2. The Controversy of Autism
The incidence of autism has steadily increased
from1/10,000 during the 1970’s to1/150 as of
2008.
This enormous increase in the diagnosis of autism
has sparked obvious questions about causality.
Possible explanations include the changing
diagnostic criteria for autism (broadening of the
autism spectrum), the ability to diagnose the
disorder at an earlier age (and therefore, the
ability to reassess those who did not receive the
autism diagnosis as a child), and environmental
contributions (e.g. from childhood vaccines).
3. Vaccines and Autism
At the same time that the incidence of autism was growing, the
number of childhood vaccines containing Thimerosal (a
mercury containing preservative) was growing, increasing the
amount of ethylmercury to which infants were exposed
threefold.
A growing number of scientists and researchers believe that a
relationship between the increase in neurodevelopmental
disorders of autism, attention deficit hyperactive disorder, and
speech or language delay, and the increased use of thimerosal
in vaccines is plausible and deserves more scrutiny.
Toxins in vaccines can have devastating effects on children
who are genetically predisposed to retain environmental toxins
and metals.
Despite the growing amount of research regarding the links
between autism and vaccinations, the Food and Drug
Administration (FDA), the Institute of Medicine (IOM), the
Center for Disease Control and Prevention (CDC) and other
government officials continue to deny any causal link.
4. Dr. Bernadine Healy
Former director of the National Institutes of Health and
member of the Institute of Medicine.
In an 2008 interview with CBS news, Healy discussed
the possibility that certain children could be more
vulnerable to the adverse side effects of vaccines.
She disagrees with the IOM’s 2004 statement that
denied any causal link with vaccines and autism
because the susceptibility of certain children to
harmful side effects has not been adequately
researched.
She does not agree with the decision to abandon
research because of the government’s fear that what
might be found may deter caregivers from obtaining
vaccinations for their children.
6. Outline of Presentation
I.
II.
III.
IV.
V.
VI.
VII.
VIII.
Mercury: Properties and Effects on the Body
Thimerosal and Vaccines
A 2008 Summary of Evidence Supporting the
Links between Mercury Exposure and ASD
Development
Pivotal Past Research
Analyses of Recently Published Studies
A Look at the Hannah Poling 2008 Court Case
Arguments Against Causal Links
Conclusions
7. Quick Facts About Mercury
Heavy metal
Widespread and persistent in
the environment.
Coal-burning power plants
are the largest humancaused source of mercury
emissions to the air in the
United States.
Mercury in the air settles in
water or on land. Once
deposited, certain
microorganisms can change
mercury into methylmercury.
Methylmercury is a highly
toxic form that builds up in
fish, shellfish and animals
that eat fish (including
humans).
8. Mercury and the Body
Mercury adversely affects multiple systems of the
body including the nervous system, the immune
system, the gastrointestinal tract, the cardiovascular
system, as well as the kidneys and liver.
Mercury interferes with serotonin release and
transport, alters dopamine metabolism, elevates
glutamate, elevates norepinephrine and epinephrine,
and causes demyelination.
“The fetus is considered much more sensitive than the
adult. Prenatal exposures interfere with the growth
and migration of neurons and have the potential to
cause irreversible damage to the developing central
nervous system”. (Toxicological Effects of
Methylmercury, 2000).
9. Major Sources of Infant Exposure to
Mercury
Maternal seafood
consumption
(methylmercury).
Maternal mercury
amalgam dental
fillings.
Environmental
mercury release
Thim e ro s a l in
childhood vaccines.
10. Thimerosal
Thimerosal is a mercury containing preservative used in some
vaccines and other products since the 1930’s.
It is 49.6% mercury by weight and is metabolized/degraded
into e thy lm e rc ury .
Studies have suggested that ethylmercury is processed
differently in the body than methylmercury. Since ethylmercury is
processed more quickly and excreted more rapidly, skeptics infer
that ethylmercury is less likely to cause harm.
The Federal Government has established no safety threshold for
ethylmercury.
In 1999, it was discovered that the amount of Thimerosal in
childhood vaccines far exceeded FDA guidelines (Adams and
Romdalvik, 2007)
Federal health officials have conceded that the amount of
thimerosal in vaccines exceeded the EPA threshold of 0.1
micrograms per kilogram of bodyweight. In fact, the amount of
mercury in one dose of DTaP or Hepatitis B vaccines (25
micrograms each) exceeded this threshold many times over.
11. Government Reactions to
Thimerosal Concerns
July
1999, U.S. Department of Health and
Human Services agencies, The American
Academy of Pediatrics; and vaccine
manufacturers agreed that thimerosal should be
reduced or eliminated in vaccines as a
precautionary measure and to reduce exposure
to mercury from all sources.
According to the FDA, as of 2001, vaccines
manufactured for the U.S. market and routinely
recommended for children ≤ 6 years of age
have contained no thimerosal or only “trace”
amounts (≤ 1 microgram of mercury per dose
remaining from the manufacturing process),
with the exception of inactivated influenza
vaccine.
13. Vaccines Containing
Thimerosal
The Influenza (Flulaval), Influenza (Fluvirin), Japanese
Encephalitis, Meningitis (Menomune), and Tetanus and Diphtheria
vaccines continue to contain more than trace amounts of thimerosal
(CDC, 2008)
For some of these vaccines, thimerosal-free options are
available.
However, the FDA, the CDC, and the IOM continue to refute that
these vaccines cause harm or have influenced the incidence of
autism.
This may prevent parents from seeking alternative thimerosalfree vaccines.
In 2008, the US CDC recommended that all pregnant women
should receive an influenza vaccine (without regard to the trimester
of pregnancy) and that all infants should receive two doses of
influenza vaccine in the first year of life, with one influenza vaccine
administered on a yearly basis thereafter until 59 months. In
addition, the CDC recommends that children under nine who only
received one influenza vaccine initially should be given 2 doses of
influenza vaccine, at least two weeks apart.
14. Summary of evidences supporting that Hg exposure during fetal
and/or early childhood periods significantly contributes to the
development of ASDs (Geier et al., 2008)
Category
Support
↑ bo d y -burd e n
Hg
* ↑ Hg in ASD baby teeth.
* ↑ Hg-associated urinary porphyrins
in ASDs.
* ↑ or ↓ Hg in ASD hair samples.
* ↑ Hg in urine & fecal samples in
ASDs.
* ↑ Hg in the brain of ASDs.
* ↑ Hg in the blood of ASDs.
Bio c he m ic a l s us c e p tibility fa c to rs
* Abnormalities in transsulfuration
metabolites among ASDs associated
with ↑ Hg toxicity.
(e . g . ↓ re d uc e d g luta thio ne , ↑ o x id iz e d
g luta thio ne , ↓ c y s te ine , ↓ s ulp ha te ,
e tc . )
* ↓ Abnormalities in antioxidant
enzymes associated with ↑ Hg toxicity.
15. Summary of evidences supporting that Hg exposure during fetal
and/or early childhood periods significantly contributes to the
development of ASDs (Geier et al., 2008) Cont’d.
Category
Support
Ep id e m io lo g ic a l s tud ie s
* Thimerosal-containing vaccines &
biologics linked to ASDs.
* Environmental Hg linked to ASDs.
A a l m o d e ls
nim
* Low-dose Hg exposure (organic or
inorganic) is associated with
neuroinflammatory pathology found in
ASD brains.
* Low-dose thimerosal exposure linked
to ASD symptoms & brain pathology in a
susceptible
(i. e . ↑ a uto im m unity & ↓ a ntio x id a nt
c a p a c ity ) m o us e m o d e l.
M le /fe m a le ra tio
a
* Testosterone co-exposure ↑ Hg
poisoning, whereas estradiol coexposure ↓ Hg poisoning.
* More males than females diagnosed
with ASDs, and have ↑ testosterone & ↓
estradiol.
16. Summary of evidences supporting that Hg exposure during fetal
and/or early childhood periods significantly contributes to the
development of ASDs (Geier et al., 2008) Cont’d.
Category
Support
Ce llula r s us c e p tibility to Hg to x ic ity
* Cultured cells of ASDs have show
significant dose- and time-dependent
greater susceptibility to Hg-induced
cellular toxicity than unaffected
controls.
* Cultured neuronal cells exposed to
low-dose Hg have similar pathology as
ASD brains.
Sim ila rity o f A & Hg p o is o ning
SD
* Hg-associated oxidative stress
markers among ASDs
Te m p o ra l a s s o c ia tio n
* Symptoms of ASDs emerge within
the first several years of life, Hg
exposure
(i. e . fe ta l & e a rly infa nc y ) proceeds
development of ASD symptoms.
17. Pivotal Past Studies on Autism and
Toxic Metals
Holmes et al. (2003)
94 children with autism matched to
45 controls
Adams et al. (2008)
Found that their first baby haircuts
had mercury levels that were
statistically significantly less than
controls and levels of mercury were
correlated with the severity of autism.
Collected information about the
levels of Hg exposure (maternal fish
consumption, vaccines, maternal
mercury amalgam dental fillings)
The children with autism had higher
levels of exposure than controls. This
study suggests that children with
autism may not be able to eliminate
Hg and thus may accumulate it
instead.
Supported the Holmes study,
found that compared to children
with higher levels of Hg, children
with lower levels of Hg in their
hair were 2.5-fold significantly
more likely to be diagnosed with
ASDs.
These researchers stated that
the lower level of Hg in the baby
hair of children with ASDs
indicates an altered metabolism
of Hg, and may be due to a
decreased ability to excrete Hg.
18. Pivotal Past Studies on Autism and
Toxic Metals Cont’d.
Hornig M., Chian D., Lipkin WI., 2004
Researchers from Columbia University reported that an autoimmune
diathesis is described in ASD patients.
Major histocompatibility complex (MHC) genes regulate risk of Hginduced autoimmunity in mice.
Exposed mice of differing autoimmunity backgrounds to thimerosal
in doses/timing equivalent to the US pediatric immunization
schedule of the 1990s.
Observed behavioral and neuropathological side effects after postnatal thimerosal exposure in mice with autoimmune sensitivity but
not in mice strains without autoimmune sensitivity.
Symptoms observed in the treated autoimmune sensitive mice were
similar to ASD symptoms, including: growth delay; reduced
locomotion; exaggerated response to novelty; and, for the brain
structure, densely packed, altered glutamate receptors and
transporters.
19. Pivotal Studies on Autism and Toxic Metals
Cont’d.
Hormones and Mercury Toxicity
Autism disproportionately affects male children (male: female
ratio is about 5:1).
Research suggests that those most vulnerable to Hg toxicity
are characterized by high testosterone.
In animal models and in human Hg poisonings, males were
found to be significantly more susceptible to Hg toxicity
(including neurotoxicity) than females (Sager et al., 1984,
Clarkson et al., 1985 and Grandjean et al., 1998)
Additionally, in a series of tissue culture experiments with
neurons, testosterone was able to potentiate the neuronal
toxicity of Hg, whereas estradiol significantly lessened the
neuronal toxicity of Hg (Olivieri et al., 2002 and Haley, 2005)
20. “Mercury, Lead, Zinc in Baby Teeth of Children
with Autism Versus Controls” (Adams,
Romdalvick, 2007)
The purpose of this study was to further investigate the
mercury/lead body burden of children with autism versus
controls by evaluating the amount of mercury/lead in
their baby teeth. Baby teeth are formed in utero and
during the first few years of life, so they provide a
measure of cumulative exposure during critical periods
of development.
Previous studies have demonstrated that mercury can
be reliably measured in teeth (Eide et al., 1993;
Tvinnereim et al., 2000).
The participants were children with autism in the state of
Arizona (n=16) and controls (n=11).
21. “Mercury, Lead, Zinc in Baby Teeth of Children with Autism
Versus Controls” (Adams, Romdalvick, 2007) Cont’d
Found that the teeth of the children with autism had a 2.1-fold
higher mean level of mercury, and a 3.1-fold higher median level of
mercury.
The teeth of the children with autism had levels of lead that were
slightly higher than the controls, but the difference was not
statistically significant. The teeth of the children with autism had
very similar levels of zinc compared to the control children.
By utilizing a medical history questionnaire, it was found that the
autism group had similar levels of maternal seafood consumption,
number of maternal dental fillings present during pregnancy, and
number of maternal dental fillings placed during pregnancy
compared to the control group.
The children with autism had significantly higher levels of antibiotic
usage at ages 6–12 mo and at ages 0–6 mo. They also had
quantitatively higher levels of oral antibiotic usage at ages 12–24
mo and 24–36 mo (though not quite statistically significant).
22. “Mercury, Lead, Zinc in Baby Teeth of Children with Autism
Versus Controls” (Adams, Romdalvick, 2007) Cont’d
“The two- to threefold higher level of mercury in
the baby teeth of children with autism is
important because it strongly suggests that they
had a higher body burden of mercury during
several years of prenatal/infant development”
Since mercury is a potent neurodevelopmental
toxin that produces many of the symptoms
observed in autism (Bernard et al., 2001), this
higher body burden of mercury may have
exacerbated or produced the development of
autism in some of the children in this study.
23. “Oxidative stress in autism: elevated cerebellar 3nitrotyrosine levels” (Sajdel-Sulkowska et al.,
2008)
Harvard University researchers
This study compared the cerebellar levels of the
oxidative stress marker 3-nitrotyrosine (3-NT), Hg and
the antioxidant selenium levels between control and
ASD subjects
Mercury has been found to strongly associate with
oxidative stress (Mutter et al., 2005).
Antioxidant deficiency has been implicated in the
pathophysiology of autism (McGinnis, 2004).
Analyzed frozen cerebellum tissue samples
24. “Oxidative stress in autism: elevated cerebellar 3nitrotyrosine levels” (Sajdel-Sulkowska et al., 2008) Cont’d
They found an increase in 3-NT levels (a measure of
oxidative stress) in the autistic cerebellum, along with a
positive correlation between elevated cerebellar 3-NT
and high mercury levels.
This suggests that increased oxidative stress in brains of autistic
subjects may be related in part to the increased mercury. It is
possible that increased levels of Hg in the autistic brain may be
caused by defects in the detoxification mechanisms as
suggested by studies of Geier and Geier (2006).
Additionally, observed that levels of the antioxidant Se
were lower in autistic individuals compared to controls
(similar results were found in Audhya and McGinnis,
2004 study).
A function of Se is its ability to counteract the neurotoxicity of
25. “Biomarkers of environmental toxicity and susceptibility in
autism” (Geier et al., 2009)
Hypothesized that autism may be the result of a genetic
susceptibility to a decreased ability to excrete mercury
and/or a environmental exposure at key times of
development.
Purpose of the study was to evaluate potential
biomarkers for evidence of mercury susceptibility and
toxicity in the transsulfuration and porphyrin pathways in
a cohort of participants diagnosed with autism spectrum
disorders (ASDs).
Geier et al. conducted a similar study in 2008 and
found a significant abnormalities in the biochemical
markers in the transsulfuration pathway among
participants diagnosed with ASDs in comparison to
26. “Biomarkers of environmental toxicity and susceptibility in
autism” (Geier et al., 2009) Cont’d
28 autistic children between the ages 2-16 were recruited from the
Dallas/Fort Worth area.
The severity of the children’s autism was measured using the
Childhood Autism Rating Scale (CARS) and blood and urine
samples were collected and tested for transsulfuration metabolites
and urinary porphyrins.
Previously demonstrated that the transsulfuration pathway
products of glutathione (Ballatori, Clarkson 1985) and sulfate
(Ahearn et al., 2004) were related to mercury excretion
rates/mercury intoxification and that urinary porphyrins (Woods,
1996) can provide specific profiles that reflect mercury toxicity.
Concentrations of transsulfuration products and urinary
porphyrins were compared to neurotypical control children.
27. “Biomarkers of environmental toxicity and susceptibility in
autism” (Geier et al., 2009) Cont’d
Overall results showed that children with
ASDs had decreased transsulfuration
metabolites and increased urinary porphyrin
metabolites associated with mercury toxicity
and susceptibility.
There was a significant correlation in the
severity of autism (measured by CARS) and
urinary porphyrins associated with mercury
toxicity.
“…it is apparent that an increased mercury bodyburden and toxicity may contribute overall to the
28. “Proximity to point sources of environmental mercury
release as a predictor of autism prevalence” (Palmer,
Blanchard, Wood, 2009)
The objective of the study was to determine if
proximity of mercury pollution in 1998 related
to autism prevalence in 2002 in Texas.
Built on two past studies demonstrating an
association between environmental mercury
release and autism rates (Palmer et al., 2006,
Windham et al., 2006)
Autism count data retrieved from the Texas
Educational Agency and environmental
mercury release information retrieved from the
Environmental Protection Agency (EPA).
29. “Proximity to point sources of environmental mercury
release as a predictor of autism prevalence” (Palmer,
Blanchard, Wood, 2009) Cont’d.
Found that for every 1000 lbs of industrial mercury release, there
was a 2.6% increase in autism rates and a 3.7% increase
associated with power plant emissions.
For every 10 miles from industrial or power plant sources, there was
an associated decrease in autism incident risk (2.0% from
industrial, 1.7% from power plants).
Release in pounds from industrial sites were correlated with
accelerated autism risk.
Major limitation: Cannot verify exposure at the individual level
In agreement with past plant, animal, and human studies, this study
demonstrates that proximity to sources of environmental mercury
increases the mercury burden on the body.
Researchers advise that this study should be viewed as “hypothesis
generating”
30. The Hannah Poling Case
(2008)
In 2000, when Hannah was
19 months old, she received
five shots against nine
infectious diseases.
Two days later, she
developed a fever, became
hysterical and refused to
walk. Over the next seven
months she spiraled
downward, and in 2001 she
was given a diagnosis of
autism.
In addition, she was
diagnosed with a
mitochondrial disorder.
31. The Hannah Poling Case (2008)
Cont’d.
On March 6, 2008, government health officials conceded that
childhood vaccines worsened a rare, underlying disorder that
ultimately led to autism-like symptoms in Hannah, and that she
should be paid from a federal vaccine-injury fund.
First case in which the government has compensated a family for
vaccine-induced autism.
Two theories have been posed to describe what happened to
Hannah. The first is that she had an underlying mitochondrial
disorder that vaccinations aggravated. The second is that
vaccinations caused this disorder.
“The government chose to believe the first theory…we don’t
know that she had an underlying disorder” Terry Poling
''This decision gives people significant reason to be cautious
about vaccinating their children,'' John Gilmore, executive
director of the group Autism United.
32. Arguments Against the Correlation Between
Autism and Vaccinations
Argument
Response
Thim
erosal has been
rem
oved from
vaccines since 2001
but the rates of
autism continue to
rise.
As of 2008, the CDC lists several
vaccinations that still contain more than
trace amounts of Thimerosal. Moreover,
the introduction of influenza vaccines
has provided a full complement of
Thimerosal. When Thimerosal was
initially removed from vaccines, rates of
autism in California significantly
decreased. However, after the
introduction of the flu vaccine, numbers
began to rise again (Cave, 2008).
Moreover, environmental mercury
exposure may be linked to autism.
33. Arguments Against the Correlation Between
Autism and Vaccinations Cont’d.
Argument
M
any studies
have found no
link between
autism incidence
and vaccines.
Response
Four frequently-cited studies failed to find a link
(Andrews et al., 2004; Hviid et al., 2003; Madsen
et al., 2003; Stehr-Green et al., 2003). Three of
these studies were in countries with much lower
usage of Thimerosal in vaccines than in the
United States, and they had much lower rates of
autism in those countries. Additionally, many
studies that claim no link between vaccinations
and autism fall just short of statistical significance
(therefore, almost significant). W can’t discount
e
past and emerging studies that are finding a
causal link. These studies tell us that more
research is necessary to determine the real
effects of toxins in vaccines on children who are
genetically predisposed to retain heavy metals.
34. Conclusions
The autism epidemic is real and can not be explained by changing
diagnostic criteria or early diagnoses alone.
Emerging evidence supports the theory that some autism spectrum
disorders may result from a combination of genetic/biochemical
susceptibility, specifically a reduced ability to excrete Hg, and
exposure to Hg at critical developmental periods.
Government agencies maintain that there is no link between the
development of autism and the toxins in vaccines.
Despite the introduction of Thimerosal-free vaccines, the public may not
be swayed to pursue these options because of the government’s efforts
to minimize evidence that supports the causal link.
By recognizing that physiological functions are altered by mercury
intoxification through vaccines during critical periods of
development, more research can be conducted to determine the
exact causes of the autism epidemic.
35. References
Holmes AS, Blaxill MF, Haley BE (2003). Reduced levels of mercury in the first baby haircuts of autistic children.
I rna tio na l Jo urna l o f To x ic o lo g y 2 2 : 2 7 7 -8 5 .
nte
Toxicological Effects of Methylmercury (2008). Co m m itte e o n the To x ic o lo g ic a l Effe c ts o f M thy lm e rc ury , Bo a rd o n
e
Enviro nm e nta l Stud ie s a nd To x ic o lo g y , N tio na l Re s e a rc h Co unc il.
a
Cave SF (2008). The history of vaccinations in light of the autism epidemic. A rna te The ra p ie s in He a lth a nd
lte
M d ic ine , 14(6), 54-57.
e
Adams JB, Romdalvick J, Ramanujam YM, Legator MS (2007). Mercury, Lead, and Zinc in Baby Teeth of Children
with Autism Versus Controls. Jo urna l o f To x ic o lo g y a nd Enviro nm e nta l He a lth, 70(12), 1046-1051.
Palmer RF (2009). Proximity to point sources of environmental mercury release as a predictor of autism prevalence.
He a lth & p la c e , 15(1), 18-24.
Geier DA (2009). Biomarkers of environmental toxicity and susceptibility in autism. Jo urna l o f the ne uro lo g ic a l
s c ie nc e s , 280(1-2), 101-108.
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m
Jo urna l o f Bio c he m is try a nd Bio te c hno lo g y , 4(2), 73-84.
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36. References Cont’d
Clarkson TW, Nordberg GF, Sager PR. Reproductive and developmental toxicity of metals (1985). S c a nd J Wo rk
Enviro n He a lth, 11, 145-54.
Sager PR, Aschner M, Rodier PM (1984). Persistent, differential alterations in developing cerebellar cortex of male
and female mice after methylmercury exposure. Bra in Re s , 314, 1-11.
Haley BE (2005). Mercury toxicity: genetic susceptibility and synergistic effects. M d Ve rita s , 2 , 535(42),
e
122.
Olivieri G, Novakovic M, Savaskan E, Meier F, Baysang G, Brockhaus M, e t a l (2002). The effects of beta-estradiol on
SHSY5Y neuroblastoma cells during heavy metal induced oxidative stress, neurotoxicity and beta-amyloid
secretion. N uro s c ie nc e , 113, 849-55.
e
Adams JB, Romdalvik G, Levine KE, Hu LW (2008). Mercury in first cut baby hair of children with autism vs. typicallydeveloping children. Enviro nm e nta l To x ic o lo g y Che m is try , 90 : 739-53.
Geier DA (2008). A comprehensive review of mercury provoked autism. I ia n Jo urna l o f M d ic ine , 128, 383-411
nd
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Vaccine Excipient & Media Summary, Part 2. Retrieved April 22, 2009, from Center for Disease Control and
Prevention Web site: http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/appendices/B/excipient-table-2.pdf
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http://www.medicinenet.com/mercury_poisoning/page2.htm
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