Aluminum Toxicity References
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Aluminum neurotoxicity in pre-term infants receiving intravenous-feeding solutions.
Author: Bishop N.J. – Morley R. – Day J.P. – Lucas A.
Source: N Engl J Med (1997 May 29) 336(22):1557-61
Aluminum, a contaminant of commercial intravenous–feeding solutions, is potentially
neurotoxic. We investigated the effect of prenatal exposure to intravenous aluminum on
the neurotoxic. We investigated the effect of prenatal exposure to intravenous aluminum
on the neurological 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 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 neurological development.
Aluminum-containing emboli in infants treated with extracorporeal membrane oxygenation.
Author: Vogler C. – Sotelo-Avila C. – Lagunoff D. – Braun P. – Schreifels J.A. – Weber T.
Source: 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.
Sequential serum aluminum and urine aluminum: creatinine ratio and tissue aluminum
loading in infants with fractures/rickets.
Author: Koo W.W. – Krug-Wispe S.K. – Succop P. – Bendon R. – Kaplan L.A.
Source: 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.
Aluminum in parenteral solutions revisited - again
Author: Klein G.L.
Source: 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 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.
Aluminum-induced anemia
Source: 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.
Source: 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. Persistent subcutaneous nodules in
patients hyposensitized with aluminum -containing allergen extracts.
Persistent subcutaneous nodules in patients hyposensitized with aluminum-containing
allergen extracts
Author: Garcia-Patos V. – Pujol R.M. – Alomar A. – Cistero A. – Curell R. – Fernandez-
Figueras M.T. – de Moragas J.M.
Source: 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 hypo sensitization
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.
Trace metals and degenerative diseases of the skeleton
Author: Savory J. – Bertholf R.L. – Wills M.R.
Source: 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.
Postvaccinal sarcomas in the cat: epidemiology and electron probe micro analytical
identification of aluminum
Author: Hendrick M.J. – Goldschmidt M.H. – Shofer F.S. – Wang Y.Y. – Somlyo A.P.
Source: 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.
Aspects of aluminum toxicity
Author: Hewitt C.D. – Savory J. – Wills M.R.
Source: 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.
Soft tissue sarcoma associated with aluminum oxide ceramic total hip arthroplasty. A case
report.
Author: Ryu R.K. – Bovill E.G. Jr – Skinner H.B. – Murray W.R.
Source: 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.
Aluminum-induced granulomas in a tattoo.
Author: McFadden N. – Lyberg T. – Hensten-Pettersen A.
Source: 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 chloride solution. A
histologic study with evaporimetry correlation.
Author: Sawchuk W.S. – Friedman K.J. – Manning T. – Pinnell S.R.
Source: 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.
Aluminium and injection site reactions.
Author: Culora G.A. – Ramsay A.D. – Theaker J.M.
Source: 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 microscopically 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
emphasizes 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.
Author: Vogh B.P. – Godman D.R. – Maren T.H.
Source: 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.
Aluminum toxicity and albumin.
Author: Kelly A.T. – Short B.L. – Rains T.C. – May J.C. – Progar J.J.
Source: 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.
The role of aluminium for adverse reactions and immunogenicity of diphtheria-tetanus
booster vaccine.
Author: Mark A. – Granstrom M.
Source: 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.
Author: Heyer N.J.
Source: 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.
Reducing aluminum: an occupation possibly associated with bladder cancer
Author: Theriault G. – De Guire L. – Cordier S.
Source: 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)
Immunohistochemical study of microtubule-associated protein 2 and ubiquitin in
chronically aluminum-intoxicated rabbit brain.
Author: Takeda M. – Tatebayashi Y. – Tanimukai S. – Nakamura Y. – Tanaka T. – Nishimura
T.
Source: 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.
Source: 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.
Aluminium in tooth pastes and Alzheimer's disease.
Author: Verbeeck R.M. – Driessens F.C. – Rotgans J.
Source: 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
allergen extracts.
Author: Frost L. – Johansen P. – Pedersen S. – Veien N. –
Ostergaard P.A. – Nielsen M.H.
Source: Allergy (1985 Jul) 40(5):368-72
A follow-up study of 202 children who had received hyposensitization with aluminium-
containing allergens 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.
Contact sensitivity to aluminium in a patient hyposensitized with aluminium precipitated
grass pollen.
Author: Clemmensen O. – Knudsen H.E.
Source: 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.
Behavioural effects of gestational exposure to aluminium.
Author: Rankin J. – Sedowofia K. – Clayton R. – Manning A.
Subject: 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.
The absence of extracellular calcium potentiates the killing of cultured hepatocytes by
aluminum maltolate.
Author: Snyder J.W. – Serroni A. – Savory J. – Farber J.L.
Source: Arch Biochem Biophys (1995 Jan 10) 316(1): 434-42
This data defines a new model in which aluminum kills liver cells by a mechanism 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.
Sensitization to aluminium by aluminium-precipitated dust and pollen extracts.
Author: Castelain P.Y. – Castelain M. – Vervloet D. – Garbe L. – Mallet B.
Subject: 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.
Allergy to non-toxoid constituents of vaccines and implications for patch testing.
Author: Cox N.H. – Moss C. – Forsyth A.
Subject: 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.
Aluminium allergy in patients hyposensitized with aluminium-precipitated antigen extracts.
Author: 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.
Aluminium allergy.
Author: Veien N.K. – Hattel T. – Justesen O. – Norholm A.
Source: 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).
Vaccination granulomas and aluminium allergy: course and prognostic factors.
Author: Kaaber K. – Nielsen A.O. – Veien N.K.
Source: 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.
Short-term experimental acidification of a Welsh stream: toxicity of different forms of
aluminium at low pH to fish and invertebrates.
Author: McCahon C.P. – Pascoe D.
Source: 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.
Differentiated neuroblastoma cells are more susceptible to aluminium toxicity than
developing cells.
Author: E. Meiri
Source: 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.
Reversal of an aluminum-induced behavioral deficit by administration of deferoxamine.
Author: 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.
Aluminum-induced neurofibrillary degeneration disrupts acquisition of the rabbit's
classically conditioned nictitating membrane response.
Author: Pendlebury W.W. – Perl D.P. – Schwentker A. – Pingree T.M. – Solomon P.R.
Source: 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.
Aluminum, a neurotoxin which affects diverse metabolic reactions.
Author: Joshi J.G.
Source: 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.
Distribution of aluminum in different brain regions and body organs of rat.
Author: Vasishta R.K. – Gill K.D.
Source: 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.
Ti-6Al-4V ion solution inhibition of osteogenic cell phenotype as a function of
differentiation timecourse in vitro.
Author: Thompson G.J. – Puleo D.A.
Source: 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.
Aluminium release from glass ionomer cements during early water exposure in vitro.
Author: Andersson O.H. – Dahl J.E.
Source: 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.
Impaired control of information transfer at an isolated synapse treated by aluminum: is it
related to dementia?
Author: Banin E. – Meiri H.
Source: 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.
Chronic aluminum-induced motor neuron degeneration: clinical, neuropathological and
molecular biological aspects.
Author: Strong M.J. – Garruto R.M.
Source: 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.
Some commonly unrecognized manifestations of metabolic arthropathies.
Author: Cobby M.J. – Martel W.
Source: 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.
Sepsis: a cause of aluminum release from tissue stores associated with acute
neurological dysfunction and mortality.
Author: Davenport A. – Williams P.S. – Roberts N.B. – Bone J.M.
Source: 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.
Estimates of dietary exposure to aluminium.
Author: Pennington J.A. – Schoen S.A.
Source: 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.
Transverse fractures of the spinous process of the 7th cervical vertebra in RDT patients:
an Al related disease?
Source: 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.
Risk of aluminum accumulation in patients with burns and ways to reduce it.
Author: Klein G.L. – Herndon D.N. – Rutan T.C. – Barnett
J.R. – Miller N.L. – Alfrey A.C.
Source: 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.
Aluminum concentrations in tissues of rats: effect of soft drink packaging.
Author: Kandiah J. – Kies C.
Source: 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.
Environmental Effects of Aluminum.
CT Aluminum in acidic surface waters: chemistry, transport, and effects.
Source: 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.
Inhibition of Ca2+ uptake in freshwater carp, Cyprinus carpio, during short-term exposure
to aluminum.
Author: Verbost P.M. – Lafeber F.P. – Spanings F.A. – Aarden E.M. – Wendelaar Bonga S.E.
Source: 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.
A mechanism for acute aluminium toxicity in fish
Author: Exley C. – Chappell J.S. – Birchall J.D.
Source: 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.
Can the mechanisms of aluminum neurotoxicity be integrated into a unified scheme?
Author: Strong M.J. – Garruto R.M. – Joshi J.G. – Mundy W.R. – Shafer T.J.
Source: 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 Research: Department of Clinical Neurological Sciences, University of
Western Ontario, London, Canada (Mstrong@julian.uwo.ca).
Aluminum toxicity following intravesical alum irrigation for hemorrhagic cystitis.
Author: Kanwar V.S. – Jenkins J.J. 3rd – Mandrell B.N. – Furman W.L.
Source: 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.
Progressing encephalomyelopathy with muscular atrophy, induced by aluminum powder.
Author: Bugiani O. – Ghetti B.
Source: 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.
Aluminium foil as a wound dressing
Author: Poole M.D. – Kalus A.M. – von Domarus H.
Source: 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.
History of crime against the Food Laws (1929)
Dr. Riley was the prime mover behind the original Pure Food Law and Director of the FDA.
He resigned 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.
Sources of Aluminum:
Over the Counter: Deodorants, vaginal douches, baby wipes, skin creams, suntan lotions,
toothpaste, buffered aspirin, some hemorrhoid and diarrhea products.
Medical; Vaccinations, allergy testing, intravenous solutions, allergens, wound and
antacid irrigation, ulcer treatment, blood oxygenation, 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.