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Vaccines: Childhood Vaccinations: Mercury in Vaccines, Thimerosal Controversy, Possible Links to Autism in Children

For ease of navigation and reference in this very comprehensive and extensive section on vaccines we are posting the "Quick Index on Vaccines" for the entire contents at the beginning of each page.

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Information on Vaccines and Mercury and Possible Risks to Children

Support Resesearch Studies on Vaccines for Children and Autism

autism linked to vaccines

Controversy Linking Mercury in Vaccines to Austism

Origins of the Mercury / Vaccine Controversy

The mercury / vaccine controversy began in 1997, when Frank Pallone, a Democratic congressman from New Jersey, attached an amendment to an FDA reauthorization bill, requiring the FDA to "compile a list of drugs and foods that contain intentionally introduced mercury compounds and [to] provide a quantitative and qualitative analysis of the mercury compounds in the list." The bill later evolved into the landmark FDA Modernization Act of 1997 (FDAMA) and was signed into law on November 21, 1997.

The act also authorized the FDA to review and assess the risk of all mercury-containing food and drugs. In line with this review, U.S. vaccine manufacturers responded to a two requests in 1988 and 1989 FDA request to provide more detailed information about the thimerosal content of their preparations that included this compound as a preservative. Thimerosal has been used as an additive to biologics and vaccines since the 1930s because it is very effective in killing bacteria used in several vaccines and in preventing bacterial contamination, particularly in opened multidose containers. Some but not all of the vaccines recommended routinely for children in the United States contain thimerosal.

In 1999 the Public Health Service, US Dept of Health and Human Services and the American Academy of Pediatrics put out a "joint statement", Thimerosal in Vaccines: A Joint Statement of the American Academy of Pediatrics and the Public Health Service, stating: "PHS and AAP continue to recommend that all children should be immunized against the diseases indicated in the recommended immunization schedule. Given that the risks of not vaccinating children far outweigh the unknown and much smaller risk, if any, of exposure to thimerosal-containing vaccines over the first 6 months of life, clinicians and parents are encouraged to immunize all infants even if the choice of individual vaccine products is limited for any reason." However, in their research on mercury toxicity to the developing brain, Trasande, Landrigan and Schechter assert that "There is no evidence to date validating the existence of a threshold blood mercury concentration below which adverse effects on cognition are not seen".

Thimerosal is a compound that is 49.6% mercury by weight. When pregnant women eat foods or take medicines that contain mercury, the mercury can be transferred to the developing fetus through the placenta. Infants can be exposed to mercury through foods, including breast milk, or medicines. Developing fetuses and young children are more susceptible to mercury exposure than adults because mercury can interfere with the developing nervous system.

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Childhood Vaccinaions and Mercury Toxicity

Childhood Vaccinaions and Mercury Toxicity

Vaccines and Mercury Neurotoxicity in Children

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).

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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 multi-dose 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]

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.

A 2005 research study on thimerosal citing the Institute of Medicine (IOM), noted that "recent publications have proposed a direct link between the use of thimerosal-containing vaccines and the significant rise in the number of children being diagnosed with autism, a serious and prevalent developmental disorder (for review, see IOM 2001). Results from an initial IOM review of the safety of vaccines found that there was not sufficient evidence to render an opinion on the relationship between ethylmercury exposure and developmental disorders in children (IOM 2001).

The IOM review did, however, note the possibility of such a relationship and recommended further studies be conducted. A recently published second review (IOM 2004) appears to have abandoned the earlier recommendation as well as backed away from the American Academy of Pediatrics goal. This approach is difficult to understand, given our current limited knowledge of the toxicokinetics and developmental neurotoxicity of thimerosal, a compound that has been (and will continue to be) injected in millions of newborns and infants."

The key findings of the present study are the differences in the disposition kinetics and demethylation rates of thimerosal and Monomethylmercury (MeHg). Consequently, the researchers conclude that MeHg is not a suitable reference for risk assessment from exposure to thimerosal-derived Hg. The authors go on to state: "Knowledge of the biotransformation of thimerosal, the chemical identity of the Hg-containing species in the blood and brain, and the neurotoxic potential of intact thimerosal and its various biotransformation products, including ethylmercury, is urgently needed to afford a meaningful interpretation of the potential developmental effects of immunization with thimerosal-containing vaccines in newborns and infants. This information is critical if we are to respond to public concerns regarding the safety of childhood immunizations."

[Return to "Quick-Index" of Mercury and Vaccines]

Ethylmercury and the DPT Vaccine

Ethylmercury is a metabolite of thimerosal (ethyl(2-mercaptobenzoato-(2)-O,S). Ethyl mercury derivatives are virulent neurotoxins on either acute or chronic exposure. They are especially hazardous because of their volatility, their ability to penetrate epithelial and blood-brain barriers and their persistence in vivo.

For ethylmercury, the exposure pathway of concern to children has been via vaccines. It has been suggested that there may be neurological effects of ethylmercury exposure from use of thimerosal in vaccines, though studies have reported conflicting results. Ethylmercury exposure from thimerosal in some vaccines has been associated, in some studies and not others , with autism and other neurological disorders in children.

Ethylmercury has been a component of the DPT vaccine. Some believe that this compound also exacerbates any tendencies of the DPT vaccine to contribute to epileptiform activity.

A main theoretical concern is that infants, because of smaller body mass, will have a still small but higher concentration of ethyl mercury than older children or adults when thimerosal is metabolized. Because infants are still in the phase of neurodevelopment, it is theoretically possible that the potential effects of organic mercury may be greater,

Thimerosal-free vaccines have been slowly becoming the norm, but it is still often difficult for most parents to find reliable current data on what vaccines still contain thimerosal (which contains ethylmercury). Updated January 28, 2008, a Table Showing Which Vaccines Contain Thimerosal (Thimerosal Content in Some U.S. Licensed Vaccines), still notes (in fine print), that a number of these products "...should be considered considered equivalent to thimerosal-free products. This vaccine may [ still ] contain trace amounts (<0.3 mcg) of mercury left after post-production thimerosal removal" — and goes on to assert that "these amounts have no biological effect" [according to JAMA 1999;282(18) and JAMA 2000;283(16)].

Other researchers assert that "there is no evidence to date validating the existence of a threshold blood mercury concentration below which adverse effects on cognition are not seen". 10

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Other Sources of Mercury and its Effects on the Developing Brain

In February of 2005, Leonardo Trasande1,2,3,4, Philip J. Landrigan1,2, and Clyde Schechter5  [1Center for Children's Health and the Environment, Department of Community and Preventive Medicine; 2Department of Pediatrics, Mount Sinai School of Medicine, New York; 3Division of General Pediatrics, Children's Hospital, Boston; 4Department of Pediatrics, Harvard Medical School, Boston; 5Department of Family Medicine, Albert Einstein College of Medicine, New York ] published a research article, Public Health and Economic Consequences of Methyl Mercury Toxicity to the Developing Brain, where in the Abstract it is noted that "Methyl mercury is a developmental neurotoxicant. Exposure results principally from consumption by pregnant women of seafood contaminated by mercury from anthropogenic (70%) and natural (30%) sources. Throughout the 1990s, the U.S. Environmental Protection Agency (EPA) made steady progress in reducing mercury emissions from anthropogenic sources, especially from power plants, which account for 41% of anthropogenic emissions. However, the U.S. EPA recently proposed to slow this progress, citing high costs of pollution abatement."

To put into perspective the costs of controlling emissions from American power plants, they estimated the economic costs of methyl mercury toxicity attributable to mercury from these plants. The researchers used an environmentally attributable fraction model and limited their analysis to the neurodevelopmental impacts — specifically loss of intelligence.

Using national blood mercury prevalence data from the Centers for Disease Control and Prevention, we found that between 316,588 and 637,233 children each year have cord blood mercury levels > 5.8 μg/L, a level associated with loss of IQ. They concluded that the resulting loss of intelligence caused diminished economic productivity that persists over the entire lifetime of these children, and that this lost productivity is the major cost of methyl mercury toxicity, amounting to $8.7 billion annually (range, $2.2­43.8 billion. Of this total, $1.3 billion (range, $0.1­6.5 billion) each year is attributable to mercury emissions from American power plants. The authors go on to state: "This significant toll threatens the economic health and security of the United States and should be considered in the debate on mercury pollution controls."

Mercury is a ubiquitous environmental toxicant (Goldman et al. 2001). It exists in three forms, each of which possesses different bioavailability and toxicity: the metallic element, inorganic salts, and organic compounds (methyl mercury, ethyl mercury, and phenyl mercury) (Franzblau 1994). Although volcanoes and other natural sources release some elemental mercury to the environment, anthropogenic emissions from coal-fired electric power generation facilities, chloralkali production, waste incineration, and other industrial activities now account for approximately 70% of the 5,500 metric tons of mercury that are released into the earth's atmosphere each year (United Nations Environmental Programme (UNEP) 2002).

Elemental mercury is readily aerosolized because of its low boiling point, and once airborne it can travel long distances to eventually deposit into soil and water. In the sediments of rivers, lakes, and the ocean, metallic mercury is transformed within microorganisms into methyl mercury (Guimaraes et al. 2000). This methyl mercury biomagnifies in the marine food chain to reach very high concentrations in predatory fish such as swordfish, tuna, king mackerel, and shark (Dietz et al. 2000; Gilmour and Riedel 2000; Mason et al. 1995; Neumann and Ward 1999). Consumption of contaminated fish is the major route of human exposure to methyl mercury.

The toxicity of methyl mercury to the developing brain was first recognized in the 1950s in Minamata, Japan, where consumption of fish with high concentrations of methyl mercury by pregnant women resulted in at least 30 cases of cerebral palsy in children; exposed women were affected minimally if at all (Harada 1968).

A similar episode followed in 1972 in Iraq when the use of a methyl mercury fungicide led to poisoning in thousands of people (Bakir et al. 1973); again, infants and children were most profoundly affected (Amin-Zaki et al. 1974, 1979). The vulnerability of the developing brain to methyl mercury reflects the ability of lipophilic methyl mercury to cross the placenta and concentrate in the central nervous system (Campbell et al. 1992). Moreover, the blood­brain barrier is not fully developed until after the first year of life, and methyl mercury can cross this incomplete barrier (Rodier 1995).

As mentioned in the previous section, a study in the Seychelles Islands in the Indian Ocean found only one adverse association with maternal hair mercury concentration among 48 neurodevelopmental end points examined (prolonged time to complete a grooved pegboard test with the nonpreferred hand) (Myers et al. 2003). However, the grooved pegboard test was one of the few neurobehavioral instruments in the Seychelles study not subject to the vagaries of translation that can degrade the validity of culture-bound tests of higher cognitive function when they are applied in developing nations (Landrigan and Goldman 2003).

A third prospective study in the Faroe Islands, a component of Denmark inhabited by a Scandinavian population in the North Atlantic, has followed a cohort of children for 14 years and collected data on 17 neurodevelopmental end points, as well as on the impact of methyl mercury on cardiovascular function. The Faroes researchers found significant dose-related, adverse associations between prenatal mercury exposure and performance on a wide range of memory, attention, language, and visual-spatial perception tests (Grandjean et al. 1997). Methyl mercury exposure was also associated with decreased sympathetic- and parasympathetic-mediated modulation of heart rate variability (Grandjean et al. 2004) and with persistent delays in peaks I­III brainstem evoked potentials (Murata et al. 2004).

Recent data suggest that the cord blood mercury concentration may on average be 70% higher than the maternal blood mercury concentration (Stern and Smith 2003), and a recent analysis suggests that a modification of the U.S. EPA reference dose for methyl mercury be made to reflect a cord blood:maternal blood ratio that is > 1 (Stern 2005). If the developmental effects of mercury exposure do, in fact, begin at 5.8 μg/L in cord blood, as suggested by the Faroes (Grandjean et al. 1997) and New Zealand (Kjellstrom et al. 1986, 1989) data and by the NAS report (National Research Council 2000), then effects would occur in children born to women of child-bearing age with blood mercury concentrations ≥3.41 (ratio, 5.8:1.7) μg/L. National population data from the 1999­2000 National Health and Nutrition Examination Survey (NHANES) found that 15.7% of American women of childbearing age have total blood mercury concentrations ≥3.5 μg/L (Mahaffey et al. 2004).

Some commentators have used data from the Seychelles study to argue that methyl mercury is not toxic to the fetus at low concentrations and to suggest that fear of mercury exposure is needlessly preventing women from ingesting fish and thus denying them access to beneficial long-chain polyunsaturated fatty acids (LCPUFAs), especially docosahexaenoic acid (DHA).

There is no evidence to date validating the existence of a threshold blood mercury concentration below which adverse effects on cognition are not seen. The U.S. EPA has, however, set a benchmark dose level (BMDL) for cord blood mercury dose concentration of 58 μg/L.

In the results of the research's base-case analysis, it was determined that each year in the United States, between 316,588 (7.8% of the annual birth cohort) and 637,233 babies are born with cord blood mercury levels > 5.8 μg/L. The lower-bound estimate of 316,588 babies is based on the very conservative assumption that maternal and cord blood mercury concentrations are equal. But if the cord blood mercury concentration is on average 70% higher than the maternal blood mercury concentration, as suggested by recent research (Stern and Smith 2003), 637,233 babies, or 15.7% of the birth cohort, experience cord blood mercury levels > 5.8 μg/L. Fetal blood mercury levels > 5.8 μg/L are associated with small but significant loss of IQ. This decrement in IQ appears to be permanent and irreversible, and it adversely affects a significant portion of the annual birth cohort's economic productivity over a lifetime.

Since January 2003, the issue of early life exposure to methyl mercury has become the topic of intense debate after the U.S. Environmental Protection Agency (EPA) announced a proposal to reverse strict controls on emissions of mercury from coal-fired power plants. This proposed "Clear Skies Act" would slow recent progress in controlling mercury emission rates from electric generation facilities and would allow these releases to remain as high as 26 tons/year through 2010 (U.S. EPA 2004a). By contrast, existing protections under the Clean Air Act will limit mercury emissions from coal-fired power plants to 5 tons/year by 2008 (U.S. EPA 2004b).

[Return to "Quick-Index" of Mercury and Vaccines]

Testing for Mercury Toxicity in Children

Tests thought to indicate a high potential for heavy metal poisoning (including mercury) include the following:

  1. On the CBC - elevated MCH and MCV
  2. Immune tests - low CD8 cells, elevated CD4/CD8 ratio
  3. Low absolute number of NK cells
  4. Serum IgE elevated above normal range
  5. Elevated urinary d-glucaric acid>
  6. Elevated urinary 3-methylhistidine
  7. Elevated serum ALT and/or AST
  8. 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.


  1. Data presented by Dr. Stanley Plotkin at an August, 1999, workshop on thimerosal safety held at the National Institutes of Health (NIH).
  2. J Pediatr 2000;136;679-81.
  3. Hg statistical calculations for Thimerosal: from a US government analysis of thimerosal.
  4. Washington, May 04, 2000 (Reuters Health). FDA Endorses single virus vaccines without preservatives.
  5. 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.
  6. Templeton DM, Chaitu N. Effects of divalent metals on the isolated rat glomerulus. Toxicology. 61(2):119-33, 1990 Apr 17.
  7. Templeton DM, Chaitu N. Effects of divalent metals on the isolated rat glomerulus. Toxicology. 61(2):119-33, 1990 Apr 17.
  8. From: Amy Holmes; To secretin-discussion@egroups.com , Thursday, June 08, 2000 7:56 PM, Re: [secretin-discussion] Re: Porphyrin metabolism as a biomarker of mercury exposure and toxicity.
  9. 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.

Written and overseen by Lewis Mehl-Madrona, M.D., Ph.D.

Associate Professor of Family Medicine and Psychiatry
Department of Family Medicine / University of Saskatchewan College of Medicine


Coordinator for Integrative Psychiatry and System Medicine
Program in Integrative Medicine / University of Arizona College of Medicine

Clinical Program Director, Continuum Center for Health and Healing,
Beth Israel Hospital / Albert Einstein School of Medicine

Medical Director
Center for Complementary Medicine / University of Pittsburgh Medical Center

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