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? Is he an iatrogenecist
who intentionally supports deliberately iatrogenic medicine?
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
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
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
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
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
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
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
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
10. Mercury levels in newborns and infants after receipt of
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.
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
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
Parran DK et al. Toxicol Sci. 2005 Jul;86(1):132-40.
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.
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
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.
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
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.
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
24. Part II: Squalene laced H1N1
Binstock by email
index of essays by TCeresa Binstock