al = aluminum - a toxic element - linked to many diseases in humans

11/13/15 12:01 PMAl = Aluminum - a Toxic Element - Linked to many diseases in humans

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Al Aluminum

atomic no. 13, atomic wt. 26.98, metal, row 4, col.3A, val. 3, orbits 2-8-3

{Merck Index - © 1952 by Merck & Co., Inc.}

Aluminum. Al; at. wt. 26.98; at. no. 13; valence 3. Discovered by Wöhler in 1827. Obtained from cryolite(double sod. and aluminum fluoride) or bauxite (native aluminum hydroxide) by electrolysis in electricfurnace.

Tin-white, malleable, ductile metal, with somewhat bluish tint; capable of taking brilliant polish which isretained in dry air. In moist air gradually oxidizes superficially. Available in bars, leaf, powder, sheets orwire. d. 2.70. m. 660°. b. 1800°. Does not vaporize even at high temps., but finely divided aluminum dust iseasily ignited, and may cause explosions. Soluble in dil. HCl, H2SO4, in soln. KOH and NAOH withevolution of hydrogen; almost insoluble in HNO3 or acetic acid when hot.

Reduces the cations of many heavy metals to the metallic state. Solns. of the metal in dil. HCl or neutralor slightly acid solns. of most aluminum salts, yield with Na2S a white ppt. soluble in excess of Na2S. Dil.neutral soln. of aluminum salts yield white gelatinous ppt. on boiling with sod. acetate.

Use: As the pure metal or as alloys (magnalium, aluminum bronze, etc.) for aircraft, utensils, apparatus,electrical conductors; instead of copper in dental alloys. The coarse powder is used in aluminothermics(thermite process); the fine powder as flashlight in Photography, in explosives, fireworks and inaluminum paints; for absorbing occluded gases in manuf. of steel. In testing for Au, As, Hg; coagulatingcolloidal solns. of As or Sb; pptg. Cu; reducer for determining nitrates and nitrites; instead of Zn forgenerating hydrogen in testing for As.

Grades available: Reagent, technical.

Med. Use: Inhalation of finely divided aluminum dust proposed as a means of "binding" silica to preventand reverse lung changes caused by silica dust.

Aluminum ToxicityThe following information was compiled and submitted by Frank Hartman.

"From the earliest days of food regulation, the use of alum (aluminum sulphate) in foods has beencondemned. It is universally acknowledged as a poison in all countries. If the Bureau of Chemistry hadbeen permitted to enforce the law ... no food product in the country would have any trace of ... anyaluminum or saccarin. No soft drink would contain caffeine or hebromin; no bleached flour would be ininterstate commerce. Our food and drugs would be wholly without adulteration ... and the health of ourpeople would be vastly improved and their life greatly extended."

From History of crime against the Food Laws (1929) by Dr. Wiley, the prime mover behind the originalPure Food Law and Director of the FDA. He resigned in disgust in 1912 over exceptions granted to thelaw and lack of enforcement.

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Aluminum has been exempted from tesitng for safety by the FDA under a convoluted logic wherein it isclassified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety andthere are NO restrictions whatever on the amount or use of aluminum.

There are over 2000 references in the National Library of Medicine on adverse effects of alumium. Thefollowing were extracted to provide a small sample of the range of toxicity of aluminum.

Chemical Registry

Aluminum toxicity has been recognized in many settings where exposure is heavy or prolonged, whererenal function is limited, or where apreviously accumulated bone burden is released in stress or illness.Toxicity may include: encephalopathy (stuttering, gait disturbance, myoclonic jerks, seizures, coma,abnormal EEG) osteomalacia or aplastic bone disease ( associated with painful spontaneous fractures,hypercalcemia, tumorous calcinosis ) proximal myopathy, increased risk of infection, increased leftventricular mass and decreased myocardial function microcytic anemia with very high levels, suddendeath.

Aluminum is ubiquitous in our environment; it is the third most prevalent element in the earth's crust.The gastrointestinal tract is relatively impervious to aluminum, absorption normally being only about 2%.Aluminum is absorbed by a mechanism related to that for calcium. Gastric acidity and oral citrate favorsabsorption, and H2-blockers reduce absorption. As is true for several trace elements, transferrin is theprimary protein binder and carrier for aluminum in the plasma, where 80% is protein bound and 20% isfree or complexed to small molecules such as citrate.

Cells appear to take up aluminum from transferrin rather than from citrate. Purified preparations offerritin from brain and liver have been found to contain aluminum.

It is not known if ferritin has a specific binding site for aluminum. Factors regulating the migration ofaluminum across the blood–brain barrier are not well understood.

Serum aluminum correlates with encephalopathy; red cell aluminum correlates with microcytic anemia,and bone aluminum correlates with aluminum bone disease.

Basal PTH when elevated appears to protect bone and thereby favor CNS toxicity.

Other factors favoring one form of toxicity over another are not well understood.

Aluminum toxicity has been reported to impair the formation and release of parathyroid hormone. Theparathyroid glands concentrate aluminum above levels in surrounding tissues. Treatment of aluminumtoxicity in renal failure patients often reactivates hyperparathyroidism, which to a certain extent is helpfulfor bone remodeling and healing.

Distilled Water Placed in Various Containers



Distilled water was placed in metal containers and the amount of the "Metal Can" thatdisolved into the distilled water was measured daily using Specific Conductance readings.You can divide the SC number by 2 to get the approxamite amount of atoms in ppm ( mg / l ).

4 ppm of aluminum in human blood can cause it to colagulate. Aluminum in humans is documented to Inhibit Learning. See Below ...

Aluminum neurotoxicity in preterm infants receiving intravenous-feeding solutions.

Bishop N.J. – Morley R. – Day J.P. – Lucas A.

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

Aluminum, a contaminant of commercial intravenous–feeding solutions, is potentially neurotoxic. Weinvestigated the effect of perinatal exposure to intravenous aluminum on the neurologic development ofinfants born prematurely.

RESULTS: The 90 infants who received the standard feeding solutions had a mean (± SD) Bayley MentalDevelopment Index of 95 ±22, as compared with 98 ±20 for the 92 infants who received the aluminum-depleted solutions (P=0.39). The former were significantly more likely (39 percent, vs. 17 percent of thelatter group; P=0.03) to have a Mental Development Index of less than 85, increasing their risk ofsubsequent educational problems. For all 157 infants without neuromotor impairment, increasingaluminum exposure was associated with a reduction in the Mental Development Index (P=0.03), with anadjusted loss of one point per day of intravenous feeding for infants receiving the standard solutions. Inpreterm infants, prolonged intravenous feeding with solutions containing aluminum is associated with

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impaired neurologic development.

Aluminum-containing emboli in infants treated with extracorporeal membrane oxygenation.

Vogler C. – Sotelo-Avila C. – Lagunoff D. – Braun P. – Schreifels J.A. – Weber T.

From: N Engl J Med (1988 Jul 14) 319(2):75-9

We found fibrin thrombi or thromboemboli at autopsy in 22 of 23 infants with respiratory failure who hadbeen treated with venoarterial extracorporeal membrane oxygenation (ECMO). In addition, distinctivebasophilic aluminum-containing emboli were found in 12 of the infants; the distribution of these emboliwas similar to that of the thromboemboli, except that an aluminum-containing embolus was found in alung in only 1 infant. Sixteen infants had pulmonary thrombi or thromboemboli. We also found friablealuminum-containing concretions adhering loosely to the mixing rods of heat exchangers that had beenused to warm the blood flowing through the ECMO circuit; such concretions were not present on unusedmixing rods. We propose that these aluminum-containing concretions developed as the silicone coatingof the heat exchanger wore away and aluminum metal was exposed to warm, oxygenated blood and thatfragments of aluminum-containing concretions formed emboli. This hypothesis is supported by the factthat aluminum-containing emboli were generally not present in the lungs, which are bypassed by ECMO.

Sequential serum aluminum and urine aluminum: creatinine ratio and tissue aluminum loading in infantswith fractures/rickets.

Koo W.W. – Krug-Wispe S.K. – Succop P. – Bendon R. – Kaplan L.A.

From: Pediatrics (1992 May) 89(5 Pt 1):877-81

Aluminum toxicity is associated with the development of bone disorders, including fractures, osteopenia,and osteomalacia. Fifty-one infants with a mean (± SEM) birth weight of 1007 ±34 g, gestational age of28.5 +/-0.3 weeks, and serial radiographic documentation at 3, 6, 9, and 12 months for the presence (n =16) or absence (n = 35) of fractures and/or rickets were studied at the same intervals to determine theserial changes in serum aluminum concentrations and urine aluminum-creatinine ratios. Autopsy bonesamples were used to determine the presence of tissue aluminum. One infant who received aluminum-containing antacid had marked increase in serum aluminum to 83 micrograms/L while urine aluminum-creatinine ratio increased from 0.09 to a peak of 8.53. Vertebrae from three infants at autopsy (full enteralfeeding was tolerated for 37 and 41 days in two infants, respectively) showed aluminum deposition in thezone of provisional calcification and along the newly formed trabecula.

Aluminum in parenteral solutions revisited — again.

Klein G.L.

From: Am J Clin Nutr (1995 Mar) 61(3):449-56

It has been a dozen years since aluminum was first shown to contaminate parenteral nutrition solutionsand to be a contributing factor in the pathogenesis of metabolic bone disease in parenteral nutritionpatients as well as in uremic patients. However, there are no regulations in place to effectively reducealuminum contamination of various parenterally administered nutrients, drugs, and biologic products.The purpose of this review is fourfold: 1.) to summarize our knowledge of the adverse effects ofaluminum on bone formation and mineralization in parenteral nutrition patients; 2.) to discuss thepossible role of aluminum in the osteopenic bone disease of preterm infants; 3.) to show how lack ofregulations covering aluminum content of parenteral solutions can lead to vulnerability of new groups of



patients to aluminum toxicity, the example being given here is that of burn patients

Aluminum-induced anemia.

From: Am J Kidney Dis (1985 Nov) 6(5):348-52

... many questions still remain unanswered, it is clear that aluminum causes a microcytichypoproliferative anemia and is a factor responsible for worsening anemia in patients with end-stagerenal disease.

Arch Dermatol (1984 Oct) 120(10):1318-22

Three patients had subcutaneous nodules at the sites of previous injections of vaccine containingtetanus toxoid, showed aluminum crystals in the nodules from two patients. From the evidence available,we believe that these nodules are a complication of inoculations with aluminum-containing vaccines.

Persistent subcutaneous nodules in patients hyposensitized with aluminum-containing allergen extracts.

Garcia-Patos V. – Pujol R.M. – Alomar A. – Cistero A. – Curell R. – Fernandez-Figueras M.T. – de MoragasJ.M.

From: Arch Dermatol (1995 Dec) 131(12):1421-4

These lesions have been mainly attributed to a hypersensitivity reaction to aluminum hydroxide, which isused as an absorbing agent in many vaccines and hyposensitization preparations. Patch tests withstandard antigens and aluminum compounds and histopathologic and ultrastructural studies wereperformed on 10 patients with persistent subcutaneous nodules on the upper part of their arms afterinjection of aluminum-adsorbed dust and/or pollen extracts. The nodules appeared 1 month to 6.5 yearsafter injections.

Trace metals and degenerative diseases of the skeleton.

Savory J. – Bertholf R.L. – Wills M.R.

From: Acta Pharmacol Toxicol (Copenh) (1986) 59 Suppl 7:282-8

Aluminum related osteodystrophy is the most important manifestation of trace metal toxicity related todegenerative diseases of the skeleton.

Postvaccinal sarcomas in the cat: epidemiology and electron probe microanalytical identification ofaluminum.

Hendrick M.J. – Goldschmidt M.H. – Shofer F.S. – Wang Y.Y. – Somlyo A.P.

From: Cancer Res (1992 Oct 1) 52(19):5391-4

An increase in fibrosarcomas in a biopsy population of cats in the Pennsylvania area appears to berelated to the increased vaccination of cats following enactment of a mandatory rabies vaccination law.

The majority of fibrosarcomas arose in sites routinely used by veterinarians for vaccination, and 42 of198 tumors were surrounded by lymphocytes and macrophages containing foreign material identical to



that previously described in postvaccinal inflammatory injection site reactions. Some of the vaccinesused have aluminum-based adjuvants, and macrophages surrounding three tumors contained aluminumoxide identified by electron probe microanalysis and imaged by energy-filtered electron microscopy.Persistence of inflammatory and immunological reactions associated with aluminum may predispose thecat to a derangement of its fibrous connective tissue repair response, leading to neoplasia.

Aspects of aluminum toxicity.

Hewitt C.D. – Savory J. – Wills M.R.

From: Clin Lab Med (1990 Jun) 10(2):403-22

Attention was first drawn to the potential role of aluminum as a toxic metal over 50 years ago, but wasdismissed as a toxic agent as recently as 15 years ago. The accumulation of aluminum, in some patientswith chronic renal failure, is associated with the development of toxic phenomena; dialysisencephalopathy, osteomalacic dialysis osteodystrophy, and an anemia. Aluminum accumulation alsooccurs in patients who are not on dialysis, predominantly infants and children with immature or impairedrenal function. Aluminum has also been implicated as a toxic agent in the etiology of Alzheimer'sdisease, Guamiam amyotrophic lateral sclerosis, and parkinsonism-dementia.

Soft tissue sarcoma associated with aluminum oxide ceramic total hip arthroplasty. A case report.

Ryu R.K. – Bovill E.G. Jr – Skinner H.B. – Murray W.R.

From: Clin Orthop (1987 Mar)(216):207-12

Malignant tumors around fracture fixation implants have been reported sporadically for many years.Recently, however, reports of sarcomatous degeneration around a standard cemented hip arthroplastyand around cobalt-chromium-bearing hip arthroplasties raise new questions of the malignant potential ofmetallic ends prostheses. Sarcomatous changes around aluminum oxide ceramics seem not to havebeen reported in the literature. The present report may be the first documented case of an aggressive softtissue sarcoma detected 15 months after the patient had an uncemented ceramic total hip arthroplasty. Ifa causal relationship exists, the incidence of this phenomenon in the United States is 250 times greaterthan would be expected from statistics on soft tissue sarcoma at the hip.

Aluminum-induced granulomas in a tattoo.

McFadden N. – Lyberg T. – Hensten-Pettersen A.

From: J Am Acad Dermatol (1989 May) 20(5 Pt 2):903-8

Aluminum was the only nonorganic element present in the test site tissue. This is the first report ofconfirmed aluminum-induced, delayed-hypersensitivity granulomas in a tattoo.

Delayed healing in full-thickness wounds treated with aluminum chloride solution. A histologic study withevaporimetry correlation.

Sawchuk W.S. – Friedman K.J. – Manning T. – Pinnell S.R.

From: J Am Acad Dermatol (1986 Nov) 15(5 Pt 1):982-9



Wounds were treated either with 30% aluminum chloride solution or ferric subsulfate solution or wereallowed to clot with minimal pressure from a gauze pad. Delay in reepithelialization was notedhistologically both in wounds treated with aluminum chloride and in those treated with ferric subsulfatecompared to controls. Presumably this delay was the result of tissue necrosis caused by thesehemostatic agents, resulting in slightly larger and less cosmetically acceptable scars. Plots ofevaporimetry data revealed a biphasic pattern of water loss during healing, with an initial rapid decline inwater loss followed by a much slower decline.

Aluminium and injection site reactions.

Culora G.A. – Ramsay A.D. – Theaker J.M.

From: J Clin Pathol (1996 Oct) 49(10):844-7

To alert pathologists to the spectrum of histological appearances that may be seen in injection sitereactions related to aluminium, showed unusual features not described previously. In one, there was asclerosing lipogranuloma-like reaction with unlined cystic spaces containing crystalline material. Theother case presented as a large symptomatic subcutaneous swelling which icroscopically showeddiffuse and wide-spread involvement of the subcutis by a lymphoid infiltrate with prominent lymphoidfollicles.

CONCLUSIONS: This report highlights the changes encountered in aluminium injection site reactions andemphasises that the lesions have a wider range of histological appearances than described previously.

Aluminum and gallium arrest formation of cerebrospinal fluid by the mechanism of OH- depletion.

Vogh B.P. – Godman D.R. – Maren T.H.

From: J Pharmacol Exp Ther (1985 Jun) 233(3):715-21

AlCl3 or GaCl3 was added to artificial cerebrospinal fluid and perfused through the cerebral ventricles ofthe rat. Depending on the metal and its concentration (1-10 mM) the pH of the perfusate ranged from 7.2to 3.5. At 10 mM metal chloride, yielding pH 4.7 (Al) or 3.5 (Ga), formation of cerebrospinal fluid wassuppressed 100%. This mechanism may also account for the antiperspirant action of Al salts.

Aluminum toxicity and albumin.

Kelly A.T. – Short B.L. – Rains T.C. – May J.C. – Progar J.J.

From: ASAIO Trans (1989 Jul-Sep) 35(3):674-6

During a study of priming solutions for extracorporeal membrane oxygenation (ECMO) in the intensivecare nursery, it was discovered that those solutions using certain brands of 25% albumin containedaluminum levels within the toxic range. When the brand was changed to a brand known to have a loweraluminum (Al) content, a marked drop in priming solution Al levels was measured.

The role of aluminium for adverse reactions and immunogenicity of diphtheria-tetanus booster vaccine.

Mark A. – Granstrom M.

From: Acta Paediatr (1994 Feb) 83(2):159-63



235 schoolchildren aged 10 years received either a regular, aluminium-adsorbed diphtheria-tetanusvaccine or the same vaccine in fluid form, in order to investigate if local side effects could be diminishedby exclusion of aluminium. System reactions were rare and local reactions frequent in both groups butlarger local reactions were even more pronounced in the non-adsorbed vaccine group.

Potroom palsy? Neurologic disorder in three aluminum smelter workers.

Heyer N.J.

From: Arch Intern Med (1985 Nov) 145(11):1972-5

We studied three patients with a progressive neurologic disorder, all of whom had worked for over 12years in the same potroom of an aluminum smelting plant. All had incoordination and an intention tremor.Two of the three patients had cognitive deficits, and the most severely affected patient also had spasticparaparesis. None had involvement of the peripheral nervous system. Despite extensive evaluations, thecause of these patients' problems remains obscure.

Neurotoxic effects of aluminum in animals are directed at the central nervous system, and theoreticallylong-term low-level exposure to aluminum in the potroom could explain the findings in our patients.

Reducing aluminum: an occupation possibly associated with bladder cancer

Theriault G. – De Guire L. – Cordier S.

From: Can Med Assoc J (1981) 124(4):419-422,425

These findings suggest that employment in an aluminum reduction plant accounts for part of the excessof bladder cancer in the region studied. (Author abstract) (85 Refs)

Immunohistochemical study of microtubule-associated protein 2 and ubiquitin in chronically aluminum-intoxicated rabbit brain.

Takeda M. – Tatebayashi Y. – Tanimukai S. – Nakamura Y. – Tanaka T. – Nishimura T.

From: Acta Neuropathol (Berl) (1991) 82(5):346-52

Experimental neurofibrillary change was produced in rabbit brain by daily subcutaneous aluminumtartrate injection for 40 days.

Neurotoxic effects of aluminium on embryonic chick brain cultures.

From: Acta Neuropathol (Berl) (1994) 88(4):359-66

Toxic damage of brain cells by aluminium (Al) is discussed as a possible factor in the development ofneurodegenerative disorders in humans. Effects of Al on cell viability (lysosomal and mitochondrialactivity) and differentiation (synthesis of cell-specific proteins) were found to the brain area specific withthe highest sensitivity observed in optic tectum.

Aluminium in tooth pastes and Alzheimer's disease.



Verbeeck R.M. – Driessens F.C. – Rotgans J.

From: Acta Stomatol Belg (1990 Jun) 87(2):141-4

The role of aluminium from tooth pastes may be even more important than that from the drinking water.

Persistent subcutaneous nodules in children hyposensitized with aluminium-containing allergenextracts.

Frost L. – Johansen P. – Pedersen S. – Veien N. – Ostergaard P.A. – Nielsen M.H.

From: Allergy (1985 Jul) 40(5):368-72

A follow-up study of 202 children who had received hyposensitization with aluminium-containingallergens showed that 1-3 years after cessation of hyposensitization 13 children still hadseverely treatment-resistant subcutaneous nodules in their forearms. Because of their long persistencethe nodules of six children were studied in detail. Histologically, the nodules showed infiltration withlymphocytes (forming germinal centres), macrophages, plasma cells, mast cells and a few eosinophils.

In five patients aluminium crystals were found scattered between the cells and, in addition, thephagosomes of the macrophages contained aluminium. Patch tests for aluminium were positive in four ofthe six patients.

Contact sensitivity to aluminium in a patient hyposensitized with aluminium precipitated grass pollen.

Clemmensen O. – Knudsen H.E.

From: Contact Dermatitis (1980 Aug) 6(5):305-8

Standard patch testing of a patient with eczema revealed positive reactions to the aluminium discs usedfor testing.

Behavioural effects of gestational exposure to aluminium.

Rankin J. – Sedowofia K. – Clayton R. – Manning A.

From: Ann Ist Super Sanita (1993) 29(1):147-52

The involvement of aluminium in the aetiology of a number of human pathological diseases has alteredits status from being a nontoxic, nonabsorbable, harmless element. This maybe of particular concern tothe developing foetus which is more susceptible to agents and at lower levels than the adult. Littleattention has been given to aluminium's potential reproductive toxicity until recently and further researchis required for a full evaluation of its toxicity. Our preliminary results demonstrate behavioural andneurochemical alterations in the offspring of mice exposed to aluminium during gestation. Further, theeffects of such exposure are also present in the adult animal suggesting persistent changes in behaviourfollowing prenatal exposure.

The absence of extracellular calcium potentiates the killing of cultured hepatocytes by aluminummaltolate.

Snyder J.W. – Serroni A. – Savory J. – Farber J.L.



From: Arch Biochem Biophys (1995 Jan 10) 316(1):434-42

This data defines a new model in which aluminum kills liver cells by a mechanisms distinct frompreviously recognized pathways of lethal cell injury. It is hypothesized that aluminum binds tocytoskeletal proteins intimately associated with the plasma membrane. This interaction eventuallydisrupts the permeability barrier function of the cell membrane, an event that heralds the death of thehepatocyte.

Sensitization to aluminium by aluminium-precipitated dust and pollen extracts.

Castelain P.Y. – Castelain M. – Vervloet D. – Garbe L. – Mallet B.

From: Contact Dermatitis (1988 Jul) 19(1):58-60

... the means of sensitization was the inoculation of aluminium-precipitated pollen or dust extracts forhyposensitization. We conclude that aluminium allergy is not exceptional.

Allergy to non-toxoid constituents of vaccines and implications for patch testing.

Cox N.H. – Moss C. – Forsyth A.

From: Contact Dermatitis (1988 Mar) 18(3):143-6

Aluminium allergy causes false positive patch test reactions and we propose methods of patch testingpatients with symptoms at vaccination sites in order to avoid this problem.

Aluminium allergy in patients hyposensitized with aluminium-precipitated antigen extracts.

Lopez S. – Pelaez A. – Navarro L.A. – Montesinos E. – Morales C. – Carda C.

Aluminum precipitated antigen solutions, a small percentage of patients develop persistentsubcutaneous nodules at the injection site; the existence of delayed sensitivity to aluminium has beenimplicated in the pathogenesis of these nodules.

Aluminium allergy.

Veien N.K. – Hattel T. – Justesen O. – Norholm A.

From: Contact Dermatitis (1986 Nov) 15(5):295-7

13 children ranging in age from 1 to 13 years and 1 adult patient had positive patch tests to 2% AlCl3 inwater. 13 of them had pruritic excoriated papules, 9 at sites of hyposensitization therapy with aluminium-bound pollen extracts, and 4 at sites of childhood immunization with an aluminium-bound vaccine (Di-Te-Pol).

Vaccination granulomas and aluminium allergy: course and prognostic factors.

Kaaber K. – Nielsen A.O. – Veien N.K.

From: Contact Dermatitis (1992 May) 26(5):304-6



21 children who had cutaneous granulomas following immunization with a vaccine containing aluminiumhydroxide, and who had positive patch tests to aqueous aluminium chloride and/or to a Finn Chamber,were followed for 1 to 8 years. During the period of observation, the symptoms cleared in 5 children,improved in 11, and remained unchanged in 5.

Short-term experimental acidification of a Welsh stream: toxicity of different forms of aluminium at lowpH to fish and invertebrates.

McCahon C.P. – Pascoe D.

From: Arch Environ Contam Toxicol (1989 Jan-Apr) 18(1-2):233-42

Minimal effects were observed in the control and acid zones whilst large mortalities and reduced feedingwere recorded in the acid and aluminium zone.

H Differentiated neuroblastoma cells are more susceptible to aluminium toxicity than developing cells.

E. Meiri

From: Arch Toxicol (1989) 63(3):231-7

Two specific questions were addressed: 1.) Can differentiated cells maintain their normal excitablefunction when exposed to aluminium? 2.) Can proper development of electrophysiological properties beachieved in its presence? We report that aluminium caused premature onset of deterioration in fullydifferentiated cells. Within 4-6 days they depolarized from -29.3 ±0.9 mV to levels lower than -15 mV;compound polyphasic action potentials were gradually replaced by slow monophasic spikes before thefinal loss of excitable properties and structural deformations was noticed.

Reversal of an aluminum-induced behavioral deficit by administration of deferoxamine.

Connor D.J. – Harrell L.E. – Jope R.S.

From: Behav Neurosci (1989 Aug) 103(4):779-83

The behavioral deficit was not due to nonspecific effects caused by lower fluid consumption. Partialreversal of the deficit was produced by discontinuing aluminum treatment, 2 weeks prior to testing.

Aluminum-induced neurofibrillary degeneration disrupts acquisition of the rabbit's classicallyconditioned nictitating membrane response.

Pendlebury W.W. – Perl D.P. – Schwentker A. – Pingree T.M. – Solomon P.R.

From: Behav Neurosci (1988 Oct) 102(5):615-20

Aluminum intoxicated rabbits, in contrast, did not acquire the conditioned response over the 4 days oftesting. This disruption of conditioning in aluminum-treated rabbits could not be attributed to deficits insensory or motor processes or to illness. Neuropathological analysis revealed widespread neurofibrillarytangle formation in aluminum-treated animals.

Aluminum, a neurotoxin which affects diverse metabolic reactions.



Joshi J.G.

From: Biofactors (1990 Jul) 2(3):163-9

Experimental evidence is summarized to support the hypothesis that chronic exposure to low levels ofaluminum may lead to neurological disorders.

Distribution of aluminum in different brain regions and body organs of rat.

Vasishta R.K. – Gill K.D.

From: Biol Trace Elem Res (1996 May) 52(2):181-92

In the present study, an attempt has been made to investigate the distribution of aluminum in differentregions of brain and body organs of male albino rats, following subacute and acute aluminum exposure.Aluminum was observed to accumulate in all regions of the brain with maximum accumulation in thehippocampus. Aluminum was also seen to compartmentalize in almost all the tissues of the body tovarying extents, and the highest accumulation was in the spleen.

Ti-6Al-4V ion solution inhibition of osteogenic cell phenotype as a function of differentiation timecoursein vitro.

Thompson G.J. – Puleo D.A.

From: Biomaterials (1996 Oct) 17(20):1949-54

These results indicate that ions associated with Ti-6Al-4V alloy inhibited the normal differentiation ofbone marrow stromal cells to mature osteoblasts in vitro, suggesting that ions released from implants invivo may contribute to implant failure by impairing normal bone deposition.

Aluminium release from glass ionomer cements during early water exposure in vitro.

Andersson O.H. – Dahl J.E.

From: Biomaterials (1994 Sep) 15(11):882-8

Aluminium is a major constituent of glass ionomer cements. During mixing and setting aluminium isreleased from the glass into the polyalkeonic acid solution. Part of this aluminium may not combine withthe polyalkeonic acid, but may be released from the cement. The aluminium release from auto-cured andlight-cured glass ionomer cements during early water exposure was studied. The former cementsreleased more aluminium than the latter. It is suggested that the considerable release of aluminium fromglass ionomer cements during early water exposure may explain the reported lack of mineralization ofpredentin in the pulp beneath glass ionomer cements. This would correspond to the inhibiting effect ofaluminium on bone mineralization.

Impaired control of information transfer at an isolated synapse treated by aluminum: is it related todementia?

Banin E. – Meiri H.

From: Brain Res (1987 Oct 13) 423(1-2):359-63



These results indicate that aluminum at concentrations similar to those found in the diseased brain ofdemented patients modulates synaptic transmission.

Chronic aluminum-induced motor neuron degeneration: clinical, neuropathological and molecularbiological aspects.

Strong M.J. – Garruto R.M.

From: Can J Neurol Sci (1991 Aug) 18(3 Suppl):428-31

Aluminum chloride induces aggregates of phosphorylated neurofilament that mimics the intraneuronalinclusions of amyotrophic lateral sclerosis.

Some commonly unrecognized manifestations of metabolic arthropathies.

Cobby M.J. – Martel W.

From: Clin Imaging (1992 Jan-Mar) 16(1):1-14

The metabolic arthropathies are characterized by the deposition of abnormal substances in or aroundjoints. Certain features of some of these arthropathies and their significance have only recently beenrecognized and others have been insufficiently emphasized. An important group of conditions are thearthropathies related to renal failure and its treatment, namely, aluminum toxicity, periarticularcalcification and crystal deposition, hyperparathyroidism, and dialysis-related amyloidosis. Crystaldeposition diseases, specifically, gouty arthritis, calcium pyrophosphate deposition, and calciumhydroxyapatite deposition, are also reviewed.

Sepsis: a cause of aluminum release from tissue stores associated with acute neurological dysfunctionand mortality.

Davenport A. – Williams P.S. – Roberts N.B. – Bone J.M.

From: Clin Nephrol (1988 Jul) 30(1):48-51

We report six cases of patients with renal failure and exposure to aluminum who developed septicemia.In all cases the serum aluminum increased markedly. This may have contributed to the neurologicaldysfunction seen in five, and the deaths of four of the patients. We suggest that the rise in serumaluminum was due to the release of tissue-bound aluminum, resulting in an increase in free, diffusablealuminum and that this jeopardized both neurological function and immunocompetence.

Estimates of dietary exposure to aluminium.

Pennington J.A. – Schoen S.A.

From: Food Addit Contam (1995 Jan-Feb) 12(1):119-28

Daily intakes of aluminium were estimated for 14 age-sex groups based on the Food and DrugAdministration's (FDA) Total Diet Study dietary exposure model. Estimates of aluminium intakes rangedfrom 0.7 mg/day for 6-11-month-old infants to 11.5 mg/day for 14-16-year-old males. Average intakes foradult men and women were 8-9 and 7 mg/day, respectively. The major contributors to daily intake ofaluminium were foods with aluminium-containing food additives, e.g. grain products and processed



cheese.

Transverse fractures of the spinous process of the 7th cervical vertebra in RDT patients: an Al relateddisease?

From: Int J Artif Organs (1987 Mar) 10(2):93-6

The bone fractures had occurred suddenly while the patients were going about their daily work. Theseobservations indicate that Al- or iron- related bone disease with secondary hyperparathyroidism caninduce bone fracture by only slight stress in patients maintained on hemodialysis.

Risk of aluminum accumulation in patients with burns and ways to reduce it.

Klein G.L. – Herndon D.N. – Rutan T.C. – Barnett J.R. – Miller N.L. – Alfrey A.C.

From: J Burn Care Rehabil (1994 Jul-Aug) 15(4):354-8

Severely burned patients experience a bone lesion consisting of markedly reduced bone formation andevidence of decreased resportion. The cause of the lesion may be multifactorial, but aluminum loading,which also occurs in patients with burns, has been documented to produce this type of injury in bothhumans and animals.

Cutaneous exposure to aluminum is greatest from baths, which may provide up to 8 mg aluminum.However, the dynamics of aluminum entry into the blood via a damaged skin barrier are unclear. Enteralexposure to aluminum is no greater than daily dietary exposure. Parenteral sources of aluminum,especially 25% human serum albumin and calcium gluconate, provide the most significant risk of loadingbecause of direct introduction of aluminum into the circulation.

Substitution with a different brand of albumin and calcium chloride can reduce the parenteral aluminumload by as much as 95% and minimize any role aluminum may play in the pathogenesis of this bonelesion.

Aluminum concentrations in tissues of rats: effect of soft drink packaging.

Kandiah J. – Kies C.

From: Biometals (1994 Jan) 7(1):57-60

Canned soft drink fed rats had significantly higher blood, liver and bone aluminum concentration thanrats that were given glass bottled soft drink.

Sources of AluminumOver the Counter; Deoderants, vaginal douches, baby wipes, skin creams, suntan lotions, toothpaste,buffered asprin, some haemorrhoid and diarrhea products.

Medical; Vaccinations, allergy testing, intervenous solutions, allergens, wound and antacid irrigation,ulcer treatment, blood oxygenization, bone or joint replacement and burn treatment.

Foods; Aluminum cans, foils, containers, baking powder, cake mixes, frozen dough, pancake mixes, self-rising flour, grains, processed cheese.



Environmental Effects of Aluminum

CT Aluminum in acidic surface waters: chemistry, transport, and effects.

From: Environ Health Perspect (1985 Nov) 63:93-104

Ecologically significant concentrations of Al have been reported in surface waters draining "acid-sensitive" watersheds that are receiving elevated inputs of acidic deposition. It has been hypothesizedthat mineral acids from atmospheric deposition have remobilized Al previously precipitated within thesoil during soil development. This Al is then thought to be transported to adjacent surface waters.Dissolved mononuclear Al occurs as aquo Al, as well as OH-, F-, SO4(2-), and organic complexes.

Although past investigations have often ignored non-hydroxide complexes of Al, it appears that organicand F complexes are the predominant forms of Al in dilute (low ionic strength) acidic surface waters. Theconcentration of inorganic forms of Al increases exponentially with decreases in solution pH. Thisresponse is similar to the theoretical pH dependent solubility of Al mineral phases.

The concentration of organic forms of Al, however, is strongly correlated with variations in organiccarbon concentration of surface waters rather than pH. Elevated concentrations of Al in dilute acidicwaters are of interest because: Al is an important pH buffer; Al may influence the cycling of importantelements like P, organic carbon, and trace metals; and Al is potentially toxic to aquatic organisms.

Inhibition of Ca2+ uptake in freshwater carp, Cyprinus carpio, during short-term exposure to aluminum.

Verbost P.M. – Lafeber F.P. – Spanings F.A. – Aarden E.M. – Wendelaar Bonga S.E.

From: J Exp Zool (1992 Jun 1) 262(3):247-54

In carp exposed to pH 5.2 in fresh water, the Ca2+ influx from the water is reduced by 31% whencompared to fish in water of neutral pH. At pH 5.2, the Ca2+ influx but not Na+ uptake is decreased byaluminum (Al). Al reduces Ca2+ influx dose-dependently: a maximum 55% reduction was observed after1-2 h exposure to 200 micrograms .1(-1) (7.4 microM) Al.

A mechanism for acute aluminium toxicity in fish

Exley C. – Chappell J.S. – Birchall J.D.

From: J Theor Biol (1991 Aug 7) 151(3):417-28

Aluminium is acutely toxic to fish in acid waters. The gill is the principal target organ and death is due toa combination of ionoregulatory, osmoregulatory and respiratory dysfunction. The mechanism ofepithelial cell death is proposed as a general mechanism of aluminium-induced accelerated cell death.

Can the mechanisms of aluminum neurotoxicity be integrated into a unified scheme?

Strong M.J. – Garruto R.M. – Joshi J.G. – Mundy W.R. – Shafer T.J.

From: J Toxicol Environ Health (1996 Aug 30) 48(6):599-613

Regardless of the host, the route of administration, or the speciation, aluminum is a potent neurotoxicant.



In the young adult or developmentally mature host, the neuronal response to Al exposure can bedichotomized on morphological grounds. In one, intraneuronal neurofilamentous aggregates are formed,whereas in the other, significant neurochemical and neurophysiological perturbations are inducedwithout neurofilamentous aggregate formation.

Evidence is presented that the induction of neurofilamentous aggregates is a consequence of alterationsin the posttranslational processing of neurofilament (NF), particularly with regard to phosphorylationstate. Although Al has been reported to impact on gene expression, this does not appear to be critical tothe induction of cytoskeletal pathology.

In hosts responding to Al exposure without the induction of cytoskeletal pathology, impairments inglucose utilization, agonist-stimulated inositol phosphate accumulation, free radical-mediatedcytotoxicity, lipid peroxidation, reduced cholinergic function, and altered protein phosphorylation havebeen described. The extent to which these neurochemical modifications correlate with the induction of acharacteristic neurobehavioral state is unknown.

In addition to these paradigms, Al is toxic in the immediate postnatal interval. Whether uniquemechanisms of toxicity are involved during development remains to be determined. In this article, themechanisms of Al neurotoxicity are reviewed and recommendations are put forth with regard to futureresearch.

Institutional address:

Department of Clinical Neurological Sciences

University of Western Ontario

London, Canada.

[email protected]

Aluminum toxicity following intravesical alum irrigation for hemorrhagic cystitis.

Kanwar V.S. – Jenkins J.J. 3rd – Mandrell B.N. – Furman W.L.

From: Med Pediatr Oncol (1996 Jul) 27(1):64-7

Mental status changes in an immunosuppressed child can be due to a variety of causes; aluminumtoxicity is rarely considered. We report a teenage girl with acute lymphoblastic leukemia who developedmental status changes, speech disturbance, coarse tremor, and abnormal EEG findings followingintravesical 1% alum irrigation and administration of aluminum-containing antacids. All abnormalitiesresolved after a nine-week course of intravenous deferoxamine.

Progressing encephalomyelopathy with muscular atrophy, induced by aluminum powder.

Bugiani O. – Ghetti B.

From: Neurobiol Aging (1982 Fall) 3(3):209-22

The injection of aluminum powder into the cerebrospinal fluid of adult rabbits induced a slowlyprogressing encephalomyelopathy characterized at first by alteration of posture and then by myoclonicjerks and muscle weakness.



Neurofibrillary degeneration was the hallmark of the disease and involved most of the gray areas.Neurogenic muscular atrophy appeared in animals sacrificed in the second and third month afterinjection.

Aluminium foil as a wound dressing

Poole M.D. – Kalus A.M. – von Domarus H.

From: Br J Plast Surg (1979 Apr) 32(2):145-6

ISBN: 0007-1226

Aluminium foil has been found to be an extremely useful and painless way of dressing wounds prior todelayed skin grafting. However, it is not recommended for use on skin-graft donor sites as it delaysepithelial healing.

From: History of crime against the Food Laws (1929)

by Dr. Riley, the prime mover behind the original Pure Food Law and Director of the FDA. He resigned indisgust in 1912 over exceptions granted to the law and lack of enforcement.

Aluminum has been exempted from testing for safety by the FDA under a convoluted logic wherein it isclassified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety andthere are NO restrictions whatever on the amount or use of aluminum.

Diseases Associated with Aluminium Intoxication H. Tomlinson, M.B., Ch.B., MRCS., LRCP

Aluminum is known to inhibit cell division during the "S Phase" at levels less than 4 ppm.

Aluminum toxicity is a widespread problem in all forms of life, including humans, animals, fish, plantsand trees, and causes widespread degradation of the environment and health. Over 7,000 referencearticles on aluminum toxicity existed in various data bases as of 1936, (Today, there are more than amillion.) all recognizing the toxicity.

Link to Chemical Elements.com

Aluminum and Colloidal Suspensions

The Problem With Mercury

Heavy Metal Toxicology

Chelation Therapy

Symptoms of Elemental Toxicities

Hydroponic Reference Center

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