Toxicity of adjuvants and preservatives in vaccines  E-mail
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Body - Vaccination
Tuesday, 01 January 2008 11:37


Immunizations for infants and children are facing a controversy. Pediatricians are strongly concerned about preventing epidemics and immunize babies with up to 27 immunizations against 15 diseases before age two, while parents see the long-term adverse events as a threat to their children. There are three components of vaccines thimerosal, formaldehyde, and aluminum salts that have been of special interest to the public because of the increasing awareness of their toxicity to humans. The objective of this study was to summarize existing data on the effects of adjuvants and preservatives found in vaccines on humans.

Accumulation of mercury, which is the main ingredient of thimerosal, occurred mainly in the brain but not in the blood. Mercury crosses the blood-brain barrier and binds to lipoproteins in the brain. Inorganic mercury increased the number of microglia in the brain, while decreased the number of astrocytes. Thimerosal retarded growth and caused hypoactivity in autoimmune disease sensitive mice. The exposure to ethylmercury caused genetic and neurological alterations. Formaldehyde has been shown to cause cytotoxicity and genotoxicity. It also induced DNA-protein crosslinks in proliferating and non-proliferating cells. Blood cells exposed to formaldehyde with raised levels of DNA-protein crosslinks resulted in an increase in sister chromatid exchange rather than micronuclei. An allergic skin reaction was observed after the injection of adjuvants. The administration of aluminum hydroxide resulted in lack of behavioral and motor reactions and a high number of apoptotic neurons. Additionally, high numbers of reactive astrocytes implicated an inflammatory response. Aluminum was shown to induce toxicity in neurons.

Index Entries: vaccine, adjuvant, thimerosal, formaldehyde, adverse event


Every baby born in the United States receives up to 27 immunizations against 15 diseases before age two. The number of required vaccines varies in different states and the number of injections depends on the manufacturing brand. The Center for Disease Control suggests immunizing against hepatitis B, rotavirus, diphtheria, tetanus, pertussis, haemophilus influenzae type b (HiB), pneumonia, polio, influenza, mumps, measles, rubella, chicken pox, meningococcal disease, and hepatitis A (CDC, 2007). To reduce the number of injections several combinations of vaccines have been developed, such as Prevnar and ProQuad. Prevnar contains capsular antigen saccharides from seven serotypes of Streptococcus pneumoniae, while ProQuad combines the Measles, Mumps, and Rubella (MMR) with the chickenpox vaccine (Wyeth, 2005).

Prophylactic vaccines can contain attenuated viruses or bacteria that are alive, such as in MMR, inactivated microorganisms as in polio, toxic particles, also known as toxoids, from the microorganism as in diphtheria and tetanus, or subunits of a microorganism such as membrane proteins of the hepatitis B virus (Aventis Pasteur, 2005). Other types include conjugate vaccines that are made out of saccharides of the capsular antigen conjugated to proteins in the pneumococcal vaccine, recombinant vaccines that contain the genome from one and another part from a different microorganism, or DNA vaccines that contain the DNA of viruses or bacteria inserted into a human or animal cell (Wyeth, 2007).

Viruses are grown in fetal bovine serum, human diploid lung fibroblasts, monkey kidney cells, or chicken embryos (Romm, 2001). The growth medium contains amino acids, vitamins, and a stabilizer that consists of sucrose, phosphate, glutamate, and human albumin. Vaccines contain a large variety of additional ingredients such as sorbitol, sodium chloride, hydrolyzed gelatin, neomycin, which is an antibiotic, streptomycin, and polymyxin B. Formaldehyde, also known as formalin or methanal, 2-phenoxyethanol, and thimerosal are added as preservatives to some vaccines. Aluminum hydroxide, aluminum phosphate, alum, calcium phosphate, and magnesium hydroxide are some of the adjuvants used (Little, 2007). Thimerosal, formalin, and aluminum salts are of special interest to the public due to the increasing awareness of their toxicity to humans.


Thimerosal contains 49.6% of mercury by weight (Burbacher, 2005). It breaks apart into ethylmercury and thiosalicylate in the body. Thimerosal is added as a preservative to hepatitis B, HiB, and meningococcal vaccines. According to the sample calculation of mercury the cumulative amount is 4.8 mg that is currently injected into a baby in the first 24 months of its life (Table 1). This amount is highly variable since different brands of vaccines contain different amounts of thimerosal. Other studies found that both ethylmercury and methylmercury are added as preservatives to intramuscular injected and oral vaccines (Burbacher, 2005). An infant is injected with 187.5 mg of ethylmercury during the first 14 weeks of life, which exceeds the U.S. Environmental Protection Agency criterion for methylmercury (MeHg) consumption during pregnancy of 0.1 mg/kg of body weight/day. A single injection can increase blood mercury levels more than ten-fold in preterm infants. Mercury was detected in the blood of infants who were immunized with the Hepatitis B vaccine containing 12.5mg mercury/dose within 48 to 72 hours. In the infant primates, Macaca fascicularis, who were administered 20 mg/kg of mercury on days 0, 7, 14, and 21 orally or intramuscularly, mercury was detected in blood 48 to 72 hours after each injection. Mercury levels in the blood were highest around day 22 with a concentration of 38 ng/mL in the treatment group administered MeHg. The concentration of mercury in the brain was 1.7- to 3-fold higher than in the blood in the MeHg injected group. In the group injected with thimerosal the blood mercury concentration increased to 12 ng/mL after injection and dropped to 4 ng/mL after seven days. This response was consistent after all four injections. Monkeys, which were injected with thimerosal showed a 2.6- to 4.6-fold higher mercury concentration in the brain than in the blood. Accumulation of mercury occurs predominantly in the brain instead of in the blood, because of mercury’s affinity to lipoproteins that are found in the brain. Total mercury in the brain varies from 21 to 86 % inorganic mercury, depending on the time from thimerosal injection, with the remainder of mercury organically bound. Organic mercury is eliminated from the body faster than inorganic mercury. The concentration of inorganic mercury in the brain remained constant at 16 ng/mL over the course of the study. In adult monkeys the half-life of organic mercury was 37 days in the brain and was equally distributed in all brain regions. However, inorganic mercury was unequally distributed and the half-life varied from 227 to 540 days, depending on the brain region. The concentration of inorganic mercury in the thalamus stayed constant, while it doubled in the pituitary, six months following the last mercury exposure. The longer inorganic mercury stays in the brain the more it can damage the tissues. Inorganic mercury increases the number of microglia in the brain, while decreasing the number of astrocytes. A similar occurrence of neuroinflammation, together with active microglia has been observed in people with autism (Burbacher, 2005).

Another study found that thimerosal retarded growth and weight, generated overwhelming reactions to new environments, and caused hypoactivity in autoimmune disease-sensitive mice (Hornig, 2004). These effects were dependent upon the sex and strain of mice. No effects were observed in autoimmunity resistant strains after thimerosal exposure. Mice were injected with thimerosal-only, thimerosal-vaccine, or phosphate-buffered saline. Since thimerosal-only and thimerosal-vaccine treatment groups exhibited the same pattern of effects, they were evaluated together. The timing of injections was adjusted to mimic the equivalent maturation of the central nervous and immune systems including neuronal migration and window of immune tolerance of an infant receiving Hepatitis B, DTaP, and HiB vaccines, according to the 2001 US Immunization Schedule. The dose of ethylmercury was calculated for the 10th percentile weight of boys and was 62.5 mg/kg for the first three immunizations and 50.0 mg/kg for the last immunization. At week four, growth, total distance traveled, exploratory rearing, total and center ambulatory distance, and XY and Z plane stereotypy episodes were significantly lower in male and female autoimmune-disease sensitive mice that were injected with thimerosal than in the other strains. There was a significant time and ethylmercury interaction effect on ambulatory distance. At week ten, exploratory rearing was lower in both males and females, while center ambulatory distance was lower in male mice only. In autoimmune disease-sensitive mice, the hippocampal structures were found to be bigger than normal and had changed glutamate receptors and transporters. This is also known to occur in Rett syndrome, which has similar symptoms as autism. The number and density of neurons increased in the dentate gyrus, Cornu Ammonis fields one and two in mice exposed to thimerosal. The number of pyramidal neurons in Cornu Ammonis field three increased and spread in a wide arc. The infrapyramidal blade of the dentate gyrus was less deformed than the suprapyramidal blade. The infrapyramidal blade was also enlarged. Exposure to ethylmercury caused genetic and neurological alterations. There is a need for research testing long-term effects of mercury on the brain. According to the authors of the study on M. fascicularis there are thimerosal-free vaccines that are given to children less than six years old (Burbacher, 2005); however, this is not normal practice. Pediatricians, knowing little about toxicokinetics and developmental neurotoxicity of mercury still immunize children and babies with thimerosal containing vaccines, such as HiB and Hepatitis B. Little is known about the acute and long-term effects of toxic mercury in the developing brain of an infant or a fetus. To reduce the exposure of fetuses to mercury, the U.S. Food and Drug Administration warn pregnant women about the consumption of mercury containing fish. Ingested MeHg is absorbed in the intestine. Since it binds to cystein the body perceives MeHg as methionine and transports it across the blood-brain barrier and across the placenta. Newborns who have been exposed to mercury showed motor and sensory deficiencies and mental retardation. When adults have been exposed to high levels of methylmercury they experienced hearing impairment, speech difficulties, narrowing of the visual field, blindness or death as it happened in Japan and Iraq. Since fish in our diet are a major source of mercury the US Environmental Protection Agency calculated a maximum level of methylmercury that a person could consume before toxicity is reached. The criterion is 0.3 mg methylmercury per kilogram of fish (USEPA, 2007).

Mercury is a byproduct of acetaldehyde, paint, and electrical equipment manufacturing, as well as waste incineration. The primary source of mercury in the environment is from coal combustion. It is transported in the air and deposited in water bodies where it accumulates in the benthos. Ionic mercury binds to organic matter and is consumed by plankton, a major food source of fish. In the aquatic environment mercury is bioaccumulated and biomagnified up the food chain.


Another way to preserve vaccines is the addition of formaldehyde. Formaldehyde is used to kill viruses or bacteria, which can then be incorporated into vaccines. Additionally, it may be used as an adjuvant (Little, 2007). One thousand micrograms of formaldehyde are injected into a child before it reaches two years of age (Table 1). Formaldehyde exists in small quantities as a byproduct of metabolism in the human body. Since formaldehyde is a gas at room temperature it is combined with water to form the hydrate CH2(OH)2. Formaldehyde irreversibly cross-links primary amine groups in proteins with nitrogen atoms in protein or DNA. It also prevents RNA from forming secondary structures. Formaldehyde in the air irritates the eye and mucous membranes. It results in a headache, burning in the throat, labored breathing, and asthma when inhaled. The USEPA set a limit of 0.016 ppm formaldehyde in the air. High amounts of formaldehyde through ingestion are lethal, because it becomes formic acid in the human body. Formic acid may cause acidosis, hypothermia, blindness, coma, or death. Chronic formaldehyde exposure can lead to cancer. The International Agency for Research on Cancer states that it causes nasopharyngeal cancer in humans. It can also cause allergies and dermatitis upon skin contact.

Formaldehyde has been shown to induce DNA-protein crosslinks in proliferating and non-proliferating cells (Schmid, 2007). Spontaneous hydrolysis and active DNA repair has been shown to remove crosslinks in 12 to 18 hours (Schmid, 2007). DNA-protein crosslinks in proliferating cells can replicate and cause sister chromatid exchanges. If DNA-protein crosslinks are incompletely repaired mutations will result. Chromosome aberrations and micronuclei will occur. A significant induction of DNA-protein crosslinks in human blood culture occurred when exposed to ³ 25 mM formaldehyde. The removal of formaldehyde induced DNA-protein crosslinks occurred more rapidly after the exposure to 100 mM formaldehyde, which is completely removed by 24 hours, as compared to 200 mM and 300 mM formaldehyde exposures, in which formaldehyde induced DNA-protein crosslinks are still present. Lymphocytes enter S-phase of their cell cycle after 24 hours from the start of cell culture. A 200 mM formaldehyde concentration significantly increases sister chromatid exchange. This concentration also caused strong cytotoxicity, as does 100 mM concentration. Depending on formaldehyde concentrations, cytotoxic effects may occur before genotoxic effects. Formaldehyde concentrations above 300 mM caused induction of the micronuclei. Due to the volatility and reactivity with cell membrane and cytoplasm of formaldehyde its concentration is lower in the cell nucleus. Formaldehyde-induced cytotoxicity may also be the result of other reactions besides the DNA-protein crosslinks. For the increase in sister chromatid exchange in human blood cultures to occur a high formaldehyde concentration of 200 mM must be present. When lymphocytes are exposed to formaldehyde during their last cell cycle micronuclei are increased. Formaldehyde is a week micronuclei inducer in human blood cultures, because it needs blood cells with increased DNA-protein crosslinks. Formaldehyde-induced micronuclei are 81 % centromere-negative. Blood cells exposed to formaldehyde with raised levels of DNA-protein crosslinks, result in an increase in sister chromatid exchange rather than micronuclei.


Vaccines consist of an antigen and an adjuvant, such as aluminum hydroxide or aluminum phosphate, that increases the effectiveness of the antigen (Flarend, 1997). The possible cumulative amount is 3070 mg in the first 24 months of life (Table 1). An adjuvant acts similar to a chemical catalyst amplifying the vaccine, but has no effect if injected alone. An immunologic adjuvant does not have any antigenic properties. It stimulates the immune system by releasing the vaccine slowly into the interstitial fluid increasing the exposure time to lymphocytes (Ulanova, 2001). Because aluminum adjuvants localize the deposition of the antigen, they cause local inflammation (Goto, 1997). Aluminum salts, QS21 that is a plant extract from the Quillaja saponaria tree, MF59 that is an oil-in-water emulsion, and virosomes are used as adjuvants. Aluminum adjuvants enhance the processing of desorbed and adsorbed antigens by antigen-presenting cells and stimulate the response of type 2 T helper cells, which are lymphocytes (Ulanova, 2001, Little, 2007). Antigen-presenting cells take up antigen faster in the presence of aluminum hydroxide in vitro (Ulanova, 2001). Accessory properties of monocytes are enhanced through aluminum hydroxide (Al(OH)3). Cultures treated with Al(OH)3 contained mRNA for interleukin-4, which regulates several immunological processes. Interleukin-4 causes the expression of major histocompatibility complex class II compounds on the cell surface. Human monocytes of peripheral blood mononuclear cells show an increase of major histocompatibility complex class II, CD40, CD54, CD58, CK83, and CD86 on the cell membrane. Monocytes developed dentritic characteristics after being exposed to Al(OH)3 for 48 hours (Ulanova, 2001). Another study found that the aluminum concentration of 500 mg per dose had to be present to achieve a high serological response in rabbits (Little, 2007). An injection of 25 mg of Bacillus anthracis recombinant protective antigen adsorbed to 500 mg of aluminum resulted in 31.0 mg of anti-recombinant protective antigen Immunoglobulin G (IgG) per ml at week two. When the amount of aluminum was reduced to 158 mg the anti-recombinant protective antigen IgG dropped eight-fold to 4.0 mg per ml. Every other reduction in the aluminum concentration in the study led to a two-fold decline in IgG. The test for serological response and the protective efficacy showed that rabbits injected recombinant protective antigen with or without aluminum experienced a peak at week six after two doses were given. The treatment group that was injected with Al(OH)3 exhibited higher IgG antibody responses. IgG titers declined over time, but increased significantly after the second dose and declined again until the challenge with the pathogen. This difference was significant between the two groups over time and at each week. Both treatment groups of rabbits were exposed to aerosol B. anthracis spores six weeks after the booster injection. Rabbits that received the inoculation containing aluminum were 100 % immune, while rabbits without the aluminum adjuvant were 92 % immune. The control animals died. The post-challenge IgG titers were higher in the rabbits that did not receive aluminum than in rabbits that received aluminum in the vaccine. The anti-recombinant protective antigen IgG titer was 158 mg at week ten and increased to 322 mg after the exposure to the pathogen in rabbits with aluminum. This is a two-fold increase. The increase was more pronounced from 31.8 mg at week ten to 511 mg in rabbits that were not exposed to aluminum. This is a seven-fold increase. The post-challenge value of 322 mg is similar to the value of 342 mg that was seen after the second injection with aluminum. However, the post-challenge value of 511 mg was drastically higher than the 72 mg anti-recombinant protective antigen IgG per ml that was obtained 2 weeks after the booster shot. This increase points towards the lack of sterile immunity.

The United States Food and Drug Administration approves less than 0.85 mg aluminum per dose (Flarend, 1997, Little, 2007). Aluminum is present in blood one hour after intramuscular injection. Therefore, aluminum adjuvants dissolve fast in interstitial fluid, while aluminum hydroxide (AH) dissolves faster in the first 24 hours and aluminum phosphate (AP) after 48 hours (Flarend, 1997). The concentration of aluminum in blood stays constant from day two. Seventeen percent of AH and 51 % of AP are absorbed in 28 days. The rabbits excreted six percent of the aluminum from AH and 22 % from AP through urine during 28 days. The mean residence time was longer for AH. Tissue samples contained 2.9 times more aluminum in rabbits with AP than AH adjuvants. The highest concentration was in the kidney, than spleen, liver, heart, lymph node, and the brain contained the lowest. Repository effect explain the mechanism of the aluminum adjuvant taking up and holding the antigen until it is injected and then freeing it. In humans aluminum concentration rises by 0.04 ng/ml after the injection of a 0.85 mg aluminum dose. Since the normal value is 5 ng/ml the plasma aluminum concentration increases 0.8 % (Flarend, 1997).

Subcutaneous nodules, granulomatous inflammation, and sterile abscesses have been observed as local side reactions after injection of aluminium adjuvants (Goto, 1997). Guinea pigs exhibited local histopathological reactions when injected with vaccines containing calcium phosphate or aluminum hydroxide (Goto, 1997). Calcium phosphate and aluminum hydroxide injected as gel caused infiltration of neutrophils and edema in the interstitial connective tissue. Al(OH)3 suspension initiated collection of neutrophils and phagocytosis of a little aluminum suspension. Calcium (Ca) suspension induced infiltration of many injured neutrophils. Suspensions were responsible for more serious damage to neutrophils. The injection site of aluminum (Al) gel showed an inflammatory response with macrophages consisting of foamy cytoplasm, epithelioid cells, small lymphocytes, and giant cells with many nuclei that continued for longer than eight weeks. Al suspension caused a rapid increase of macrophages that remained until eight weeks. However, Al residue dissolved by the fifth week. Al gel and Al suspension have a toxic effect on macrophages, while Ca gel and Ca suspension do not. Macrophages degrade after being exposed to the Al suspension for two hours and die after 24 hours. The adjuvant entered the cell via phagocytosis. The combination of Al gel with ovalbumin initiated the most effective antibody response. The same was observed with tetanus toxoid. The suspension type caused a bigger damage to neutrophils than did the gel type. The number of IgG antibodies is initially higher with the aluminum adjuvant. However, the difference is minimal after 16 weeks between the soluble ovalbumin and the combination of al adjuvant and ovalbumin. Similar results were obtained for tetanus toxoid. Local tissue adverse effect is shorter in Ca, because it is a non-toxic chemical and is therefore eliminated faster. Al is toxic to phagocytes and has therefore affected the injection site for a longer period (Goto, 1997).

Dialysis encephalopathy, osteomalacia, microcytic anemia, b2-microglobulin-associated amyloidosis, amyotrophic lateral sclerosis, and parkinsonismdementia, and Alzheimer’s disease are associated with aluminum (Kawahara, 2001). Lipophilic Al compounds, to which Al(acac)3 and Al(malt)3 belong, cross the cell membrane and initiate adverse effects, because of their extremely toxic characteristics. Degeneration of neurons occurs when they are subjected to Al(acac)3 or Al(malt)3. The axonal transport in cultured rat cortical neurons is vulnerable to Al(malt)3. Long-term exposure to AlCl3 changed the morphology in depositions immunopositive to tau proteins, neurofilaments, and AbP in neurons. A similar phenomenon occurs in Alzheimer’s disease. AbP is assimilated into neuronal membranes and produces cation-selective ion channels. Aluminum inhibits phosphorylation, dephosphorylation, metabolism, and DNA transcription and alters axonal flows (Kawahara, 2001).

Aluminum hydroxide when injected causes a decline in muscular strength and endurance in mice (Petrik, 2007). An increase in anxiety has also been observed. Mice that received a combination of aluminum hydroxide and squalene showed late stage, long-term memory loss suggesting neuronal apoptosis in the red nucleus and DG region of the hippocampus. Aluminum hydroxide increases activated caspase-3 in single labeling by 255 %, which points to apoptosis of non-neural cells, and by 233 % in double labeling with NeuN in the ventral lumbar spinal cord of mice. In the primary motor cortex the increase is 192 % for single labeling and 185 % for double labeling. Aluminum causes a decline in motor neurons by 35 % in the lumbar spinal cord. The expression of GFAP-positive astrocytes rises by 350 %. Some mice showed hair loss at the site of injection. An allergic skin reaction was observed after the injection of both adjuvants. The injection of aluminum hydroxide results in lack of behavioral and motor reactions and a high number of apoptotic neurons. High numbers of reactive astrocytes implicate an inflammatory response.

Aluminum hydroxide is used in vaccines, like DPT, Hepatitis A and B, as an adjuvant (Braun, 2000). Even though, many studies prove the toxicity of aluminum adjuvants and urge to abolishment, they are still in use.

The Vaccine Adverse Event Reporting System is a passive national surveillance system that has received many adverse events reports. However, they are not linked to a specific ingredient of the vaccine, just to the vaccine itself.

The diphtheria-tetanus-whole-cell pertussis vaccine caused acute encephalopathy and several chronic nervous system dysfunctions (Braun, 2000). Some adverse events that occur months or years later are not linked to the vaccine. Fever, agitation, screaming syndrome, convulsion, abnormal cry, stupor, somnolence, vomit, rash, urticaria, and hypotonia have been reported as adverse events caused by the diphtheria-tetanus-acellular pertussis vaccine. The DTP and DTPH vaccines were responsible for eighty-five deaths in 1995.

The pertussis vaccine causes adverse effects (Burstyn, 1983). It can be even deadly for newborn babies. The number of babies dieing from pertussis is small, because of improved housing and nutrition. Passively acquired antibodies in babies prevent their immune system to properly utilize the pertussis vaccine. The time of vaccination should be readjusted.

Trivalent influenza vaccine caused fever, seizures, injection site reaction, urticarial rash, cough, rhinitis, vomiting, flu syndrome, and agitation when administered alone (McMahon, 2005). When TIV was administered in combination with other vaccines diarrhea and lethargy were also observed. Death occurred in three children.


The future of our children is shaped by aluminum, mercury, and formaldehyde circulating in their arteries and veins affecting significant organs in their developing bodies. There have been only a few studies conducted that tested long-term effects of vaccine ingredients. Therefore, there is not enough evidence to draw a conclusion of their effects. The evidence provided in the discussed studies suggests that long-term toxicity of vaccine ingredients has been associated with many serious chronic diseases. A known fact is if a child receives immunization while having a mild respiratory infection it is likely to die. Adverse events, such as fever, high pitch screaming, vomiting, and convulsion are normal symptoms that occur after receiving a vaccination, but if an unvaccinated child exhibits these symptoms the doctor will diagnose the child with meningitis. If a child missed pertussis vaccines it is less likely to develop asthma, missed measles vaccines means less likely to develop inflammatory bowel disease, missed HiB vaccines less likely to develop diabetes, and without rubella vaccine less probability of suffering arthritis.

Homeopathic vaccine alternatives have not been linked to any adverse events or chronic diseases and should be considered by parents. However, the efficacy of homeopathic vaccines has not yet been tested since studies including purposeful exposure to pathogens on human subjects are prohibited.

Thimerosal free vaccines should be used for autoimmune disease sensitive children, since their brains are sensitive to mercury. Adjuvants such as calcium phosphate or QS21 should be used as alternatives. Calcium is eliminated faster from the body.



Aventis Pasteur. (2005) Poliovirus vaccine inactivated. Package insert.

Braun M. M., Mootrey G. T., Salive M. E., Chen R. T., and Ellenberg S. S. (2000) Infant immunization with acellular pertussis vaccines in the United States: Assessment of the first two years' data from the vaccine adverse event reporting system (VAERS). Pediatrics.106, 51-58.

Burbacher T. M., Shen D. D., Liberato N., Grant K. S., Cernichiari E., and Clarkson T. (2005) Comparison of blood and brain mercury levels in infant monkeys exposed to methylmercury or vaccines containing thimerosal. Environmental Health Perspectives 113, 1015-1021.

Burstyn D. G., Baraff L. J., Peppler M. S., Leake R. D., St Geme J., and Manclark C. R. (1983) Serological response to filamentous hemagglutinin and lymphocytosis-promoting toxin of bordetella pertussis. Infection and immunity. 41, 1150-1156.

Center for Disease Control. (2007) Recommended Immunization Schedule for Persons Aged 0-6 Years. http://www.cdc.gov/nip/recs/child-schedule-color-print.pdf.

Flarend R. E., Hem S. L., White J. L., Elmore D., Suckow M. A., Rudy A. C., and Dandashli E. A. (1997) In vivo absorption of aluminium-containing vaccine adjuvants using 26Al. Vaccine. 15, 1314-1318.

Goto N., Kato H., Maeyama J., Maeyama J., Shibano M., Saito T., Yamaguchi J., and Yoshihara S. (1997) Local tissue irritating effects and adjuvant activities of calcium phosphate and aluminium hydroxide with different physical properties. Vaccine. 15, 1364-1371.

Hornig M., Chian D., and Lipkin W. I. (2004) Neurotoxic effects of postnatal thimerosal are mouse strain dependent. Molecular psychiatry. 9, 833-845.

Kawahara M., Kato M., and Kuroda Y. (2001) Effects of aluminum on the neurotoxicity of primary cultured neurons and on the aggregation of β-amyloid protein. Brain Research Bulletin. 55, 211-217.

Little S.F., Ivins B.E., Webster W.M., Norris S.L.W., and Andrews G.P. (2007) Effect of aluminum hydroxide adjuvant and formaldehyde in the formulation of rPA anthrax vaccine. Vaccine. 25, 2771-2777

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Table 1 A cumulative example of the amount of mercury, aluminum, and formaldehyde (micrograms) that is administered to an infant in the first 24 months through vaccines recommended by the Center for Disease Control

Vaccine Trademark Doses 24 months Hg (mg) Total Hg (mg) Al (mg) Total Al (mg) Formalin (mg) Total F (mg)
Hepatitis B Engerix-B 3 3 0.5 1.5 250 750 0 0
Rotavirus RotaTeq 3 3 0 0 0 0 0 0
DTP Daptacel 5 4 0 0 330 1320 100 400
Hib ActHIB 4 4 0.3 1.2 0 0 0 0
Pneumococcal Prevnar 4 4 0 0 125 500 0 0
Inactivated Poliovirus IPOL 4 3 0 0 0 0 100 300
Influenza (yearly) FLUARIX 2 2 1 2 0 0 50 100
MMR MMR II 2 1 0 0 0 0 0 0
Varicella VARIVAX 1 1 0 0 0 0 0 0
Hepatitis A HAVRIX 2 2 0 0 250 500 100 200
Meningococcal (opt) Menomune 1 1 0.1 0.1 0 0 0 0
approved maximum           850      
Total   31 28 1.9 4.8 955 3070 350 1000
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