Lesson 7D, Part 5 - Vaccines & Mercury
http://www.healing-arts.org/children/vaccines/vaccines-mercury.htm
At high exposure levels, mercury causes neurotoxicity in humans, especially in fetuses and small infants whose
brains are still developing.
The major toxicity of mercury is manifested in the central nervous system. Forty years ago, when women at
Minamata Bay, Japan, ate fish contaminated with methylmercury from pollutants, their children were exposed to
high levels in utero and were born with developmental and neurologic disorders.
Methylmercury poisoning also occurred in Iraq following consumption of seed grain that had been treated with a
fungicide containing methylmercury. In both the Japanese and Iraqi episodes, exposures to methylmercury were
high.
Two population-based studies are often cited as the basis for calculations on the neurotoxicity of mercury in utero.
In the first, a study from the Seychelles, infants were exposed to mercury in utero when their mothers ate a high
daily consumption of methylmercury-containing fish. The mothers had mean mercury levels in hair of 6.8 ppm.
No developmental defects were detected.
In the second, a study from the Faroe Islands, infants were born to mothers with mean hair levels of 4.3 ppm. In
contrast to the Seychelles mothers, these mothers were exposed to mercury through intermittent "bolus"
consumption of pilot whale meat. Lower scores on memory, attention, and language tests were associated with
methylmercury exposure in the children (see the Mercury Study Report to Congress, EPA, 1997).
[Return to "Quick-Index" of Mercury and Vaccines]
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Thimerosal and Neurotoxicity
The mercury compound, thimerosal, was used as a vaccine preservative since the 1930s, and was viewed as a
safe, reliable, and somewhat drab defender against bacterial and fungal contamination. Thimerosal was sometimes
added to vaccines during manufacturing to offset production-related contamination. It was thought to have its
greatest value in the field, where it acted as a fail-safe against imperfect aseptic handling, especially for multidose vaccines, in which the re-entry of needles increases the risk of bacterial contamination. Thimerosal's only
competitor, 2-phenoxyethanol, was less effective in suppressing potential contaminants like Pseudomonas
aeruginosa, E. coli, and Staph. Aureus.1 Thimerosal contains 49.6% mercury by weight.
Thimerosal is a water-soluble, cream-colored, crystalline powder. . In the human body, thimerosal is metabolized
to ethylmercury and thiosalicylate. Toxicological information on the chief metabolite of thimerosal, ethylmercury,
is extremely limited.
Total mercury levels before and after the administration of hepatitis B vaccine (which contains thimerosal) was
measured in 15 preterm and 5 term infants. Comparison of pre- and post-vaccination mercury levels showed a
significant increase in both preterm and term infants after vaccination. Additionally, post-vaccination mercury
levels were significantly higher in preterm infants as compared with term infants.2
During the recent controversy over the safety of thimerosal in vaccines, toxicologists have assumed that the
toxicity of ethylmercury is equivalent to the toxicity of methylmercury. The primary environmental exposure is
through consumption of predator fish. A 6-ounce can of tuna fish contains an average of 17 micrograms of
mercury. A pediatric dose of hepatitis B vaccine contains very little more mercury than that.3
Thimerosal surfaced as a safety issue in Europe in June, 1999, when the Agency for the Evaluation of Medicinal
Products (EMEA), completed an 18-month inquiry into the risks and benefits of using thimerosal in vaccines. The
EMEA concluded that: "Although there is no evidence of harm caused by the level of exposure from vaccines, it
would be prudent to promote the general use of vaccines without thimerosal."
The FDA's Center for Biologics Evaluation & Research (CBER) began by adding up the total amount of mercury
given to children through vaccines in the U.S. immunization schedule. Thimerosal was present in over 30 licensed
vaccines in the U.S. in concentrations of 0.003% to 0.01%. According to the agency's calculations, an infant six
months old, receiving all vaccine doses on schedule, would receive:
75 micrograms of mercury from three doses of DTP,
75 micrograms from three doses of Hib, and
37.5 micrograms from three doses of hepatitis B vaccine;
for a total of 187.5 micrograms of mercury.
Thimerosal is metabolized in humans to ethylmercury, but guidelines for safe mercury intake relate only to
methylmercury. The literature on ethylmercury toxicity was so scant that toxicologists did not know if
ethylmercury was more or less toxic than methylmercury. Left with no choice, CBER analysts assumed that the
toxicity of the ethyl compound was equivalent to the methyl compound.
Given this assumption, the mercury intake from vaccines in children six months old, 187.5 micrograms, was
compared to the suggested safe limits for methylmercury intake published by three federal agencies: EPA, FDA,
and the Agency for Toxic Substances and Disease Registry (ATSDR). Mercury intake through vaccination during
the first six months of life exceeded the limit set by the EPA.
However, the EPA's reference dose, or RfD, was truly cautious, based on a single episode of methylmercury
poisoning in Iraq in which 81 children were exposed to high levels of mercury in utero. The EPA calculated the
RfD by determining the dose that produced a 10% prevalence of adverse neurological effects in the affected
children, including late walking, late talking, and abnormal neurological scores. The agency then placed a 95%
confidence interval around this dose and divided the lower bound of the interval by an "uncertainty factor" of 10
to arrive at the RfD.
Nevertheless, the Iraqi finding strengthened the anti-mercury argument, since its proponents maintained that
mercury was most hazardous among children already susceptible for autism. Since most children are not
susceptible, mercury might be acceptable for the majority, but devastating for the small minority.
The Iraqi children sustained long-term daily prenatal exposures, while vaccinated children have intermittent
intramuscular doses later in life, as infants. No one knew how these exposure differences affected the potential
neurotoxicity of mercury, or if they would.
Only two single-antigen pediatric hepatitis B vaccines exist on the U.S. market - Engerix-B (SmithKline
Beecham) and Recombivax HB (Merck). Both contain thimerosal and 12.5 micrograms of mercury per 0.5 ml
dose. The American Academy of Pediatrics pressed CDC to agree to a delay of the hepatitis B vaccination series,
usually started at birth, for children born to hepatitis B surface antigen (HBsAg)-seronegative mothers. The
Academy argued that the delay would only be temporary, because both Merck and SmithKline Beecham had
promised that they could quickly shift manufacturing to thimerosal-free vaccine, perhaps in just a few months (the
FDA had already promised to review applications for thimerosal-free hepatitis B vaccine within 30 days).
The US Food and Drug Administration (FDA) is moving in the pharmacological direction of "single dose
presentations of vaccines without preservatives", said the FDA's Dr. William M. Egan at the Third Annual
Conference on Vaccine Research in Washington, DC, May 4, 2000.4
Dr. Egan, acting director of the Center for Biological Evaluation and Research's office of vaccines research and
review, centered his talk on thimerosal, a common preservative in vaccines, including childhood vaccines. The
American Academy of Pediatrics and the Public Health Service released a joint statement saying that the risks of
not vaccinating far outweighed the potential risk of thimerosal. But the statement - as Dr. Egan pointed out - also
recommended that thimerosal should be removed from vaccines as soon as possible.
As of May, 2000, it is possible to get the entire course of childhood vaccines without thimerosal, since some
manufacturers have developed thimerosal-free vaccines.
Mercury and other heavy metals have an adverse effect on the sulfate transport mechanism which helps reabsorb
sulfate at the level of the kidneys.5 This transporter provides a mechanism to prevent excess loss of sulfate. Two
heavy metals, chromium and mercury, are especially talented at preventing the transporter from doing its job:
mercury could stop the retention of sulfate almost completely.6
Heavy metals are nephrotoxic, with the glomerulus a primary site of damage in some cases. In order to separate
the direct effects of metal ions from those occurring secondary to systemic or post-glomerular toxicity, Templeton
and Chaitu studied the effects of divalent salts of Hg, Cd, Cu, Zn, Mn, Ni and Co on freshly isolated rat
glomeruli.7
The concentration of the metal ion causing a 50% reduction in the incorporation of [3H]leucine into protein over
16 hours varied from 30 microM with Cd to about 2 mM with Ni and Mn. The log of the concentration was
significantly correlated with the softness of the metal ion, indicating greater toxicity of ions such a Cd2+ and
Hg2+ that prefer sulphur as a ligand. Incorporation of [3H]sulphate into proteoglycans was affected in a
comparable manner to total protein synthesis. However, the softer metals caused a preferential decrease in the
production of more highly charged dermatan sulphate, indicative of an effect on mesangial cells.
Various writers have theorized that heavy metal exposure might have the most deleterious effects on the
differentiation of highly sulfated tissues like O2A cells, the precursors of type 2 astrocytes and for
oligodendrocytes, the myelinating cells of the central nervous system. This provides one potential explanation for
how heavy metals might contribute to autism.
A similar transporter in the gut facilitates the absorption of sulfate from the contents of the gut, and is so similar
structurally to the kidney and liver transporter that one would also expect mercury would pose similar problems
regarding the acquisition of sulfate from the diet. Because mercury could pose problems both in absorption and
retention of sulfate, it shouldn't be surprising that the symptoms of mercury poisoning are so similar to the
symptoms of autism.
Dr. Rosemary Waring's work in autism found high levels of sulfate in the urine despite low blood levels. Dr.
Waring also found evidence for a loss of sulfur detoxification ability. When the glomerular basement membrane
itself becomes undersulfated, the result is increasing loss of sulfate, associated with peptiduria and proteinuria common findings in autism.
If the body is wasting protein and amino acids, then it is also wasting its own metabolic source of sulfate. On the
cellular level, sulfated amino acids can compensate for the loss of sulfate transporter function if these amino acids
are available in adequate quantity for the cell to use. This assumes a lack of inherited problems in the cysteine to
sulfate pathway - errors that are more common in autism than in controls.
[Return to "Quick-Index" of Mercury and Vaccines]
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Is There a Link betwen Mercury Exposure and Autism?
Purported links between mercury and autism still remain speculative, although new research shows that
treatments for mercury toxicity are promising (see Dr. Amy Holmes article, The Chelation of Mercury in the
Treatment of Autism). Mercury does affect microtubules, which participate in neuronal function and in
synaptogenesis. The timing of infant and toddler thimerosal injections corresponds to major neuronal
development and synaptogenesis (the making of synapses) that occurs postnatally in the human. Synaptogenesis is
important with regard to eye-contact, smiling, early language, and other traits central to the diagnostic criteria for
autism.
Why are only some children affected and not others? Proponents of the mercury hypothesis argue that numerous
studies have documented a range of mercury responses, from not-affected to severely affected - in all species thus
far studied. This range of reactions derives from genetic predispositions and/or from altered detoxification
capabilities, which themselves involve liver function and glutathione.
Many factors can affect liver function and glutathione availability in infants and toddlers. For instance, a recent or
chronic-active infection can deplete glutathione. The factors which predispose towards mercury neurotoxicity and
their primary citations are reviewed in Bernard et al. Similarly, thalidomide and Pink Disease provide human
examples wherein only some individuals within exposed populations developed adverse effects.
[Return to "Quick-Index" of Mercury and Vaccines]
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Ethylmercury and the DPT Vaccine
Ethylmercury has been a component of the DPT vaccine. Some believe that this compound exacerbates any
tendencies of the DPT vaccine to contribute to epileptiform activity.
[Return to "Quick-Index" of Mercury and Vaccines]
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Testing for Mercury Toxicity
Tests thought to indicate a high potential for heavy metal poisoning (including mercury) include the following:
On the CBC - elevated MCH and MCV
Immune tests - low CD8 cells, elevated CD4/CD8 ratio
Low absolute number of NK cells
Serum IgE elevated above normal range
Elevated urinary d-glucaric acid
Elevated urinary 3-methylhistidine
Elevated serum ALT and/or AST
Low serum superoxide dismutase (SOD)8
Changes in fractionated urine porphyrins is also good test for heavy metal toxicity, but is not completely specific
for mercury.9 The specimen must be protected from light. The containers should be wrapped in aluminum foil
and kept in the refrigerator. Coproporpyrin is elevated along with, sometimes, uroporphyrin.
Urinary mercapturic acid levels may also be high. In rats, exposure for a prolonged period to mercury as methyl
mercury hydroxide was associated with urinary porphyrin changes, which were uniquely characterized by highly
elevated levels of 4- and 5-carboxyl porphyrins and by the expression of an atypical porphyrin
(''precoproporphyrin'') not found in the urine of unexposed animals.
These distinct changes in urinary porphyrin concentrations were observed as early as 1-2 weeks after initiation of
mercury exposure, and increased in a dose- and time-related fashion with the concentration of mercury in the
kidney, a principal target organ of mercury compounds. Following cessation of mercury exposure, urinary
porphyrin concentrations reverted to normal levels, consistent with renal mercury clearance.
Changes in the urinary porphyrin profile has been observed among human subjects with occupational exposure to
mercury vapor sufficient to elicit urinary mercury levels greater than 20 micrograms/l. Urinary porphyrin profiles
also correlate significantly with mercury body burden and with specific neurobehavioral deficits associated with
low level mercury exposure.
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References
Data presented by Dr. Stanley Plotkin at an August, 1999, workshop on thimerosal safety held at the National
Institutes of Health (NIH).
J Pediatr 2000;136;679-81.
Hg statistical calculations for Thimerosal: from a US government analysis of thimerosal.
Washington, May 04, 2000 (Reuters Health). FDA Endorses single virus vaccines without preservatives.
From: Susan Owens; To: secretin-discussion@egroups.com; Date: Friday, June 02, 2000 5:13 PM; Subject: Re:
[secretin-discussion] Autism Mimics The Exact Same Symptoms As Mercury Poisoning.
Templeton DM, Chaitu N. Effects of divalent metals on the isolated rat glomerulus. Toxicology. 61(2):119-33,
1990 Apr 17.
Templeton DM, Chaitu N. Effects of divalent metals on the isolated rat glomerulus. Toxicology. 61(2):119-33,
1990 Apr 17.
From: Amy Holmes; To secretin-discussion@egroups.com , Thursday, June 08, 2000 7:56 PM, Re: [secretindiscussion] Re: Porphyrin metabolism as a biomarker of mercury exposure and toxicity.
Woods JS. Altered porphyrin metabolism as a biomarker of mercury exposure and toxicity. Can J Physiol
Pharmacol 1996 Feb 74:2 210-5 and Can J Physiol Pharmacol bull; Volume 74 bull; Issue 2.
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Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.
Program Director, Continuum Center for Health and Healing,
Beth Israel Hospital / Albert Einstein School of Medicine
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