children in developing countries." (17)Needless to say, I and others are perplexed. Why do most vaccinologists and many health officials proclaim the safety of vaccines containing aluminum compounds and/or thimerosal? Why do reporters such as Melissa Healy and spokespersons for the CDC and FDA turn our attention away from peer-reviewed studies demonstrating adverse effects from aluminum and thimerosal? Why must myriad children and their families live with adverse effects of vaccinations whose ingredients cause neurodegeneration and developmental disabilities?

References:1. Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brainPendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL.Neurotoxicology. 1997;18(2):315-24.

Hg2+ interacts with brain tubulin and disassembles microtubules that maintain neurite structure. Since it is well known that Hg vapor (Hg0) is continuously released from "silver" amalgam tooth fillings and is absorbed into brain, rats were exposed to Hg0 4h/day for 0, 2, 7, 14 and 28 d at 250 or 300 micrograms Hg/m3 air, concentrations present in mouth air of some humans with many amalgam fillings. Average rat brain Hg concentrations increased significantly (11-47 fold) with duration of Hg0 exposure. By 14 d Hg0 exposure, photoaffinity labelling on the beta-subunit of the tubulin dimer with [alpha 32P] 8N3 GTP in brain homogenates was decreased 41-74%, upon analysis of SDS-PAGE autoradiograms. The identical neurochemical lesion of similar or greater magnitude is evident in Alzheimer brain homogenates from approximately 80% of patients, when compared to human age-matched neurological controls. Total tubulin protein levels remained relatively unchanged between Hg0 exposed rat brains and controls, and between Alzheimer brains and controls. Since the rate of tubulin polymerization is dependent upon binding of GTP to tubulin dimers, we conclude that chronic inhalation of low-level Hg0 can inhibit polymerization of brain tubulin essential for formation of microtubules.

2. Reduced levels of mercury in first baby haircuts of autistic childrenHolmes AS, Blaxill MF, Haley BE.Int J Toxicol. 2003 Jul-Aug;22(4):277-85.

Reported rates of autism have increased sharply in the United States and the United Kingdom. One possible factor underlying these increases is increased exposure to mercury through thimerosal-containing vaccines, but vaccine exposures need to be evaluated in the context of cumulative exposures during gestation and early infancy. Differential rates of postnatal mercury elimination may explain why similar gestational and infant exposures produce variable neurological effects. First baby haircut samples were obtained from 94 children diagnosed with autism using Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV) criteria and 45 age- and gender-matched controls. Information on diet, dental amalgam fillings, vaccine history, Rho D immunoglobulin administration, and autism symptom severity was collected through a maternal survey questionnaire and clinical observation. Hair mercury levels in the autistic group were 0.47 ppm versus 3.63 ppm in controls, a significant difference. The mothers in the autistic group had significantly higher levels of mercury exposure through Rho D immunoglobulin injections and amalgam fillings than control mothers. Within the autistic group, hair mercury levels varied significantly across mildly, moderately, and severely autistic children, with mean group levels of 0.79, 0.46, and 0.21 ppm, respectively. Hair mercury levels among controls were significantly correlated with the number of the mothers' amalgam fillings and their fish consumption as well as exposure to mercury through childhood vaccines, correlations that were absent in the autistic group. Hair excretion patterns among autistic infants were significantly reduced relative to control. These data cast doubt on the efficacy of traditional hair analysis as a measure of total mercury exposure in a subset of the population. In light of the biological plausibility of mercury's role in neurodevelopmental disorders, the present study provides further insight into one possible mechanism by which early mercury exposures could increase the risk of autism3. Mercury toxicity presenting as chronic fatigue, memory impairment and depression: diagnosis, treatment, susceptibility, and outcomes in a New Zealand general practice setting (1994-2006)Wojcik DP, Godfrey ME, Christie D, Haley BE.Neuro Endocrinol Lett. 2006 Aug;27(4):415-23.In a group of 465 patients diagnosed as having chronic mercury toxicity (CMT), 32.3% had severe fatigue, 88.8% had memory loss, and 27.5% had depression. A significant correlation was found between CMT and the Apo-lipoprotein E4 genotype (p=0.001). An investigation into an additional 864 consecutively seen general practice patients, resulted in 30.3% having evidence consistent with CMT, and once again a significant correlation was found with the APO-E4 genotype (p=0.001). Removal of amalgam mercury fillings when combined with appropriate treatment resulted in a significant symptom reduction (p<0.001)>

4. Aluminum in vaccination-associated cognitive decline, motor neuron disease, autismTeresa Binstock; Sept 28, 2009

http://www.generationrescue.org/binstock/090928-aluminum-als-alzheimer-autism.htm

5. Autism's genetic roots examined in new government-funded studyMelissa Healy, Los Angeles Times September 30, 2009 http://latimesblogs.latimes.com/booster_shots/2009/09/autisms-genetic-roots-probed-by-new-governmentfunded-study.html

6. Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years Gallagher C, Goodman M. Toxicol Environ Chem 2008 90(5):997-1008.{free online}

http://fourteenstudies.org/pdf/hep_b.pdf

7. Hepatitis B vaccination of male neonates and autismCM Gallagher, MS GoodmanAnnals of EpidemiologyVol. 19, No. 9

ABSTRACTS (ACE)September 2009: p. 659
Stony Brook University Medical Center, NY

PURPOSE: Universal newborn immunization with hepatitis B vaccine was recommended in 1991; however, safety findings are mixed. The Vaccine Safety Datalink Workgroup reported no association between hepatitis B vaccination at birth and febrile episodes or neurological adverse events. Other studies found positive associations between hepatitis B vaccination and ear infection, pharyngitis, and chronic arthritis; as well as receipt of early intervention/special education services (EIS); in probability samples of U.S. children. Children with autistic spectrum disorder (ASD) comprise a growing caseload for EIS. We evaluated the association between hepatitis B vaccination of male neonates and parental report of ASD.


METHODS: This cross-sectional study used U.S. probability samples obtained from National Health Interview Survey 1997–2002 datasets. Logistic regression modeling was used to estimate the effect of neonatal hepatitis B vaccination on ASDrisk amongboys age 3–17 years with shot records, adjusted for race, maternal education, and two-parent household.

RESULTS:Boys who received the hepatitis B vaccine during the first month of life had 2.94 greater odds for ASD (nZ31 of 7,486; OR Z 2.94; p Z 0.03; 95% CI Z 1.10, 7.90) compared to later- or unvaccinated boys. Non-Hispanicwhite boys were 61% less likely to have ASD(ORZ0.39; pZ0.04; 95% CIZ0.16, 0.94) relative to non-white boys.

CONCLUSION: Findings suggest that U.S. male neonates vaccinated with hepatitis B vaccine had a 3-fold greater risk of ASD; risk was greatest for non-white boys.

8. [Synopsis & review]Blockbuster primate Study Shows Significant Harm from One Birth Dose of a Mercury-containing Vaccine By Mark Blaxill; Sept 30, 2009

http://tinyurl.com/y9dvzae

9. Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration Yokel RA. J Alzheimers Dis. 2006 Nov;10(2-3):223-53.

10: Aluminum complexing enhances amyloid beta protein penetration of blood-brain barrierBanks WA et al.Brain Res. 2006 Oct 20;1116(1):215-21.

11: Some aspects of astroglial functions and aluminum implications for neurodegeneration Aremu DA, Meshitsuka S. Brain Res Rev. 2006 Aug 30;52(1):193-200.

12: Nanomolar aluminum induces pro-inflammatory and pro-apoptotic gene expression in human brain cells in primary culture, Lukiw WJ et al. J Inorg Biochem. 2005 Sep;99(9):1895-8.

13. Long-term persistence of vaccine-derived aluminum hydroxide is associated with chronic cognitive dysfunction, Maryline Couette et al. Journal of Inorganic Biochemistry (2009) in press

14. Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration Christopher A. Shaw; Michael S. Petrik.Journal of Inorganic Biochemistry (2009) in press

15. Biochemical and molecular basis of thimerosal-induced apoptosis in T cells: a major role of mitochondrial pathway Makani S et al. Genes Immun. 2002 Aug;3(5):270-8.{free online}

http://www.nature.com/gene/journal/v3/n5/abs/6363854a.html

16. Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria, Yel L et al. Int J Mol Med. 2005 Dec;16(6):971-7.

17. Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursorsJames SJ et al.Neurotoxicology. 2005 Jan;26(1):1-8.

Thimerosol is an antiseptic containing 49.5% ethyl mercury that has been used for years as a preservative in many infant vaccines and in flu vaccines. Environmental methyl mercury has been shown to be highly neurotoxic, especially to the developing brain. Because mercury has a high affinity for thiol (sulfhydryl (-SH)) groups, the thiol-containing antioxidant, glutathione (GSH), provides the major intracellular defense against mercury-induced neurotoxicity.

Cultured neuroblastoma cells were found to have lower levels of GSH and increased sensitivity to thimerosol toxicity compared to glioblastoma cells that have higher basal levels of intracellular GSH. Thimerosal-induced cytotoxicity was associated with depletion of intracellular GSH in both cell lines. Pretreatment with 100 microM glutathione ethyl ester or N-acetylcysteine (NAC), but not methionine, resulted in a significant increase in intracellular GSH in both cell types. Further, pretreatment of the cells with glutathione ethyl ester or NAC prevented cytotoxicity with exposure to 15 microM Thimerosal. Although Thimerosal has been recently removed from most children's vaccines, it is still present in flu vaccines given to pregnant women, the elderly, and to children in developing countries. The potential protective effect of GSH or NAC against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccinations.

Further studies on thimerosal neurotoxicity:

Dórea JG, Marques RC.Modeling neurodevelopment outcomes and ethylmercury exposure from thimerosal-containing vaccines. Toxicol Sci. 2008 Jun;103(2):414-5;

Mutter J, Yeter D. Kawasaki's disease, acrodynia, and mercury. Curr Med Chem. 2008;15(28):3000-10.

Berman RF, Pessah IN,
Low-level neonatal thimerosal exposure: further evaluation of altered neurotoxic potential in SJL mice. Toxicol Sci. 2008 Feb;101(2):294-309.

Herdman ML, Marcelo A,
Thimerosal induces apoptosis in a neuroblastoma model via the cJun N-terminal kinase pathway. Toxicol Sci. 2006 Jul;92(1):246-53.

Humphrey ML, Cole MP,
Mitochondrial mediated thimerosal-induced apoptosis in a human neuroblastoma cell line (SK-N-SH). Neurotoxicology. 2005 Jun;26(3):407-16

James SJ, Slikker W 3rd,
Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors. Neurotoxicology. 2005 Jan;26(1):1-8

Parran DK, Barker A, Ehrich M.
Effects of thimerosal on NGF signal transduction and cell death in neuroblastoma cells. Toxicol Sci. 2005 Jul;86(1):132-40.

Blaxill MF, Redwood L,
Thimerosal and autism? A plausible hypothesis that should not be dismissed. Med Hypotheses. 2004;62(5):788-94.

Sorbitol: cardiac toxin, causes neuropathy in diabetes

Sorbitol: cardiac toxin, diabetes exacerbater, warned by our own government the substance is not to be injected!

http://www.drugs.com/pro/sorbitol.html

This is the official FDA information on sorbitol:

Warnings
Not for injection.

Pediatric Use
Safety and effectiveness in pediatric patients have not been established.

http://www.sailhome.org/Concerns/Vaccines.html

The sudden injection of extra sorbitol can ruin the equilibrium of enzymes that regulate the conversion of glucose to fructose in a process associated with the onset of diabetes and its complications. Further, the polyol pathway is involved with a complex network of metabolic activities; disruption leads to a cascade of problems (citations here, here and here) such as mitochondrial failure, cell apoptosis (cell death), and DNA fragmentation. In general, sorbitol induces cell hyperosmotic stress resulting in phosphorylation (uptake of phosphorus into cell) -- an important on/off switch regulating enzymes and signaling networks. This government record prominently states under Drug Warnings that sorbitol is not to be injected.

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/r?dbs+hsdb:@term+@rn+50-70-4

http://medical-dictionary.thefreedictionary.com/sorbitol

A sugar alcohol found in various berries and fruits; in mammals, sorbitol is an intermediate in the conversion of glucose to fructose. It is found in lens deposits in diabetes mellitus. A 50% solution is used as an osmotic diuretic.

http://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/Meds/Sorbitol.htm

Precautions:
Significant cardiopulmonary,renal dysfunction, diabetes mellitus, hyponatremia, hypovolemia

Adverse Reactions (Side Effects):
CNS: seizures, vertigo
CV: angina, hypotension, congestive heart failure
EENT:Blurred vision, rhinitis, thirst
GI: Colonic necrosis, diarrhea, nausea, vomiting
GU: Acidosis, diuresis, edema, urinary retention
METAB: acidosis, hyperglycemia, hypernatremia, hyponatremia
Skin: rash, urticaria

http://doublecheckmd.com/EffectsDetail.do?dname=sorbitol&sid=13713&eid=2084

Gastrointestinal side effects have included sudden severe abdominal bloating, abdominal cramping, vomiting, and osmotic diarrhea.

The use of sorbitol is contraindicated in patients with anuria. Sorbitol should not be used in patients with suspected or documented fructose intolerance. Sorbitol should not given by injection.

Sudden severe abdominal bloating and diarrhea have been reported in patients ingesting sorbitol.

http://www4.wiwiss.fu-berlin.de/dailymed/page/drugs/2992

Life threatening adverse reactions with intravenous sorbitol infusions have been reported in patients with fructose intolerance. The literature reports occasional adverse reactions for intravenous sorbitol infusions. These include disturbances such as acidosis, electrolyte loss, marked diuresis, urinary retention, edema, dryness of mouth and thirst, and dehydration; cardiovascular/pulmonary disorders such as pulmonary congestion, hypotension, tachycardia, angina-like pains, and other general reactions such as blurred vision, convulsions, nausea, vomiting, diarrhea, rhinitis, chills, vertigo, and backache. Allergic reactions reported to occur from sorbitol include urticaria. Should adverse reactions occur, discontinue the irrigant and reevaluate the clinical status of the patient.

http://www.wellsphere.com/exercise-article/sorbitol-poison-in-your-body-ok-in-foods/237070

(this article lays it flat out: sorbitol in your blood stream is vastly more dangerous than sorbitol in food!)

Sorbitol: Poison in Your Body, OK in Foods
Posted Aug 26 2008 by Dr. Mirkin

When blood sugar levels rise too high, sugar sticks to the surface membranes of cells. The sugar, glucose, is converted into another sugar, fructose, and eventually to sorbitol, which destroys the cells. This cell damage leads to heart attacks, strokes, blindness, deafness, kidney damage and the other harmful effects of diabetes. The same chemical is harmless when it is used in foods because you do not absorb it.

Studies supporting causation of sorbitol to exacerbating diabetes or causing neuropathy in diabetes patients:

Sim HJ, Jeong JS,
HPLC with pulsed amperometric detection for sorbitol as a biomarker for diabetic neuropathy.

J Chromatogr B Analyt Technol Biomed Life Sci. 2009 May 15;877(14-15):1607-11

Ido Y, Nyengaard JR, Early Neural and Vascular Dysfunction in Diabetic Rats are Largely Sequelae of Increased Sorbitol Oxidation. Antioxid Redox Signal. 2009 Jul 22.

Jakić M, Diabetic nephropathy and prevention of diabetic nephropathy caused chronic renal insufficiency, Lijec Vjesn. 2009 Jul-Aug;131(7-8):218-25.

Excerpt: Pathogenesis of diabetic nephropathy is based on hyperglycemia and distinct hemodynamic changes, glomerular hyperfiltration and high intraglomerular pressure. The important role have oxidative stress, advanced glycation end products, some cytokines, growth factors and sorbitol pathway.

LIU Tsang-Pai ; JUANG Shiow-Wen; The role of sorbitol pathway and treatment effect of aldose reductase inhibitor ONO2235 in the up-regulation of cardiac M2-muscarinic receptors in streptozotocin-induced diabetic rats; Neuroscience letters, 2005, vol. 383, no1-2, pp. 131-135 .

Emanuela Ciuchi, Patrizio Odetti; Relationship between glutathione and sorbitol concentrations in erythrocytes from diabetic patients; Metabolism, Volume 45, Issue 5, May 1996

Saraswat M, Muthenna P, Dietary sources of aldose reductase inhibitors: prospects for alleviating diabetic complications, Asia Pac J Clin Nutr. 2008;17(4):558-65.

Excerpt: The ex vivo incubation of erythrocytes in high glucose containing medium was used to underscore the significance in terms of prevention of intracellular sorbitol accumulation.

Polysorbate 80 aka "Tween 80": Allows Vaccine Toxins to Cross the BBB, Anaphylaxis risk also


http://www.sailhome.org/Concerns/Vaccines.html

Emulsifiers

Generally listed as Polysorbate 80 or 20, these chemicals have an ability to increase cell permeability, damage, and bursting. After injection they can rapidly metabolize into sorbitol and ethylene oxide which is much more toxic than the original chemical. When Polysorbate 80 breaks down there are 20 moles of ethylene oxide for every mole of sorbitol. These polysorbates have been shown to cause dangerous, sometimes fatal effects, when given through a needle. Changes in heart function can occur immediately. The blood-brain-barrier (BBB) can be weakened and penetrated, followed by seizures and even death. Anaphylactic and other reactions can occur. Infants are particularly susceptible. These polysorbates also demonstrate synergistic toxicity with a range of chemicals including lindane, thalidomide -- even Polymyxin B. ((ICAV notes: polymyxyin b is also a vaccine ingredient))

http://infertility.suite101.com/article.cfm/polysorbate_80_causes_infertility

Polysorbate 80 (also known as tween 80) is a stabilizer used in a wide variety of products including ice cream, milk products, vitamin tablets, lotions and creams and medical products like vaccines and anti-cancer medications.

It is toxic and should not be eaten, drunk, put on the skin or injected.

According to Annals of Allergy, Asthma and Immunology, Volume 95, Number 6, December 2005 , pp. 593-599(7), "it is of current relevance as a 'hidden' inductor of anaphylactoid reactions", and "Polysorbate 80 was identified as the causative agent for the anaphylactoid reaction of nonimmunologic origin in the patient. Conclusions: Polysorbate 80 is a ubiquitously used solubilizing agent that can cause severe nonimmunologic anaphylactoid reactions."

Put in plain English, polysorbate 80 can affect your immune system and cause severe anaphylactic shock which can kill.

http://www.drugs.com/cdi/darbepoetin-alfa-polysorbate-80.html

Clinical studies have shown Darbepoetin Alfa (Polysorbate 80) to increase the risk of serious side effects (eg, blood clots, stroke, heart attack, heart failure) and death in some cases. It has also been shown to shorten overall survival and/or increase the risk of tumor growth or recurrence in patients with certain types of cancer. Talk with your doctor about the risks and benefits of using Darbepoetin Alfa (Polysorbate 80) . Do not use more than the recommended dose without checking with your doctor.

http://www.associatedcontent.com/article/907819/polysorbate_80_in_vaccines_a_potentially.html?cat=70

Polysorbate 80 in Vaccines - A Potentially Toxic Vaccine Stabilizer

Polysorbate 80 in vaccines has become a controversial topic. According to the MSDS sheet at Science lab.com, section 11: Toxicological Information, it was tested for inhalation and ingestion and was shown to be slightly hazardous on skin contact, ingestion and inhalation. however these are minor compared to other potential side effects of it's use especially in an intravenous or immunologic setting.

In the same section of toxicological information it states that it may cause reproductive effects, it may cause cancer, and may be a mutagenic, (change the genetics), in animals but this is followed up with the statement, no human data found. Well, unless they use people as lab rats, they won't find this data until it is used on humans to an extent to present this data.

According to PubMed.Gov a service of the U.S. Library of Medicine and the National Institute of Health, a report shows that neonatal rats were injected with small doses of polysorbate 80 and the results were major effects on the reproductive organs of the rats, resulting in infertility. (see the PubMed link below). Considering this is a component of the Gardasil HPV vaccine, (not to mention other vaccines), and they are recommending this to girls at prepubescent ages, there should be some concern to any parent that this could possibly lead to infertility in your child.

The Blood Brain Barrier: information

http://faculty.washington.edu/chudler/bbb.html

Functions of the BBB

The BBB has several important functions:
Protects the brain from "foreign substances" in the blood that may injure the brain.
Protects the brain from hormones and neurotransmitters in the rest of the body.
Maintains a constant environment for the brain.

The BBB can be broken down by:
Hypertension (high blood pressure): high blood pressure opens the BBB.
Development: the BBB is not fully formed at birth.
Hyperosmolitity: a high concentration of a substance in the blood can open the BBB.
Microwaves: exposure to microwaves can open the BBB.
Radiation: exposure to radiation can open the BBB.
Infection: exposure to infectious agents can open the BBB.
Trauma, Ischemia, Inflammation, Pressure: injury to the brain can open the BBB.

http://en.wikipedia.org/wiki/Blood-brain_barrier

The blood-brain barrier (BBB) is a separation of circulating blood and cerebrospinal fluid (CSF) maintained by the choroid plexus in the central nervous system (CNS). Endothelial cells restrict the diffusion of microscopic objects (e.g. bacteria) and large or hydrophilic molecules into the CSF, while allowing the diffusion of small hydrophobic molecules (O2, hormones, CO2). Cells of the barrier actively transport metabolic products such as glucose across the barrier with specific proteins.

This "barrier" results from the selectivity of the tight junctions between endothelial cells in CNS vessels that restricts the passage of solutes. At the interface between blood and brain, endothelial cells and associated astrocytes are stitched together by these tight junctions, which are composed of smaller subunits, frequently dimers, that are transmembrane proteins such as occludin, claudins, junctional adhesion molecule (JAM), ESAM and others. Each of these transmembrane proteins is anchored into the endothelial cells by another protein complex that includes zo-1 and associated proteins.The blood-brain barrier is composed of high density cells restricting passage of substances from the bloodstream much more than endothelial cells in capillaries elsewhere in the body. Astrocyte cell projections called astrocytic feet (also known as "glia limitans") surround the endothelial cells of the BBB, providing biochemical support to those cells. The BBB is distinct from the similar blood-cerebrospinal fluid barrier, a function of the choroidal cells of the choroid plexus, and from the blood-retinal barrier, which can be considered a part of the whole.[1]

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author's translation: the BBB keeps bad stuff out of the brain. Polysorbate 80 or "tween 80" in crossing the blood brain barrier, serves as a mode of transport for both positive chemicals to enter the brain (to aide in healing disease), as well as negative ones (such as the toxins in vaccinations). Shockingly enough, although polysorbate 80 is being used to aide other chemicals access beyond the BBB that would not normally be able to get through, absolutely no research has been done on whether polysorbate 80 in vaccinations also allows the chemicals of vaccinations to cross the BBB as well.

Studies on polysorbate 80 crossing the blood brain barrier (permeability):

Olivier JC, Fenart L, Indirect evidence that drug brain targeting using polysorbate 80-coated polybutylcyanoacrylate nanoparticles is related to toxicity. Pharm Res. 1999 Dec;16(12):1836-42.

Kreuter J, Ramge P, Direct evidence that polysorbate-80-coated poly(butylcyanoacrylate) nanoparticles deliver drugs to the CNS via specific mechanisms requiring prior binding of drug to the nanoparticles. Pharm Res. 2003 Mar;20(3):409-16.

Alyautdin RN, Petrov VE, Delivery of loperamide across the blood-brain barrier with polysorbate 80-coated polybutylcyanoacrylate nanoparticles. Pharm Res. 1997 Mar;14(3):325-8.

Gao K, Jiang X.Influence of particle size on transport of methotrexate across blood brain barrier by polysorbate 80-coated polybutylcyanoacrylate nanoparticles. Int J Pharm. 2006 Mar 9;310(1-2):213-9.

Wilson B, Samanta MK, Targeted delivery of tacrine into the brain with polysorbate 80-coated poly(n-butylcyanoacrylate) nanoparticles. Eur J Pharm Biopharm. 2008 Sep;70(1):75-84

Studies of polysorbate 80 and anaphylaxis:

Coors EA, Seybold H, Polysorbate 80 in medical products and nonimmunologic anaphylactoid reactions. Ann Allergy Asthma Immunol. 2005 Dec;95(6):593-9.

CONCLUSIONS: Polysorbate 80 is a ubiquitously used solubilizing agent that can cause severe nonimmunologic anaphylactoid reactions

Julia M.L. Brotherton, MD MPH, Mike S. Gold, MD, Anaphylaxis following quadrivalent human papillomavirus vaccination. CMAJ • September 9, 2008; 179 (6).

(this article *does* specify polysorbate 80 in the details as the causative agent of anaphylaxis)

Neal A. Halsey, MD The human papillomavirus vaccine and risk of anaphylaxis, CMAJ • September 9, 2008; 179 (6).

Marléne Isaksson and Lennart Jansson, Contact allergy to Tween 80 in an inhalation suspension, Contact Dermatitis Volume 47 Issue 5, Pages 312 - 313. Jan 2003

Price, Kursteen S.1; Hamilton, Robert G, Anaphylactoid reactions in two patients after omalizumab administration after successful long-term therapy, Allergy and Asthma Proceedings, Volume 28, Number 3, May-June 2007 , pp. 313-319

Excerpt: The in vitro and in vivo immunologic data support the conclusion that the adverse reactions experienced by two patients after omalizumab administration after more than a year of successful omalizumab therapy for asthma were likely anaphylactoid in nature. Polysorbate, an excipient in omalizumab, is known to cause similar reactivity to other medicines and is the most likely cause of these reactions.

http://www.sailhome.org/Concerns/Vaccines/MAC.html

Understanding the mechanism of detergents (polysorbate 80) in the human body:

Injected detergents trespass on an immune process that holds life and death control over cells... There are two major aspects to the body's immune system:
• The 'adaptive' immune system -- this includes various lymphocytes, such as B cell and T cells, and antibodies
• The 'innate' immune system -- this includes various leukocytes, such as phagocytes and natural killer cells, and the use of inflammation and the Complement system

The Complement system is a chain-reaction of biochemical events that help remove pathogens from the body. The Membrane Attack Complex (MAC) is part of the Compliment system -- and it is one of the immune system's ultimate weapons.

When an invading pathogen is identified, signals are sent causing MAC proteins to collect onto the pathogen's surface membrane. These proteins form ring structures which tunnel through the membrane. In other words, the MAC puts holes in the invading cell. These holes cause the cell to leak or explode by weakening its membrane. The cell dies quickly. Killing cells by punching holes into them makes the MAC extremely potent -- and also extremely destructive if it runs out of control. For this reason the MAC (and the Complement system in general) is tightly regulated by additional proteins. Detergents are used during the manufacture of flu vaccines. These chemicals are not completely purified out of the final product, so they enter the body at the time of injection.

Understanding the MAC helps explain the harm caused by injected detergents. Just like the MAC, detergents cause cells to leak or explode. But detergents are unregulated. Detergents act like the MAC out of control. The MAC targets foreign cells and avoids self-cells -- detergents hit cells at random. The MAC responds to signals which call off the attack -- detergents continue destroying cells. The MAC is integrated into the complex (and sensitive) signaling and feedback relationships between the Compliment system, the overall immune system, and other bodily functions in general -- detergents are foreign to these relationships and disrupt them.

The MAC operates as part of the Complement system. When activated, the Complement system triggers events such as:

• Increased arachidonic acid metabolism leading to acute inflammation and damage to nearby tissue
• Histamine release with its effects on allergic response, digestion, and neurotransmitter function
• Pyrogen release and the onset of fever

These are normal immune responses, but autoimmune disorders and other diseases arise when the responses become overactive. Examples of illnesses directly linked to severe MAC activity include:

Demyelination
Microvascular injury leading to blindness, kidney failure, and
neuropathy
Progressive muscle damage (
dysferlinopathy)
Beta-amyloid growth and Alzheimer's disease
Reperfusion injury (for instance following heart failure or stroke)
Myasthenia gravis
Brain swelling

These maladies illustrate the consequences of MAC overactivity -- and hence illustrate consequences to be expected from injected detergents. Detergents represent the worst kind of autoimmune dysfunction -- they randomly destroy *any* kind of host cell with no mechanism for regulating destructive activity.

As mentioned above, the MAC is regulated by certain proteins. One of these proteins is labeled CD59. It protects a host cell by binding to its surface and preventing MAC structures from assembling. Loss of CD59 protection leaves the cell vulnerable to damage and lysis (a ruptured membrane).

Here are some examples of conditions directly linked to loss of CD59:

Damaged neuromuscular transmission junctions
Rheumatoid arthritis
Kidney disease
Stroke
Fatal cerebral hemorrhage

These conditions indicate the kind of damage that can be done by injected detergents -- they have no regard for cells protected by CD59 or other regulating proteins. How fast do detergents leave the body? Do they just keep causing damage until they are somehow metabolized and eliminated? Carrying out studies to investigate the metabolic fate of detergents injected into humans would be unethical. Clues must be gathered from other kinds of studies in order to understand the rate at which injected detergents leave the body.

These studies indicate:
• Detergents are not easily metabolized and may remain in the system for lengthy periods
• Elimination is dependent on P450 enzymes and the liver -- which may also be damaged in the process
• Breakdown products include octylphenols which:
Are more persistent
Are endocrine disruptors
Depress immune function
Deplete glutathione
Induce cell death (apoptosis)
Pass through breast milk

According to GlaxoSmithKline a 0.5 ml dose of Fluarix may contain up to 0.085 mg of Triton X-100. It proved too difficult to find the specific gravity for Fluarix so calculating the level of Triton X-100 in parts per million (ppm) isn't easily possible. However, this gives the molecular weight of Triton X-100 as 250.376 g/mol. That's 200 thousand trillion molecules of Triton X-100 injected in a dose. That's an opportunity for trillions of self-cells to be injured or killed by the detergent, resulting in symptoms and diseases in line with what is described above. Exposure is likely to be similar with other vaccines containing detergents. If someone has a SNP (single nucleotide polymorphism) of -/+, +/-, or -/- for HGNC:1689 expression of CD59 they may be especially vulnerable to disruptions and damage caused by detergents. SNPs in other Complement system regulators would also make a person more vulnerable to these effects.

Normally, phagocytes consume injured cells, dead cells and their fragments after MAC activity. But phagocytosis will not necessarily take place after a self-cell is injured (not completely destroyed) by a detergent. Just postulating for a moment: What if the detergent weakens but does not destroy a cell. And what if this injured cell (perhaps it's a stem cell) becomes cancerous? Further, what if this cell is self-protected by CD59 or other control proteins? In that scenario the self-protected cancer cell could have favorable conditions to proliferate. That would offer a mechanism for explaining why detergents have been observed to promote tumors (as cited here). That idea is not so far-fetched when considering that cancer cells express CD59 and other MAC inhibitors. Sea anemones and malaria-transmitting mosquitoes also make use of MAC-like proteins to breach their victim's cells. It has been demonstrated that antibiotics work by disrupting cell membranes, too.

Detergents are used extensively in cell research precisely because of their ability to break cells open for further analysis.

Does it really make sense to knowingly inject these chemicals into pregnant women, babies, children, the immune compromised, the elderly --- or anyone else?

A note on Polysorbate 20- found in the Havrix vaccine (this is much weaker than polysorbate 80 it turns out)

http://www.associatedcontent.com/article/906301/toxic_chemicals_in_vaccines_polysorbate.html?cat=58

A Slightly Toxic Emmulsifier and Delivery Vehicle for Antigens

Polysorbate 20 is only Mildly toxic as compared to many of the vaccine ingredients. According to the MSDS sheet it is slightly hazardous in short term contact and may be an irritant to skin and eyes, as well as inhalation and ingestion. There is no available information pertaining to it's carcinogenic, Mutagenic, Teratogenic effects or developmental effects.Unlike polysorbate 80, it appears as though polysorbate 20 is relatively safe, at least with the limited research into it.

My biggest concern with ingredients that show mild irritation to skin and eyes is that these contact exposures differ widely from injected polysorbate 20 in vaccines exposure. Skin and eye contact are presumably washed off before or when irritation occurs, where as if this ingredient causes internal irritation not only may it go unnoticed, but you cannot wash it away. It will not be filtered out by the normal biological processes since it was not introduced into the body through normal exposure.Polysorbate 80 has been shown to cause infertility in mice, which will be covered in the polysorbate 80 article, but polysorbate 20 is a family chemical even though it is different. I certainly would feel better about this ingredient than I do most of the ingredients I have written on so far. The only vaccine I've found polysorbate 20 in is the Havrix Hepatitis A vaccine manufactured by GlaxoSmithKline

MSDS:

http://www.sciencelab.com/xMSDS-Polysorbate_20-9926640

Informed Choice:

http://www.informedchoice.info/cocktail.html

2-phenoxyethanol: Neurotoxin, CNS toxin

Also known as ethylene glycol monomethyl ether (EGME).

Note: While this substance was classified by the author as a neurotoxicant and CNS toxicant, it is also linked to reproductive effects in women and men and renal failure/kidney damage. This has not been causally proven by substantive evidence.The developmental effects and neurological damage to fetuses and children and adults is causally proven, however, in addition to the neurotoxic (CNS in particular) effects of the ingredient.

http://www.novaccine.com/vaccine-ingredients/results.asp?sc=17

Used as an insect repellent, a topical antiseptic, a solvent for cellulose acetate, dyes, inks and resins, in organic synthesis of plasticizers, in germicides. In vaccines, 2-Phenoxyethanol is an alternative to thiomersal.

Classed as "Very Toxic Material". May lead to kidney, liver, blood and central nervous system (CNS) disorders. Harmful or fatal if swallowed. Effects include behavioural disorders, drowsiness, vomiting, diarrhoea, visual disturbances, thirst, convulsions, cyanosis, and rapid heart rate, CNS stimulation, depression, cardiopulmonary effects, kidney disorders. May also lead to liver and blood disorders. Produces reproductive and developmental effects in experimental animals. May cause reproductive defects. Severe eye and skin irritant. Harmful if swallowed, inhaled or absorbed through the skin. One report describes generalised eczema occurring after vaccination where 2-phenoxyethanol was found to be the sensitising agent.

www.hazard.com/msds, which provides three search options:

Search by manufacturer, which you may not know
Search the database by keying in the chemical ingredient
Search the Chemical Toxicity Database.
Enter phenoxyethanol into the database, and five MSDSs are listed. Enter phenoxyethanol into the Chemical Toxicity Database, and seven entries are listed. A sample of information found on phenoxyethanol includes:
Hazards Identification

EMERGENCY OVERVIEW WARNING!

Harmful if swallowed
Causes skin irritation
May cause central nervous system depression
May cause kidney damage
May cause respiratory and digestive tract irritation
Target Organs: Kidneys, central nervous system

POTENTIAL HEALTH EFFECTS

Skin Contact: Severe irritation or burns
Eye Contact: Severe irritation or burns
Ingestion: May cause gastrointestinal irritation with nausea, vomiting and diarrhoea
May cause central nervous system depression
May cause headache, dizziness, drowsiness, and nausea
Advanced stages may cause collapse, unconsciousness
May cause coma and possible death due to respiratory failure
May cause kidney failure
May be harmful if swallowed
Lesions may appear in the brain, lungs, liver, meninges and heart

http://msds.chem.ox.ac.uk/PH/2-phenoxyethanol.html

Harmful if swallowed, inhaled or absorbed through the skin. May cause reproductive defects.

Studies confirming 2-phenoxyethanol/ethylene glycol monomethyl ether toxicity:

El-Zein R, Albrecht T, Reduction in telomere length in individuals exposed in utero to glycol ether, Arch Environ Occup Health. 2007 Fall;62(3):161-3.

Excerpt: Little is known about the mechanism by which ethylene glycol monomethyl ether (EGME) produces genotoxic effects in humans. The authors found that individuals exposed in utero to EGME showed characteristic dysmorphic features, unexplained mental retardation, and persistent cytogenetic damage.... Findings suggest that exposure to EGME in utero could result in terminal chromosome rearrangements and shortening of telomere length, leading to the observed dysmorphic features and idiopathic mental retardation.

El-Zein RA, Abdel-Rahman SZ, Exposure to ethylene glycol monomethyl ether: clinical and cytogenetic findings, Arch Environ Health. 2002 Jul-Aug;57(4):371-6.

Excerpt: Glycol ethers are known reproductive and developmental toxins in laboratory animals, but little is known about their genotoxic effects in humans. In the current article, the authors tested the hypothesis that human in utero exposure to ethylene glycol monomethyl ether (EGME) is associated with the development of specific congenital anomalies and elevated levels of chromosome aberrations...The study characterizes EGME as a human teratogen, as indicated by the prevalence of characteristic dysmorphic features and persistent cytogenetic damage in individuals exposed in utero to this chemical.

Cecilia Anselmi, Anna Ettorre, In vitro induction of apoptosis vs. necrosis by widely used preservatives: 2-phenoxyethanol, a mixture of isothiazolinones, imidazolidinyl urea and 1,2-pentanediol, Biochemical Pharmacology Volume 63, Issue 3, 1 February 2002, Pages 437-453

Excerpt: Preservatives are added to many final products, such as detergents, cosmetics, pharmaceuticals and vaccines. We conducted an in vitro investigation of the apoptosis- and necrosis-inducing potential of brief applications (10 min) of four common preservatives: ethylene glycol monophenyl ether, 2-phenoxyethanol (EGPE), imidazolidinyl urea (IMU), a mixture of 5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one (CMI/MI), and 1,2-pentanediol, a "preservative-non-preservative" best known as pentylene glycol. Externalization of PS, a hallmark of apoptosis, occurred early in HL60 treated with low concentrations of CMI/MI and EGPE and was concomitant with the subdiploid peak in HL60 treated with PG. However, it did not occur in HL60 treated with IMU. In conclusion, at appropriate concentrations, each of the four preservatives modulates the apoptotic machinery by a caspase-dependent mechanism. Thus, apoptosis could be a good parameter to evaluate the cytoxicity of these chemical compounds.

Ulrich Mußhoff, Michael Madeja, Effects of 2-phenoxyethanol on N-methyl-d-aspartate (NMDA) receptor-mediated ion currents, Analytics of Toxicology, Volume 73, Number 1 / March, 1999, pages 55-59

Excerpt: Most of the 17 glycol ethers exerted no effects on the glutamate subreceptors activated by kainate and N-methyl-d-aspartate (NMDA), whereas 2-phenoxyethanol (ethylene glycol monophenyl ether) caused a considerable reduction of NMDA-induced membrane currents in a reversible and concentration-dependent manner. The results indicate a neurotoxic potential for 2-phenoxyethanol.

Johanson G., Toxicity review of ethylene glycol monomethyl ether and its acetate ester, Crit Rev Toxicol. 2000 May;30(3):307-45.

Starek A, Szabla J. [Ethylene glycol alkyl ethers--the substances noxious to health], Med Pr. 2008;59(2):179-85.

Excerpt: Ethylene glycol alkyl ethers (EGAE), 2-methoxyethanol, 2-ethoxyethanol, 2-isopropoxyethanol, and 2-butoxyethanol, are widely used in a variety of industrial and household products. They are found in a number of paints, varnishes, engine fuels, hydraulic fluids, and also in many household products, including floor polishes and glass, leather, and upholstery cleaners. Human and animal studies have shown that EGAE can cause adverse reproductive, developmental, and hematological effects. The oxidation of these chemicals to appropriate aldehydes and alkoxyacetic acids is responsible for their toxic effects. The central nervous system, blood and blood-forming organs, and reproduction are the targets in acute and chronic intoxications with EGAE. Data on exposure, metabolism, biomonitoring, and toxic effects ofEGAE, especially those on hematological disorders in human and laboratory animals are presented in this paper.

Holladay SD, Comment CE, Fetal hematopoietic alterations after maternal exposure to ethylene glycol monomethyl ether: prolymphoid cell targeting, Toxicol Appl Pharmacol. 1994 Nov;129(1):53-60.

Excerpt: Ethylene glycol monomethyl ether (EGME), which is extensively used in the chemical industries, has been associated with hematologic disorders in both humans and experimental animals. EGME is metabolized to the active compound methoxy-acetic acid (MAA), which readily crosses the placenta and impairs fetal development. However, little is known about the effect of maternal EGME exposure on the development of fetal immunity. In the present report, in utero treatment with EGME was found to alter expression of murine thymocyte and liver fetal cell-surface markers. These data suggest that EGME, in addition to producing thymic hypocellularity, may inhibit thymocyte maturation. EGME also reduced the percentage of CD45+ leukocytic cells present in fetal liver, an alteration that appeared to be largely manifested by decreased numbers of CD45R+ and CD44dim prolymphoid cells. In vitro MAA exposure of fetal liver cells enriched for lymphoid precursors resulted in significant inhibition of proliferation. Reconstitution of irradiated hosts with gd 18 fetal liver cells from vehicle and EGME-exposed syngeneic donors demonstrated impaired ability of the EGME-treated fetal liver to repopulate the host spleen with B or T lymphocytes. These data suggest that EGME-induced immunosuppression may result from targeting of multiple hematopoietic compartments. Further, the present data indicate that fetal liver prolymphocytes may represent sensitive targets of EGME exposure.

G. Schmuk, W. Steffens, 2-Phenoxyethanol: a neurotoxicant?, Archives of Toxicology, Volume 74, Numbers 4-5 / July, 2000, pages 281-283

Bagchi G, Waxman DJ., Toxicity of ethylene glycol monomethyl ether: impact on testicular gene expression., Int J Androl. 2008 Apr;31(2):269-74.

Wang W, Chapin RE., Differential gene expression detected by suppression subtractive hybridization in the ethylene glycol monomethyl ether-induced testicular lesion., Toxicol Sci. 2000 Jul;56(1):165-74.

Browning RG, Curry SC. Clinical toxicology of ethylene glycol monoalkyl ethers, Hum Exp Toxicol. 1994 May;13(5):325-35.

Chemical Descriptions:United States National Library of Medicine: PubChem

>http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=103372

http://www.associatedcontent.com/article/887293/2phenoxyethanol_a_toxic_vaccine_antibacterial.html?cat=5

http://www.inspiredliving.com/organic/a~chemicaldetection.htm

http://journals.lww.com/joem/Abstract/1990/01000/Occupational_Phenoxyethanol_Neurotoxicity__A.12.aspx