Aluminium Deseases

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"From the earliest days of food regulation, the use of alum (aluminumsulphate) in foods has been condemned. It is universally acknowledged as a

poison in all countries. If the Bureau of Chemistry had been permitted toenforce the law ... no food product in the country would have any trace of ...

any aluminum or saccarin. No soft drink would contain caffeine or hebromin;no bleached flour would be in interstate commerce. Our food and drugs would

be wholly without adulteration ... and the health of our people would be vastlyimproved and their life greatly extended."

From History of crime against the Food Laws (1929) by Dr. Wiley, the primemover behind the original Pure Food Law and Director of the FDA. He resignedin disgust in 1912 over exceptions granted to the law and lack of enforcement.

Aluminum has been exempted from tesitng for safety by the FDA under aconvoluted logic wherein it is c lassified as GRAS. (Generally Regarded AsSafe.) It has never been tested by the FDA on its safety and there are NOrestrictions whatever on the amount or use of aluminum.

There are over 2000 references in the National Library of Medicine on adverseeffects of alumium. The following 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, where renal function is limited, or where apreviouslyaccumulated bone burden is released in stress or illness. Toxicity may

include: encephalopathy (stuttering, gait dist urbance, myoclonic jerks,seizures, coma, abnormal EEG) osteomalacia or aplastic bone disease (

associated with painful spontaneous fractures, hypercalcemia, tumorouscalcinosis ) proximal myopathy, increased risk of infection, increased leftventricular mass and decreased myocardial function microcytic anemia withvery high levels, sudden death.

Aluminum is ubiquitous in our environment; it is the third most prevalentelement in the earth's crust. The gastrointestinal tract is relatively imperviousto aluminum, absorption normally being only about 2%. Aluminum is absorbedby a mechanism related to that for calcium. Gastric acidity and oral citratefavors absorption, and H2-blockers reduce absorption. As is true for severaltrace elements, transferrin is th e primary protein binder and carrier for aluminum in the plasma, where 80% is protein bound and 20% is free or

complexed to small molecules such as citrate.

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

It is not known if ferritin has a specific binding site for aluminum. Factorsregulating the migration of aluminum across the blood ±brain barrier are notwell understood.



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

disease.

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

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

Aluminum toxicity has been reported to impair the formation and release of

parathyroid hormone. The parathyroid glands concentrate aluminum abovelevels in surrounding tissues. Treatment of aluminum toxi city in renal failure

patients often reactivates hyperparathyroidism, which to a certain extent ishelpful for bone remodeling and healing.

Distilled Water Placed in Various Containers

Distilled water was placed in metal containers and the amount of the "Metal

Can" that disolved into the distilled water was measured daily using SpecificConductance readings. You can divide the SC number by 2 to get theapproxamite 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 -feedingsolutions.

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, ispotentially neurotoxic. We investigated the effect of perinatal exposure to

intravenous aluminum on the neurologic development of infants bornprematurely.

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).

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 of subsequent educational problems. For all 1 57 infants

without neuromotor impairment, increasing aluminum exposure wasassociated with a reduction in the Mental Development Index (P=0.03), with anadjusted loss of one point per day of intravenous feeding for infants receivingthe standard solutions. In preterm infants, prolonged intravenous feeding withsolutions containing aluminum is associated with impaired neurologicdevelopment.

Aluminum-containing emboli in infants treated with extracorporeal membraneoxygenation.

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 withrespiratory failure who had been treated with venoarterial extracorporealmembrane oxygenation (ECMO). In addition, distinctive basophilic aluminum -containing emboli were found in 12 of the infants; the distribution of theseemboli was similar to that of the thromboemboli, except that an aluminum -containing embolus was found in a lung in only 1 infant. Sixteen infants hadpulmonary thrombi or thromboemboli. We also found friable aluminum -

containing concretions adhering loosely to the mixing rods of heat exchangersthat had been used to warm the blood flowing through the ECMO circ uit; suchconcretions were not present on unused mixing rods. We propose that thesealuminum-containing concretions developed as the silicone coating of theheat exchanger wore away and aluminum metal was exposed to warm,oxygenated blood and that fragments of aluminum-containing concretionsformed emboli. This hypothesis is supported by the fact that aluminum -containing emboli were generally not present in the lungs, which are bypassedby ECMO.



Sequential serum aluminum and urine aluminum: creatinine ra tio and tissue

aluminum loading in infants with 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 amean (± SEM) birth weight of 1007 ±34 g, gestational age of 28.5 +/ -0.3 weeks,

and serial radiographic documentation at 3, 6, 9, and 12 months for thepresence (n = 16) or absence ( n = 35) of fractures and/or rickets were studied

at the same intervals to determine the serial changes in serum aluminumconcentrations and urine aluminum-creatinine ratios. Autopsy bone samples

were used to determine the presence of tissue aluminum. One i nfant whoreceived 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) showedaluminum deposition in the zone of provisional calcification and along thenewly formed trabecula.

Aluminum in parenteral solutions revisited ² 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 contaminateparenteral nutrition solutions and to be a contributing factor in thepathogenesis of metabolic bone disease in parenteral nutrition patients as wellas in uremic patients. However, there are no regulations in place to effectivelyreduce aluminum contamination of various parenterally administerednutrients, drugs, and biologic products. The purpose of this review is fourfold:1.) to summarize our knowledge of the adverse effects of aluminum on boneformation 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 of regulations covering aluminum content of par enteralsolutions 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 amicrocytic hypoproliferative anemia and is a factor responsible for worsening

anemia in patients with end-stage renal disease.

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

Three patients had subcutaneous nodules at the sites of previous injections of vaccine containing tetanus toxoid, showed aluminum crystals in the nodulesfrom two patients. From the evidence available, we believe that these nodulesare 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 Moragas J.M.

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

These lesions have been mainly attributed to a hypersensitivity reaction toaluminum hydroxide, which is used as an absorbing agent in many vaccines

and hyposensitization preparations. Patch tests with stand ard antigens andaluminum compounds and histopathologic and ultrastructural studies were

performed on 10 patients with persistent subcutaneous nodules on the upper part of their arms after injection of aluminum -adsorbed dust and/or pollen

extracts. The nodules appeared 1 month to 6.5 years after 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 tracemetal toxicity related to degenerative diseases of the skeleton.

Postvaccinal sarcomas in the cat: epidemiology and electron probemicroanalytical identification of aluminum.

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 thePennsylvania area appears to be related to the increased vaccination of catsfollowing enactment of a mandatory rabies vaccination law.



The majority of fibrosarcomas arose in sites routinely used by veterinariansfor vaccination, and 42 of 198 tumors were surrounded by lymphocytes and

macrophages containing foreign material identical to that previously descri bedin postvaccinal inflammatory injection site reactions. Some of the vaccines

used have aluminum-based adjuvants, and macrophages surrounding threetumors contained aluminum oxide identified by electron probe microanalysis

and imaged by energy-filtered electron microscopy. Persistence of inflammatory and immunological reactions associated with aluminum maypredispose the cat 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 metalover 50 years ago, but was dismissed as a toxic agent as recently as 15 yearsago. The accumulation of aluminum, in some patients with chronic renalfailure, is associated with the development of toxic phenomena; dialysisencephalopathy, osteomalacic dialysis osteodystrophy, and an anemia.Aluminum accumulation also occurs in patients who are not on dialysis,predominantly infants and children with immature or impaired renal function.Aluminum has also been implicated as a toxic agent in the etiology of Alzheimer's disease, Guamiam amyotrophic lateral sclerosis, andparkinsonism-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 reportedsporadically for many years. Recently, however, reports of sarcomatousdegeneration around a standard cemented hip arthroplasty and around cobalt -chromium-bearing hip arthroplasties raise new questions of the malignant

potential of metallic ends prostheses. Sarcomatous changes around aluminumoxide ceramics seem not to have been reported in the literature. The presentreport may be the first documented case of an aggressive soft tissue sarcomadetected 15 months after the patient had an uncemented ceramic total hiparthroplasty. If a causal relationship exists, the incidence of this phenomenonin the United States is 250 times greater than would be expected fromstatistics on soft tissue sarcoma at the hi p.



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 of confirmed aluminum-induced, delayed-hypersensitivity granulomas in a tattoo.

Delayed healing in full-thickness wounds treated with aluminum chloridesolution. A histologic study with evaporimetry 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 ferricsubsulfate solution or were allowed to clot with minimal pressure from a gauzepad. Delay in reepithelialization was noted histologically both in woundstreated with aluminum chloride and in those treated with ferric subsulfate

compared to controls. Presumably this delay was the result of tissue necrosiscaused by these hemostatic agents, resulting in slightly larger and less

cosmetically acceptable scars. Plots of evaporimetry data revealed a biphasicpattern of water loss during healing, with an initial rapid decline in water 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 beseen in injection site reactions related to aluminium, showed unusual features

not described previously. In one, there was a sclerosing lipogranuloma -likereaction with unlined cystic spaces containing crystalline material. The other

case presented as a large symptomatic subcutaneous swelling whichicroscopically showed diffuse and wide -spread involvement of the subcutis by

a lymphoid infiltrate with prominent lymphoid follicles.

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

Aluminum and gallium arrest formation of cerebrospinal fluid by themechanism 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 throughthe cerebral ventricles of the rat. Depending on the metal and its concentration

(1-10 mM) the pH of the perfusate ranged from 7.2 to 3.5. At 10 mM metalchloride, yielding pH 4.7 (Al) or 3.5 (Ga), formation of cerebrospinal fluid wassuppressed 100%. This mechanism may also account for the antiperspirantaction 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 intensive care nursery, it was discovered that those solutionsusing certain brands of 25% albumin contained aluminum levels within thetoxic range. When the brand was changed to a brand known to have a lower

aluminum (Al) content, a marked drop in priming solution Al levels wasmeasured.

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-tetanus vaccine or the same vaccine in fluid form, in

order to investigate if local side effects could be diminished by exclusion of aluminium. System reactions were rare and local reactions frequent in both

groups but larger 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 whomhad worked for over 12 years in the same potroom of an aluminum sme ltingplant. 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, the cause of these patients' problems remains obscure.

Neurotoxic effects of aluminum in animals are directed at the central nervoussystem, and theoretically long-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 plantaccounts for part of the excess of bladder cancer in the region studied.

(Author abstract) (85 Refs)

Immunohistochemical study of microtubule -associated protein 2 and ubiquitinin 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 aluminum tartrate 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 possiblefactor in the development of neurodegenerative disorders in humans. Effec tsof Al on cell viability (lysosomal and mitochondrial activity) 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 thatfrom the drinking water.

Persistent subcutaneous nodules in chil dren hyposensitized with aluminium-containing allergen extracts.

Frost L. ± Johansen P. ± Pedersen S. ± Veien N. ± Ostergaard P.A. ± NielsenM.H.

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

A follow-up study of 202 children who had received hyposensitizatio n with

aluminium-containingallergens showed that 1 -3 years after cessation of hyposensitization 13 children still had severely treatment -resistant

subcutaneous nodules in their forearms. Because of their long persistence thenodules of six children were studied in detail. Histologically, the nodules

showed infiltration with lymphocytes (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, the phagosomes of the macrophages contained aluminium. Patchtests for aluminium were positive in four of the 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 tothe aluminium discs used for 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 humanpathological diseases has altered its status from being a nontoxic,nonabsorbable, harmless element. This maybe of particular concern to thedeveloping foetus which is more susceptible to agents and at lower levels thanthe adult. Little attention has been given to aluminium's potential reproductivetoxicity until recently and further resear ch is required for a full evaluation of its

toxicity. Our preliminary results demonstrate behavioural and neurochemicalalterations in the offspring of mice exposed to aluminium during gestation.



Further, the effects of such exposure are also present in th e adult animalsuggesting persistent changes in behaviour following prenatal exposure.

The absence of extracellular calcium potentiates the killing of culturedhepatocytes by aluminum maltolate.

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 amechanisms distinct from previously recognized pathways of lethal cell injury.

It is hypothesized that aluminum binds to cytoskeleta l proteins intimatelyassociated with the plasma membrane. This interaction eventually disrupts the

permeability barrier function of the cell membrane, an event that heralds thedeath of the hepatocyte.

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 for hyposensitization. We conclude that aluminiumallergy is not exceptional.

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

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 proposemethods of patch testing patients with symptoms at vaccination sites in order to avoid this problem.

Aluminium allergy in patients hyposensitized with aluminium -precipitatedantigen extracts.

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

Aluminum precipitated antigen solutions, a small percentage of patientsdevelop persistent subcutaneous nodules at the injection site; the existence of



delayed sensitivity to aluminium has been implicated 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 in water. 13 of them had pruritic excoriated papules, 9at 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 avaccine containing aluminium hydroxide, and who had positive patch tests to

aqueous aluminium chloride and/or to a Finn Chamber, were followed for 1 to8 years. During the period of observation, the symptoms cleared in 5 chil dren,

improved in 11, and remained unchanged in 5.

Short-term experimental acidification of a Welsh stream: toxicity of differentforms of aluminium at low pH 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 largemortalities and reduced feeding were recorded in the acid and aluminiumzone.

H Differentiated neuroblastoma cells are more susceptible to aluminiumtoxicity than developing cells.

E. Meiri

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



Two specific questions were addressed: 1.) Can differentiated cells maintaintheir normal excitable function when exposed to aluminium? 2.) Can proper

development of electrophysiological properties be achieved in its presence?We report that aluminium caused premature onset of deterioration in fully

differentiated cells. Within 4 -6 days they depolarized from -29.3 0.9 mV tolevels lower than -15 mV; compound polyphasic action potentials were

gradually replaced by slow monophasic spikes before the final 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. Partial reversal of the deficit was produced by discontinuingaluminum treatment, 2 weeks prior to testing.

Aluminum-induced neurofibrillary degeneration disrupts acquisition of therabbit's classically conditioned 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 conditionedresponse over the 4 days of testing. This disruption of conditioning inaluminum-treated rabbits could not be attributed to deficits in sensory or

motor processes or to illness. Neuropathological analysis revealedwidespread neurofibrillary tangle 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 chronicexposure to low levels of aluminum 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 distributionof aluminum in different regions of brain and body organs of male albino rats,

following subacute and acute aluminum exposure. Aluminum was observed toaccumulate in all regions of the brain with maximum accumulation in the

hippocampus. Aluminum was also seen to compartmentalize in almost all thetissues of the body to varying extents, and the highest accumu lation was inthe spleen.

Ti-6Al-4V ion solution inhibition of osteogenic cell phenotype as a function of differentiation timecourse in 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 thenormal differentiation of bone marrow stromal cells to mature osteoblasts invitro, suggesting that ions released from implants in vivo may contribute toimplant failure by impairing normal bone deposition.

Aluminium release from glass ionomer cements during early water exposure invitro.

Andersson O.H. ± Dahl J.E.

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

Aluminium is a major constituent of glass ionomer cements. During mixingand setting aluminium is released from the glass into the polyalkeonic acidsolution. Part of this aluminium may not combine with the polyalkeonic acid,but may be released from the cement. The aluminium release from auto -cured

and light-cured glass ionomer cements during early wa ter exposure wasstudied. The former cements released more aluminium than the latter. It is

suggested that the considerable release of aluminium from glass ionomer cements during early water exposure may explain the reported lack of

mineralization of predentin in the pulp beneath glass ionomer cements. Thiswould correspond to the inhibiting effect of aluminium on bone mineralization.

Impaired control of information transfer at an isolated synapse treated byaluminum: is it related to dementia?

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 foundin the diseased brain of demented patients modulates synaptic transmission.

Chronic aluminum-induced motor neuron degeneration: clinical,neuropathological and molecular biological 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 thatmimics the intraneuronal inclusions 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 deposit ion of abnormalsubstances in or around joints. Certain features of some of thesearthropathies and their significance have only recently been recognized and

others have been insufficiently emphasized. An important group of conditionsare the arthropathies related to renal failure and its treatment, namely,

aluminum toxicity, periarticular calcification and crystal deposition,hyperparathyroidism, and dialysis-related amyloidosis. Crystal deposition

diseases, specifically, gouty arthritis, calcium pyrophosp hate deposition, and

calcium hydroxyapatite deposition, are also reviewed.

Sepsis: a cause of aluminum release from tissue stores associated with acuteneurological dysfunction and 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 aluminumwho developed septicemia. In all cases the serum aluminum increased

markedly. This may have contributed to the neurological dysfunction seen infive, 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 anincrease in free, diffusable aluminum and that this jeopardized bothneurological function an d 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 theFood and Drug Administration's (FDA) Total Diet Study dietary exposure

model. Estimates of aluminium intakes ranged from 0.7 mg/day for 6 -11-month-old infants to 11.5 mg/day for 14 -16-year-old males. Average intakes for adult men and women were 8-9 and 7 mg/day, respectively. The major contributors to daily intake of aluminium 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 inRDT patients: an Al related disease?

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

The bone fractures had occurred suddenly while the patients were going abouttheir daily work. These observations indicate that Al - or iron- related bonedisease with secondary hyperparathyroidism can i nduce bone fracture by onlyslight 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 markedlyreduced bone formation and evidence of decreased resportion. The cause of the lesion may be multifactorial, but aluminum loading, which al so occurs inpatients with burns, has been documented to produce this type of injury inboth humans 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 bloodvia a damaged skin barrier are unclear. Enteral exposure 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 loading be cause of direct introduction of aluminuminto the circulation.

Substitution with a different brand of albumin and calcium chloride can reduce

the parenteral aluminum load by as much as 95% and minimize any rolealuminum may play in the pathogenesis of this bone lesion.

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, liv er and bonealuminum concentration than rats that were given glass bottled soft drink.

Sources of Aluminum

Over 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 jointreplacement and burn treatment.

Foods; Aluminum cans, foils, containers, baking powder, cake mixes, frozendough, 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 inputsof acidic deposition. It has been hypothesized that mineral acids fromatmospheric deposition have re mobilized Al previously precipitated within thesoil during soil development. This Al is then thought to be transported toadjacent surface waters. Dissolved mononuclear Al occurs as aquo Al, as wellas OH-, F-, SO4(2-), and organic complexes.

Although past investigations have often ignored non-hydroxide complexes of

Al, it appears that organic and F complexes are the predominant forms of Al indilute (low ionic strength) acidic surface waters. The concentration of

inorganic forms of Al increases exponenti ally with decreases in solution pH.This response is similar to the theoretical pH dependent solubility of Al

mineral phases.

The concentration of organic forms of Al, however, is strongly correlated withvariations in organic carbon concentration of surf ace waters rather than pH.Elevated concentrations of Al in dilute acidic waters are of interest because: Alis an important pH buffer; Al may influence the cycling of important elementslike 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 isreduced by 31% when compared to fish in water of neutral pH. At pH 5.2, the

Ca2+ influx but not Na+ uptake is decreased by aluminum (Al). Al reducesCa2+ influx dose-dependently: a maximum 55% reduction was observed after

1-2 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 targetorgan and death is due to a combination of ionoregulatory, osmoregulatory

and respiratory dysfunction. The mechanism of epithelial cell death isproposed as a general mechanism of aluminium -induced accelerated cell

death.

Can the mechanisms of aluminum neurotoxicity be integrated into a unifiedscheme?

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 developmentallymature host, the neuronal response to Al exposure can be dichotomized on

morphological grounds. In one, intraneuronal neurofilamentous aggregatesare formed, whereas in the other, significant neurochemical and

neurophysiological perturbations are induced wi thout neurofilamentousaggregate formation.

Evidence is presented that the induction of neurofilamentous aggregates is aconsequence of alterations in the posttranslational processing of neurofilament (NF), particularly with regard to phosphorylation stat e. AlthoughAl has been reported to impact on gene expression, this does not appear to be

critical to the induction of cytoskeletal pathology.



In hosts responding to Al exposure without the induction of cytoskeletalpathology, impairments in glucose utilization, agonist -stimulated inositol

phosphate accumulation, free radical -mediated cytotoxicity, lipid peroxidation,reduced cholinergic function, and altered protein phosphorylation have been

described. The extent to which these neurochemical modifications correlatewith the induction of a characteristic neurobehavioral state is unknown.

In addition to these paradigms, Al is toxic in the immediate postnatal interval.Whether unique mechanisms of toxicity are involved during developmentremains to be determined. In this article, the mechanisms of Al neurotoxicityare 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 hemorrhagiccystitis.

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 varietyof causes; aluminum toxicity is rarely considered. We report a teenage girlwith acute lymphoblastic leukemia who developed mental status changes,speech disturbance, coarse tre mor, and abnormal EEG findings following

intravesical 1% alum irrigation and administration of aluminum -containingantacids. All abnormalities resolved after a nine -week course of intravenous

deferoxamine.

Progressing encephalomyelopathy with muscular a trophy, 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 rabbitsinduced a slowly progressing encephalomyelopathy characterized at first byalteration of posture and then by myoclonic jerks and muscle weakness.



Neurofibrillary degeneration was the hallmark of the disease and involvedmost of the gray areas. Neurogenic muscular atrophy appeared in animals

sacrificed in the second and third month after injection.

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 to delayed skin grafting. However, it is not

recommended for use on skin-graft donor sites as it delays epithelial 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 in disgust in 1912 over exceptions granted to the law

and lack of enforcement.

Aluminum has been exempted from testing for safety by the FDA under aconvoluted logic wherein it is classified as GRAS. (Generally Regarded As

Safe.) It has never been tested by the FDA on its safety and there are NOrestrictions 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 lessthan 4 ppm.

Aluminum toxicity is a widespread problem in all forms of life, including

humans, animals, fish, plants and trees, and causes widespread degradationof the environment and health. Over 7,000 reference articles on aluminum

toxicity existed in various data bases as of 1936,(Today, there are more than a

million.) all recognizing the toxicity.



Second article Aluminum - Al

Properties - Health effects of aluminum -Environmentaleffects of aluminum

Atomic number 13

Atomic mass 26.98154 g.

Electronegativity according to Pauling 1.5

Density 2.7 g.cm -3 a

Melting point 660.4 °C

Boiling point 2467 °C

Vanderwaals radius 0.143 nm

Ionic radius 0.05 nm

Isotopes 3

Artificial isotopes 16

Electronic shell 1s2 2s2 2p6 3

Energy of first ionization 577.4 kJ.mo

Energy of second ionization 1816.1 kJ.mEnergy of third ionization 2744.1 kJ.m

Standard potential - 1.67 V

Discovered by Hans Christi

Aluminum

The name aluminum is derived from the ancient name for a

(Latin, meaning bitter salt). Aluminum was the original namcalled it aluminum and that became the accepted name in E

aluminum and when the American Chemical Society debate

aluminum.

Aluminum is a soft and lightweight metal. It has a dull silve

forms quickly when it is exposed to air. Aluminum is nontox



Aluminum has only one naturally occurring isotope, alumini

Applications

A silvery and ductile member of the poor metal group of eleand is remarkable for its resistance to oxidation (aluminum

in this form unlike most metals), its strength, and its light w

millions of different products and is very important to the w

aluminum are vital to the aerospace industry and very impo

which light weight, durability, and strength are needed.The use of aluminum exceed that of any other metal except

elements such as copper, zinc, magnesium, manganese and

N early all modern mirrors are made using a thin reflective cfloat glass. Telescope mirrors are also coated with a thin lay

Other applications are electrical transmission lines, and pac

Because of its high conductivity and relatively low price com

household electrical wiring to a large degree in the US in the

caused by its greater coefficient of thermal expansion and it

both eventually causing loosening the connection; galvanic c

The most recent development in aluminum technology is th

metal a compound (a metal hybrid), which releases hydrogethis is done and this is achieved by adding aluminum oxide

is used in traffic tunnels and in space shuttle.

Aluminum in the environment

Aluminum is an abundant element in Earth's crust: it is belie

8.1%. Aluminum is very rare in its free form. Aluminum con

present mainly as insoluble aluminum hydroxide.

Aluminum is a reactive metal and it is hard to extract it from

the most difficult metals on earth to refine, the reason is th

an extremely stable compound that, unlike rust on iron, doeused in many applications is why it is so hard to produce.

Several gemstones are made of the clear crystal form of alu



traces of other metals creates various colors: cobalt creates

these are now easy and cheap to manufacture artificially. To

iron.

Recovery of this metal from scrap (via recycling) has becomIndustrial production world-wide of new metal is around 20

Known reserves of ores are 6 billion tones.

Health effects of aluminum

Aluminum is one of the most widely used metals and also o

crust. Due to these facts, aluminum is commonly known as

high concentrations, it can cause health problems. The wate

these particles are called ions. They are usually found in a sinstance as aluminum chlorine.

The uptake of aluminum can take place through food, throu

significant concentrations of aluminum can lead to serious h

- Damage to the central nervous system

- Dementia

- Loss of memory- Listlessness

- Severe trembling

Aluminum is a risk in certain working environments, such as

in factories where aluminum is applied during production pr

aluminum dust. Aluminum can cause problems for kidney pa

Inhalation of finely divided aluminum and aluminum oxide pfibrosis and lung damage. This effect, know as Shaver¶s Dis

silica and oxides of iron. May also be implicated in Alzheime

Environmental effects of aluminum



The effects of aluminum have drawn our attention, mainly d

accumulate in plants and cause health problems for animals

The concentrations of aluminum appear to be highest in acidamphibians is declining due to reactions of aluminum ions w

High aluminum concentrations do not only cause effects upo

consume contaminated fish and insects and upon animals th

for birds that consume contaminated fish are eggshell thinn

for animals that breathe in aluminum through air may be lu

Another negative environmental effect of aluminum is that i

phosphates to be less available to water organisms.

High concentrations of aluminum may not only be found in a

acidified soils. There are strong indications that aluminum c

groundwater.

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Aluminium Deseases

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