Toxicity Profiles
Toxicity Summary for ALUMINUM
NOTE:
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- EXECUTIVE SUMMARY
- 1. INTRODUCTION
- 2. METABOLISM AND DISPOSITION
- 2.1 ABSORPTION
2.2 DISTRIBUTION
2.3 METABOLISM
2.4 EXCRETION
- 3. NONCARCINOGENIC HEALTH EFFECTS
- 3.1 ORAL EXPOSURES
3.2 INHALATION EXPOSURES
3.3 OTHER ROUTES OF EXPOSURE
3.4 TARGET ORGANS/CRITICAL EFFECTS
- 4. CARCINOGENICITY
- 4.1 ORAL EXPOSURES
4.2 INHALATION EXPOSURES
4.3 OTHER ROUTES OF EXPOSURE
4.4 EPA WEIGHT-OF-EVIDENCE
4.5 CARCINOGENICITY SLOPE FACTORS
- 5. REFERENCES
September 1993
Prepared by Cheryl B. Bast, Chemical Hazard Evaluation Group, Biomedical Environmental Information Analysis Section, Health Sciences Research Division, *, Oak Ridge, Tennessee.
Prepared for OAK RIDGE RESERVATION ENVIRONMENTAL RESTORATION PROGRAM.
*Managed by Martin Marietta Energy Systems, Inc., for the U.S. Department of Energy under Contract No. DE-AC05-84OR21400.
EXECUTIVE SUMMARY
Aluminum is a silver-white flexible metal with a vast number of uses. It is poorly absorbed and
efficiently eliminated; however, when absorption does occur, aluminum is distributed mainly in bone, liver,
testes, kidneys, and brain (ATSDR, 1990).
Aluminum may be involved in Alzheimer's disease (dialysis dementia) and in Amyotrophic Lateral
Sclerosis and Parkinsonism-Dementia Syndromes of Guam (Guam ALS-PD complex) (ATSDR, 1990;
Goyer, 1991). Aluminum content of brain, muscle, and bone increases in Alzheimer's patients.
Neurofibrillary tangles (NFTs) are found in patients suffering from aluminum encephalopathy and
Alzheimer's disease. Symptoms of "dialysis dementia" include speech disorders, dementia, convulsions, and
myoclonus. People of Guam and Rota have an unusually high incidence of neurodegenerative diseases. The
volcanic soil in the region of Guam where the high incidence of ALS-PD occurs contains high levels of
aluminum and manganese. Neurological effects have also been observed in rats orally exposed to aluminum
compounds.
The respiratory system appears to be the primary target following inhalation exposure to aluminum.
Alveolar proteinosis has been observed in guinea pigs, rats, and hamsters exposed to aluminum powders
(Gross et al., 1973). Rats and guinea pigs exposed to aluminum chlorohydrate exhibited an increase in
alveolar macrophages, increased relative lung weight, and multifocal granulomatous pneumonia (Cavender
et al., 1978).
No decrease in reproductive capacity, hormonal abnormalities, or testicular histopathology was
observed in male rats exposed to aluminum in drinking water for 90 days (Dixon et al., 1979).
However, male rats exposed to aluminum (as aluminum chloride) via gavage for 6 months exhibited
decreased spermatozoa counts and sperm motility, and testicular histological and histochemical changes
(Krasovskii et al., 1979).
Subchronic and chronic reference doses and reference concentrations have not been derived for
aluminum.
Male rats exposed to drinking water containing aluminum (as aluminum potassium sulfate) for a
lifetime exhibited increases in unspecified malignant and nonmalignant tumors (Schroeder and Mitchener,
1975a), and similarly exposed female mice exhibited an increased incidence of leukemia (Schroeder and
Mitchener, 1975b). Rats and guinea pigs exposed via inhalation to aluminum chlorohydrate developed lung
granulomas (Cavender et al., 1978), while granulomatous foci developed in similarly exposed male hamsters
(Drew et al., 1974).
The U.S. EPA has not evaluated aluminum or aluminum compounds for carcinogenicity, and a
weight-of-evidence classification is currently not assigned.
1. INTRODUCTION
Aluminum (CAS registry number 7429-90-5) is a silver-white, flexible metal (ATSDR, 1990). It
makes up about 8% of the earth's crust in undecomposed rock fragments and in secondary aluminosilicate
clays. The aluminum content of seawater ranges from 3 to 2400 ppb (Venugopal and Luckey, 1978). Until
recently, aluminum has existed in forms not available to humans and most other species. However, acid rain
has increased the availability of aluminum to biological systems and has resulted in destructive effects on
fish and plant species. It is unknown if humans are susceptible to this increased bioavailability (Goyer,
1991). Aluminum is not an essential element for mammals (Venugopal and Luckey, 1978).
Aluminum metal is used as a structural material in the construction, automotive, and aircraft
industries, in the production of metal alloys, and in the electrical industry in power lines, insulated cables
and wiring. Other uses of aluminum metal include cooking utensils, decorations, fencing, highway signs,
cans, food packaging, foil, and dental crowns and dentures (ATSDR, 1990).
Aluminum compounds and materials also have a number of uses. Aluminum powder is used in paints
and fireworks, and natural aluminum minerals are used in water purification, sugar refining, and in the
brewing and paper industries. Aluminum borate is used in the production of glass and ceramics, and
aluminum chloride is used to make rubber, lubricants, wood preservatives, and cosmetics. Aluminum
chlorohydrate is the active ingredient in antiperspirants and deodorants, while aluminum hydroxide is used
as a pharmaceutical to lower plasma phosphorus levels of patients with kidney failure. Aluminum silicate
is a component of dental cement, and various other aluminum compounds are used as tanning agents in the
leather industry, and as components of veterinary medicines, glues, and disinfectants (ATSDR, 1990).
2. METABOLISM AND DISPOSITION
2.1. ABSORPTION
In mammals, gastrointestinal absorption of ingested aluminum is poor due to the conversion of
aluminum salts into insoluble aluminum phosphate in the digestive tract. This is the result of pH changes
and the presence of phosphate in the diet (Venugopal and Luckey, 1978). Absorption from oral exposure
is also affected by the chemical form of the aluminum, vitamin D, parathyroid hormone, and other ions
(ATSDR, 1990). At high doses, such as 200 mg aluminum/kg as Al2(SO4)3, intestinal absorption in rats has been shown to be 10% (Kortus, 1967). Aluminum compounds can affect absorption of other elements in the
gastrointestinal tract; aluminum inhibits fluoride absorption and may decrease the absorption of calcium and
iron compounds. It may possibly decrease the absorption of cholesterol by forming an aluminum pectin
complex that binds fats to nondigestable vegetable fibers (Nagyvary and Bradbury, 1977). Absorption from
intramuscular, subcutaneous, and peritoneal cavity injection of aluminum compounds is slow, occurring
mainly through phagocytosis by macrophages (Venugopal and Luckey, 1978). When aluminum compounds
are intravenously injected, a small portion of ionic aluminum is bound to albumin and is transported out of
the blood into soft tissues, including the brain. Following inhalation, most insoluble aluminum salts are
retained in the lung, while soluble compounds are slowly absorbed into the blood. Aluminum measured in
the lung tissue of aluminum refinery workers increases with duration of exposure (Venugopal and Luckey,
1978). Aluminum is not readily absorbed through the skin (Venugopal and Luckey, 1978).
2.2. DISTRIBUTION
Following absorption, aluminum is distributed mainly in the skeleton, liver, testes, kidneys, and brain,
and in smaller amounts in other soft tissues (Venugopal and Luckey, 1978). Retention of aluminum in bone
is prolonged; however, it is transient in soft tissues. Renal failure increases aluminum deposition in the bone
(Thurston et al., 1972). Rats fed diets containing aluminum hydroxide exhibited increased aluminum levels
in bone, muscle, and kidneys. Aluminum concentrations in these tissues decreased 3 days after withdrawal
of aluminum hydroxide from the diet (Greger and Donnaubauer, 1986). There is limited evidence to suggest
that aluminum administered orally to rabbits can cross the placenta, accumulate in the fetus, and be
transferred to the neonate via milk (Cranmer et al., 1986; Yokel and McNamara, 1985). When aluminum
hydroxide was injected intraperitoneally in rats, the highest aluminum concentration was observed in the
liver. High aluminum levels were also observed in muscle, brain, bone, and heart (Berlyne et al., 1972).
Following inhalation exposure, aluminum accumulates in the lungs as particulates of poorly soluble
compounds (Ganrot, 1986).
2.3. METABOLISM
Aluminum, itself, does not undergo metabolism in that it is absorbed and excreted unchanged.
However, it is found attached to other chemicals, and these moieties can change within the body. The
aluminum ion is easily bound to many substances and structures in the organism, and its fate is determined
by its affinity to each of the ligands and their metabolism (ATSDR, 1990).
2.4. EXCRETION
In orally exposed humans, absorbed aluminum is eliminated through the urine, and unabsorbed
aluminum is excreted in the feces (ATSDR, 1990), while in dogs and pigs injected with aluminum, the major
excretion route is the kidney (Kolvalchik et al, 1978; Monteagudo et al, 1988). After inhalation exposure
to aluminum, the urine is the major route of excretion (ATSDR, 1991). Small amounts of aluminum may
also be excreted through sweat (Venugopal and Luckey, 1978).
3. NONCARCINOGENIC HEALTH EFFECTS
3.1. ORAL EXPOSURES
3.1.1. Acute Toxicity
3.1.1.1. Human
No information was available regarding the acute toxicity of aluminum in humans.
3.1.1.2. Animal
Due to the poor absorption and efficient excretion of aluminum, acute oral toxicity is observed only
after relatively large doses. The LD50 for aluminum nitrate in rats is 261 mg aluminum/kg (Llobet et al.,
1987), and the LD50 for aluminum chloride in mice is 770 mg aluminum/kg (Ondreicka et al., 1966).
3.1.2. Subchronic Toxicity
3.1.2.1. Human
Greger and Baier (1983) gave 4 healthy men a control diet containing 4.6 mg aluminum/day for 20
days, while 4 other men received a test diet of 125 mg aluminum/day as aluminum lactate. The diets were
then exchanged for an additional 20 days, and each subject acted as his own control. Fecal, urine, and serum
albumin measurements indicated that absorption and rapid excretion occurred. No adverse effects were
observed.
3.1.2.2. Animal
Male rats and male guinea pigs were given 0, 6, 17, or 50 mg aluminum/kg/day as aluminum chloride
in water by gavage for 20-30 days. Male rabbits were similarly exposed to 0, 3, 9, or 27 mg
aluminum/kg/day (Krasovskii et al., 1979). Decreased serum alkaline phosphatase activity was observed
at > 17 mg/kg/day in the rats and guinea pigs, and > 9 mg/kg/day in the rabbits. Serum ATP, ADP, and AMP
levels were decreased at > 17 mg/kg/day in the rats and guinea pigs, and > 27 mg/kg/day in the rabbits. Rats
were also similarly exposed to 0.0025, 0.25, or 2.5 mg aluminum/kg/day for 6-12 months (Krasovskii et al.,
1979). Decreased serum alkaline phosphatase and decreased motor reflexes were observed at the high dose.
Alkaline phosphatase activity was also decreased at 0.25 mg/kg, but only during the first month of exposure.
Eight male Fischer rats and eight female Sprague-Dawley rats were fed a diet containing 0.2% aluminum
(as aluminum chloride) for 12 weeks (Commissaris et al., 1982). Significantly decreased locomotor activity
was observed in the female rats, while the males exhibited a trend in this effect. Sprague-Dawley rats
administered 0.1% aluminum (as aluminum chloride) for 11 months exhibited decreased locomotor activity
and learning (Commissaris et al., 1982).
3.1.3. Chronic Toxicity
3.1.3.1. Human
Aluminum may be involved in Alzheimer's disease, "dialysis dementia", and Amyotrophic Lateral
Sclerosis and Parkinsonism-Dementia Syndromes of Guam (Guam ALS-PD complex) but the causal link
between aluminum and these diseases is tenuous at best (ATSDR, 1990; Goyer, 1991). Increased amounts
of aluminum have been observed in the brains of persons dying of Alzheimer's disease, however aluminum
content varies greatly in these patients. Also, neurofibrillary tangles (NFTs) are found in patients suffering
from aluminum encephalopathy and Alzheimer's disease. The formation of NFTs is associated with loss of
synapsis and atrophy of the dendritic tree (Goyer, 1991). Although Alzheimer's patients often have more
aluminum than usual in the NFTs, there are no significant differences between Alzheimer's patients and
controls in the aluminum content of hair, serum or spinal fluid (Shore and Wyatt, 1986). This may indicate
that Alzheimer's patients have a decreased blood-brain barrier for aluminum that may be the result of genetic
factors, viral, or immune mediated damage (Goyer, 1991). "Dialysis dementia" occurs in patients on renal
dialysis who receive large amounts of aluminum orally or intravenously (ATSDR, 1990; Goyer, 1991).
Symptoms include speech disorders, dementia, convulsions, and myoclonus. These symptoms usually occur
after 3 to 7 years of dialysis treatment and may be due to aluminum intoxication. Aluminum content of
brain, muscle, and bone increases in these patients (Goyer, 1991).
People of Guam and Rota have an unusually high incidence of neurodegenerative diseases associated
with nerve cell loss and neurofibrillary degeneration of the Alzheimer type termed Amyotrophic Lateral
Sclerosis and Parkinsonism-Dementia Syndromes of Guam (Guam ALS-PD complex). The volcanic soil
in the region of Guam where the high incidence of ALS-PD occurs, contains high levels of aluminum and
manganese and low levels of calcium and magnesium. It is hypothesized that low calcium and magnesium
intake induce secondary hyperparathyroidism resulting in an increase in aluminum and other toxic metals.
It is unknown how aluminum enters the brains of the ALS-PD patients (Goyer, 1991).
3.1.3.2. Animal
Aluminum chloride was administered to groups of 10 mice at concentrations of 0 or 19.3 mg
aluminum/kg/day in drinking water in a 3 generation study (Ondreicka et al.,1966). The parental generation
was treated for 180-390 days, and weanlings were similarly treated from 4 weeks of age. Decreased body
weight was observed in the second and third generations; however, the significance of this effect is difficult
to assess since food consumption was not reported. Zero or 5 ppm aluminum (as aluminum chloride) was
administered to 52 Long-Evans rats/sex (Schroeder and Mitchener, 1975a) and 54 Swiss mice/sex (Schroeder
and Mitchener, 1975b) for life. No adverse effects were observed in either species.
3.1.4. Developmental and Reproductive Toxicity
3.1.4.1. Human
No information was available regarding the developmental and reproductive toxicity of aluminum
in humans.
3.1.4.2. Animal
Dixon et al. (1979) exposed male Sprague-Dawley rats (31/group) to 0, 5, 50, or 500 mg aluminum/L
(as aluminum chloride) in drinking water for 30, 60, or 90 days. Seven rats from each group were sacrificed
at each time point for hormone determination and histological examination of the testes. The remaining
males from each group were mated after 90 days of treatment; a different female was paired with each male
every 7 days for a total of 70 days. No adverse effects were observed. Krasovskii et al. (1979) exposed male
rats to 0, 0.025, 0.25 or 2.5 mg aluminum/kg/day (as aluminum chloride) by gavage for 6 months. Decreased
spermatozoa counts and sperm motility, and testicular histological and histochemical changes were observed
at 2.5 mg/kg/day. As described in section 3.1.3.2, Ondreicka et al. (1966) administered aluminum chloride
in drinking water to groups of 10 mice at concentrations of 0 or 19.3 mg aluminum/kg/day for 3 generations.
Decreased body weight was observed in the second and third generations; however, food consumption was
not reported so this effect may not be significant.
3.1.5. Reference Dose
3.1.5.1. Subchronic
An oral, subchronic reference dose has not been calculated for aluminum.
3.1.5.2. Chronic
An oral, chronic reference dose has not been calculated for aluminum.
3.2. INHALATION EXPOSURES
3.2.1. Acute Toxicity
3.2.1.1. Human
No information was available regarding the acute toxicity of aluminum in humans.
3.2.1.2. Animal
No information was available regarding the acute toxicity of aluminum in animals.
3.2.2. Subchronic Toxicity
3.2.2.1. Human
No information was available regarding the subchronic toxicity of aluminum in humans.
3.2.2.2. Animal
Gross et al. (1973) exposed groups of 14-30 guinea pigs, rats, and hamsters to metallic aluminum
powders at air concentrations of 15, 30, 50, or 100 mg/m3, 6 hours/day, 5 days/week for 6 months. Alveolar
proteinosis was observed in all 3 species. Groups of 35 Fischer rats/sex and 35 Hartley guinea pigs/sex were
exposed to 0.25, 2.5, or 25 mg/m3 aluminum chlorohydrate, 6 hours/day, 5 days/week, for 6 or 12 months
(Cavender et al., 1978). At 6 months (in both species), alveolar macrophages were increased at all dose
levels. Decreased body weight, increased relative lung weight, and multifocal granulomatous pneumonia
were observed at 25 mg/m3. At 12 months granulomas were observed in the lungs of both species exposed
to 25 mg/m3.
3.2.3. Chronic Toxicity
3.2.3.1. Human
Pulmonary fibrosis has been associated with occupational exposure to aluminum powder and dust
(ATSDR, 1990; U.S. EPA, 1987). However, this association is inconclusive because of concurrent exposure
to other irritants, cigarette smoking, or previous occupational exposures. The U.S. EPA reports that there
is no evidence of fibrogenic activity of aluminum at exposure levels recommended by the ACGIH (10 mg/m3
for dust and 5 mg/m3 for powder) and classifies aluminum dust and powder as inert particles (U.S. EPA,
1987). Workers were treated with 350 mg/m3 of respirable alumina powder for 10 minutes/day as a
treatment for silicosis (Stokinger, 1981). Over 42,000,000 treatments were given over a 27-year period, and
no adverse effects were observed.
3.2.3.2. Animal
Pigott et al. (1981) exposed a group of 50 Aderly Park rats to 2.18 mg/m3 aluminum fibers, 6
hours/day, 5 days/week for 86 weeks. Slight increases in alveolar macrophages and irritation of the nasal
passages were observed. However, these responses are typical of exposure to inert, irritant particles, and thus
may be due to physical irritation rather than the composition of the aluminum itself.
3.2.4. Developmental and Reproductive Toxicity
3.2.4.1. Human
No information was available regarding the developmental and reproductive toxicity of aluminum
in humans.
3.2.4.2. Animal
No information was available regarding the acute developmental and reproductive toxicity of
aluminum in animals.
3.2.5. Reference Concentration
3.2.5.1. Subchronic
An inhalation, subchronic reference concentration has not been calculated for aluminum.
3.2.5.2. Chronic
An inhalation, chronic reference concentration has not been calculated for aluminum.
3.3. OTHER ROUTES OF EXPOSURE
3.3.1. Acute Toxicity
3.3.1.1. Human
Aluminum compounds are used in antiperspirant products without harmful effects to the skin or other
organs. However, some people are unusually sensitive to these products and may develop skin rashes
(ATSDR, 1990). Children who had injections of vaccines or allergens in an aluminum-based vehicle showed
hypersensitivity to aluminum chloride in a patch test (ATSDR, 1990).
3.3.1.2. Animal
Mice, pigs, and rabbits exhibited skin hyperplasia, microabscess formation, dermal inflammatory cell
infiltration, and ulceration from the dermal application of 10% aluminum chloride and aluminum nitrate
applied for 5 days. No effects were observed with similarly applied aluminum sulfate, hydroxide,
chlorohydrate, or acetate (Lansdown, 1973).
3.3.2. Subchronic Toxicity
3.3.2.1. Human
No information was available regarding the subchronic toxicity of aluminum by other routes of
exposure in humans.
3.3.2.2. Animal
No information was available regarding the subchronic toxicity of aluminum by other routes of
exposure in animals.
3.3.3. Chronic toxicity
3.3.3.1. Human
No information was available regarding the chronic toxicity of aluminum by other routes of exposure
in humans.
3.3.3.2. Animal
No information was available regarding the chronic toxicity of aluminum by other routes of exposure
in animals.
3.3.4. Developmental and Reproductive Toxicity
3.3.4.1. Human
No information was available regarding the developmental and reproductive toxicity of aluminum
by other routes of exposure in humans.
3.3.4.2. Animal
No information was available regarding the developmental and reproductive toxicity of aluminum
by other routes of exposure in animals.
3.4. TARGET ORGANS/CRITICAL EFFECTS
3.4.1. Oral Exposures
3.4.1.1. Primary Target Organs
Central Nervous System: Aluminum may be involved in Alzheimer's disease, "dialysis dementia",
and Amyotrophic Lateral Sclerosis and Parkinsonism-Dementia Syndromes of Guam (Guam ALS-PD
complex). Increased amounts of aluminum have been observed in the brains of persons dying of Alzheimer's
disease and neurofibrillary tangles (NFTs) are found in patients suffering from aluminum encephalopathy
and Alzheimer's disease. Significantly decreased locomotor activity was observed in female rats fed
aluminum in the diet for 12 weeks, and Sprague-Dawley rats administered aluminum for 11 months exhibited
decreased locomotor activity and learning.
3.4.1.2. Other Target Organs
Reproductive System: Male rats exposed to aluminum chloride by gavage for 6 months exhibited
decreased spermatozoa counts and sperm motility, and testicular histological and histochemical
changes.
3.4.2. Inhalation Exposures
3.4.2.1. Primary Target Organs
Respiratory System: Alveolar proteinosis was observed in guinea pigs, rats, and hamsters exposed
to aluminum powders for 6 months. Rats and guinea pigs exposed to aluminum chlorohydrate for 6 months
exhibited an increase in alveolar macrophages, increased relative lung weight, and multifocal granulomatous
pneumonia. After 12 months exposure, granulomas were observed in the lungs of both rats and guinea pigs.
4. CARCINOGENICITY
4.1. ORAL EXPOSURES
4.1.1. Human
No information was available regarding the carcinogenicity of aluminum by the oral route in humans.
4.1.2. Animal
Schroeder and Mitchener (1975a) exposed Long-Evans weanling rats (52/sex) to drinking water
containing 5 mg/L aluminum (as aluminum potassium sulfate) for life. Specific tumor types were not
specified; the incidence of total tumors was 13/25 in treated males and 4/26 in control males. The incidence
of malignant tumors was 6/25 in treated males and 2/26 in control males. In another study, groups of 54
Swiss mice/sex were given 5 mg aluminum/L (as aluminum potassium sulfate) in the drinking water for life
(Schroeder and Mitchener, 1975b). The incidence of leukemia in treated females was 10/41, while the
incidence in control females was 3/47.
4.2. INHALATION EXPOSURES
4.2.1. Human
No information was available regarding the carcinogenicity of aluminum by the inhalation route in
humans.
4.2.2. Animal
Rats and guinea pigs (35/sex/group) were exposed to 0.25, 2.5, or 25 mg/m3 of aluminum
chlorohydrate, 6 hours/day, 5 days/week for 6-12 months (Cavender et al., 1978). Lung granulomas were
observed in both species following exposure to 25 mg/m3 for 6 months and 2.5 mg/m3 for 12 months. Drew
et al. (1974) exposed male hamsters to 52 mg/m3 aluminum chlorohydrate, 6 hours/day, 5 days/week for 20
or 30 exposures. Granulomatous foci developed at the bifurcation of the bronchioalveolar ducts.
4.3. OTHER ROUTES OF EXPOSURE
4.3.1. Human
No information was available regarding the carcinogenicity of aluminum by the other routes of
exposure in humans.
4.3.2. Animal
No information was available regarding the carcinogenicity of aluminum by other routes of exposure
in animals.
4.4. EPA WEIGHT-OF-EVIDENCE
4.4.1. Oral
No weight-of-evidence classification has been assigned.
4.4.2. Inhalation
No weight-of-evidence classification has been assigned.
4.5. CARCINOGENICITY SLOPE FACTORS
4.5.1. Oral
An oral carcinogenicity slope factor has not been derived for aluminum.
4.5.2. Inhalation
An oral carcinogenicity slope factor has not been derived for aluminum.
5. REFERENCES
ATSDR (Agency for Toxic Substances and Disease Registry). 1990. Toxicological Profile for
Aluminum. U.S. Department of Health and Human Services. Public Health Service.
Berlyne, G.M., J. Ben Ari, E. Knopf, et al. 1972. Aluminum toxicity in rats. Lancet. 1: 564-567.
Cavender, F.L., W.H. Steinhagen, and B.Y. Cockrell. 1978. Chronic toxicity of aluminum chlorohydrate.
Clin. Toxicol. 12:606.
Commissaris, R.L., J.J. Gordon, S. Sprague, et al. 1982. Behavioral changes in rats after chronic aluminum
and parathyroid hormone administration. Neurobehavior. Toxicol. Teratol. 4: 403-410.
Cranmer, J.M., J.D. Wilkins, D.J. Cannon, et al. 1986. Fetal-placental-maternal uptake of aluminum in mice
following gestational exposure: effect of dose and route of administration. Neurotoxicology. 7: 601-608.
Dixon, R.L., R.J. Sherins, and I.P. Lee. 1979. Assessment of environmental factors affecting male fertility.
Environ. Health Perspect. 30: 53-68.
Drew, R., N. Bhola, J. Bend, and G. Hook. 1974. Inhalation studies with a glycol complex of aluminum
chloride hydroxide. Arch. Environ. Health. 28: 321.
Ganrot, P.O. 1986. Metabolism and possible health effects of aluminum. Environ. Health Perspect. 65: 363-441.
Goyer, R.A. 1991. Toxic Effects of Metals. In: Casarett and Doull's Toxicology. The Basic Science of
Poisons. Fourth Edition. M.O. Amdur, J. Doull, and C.D. Klaassen, Ed. Permagon Press. pp. 662-663.
Greger, J.L. and M.J. Baier. 1983. Excretion and retentionof low or moderate levels of aluminum by human
subjects. Food Chem. Toxicol. 21: 473-477.
Greger, J.L. and S.E. Donnaubauer. 1986. Retention of aluminum in the tissues of rats after discontinuation
of oral exposure to aluminum. Food Chem. Toxicol. 24: 1131-1134.
Gross, P., R.H. Harley, and R.T.P. deTreville. 1973. Pulmonary reaction to metallic aluminum powders.
Arch. Environ. Health. 26: 227-236.
Kolvachik, M.T., W.D. Kaehny, A.P. Hegg, et al. 1978. Aluminum kinetics during hemodialysis. Lab. Clin.
Med. 92:712.
Kortus, J. 1967. The carbohydrate metabolism accompanying intoxication by aluminum salts in the rat.
Experientia. 23: 912-915.
Krasovskii, G.N., L.Y. Vasulovich and O.G. Charie. 1979. Experimental study of biological effects of lead
and aluminum following oral administration. Environ. Health Perspect. 30: 47-51.
Lansdown, A.B. 1973. Production of epidermal damage in mammalian skins by some simple aluminum
compounds. Br. J. Dermatol. 89: 67-76.
Llobet, J.M., J.L. Domingo, M. Gomez, et al. 1987. Acute toxicity studies of aluminum compounds-
antidotal efficacy of several chelating agents. Pharmacology and Toxicology. 60: 280-283.
Monteagudo, F.S.E., L.C. Isaacson, G. Wilson, et al. 1988. Aluminum excretion by the distal tubule of the
pig kidney. Nephron. 49: 245-250.
Nagyvary, J. and E.L. Bradbury. 1977. Hypocholesterolemic effects of Al3+ complexes. Biochem. Res.
Commun. 2: 592-598.
Ondreicka, R., E. Ginter, and J. Kortus. 1966. Chronic toxicity of aluminum in rats and mice and its effects
on phosphorus metabolism. Brit. J. Ind. Med. 23: 305-312.
Pigott, G.H., B.A. Gaskell, and J. Ishmael. 1981. Effects of long-term inhalation of aluminum fibres in rats.
Br. J. Exper. Pathol. 62: 323-331.
Schroeder, H.A. and M. Mitchener. 1975a. Life-term studies in rats: Effects of aluminum, barium, beryllium,
and tungsten. J. Nutr. 105: 421-427.
Schroeder, H.A. and M. Mitchener. 1975b. Life-term effects of mercury, methyl mercury and nine other trace
metals on mice. J. Nutr. 105: 452-458.
Shore, D. and R.J. Wyatt. 1983. Aluminum and Alzheimer's disease. J. Nerv. Ment. Dis. 171: 553-558.
Stokinger, H.A. 1981. Aluminum. The metals. In: Patty's Industrial Hygiene and Toxicology, 3rd rev. ed.,
Vol. IIA, G.D. Clayton and F.E. Clayton, Ed. John Wiley and Sons, NY. p. 1493-1504.
Thurston, H., G.R. Gilmore, and J.E. Swalws. 1972. Aluminum retention and toxicity in renal failure. Lancet.
1: 881-883.
U.S. EPA. 1987. Health Effects Assessment Document for Aluminum. Prepared for the Office of Solid
Waste and Emergency Response by the Environmental Criteria and Assessment Office, Cincinnati, OH.
ECAO-CIN-H114.
Venugopal, B. and T.D. Luckey. 1978. Metal Toxicity in Mammals-2. Chemical Toxicity of Metals and
Metalloids. Plenum Press. pp. 104-112.
Yokel, R.A. and P.J. McNamara. 1985. Aluminum bioavailability and disposition in adult and immature
rabbits. Toxicology and Applied Pharmacology. 77: 344-352.
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