Home Contact Us Search Toxic Exposure Study Trust Foundation

Aluminum & Vaccines

Mercury Amalgam Thimerosal Founders Donations

Thimerosal Toxicity
Thimerosal Content
Published  Studies
Thimerosal Vs. Hg(II)
Vaccine Hg Exposure
FDA Hypocracy
Experts Speak Out
Vaccines & Development
IOM Conference
Neurodevelopmental Effects
Autism & Mercury
Thimerosal Links
Mothering & Autism
Homeland Insecurity
Records Sealed
Government Knew
Known Effects
Vaccine Lawsuits
Eli Lilly & Thimerosal
Vaccine Booster
Hg Free Vaccines
Vaccine Assessment
Metals & Autism
Congressional Acts
WHO & Thimerosal
Flu Vaccines
Autism & Vaccines
Autism & Detoxification
Childhood Immunizations
Aluminum & Vaccines
Vaccine Adjuvants
Allergic Components
Thimerosal & Autism
AAPS Opposition
Toxic Vaccines
Mercury Exposure
Hg in Medicines
Vaccines-Pro & Con
Candida & Autism
Thimerosal Effects
Gulf War Syndrome
Dr. Synder Responds
Myth From Reality
Vaccine History
Developmental Disorders
Polio Vaccine
Safe Minds
Why So Long?
1st Vaccine Conference
2nd Vaccine Conference
Vaccine Injury

Safety of Aluminum Added to Vaccines as a Vaccine Adjuvant

E-mail from Dr. Philip Rudnick Ph.D.
Professor Emeritus, Chemistry
West Chester University of Pennsylvania

Date: Sun, 08 Dec 2002 15:08:06 -0500
From: pbrudnick@netscape.net
To: bhaley@altcorp.com
Subject: Aluminum Neurotoxicity



Thimerosal is certainly a very potent neurotoxin. It should never have been used in vaccines, particularly for infants and children. But what about aluminum INJECTED into the body not as a vaccine preservative but as a vaccine adjuvant? (Aluminum is not readily absorbed from the GI tract.) Aluminum, also is a neurotoxin. This has been known for over 100 years. And what safety studies have ever been done about the possible neurotoxic interaction/synergism of thimerosal and aluminum?


Philip Rudnick, PhD

Professor Emeritus, Chemistry

West Chester University of Pennsylvania


Some Refences:

Redhead K, Quinlan GJ, Das RG, Gutteridge JM. Pharmacol Toxicol 1992 Apr;70(4):278-80.

Aluminium-adjuvanted vaccines transiently increase aluminium levels in murine brain tissue.

Division of Bacteriology, National Institute for Biological Standards and Control, Herts., UK.

Aluminum is widely used as an adjuvant in human vaccines, and children can often receive up to 3.75 mg of parenteral aluminum during the first six months of life. We show that intraperitoneal injection of aluminum adsorbed vaccines into mice causes a transient rise in brain tissue aluminum levels peaking around the second and third day after injection. This rise is not seen in the saline control group of animals or with vaccine not containing aluminum. It is likely that aluminum is transported to the brain by the iron-binding protein transferrin and enters the brain via specific transferrin receptors. PMID: 1608913, UI: 92302160



Gupta RK, Relyveld EH.

Adverse reactions after injection of adsorbed diphtheria-pertussis-tetanus (DPT) vaccine are not due only to pertussis organisms or pertussis components in the vaccine.

Vaccine. 1991 Oct;9(10):699-702. Review.PMID: 1759487; UI: 92101590

Aluminum compounds such as aluminum phosphate and aluminum hydroxide are the most commonly used adjuvants with vaccines for human use. Due to the increasing concern about the toxicity of aluminum, other adjuvants like calcium phosphate may be evaluated as an alternative to aluminum adjuvants. To minimize reactions after immunization with DPT vaccine due to impurities in the toxoids, the use of toxoided purified toxins is suggested.


Neurotoxicology of the brain barrier system: new implications.

Zheng W.

J Toxicol Clin Toxicol. 2001;39(7):711-9.

College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. wz18@columbia.edu

The concept of a barrier system in the brain has existed for nearly a century. The barrier that separates the blood from the cerebral interstitial fluid is defined as the blood-brain barrier, while the one that discontinues the circulation between the blood and cerebrospinal fluid is named the blood-cerebrospinal fluid barrier. Evidence in the past decades suggests that brain barriers are subject to toxic insults from neurotoxic chemicals circulating in blood. The aging process and some disease states render barriers more vulnerable to insults arising inside and outside the barriers. The implication of brain barriers in certain neurodegenerative diseases is compelling, although the contribution of chemical-induced barrier dysfunction in the etiology of any of these disorders remains poorly understood. This review examines what is currently understood about brain barrier systems in central nervous system disorders by focusing on chemical-induced neurotoxicities including those associated with nitrobenzenes, N-methyl-D-aspartate, cyclosporin A, pyridostigmine bromide, aluminum, lead, manganese, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, and 3-nitropropionic acid. Contemporary research questions arising from this growing understanding show enormous promises for brain researchers, toxicologists, and clinicians.


Aluminum, NO, and nerve growth factor neurotoxicity in cholinergic neurons.

Szutowicz A.

J Neurosci Res. 2001 Dec 1;66(5):1009-18.

Chair of Clinical Biochemistry, Department of Laboratory Medicine, Medical University of Gdańsk, Debinki 7, 80-211 Gdańsk, Poland. aszut@amg.gda.pl

Several neurotoxic compounds, including Al, NO, and beta-amyloid may contribute to the impairment or loss of brain cholinergic neurons in the course of various neurodegenerative diseases. Genotype and phenotypic modifications of cholinergic neurons may determine their variable functional competency and susceptibility to reported neurotoxic insults. Hybrid, immortalized SN56 cholinergic cells from mouse septum may serve as a model for in vitro cholinotoxicity studies. Differentiation by various combinations of cAMP, retinoic acid, and nerve growth factor may provide cells of different morphologic maturity as well as activities of acetylcholine and acetyl-CoA metabolism. In general, differentiated cells appear to be more susceptible to neurotoxic signals than the non-differentiated ones, as evidenced by loss of sprouting and connectivity, decreases in choline acetyltransferase and pyruvate dehydrogenase activities, disturbances in acetyl-CoA compartmentation and metabolism, insufficient or excessive acetylcholine release, as well as increased expression of apoptosis markers. Each neurotoxin impaired both acetylcholine and acetyl-CoA metabolism of these cells. Activation of p75 or trkA receptors made either acetyl-CoA or cholinergic metabolism more susceptible to neurotoxic influences, respectively. Neurotoxins aggravated detrimental effects of each other, particularly in differentiated cells. Thus brain cholinergic neurons might display a differential susceptibility to Al and other neurotoxins depending on their genotype or phenotype-dependent variability of the cholinergic and acetyl-CoA metabolism.

Copyright 2001 Wiley-Liss, Inc.


Aluminium impairs the glutamate-nitric oxide-cGMP pathway in cultured neurons and in rat brain in vivo: molecular mechanisms and implications for neuropathology.

Canales JJ, Corbalan R, Montoliu C, Llansola M, Monfort P, Erceg S, Hernandez-Viadel M, Felipo V.

J Inorg Biochem. 2001 Nov;87(1-2):63-9.

Laboratory of Neurobiology, Instituto de Investigaciones Citológicas, Fundación Valenciana de Investigaciones Biomédicas, Amadeo de Saboya 4, 46010 Valencia, Spain.

Aluminium (Al) is a neurotoxicant and appears as a possible etiological factor in Alzheimer's disease and other neurological disorders. The mechanisms of Al neurotoxicity are presently unclear but evidence has emerged suggesting that Al accumulation in the brain can alter neuronal signal transduction pathways associated with glutamate receptors. In cerebellar neurons in culture, long term-exposure to Al added 'in vitro' impaired the glutamate-nitric oxide (NO)-cyclic GMP (cGMP) pathway, reducing glutamate-induced activation of NO synthase and NO-induced activation of the cGMP generating enzyme, guanylate cyclase. Prenatal exposure to Al also affected strongly the function of the glutamate-NO-cGMP pathway. In cultured neurons from rats prenatally exposed to Al, we found reduced content of NO synthase and of guanylate cyclase, and a dramatic decrease in the ability of glutamate to increase cGMP formation. Activation of the glutamate-NO-cGMP pathway was also strongly impaired in cerebellum of rats chronically treated with Al, as assessed by in vivo brain microdialysis in freely moving rats. These findings suggest that the impairment of the Glu-NO-cGMP pathway in the brain may be responsible for some of the neurological alterations induced by Al.


Effects of aluminium exposure on brain glutamate and GABA systems: an experimental study in rats.

Nayak P, Chatterjee AK.

Food Chem Toxicol. 2001 Dec;39(12):1285-9.

Biochemistry and Nutrition Research Laboratory, Department of Physiology, University of Calcutta, 92 A.P.C. Road, 700 009, Calcutta, India. nprasunpriya@hotmail.com

It has been postulated that the neurotoxic effects of aluminium could be mediated through glutamate, an excitatory amino acid. Hence the effects of aluminium administration (at a dose of 4.2mg/kg body weight daily as aluminium chloride, hexahydrate, intraperitoneally, for 4 weeks) on glutamate and gamma-amino butyrate (GABA), an inhibitory amino acid, and related enzyme activities in different regions of the brain were studied in albino rats. The glutamate level increased significantly in the cerebrum, thalamic area, midbrain-hippocampal region and cerebellum in response to in vivo aluminium exposure. The aluminium insult also caused significant increases in glutamate alpha-decarboxylase activity in all the brain regions. However, on aluminium insult, the GABA content was not significantly changed except in the thalamic area, where it was elevated. On the contrary, the GABA-T activities of all the regions were reduced significantly in all regions except the midbrain-hippocampal region. However, the succinic semi-aldehyde content of all brain regions increased, often significantly. The aluminium-induced modification of the enzyme activities may be either due to the direct impact of aluminium or due to aluminium-induced changes in the cellular environment. The aluminium-induced differential regional accumulation of glutamate or other alterations in enzymes of the glutamate-GABA system may be one of the causes of aluminium-induced neurotoxicity.


Dementia in patients undergoing long-term dialysis: aetiology, differential diagnoses, epidemiology and management.

Rob PM, Niederstadt C, Reusche E.

CNS Drugs. 2001;15(9):691-9.

Nephrologisches Zentrum am Klinikum Süd, Kalhlhorststrasse 31, D-23552 Lübeck, Germany. prof-rob@gmx.de

Dementia in patients undergoing long-term dialysis has not been clearly defined; however, four different entities have been described. Uraemic encephalopathy is a complication of uraemia and responds well to dialysis. Dialysis encephalopathy syndrome, the result of acute intoxication of aluminium caused by the use of an aluminium-containing dialysate, was a common occurrence prior to 1980. However, using modern techniques of water purification, such acute intoxication can now be avoided. Dialysis-associated encephalopathy/dementia (DAE) is always associated with elevated serum aluminium levels. Pathognomonic morphological changes in the brain have been described, but the mechanism for the entry of aluminium into the CNS is incompletely understood. The mechanisms involved in the pathogenesis of the neurotoxicity associated with aluminium are numerous. Although only a very small fraction of ingested aluminium is absorbed, the continuous oral aluminium intake from aluminium-based phosphate binders, and also of dietary or environmental origin, is responsible for aluminium overload in dialysis patients. Age-related dementia, especially vascular dementia, occurs in patients undergoing long-term dialysis as frequently as it does in the general population. The differential diagnoses of dialysis-associated dementias should include investigation for metabolic encephalopathies, heavy metal or trace element intoxications, and distinct structural neurological lesions such as subdural haematoma, normal pressure hydrocephalus, stroke and, particularly, hypertensive encephalopathy and multi-infarct dementia. To prevent DAE, dietary training programmes should aim to achieve the lowest phosphate intake and pharmacological tools should be used to keep serum phosphate levels below 2 mmol/L. To prevent vascular dementia, lifestyle modification should be undertaken, including optimal physical activity and fat intake, nicotine abstinence, and targeting optimal blood glucose, cholesterol and triglyceride levels, and blood pressure, to those outlined in current recommendations.


The toxicology of aluminum in the brain: a review.

Yokel RA.

Neurotoxicology. 2000 Oct;21(5):813-28.

College of Pharmacy and Graduate Center for Toxicology, University of Kentucky Medical Center, Lexington, USA. ryokel1@pop.uky.edu

Aluminum is environmentally ubiquitous, providing human exposure. Usual human exposure is primarily dietary. The potential for significant Al absorption from the nasal cavity and direct distribution into the brain should be further investigated. Decreased renal function increases human risk of Al-induced accumulation and toxicity. Brain Al entry from blood may involve transferrin-receptor mediated endocytosis and a more rapid process transporting small molecular weight Al species. There appears to be Al efflux from the brain, probably as Al citrate. There is prolonged retention of a fraction of Al that enters the brain, suggesting the potential for accumulation with repeated exposure. Al is a neurotoxicant in animals and humans. It has been implicated in the etiology of sporadic Alzheimer's disease (AD) and other neurodegenerative disorders, although this is highly controversial. This controversy has not been resolved by epidemiological studies, as only some found a small association between increased incidence of dementia and drinking water Al concentration. Studies of brain Al in AD have not produced consistent findings and have not resolved the controversy. Injections of Al to animals produce behavioral, neuropathological and neurochemical changes that partially model AD. Aluminum has the ability to produce neurotoxicity by many mechanisms. Excess, insoluble amyloid beta protein (A beta) contributes to AD. Aluminum promotes formation and accumulation of insoluble A beta and hyperphosphorylated tau. To some extent, Al mimics the deficit of cortical cholinergic neurotransmission seen in AD. Al increases Fe-induced oxidative injury. The toxicity of Al to plants, aquatic life and humans may share common mechanisms, including disruption of the inositol phosphate system and Ca regulation. Facilitation of Fe-induced oxidative injury and disruption of basic cell processes may mediate primary molecular mechanisms of Al-induced neurotoxicity. Avoidance of Al exposure, when practical, seems prudent.


Aluminum neurotoxicity in preterm infants receiving intravenous-feeding solutions.

Bishop NJ, Morley R, Day JP, Lucas A.

N Engl J Med. 1997 May 29;336(22):1557-61.

Comment in:

N Engl J Med. 1997 Oct 9;337(15):1090-1 PMID: 9324646

Medical Research Council (MRC) Dunn Nutrition Unit, Cambridge, United Kingdom.

BACKGROUND: Aluminum, a contaminant of commercial intravenous-feeding solutions, is potentially neurotoxic. We investigated the effect of perinatal exposure to intravenous aluminum on the neurologic development of infants born prematurely. METHODS: We randomly assigned 227 premature infants with gestational ages of less than 34 weeks and birth weights of less than 1850 g who required intravenous feeding before they could begin enteral feeding to receive either standard or specially constituted, aluminum-depleted intravenous-feeding solutions. The neurologic development of the 182 surviving infants who could be tested was assessed by using the Bayley Scales of Infant Development at 18 months of age. RESULTS: The 90 infants who received the standard feeding solutions had a mean (+/-SD) Bayley Mental Development Index of 95+/-22, as compared with 98+/-20 for the 92 infants who received the aluminum-depleted solutions (P=0.39). In a planned subgroup analysis of infants in whom the duration of intravenous feeding exceeded the median and who did not have neuromotor impairment, the mean values for the Bayley Mental Development Index for the 39 infants who received the standard solutions and the 41 infants who received the aluminum-depleted solutions were 92+/-20 and 102+/-17, respectively (P=0.02). The former were significantly more likely (39 percent, vs. 17 percent of the latter group; P=0.03) to have a Mental Development Index of less than 85, increasing their risk of subsequent educational problems. For all 157 infants without neuromotor impairment, increasing aluminum exposure was associated with a reduction in the Mental Development Index (P=0.03), with an adjusted loss of one point per day of intravenous feeding for infants receiving the standard solutions. CONCLUSIONS: In preterm infants, prolonged intravenous feeding with solutions containing aluminum is associated with impaired neurologic development.


Aluminum neurotoxicity in experimental animals.

Erasmus RT, Savory J, Wills MR, Herman MM.

Ther Drug Monit. 1993 Dec;15(6):588-92.

Department of Pathology, University of Virginia Health Sciences Center, Charlottesville 22908.

Neurotoxic effects of aluminum (Al) were recognized > 100 years ago, but have only recently been studied in detail. By far, the most dramatic effect of Al is that of producing intraneuronal perikaryal neurofilamentous aggregates, which consist of phosphorylated neurofilaments. Several species have been used to demonstrate this effect, rabbit being most common; the effect also is seen in in vitro systems. Besides its role in producing neurofibrillary pathology, Al appears to modify the blood-brain barrier and exert cholinergic and noradrenergic effects. Possible mechanisms of Al neurotoxicity could be related to cell damage via free radical production, impairment of glucose metabolism, and effects on signal transduction.


Effects of metals on the nervous system of humans and animals.

Carpenter DO.

Int J Occup Med Environ Health. 2001;14(3):209-18.

School of Public Health University at Albany Rensselaer, NY 12144, USA.

Several metals have toxic actions on nerve cells and neurobehavorial functioning. These toxic actions can be expressed either as developmental effects or as an increased risk of neurodegenerative diseases in old age. The major metals causing neurobehavioral effects after developmental exposure are lead and methylmercury. Lead exposure in young children results in a permanent loss of IQ of approximately 5 to 7 IQ points, and also results in a shortened attention span and expression of anti-social behaviors. There is a critical time period (<2 years of age) for development of these effects, after which the effects do not appear to be reversible even if blood lead levels are lowered with chelation. Methylmercury has also been found to have effects on cognition at low doses, and prenatal exposure at higher levels can disrupt brain development. Metals have also been implicated in neurodegenerative diseases, although it is unlikely that they are the sole cause for any of them. Elevated aluminum levels in blood, usually resulting from kidney dialysis at home with well water containing high aluminum, result in dementia that is similar to but probably different from that of Alzheimer's disease. However, there is some epidemiological evidence for elevated risk of Alzheimer's in areas where there is high concentration of aluminum in drinking water. Other metals, especially lead, mercury, manganese and copper, have been implicated in amvotrophic lateral sclerosis and Parkinson's disease.



Cancer in Cats and Dogs
In pets, researchers have working models for human diseases

The Scientist 14[11]:18, May. 29, 2000


Vaccine-Associated Feline Sarcoma

All of the above methods could find their ways into human cancer treatment regimens. But there is one baffling cancer that is uniquely feline and for which the specific etiology is unknown: vaccine-associated feline sarcoma.

As any cat owner knows, cats receive two or three combination vaccinations during their first year of life and then, depending on the vaccine and the recommendation of the veterinarian, annual vaccination against some infections and triennial vaccination against others. This works out to a lot of vaccinations during the approximately 12-year lifespan of the average cat. In 1991, University of Pennsylvania School of Veterinary Medicine pathologist Mattie Hendrick coauthored a letter to the editor in the Journal of the American Veterinary Medical Association1 describing increased numbers of fibrosarcomas in the interscapular area in cats seen by her service at the university. Cats usually are vaccinated over their shoulder blades.

"She was finding increased inflammatory reaction at the sites and also found foreign material," notes James R. Richards, director of the Cornell Feline Health Center at Cornell's College of Veterinary Medicine. He is one of 10 members of a group organized to aid in investigating and preventing these malignancies and educating veterinarians and the public about them: the Vaccine-Associated Feline Sarcoma Task Force (VAFSTF). "This was indeed a foreign substance that contained aluminum and oxygen," says Richards. Aluminum is a common adjuvant in vaccines. But, Richards adds, it's not known "if this is a cause-and-effect situation or whether the adjuvant was there and showed up" but did not cause the tumors.

Veterinary oncologist Barbara E. Kitchell of the University of Illinois College of Veterinary Medicine in Urbana, who has been studying the etiopathogenesis of these tumors, notes that they have been reported to occur "as close as one month after vaccination and after 10 years. Ninety percent of cats who develop tumors do so within four years of vaccine; 59 percent developed within one year."

There have been a number of theories about what is causing these tumors, from macrophage ingestion of aluminum resulting in fibroblast production to activation of exogenous or endogenous (within the feline genome) retroviral elements, to mutations of the p53 gene predisposing some cats to develop these tumors.

Kass has been studying the epidemiology of the tumors with financial support from VAFSTF. (VAFSTF awards grants for research from money donated by vaccine companies, especially Pfizer Animal Health, veterinary associations such as the American Animal Hospital Association Foundation, and research groups such as the Cornell Feline Health Center.) Although he has not yet analyzed the data--supplied by several hundred veterinarians who have reported on the numbers, types, and brands of vaccines used; their vaccination technique; and any adverse effects--he estimates that between one and three cats per 10,000 develop vaccine-associated sarcoma per year. One of the problems in even estimating the extent of the problem is "the underreporting is just vast."

In 1994, the U.S. Pharmacopeia (USP), Rockville, Md., a nonprofit public health organization, launched the Veterinary Practitioners' Reporting Program to which veterinarians could report adverse events and other problems associated with the use of vaccines, drugs, and pesticides in animals. Reporting is purely voluntary, and the information veterinarians supply on vaccine-associated sarcomas to the USP is limited to the last vaccine given at the site of sarcoma development, notes veterinarian E. Kathryn Meyer, who coordinates the program. From April 30, 1996, through May 8, 2000, veterinarians reported 586 cases of vaccine-associated sarcomas in cats to the USP, says Meyer. "Not every sarcoma that develops is reported," she says. But 190 veterinarians reporting these sarcomas to USP in 1998 and early 1999 were invited to enroll in Kass' epidemiological study, and 72 participated.

"Cats," Kass observes, "are totally different organisms than dogs. They just react strangely to chemicals," differently from dogs, horses, other animals, and humans. Yet the desire to find cures to human disease is a big motivator for veterinary oncologists. Says MacEwen: "They [the dog and the cat] provide an opportunity for enhancing the effectiveness of treatment in humans. That's why I went into the field in the first place."

Myrna E. Watanabe is editor of Cornell University's newsletters for pet owners, CatWatch and DogWatch.

1. M. Hendrick and M.H. Goldschmidt, "Do injection site reactions induce fibrosarcomas in cats?" Journal of the American Veterinary Medical Association, 199:968, 1991.


Back Home Up Next