Ilena Rose
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 Posted: Mon Oct 06, 2008 12:43 am Post subject: Aluminium induced electrophysiological, biochemical and cogn |
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From Health Lover, Ilena Rosenthal:
Thank you for posting this.
Until I began posting about the dangers of aluminum and Gardasil ... I
didn>t realize that there was a cover-up of aluminum dangers as deep
as silicone and mercury. The same shills and flacks began their same
idiotic rants about aluminum.
Here are some other studies I found:
~~~~~~~~~~~~~~~~~
http://www.hbci.com/~wenonah/hydro/al.htm
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 in aluminum paints; for absorbing occluded
gases in manuf. of steel. In testing for Au, As, Hg; coagulating
colloidal solns. of As or Sb; pptg. Cu; reducer for determining
nitrates and nitrites; instead of Zn for generating hydrogen in
testing for As.
Grades available: Reagent, technical.
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Aluminum Toxicity
The 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 been condemned. It is universally acknowledged
as a poison in all countries. If the Bureau of Chemistry had been
permitted to enforce 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 vastly improved and their life
greatly extended."
From History of crime against the Food Laws (1929) by Dr. Wiley, 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 tesitng for safety by the FDA under a
convoluted 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 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. 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
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 left ventricular mass and decreased myocardial
function microcytic anemia with very high levels, sudden death.
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 favors absorption, and
H2-blockers reduce absorption. As is true for several trace elements,
transferrin is the 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 to contain aluminum.
It is not known if ferritin has a specific binding site for aluminum.
Factors regulating the migration of aluminum across the bloodbrain
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. The parathyroid glands concentrate
aluminum above levels in surrounding tissues. Treatment of aluminum
toxicity in renal failure patients often reactivates
hyperparathyroidism, which to a certain extent is helpful 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 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 ...
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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 intravenousfeeding solutions,
is potentially neurotoxic. We investigated the effect of perinatal
exposure to intravenous aluminum on the neurologic development of
infants born prematurely.
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 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. In preterm infants, prolonged
intravenous feeding with solutions containing aluminum is associated
with impaired neurologic development.
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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 had been treated with
venoarterial extracorporeal membrane oxygenation (ECMO). In addition,
distinctive basophilic aluminum-containing emboli were found in 12 of
the infants; the distribution of these emboli was similar to that of
the thromboemboli, except that an aluminum-containing embolus was
found in a lung in only 1 infant. Sixteen infants had pulmonary
thrombi or thromboemboli. We also found friable aluminum-containing
concretions adhering loosely to the mixing rods of heat exchangers
that had been used to warm the blood flowing through the ECMO circuit;
such concretions were not present on unused mixing rods. We propose
that these aluminum-containing concretions developed as the silicone
coating of the heat exchanger wore away and aluminum metal was exposed
to warm, oxygenated blood and that fragments of aluminum-containing
concretions formed emboli. This hypothesis is supported by the fact
that aluminum-containing emboli were generally not present in the
lungs, which are bypassed by ECMO.
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Sequential serum aluminum and urine aluminum: creatinine ratio 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 a mean (± 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 the presence (n = 16) or
absence (n = 35) of fractures and/or rickets were studied at the same
intervals to determine the serial changes in serum aluminum
concentrations and urine aluminum-creatinine ratios. Autopsy bone
samples 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 enteral feeding was tolerated for 37 and 41
days in two infants, respectively) showed aluminum deposition in the
zone of provisional calcification and along the newly formed
trabecula.
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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 solutions and to be a contributing
factor in the pathogenesis of metabolic bone disease in parenteral
nutrition patients as well as in uremic patients. However, there are
no regulations in place to effectively reduce aluminum 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 of aluminum on bone formation and
mineralization in parenteral nutrition patients; 2.) to discuss the
possible role of aluminum in the osteopenic bone disease of preterm
infants; 3.) to show how lack of regulations 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
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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 microcytic 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 nodules from two patients. From the evidence
available, we believe that these nodules are a complication of
inoculations with aluminum-containing vaccines.
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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 to aluminum hydroxide, which is used as an absorbing agent in
many vaccines and hyposensitization preparations. Patch tests with
standard antigens and aluminum 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.
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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 to degenerative diseases of the skeleton.
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Postvaccinal sarcomas in the cat: epidemiology and electron probe
microanalytical 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 the
Pennsylvania area appears to be related 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 of 198 tumors were surrounded by
lymphocytes and macrophages containing foreign material identical to
that previously described in postvaccinal inflammatory injection site
reactions. Some of the vaccines used have aluminum-based adjuvants,
and macrophages surrounding three tumors contained aluminum oxide
identified by electron probe microanalysis and imaged by
energy-filtered electron microscopy. Persistence of inflammatory and
immunological reactions associated with aluminum may predispose the
cat to a derangement of its fibrous connective tissue repair response,
leading to neoplasia.
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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 was dismissed as a toxic agent as
recently as 15 years ago. The accumulation of aluminum, in some
patients with chronic renal failure, is associated with the
development of toxic phenomena; dialysis encephalopathy, 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, and
parkinsonism-dementia.
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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 arthroplasty and around
cobalt-chromium-bearing hip arthroplasties raise new questions of the
malignant potential of metallic ends prostheses. Sarcomatous changes
around aluminum oxide ceramics seem not to have been reported in the
literature. The present report may be the first documented case of an
aggressive soft tissue sarcoma detected 15 months after the patient
had an uncemented ceramic total hip arthroplasty. If a causal
relationship exists, the incidence of this phenomenon in the United
States is 250 times greater than would be expected from statistics on
soft tissue sarcoma at the hip.
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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.
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Delayed healing in full-thickness wounds treated with aluminum
chloride solution. 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
ferric subsulfate solution or were allowed to clot with minimal
pressure from a gauze pad. Delay in reepithelialization was noted
histologically both in wounds treated with aluminum chloride and in
those treated with ferric subsulfate compared to controls. Presumably
this delay was the result of tissue necrosis caused by these
hemostatic agents, resulting in slightly larger and less cosmetically
acceptable scars. Plots of evaporimetry data revealed a biphasic
pattern of water loss during healing, with an initial rapid decline in
water loss followed by a much slower decline.
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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 site reactions related to aluminium, showed
unusual features not described previously. In one, there was a
sclerosing lipogranuloma-like reaction with unlined cystic spaces
containing crystalline material. The other case presented as a large
symptomatic subcutaneous swelling which icroscopically 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
aluminium injection site reactions and emphasises that the lesions
have a wider range of histological appearances than described
previously.
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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 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 metal chloride, yielding pH 4.7 (Al) or 3.5
(Ga), formation of cerebrospinal fluid was suppressed 100%. This
mechanism may also account for the antiperspirant action of Al salts.
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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 solutions using certain brands of 25% albumin contained
aluminum levels within the toxic 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 was measured.
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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.
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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 12 years 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 spastic paraparesis. 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
nervous system, and theoretically long-term low-level exposure to
aluminum in the potroom could explain the findings in our patients.
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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 excess of bladder cancer in the region
studied. (Author abstract) (85 Refs)
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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 aluminum tartrate injection for 40 days.
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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 of neurodegenerative disorders in
humans. Effects of Al on cell viability (lysosomal and mitochondrial
activity) and differentiation (synthesis of cell-specific proteins)
were found to the brain area specific with the highest sensitivity
observed in optic tectum.
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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.
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Persistent subcutaneous nodules in children hyposensitized with
aluminium-containing allergen extracts.
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 had severely
treatment-resistant subcutaneous nodules in their forearms. Because of
their long persistence the nodules 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. Patch tests for aluminium were positive in four of the six
patients.
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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 used for testing.
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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 altered its status from being a nontoxic,
nonabsorbable, harmless element. This maybe of particular concern to
the developing foetus which is more susceptible to agents and at lower
levels than the adult. Little attention has been given to aluminium>s
potential reproductive toxicity until recently and further research is
required for a full evaluation of its toxicity. Our preliminary
results demonstrate behavioural and neurochemical alterations in the
offspring of mice exposed to aluminium during gestation. Further, the
effects of such exposure are also present in the adult animal
suggesting persistent changes in behaviour following prenatal
exposure.
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The absence of extracellular calcium potentiates the killing of
cultured hepatocytes 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 a
mechanisms distinct from previously recognized pathways of lethal cell
injury. It is hypothesized that aluminum binds to cytoskeletal
proteins intimately associated with the plasma membrane. This
interaction eventually disrupts the permeability barrier function of
the cell membrane, an event that heralds the death of the hepatocyte.
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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 aluminium allergy is not exceptional.
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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 testing patients with symptoms at vaccination
sites in order to avoid this problem.
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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 persistent subcutaneous nodules at the injection
site; the existence of delayed sensitivity to aluminium has been
implicated in the pathogenesis of these nodules.
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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, 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).
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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 aluminium hydroxide, 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.
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Short-term experimental acidification of a Welsh stream: toxicity of
different forms 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
large mortalities and reduced feeding were recorded in the acid and
aluminium zone.
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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 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 to levels 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.
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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 discontinuing aluminum treatment, 2 weeks prior to testing.
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Aluminum-induced neurofibrillary degeneration disrupts acquisition of
the rabbit>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
conditioned response over the 4 days of testing. This disruption of
conditioning in aluminum-treated rabbits could not be attributed to
deficits in sensory or motor processes or to illness.
Neuropathological analysis revealed widespread neurofibrillary tangle
formation in aluminum-treated animals.
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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 of aluminum may lead to neurological
disorders.
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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 different regions 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 the hippocampus. Aluminum was also seen to
compartmentalize in almost all the tissues of the body to varying
extents, and the highest accumulation was in the spleen.
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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 the normal differentiation of bone marrow stromal cells to
mature osteoblasts in vitro, suggesting that ions released from
implants in vivo may contribute to implant failure by impairing normal
bone deposition.
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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 is released from the glass into the
polyalkeonic acid solution. 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 water exposure was studied. 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. This would
correspond to the inhibiting effect of aluminium on bone
mineralization.
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Impaired control of information transfer at an isolated synapse
treated by aluminum: 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 found in the diseased brain of demented patients modulates
synaptic transmission.
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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
that mimics the intraneuronal inclusions of amyotrophic lateral
sclerosis.
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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 around joints. Certain features of some of
these arthropathies and their significance have only recently been
recognized and others have been insufficiently emphasized. An
important group of conditions are 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 pyrophosphate deposition, and
calcium hydroxyapatite deposition, are also reviewed.
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Sepsis: a cause of aluminum release from tissue stores associated with
acute neurological 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
aluminum who developed septicemia. In all cases the serum aluminum
increased markedly. This may have contributed to the neurological
dysfunction seen in five, and the deaths of four of the patients. We
suggest that the rise in serum aluminum was due to the release of
tissue-bound aluminum, resulting in an increase in free, diffusable
aluminum and that this jeopardized both neurological function and
immunocompetence.
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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 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.
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Transverse fractures of the spinous process of the 7th cervical
vertebra in RDT 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
about their daily work. These observations indicate that Al- or iron-
related bone disease with secondary hyperparathyroidism can induce
bone fracture by only slight stress in patients maintained on
hemodialysis.
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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 and evidence 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 both 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 blood via 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
because of direct introduction of aluminum into 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 role aluminum may play in the pathogenesis of this bone lesion.
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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 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 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
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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 hypothesized that
mineral acids from atmospheric deposition have remobilized Al
previously precipitated within the soil 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 organic and F complexes are the
predominant forms of Al in dilute (low ionic strength) acidic surface
waters. The concentration of inorganic forms of Al increases
exponentially 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 with variations in organic carbon concentration of surface
waters rather than pH. Elevated concentrations of Al in dilute acidic
waters are of interest because: Al is an important pH buffer; Al may
influence the cycling of important elements like P, organic carbon,
and trace metals; and Al is potentially toxic to aquatic organisms.
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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% 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 reduces Ca2+ influx dose-dependently: a maximum 55% reduction
was observed after 1-2 h exposure to 200 micrograms .1(-1) (7.4
microM) Al.
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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 to a combination of
ionoregulatory, osmoregulatory and respiratory dysfunction. The
mechanism of epithelial cell death is proposed as a general mechanism
of aluminium-induced accelerated cell death.
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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
be dichotomized on morphological grounds. In one, intraneuronal
neurofilamentous aggregates are formed, whereas in the other,
significant neurochemical and neurophysiological perturbations are
induced without neurofilamentous aggregate formation.
Evidence is presented that the induction of neurofilamentous
aggregates is a consequence of alterations in the posttranslational
processing of neurofilament (NF), particularly with regard to
phosphorylation state. Although Al 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
cytoskeletal pathology, 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 correlate with 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
development remains to be determined. In this article, the mechanisms
of Al neurotoxicity are reviewed and recommendations are put forth
with regard to future research.
Institutional address:
Department of Clinical Neurological Sciences
University of Western Ontario
London, Canada.
mstrong@julian.uwo.ca
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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; aluminum toxicity is rarely considered. We report a
teenage girl with acute lymphoblastic leukemia who developed mental
status changes, speech disturbance, coarse tremor, and abnormal EEG
findings following intravesical 1% alum irrigation and administration
of aluminum-containing antacids. All abnormalities resolved after a
nine-week course of intravenous deferoxamine.
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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 slowly progressing encephalomyelopathy characterized
at first by alteration of posture and then by myoclonic jerks 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 after injection.
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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.
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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 a
convoluted 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 NO restrictions whatever on the amount or use of aluminum.
Diseases Associated with Aluminium Intoxication
H. Tomlinson, M.B., Ch.B., MRCS., LRCP
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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, plants and trees, and causes
widespread degradation of 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. |
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