ALUMINUM CHLORIDE, ANHYDROUS
ALUMINUM CHLORIDE
Human Health Effects:
Human Toxicity Excerpts:
... /IT/ IS CAUSTIC & IRRITATING TO EYES ... BUT IN ONLY 1 OUT OF 5
INSTANCES OF INDUSTRIAL CORNEAL BURNS HAS HEALING BEEN DELAYED BEYOND TWO DAYS
...
A case study of a 21 year old man with delayed hypersensitivity granuloma
formation in a tattoo is reported. Four weeks after tattooing, three separate
tumorous areas appeared in the violet areas of the tattoo. These intermittently
pruritic but never painful lesions had existed for five months by the time of
the first examination. Microscopic examination of the excised tumor indicated
the presence of titanium and aluminum pigments in the tissue. Pigment particles
were both extracellular and intracellular. Moderate hyperkeratosis with
parakeratosis was present. Provocation testing with a sterile suspension of
aluminum was performed by intradermal injection into the arm. The aluminum
suspension consisted of 100 ml of a solution composed of a 2% aqueous solution
of disodium hydrogen phosphate-12-hydrate and 10% aqueous aluminum
chloride at pH 4.1 which was centrifuged and the sediment added
to a 0.9% saline solution. The pH of the suspension was adjusted to pH 7.0 by
addition of 5M sodium hydroxide. After 2 weeks, an erythematous nodular reaction
appeared in the test site. A biopsy was performed 3 months after the provocation
testing. It revealed a perifollicular and perivascular lymphocytic infiltrate
with scattered plasma cells and pigment particles in the reticular and papillary
dermis. A mild fibrosis was present, but no giant cells or necrosis were
detected.
/Anhydrous aluminum chloride is a/
powerful irritant to tissue; moderately toxic by ingestion. Reacts violently
with water evolving hydrogen chloride gas.
A 23 yr old woman whose unilateral segmental hyperhidrosis had been
controlled by weekly occlusive therapy with aluminium chloride 20% in dehydrated
alcohol, developed miliaria over the treated area after exertion. The miliaria
resolved on discontinuation of treatment but the hyperhidrosis returned.
A solution of aluminium chloride 20% in dehydrated alcohol was effective in
relieving axillary hyperhidrosis in 64 of 65 patients. The solution was applied
at night to the dry axilla, the axilla being washed with soapand water in the
morning. After a week, applications were made only when necessary, usually every
7 to 21 days. Irritation was the only side-effect. Occlusion was not necessary.
/Aluminum chloride (anhydrous)/ causes
severe eye & skin burns. Irritating to skin, eye, & respiratory system.
A pilot study with aluminum chloride demonstrated
the virtually complete protective action of aluminum against the fibrogenic and
alveolar damaging effects of inhaled silica dusts. McIntyre aluminum powder,
however, did not inhibit pulmonary fibrosis, while powdered aluminum by itself
produced collagen as measured by total hydroxyproline in the lung. Aluminum
chlorohydroxyallantoinate reduced experimental silicosis and anthracosilicosis
in rats and monkeys. In coal workers' pneumoconiosis, this compound delayed
progression during a 5 yr therapy.
PRELIMINARY EVIDENCE SUGGESTS THAT THERE MIGHT BE A RELATIONSHIP BETWEEN
DEGREE OF DISSOCIATION OF ALUMINUM SPECIES ... IN CONJUNCTION WITH ITS CHARGE
VALUE, & ITS ABILITY TO REDUCE OR INHIBIT PERSPIRATION. /ALUMINUM/
Patients who had died with dialysis encephalopathy syndrome had brain gray
matter aluminum levels that were 3 times higher (approximately 12 mg/kg dry
weight) than those seen in patients who had been comparably dialyzed but did not
have dialysis encephalopathy syndrome (approximately 4 mg/kg dry weight). Both
of these groups were markedly higher than the 1 mg/kg dry weight level seen in
controls. These data clearly indicate elevated brain levels of aluminum in
dialyzed patients and emphasize the fact that only the highest levels of brain
aluminum are associated with dialysis encephalopathy syndrome. /Aluminum/
X-ray spectrometric evidence of aluminum accumulation in neurofibrillary
tangle-bearing neurons of human brains was reported. Quite in contrast to the
extensive literature on aluminum in dialysis encephalopathy syndrome, there
appears to be only a small amount of additional corroborating evidence for
elevated brain levels of aluminum in Alzheimer's disease patients. ... Much of
the argument for a role of aluminum in Alzheimer's disease has been built on the
fact that in experimental animals, such as cat and rabbit, intracerebral
injections of small amounts of aluminum result in neural degeneration which is
characterized by the development of neurofibrillary tangles. ...
Aluminum-induced tangles in experimental animals are composed of single 10 nm
filaments while those from Alzheimer's disease are paired, helically wound
filaments. ... In spite of the apparent similarities in the two types of
tangles, there are sufficient differences to warrant caution in interpreting
that the tangles in humans are caused by aluminum as they are in experimental
animals. /Aluminum/
Genetic predisposition to Alzheimer's disease and other similar
neuroencephalopathies has become more widely appreciated. For example, PHF-containing
neurons have been found to be common in patients on the island of Guam who have
been diagnosed with a particular type of encephalopathy, referred to as
amyotrophic lateral sclerosis with Parkinsonism dementia complex (ALS-PD complex
of Guam). Elevation of aluminum levels of drinking water in Guam have been
associated with the high incidence of this complex, but it appears that only the
indigenous population of Guam is affected suggesting a genetic predisposition.
/Aluminum/
THERE IS SOME EVIDENCE THAT @ INTAKE LEVELS CONSIDERABLY HIGHER THAN NORMAL
THERE IS TENDENCY FOR BODY TO BECOME DEPLETED OF /PHOSPHORUS/, OWING TO BINDING
OF DIETARY PHOSPHATE BY ALUMINUM IN DIGESTIVE TRACT. /ALUMINUM/
LOCALLY IN SOLN ... /ALUM IS/ RARELY IRRITATING BUT THE DRY POWDER MAY CAUSE
MARKED INFLAMMATION OR CORROSION OF THE SKIN & MUCOUS MEMBRANES. WHEN
INGESTED AS CONCN SOLN OR AS SOLID ... THERE IS GI IRRITATION OR CORROSION, WITH
NAUSEA, VOMITING, ABDOMINAL PAIN & DIARRHEA. /ALUM/
Nineteen young male workers exposed occupationally from 1975-1977 to inhaled
particles of aluminum ... Breathlessness with reversible airways obstruction
after an average of 4 mo employment. At standardized methacholine provocation
tests, 17 of 19 workers with normal spirometry showed airway hyperreactivity
with a fall of forced expiratory volume in 1 sec of: greater than or equal to
15% after 0.1% methacholine. Fifteen initially asthmatic workers were followed
for 2-5 yr with methacholine provocation tests. Mean threshold dose 15% forced
expiratory volume in 1 sec in 11 workers did not change significantly after an
average of 41 mo of nonexposure. Six workers continuously exposed for 48 mo also
failed to change normal airway reactivity. /Aluminum salts/
Literature describing serum and cerebrospinal fluid aluminum concn in
patients with Alzheimer's disease and elderly normal controls is reviewed, and
results of a comparative study in ten patients and ten controls are presented.
Aluminum concn in the hair of study subjects was measured by plasma emission
spectrometry. There were no significant differences in the concn of aluminum in
hair, serum, or cerebrospinal fluid between patients and controls. The
implications of previous reports of elevated aluminum concn in patients with
Alzheimer's disease for the treatment of the disease are reviewed. At the
present time, there is no conclusive evidence that active attempts to alter
aluminum concn in diet or medicines produce any beneficial effect in Alzheimer's
disease. /Aluminum/
Nuclear and chromatin fractions were prepared from the cerebral cortex of 34
human and 37 animal brains. Chromatin was separated into a heavy heterochromatin
fraction and two euchromatin fractions: intermediate euchromatin and light
euchromatin. Compared to age-matched controls, aluminum content expressed per
gram of DNA was significantly increased in nuclear and heterochromatin fractions
in pre-senile Alzheimer's disease. In contrast, nuclear preparations from brains
of patients who had died with dialysis encephalopathy contained less aluminum
than controls, although whole tissue concn were elevated ten to fifteen times
above the control concn. Direct injection of aluminum into the cerebrospinal
fluid of cats resulted in a progressive encephalopathy with neurofibrillary
degeneration and increased intranuclear aluminum content. It is speculated that
in Alzheimer's disease, the normal blood-brain and cytoplasmic barriers for this
neurotoxic metal are defective, permitting aluminum to gain access to
DNA-containing constituents of the nuclei. /Aluminum/
Though the etiology of the dialysis dementia has not been conclusively
established, there is ample evidence to implicate aluminum as the causative
agent for this fatal syndrome. ... Dialysis dementia is a severe syndrome
characterized by progressive neurological impairment, speech disorders,
dysarthria, dyspraxia, dysphasia, aphemia, amnesia, mutism, facial grimacing and
myoclonus. Of sixty dialysis dementia cases recently reviewed, 87% exhibited
disturbances in communication, 66% in cognition and 93% in movement. The onset
is usually insidious, with the first symptoms occurring after a mean of 37 mo
from the beginning of the dialysis treatment. Hesitant, stuttering,
misarticulated and non-fluent speech, difficulty in concentration, diurnal
drowsiness, reduction of attention span, poor memory, dysgraphia and twitching
of limbs are usually the earliest signs. Patients exhibit a very characteristic
electroencephalogram demonstrating paroxysmal slowing, diffuse rhythmical
bursts, with diphasic or triphasic spiked waves in the high-voltage delta
frequency range in the initial early stages and only pronounced generalized
delta and theta activity late in the course of the dialysis dementia. Reports
exist on possible epileptogenic activity arising in the middle diencephalon and
a few indicate localized cortical atrophy. Low protein content in the frontal
grey matter may indicate that dialysis encephalopathy is accompanied by defects
in the blood-brain barrier. Episodic apnea was also related to the EEG
abnormality with intermittent respiratory arrest occurring simultaneously with
paroxysmal slowing. ... The actual pathogenesis is complicated, since the
symptoms are developed in some patients and not in other equally exposed
patients. This can be attributed to the rate of exposure or peak free aluminum
concn as well as other factors, such as parathyroid hormone, that affects
aluminum absorption and/or distribution, and the impairment of some functions of
the central nervous system. /Aluminum/
On occasion workers chronically exposed to aluminum-containing dusts or fumes
have developed severe pulmonary reactions including fibrosis, emphysema and
pneumothorax. A much rarer encephalopathy has also been described. The factors
which predispose to lung damage are not well characterized. ... /Aluminum (dust
or fumes)/
May cause minor irritation to lungs & eyes. /Aluminum (dust or powder)/
Aluminum deposition in bone is a major cause of osteomalacia in long-term
dialysis patients. Aluminum is deposited at the mineralization front and thus
prevents normal calcium deposition ... . Other factors that may contribute to
osteomalacia in patients with chronic renal failure are metabolic acidosis and
hypophosphatemia due to excessive use of phosphate-binding antacids. /Aluminum/
The high levels of aluminum found in the brain tissue of uremic patients who
died are thought to be the cause of dialysis encephalopathy. Aluminum in the
water supply and in phosphate binding gels is the likely source. Aluminum
toxicity also is manifested by abnormal accumulation in bone. Osteomalacia is
rare when aluminum-free dialysate is used and oral aluminum ingestion is
minimized. /Aluminum/
Certain dusts produce primarily interstitial fibrotic disease (eg, acute
berylliosis, aluminosis, asbestosis) rather than the focal nodular lesions seen
in simple pneumoconiosis. Fibrotic lesions appear out of proportion to the
presence of dust-laden macrophages. /Aluminum dust/
Chronic renal failure patients on long-term dialysis develop high aluminum
serum and tissue concentrations, especially in bone. Aluminum toxicity occurs
almost exclusively in patients who are unable to excrete dietary aluminum. In
addition, a subset of dialysis patients may exist who absorb aluminum
excessively for unknown reasons. Elevated aluminum levels appear to be an
important factor in the pathogenesis of dialysis encephalopathy and in one type
of dialysis osteomalacia that requires 3 to 7 years of dialysis for clinical
expression. /Aluminum/
Accumulation of aluminum in bone appears to reduce the positive effects of
vitamin D on uremic osteodystrophy. The deposition of aluminum in bone may block
incorporation of calcium into osteoid, leading to osteomalacia. The prevention
of calcium deposition in both leads to return of the calcium to the circulation
with a rise in the serum calcium level. The elevated levels in turn inhibit the
release of parathyroid hormone by the parathyroid glands. In addition, aluminum
may be one factor in the etiology of anemia in chronic renal failure. /Aluminum/
Amyotrophic lateral sclerosis, another severe neurological disease, has also
been related to aluminum accumulation in the brain. This disease is epidemic in
certain areas of the world where intake of calcium and magnesium from food and
water are very low and where at the same time the relative intake of aluminum
appears to be comparably high. /Aluminum/
Fumes from an aluminum soldering flux have been reported to result in a
delayed type of asthma resembling pollen-sensitivity asthma, rather than the
infiltrative type seen in farmer's lung. Delayed and prolonged
bronchoconstriction was investigated by serial spirometry, peak flow rates, and
body plethysmography after the inhalation of small amounts of flux fumes.
Because similar responses were obtained after inhalation of (aminoethyl)
ethanolamine, one of the major flux constituents, it was presumed to be the
active allergic agent. If the inert-gas, tungsten-ore process is used in
aluminum welding the asthma problem is eliminated, but this process can lead to
upper respiratory symptoms (chest tightness and wheezing from edema) unless
ozone exposures are kept below 0.2 ppm. /Aluminum/
Recently reported adverse effects of aluminum in humans have resulted from
inhalation or ingestion of aluminum in concentrations many times greater than
the amounts present in normal circumstances. Following large oral doses of
aluminum, toxic syndromes involve gastrointestinal tract irritation and
eventually, interference with phosphate absorption, which results in rickets.
Industrial exposure to high concentrations of aluminum-containing airborne dusts
has resulted in a number of cases of occupational pneumoconiosis. Most of these
exposures were chronic, and other substances were involved in nearly all
instances. For example, an asthma-like disease has been reported in workers
engaged in the production of aluminum from its oxide. This condition may result
from the hydrogen fluoride that evolves from the use of fluorine-bearing
materials in the production of metallic aluminum. Silicosis, aluminosis,
aluminum lung, and bauxite pneumoconiosis are the result of pulmonary fibrotic
reactions to silical and aluminum-containing compounds, which have been observed
in the lung tissue in humans. Paradoxically, aluminum powder has been used in
the prevention and therapy of silicosis. The rationale is that small amounts of
metallic aluminum inhibit the solubility of siliceous materials in the lungs or
diminish their fibrogenic properties. There is no unequivocable evidence that
the procedure is clinically effective. /Aluminum/
Serum aluminum levels and dihydropteridine reductase levels in erythrocytes
of 38 patients on hemodialysis were studied. None of the patients showed
clinical evidence of aluminum encephalopathy. The serum aluminum level of
dialysis patients averaged 67.6 ug/l (range 15 to 190 ug/l) and that of 18
control patients averaged 4.9 ug/l. Dihyropteridine reductase activity was
inversely related to the serum aluminum concentration and was less than that
predicted from hemoglobin concentrations. Serum biopterin derivatives were
markedly elevated in dialysis patients, indicating a disturbance of
neurotransmitter metabolism, but were not correlated with hemoglobin or serum
aluminum concentrations. /Aluminum/
Laser microprobe mass analysis was used to study the neurofibrillary
tangle-bearing and tangle-free neurons from the brain tissue of the native
population of Guam. This population has a remarkably high tendency to develop
neurodegenerative disease, particularly amyotropic lateral sclerosis and a form
of parkinsonism associated with severe dementia. The concentration of
intracellular aluminum in the tangle-bearing neurons was about 300-600 ppm.
/Aluminum/
Serum aluminum was determined in 7 patients diagnosed with Alzheimer's
dementia and 5 patients with multiinfarct dementia. The mean age was 80.6 + or -
4.9 years. Serum aluminum was 0.099 + or - 0.01 ug/ml in the Alzheimer's group
and 0.084 + or - 0.012 ug/ml in the multiinfarct group. This was significantly
different at the p <0.03 level (Mann Whitney U test, 2 tail). /Aluminum/
In group of 19 rheumatoid arthritis patients with normal renal function,
serum levels of aluminum were monitored during treatment with drugs containing
aluminum. The serum aluminum levels during treatment were significantly higher
than those before treatment, ie 19.4 (SEM 2.3) ug/l and 12.3 (1.7),
respectively. This incr in serum aluminum levels of was significantly correlated
with the pretreatment serum creatinine level (mean value for the whole group
80.5 (SEM 4.7) uM/l), but showed no correlation with the predicted creatinine
clearance. /Aluminum/
The psychomotor function of 27 long term hemodialysis patients with
apparently normal cerebral function, who had only mildly raised serum aluminum
(mean 59 ug/l), was measured by means of a computerized version of the symbol
digit coding test. Compared with those of control subjects matched for age and
the patients estimated premorbid IQ, the patients response times were
significantly longer (2.51 vs 1.88 sec). Abnormalities were also detected in 5
other computerized tests of psychomotor function. The mean activity of
erythrocyte dihydropteridine reductase, which is inhibited by aluminum, rose
during 3 mo of desferrioxamine treatment in most of the 15 patients so treated.
Although there was no relation between baseline psychomotor function and either
indices of cumulative aluminum exposure or erythrocyte dihydropteridine
reductase activity, changes in dihyropteridine reductase induced by
desferrioxamine correlated with changes in psychomotor performance. The flash
stimulated visual evoked potential (measured in 10 patients) was delayed (133.4
millisec), although the pattern stimulated visual evoked potential remained
normal (101.8 millisec). The difference between the visual evoked potentials
stimulated by flash and pattern was significantly greater in the patients than
in the controls (31.6 vs 19.4 millisec) and was significantly related to the
symbol digit coding response times and to the oral aluminum intake. /Aluminum/
Skin, Eye and Respiratory Irritations:
Irritating to eyes, nose and throat. Will burn skin and eyes.
May cause minor irritation to lungs & eyes. /Aluminum (dust or powder)/
Drug Warnings:
Aluminum salts may cause phosphorus depletion which is generally negligible.
However, with prolonged administration or large doses, hypophosphatemia may
occur, especially in patients with inadequate dietary intake of phosphorus;
hypercalciuria secondary to bone resorption and increased intestinal absorption
of calcium results. This phosphorus depletion syndrome is characterized by
anorexia, malaise, and muscle weakness, and prolonged aluminum antacid therapy
may cause urinary calculi, osteomalacia, and osteoporosis. A low-phosphorus
diet, diarrhea, excessive phosphorus losses from malabsorption, and restoration
of renal function after a kidney transplant increase the likelihood of the
syndrome. Serum phosphate concentrations should be monitored at monthly or
bimonthly intervals in patients on maintenance hemodialysis who are receiving
chronic aluminum antacid therapy. /Aluminum salts/
Medical Surveillance:
Employment and periodic physical examinations should give special
consideration to the skin, eyes and lungs. Lung function should be followed.
Probable Routes of Human Exposure:
INTAKE OF ALUMINUM IS CHIEFLY BY MOUTH, FROM FOODS AND BEVERAGES, ALSO BY
LUNGS, FROM THE ATMOSPHERIC DUST CONTENT. IT IS PRESENT IN NATURAL DIET, IN AMT
VARYING FROM VERY LOW IN ANIMAL PRODUCTS TO RELATIVELY HIGH IN PLANTS.
/ALUMINUM/
Body Burden:
Aluminum content of normal human brain ranged from 0.1-3.9 ug/g dry weight.
In a study of 208 samples taken from 7 patients, ... a mean aluminum content of
1.9 + or - 0.07 ug/g dry weight of gray matter /was found/ to be abnormal. In a
study of 585 areas sampled from the brain tissue of 10 patients with Alzheimer's
disease they found 28% had an aluminum concn > 4 ug/g. The range of the 585
samples was 0.4-107 ug/g. /Aluminum/
Average Daily Intake:
The daily ingestion of aluminum by humans was estimated to be 30-50 mg.
/Aluminum/
Antidote and Emergency Treatment:
/Exposure to aluminum chloride:/ Dust:
Irritating to eyes, nose and throat. Harmful if inhaled. Move to fresh air if
beathing has stopped, give artificial respiration. If breathing is difficult,
give oxygen. Solid: Will burn skin and eyes. Harmful if swallowed. Remove
contaminated clothing and shoes. Flush affected areas with plenty of water. If
in eyes, hold eyelids open and flush with plenty of water. If swallowed and
victim is conscious, have victim drink water or milk. Do not induce vomiting.
TREATMENT: TO RELIEVE THE GI DISTRESS /CAUSED BY SWALLOWING ALUMINUM
SALTS/... THE DEGREE OF DEHYDRATION & ELECTROLYTE LOSS CAUSED BY VOMITING
& DIARRHEA MUST BE DETERMINED, & CORRECTED BY IV INFUSIONS OF
APPROPRIATE SOLUTIONS. /ALUMINUM SALTS/
DIAGNOSIS: WHEN HISTORY IS UNATTAINABLE, DIAGNOSIS DEPENDS ON THE
DEMONSTRATION OF LARGE AMT OF ALUMINUM IN VOMITUS, STOMACH CONTENTS OR FECES.
/ALUMINUM CMPD/
Deferoxamine has been used to treat dialysis encephalopathy and osteomalacia
with symptomatic relief reported. The use of deferoxamine for aluminum-toxic
dialysis patients has been suggested for serum levels of aluminum between 100
and 200 ug/ml. Deferoxamine also has been used to diagnose aluminum-related
osteodystrophy. After a deferoxamine infusion of 40 mg/kg over 2 hours, an
increment in plasma aluminum concentration of 200 ug/l identified 35 of 37
patients with biopsy-proven aluminum-related osteodystrophy (sensitivity, 94%;
specificity, 50%). Calcium disodium ethylenediaminetetraacetic acid does not
appear as effective as deferoxamine in chelating aluminum. Especially in
dialysis patients, aluminum-containing medications should be reduced. /Aluminum/
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
CHROMOSOME ABERRATIONS IN MICE INDUCED BY ALUMINUM
CHLORIDE. HIGHER CONCN INDUCED HIGHER FREQUENCY OF ABERRATIONS
BUT THE INCR WAS NOT PROPORTIONAL.
BONE MARROW CELLS OF MICE INJECTED WITH 0.1, 0.05 & 0.01 MOLAR SOLN OF ALUMINUM
CHLORIDE @ 1 ML/30 G BODY WT, EROSION, STICKINESS, SUB-CHROMATID,
CHROMATID & CHROMOSOME BREAKS, TRANSLOCATIONS, GAPS & CONSTRICTIONS IN
INDIVIDUAL CHROMOSOMES WERE OBSERVED.
TERATOGENIC EFFECTS OF ALUMINUM IN RATS. ALUMINUM
CHLORIDE; MAMMAL, RAT; RATTUS, SPRAGUE-DAWLEY.
TERATOLOGICAL STUDIES WITH ALUMINUM IN THE RAT. ALUMINUM
CHLORIDE; MAMMAL, RAT; RATTUS, HOLTZMAN.
IN INHALATION STUDIES LUNGS OF HAMSTERS GIVEN 20 OR MORE EXPOSURES TO 50
MG/CU M OF PROPYLENE GLYCOL COMPLEX OF ALUMINUM-CHLORIDE-HYDROXIDE
SHOWED GRANULOMATOUS LESION IN RESP BRONCHIOLES THAT PERSISTED THROUGHOUT 6-WK
POSTEXPOSURE PERIOD. /ANTIPERSPIRANTS/
IN INHALATION STUDIES WITH PROPYLENE GLYCOL COMPLEX OF ALUMINUM-CHLORIDE-HYDROXIDE,
ALVEOLAR THICKENING & INCR NUMBER OF MACROPHAGES WERE SEEN IN LUNGS OF
HAMSTER SOON AFTER 3 EXPOSURES TO 150 MG/CU M BUT WITH TIME TO 35 MG/CU M OR
HIGHER WERE INCR ON 4TH DAY.
ALUMINUM CHLORIDE ADMIN IP TO
PREGNANT RATS @ DIFFERENT DOSE LEVELS & @ DIFFERENT STAGES OF GESTATION.
HIGH INCIDENCE OF MATERNAL DEATH @ HIGH DOSE-LEVELS. MATERNAL WT GAIN DURING
GESTATIONAL PERIOD WAS LESS AS COMPARED TO CONTROLS. ... ALUMINUM
CHLORIDE ADMIN IP TO PREGNANT RATS @ DIFFERENT STAGES OF
GESTATION. MATERNAL LIVER WAS SEVERELY DAMAGED, OFFSPRING SHOWED GROWTH
RETARDATION & SKELETAL DEFECTS. INCIDENCE OF FETAL DEATHS & RESORPTION
WAS SIGNIFICANTLY INCR.
Dietary levels of 100 to 200 mg/kg of aluminum
chloride fed to experimental animals for extended periods led to
retardation of growth and disturbances of phosphate metabolism.
Three groups of pregnant Wistar rats were fed aluminum
chloride. The first group (14 rats) received diet supplemented
with 160 mg aluminum/kg body weight/day from day 8 of gestation to parturition
and the second group (13 rats) was given 200 mg aluminum/kg body weight/day.
Control rats (12 animals) received the diet at the same time periods. Results
indicated that aluminum at both doses had no effect on maternal weight or
behavior. Pre-weaning mortality was increased in offspring, and surviving pups
showed a delay in their neuromotor development and in postnatal weight gain.
/Aluminum/
Male Sprague-Dawley rats (three per treatment group) were administered 0, 2,
10, 20, or 40 mg aluminum per kilogram ip per day for 3 days as aluminum
chloride in saline. Animals were killed 24 hr later. Aluminum
was found to inhibit hepatic drug metabolism in a dose-dependent fashion. The
lowest dose (2 mg or 75 umol/kg) had no effect on the parameters measured,
whereas the highest dose (40 mg or 1.5 mmol/kg) caused a 52% decrease in
cytochrome p450, a 71% decrease in p-nitrophenetole O-deethylase activity, and a
77% decrease in ethylmorphine N-demethylase activity. Hepatic glutathione levels
were unaffected by aluminum, whereas metallothionein was induced in both liver
and kidney. The distribution of endogenous metals normally associated with
metallothionein was altered by aluminum administration. At the highest dose of
aluminum (40 mg/kg), zinc levels were increased in liver cytosol (154%), while
copper levels were unchanged in liver, but decreased in kidney (70%). Aluminum
was present in the liver and kidney. Of the aluminum in the liver, less than 5%
was in the cytosol, bound to a metallothionein-like protein. /Aluminum/
Rainbow trout (Salmo gairdneri) fitted with dorsal aortic cannulae were
exposed in a flow-through soft water system to three acidities (pH 5.2, 4.8, or
4.4) and two concentrations of calcium (45 or 410 uequiv/l), in the presence
(105 ug/l) or absence of aluminum in the form of aluminum
chloride. Mortalities were recorded and blood was sampled for
respiratory gases, ions, metabolites, and hematology before and at 4, 18, 28,
42, and 66 hr. Aluminum was most toxic to cannulated rainbow trout at pH 5.2 and
least toxic at pH 4.4. Higher water calcium concentrations reduced mortality
owing to aluminum at pH 5.2 and 4.8, but had no significant effect at pH 4.4,
where mortality was 0-35% in the presence or absence of aluminum. Most fish
deaths occurred between 42 and 66 hr, with the exception of the aluminum
exposure at pH 5.2, low calcium treatment, where 4 of 10 fish died at about 30
hr. Two toxic mechanisms of aluminum and acidity were seen: ionoregulatory
toxicity, which was caused by aluminum at pH 5.2 and 4.8 and by acidity at pH
4.4, and respiratory toxicity, which was caused solely by aluminum, and was
greatest at higher pH. Ionoregulatory toxicity involved decreases in plasma
sodium + and chlorine -, red cell swelling, and hemoconcentration. Respiratory
toxicity involved reduced blood oxygen tension, elevated blood carbon dioxide
tension, and increases in blood lactate.
Honeylocust (Gleditsia triacanthos L) seedlings were grown for 72 days in
soil from a BC horizon of a Spodosol altered by adding four levels of aluminum
chloride hexahydrate. At harvest, soils at field moisture
capacity were mixed with additional water (equivalent to 1.0 g dry soil:0.4 g
water) or with 0.01 M strontium chloride (equivalent to 1.0 g dry soil:1.4 g
0.008 M strontium chloride . Mixtures were centrifuged and the supernatant
filtered. Saturated paste (water) extracts from controls to the highest aluminum
chloride treatment contained, respectively, 85 to 831 uM
aluminum, 834 to 163 uM calcium, and 316 to 35 uM magnesium and had a pH of 4.4
to 4.0. Leaf, stem, and root concn of aluminum and phosphorus increased while
those of magnesium, calcium, and zinc decreased with increasing levels of
aluminum. Growth decreased as aluminum, aluminum/calcium, and aluminum/magnesium
ratios in the extract increased. Growth was negatively related to tissue concn
of aluminum, phosphorus, zinc and positively related to tissue magnessium and
calcium. /Aluminum chloride hexahydrate/
The effects of aluminum were compared in sham-operated (n= 4) and
thyroparathyroidectomized beagles (n= 4). Thyroparathyroidectomized dogs
received sufficient calcium carbonate (5 g/day) and calcitriol (0.125 ug/day) to
maintain normal plasma calcium and calcitriol levels, but developed evidence of
decr osteoblast recruitment and activity, including diminished osteoid covered
trabecular bone surface (3.22 + or - 0.21 vs 10.95 + or - 1.30%) and a decr
osteoblast number (27.8 + or - 8.1 vs 139.0 + or - 26.0/mm). 2 mo after surgery,
admin of aluminum (1.25 mg/kg iv, 3 times/wk for 8 wk) increased the serum
aluminum levels in both sham (1,087.0 + or - 276.0 vs 2.7 + or - 0.8 ug/l) and
thyroparathyroidectomized animals (2,786.0 + or - 569.0 vs 3.6 + or - 0.8 ug/l)
above normal, but did not alter the plasma calcium, creatinine, or parathyroid
hormone from control levels in either sham or thyroparathyroidectomized dogs.
After 9 wk of therapy, however, bone biopsies from sham-operated beagles
displayed evidence of neoosteogenesis including an increased bone volume (47.0 +
or - 1.0 vs 30.4 + or - 0.9%) and trabecular number 4.1 + or - 0.2 vs 3.2 + or -
0.2/mm). Much of the enhanced volume resulted from deposition of poorly
mineralized woven bone (9.9 + or - 2.7%). In contrast, biopsies from aluminum
treated thyroparathyroidectomized animals exhibited significantly less evidence
of ectopic bone formation. In this regard, bone (35.5 + or - 1.7%) and woven
tissue volume (1.4 + or - 0.8%) as well as trabecular number (3. + or - 0.1/mm)
were significantly less than those of the aluminum treated controls. /Aluminum/
The neurotransmitter alterations which accompany aluminum induced
neurofibrillary degeneration were examined in order to assess how closely they
mimic those of Alzheimer's disease. Ten New Zealand white rabbits were
administered 100 ul of 1% aluminum chloride iv;
control rabbits received 0.9% sodium chloride iv. There was a significant
reduction in choline acetyltransferase activity in entorhinal cortex and
hippocampus as well as significant reductions in cortical concn of serotonin and
norepinephrine in the aluminum treated rabbits. Significant reductions in
glutamate, aspartate and taurine were found in frontoparietal and posterior
parietal cortex. Concn of gamma aminobutyric acid were unchanged in cerebral
cortex. Both substance P and cholecystokinin immunoreactivity were significantly
reduced in entorhinal cortex but there were no significant changes in
somatostatin, neuropeptide Y and vasoactive intestinal polypeptide. The five
neuropeptides were unaffected in striatum, thalamus, cerebellum and brainstem.
Neurochemical changes were found in the regions with the most neurofibrillary
degeneration while regions with little or no neurofibrillary degeneration were
unaffected.
Honey locust and loblolly pine were grown in solution culture with 250 to
1500 uM aluminum (applied as a 1:1 mixture of aluminum
chloride and aluminum sulfate). In both species aluminum reduced
primary root elongation, more severely in the honey locust. The decrease was
most evident in the second mm root segment after 24 hr. The decrease in
elongation was not accompanied by a decrease in cell size. The cytological
appearance of cells in the meristems of treated and untreated honey locust and
loblolly pine also differed. In honey locust, the meristems of control roots 72
hr after treatment were dividing actively and were densely cytoplasmic. In roots
treated with 600 uM aluminum, cell division had almost ceased and the cells were
much more vacuolate. In loblolly pine, cells in the meristem of control roots
were actively dividing and densely protoplasmic. In treated roots, the impact of
aluminum was less pronounced, mitotic divisions were still present, and
vacuolation increased mainly in the differentiating cells distal to the
meristem. Aluminum drastically reduced mitotic activity in honey locust; this
was irreversible with time. A less marked decline was seen in loblolly pine,
with mitotic activity returning to control levels after 72 hr. /Aluminum salts/
Pregnant Wistar rats were divided into 8 groups. Rats in the first 4 groups
received from day 1 of gestation to parturition a standard diet supplemented
with 0 (group 1, control, n= 11), 100 (group 2, n= 12), 300 (group 3, n= 6), and
400 (group 4, n= 8) mg aluminum (as aluminum
trichloride)/kg/day. Rats in groups 5 (control, n= 6), 6 (n= 7),
7 (n= 10) and 8 (n= 6) received during the same period a standard diet
supplemented with 0, 100, 200, and 400 mg aluminum (as aluminum lactate)/kg/day.
No effect of treatment on litter size was detected, but an increased mortality
of pups appeared during the first wk. In groups 3 and 4, the mortality was
already very high on day 1 after parturition (25.2 and 33.8%, respectively) and
reached the maximum value on day 14 in groups 3 (48.7%) and at day 9 in group 4
(57.1%). The neuromotor maturation of surviving pups treated with aluminum
showed an important impairment during the first 2 wk of postnatal life. The time
necessary for pups to return to normal dorsoventral position increased
significantly with the dose of aluminum received by the mother (p< 0.001).
With aluminum chloride, the
performance of young from control groups was superior to that of the treated
groups in tests for negative geotaxis and locomotor coordination. Statistical
analysis showed no difference among the 8 groups for a grasping reflex test on
day 6 and a suspension test on postnatal day 12. /Aluminum/
Groups of 41 juvenile fathead minnows (Pimephales promelas) were exposed (in
duplicate) to a pH of 8.0, 7.5, 6.0, 5.5 and 5.2 and aluminum (Aluminum; as aluminum
trichloride) concn in soft water (8 mg calcium/l) to determine
effect levels at various life stages. Aluminum levels were 15, 30, 35, and 60
ug/l. Reproductive processes including spawning, embryogenesis and early larval
survival were more sensitive to acid stress than were juvenile growth and
survival. Juvenile survival was significantly reduced at pH 5.2 + 60 ug
aluminum/l (p< 0.05). Spawning success was reduced at pH 6.0 and 5.5 (p<
0.10) and failed completely at pH 5.2, regardless of aluminum concn. An apparent
beneficial effect of added aluminum was observed during spawning at pH 7.5 + 35
ug aluminum/l, but this effect was not significantly greater than at pH 7.5 + 15
ug aluminum/l. A significant (p< 0.05) decr in larval survival occurred at pH
6.0 + 15 ug aluminum/l and lower compared to the survival at pH 7.5 + 15 ug
aluminum/l. Aluminum at 30 ug/l provided protection resulting in short term incr
embryo-larval survival at pH 5.5 (survival of 38 vs 0%, p< 0.05). The effect
of parental exposure on progeny survival was assessed by an interchange of
embryos from the spawning treatment to all tested exposure conditions. When
reared at pH 8.0 + 15 ug aluminum/l through 6.0 + 15 ug aluminum/l or at pH 5.5
+ 30 ug aluminum/l, parental exposure did not significantly influence progeny
survival. However, survival was significantly reduced among progeny from brood
fish reared at pH 5.5 + 15 ug aluminum/l as compared to those spawned at pH 6.0
+ 15 ug aluminum/l and above, or at pH 5.5 + 30 ug aluminum/l (p< 0.05).
Juvenile or 14 day larval growth effects were not detected under any exposure
condition (p> 0.05). /Aluminum/
The antigenic composition, neuronal specificity and distribution of aluminum
induced neurofibrillary degeneration were examined in regions of New Zealand
white rabbit brain analogous to those that develop neurofibrillary tangles in
Alzheimer's disease. Neurofibrillary degeneration was induced by
intraventricular instillation of aluminum chloride. In
aluminum treated rabbits, intensely immunoreactive filamentous aggregates were
seen in affected neuronal perikarya after staining with an antiphosphorylated
neurofilament antibody (SMI 31), while in controls immunoreactivity was confined
to axon like elements. Monoclonal antibodies against microtubule associated
protein 2 and tau, which stain neurons exhibiting neurofibrillary degeneration,
formed a discrete linear pattern in layers III and V of cortex. Cortical
somatostatin and nicotinamide adenine dinucleotide phosphate diaphorase reactive
neurons identified in double stained sections were unaffected. Large perikarya
in the vicinity of the globus pallidus, some of which contained AChE, were
frequently SMI 31-immunoreactive. Among the cell groups affected in the upper
brainstem were the nucleus raphe dorsalis and locus coeruleus.
Differential effects of low pH and aluminum on the caudal neurosecretory
system of the brook trout, Salvelinus fontinalis, were studied. The fish were
subjected to soft water at pH 6.5, 5.5 or 5.0 without aluminum added, or to
water pH 5.5 with 200, 300 or 500 ug/l aluminum (as aluminum
chloride) added. Using radioimmunoassay, the concentrations of
urotensin I and urotensin II in the urophysis were measured. A positive
correlation was found between urotensin I concentrations and acidity, and a
negative correlation was found between urotensin II concentrations and total
aluminum in the water. Morphometric analysis revealed that the mean size of
caudal neurosecretory cells tended to be slightly smaller in fish kept in water
at pH 6.5 than in fish at pH 5.5 or at pH 5.5 with 500 ug/l aluminum added. A
smaller proportion of lobed nuclei was observed in caudal neurosecretory cells
of fish at pH 6.5 than at 5.5, and at pH 5.5 with 500 ug/l aluminum added (P<
or = 0.05).
NB2a/dl mouse neuroblastoma cells were exposed to aluminum
chloride (0, 0.1, 0.4, and 1 mM) for 3 and 6 days. Additional
cultures were exposed to aluminum chloride and
the cells were stimulated to elaborate axonal neurites by dibutyryl cyclic AMP.
By phase-contrast microscopy, Aluminum chloride had
no effect on the morphology of undifferentiated (NB2a(-)) or differentiated
(NB2a(+)) cells, or on neuritic elaboration and maintenance. Silver staining by
the Bielschowsky method, however, demonstrated argyrophilic accumulations in
perikarya of many treated NB2a(-) and NB2a(+) cells. The effect was dose
dependent, and 1 mM aluminum chloride incr
by approx 5-fold the percentages of Bielschowsky positive NB2a(-) and (+) cells
over those of untreated cells. At the ultrastructural level, whorls of
intermediate filaments were the most prominent abnormalities in neuronal
perikarya. Although phosphorylated high molecular wt neurofilament subunits are
normally detected by immunocytochemical analyses only within axonal neurites of
NB2a/dl cells, aluminum chloride treatment
caused the detection of phosphorylated epitopes of neurofilament subunits within
perikaryal of NB2a(-) and NB2a(+) cytoskeletons.
Fathead minnow (Pimephales promelas) 1 day post hatch larvae, 12 day post
hatch larvae, and 4 wk post hatch juveniles were exposed to combinations of acid
and inorganic aluminum (aluminum, as aluminum
trichloride) for 96 hr in the laboratory. Life stages were
exposed, under flow through conditions, to 4 nominal pH levels: 4.5, 5.5, 6.5
and 7.5 (control), and 5 nominal aluminum concn: 0 (control) 50, 100, 200, and
400 ug/l in fresh water with a total hardness of 20 to 24 mg/l as calcium
chloride Theoretical speciation of the measured total dissolved monomeric
aluminum was performed in order to estimate the toxic forms of aluminum. The
ranking of life stage sensitivities to acid alone was 1 day larvae, most
sensitive, followed by 12 day larvae and juveniles. At pH 4.5, all three stages
exhibited 100% mortality in all aluminum treatments and controls. At pH 4.5 and
400 ug/l nominal aluminum (total dissolved monomeric aluminum= 384 ug/l), 12 day
larvae experienced 95.5% mortality after only 6 hr exposure. At pH 5.5, 90 to
100% mortality occurred in all but the 50 ug/l aluminum treatment and the no
aluminum control. At pH 5.5, hydroxoid species of aluminum were the predominate
forms of the total dissolved monomeric aluminum. At pH 6.5 and 7.5, aluminum was
not toxic to the 1 day larvae and juveniles, but the mortality of 12 day larvae
exposed to aluminum (predominately hydroxy species) ranged from 18 to 68% with
no clear dose response. Addition of inorganic aluminum to the 4 pH conditions
significantly increased mortality of all 3 life stages (P< 0.001). /Aluminum/
Mouse neuroblastoma clone N1E-115 cells were exposed to either 2%
dimethylsulfoxide medium or dimethylsulfoxide supplemented with aluminum
chloride (aluminum chloride, at 20 to 50 ug/ml aluminum). Cells
were exposed to aluminum chloride either
the day following cell plating in dimethylsulfoxide medium, when proliferation
had been arrested but no differentiation was noticed, or after 10 days in
dimethylsulfoxide when cells were fully differentiated. Aluminum caused
premature onset of deterioration in fully differentiated cells. Toxic effects
were evident only after 24 to 48 hr in different expt. Using microelectrodes,
cells were seen to depolarize from -29.3 + or - 0.9 mV to levels lower than -15
mV in 4 to 6 days; compound polyphasic action potentials were gradually replaced
by slow monophasic spikes before the final low of excitable properties and
structural deformations was noticed. Developing cells followed the normal
pattern of differentiation in the presence of aluminum: within 7 days they
extended neurites, hyperpolarized and exhibited polyphasic spikes. Cells grown
in dimethylsulfoxide medium had a mean lifespan of 20.5 days in 13 expt. Cells
grown in dimethylsulfoxide medium exposed to aluminum from day 1 on had a mean
lifespan of 10.7 days, and those exposed to aluminum from day 10 survived, on
avg, an additional 5.7 days.
The influence of repeated aluminum administration (0.05 or 0.5 mg/100 g of
body wt ip 5 times weekly for 12 wk) on the lysosomal enzyme
N-acetyl-beta-D-glucosaminidase and beta-glucuronidase in the liver and kidneys
of adult female rats with intact kidneys, or following partial nephrectomy (5.6
NX) was investigated. After aluminum loading the aluminum content of the liver
incr 15-30 fold, that of the kidneys 5-8 fold in comparison to control animals.
At the high aluminum dose only the free N-acetyl-beta-D-glucosaminidase in the
kidneys incr. Latent N-acetyl-beta-D-glucosaminidase levels decr in both organs,
the effect being dose related and reflecting lysosomal damage. With one
exception, no elevation in total enzyme activity was observed following aluminum
loading. The liver of both groups of animals showed an incr in free and a decr
of latent beta-glucuronidase activity after high aluminum loading in a similar
manner as N-acetyl-beta-D-glucosaminidase. /Aluminum/
... Studied the effect of various metals on the in-vitro morphological
transformation of Syrian hamster embryo cells. The results for aluminum
chloride administered in concentrations up to 20 ug/ml were
negative. In shorter experiments (20 to 30 days), aluminum
chloride was given orally to rats, guinea pigs, and rabbits in
doses ranging from 3 to 50 mg/kg/day, and in chronic experiments (6 to 12
months) it was given to rats in oral doses ranging from 0.025 to 2.5 mg/kg. No
chromosomal aberrations were found in bone marrow cells as a result of these
exposures.
ALUMINUM CHLORIDE SHOWN TO EXHIBIT
GOOD ANTIPERSPIRANT ACTION IN PILOCARPINE-INDUCED SWEATING IN RAT FOOT PADS
& THIS RESULT IS IN ACCORDANCE WITH OBSERVATIONS IN HUMAN TESTS.
The acute toxic response is confined to the more soluble forms of aluminum,
the chloride and simple and complex sulfates for which the acute
toxicity for laboratory animals has been determined. The oral LD50 of aluminum
chloride for mice is reported to be 770 mg/kg as aluminum ... .
Acute aluminum chloride poisoning
resulted in increased blood glucose, decreased liver glycogen; and increased
incorporation of 32P in the liver of rats. ...
In one study, concentrations of aluminum ranging from 500 to 1,000 ug/g body
weight were added to the diets of pregnant rats from day 6 to day 19 of
gestation, when the fetuses were removed by Caesarean section. Aluminum in the
diet did not affect embryo or fetal mortality rate, litter size, fetal body
weight, or length. However, in a similarly designed experiment in which the
pregnant mothers received subcutaneous injections of parathyroid hormone (68
U/kg) on days 6, 9, 12, 15, or 18 of gestation, there was an increase only in
the resorption rate in those animals receiving aluminum at 1,000 ug/g body
weight. /Aluminum/
... Animal studies show that aluminum particles, in particular stamped
aluminum powder, may cause fibrosis of the lung whereas particles of aluminum
compounds appear to be less reactive. /Aluminum/
Severe aluminum intoxication following parenteral or oral administration of
aluminum hydroxide, chloride, or sulfate to rats is characterized by lethargy,
anorexia, or death. Other authors have found that intratracheal instillation of
aluminum salts or metallic aluminum powder has produced pulmonary fibroses.
Injected intraperitoneally, aluminum compounds produce fibrotic peritonitis.
/Aluminum cmpd/
... Aluminum salts are much more toxic intravenously than by mouth to
animals. The mechanism of this presumable systemic effect of aluminum is not
known. /Aluminum hydroxide/
Because aluminum is only sparingly absorbed from the gut, LD50 values for
aluminum ingestion are unavailable, since death occurs from intestinal blockage
due to precipitated aluminum species rather than systemic aluminum toxicity.
/Aluminum/
... Fingerling brook trout weighing from 1.5 to 4.0 g ... exposed to high
aluminum /ion/ concn (> 0.2 mg/l) in the lab, experienced a 3.2 to 3.5%/hr
reduction in sodium content during the first 8 hr exposure at pH 5.0. A pH of
4.6 resulted in sodium loss at a similar rate. ... The presence of aluminum can
accelerate net sodium loss in brook trout at pH 5.0. Field experiments indicated
that substantial net sodium loss can also occur in natural settings where
aluminum concn is high. Body sodium concn data subjected to two-way analysis of
variance showed significant effects due to exposure site and time for each
species /of trout/ tested. /Aluminum/
Groups of ten 2-yr-old brown trout (Salmo trutta fario) were exposed for up
to 96 hr using Synthetic Laiozza, a media made up from deionized water and salts
added according to concn found in Lake Laiozza, a poorly buffered mountain lake
(pH 5.3) in the Swiss alps (containing 105 + or - 9 ug total aluminum/l; 45 + or
- 18 ug labile aluminum/l). Synthetic Laiozza was enriched with 0, 0.125, 0.25,
0.5, and 4.0 meq sodium chloride/l media. Addition of sodium chloride to the
Synthetic Laiozza media significantly increased the MT50 (when 50% of the
exposed fish had turned over) value only when 4 meq sodium chloride was added
(MT50 = 85 hr). /Aluminum/
New Zealand white rabbits (n= 10) were given daily iv injections of an
aqueous solution containing 3.7 umol aluminum acetylacetonate which corresponded
to 100 ug of aluminum (about 30 ug/kg). Blood creatine kinase and lactate
dehydrogenase activities were measured every 2 days. Controls (n= 3) received
comparable molar quantities of free acetylacetone (300 ug/day for 16 days). All
rabbits of the treatment group died of congestive cardiac failure 9 to 10 days
after the beginning of treatments. After 2 days of treatment, blood creatine
kinase values ranged from 1500-1800 IU and increased to 2000-2300 IU after 5-7
days of treatment. Blood creatine kinase values for controls were not provided
although a normal value of 330 + or - 76 IU was cited from a previous study. No
experimental lactate dehydrogenase values were provided. Histological
alterations of the heart consisted of interstitial hyperplasia, muscle cell
necrosis, and myocarditis all involving both ventricles. Increased eosinophilia,
nuclear picnosis, and homogeneous-appearing cytoplasm were observed in
myocardial cells. Cells exhibiting microvacuolation or contraction bands were
noted. Multifocal myocarditis associated with interstitial hyperplasia, and
myocardial necrosis were also observed. Myocardial aluminum accumulation
(1.3-2.1 ug aluminum/g lyophilized tissue) representing a 3-4 fold increase over
controls was found for aluminum acetylacetonate treated rabbits. No indication
of clinical or histopathological alterations were observed for control rabbits.
/Aluminum acetylacetonate/
Total NAD kinase activity is twice as high in the aluminum tolerant wheat
strain (BHG) than in the aluminum sensitive variety (Grana). In the former the
calmodulin-dependent enzyme constitutes about 50% of the total activity, whereas
in the latter it does not exceed 30%. Aluminum induced NAD kinase activity 2.5
fold in the sensitive variety Grana and six fold in the aluminum tolerant BHG
upon 10 hr incubation in 0.74 mM aluminum. The induction, abolished by
cycloheximide, involves both calmodulin-dependent and calmodulin-independent
enzymes in Grana, whereas in the aluminum tolerant genotype BHG, the induction
involves only the calmodulin-independent form, and the activity of the
calmodulin-dependent enzyme becomes marginal. Changes in the activity of NAD
kinase are paralleled by the shift in the NADP/NAD ratio. /Aluminum/
Effects of a low calcium, high aluminum diet were studied in juvenile
Cynomolgus monkeys (Macaca fascicularis). After being fed a specially formulated
diet containing 0.32% calcium, with or without supplemental aluminum (150 mg
daily) and manganese (50 daily) for 41-46 mo, the animals exhibited mild calcium
and aluminum deposition and degenerative changes compatible with those of
amyotrophic lateral sclerosis and parkinsonism, dementia in motor neurons of the
spinal cord, brain stem, substantia nigra and cerebrum. The highest number of
neurons with abnormally phosphorylated neurofilaments was observed in the two
monkeys fed the low calcium diet supplemented with aluminum and manganese. In
contrast, these abnormal neurons were not observed in a control monkey fed a
normal calcium diet. /Aluminum/
Female Swiss Webster mice (6 to 8 wk old) were fed diets containing 25, 100,
500 or 1000 ug/g aluminum for up to 10 wk. After mice had consumed their diets
for either 7 or 10 wk they were killed and their brains removed. No differences
in body wt gain were observed among the groups. After 10 wk, liver aluminum
concn was significantly higher in the 1000 ug/g aluminum group, compared to the
25 and 100 ug/g groups (p< 0.05). Levels of aluminum in brain supernatants
were below assay detection limits (10 ug/g). Tubulin polymerization in
high-speed brain supernatants was not found to be affected by dietary aluminum.
However, the addition of aluminum (1 to 50 uM, as aluminum sulfate in vitro
stimulated microtubule assembly in brain supernatants from mice fed control
diets. The lowest aluminum concn that produced significant stimulation was 10 uM
(27 + or - 7%, n= 6, p< 0.05); at 25 uM the incr of the initial velocity was
65 + or - 12% (n= 6, p< 0.01). /Aluminum/
Aluminum compounds have been evaluated as non-mutagenic by most standard
methods of mutagenic assays. /Aluminum cmpd/
Non-Human Toxicity Values:
LD50 Rat oral 380 mg/kg. /From table/
LD50 Guinea pig oral 400 mg aluminum chloride/kg.
/From table/
LD50 Rabbit oral 400 mg aluminum chloride/kg.
/From table/
Metabolism/Pharmacokinetics:
Absorption, Distribution & Excretion:
Rainbow trout (9 to 220 g) were individually placed in 1 liter chambers
having aerated, fresh flowing water for 1 hr (control conditions, aluminum
concn= 0.033 mg/l, pH 4.61). They were then exposed to an aerated artificial
medium (flow rate= 297 + or - 11 ml/min, pH= 5.4) containing 0.954 + or - 0.133
mg/l aluminum (as aluminum chloride) for
up to 1 hr. There was no significant difference (p= 0.05) between episodic
aluminum levels and episodic blank (no fish) aluminum levels, indicating that
the flow rate through the chambers was sufficient to maintain aluminum levels
such that absorption of aluminum from the apparatus was negligible. Fish were
removed for tissue sampling after 5, 10, 20, 30, and 60 min exposure. Skin and
blood showed no significant incr in aluminum content (p= 0.05). Gill tissue
episodic aluminum values were significantly higher (p= 0.05)) than control
levels at 30 and 60 min, having incr from 8 ug/g to 50 ug/g wet weight in 1 hr.
Mucous aluminum content was significantly higher (p= 0.05) than control values
after 5 min of exposure incr to 4.5 mg/l from 0.2 mg/l. Mucous cells on the
secondary lamellae showed discharged mucous globules on the gill surface after 1
hr of episodic exposure, a feature not shown by unexposed gill lamellae.
It was calculated that a dialysate aluminum concn of 0.2-1.0 mg/l (a concn
readily found in many water supplies) would result in the direct transfer of
aluminum into the blood of 3-16 mg for each dialysis treatment or 42-211 mg/mo.
/Aluminum/
A given oral dose of aluminum results in significantly higher serum and
tissue levels of the metal in nephrectomized rats than in intact controls in
spite of the fact that only minimal amounts of aluminum are normally excreted in
the urine. /Aluminum/
It was found that 70-90% of total aluminum bound to plasma proteins (60-70%
to a high molecular weight protein and 10-20% to albumin while only 10-30% was
unbound). This high affinity of aluminum for plasma proteins strongly suggests
high levels of binding of aluminum to a variety of tissue proteins. /Aluminum/
It was shown that the uptake of aluminum into the blood during renal dialysis
was due to the extensive binding of aluminum to plasma proteins leaving very
little aluminum in the non-bound state in plasma. Thus, the plasma proteins
served as a trap for accumulating the metal. It was shown that the component of
plasma protein that binds aluminum is saturable. Consistent with this ... is the
fact that, during dialysis with aluminum-containing dialysate, plasma aluminum
levels reach a plateau. /Aluminum/
Renal clearance of aluminum has been shown to be approximately 5-10% of that
of urea or creatinine clearance. This is entirely consistent with the marked
protein binding of aluminum in plasma, thus leaving only a small fraction of the
total aluminum available for filtration in the kidney. /Aluminum/
That the kidney is responsible for the elimination of a major portion of
absorbed aluminum is reflected in the fact that, in dogs undergoing renal
dialysis ligation of the ureter (resulting in cessation of urinary output)
causes a greater increase in plasma aluminum concn than in intact dogs
undergoing comparable dialysis. /Aluminum/
The 200-300 mg of aluminum/kg tissue weight is most likely due to local
deposition of particulate aluminum from the air following inhalation and not due
to a specific predilection of lung tissue for aluminum. Aluminum has been
reported in both non-urban and urban air with the latter containing as much as
10 ug/cu m. /Aluminum/
The aluminum content of gray matter of brain (essentially the inner cellular
mass of the brain) was not significantly different than that in the white matter
(the outer myelinated fibers of the brain). /Aluminum/
SINCE LITTLE ALUMINUM IS ABSORBED, IT IS EXCRETED IN THE FECES, MUCH OF IT IN
THE FORM OF ALUMINUM PHOSPHATE. THERE IS NO INCR IN THE AMT OF ALUMINUM IN
TISSUES, EXCEPT IN BONE (ANIMAL EXPERIMENTS). /ALUMINUM/
AMT OF ALUMINUM IN TISSUES, ORGANS, BLOOD & URINE IS SMALL. ADULT HUMAN
BODY MAY CONTAIN 50-150 MG ... AFTER INGESTION OF LARGE AMT VERY LITTLE APPEARS
IN URINE ... BETWEEN 50 & 100 MG DAILY FOR ABOUT 70 DAYS. /ALUMINUM/
ALUMINUM SALTS ARE ABSORBED IN ... SMALL AMT FROM THE DIGESTIVE TRACT.
/ALUMINUM SALTS/
Aluminum hydroxide or oxide is slowly solubilized in the stomach and reacts
with hydrochloric acid to form aluminum chloride and
water. In addition to forming aluminum chloride, dihydroxyaluminum
sodium carbonate and aluminum carbonate form carbon dioxide, and aluminum
phosphate forms phosphoric acid. About 17-30% of the aluminum
chloride formed is absorbed and is rapidly excreted by the
kidneys in patients with normal renal functions. In the small intestine, aluminum
chloride is rapidly converted to insoluble poorly absorbed basic
aluminum salts which probably /include/ a mixture of hydrated aluminum oxide,
oxyaluminum hydroxide, various basic aluminum carbonates, and aluminum soaps.
Aluminum-containing antacids (except aluminum phosphate) also combine with
dietary phosphate in the intestine forming insoluble, nonabsorbable aluminum
phosphate which is excreted in the feces. If phosphate intake is limited in
patients with normal renal function, aluminum antacids (except aluminum
phosphate) decrease phosphate absorption and hypophosphatemia and
hypophosphaturia occur; calcium absorption is increased. In vitro studies
indicate that aluminum hydroxide binds bile salts with an affinity &
capacity similar to that of cholestyramine; aluminum phosphate binds bile salts,
but to a much lesser degree than does aluminum hydroxide. /Aluminum hydroxide or
aluminum oxide/
Cations that form insoluble phosphates interfere with the absorption of
phosphorus. For example, high intakes of aluminum decrease absorption of
phosphorus (as phosphate) by forming insoluble aluminum phosphate and increasing
the excretory loss of phosphorus. /Aluminum/
Calcium and aluminum salts decrease the absorption of fluoride from the
intestinal tract. In sheep and rats magnesium salts are somewhat less effective.
In studies of humans, Spencer and coworkers demonstrated that ingestion of
antacids containing aluminum hydroxide increased fecal excretion of fluoride by
as much as 12 times, resulting in decreased absorption and lowered plasma levels
of fluoride. On the other hand, increasing calcium and phosphorus intake did not
affect fluoride balance, although these latter minerals, as well as magnesium,
did increase fecal excretion of fluoride. /Aluminum salts/
Very few investigations have been made on the metabolism and mode of action
of aluminum compounds for the reason that it is very poorly absorbed and of low
toxicity. The existing evidence indicates that the small portion of aluminum ion
tht hydrolyzes combines with available phosphate, becomes insoluble and
unabsorbed, and so is excreted along with the un-ionized portion. In high doses
aluminum compounds have been shown to affect phosphorus metabolism of rats and
mice. At lower levels (170 and 355 ppm aluminum as aluminum
chloride) aluminum balance studies showed intake and fecal
excretion of aluminum were higher at the higher dose, but urinary excretion and
retention were not. In phosphorus balance studies made at 160 to 180 and 355 ppm
in the diet, the higher dose lowered phosphorus retention, although phosphorus
content of the liver and femur were not affected. Chronic and acute poisoning by
aluminum chloride caused, on
intraperitoneal administration of (32)H-labelled disodium hydrogen phosphate,
decreased incorporation of (32)phosphorus in the phospholipids and nucleic acids
of various rat tissues. Decreased adenosine triphosphate levels and a rise in
the adenosine diphosphate level in plasma also occurred, indicating interference
with tissue phosphorylation process.
Studies ... strongly suggest that aluminum in the gastrointestinal tract and
its subsequent distribution in tissue can be influenced by increasing the
concentration of parathyroid hormone. They fed male rats aluminum as 0.1% of
their diet for 25 days. The ready absorption of aluminum from the
gastrointestinal tract of these normal rats was enhanced by injections of
parathyroid hormone (17 U twice weekly). There was also increased deposition of
the metal in the kidney, muscle, bone, and the gray matter of the brain, but not
in the liver or in the white matter of the brain. Thus, the parathyroid hormone
exerted a specific effect on the absorption and distribution of aluminum. In
1977, these same investigators had found a positive correlation between
increased serum parathyroid hormone and serum aluminum levels in dialysis
patients ... had been reported earlier. /Aluminum/
Trace determination of aluminum was carried out in blood samples from 11
patients with chronic renal failure undergoing periodical hemodialysis
treatment. Analysis for aluminum was made by graphite furnace atomic absorption
spectrometry in samples taken at the beginning and end of dialysis, and of
dialysate from the inflow (pre) and outflow (post) lines of dialyzers. Healthy
individuals, without history of renal disease, were used as controls. The
aluminum concn in pre- and post-dialysis whole blood was 58 + or - 9 ug/l and
139 + or - 19 ug/l, respectively. The aluminum concn in pre- and post-dialysate
was 235 + or - 39 ug/l and 129 + or - 10 ug/l, respectively. Blood aluminum
concn of control subjects did not show significant differences when compared
with data reported by other authors. Aluminum was transferred to the patients'
blood during the dialysis treatments, because of the high metal content tap
water used to prepare the dialysates. /Aluminum/
ALUMINUM IN LUNGS IS PROBABLY RESULT OF LOCAL DEPOSITION FROM INHALED AIR.
/ALUMINUM/
ALUMINUM SALTS ARE ABSORBED IN ... SMALL AMT FROM THE DIGESTIVE TRACT.
/ALUMINUM SALTS/
25 Preterm infants with birth wt 540 to 2280 g (20 with birth wt < 1500 g)
and gestational ages 24 to 37 wk, were studied to determine the response to 2
levels of aluminum loading from currently unavoidable contamination of various
components of parenteral nutrition soln. The high aluminum loading group
received solutions with measured aluminum content of 306 + or - 16 ug/l and the
low aluminum loading group received solutions with 144 + or - 16 ug aluminum/l.
Urine aluminum:creatinine ratios (ug:mg) became elevated and significantly
higher in the high aluminum group (1.6 + or - 0.38 vs 0.5 + or - 0.1 at the
third sampling point (mean 19 days). Serum aluminum concn were highest at onset
in both groups and stabilized with study but remained consistently higher than
the normal median of 18 ug/l. Calculated urine aluminum excretions were
consistently low and were 34 + or - 6% vs 28 + or - 5% in the high and low
groups, respectively. In both groups, urine aluminum excretions were
significantly lower than the calculated aluminum intakes. One infant in the low
group who died 39 days after termination of the study showed the presence of
aluminum in bone trabeculae and excessive unmineralized osteoid along the
trabeculae. /Aluminum/
Biological Half-Life:
The mean plasma half-life of aluminum after iv admin in dogs is approx 4.5
hr. /Aluminum/
The shorter half-life for the urinary elimination of aluminum was about 8 hr.
/Aluminum/
Mechanism of Action:
Aluminum (10, 12.5, 17.5, 25 and 50 uM, as aluminum
trichloride) inhibited yeast glucose-6-phosphate dehydrogenase
(EC 1.1.1.49) by a pseudo-first-order reaction. The inhibition was proportional
to the incubation time (10 to 60 sec) and the concn of aluminum. Aluminum was a
better inhibitor when added to the buffered enzyme prior to the addition of
glucose-6-phosphate or NADP+. When aluminum
trichloride was added to the buffered mixture of enzyme and
glucose-6-phosphate , more than 10 times aluminum
trichloride was needed to observe a comparable inhibition. The
inhibitory effect of aluminum chloride on
glucose-6-phosphate dehydrogenase was negligible when aluminum
chloride was premixed with NADP+. Double reciprocal plots gave a
straight line with a k(inact) of 8.3/min and indicated the presence of a binding
step prior to inhibition. The kinetic study showed that 1 mol of aluminum was
bound per mol of enzyme subunit. A marked incr in sensitivity to aluminum was
observed as the pH decr. An inhibitory effect of aluminum was predominant below
pH 7.0, but above pH 8.0, aluminum did not significantly affect the reaction
rate of glucose-6-phosphate dehydrogenase.
The effect of aluminum on intestinal calcium absorption was determined in
male Sprague-Dawley rats using an everted intestinal sac technique.
Bidirectional calcium flux in the duodena and ilea of normal rats was assessed
by means of dual calcium isotopes. Addition of 2 uM aluminum (as aluminum
chloride) to the buffer solution significantly inhibited net
calcium absorption in the duodenum through suppression of mucosa-to-serosa flux.
Serosa-to-mucosa calcium flux was not similarly influenced by aluminum. In the
ileum, aluminum had no effect on any component of calcium flux. Aluminum did not
induce any suppression of glucose transport in either the duodenum or ileum,
suggesting that the effect on calcium transport is relatively specific.
ATP pools extracted from the cyanobacterium Anabaena cylindrica, grown in the
absence or presence of aluminum chloride were
measured using the luciferin-luciferase assay. Addition of low concn of aluminum
chloride (3.6-36 uM) incr the ATP pool 20-40% within 24 hr, the
effect being more marked with time. When using the Tris-EDTA boiling technique
for extraction of cellular ATP, the ATP from aluminum-exposed cells appeared
more stable during the extraction than the ATP from untreated cells. The higher
ATP pools in aluminum-exposed cells were also evident after dark treatment and
addition of the phosphorylating inhibitors carbonylcyanide
m-chlorophenylhydrazone and N,N'-dicyclohexylcarbodiimide. The formation of
elevated ATP pools in cells exposed to aluminum was curtailed by high concn of
cellular phosphate and postincubation at high pH (> 8).
Interactions:
The effect of di- and trivalent iron on the intestinal absorption of aluminum
was studied in an in situ perfusion system of rat small intestine in combination
with systemic and portal blood sampling. The small intestine of female Wistar
rats (6 animals/group) was perfused with media containing 10.0, 15.0, 20.0, and
25.0 mmol/l aluminum as aluminum chloride hexahydrate,
with or without 5 mmol/l ferrous chloride tetrahydrate (FeCl2.4H2O) or ferric
chloride hexahydrate for 60 min. The disappearance of aluminum or iron from the
perfusion medium, which is a measure for uptake from the intestinal lumen, was
calculated. After perfusion, samples of small intestine were collected. Control
tissue samples were taken from a rat perfused with saline for 60 min and from a
nonperfused rat. In the rats perfused with aluminum and/or iron there was no
morphological damage to the intestinal wall compared with the saline and
nonperfused controls. It was shown that iron(II) enhanced the uptake of aluminum
from about 30 min of perfusion onward, with all concentrations of aluminum
perfusion media tested. Significant increases were reached after 60 min of
perfusion with 10, 15, and 25 mmol aluminum/l, except for the 20 mmol
Aluminum/l. Iron(III) did not affect aluminum disappearance at any point during
perfusion. Aluminum appeared after the 60 min perfusion period in both systemic
and portal blood. Both iron(II) and iron(III) were absorbed after 60 min
perfusion, with the divalent iron being more extensively absorbed. The rise of
the aluminum level in portal blood was slightly higher than that in systemic
blood suggesting a possible liver trapping of aluminum before entering the
peripheral circulation. Iron(II) reduced the appearance of Aluminum in both
systemic and portal blood after 60 min perfusion, at all aluminum perfusion
concentrations used. Iron(III) did not affect aluminum absorption during 60 min
perfusion for all concentrations of aluminum perfusion media. /Aluminum
chloride hexahydrate/
Four factorially arranged expt of 7 wk duration were performed with weanling
Sprague-Dawley male rats. The variables in each expt were, in ug/g fresh diet,
boron supplements of 0 and 3 ug/g; aluminum (as aluminum
chloride) supplements of 0 and 1000 ug/g, and magnesium
supplements of 100 and 400 ug/g (expt 1 and 4), or 100, 200, and 400 ug/g (expt
2 and 3). All supplements were added as dry mixes to the diet. In expt 1 and 2,
20 ug manganese/g was supplemented; in expt 3 and 4 the supplement was 50 ug/g.
High dietary aluminum seemed most toxic when dietary magnesium was low enough to
cause a marked growth depression 100 ug/g. High dietary aluminum elevated the
spleen wt/body wt and liver wt/body wt ratios in magnesium deficient, but not in
magnesium adequate rats. High dietary aluminum depressed the concn of magnesium
in bone more markedly in magnesium deficient than adequate rats. On the other
hand, aluminum seemed most toxic when dietary boron was not low. Aluminum more
markedly depressed growth in boron supplemented than boron deprived rats. In the
boron deprived rats fed 400 ug magnesium/g of diet, high dietary aluminum (1000
ug/g) apparently was beneficial; in expt 2 and 3, hematocrit, and hemoglobin
were actually normalized by high dietary aluminum. Plasma magnesium was
significantly depressed by high dietary aluminum when the magnesium supplement
was 50 ug/g diet but not when it was 20 ug/g diet. However, growth was more
markedly depressed by high dietary aluminum in boron supplemented rats when the
magnesium supplement was 20 rather than 50 ug/g diet.
Male Sprague Dawley rat cerebral cortical slices were exposed to 0 (control),
10, 20, 50, 100 or 250 uM aluminum trichloride
(aluminum chloride before addition of 20 ul 2-chloroadenosine
(0-200 uM), isoproterenol (0 to 10 uM), or forskolin (0 to 10 uM). Aluminum
chloride had no effect on the cyclic adenosine monophosphate
concn in the absence of drugs that stimulate the synthesis of cyclic adenosin
monophosphate. 2-Chloroadenosine (25 to 200 uM) significantly stimulated the
synthesis of cyclic adenosine monophosphate in a concn dependent manner, and Aluminum
chloride significantly potentiated this response at 50 and 100
uM 2-chloroadenosine. This effect of aluminum chloride
was dependent on preexposure (for 30 min) of the slices to aluminum
chloride before addition of the agonist. The potentiation by aluminum
chloride of the 2-chloroadenosine induced incr in cyclic
adenosine monophosphate level was concn dependent, with significant enhancement
by 100 uM (142% of control) and 250 uM (150% of control) aluminum
chloride. Lower concn of aluminum
chloride had no significant effect on the production of cyclic
adenosine monophosphate stimulated by 2-chloroadenosine. Aluminum
chloride also potentiated the isoproterenol induced incr in
cyclic adenosine monophosphate production. Forskolin induced production of
cyclic adenosine monophosphate was unaltered by the presence of aluminum
chloride.
Plants of beech (Fagus sylvatica) were grown on nutrient solutions with
various concn of phosphate (0, 0.01, 0.1, and 1.0 mM) and aluminum (0, 0.1, and
1.0 mM) and at low pH (usually 4.2). About half of the supplied aluminum
occurred as Al(+3) under these conditions. The vacuolar inorganic phosphate
concn of excised fine roots were determined by (31)phosphorus NMR. In roots of
plants treated with 0.1 mM aluminum trichloride, the
vacuolar inorganic phosphate concn did not change over a period of 21 days. In
contrast, plants treated with 1.0 mM aluminum chloride
for about 1 day (18 to 29 hr) generally contained somewhat
higher vacuolar inorganic phosphate concn in the roots than did control plants.
Longer treatment (3 to 21 days) at the high aluminum level caused a continuously
decr vacuolar inorganic phosphate concn in the root (22% of control after 21
days). In the presence of 1.0 mM aluminum chloride, plants
with different phosphorus status showed about the same relative decr of vacuolar
inorganic phosphate concn. After transfer of control plants to a phosphorus and
aluminum free nutrient solution, vacuolar inorganic phosphate concn of roots
decr in a manner similar to that for the 1.0 mM aluminum treatment.
Female Wistar rat small intestines (n= 8 per group) were perfused in situ
with media containing 20 mmol aluminum (aluminum, as aluminum
trichloride)/l and either 5 mmol citric acid/l, 0.1 mmol/l of
the metabolic inhibitor dinitrophenol, or citric acid and dinitrophenol. Two
control groups were perfused with 5 mmol/l citric acid or 0.1 mmol/l
dinitrophenol, and one control group was not perfused at all. Luminal
disappearance of aluminum amounted to 2.4 mmol/l in the 60 min period. In the
portal blood a slight decr in aluminum was noticed after 60 min perfusion. When
citric acid was added, the aluminum disappearance was stimulated markedly
compared to aluminum disappearance without citric acid (p< 0.001). Citric
acid significantly stimulated the aluminum appearance in systemic blood and
portal blood over a 60 min period (p< 0.01). Dinitrophenol did not
significantly affect the luminal disappearance of aluminum in the absence of
citric acid, but the stimulating effect of citric acid was significantly reduced
in the presence of dinitrophenol (p< 0.001). In the portal blood, however,
dinitrophenol itself stimulated aluminum absorption in the absence of citric
acid (p< 0.02), while citric acid induced stimulation of the aluminum
absorption was counteracted. A strong negative correlation existed between
aluminum appearance in the systemic blood after 60 min perfusion with aluminum
alone, and the baseline aluminum level in the blood; the lower the baseline
level, the more aluminum appeared in the blood.
In a case study of patients on long-term dialysis, systemic aluminum
absorption with concurrent oral citrate (as an alkalinizing agent) and
aluminum-containing phosphate binder (eg, aluminum hydroxide or carbonate) was
significantly increased. Based on the proposed mechanism and pharmacologic
similarity, an interaction may be expected to occur between citric acid and
other aluminum salts (eg, aluminum phosphate, aluminum glycinate, attapulgite,
dihydroxyaluminum, kaolin, magaldrate). It has been shown that following
concurrent administration of citric acid (from lemon juice) and aluminum
hydroxide there is an increase in serum levels of a nonionized aluminum-citrate
complex, which is postulated to easily pass the gastrointestinal barrier.
Simultaneous administration of citric acid and aluminum hydroxide should be
avoided since significant systemic absorption of aluminum may occur. This may be
of additional concern in patients on long-term dialysis or with impaired renal
function. /Aluminum cmpd/
... Examined 25 dialysis patients that experienced accidental exposure to
aluminum and parathyroid hormone. At the same time as parathyroid hormone
decreased, serum calcium increased. Based on this observation it has been
suggested that aluminum is incorporated, instead of calcium, into the bone and
that this leads to the osteomalacia characteristic of aluminum-induced bone
disease. Instead of being incorporated into osteoid bone tissue, calcium returns
to the circulation which in turn inhibits the parathyroid hormone release from
the parathyroid. In support of this hypothesis, ... found a strong correlation
between bone aluminum content and the amount of bone occupied by unmineralized
osteoid in humans. Experimental support for the hypothesis of calcium-aluminum
interactions has also been provided in studies on chicks. /Aluminum/
Groups of 120 Atlantic salmon fry (Salmo salar, 1 g mass) were kept in
through-flow tanks of water (pH 5) containing various concn of aluminum and
silicic acid. The aluminum concn in all but the control tank (0.85 umol
aluminum/l) were 6-7 umol/l, at acutely toxic levels. Silicon levels were 0.66
umol/l (control), 93.06, 24.89, 5.46, and 0.60 umol/l, corresponding to
silicon:aluminum ratios of 13.0, 3.7, 0.9, and 0.1. Exchangeable aluminum, ie,
aluminum retained on Amberlite, was 6.00, 5.00, 4.11, and 1.52 umol/l in test
tanks, respectively. Fish were exposed for 96 hr, and the proportion of dead
fish was recorded at 12-hr intervals. The whole experiment was run three times;
data are from all runs combined. At a silicon:aluminum ratio of 13, acute
toxicity of aluminum was eliminated and gill structures of the fish were normal.
Percent survival versus time was higher for the higher silicon:aluminum ratio
groups. Accumulation of aluminum by fish fell sharply as the exchangeable
aluminum increased. Aluminum and silicon levels in fish were 0.44 and 0.01
(control), 0.40 and 0.54 (silicon:aluminum ratio of 13), 2.04 and 0.35
(silicon:aluminum ratio of 3.7), 2.49 and 0.33 (silicon :aluminum ratio of 0.9),
, 2.38 and 0.08 (silicon:aluminum ratio of 0.1) umol per g dry mass,
respectively. /Aluminum/
Pharmacology:
Therapeutic Uses:
Astringents
The hexahydrate /form of aluminum chloride/ used
as a topical astringent. /Aluminum chloride hexahydrate/
Some aluminum compounds are employed therapeutically, eg, aluminum hydroxide
is one component of the antacids recommended in the treatment of stomach ulcers
and gastritis. Large doses of aluminum hydroxide (in the order of grams) are
prescribed for patients who, as a result of renal dysfunction, have high blood
phosphate levels. Aluminum acetotartrate in solution is used in the treatment of
sores and for other dermatological purposes. The solution inhibits bacteria and
has astringent properties. Aluminum chloride hexahydrate
is very commonly used in deodorants, and a solution of aluminum sulfate has been
tried without significant success against stings of fire ants. /Aluminum
chloride hexahydrate/
Medicinally, aluminum and its salts are used in antacids, antidiarrheals, and
protective dermatological pastes. It is also found in cosmetics and deodorants.
/Aluminum and its salts/
Antiperspirant
Topical astringent. /Aluminum chloride hexahydrate/
Drug Warnings:
Aluminum salts may cause phosphorus depletion which is generally negligible.
However, with prolonged administration or large doses, hypophosphatemia may
occur, especially in patients with inadequate dietary intake of phosphorus;
hypercalciuria secondary to bone resorption and increased intestinal absorption
of calcium results. This phosphorus depletion syndrome is characterized by
anorexia, malaise, and muscle weakness, and prolonged aluminum antacid therapy
may cause urinary calculi, osteomalacia, and osteoporosis. A low-phosphorus
diet, diarrhea, excessive phosphorus losses from malabsorption, and restoration
of renal function after a kidney transplant increase the likelihood of the
syndrome. Serum phosphate concentrations should be monitored at monthly or
bimonthly intervals in patients on maintenance hemodialysis who are receiving
chronic aluminum antacid therapy. /Aluminum salts/
Interactions:
The effect of di- and trivalent iron on the intestinal absorption of aluminum
was studied in an in situ perfusion system of rat small intestine in combination
with systemic and portal blood sampling. The small intestine of female Wistar
rats (6 animals/group) was perfused with media containing 10.0, 15.0, 20.0, and
25.0 mmol/l aluminum as aluminum chloride hexahydrate,
with or without 5 mmol/l ferrous chloride tetrahydrate (FeCl2.4H2O) or ferric
chloride hexahydrate for 60 min. The disappearance of aluminum or iron from the
perfusion medium, which is a measure for uptake from the intestinal lumen, was
calculated. After perfusion, samples of small intestine were collected. Control
tissue samples were taken from a rat perfused with saline for 60 min and from a
nonperfused rat. In the rats perfused with aluminum and/or iron there was no
morphological damage to the intestinal wall compared with the saline and
nonperfused controls. It was shown that iron(II) enhanced the uptake of aluminum
from about 30 min of perfusion onward, with all concentrations of aluminum
perfusion media tested. Significant increases were reached after 60 min of
perfusion with 10, 15, and 25 mmol aluminum/l, except for the 20 mmol
Aluminum/l. Iron(III) did not affect aluminum disappearance at any point during
perfusion. Aluminum appeared after the 60 min perfusion period in both systemic
and portal blood. Both iron(II) and iron(III) were absorbed after 60 min
perfusion, with the divalent iron being more extensively absorbed. The rise of
the aluminum level in portal blood was slightly higher than that in systemic
blood suggesting a possible liver trapping of aluminum before entering the
peripheral circulation. Iron(II) reduced the appearance of Aluminum in both
systemic and portal blood after 60 min perfusion, at all aluminum perfusion
concentrations used. Iron(III) did not affect aluminum absorption during 60 min
perfusion for all concentrations of aluminum perfusion media. /Aluminum
chloride hexahydrate/
Four factorially arranged expt of 7 wk duration were performed with weanling
Sprague-Dawley male rats. The variables in each expt were, in ug/g fresh diet,
boron supplements of 0 and 3 ug/g; aluminum (as aluminum
chloride) supplements of 0 and 1000 ug/g, and magnesium
supplements of 100 and 400 ug/g (expt 1 and 4), or 100, 200, and 400 ug/g (expt
2 and 3). All supplements were added as dry mixes to the diet. In expt 1 and 2,
20 ug manganese/g was supplemented; in expt 3 and 4 the supplement was 50 ug/g.
High dietary aluminum seemed most toxic when dietary magnesium was low enough to
cause a marked growth depression 100 ug/g. High dietary aluminum elevated the
spleen wt/body wt and liver wt/body wt ratios in magnesium deficient, but not in
magnesium adequate rats. High dietary aluminum depressed the concn of magnesium
in bone more markedly in magnesium deficient than adequate rats. On the other
hand, aluminum seemed most toxic when dietary boron was not low. Aluminum more
markedly depressed growth in boron supplemented than boron deprived rats. In the
boron deprived rats fed 400 ug magnesium/g of diet, high dietary aluminum (1000
ug/g) apparently was beneficial; in expt 2 and 3, hematocrit, and hemoglobin
were actually normalized by high dietary aluminum. Plasma magnesium was
significantly depressed by high dietary aluminum when the magnesium supplement
was 50 ug/g diet but not when it was 20 ug/g diet. However, growth was more
markedly depressed by high dietary aluminum in boron supplemented rats when the
magnesium supplement was 20 rather than 50 ug/g diet.
Male Sprague Dawley rat cerebral cortical slices were exposed to 0 (control),
10, 20, 50, 100 or 250 uM aluminum trichloride
(aluminum chloride before addition of 20 ul 2-chloroadenosine
(0-200 uM), isoproterenol (0 to 10 uM), or forskolin (0 to 10 uM). Aluminum
chloride had no effect on the cyclic adenosine monophosphate
concn in the absence of drugs that stimulate the synthesis of cyclic adenosin
monophosphate. 2-Chloroadenosine (25 to 200 uM) significantly stimulated the
synthesis of cyclic adenosine monophosphate in a concn dependent manner, and Aluminum
chloride significantly potentiated this response at 50 and 100
uM 2-chloroadenosine. This effect of aluminum chloride
was dependent on preexposure (for 30 min) of the slices to aluminum
chloride before addition of the agonist. The potentiation by aluminum
chloride of the 2-chloroadenosine induced incr in cyclic
adenosine monophosphate level was concn dependent, with significant enhancement
by 100 uM (142% of control) and 250 uM (150% of control) aluminum
chloride. Lower concn of aluminum
chloride had no significant effect on the production of cyclic
adenosine monophosphate stimulated by 2-chloroadenosine. Aluminum
chloride also potentiated the isoproterenol induced incr in
cyclic adenosine monophosphate production. Forskolin induced production of
cyclic adenosine monophosphate was unaltered by the presence of aluminum
chloride.
Plants of beech (Fagus sylvatica) were grown on nutrient solutions with
various concn of phosphate (0, 0.01, 0.1, and 1.0 mM) and aluminum (0, 0.1, and
1.0 mM) and at low pH (usually 4.2). About half of the supplied aluminum
occurred as Al(+3) under these conditions. The vacuolar inorganic phosphate
concn of excised fine roots were determined by (31)phosphorus NMR. In roots of
plants treated with 0.1 mM aluminum trichloride, the
vacuolar inorganic phosphate concn did not change over a period of 21 days. In
contrast, plants treated with 1.0 mM aluminum chloride
for about 1 day (18 to 29 hr) generally contained somewhat
higher vacuolar inorganic phosphate concn in the roots than did control plants.
Longer treatment (3 to 21 days) at the high aluminum level caused a continuously
decr vacuolar inorganic phosphate concn in the root (22% of control after 21
days). In the presence of 1.0 mM aluminum chloride, plants
with different phosphorus status showed about the same relative decr of vacuolar
inorganic phosphate concn. After transfer of control plants to a phosphorus and
aluminum free nutrient solution, vacuolar inorganic phosphate concn of roots
decr in a manner similar to that for the 1.0 mM aluminum treatment.
Female Wistar rat small intestines (n= 8 per group) were perfused in situ
with media containing 20 mmol aluminum (aluminum, as aluminum
trichloride)/l and either 5 mmol citric acid/l, 0.1 mmol/l of
the metabolic inhibitor dinitrophenol, or citric acid and dinitrophenol. Two
control groups were perfused with 5 mmol/l citric acid or 0.1 mmol/l
dinitrophenol, and one control group was not perfused at all. Luminal
disappearance of aluminum amounted to 2.4 mmol/l in the 60 min period. In the
portal blood a slight decr in aluminum was noticed after 60 min perfusion. When
citric acid was added, the aluminum disappearance was stimulated markedly
compared to aluminum disappearance without citric acid (p< 0.001). Citric
acid significantly stimulated the aluminum appearance in systemic blood and
portal blood over a 60 min period (p< 0.01). Dinitrophenol did not
significantly affect the luminal disappearance of aluminum in the absence of
citric acid, but the stimulating effect of citric acid was significantly reduced
in the presence of dinitrophenol (p< 0.001). In the portal blood, however,
dinitrophenol itself stimulated aluminum absorption in the absence of citric
acid (p< 0.02), while citric acid induced stimulation of the aluminum
absorption was counteracted. A strong negative correlation existed between
aluminum appearance in the systemic blood after 60 min perfusion with aluminum
alone, and the baseline aluminum level in the blood; the lower the baseline
level, the more aluminum appeared in the blood.
In a case study of patients on long-term dialysis, systemic aluminum
absorption with concurrent oral citrate (as an alkalinizing agent) and
aluminum-containing phosphate binder (eg, aluminum hydroxide or carbonate) was
significantly increased. Based on the proposed mechanism and pharmacologic
similarity, an interaction may be expected to occur between citric acid and
other aluminum salts (eg, aluminum phosphate, aluminum glycinate, attapulgite,
dihydroxyaluminum, kaolin, magaldrate). It has been shown that following
concurrent administration of citric acid (from lemon juice) and aluminum
hydroxide there is an increase in serum levels of a nonionized aluminum-citrate
complex, which is postulated to easily pass the gastrointestinal barrier.
Simultaneous administration of citric acid and aluminum hydroxide should be
avoided since significant systemic absorption of aluminum may occur. This may be
of additional concern in patients on long-term dialysis or with impaired renal
function. /Aluminum cmpd/
... Examined 25 dialysis patients that experienced accidental exposure to
aluminum and parathyroid hormone. At the same time as parathyroid hormone
decreased, serum calcium increased. Based on this observation it has been
suggested that aluminum is incorporated, instead of calcium, into the bone and
that this leads to the osteomalacia characteristic of aluminum-induced bone
disease. Instead of being incorporated into osteoid bone tissue, calcium returns
to the circulation which in turn inhibits the parathyroid hormone release from
the parathyroid. In support of this hypothesis, ... found a strong correlation
between bone aluminum content and the amount of bone occupied by unmineralized
osteoid in humans. Experimental support for the hypothesis of calcium-aluminum
interactions has also been provided in studies on chicks. /Aluminum/
Groups of 120 Atlantic salmon fry (Salmo salar, 1 g mass) were kept in
through-flow tanks of water (pH 5) containing various concn of aluminum and
silicic acid. The aluminum concn in all but the control tank (0.85 umol
aluminum/l) were 6-7 umol/l, at acutely toxic levels. Silicon levels were 0.66
umol/l (control), 93.06, 24.89, 5.46, and 0.60 umol/l, corresponding to
silicon:aluminum ratios of 13.0, 3.7, 0.9, and 0.1. Exchangeable aluminum, ie,
aluminum retained on Amberlite, was 6.00, 5.00, 4.11, and 1.52 umol/l in test
tanks, respectively. Fish were exposed for 96 hr, and the proportion of dead
fish was recorded at 12-hr intervals. The whole experiment was run three times;
data are from all runs combined. At a silicon:aluminum ratio of 13, acute
toxicity of aluminum was eliminated and gill structures of the fish were normal.
Percent survival versus time was higher for the higher silicon:aluminum ratio
groups. Accumulation of aluminum by fish fell sharply as the exchangeable
aluminum increased. Aluminum and silicon levels in fish were 0.44 and 0.01
(control), 0.40 and 0.54 (silicon:aluminum ratio of 13), 2.04 and 0.35
(silicon:aluminum ratio of 3.7), 2.49 and 0.33 (silicon :aluminum ratio of 0.9),
, 2.38 and 0.08 (silicon:aluminum ratio of 0.1) umol per g dry mass,
respectively. /Aluminum/
Drug Idiosyncrasies:
Contact allergy to aluminum has been reported in a few cases. This type of
allergy must be regarded very rare, considering the common exposure to the metal
itself & the use of aluminum chloride hexahydrate
in deodorants. /Aluminum chloride hexahydrate/
Environmental Fate & Exposure:
Probable Routes of Human Exposure:
INTAKE OF ALUMINUM IS CHIEFLY BY MOUTH, FROM FOODS AND BEVERAGES, ALSO BY
LUNGS, FROM THE ATMOSPHERIC DUST CONTENT. IT IS PRESENT IN NATURAL DIET, IN AMT
VARYING FROM VERY LOW IN ANIMAL PRODUCTS TO RELATIVELY HIGH IN PLANTS.
/ALUMINUM/
Body Burden:
Aluminum content of normal human brain ranged from 0.1-3.9 ug/g dry weight.
In a study of 208 samples taken from 7 patients, ... a mean aluminum content of
1.9 + or - 0.07 ug/g dry weight of gray matter /was found/ to be abnormal. In a
study of 585 areas sampled from the brain tissue of 10 patients with Alzheimer's
disease they found 28% had an aluminum concn > 4 ug/g. The range of the 585
samples was 0.4-107 ug/g. /Aluminum/
Average Daily Intake:
The daily ingestion of aluminum by humans was estimated to be 30-50 mg.
/Aluminum/
Environmental Fate:
AQUATIC FATE: The adsorption of aluminum by fine particulates was studied in
Whitray Beck, a hill stream in England. ... Uptake of aluminum by the particles
increased with total aluminum, with pH, and with particle concentration,
although the fraction of aluminum bound at a given pH and particle concentration
decreased with total aluminum ... . /Aluminum/
TERRESTRIAL FATE: Air-dried, <2 mm fractions of 3 soil samples from The
Netherlands and 1 from New Hampshire, were taken from the surface and
sub-surface horizons of two podzols (Haplorthods) and of a recent driftsand
(Udipsamment). Duplicate samples of each emulsion soil horizon were leached ...
with aqueous hydrogen chloride (pH 3.0). ... Charge balances of the leachates
indicate that dissolved aluminum is present mainly as aquo-aluminum (+3). Only
in leachates of podzol Bhs horizons is a significant fraction (20-30%) of
dissolved aluminum organically complexed. Dissolved aluminum concn are
significantly correlated with the organic (Na4P2O7-extractable) aluminum content
of the soil sample. Mobility of aluminum in the Hubbard Brook soils is
significantly lower than in the Dutch soils, because of higher soil-solution pH
values. /Aluminum cmpd/
Albic and spodic soil horizons were sampled from old growth eastern white
pine/mixed northern hardwoods. Adirondacks, and an ochric (A) soil horizon was
sampled from the Appalachian plateau of NY State. 21 Three-horizon forest floor
and 21 forest floor/mineral soil (field moist equivalent of 12.0 oven-dry albic,
spodic, or ochric mineral soil) columns were leached in triplicate with either
10 uM nitric acid (pH 5), 5 uM sulfuric acid (pH 5), 100 uM nitric acid (pH 4),
50 uM sulfuric acid (pH 4), 1000 uM nitric acid (pH 3), 500 uM sulfuric acid (pH
3), or distilled, deionized water (pH 5.7) control treatment). Nitric acid
leached more aluminum than did sulfuric acid from forest floor/spodic soil
columns. Increasing the nitric acid concn from pH 3-5 increased total aluminum
concn in leachates from 0.70 to 0.85 mM, while increasing sulfuric acid had no
effect. Addition of pH 3 sulfuric acid to forest floor/spodic columns raised
leachate pH relative to pH 3 nitric acid and controls, and resulted in the
lowest aluminum concn of all treatments in the first 3 of 4 sequential
leachings. /Aluminum/
Albic and spodic soil horizons were sampled from old growth eastern white
pine/mixed northern hardwoods sites in the Adirondacks, and an ochric (A) soil
horizon was sampled from the Appalachian Plateau of NY State. 9 Three-horizon
forest floor, 9 mineral soil (field moist equivalent of 12.0 oven-dry albic,
spodic, or ochric mineral soil) and 9 forest floor/mineral soil columns were
leached with 60 ml of (a) 10 mM ammonium nitrate (control), (b) 1.0 mM nitric
acid in 10 mM ammonium nitrate (pH 3), and (c) 1.0 mM ammonium nitrate (pH 3) at
the rate of 10 ml/hr. The above procedure was repeated on each mineral soil
without a forest floor, except leaching soln were 0.5 mM calcium nitrate or
calcium sulfate, each in 10 mM ammonium nitrate. Adding 2 and 0.5 cmol sub c
(H+)/kg to forest floor and mineral soils, respectively, simulated snowmelt
additions. Total aluminum concn in leachates from forest floor/albic or forest
floor/ochric columns were greater than the sum of concn in leachates from the
forest floor and mineral horizon when leached separately. This positive
synergistic behavior of the forest floor-mineral horizon sequences was also
observed in the forest floor-spodic horizon sequence when leached with control
soln, but the synergism was negative for both labile and non-labile aluminum
when leached with the acids. Sulfuric acid leached less aluminum from the spodic
horizon than did nitric acid, regardless of the presence of a forest floor, but
nitric acid, sulfuric acid , and control soln leached similar concn of aluminum
from the albic and ochric horizons. The forest floor effects on the mineral soil
leachates were attributed to effects of Calcium, sulfate, nitrate, and dissolved
organic C leached from the forest floor to the mineral horizon since forest
floor removed nearly all added H+. /Aluminum/
Environmental Abiotic Degradation:
Aluminum chloride hydrolyzes in
water to aluminum hydroxide & hydrochloric acid.
Environmental Water Concentrations:
The solute and particulate aluminum chemistry of a relatively unpolluted
snowfall associated with a maritime airmass was measured by neutron activation
analysis and inductively-coupled plasma analysis (soluble fraction) and neutron
activation analysis (particulate material), to characterize background
conditions for the Scottish Highlands. Aluminum concentrations were compared to
those found in a polluted black snowfall with a trajectory that originated over
eastern Europe and to those levels found in seasonal snowpack. The variability
of the concentration of solute and the chemical composition of particulate
material is reported on an intra-and inter-site basis. The solute aluminum
content of Scottish snowfall in the inter-site survey was 19.2 ug/l, and in the
intra-site survey 52.2 ug/l. The aluminum composition of particulate matter
found within Scottish snow was 20,600 ppm in the inter-site survey, and 21,100
ppm in the intra-site survey. For the black snow, the solute aluminum content
was 84 + or - 3 ug/l, and the aluminum composition of particulate matter was
52,300 ppm. The mean concentration of aluminum in seasonal snowpack was 27,200
ppm. /Aluminum solute & particulate/
Environmental Standards & Regulations:
Acceptable Daily Intakes:
Recommended adult daily allowance for chlorine at 2-4 g. /Chlorine; from
Table 1/
Federal Drinking Water Guidelines:
EPA 50-200 ug/l /Aluminum/
State Drinking Water Standards:
(CA) CALIFORNIA 1000 ug/l /Aluminum/
State Drinking Water Guidelines:
(AZ) ARIZONA 73 ug/l /Aluminum/
(CA) CALIFORNIA 200 ug/l /Aluminum/
(ME) MAINE 1430 ug/l /Aluminum/
Chemical/Physical Properties:
Molecular Formula:
Al-Cl3
Molecular Weight:
133.34
Color/Form:
WHITE WHEN PURE; ORDINARILY GRAY OR YELLOW TO GREENISH
WHITE TO COLORLESS, HEXAGONAL
GRANULAR CRYSTALS
Odor:
STRONG ODOR OF HYDROGEN CHLORIDE
Boiling Point:
182.7 DEG C @ 752 MM HG
Melting Point:
190 DEG C @ 2.5 ATM
Density/Specific Gravity:
2.44 @ 25 DEG C; 1.31 @ 200 DEG C (LIQ)
Solubilities:
FREELY SOL IN BENZOPHENONE & BENZENE NITROBENZENE
FREELY SOL IN CARBON TETRACHLORIDE
FREELY SOL IN MANY ORG SOLVENTS
IN ABS ALC 100 G/100 CC @ 12.5 DEG C
IN CHLOROFORM 0.072 G/100 CC @ 25 DEG C
SOL IN ETHER; SLIGHTLY SOL IN BENZENE
Vapor Pressure:
1 MM HG @ 100.0 DEG C
Other Chemical/Physical Properties:
WHEN HEATED IN SMALL QUANTITIES VOLATILIZES WITHOUT MELTING
FUMES IN AIR
VERY DELIQUESCENT
Heat of fusion: 63.6 cal/g
One g dissolves in 0.9 ml water /Aluminum chloride hexahydrate/
Chemical Safety & Handling:
DOT Emergency Guidelines:
Health: TOXIC; inhalation, ingestion or contact (skin, eyes) with vapors,
dusts or substance may cause severe injury, burns, or death. Fire will produce
irritating, corrosive and/or toxic gases. Reaction with water may generate much
heat which will increase the concentration of fumes in the air. Contact with
molten substance may cause severe burns to skin and eyes. Runoff from fire
control or dilution water may cause pollution. /Aluminum
chloride, anhydrous/
Fire or explosion: Some of these materials may burn, but none ignite readily.
May ignite combustibles (wood, paper, oil, clothing, etc.). Substance will react
with water (some violently), releasing corrosive and/or toxic gases.
Flammable/toxic gases may accumulate in confined areas (basement, tanks,
hopper/tank cars etc.). Contact with metals may evolve flammable hydrogen gas.
Containers may explode when heated or if contaminated with water. Substance may
be transported in a molten form. /Aluminum chloride,
anhydrous/
Public safety: CALL Emergency Response Telephone Number on Shipping Paper
first. If Shipping Paper not available or no answer, refer to appropriate
telephone number listed on the inside back cover. Isolate spill or leak area
immediately for at least 50 to 100 meters (160 to 330 feet) in all directions.
Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate
enclosed areas. /Aluminum chloride, anhydrous/
Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical protective clothing which is specifically
recommended by the manufacturer. Structural firefighters' protective clothing is
recommended for fire situations ONLY; it is not effective in spill situations. /Aluminum
chloride, anhydrous/
Evacuation: Spill: See the Table of Initial Isolation and Protective Action
Distances for highlighted substances. For non-highlighted substances, increase,
in the downwind direction, as necessary, the isolation distance shown under
"PUBLIC SAFETY". Fire: If tank, rail car or tank truck is involved in
a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider
initial evacuation for 800 meters (1/2 mile) in all directions. /Aluminum
chloride, anhydrous/
Fire: When material is not involved in fire: do not use water on material
itself. Small fires: Dry chemical or C02. Move containers from fire area if you
can do it without risk. Large Fires: Flood fire area with large quantities of
water, while knocking down vapors with water fog. If insufficient water supply:
knock down vapors only. Fire involving tanks or car/trailer loads: Cool
containers with flooding quantities of water until well after fire is out. Do
not get water inside containers. Withdraw immediately in case of rising sound
from venting safety devices or discoloration of tank. ALWAYS stay away from the
ends of tanks. /Aluminum chloride, anhydrous/
Spill or leak: Fully encapsulating, vapor protective clothing should be worn
for spills and leaks with no fire. Do not touch damaged containers or spilled
material unless wearing appropriate protective clothing. Stop leak if you can do
it without risk. Use water spray to reduce vapors; do not put water directly on
leak, spill area or inside container. Keep combustibles (wood, paper, oil, etc.)
away from spilled material. Small spills: Cover with DRY earth, DRY sand, or
other non-combustible material followed with plastic sheet to minimize spreading
or contact with rain. Use clean non-sparking tools to collect material and place
it into loosely covered plastic containers for later disposal. Prevent entry
into waterways, sewers, basements or confined areas. /Aluminum
chloride, anhydrous/
First aid: Move victim to fresh air. Call emergency medical care. Apply
artificial respiration if victim is not breathing. Do not use mouth-to-mouth
method if victim ingested or inhaled the substance; induce artificial
respiration with the aid of a pocket mask equipped with a one-way valve or other
proper respiratory medical device. Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes. In case of contact with
substance, immediately flush skin or eyes with running water for at least 20
minutes. For minor skin contact, avoid spreading material on unaffected skin.
Removal of solidified molten material from skin requires medical assistance.
Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin
contact) to substance may be delayed. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves. /Aluminum
chloride, anhydrous/
Health: TOXIC, inhalation, ingestion, or skin contact with material may cause
severe injury or death. Contact with molten substance may cause severe burns to
skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be
delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from
fire control or dilution water may be corrosive and/or toxic and cause
pollution. /Aluminum chloride, solution/
Fire or explosion: Non-combustible, substance itself does not burn but may
decompose upon heating to produce corrosive and/or toxic fumes. Some are
oxidizers and may ignite combustibles (wood, paper, oil, clothing, etc.).
Contact with metals may evolve flammable hydrogen gas. Containers may explode
when heated. /Aluminum chloride, solution/
Public safety: CALL Emergency Response Telephone Number on Shipping Paper
first. If Shipping Paper not available or no answer, refer to appropriate
telephone number listed on the inside back cover. Isolate spill or leak area
immediately for at least 25 to 50 meters (80 to 160 feet) in all directions.
Keep unauthorized personnel away. Stay upwind. Keep out of low areas. Ventilate
enclosed areas. /Aluminum chloride, solution/
Protective clothing: Wear positive pressure self-contained breathing
apparatus (SCBA). Wear chemical protective clothing which is specifically
recommended by the manufacturer. Structural firefighters' protective clothing is
recommended for fire situations ONLY, it is not effective in spill situations. /Aluminum
chloride, solution/
Evacuation: Spill: See the Table of Initial Isolation and Protective Action
Distances for highlighted substances. For non-highlighted substances, increase,
in the downwind direction, as necessary, the isolation distance shown under
"PUBLIC SAFETY". Fire: If tank, rail car or tank truck is involved in
a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider
initial evacuation for 800 meters (1/2 mile) in all directions. /Aluminum
chloride, solution/
Fire: Small fires: Dry chemical, CO2 or water spray. Large fires: Dry
chemical, CO2, alcohol-resistant foam or water spray. Move containers from fire
area if you can do it without risk. Dike fire control water for later disposal;
do not scatter the material. Fire involving tanks or car/trailer loads: Fight
fire from maximum distance or use unmanned hose holders or monitor nozzles. Do
not get water inside containers. Cool containers with flooding quantities of
water until well after fire is out. Withdraw immediately in case of rising sound
from venting safety devices or discoloration of tank. ALWAYS stay away from the
ends of tanks. /Aluminum chloride, solution/
Spill or leak: ELIMINATE all ignition sources (no smoking, flares, sparks or
flames in immediate area). Do not touch damaged containers or spilled material
unless wearing appropriate protective clothing. Stop leak if you can do it
without risk. Prevent entry into waterways, sewers, basements or confined areas.
Absorb or cover with dry earth, sand or other non-combustible material and
transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. /Aluminum
chloride, solution/
First aid: Move victim to fresh air. Call emergency medical care. Apply
artificial respiration if victim is not breathing. Do not use mouth-to-mouth
method if victim ingested or inhaled the substance; induce artificial
respiration with the aid of a pocket mask equipped with a one-way valve or other
proper respiratory medical device. Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes. In case of contact with
substance, immediately flush skin or eyes with running water for at least 20
minutes. For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet. Effects of exposure (inhalation, ingestion or skin
contact) to substance may be delayed. Ensure that medical personnel are aware of
the material(s) involved, and take precautions to protect themselves. /Aluminum
chloride, solution/
Skin, Eye and Respiratory Irritations:
Irritating to eyes, nose and throat. Will burn skin and eyes.
May cause minor irritation to lungs & eyes. /Aluminum (dust or powder)/
Fire Fighting Procedures:
DO NOT use water. Violent reaction may result. Extinguish fire using agent
suitable, for surrounding fire. Extinguish adjacent fires with dry chemical
carbon dioxide, or foam. Use water spray to keep fire-exposed containers cool.
Toxic Combustion Products:
Reacts violently with water, liberating hydrogen chloride gas and heat.
Explosive Limits & Potential:
COMBINES WITH WATER WITH EXPLOSIVE VIOLENCE & LIBERATION OF MUCH HEAT.
Not combustible, but heating may produce irritants & toxic gases. Reacts
violently with water producing hydrochloric acid & heat.
Old containers can explode on opening
Hazardous Reactivities & Incompatibilities:
... WILL REACT WITH WATER OR STEAM TO PRODUCE HEAT, TOXIC OR CORROSIVE FUMES.
INCOMPATIBILITIES: ALKALI HYDROXIDES & CARBONATES, BORAX, & LIME
WATER PRECIPITATES ALUMINUM HYDROXIDE FROM SOLN OF ALUMINUM
CHLORIDE. IT POSSESSES INCOMPATIBILITIES OF CHLORIDES.
Reacts violently with water used in extinguishing adjacent fires.
Aluminum chloride hydrolyzes in
water to aluminum hydroxide & hydrochloric acid.
Protective Equipment & Clothing:
WEAR SPECIAL PROTECTIVE CLOTHING & POSITIVE PRESSURE SELF-CONTAINED
BREATHING APPARATUS.
Wear goggles, self-contained breathing apparatus and rubber clothing
Preventive Measures:
Remove contaminated clothing and shoes. Flush affected areas with plenty of
water.
SRP: The scientific literature for the use of contact lenses in industry is
conflicting. The benefit or detrimental effects of wearing contact lenses depend
not only upon the substance, but also on factors including the form of the
substance, characteristics and duration of the exposure, the uses of other eye
protection equipment, and the hygiene of the lenses. However, there may be
individual substances whose irritating or corrosive properties are such that the
wearing of contact lenses would be harmful to the eye. In those specific cases,
contact lenses should not be worn. In any event, the usual eye protection
equipment should be worn even when contact lenses are in place.
SRP: Contaminated protective clothing should be segregated in such a manner
so that there is no direct personal contact by personnel who handle, dispose, or
clean the clothing. Quality assurance to ascertain the completeness of the
cleaning procedures should be implemented before the decontaminated protective
clothing is returned for reuse by the workers. Contaminated clothing should not
be taken home at end of shift, but should remain at employee's place of work for
cleaning.
Shipment Methods and Regulations:
No person may /transport,/ offer or accept a hazardous material for
transportation in commerce unless that person is registered in conformance ...
and the hazardous material is properly classed, described, packaged, marked,
labeled, and in condition for shipment as required or authorized by ... /the
hazardous materials regulations (49 CFR 171-177)./
The International Air Transport Association (IATA) Dangerous Goods
Regulations are published by the IATA Dangerous Goods Board pursuant to IATA
Resolutions 618 and 619 and constitute a manual of industry carrier regulations
to be followed by all IATA Member airlines when transporting hazardous
materials.
The International Maritime Dangerous Goods Code lays down basic principles
for transporting hazardous chemicals. Detailed recommendations for individual
substances and a number of recommendations for good practice are included in the
classes dealing with such substances. A general index of technical names has
also been compiled. This index should always be consulted when attempting to
locate the appropriate procedures to be used when shipping any substance or
article.
Storage Conditions:
Always keep container closed, dry. Store in a noncombustible, nonsprinklered
building away from all combustible material. Isolate from strong acids.
KEEP TIGHTLY CLOSED & PROTECTED FROM MOISTURE.
Disposal Methods:
Cover any spills with sufficient amounts of sodium bicarbonate. Remove the
mixture into a container such as a fiber drum, plastic bag or carton box for
easy disposal in an incinerator, and dispose by burning in a furnace. Or spread
the mixture on the ground and disperse by washing or draining with plentiful
amount of water into the sewer. Wash the spilled spot thoroughly with water.
Occupational Exposure Standards:
Manufacturing/Use Information:
Major Uses:
Suitable as an acid catalyst, especially in Friedel-Crafts type reactions; in
cracking of petroleum; in manufacture of rubbers, lubricants.
CATALYST; CHEMICAL INTERMEDIATE FOR NUMEROUS ALUMINUM COMPOUNDS.
MAJOR USE IN THE ELECTROLYTIC PRODUCTION OF ALUMINIUM.
In preserving wood; disinfecting stables, slaughterhouses, etc; in deodorants
& antiperspirant prepn; refining crude oil; dyeing fabrics; manufacturing
parchment paper. /Aluminum chloride hexahydrate/
MEDICATION
Pharmaceuticals & cosmetics, pigments, roof granules, special papers,
photography, textiles (wool). /Aluminum chloride hydrate/
Manufacturers:
ACL INDUST INC, ELKTON, MD
ALLIED CHEM CORP, INDUST CHEMS DIV, RANSOMVILLE, NY
ALUMINUM CO OF AMERICA, ANDERSON COUNTY, TEX
ASCENSION CHEM OF AMERICA CORP, TONAWANDA, NY
MOR-PAK CORP, PAINESVILLE, OHIO, RAVENNA, OHIO
PEARSALL CHEM CORP, LA PORTE, TEX,
PHILLIPSBURG, NJ
STAUFFER CHEM CO, INDUST CHEM DIV, BATON ROUGE, LA
VAN DE MARK CHEM CO, INC, LOCKPORT, NY
ALCOA, 1501 ALCOA BLDG, PITTSBURGH, PA 15219, (412) 553-3204; PALESTINE, TX
CHATTEM CHEMICALS, 1715 W 38 ST, CHATTANOOGA, TN 37409, (615) 821-4571
CORTLIC CHEMICAL, BALTIMORE, MD
REHEIS, 235 SNYDER AVE, BERKELEY HEIGHTS, NJ 07922, (201) 464-1500
Methods of Manufacturing:
... FROM ALUMINUM METAL IN HEATED STREAM OF HYDROCHLORIC ACID GAS.
BY HEATING ALUMINUM IN CURRENT OF CHLORINE & ... DISSOLVING PRODUCT IN
WATER & CRYSTALLIZING, OR BY DISSOLVING FRESHLY PPT ALUMINUM HYDROXIDE IN
HYDROCHLORIC ACID & CONCENTRATING & CRYSTALLIZING.
BY REACTION OF BAUXITE WITH COKE & CHLORINE AT ABOUT 875 DEG C
CHLORINE REACTS WITH ALUMINUM OXIDE IN AN ALUMINOUS MATERIAL SUCH AS CLAY OR
BAUXITE IN THE PRESENCE OF A REDUCTANT.
By reaction of purified gaseous chlorine with molten aluminum.
Aluminum chloride /has been formed/
by reaction of aluminum and hydrogen chloride mixed with cycloalkane vapors.
General Manufacturing Information:
THE SUPPLY IN SOILS IS ABUNDANT. SOME ACID SOILS CONTAIN SUFFICIENT ALUMINUM
IN SOLUTION FORM TO KILL CERTAIN PLANTS. /ALUMINUM/
Formulations/Preparations:
ALUMINUM CHLORIDE-99.8% /GRADE
AVAILABLE/
GRADES: TECHNICAL; REAGENT
LIQUID ALUMINUM CHLORIDE, 32 DEG
BAUME, 28% GRADE
Grade: Technical, CP /chemically pure: a grade designation signifying a
minimum of impurities, but not 100% pure/; NF /National Formulary grade of
chemical/.
Impurities:
IMPURITIES: FERRIC CHLORIDE; FREE ALUMINUM; INSOLUBLES
IMPURITIES: FERRIC CHLORIDE, 0.08%; SILICON CHLORIDE, 0.02%; SODIUM CHLORIDE,
0.02%
Consumption Patterns:
35% AS A CATALYST FOR ETHYL BENZENE; 16% AS A CATALYST FOR DYESTUFF
INTERMEDIATES; 9% AS A CATALYST FOR DETERGENT ALKYLATE; 8% AS A CATALYST FOR
HYDROCARBON RESINS; 5% AS A CATALYST FOR ETHYL CHLORIDE; 27% IN NUMEROUS OTHER
APPLICATIONS AS A CATALYST & CHEMICAL INTERMEDIATE (1974)
COSMETICS & PHARMACEUTICALS, 60%; MISC, INCL PIGMENTS, ROOFINGS,
SPECIALTY PAPERS AND PHOTOGRAPHY, 40% (1980) /HYDROUS ALUMINUM
CHLORIDE/
DETERGENT ALKYLATE, 18%; ETHYLBENZENE CATALYST, 15%; HYDROCARBON RESINS, 12%;
TITANIUM DIOXIDE PROCESSING, 10%; DYESTUFF INTERMEDIATE, 10%; MISC (INCL
COSMETIC AND PHARMACEUTICAL APPLICATION, BUTYL RUBBER AND POLYBUTENES, ETHYL
CHLORIDE), 35% (1980) /ANHYDROUS ALUMINUM CHLORIDE/
U. S. Production:
(1972) 2.99X10+10 GRAMS
(1975) 2.45X10+10 GRAMS
(1984) 2.51X10+10 g /LIQUID, CRYSTAL & ANHYDROUS/
Laboratory Methods:
Clinical Laboratory Methods:
NIOSH Method 8310. Urine samples containing aluminum and its compounds are
analyzed using Inductively Coupled Argon Plasma - Atomic Emission Spectroscopy
at a wavelength of 308.2 nm. Sample preparation includes addition of a
polydithiocarbamate resin, filtration, ashing, and dissolution with concentrated
nitric/concentrated perchloric acid (4:1 v/v). This method has a detection limit
of 0.1 ug/sample and a relative standard deviation of 0.088 over a range of 0.25
to 200 ug/sample with a recovery of 100%. /Aluminum/
Procedures for aluminum determination in body fluids by flameless atomic
absorption spectrometry with a graphite furnace are described. Topics covered
include sample preparation, applicable specifications, and possible difficulties
which can arise. /Aluminum/
A microanalytical method for the measurement of aluminum in biological
samples is presented, which requires 1-500 mg of brain tissues and less than 1
ml of blood, urine, or other aqueous samples. /Aluminum/
A CATION-EXCHANGE CHROMATOGRAPHY PROCEDURE IS OUTLINED FOR THE SIMPLE AND
QUANTITATIVE DETERMINATION OF TRACE AMOUNTS OF ALUMINUM IN BIOLOGICAL MATERIAL
(URINE) EMPLOYING NEUTRON ACTIVATION ANALYSIS. /ALUMINUM/
Blood and urine aluminum concn were studied in industrially exposed workers
using electrothermal atomic absorption spectrometry. The detection limit was 5
ug/l for aluminum in blood and 3 ug/l for aluminum in urine. /Total aluminum/
Analytic Laboratory Methods:
EPA Method 9252: Titrimetric, Mercuric Nitrate. Method 9252 is applicable to
ground water, drinking, surface, and saline waters, and domestic and industrial
wastes. This method is suitable for all concentration ranges of chloride
content; however, in order to avoid large titration volume, a sample aliquot
containing not more than 10 to 20 mg chloride per 50 ml is used. An acidified
sample is titrated with mercuric nitrate in the presence of mixed
diphenylcarbazone-bromophenol blue indicator. The end point of the titration is
the formation of the blue-violet mercury diphenylcarbazone complex. In a single
laboratory, using surface water samples at an average concentration of 34 mg
chloride/l, the standard deviation was + or - 1.0. A synthetic unknown sample
containing 241 mg/l chloride ... in Type II water was analyzed in 10
laboratories by the mercurimetric method, with a relative standard deviation of
3.3% and a relative error of 2.9%. /Chloride/
Determination in air: Atomic absorption spectrometric analysis. /Aluminum and
its cmpd/
NIOSH Method 7013. Samples containing aluminum and its compounds are analyzed
using Atomic Absorption, Flame at a wave length of 309.3 nm. Sample preparation
includes filtration, ashing, and dissolution with concentrated
nitric/concentrated perchloric acid (4:1 v/v). This method has a detection limit
of 2 ug/sample and precision of 0.03 over a range of 50 to 5000 mg/sample.
/Aluminum and its cmpd/
NIOSH Method 7300. Air samples containing aluminum are analyzed using
Inductively Coupled Argon Plasma - Atomic Emission Spectroscopy at a wavelength
of 308.2. An ashing step with concentrated nitric acid/concentrated perchloric
acid (4:1 v/v) is necessary. This method has an instrumental detection limit of
14 ng/ml, a sensitivity of 0.23 ug/ml, and a precision of 0.092 at 2.5
ug/filter. /Aluminum/
USE OF ELECTRON SPECTROSCOPE TO ANALYZE ATMOSPHERIC PARTICLES CONTAINING
ALUMINUM.
NIOSH METHOD 173. ANALYTE: ALUMINUM; MATRIX: AIR; RANGE: 5-50 UG/ML, 210-2100
UG/CU M; PROCEDURE: FILTER COLLECTION, ACID DIGESTION, ATOMIC ABSORPTION
SPECTROPHOTMETRY AT 309.3 NM. /Aluminum/
Sampling Procedures:
Determination in air: Filter collection. /Aluminum and its cmpd/
Special References:
Special Reports:
DHHS/ATSDR; Toxicological Profile for Aluminum (1992) ATSDR/TP-91/01
Synonyms and Identifiers:
Related HSDB Records:
Synonyms:
ALLUMINIO(CLORURO DI) (ITALIAN)
**PEER REVIEWED**
ALUMINIUMCHLORID (GERMAN)
**PEER REVIEWED**
ALUMINUM CHLORIDE (1:3)
**PEER REVIEWED**
ALUMINUM, (CHLORURE D') (FRENCH)
**PEER REVIEWED**
ALUMINUM TRICHLORIDE
**PEER REVIEWED**
Caswell no 029
**PEER REVIEWED**
Chlorure d'aluminium (French)
**PEER REVIEWED**
EPA pesticide chemical code 013901
**PEER REVIEWED**
Pearsall
**PEER REVIEWED**
TRICHLOROALUMINUM
**PEER REVIEWED**
Associated Chemicals:
Aluminum chloride, hexahydrate;7784-13-6
Formulations/Preparations:
ALUMINUM CHLORIDE-99.8% /GRADE
AVAILABLE/
GRADES: TECHNICAL; REAGENT
LIQUID ALUMINUM CHLORIDE, 32 DEG
BAUME, 28% GRADE
Grade: Technical, CP /chemically pure: a grade designation signifying a
minimum of impurities, but not 100% pure/; NF /National Formulary grade of
chemical/.
Shipping Name/ Number DOT/UN/NA/IMO:
UN 1726; Aluminum chloride, anhydrous
UN 2581; Aluminum chloride, solution
IMO 8.0; Aluminum chloride, anhydrous
IMO 8.0; Aluminum chloride, solution
RTECS Number:
NIOSH/BD0525000
Administrative Information:
Hazardous Substances Databank Number: 607
Last Revision Date: 20020806
Last Review Date: Reviewed by SRP on 11/07/1990
Update History:
Complete Update on 08/06/2002, 1 field added/edited/deleted.
Complete Update on 01/18/2002, 6 fields added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 06/03/1999, 1 field added/edited/deleted.
Complete Update on 02/16/1999, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 03/26/1998, 5 fields added/edited/deleted.
Field Update on 02/27/1998, 1 field added/edited/deleted.
Field Update on 10/17/1997, 1 field added/edited/deleted.
Field Update on 05/08/1997, 1 field added/edited/deleted.
Field Update on 05/01/1997, 2 fields added/edited/deleted.
Complete Update on 02/26/1997, 1 field added/edited/deleted.
Complete Update on 01/24/1997, 1 field added/edited/deleted.
Complete Update on 10/12/1996, 1 field added/edited/deleted.
Complete Update on 03/21/1996, 1 field added/edited/deleted.
Complete Update on 01/19/1996, 1 field added/edited/deleted.
Complete Update on 12/21/1994, 1 field added/edited/deleted.
Complete Update on 10/19/1994, 2 fields added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 10/13/1993, 71 fields added/edited/deleted.
Field update on 12/14/1992, 1 field added/edited/deleted.
Complete Update on 08/17/1992, 70 fields added/edited/deleted.
Field Update on 01/16/1992, 1 field added/edited/deleted.
Complete Update on 05/22/1986
Record Length: 159493