Did NIAID's Anthony Fauci commit fraud or did US News & World Report misquote Dr. Fauci?

Teresa Binstock
Researcher in Developmental & Behavioral Neuroanatomy
August 29, 2009


A recent column in U.S. News & World Report described thimerosal with a statement contrary to fact. "...Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases,... said there's no evidence that Thimerosal poses any health threat..." (1)

Questions: Did Anthony Fauci, M.D., commit fraud or was he misquoted? Is there evidence that thimerosal injections injure some individuals?  If he was misquoted by U.S. News & World Report, will he ask for a correction?  Will the magazine print a correction? Furthermore, if he deliberately issued a fraudulent statement regarding thimerosal, ought his medical license be suspended? Ought his role as director of NIAID be terminated?

Needless to say, a crucial concern is, Are there data which indicate that thimerosal injections can be harmful? According to CDC and peer-reviewed studies, the answer is Yes. Thus, Dr. Fauci erred. Here is an incomplete sampling of findings which document thimerosal's adverse effects.

A. In 1999, CDC investigators led by Thomas Verstraeten reported (in house) that thimerosal injections were associated with autism, PDD, tics, speech disorders, and sleep problems. Subsequently, these discomforting findings were made to disappear by means of deliberately diluting data. Furthermore, thimerosal's adverse effects were discussed at an in-house conference attended by CDC personnel and their colleagues in the pharmaceutical industry. The CDC group's chicanery is reviewed in Evidence of Harm (2), and highlights of the CDC/pharma discussion of the findings can be found online (3-4).

B. That some individuals are sensitive to thimerosal has long been known (5). Compounding thimerosal's potential for adverse effects are the facts that (i) thimerosal inhibits a glutatione-related enzyme important for detoxification (6), and (ii) thimerosal is genotoxic (7). 

C. Although CDC loyalist Thomas Pichichero asserted that thimerosal deliberately injected into infants persists at a "safe" level (8), Waly et al found that thimerosal at levels below those described by Pichichero et al (8) was sufficient for inhibiting methionine synthase, an enzyme crucial in development (9). Needless to say, Pichichero et al keep trying to prove that thimerosal injections are non-injurious (eg, 10-11), even as another study found that thimerosal injections are particularly effective in causing mercury to enter the brain (12).

D. The U.S. Department of Health & Human Services conceded a case wherein a cocktail of vaccinations appear to have exacerbated young Hannah Poling's mitochrondrial dysfunction sufficiently so as to cause her to develop traits consistent with autism (13). That thimerosal can adversely affect mitochondria is supported by a growing number of studies (eg, 14-19).

E. In a recently published study, boys who received thimerosal injections were 9 times more likely to have received special education services than were boys who were not injected with thimerosal (20).

Preliminary conclusion:  Peer-reviewed studies indicate that Dr. Anthony Fauci, NIAID director, made a statement contrary to fact when he said "...there's no evidence that Thimerosal poses any health threat..." (1)  Is Dr. Fauci ignorant of the studies cited herein, studies which decribe thimerosal's adverse effects? Was he misquoted? 

Or is there an underlying dynamic? The CDC's 1999 thimerosal findings described associations with autism, attention, deficit, PDD, tics, speech disorders, and sleep problems (2-3). Nonetheless, in August of 2009, news media offer a chorus of recommendations for thimerosal injections via most flu and swine-flu vaccinations. Yet, Dr. Fauci and others err or stretch truth via assertions that thimerosal injections do no harm.

Consider the patented, profitable medications used for treating autism, ADHD, Tourette's, and sleep disorders.  Calculate the gross revenues generated by sales of those medications. Is it possible that a major purpose (albeit unstated) of thimerosal injections via flu (influenza) and H1N1 vaccinations is to augment thimerosal-induced pathologies associated with sales of various pharmaceuticals? 

Furthermore, consider H1N1 vaccine adjuvants, specifically squalene, which has been shown to have had a significant role in causing Gulf War Syndrome and associated rheumatic diseases. Squalene molecules occur naturally in the human body, but when squalene is injected, the person's immune system is hyperstimulated, and endogenous tissues in which squalene naturally occurs can become targets of the person's own immune reaction, thereby increasing the likelihood of generating an autoimmune pathology (eg, 21-24).

With heavy heart, I have come to the conclusion that modern medicine's profitability is dominated by the concept "Principles and Practice of Iatrogenic Medicine". Deliberately injecting thimerosal and squalene will increase the need for and sales of a wide range of pharmaceutical medications.


1. Pregnant Women, New Parents Urged to Get Swine Flu Vaccine

excerpt: "Asked if there will be swine flu vaccines available without the controversial preservative Thimerosal, Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said there would be. He said there's no evidence that Thimerosal poses any health threat, but because some people are concerned about it, a form of the vaccine without it will be available, the news service said."

2. Evidence of Harm

3. The CDC's Simpsonwood meeting...

4. As of today (Aug 29 09), the following google search is instructive:
Verstraeten cdc thimerosal 1999 Simpsonwood

5. Homozygous gene deletions of the glutathione S-transferases M1 and T1 are associated with thimerosal sensitization.
Westphal GA et al.
Int Arch Occup Environ Health. 2000 Aug;73(6):384-8.

OBJECTIVE: Thimerosal is an important preservative in vaccines and ophthalmologic preparations. The substance is known to be a type IV sensitizing agent. High sensitization rates were observed in contact-allergic patients and in health care workers who had been exposed to thimerosal-preserved vaccines. There is evidence for the involvement of the glutathione system in the metabolism of thimerosal or its decomposition products (organomercury alkyl compounds). Thus detoxification by polymorphically expressed glutathione S-transferases such as GSTT1 and GSTM1 might have a protective effect against sensitization by these substances. METHODS: To address this question, a case control study was conducted, including 91 Central European individuals with a positive patch-test reaction to thimerosal. This population was compared with 169 healthy controls and additionally with 114 individuals affected by an allergy against para-substituted aryl compounds. The latter population was included in order to test whether possible associations were due to substance-specific effects, or were a general feature connected with type IV immunological diseases. Homozygous deletions of GSTT1 and GSTM1 were determined by polymerase chain reaction. RESULTS: Glutathione S-transferase M1 deficiency was significantly more frequent among patients sensitized to thimerosal (65.9%, P = 0.013) compared with the healthy control group (49.1%) and the "para-compound" group (48%, P = 0.034). Glutathione S-transferase T1 deficiency in the thimerosal/mercury group (19.8%) was barely elevated versus healthy controls (16.0%) and the "para-compound" group (14.0%). The combined deletion (GSTT1-/GSTM1-) was markedly more frequent among thimerosal-sensitized patients than in healthy controls (17.6% vs. 6.5%, P = 0.0093) and in the "para-compound" group (17.6% vs. 6.1%, P =0.014), revealing a synergistic effect of these enzyme deficiencies (healthy controls vs. thimerosal GSTM1 negative individuals, OR = 2.0 [CI = 1.2-3.4], GSTT1-, OR = 1.2 [CI = 0.70-2.1], GSTM1/T1-, OR = 3.1 [CI = 1.4-6.5]). CONCLUSIONS: Since the glutathione-dependent system was repeatedly shown to be involved in the metabolism of thimerosal decomposition products, the observed association may be of functional relevance.

6. Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal.
Müller M et al.
Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81.

We have investigated the interaction of thimerosal, a widely used antiseptic and preservative, with the human erythrocytic GST T1 (glutathione-S-transferase T1). This detoxifying enzyme is expressed in the erythrocytes of solely the human species and it displays a genetic polymorphism. Due to this polymorphism about 25% of the individuals of the caucasian population lack this activity ("non-conjugators"), while 75% show it ("conjugators") (Hallier, E., et al., 1993). Using our newly developed HPLC-fluorescence detection assay (Müller, M., et al., 2001) we have profiled the kinetics of enzyme inhibition in erythrocyte lysates of two individuals previously identified as "normal conjugator" (medium enzyme activity) and "super-conjugator" (very high activity). For the normal conjugator we have determined a 2.77 mM thimerosal concentration to inhibit 50% of the GST T1 activity. In the case of the super-conjugator a 2.3 mM thimerosal concentration causes a 50% inhibition of the enzyme activity. For both phenotypes a 14.8 mM thimerosal concentration results in residual enzyme activities equal to those typically detected in non-conjugator lysates. Thus, sufficiently high doses of thimerosal may be able to change the phenotypic status of an individual--at least in vitro--by inhibition of the GST T1 enzyme.

7. Thimerosal induces micronuclei in the cytochalasin B block micronucleus test with human lymphocytes.
Westphal GA et al. 
Arch Toxicol. 2003 Jan;77(1):50-5.

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.

8. Mercury concentrations and metabolism in infants receiving vaccines containing thiomersal: a descriptive study.
Pichichero ME et al. 
Lancet. 2002 Nov 30;360(9347):1737-41.

BACKGROUND: Thiomersal is a preservative containing small amounts of ethylmercury that is used in routine vaccines for infants and children. The effect of vaccines containing thiomersal on concentrations of mercury in infants' blood has not been extensively assessed, and the metabolism of ethylmercury in infants is unknown. We aimed to measure concentrations of mercury in blood, urine, and stools of infants who received such vaccines. METHODS: 40 full-term infants aged 6 months and younger were given vaccines that contained thiomersal (diptheria-tetanus-acellular pertussis vaccine, hepatitis B vaccine, and in some children Haemophilus influenzae type b vaccine). 21 control infants received thiomersal-free vaccines. We obtained samples of blood, urine, and stools 3-28 days after vaccination. Total mercury (organic and inorganic) in the samples was measured by cold vapour atomic absorption. FINDINGS: Mean mercury doses in infants exposed to thiomersal were 45.6 microg (range 37.5-62.5) for 2-month-olds and 111.3 microg (range 87.5-175.0) for 6-month-olds. Blood mercury in thiomersal-exposed 2-month-olds ranged from less than 3.75 to 20.55 nmol/L (parts per billion); in 6-month-olds all values were lower than 7.50 nmol/L. Only one of 15 blood samples from controls contained quantifiable mercury. Concentrations of mercury were low in urine after vaccination but were high in stools of thiomersal-exposed 2-month-olds (mean 82 ng/g dry weight) and in 6-month-olds (mean 58 ng/g dry weight). Estimated blood half-life of ethylmercury was 7 days (95% CI 4-10 days). INTERPRETATION: Administration of vaccines containing thiomersal does not seem to raise blood concentrations of mercury above safe values in infants. Ethylmercury seems to be eliminated from blood rapidly via the stools after parenteral administration of thiomersal in vaccines.

9. Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal.
Waly M et al. 
Mol Psychiatry. 2004 Apr;9(4):358-70.

Methylation events play a critical role in the ability of growth factors to promote normal development. Neurodevelopmental toxins, such as ethanol and heavy metals, interrupt growth factor signaling, raising the possibility that they might exert adverse effects on methylation. We found that insulin-like growth factor-1 (IGF-1)- and dopamine-stimulated methionine synthase (MS) activity and folate-dependent methylation of phospholipids in SH-SY5Y human neuroblastoma cells, via a PI3-kinase- and MAP-kinase-dependent mechanism. The stimulation of this pathway increased DNA methylation, while its inhibition increased methylation-sensitive gene expression. Ethanol potently interfered with IGF-1 activation of MS and blocked its effect on DNA methylation, whereas it did not inhibit the effects of dopamine. Metal ions potently affected IGF-1 and dopamine-stimulated MS activity, as well as folate-dependent phospholipid methylation: Cu(2+) promoted enzyme activity and methylation, while Cu(+), Pb(2+), Hg(2+) and Al(3+) were inhibitory. The ethylmercury-containing preservative thimerosal inhibited both IGF-1- and dopamine-stimulated methylation with an IC(50) of 1 nM and eliminated MS activity. Our findings outline a novel growth factor signaling pathway that regulates MS activity and thereby modulates methylation reactions, including DNA methylation. The potent inhibition of this pathway by ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target of neurodevelopmental toxins.

10. Mercury levels in newborns and infants after receipt of thimerosal-containing vaccines.
Pichichero ME et al. 
Pediatrics. 2008 Feb;121(2):e208-14.

11. Mercury Levels in Premature and Low Birth Weight Newborn Infants after Receipt of Thimerosal-Containing Vaccines.
Pichichero et al. 
J Pediatr. 2009 Jun 25. [Epub ahead of print]

12. Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal.
Burbacher TM et al. 
Environ Health Perspect. 2005 Aug;113(8):1015-21.
{free online}

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 U.S. Environmental Protection Agency guidelines for methylmercury exposure, depending on the exact vaccinations, schedule, and size of the infant. In this study we compared the systemic disposition and brain distribution of total and inorganic mercury in infant monkeys after thimerosal exposure with those exposed to MeHg. Monkeys were exposed to MeHg (via oral gavage) or vaccines containing thimerosal (via intramuscular injection) at birth and 1, 2, and 3 weeks of age. Total blood 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 after thimerosal exposure was 2.1 and 8.6 days, respectively, which are significantly shorter than the elimination half-life of Hg after MeHg exposure at 21.5 days. Brain concentrations of total Hg were significantly lower by approximately 3-fold for the thimerosal-exposed monkeys when compared with the MeHg infants, whereas the average brain-to-blood concentration ratio was slightly higher for the thimerosal-exposed monkeys (3.5 +/- 0.5 vs. 2.5 +/- 0.3). A higher percentage of the total Hg in the brain was in the form of inorganic Hg for the thimerosal-exposed monkeys (34% vs. 7%). The results indicate 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.

13. Hannah Poling, see also scientific articles and news essays by her father, Jon Poling, M.D., Ph.D.

14. Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism.
James SJ et al. 
FASEB J. 2009 Aug;23(8):2374-83.

Research into the metabolic phenotype of autism has been relatively unexplored despite the fact that metabolic abnormalities have been implicated in the pathophysiology of several other neurobehavioral disorders. Plasma biomarkers of oxidative stress have been reported in autistic children; however, intracellular redox status has not yet been evaluated. Lymphoblastoid cells (LCLs) derived from autistic children and unaffected controls were used to assess relative concentrations of reduced glutathione (GSH) and oxidized disulfide glutathione (GSSG) in cell extracts and isolated mitochondria as a measure of intracellular redox capacity. The results indicated that the GSH/GSSG redox ratio was decreased and percentage oxidized glutathione increased in both cytosol and mitochondria in the autism LCLs. Exposure to oxidative stress via the sulfhydryl reagent thimerosal resulted in a greater decrease in the GSH/GSSG ratio and increase in free radical generation in autism compared to control cells. Acute exposure to physiological levels of nitric oxide decreased mitochondrial membrane potential to a greater extent in the autism LCLs, although GSH/GSSG and ATP concentrations were similarly decreased in both cell lines. These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions.

15. Effects of thimerosal on NGF signal transduction and cell death in neuroblastoma cells.
Parran DK et al.  Toxicol Sci. 2005 Jul;86(1):132-40.
{free online}

Signaling through neurotrophic receptors is necessary for differentiation and survival of the developing nervous system. The present study examined the effects of the organic mercury compound thimerosal on nerve growth factor signal transduction and cell death in a human neuroblastoma cell line (SH-SY5Y cells)...  With and without NGF, thimerosal caused elevated levels of fragmented DNA appearing at 0.01 microM (apoptosis) to decrease at concentrations >1 microM (necrosis). These data demonstrate that thimerosal could alter NGF-induced signaling in neurotrophin-treated cells at concentrations lower than those responsible for cell death.

16. Thimerosal induces DNA breaks, caspase-3 activation, membrane damage, and cell death in cultured human neurons and fibroblasts.
Baskin DS, Ngo H, Didenko VV.  Toxicol Sci. 2003 Aug;74(2):361-8.
{free online}

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... 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.

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

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.

18. 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}

The major source of thimerosal (ethyl mercury thiosalicylate) exposure is childhood vaccines. It is believed that the children are exposed to significant accumulative dosage of thimerosal during the first 2 years of life via immunization. Because of health-related concerns for exposure to mercury, we examined the effects of thimerosal on the biochemical and molecular steps of mitochondrial pathway of apoptosis in Jurkat T cells. Thimerosal and not thiosalcylic acid (non-mercury component of thimerosal), in a concentration-dependent manner, induced apoptosis in T cells as determined by TUNEL and propidium iodide assays, suggesting a role of mercury in T cell apoptosis. Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. Furthermore, thimerosal enhanced intracellular reactive oxygen species and reduced intracellular glutathione (GSH). Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. These data suggest that thimerosal induces apoptosis in T cells via mitochondrial pathway by inducing oxidative stress and depletion of GSH.

19. 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.

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.

20. Hepatitis B triple series vaccine and developmental disability in US children aged 1-9 years
Carolyn Gallagher ; Melody Goodman
Stony Brook University Medical Center
Toxicol Environ Chem 2008 90(5):997-1008.
{free online}

This study investigated the association between vaccination with the Hepatitis B triple series vaccine prior to 2000 and developmental disability in children aged 1-9 years (n = 1824), proxied by parental report that their child receives early intervention or special education services (EIS). National Health and Nutrition Examination Survey 1999-2000 data were analyzed and adjusted for survey design by Taylor Linearization using SAS version 9.1 software, with SAS callable SUDAAN version 9.0.1. The odds of receiving EIS were approximately nine times as great for vaccinated boys (n = 46) as for unvaccinated boys (n = 7), after adjustment for confounders. This study found statistically significant evidence to suggest that boys in United States who were vaccinated with the triple series Hepatitis B vaccine, during the time period in which vaccines were manufactured with thimerosal, were more susceptible to developmental disability than were unvaccinated boys.

21. Vaccine A: The Covert Government Experiment That's Killing Our Soldiers--And Why GI's Are Only The First Victims
Gary Matsumoto, 2004.

22. Squalene & Gulf War illnesses (GWI):

23.  Part 1: H1N1... vaccine and human experimentation

24. Part II: Squalene laced H1N1 vaccination