SM Bradberry BSc MB MRCP
    ST Beer BSc

    National Poisons Information Service
    (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    B18 7QH

    This monograph has been produced by staff of a National Poisons
    Information Service Centre in the United Kingdom.  The work was
    commissioned and funded by the UK Departments of Health, and was
    designed as a source of detailed information for use by poisons
    information centres.

    Peer review group: Directors of the UK National Poisons Information


    Toxbase summary

    Type of product

    Used as a component of paints and varnishes and in the manufacture of
    alloys, ceramics, glass, electrical insulators and resistors.


    Significant toxicity has been reported only following chronic
    occupational inhalation.



         -    Aluminium contact sensitivity has been described but is
              extremely rare.


         -    There are no case reports relating to acute exposure.

         -    Chronic occupational exposure causes conjunctivitis,
              pharyngitis, and nasal irritation. Occupational asthma has
              been reported in aluminium smelter workers but these
              individuals are exposed to several other potential allergens
              (including fluorides and sulphur dioxide).

         -    Chronic aluminium oxide inhalation may cause pneumoconiosis
              with cough and exertional dyspnoea, diffuse reticulonodular
              shadowing on chest X-ray and a restrictive pattern of
              pulmonary function. In severe cases death may result from
              respiratory failure or corpulmonale.

         -    There is evidence from controlled studies among aluminium
              workers that chronic aluminium oxide exposure with an
              increased body aluminium burden may be associated with
              neurocognitive dysfunction but not increased mortality.



    1.   Remove from exposure.
    2.   Treat symptomatically.


    1.   Remove from exposure.
    2.   Give supplemental oxygen by face-mask if there is evidence of
         respiratory distress.

    3.   Asthmatic symptoms respond to conventional measures.
    4.   In chronic exposure suspected pulmonary fibrosis should be
         investigated and managed conventionally.
    5.   Obtain blood and urine for aluminium concentration estimations in
         symptomatic patients. Discuss with NPIS as these analyses are not
         widely available.
    6.   Estimation of the aluminium content of CSF may be an important
         investigation in suspected aluminium-related dementia.
    7.   There is no established role for chelation therapy in chronic
         aluminium oxide poisoning. Discuss with NPIS.


    Bast-Pettersen R, Drablos PA, Goffeng LO, Thomassen Y, Torres CG.
    Neuropsychological deficit among elderly workers in aluminum
    Am J Ind Med 1994; 25: 649-62.

    Jederlinic PJ, Abraham JL, Churg A, Himmelstein JS, Epler GR, Gaensler
    Pulmonary fibrosis in aluminum oxide workers. Investigation of nine
    workers, with pathologic examination and microanalysis in three of
    Am Rev Respir Dis 1990; 142: 1179-84.

    Kongerud J, Boe J, Sœyseth V, Naalsund A, Magnus P.
    Aluminium potroom asthma: the Norwegian experience.
    Eur Resp J 1994; 7: 165-72.

    Nielsen J, Dahlqvist M, Welinder H, Thomassen Y, Alexandersson R,
    Skerfving S.
    Small airways function in aluminium and stainless steel welders.
    Int Arch Occup Environ Health 1993; 65: 101-5.

    Schwarz YA, Kivity S, Fischbein A, Ribak Y, Fireman E, Struhar D,
    Topilsky M, Greif J.
    Eosinophilic lung reaction to aluminium and hard metal.
    Chest 1994; 105: 1261-3.

    Sjögren B, Ljunggren KG, Almkvist O, Frech W, Basun H.
    A follow-up study of five cases of aluminosis.
    Int Arch Occup Environ Health 1996; 68: 161-4.

    Substance name

         Aluminium oxide

    Origin of substance

         Occurs naturally as minerals such as bauxite, corundum, diaspore
         and gibbsite.                           (CSDS, 1989)


         Aluminium sesquioxide                   (CSDS, 1989)
         Alumina                                 (DOSE, 1992)

    Chemical group

         A compound of aluminium, a group III metal.

    Reference numbers

         CAS            1344-28-1                (CSDS, 1989)
         RTECS          BD1200000                (RTECS, 1996)
         UN             NIF

    Physicochemical properties

    Chemical structure
         Aluminium oxide, Al2O3                  (DOSE, 1992)

    Molecular weight
         101.96                                  (DOSE, 1992)

    Physical state at room temperature
         Solid (powder)                          (CSDS, 1989)

         White                                   (CSDS,1989)




         Insoluble in water, practically insoluble in non-polar organic
         solvents, slowly soluble in aqueous alkaline solutions.
                                                 (CSDS, 1989)

    Autoignition temperature

    Chemical interactions
         Aluminium oxide will react vigorously with vinyl acetate vapour,
         exothermically with halogenated carbon compounds (above 200°C),
         and exothermically, possibly explosively with oxygen difluoride.

         A mixture of aluminium oxide and sodium nitrite will react
         explosively, and ignition will occur if chlorine trifluoride is
         mixed with aluminium oxide.

         Aluminium oxide should be kept well away from water, and is
         incompatible with strong oxidizers and chlorinated rubber.
                                                 (CSDS, 1989)

    Major products of combustion

    Explosive limits

         Non-flammable                           (CSDS, 1989)

    Boiling point
         2977°C                                  (CSDS, 1989)

         4.0 at 20°C/4°C                         (DOSE, 1992)

    Vapour pressure
         133.3 Pa at 2158°C                      (CSDS, 1989)

    Relative vapour density

    Flash point



         Aluminium oxide is used as an adsorbant, desiccant, as a filler
         for paints and varnishes, and as a catalyst for organic
         Aluminium oxide is employed widely in the manufacture of alloys,
         ceramics, glass, electrical insulators and resistors.
                                                 (CSDS, 1989; DOSE, 1992)

    Hazard/risk classification



    Aluminium is the most abundant metal on earth, naturally occurring in
    rocks as bauxite (aluminium oxide), mica and feldspar
    (aluminosilicates). It is a light metal which is a good conductor of
    both heat and electricity. Aluminium oxide forms as a thin surface
    layer when aluminium is exposed to air, making it resistant to
    corrosion. Aluminium oxide is used as an industrial catalyst,
    adsorbant, desiccant, and as a filler for paints and varnishes. It is
    also employed widely in the manufacture of alloys, ceramics, glass,
    electrical insulators and resistors.

    Aluminium oxide is an insoluble aluminium compound which does not
    produce an acute toxic response. The presumed low toxicity of inhaled
    aluminium oxide led in the past to its use as a prophylactic agent
    against silicotic lung disease in miners but this practice was
    abandoned in the 1970's amid concern that chronic exposure may be
    harmful. Current important sources of occupational exposure via
    inhalation are aluminium smelting and welding.


    There is experimental evidence that aluminium inhibits bone
    mineralization partly by the deposition of aluminium at the
    osteoid/calcified-bone boundary thereby directly inhibiting calcium
    influx, and partly by aluminium accumulation in the parathyroid glands
    with suppression of parathyroid hormone secretion (Visser and Van de
    Vyver, 1985; Berland et al, 1988; Firling et al, 1994).

    Proposed mechanisms of aluminium-induced neurotoxicity include
    free-radical damage via enhanced lipid peroxidation, impaired glucose
    metabolism, effects on signal transduction and protein modification
    and alterations in the axonal transport and phosphorylation state of
    neurofilaments (Birchall and Chappell, 1988; Exley and Birchall, 1992;
    Erasmus et al, 1993; Winship, 1993; Haug et al, 1994; Joshi et al,
    1994; Strong, 1994). It has also been suggested that low-level
    aluminium exposure may influence the body distribution of other
    essential metals with potential adverse metabolic effects (Röllin et
    al, 1991).



    In a healthy adult only approximately 15µg of the average daily
    dietary aluminium intake of 3-5mg is absorbed (Winship, 1992). The
    intestinal absorption of aluminium and its oxide is enhanced by
    citrate (which is found frequently in effervescent drug formulations)
    and reduced by silica. Since aluminium oxide is insoluble it is poorly
    absorbed following inhalation.


    Since aluminium oxide is insoluble some will be retained in the lung
    following inhalation. More than 90 per cent of that which is
    systematically absorbed is bound to transferrin which does not cross
    the blood-brain barrier readily. The remaining ten per cent is
    associated with low molecular weight complexes, such as citrate, which
    can accumulate in brain tissue. Systematically absorbed aluminium is
    stored mainly in bone (up to 40 per cent) and liver.


    Aluminium is excreted predominantly via the kidneys and therefore will
    accumulate in patients with renal failure (Alfrey, 1980). Following
    long-term occupational inhalation, aluminium oxide exposed workers
    with normal renal function may also accumulate aluminium. In two such
    cases the total body aluminium half-life was estimated as three years
    (Elinder et al, 1991).


    Aluminium oxide ingestion is rare and does not lead to significant
    toxicological problems; most exposures are via inhalation.

    No features following acute inhalation have been reported.


    Ocular exposure

    In one study conjunctivitis was reported significantly more frequently
    among aluminium welders (n=25) than controls (Nielsen et al, 1993).

    Dermal exposure

    Dermal toxicity

    Thériault et al (1980) described an increased number of skin
    telangiestases on the upper torso of workers in an aluminium plant.
    There were no associated clinical features and the causative agent was
    thought to be a hydrocarbon or fluoride emitted from the aluminium
    electrolytic reactors (Thériault et al, 1980).

    There are reports of contact sensitivity to aluminium but this is
    extremely rare (Kotovirta et al, 1984).


    Pulmonary toxicity

    Because metallic aluminium has an high affinity for oxygen, exposure
    to aluminium dust usually also involves exposure to aluminium oxide.
    Important sources of such exposure include aluminium smelting (among

    'potroom' workers) and welders. In some industries sub-micron sized
    aluminium particles are coated with oil to prevent surface aluminium
    oxide formation. Removal of this protective coating  in vivo however
    exposes the metal to powerful natural oxidizing agents and tissue
    damage may result (Dinman, 1987).

    Smokers are at greater risk of pulmonary complications from aluminium
    dust as they have a reduced ability to clear inhaled particles from
    the lungs.

    In a controlled study of respiratory symptoms among 25 aluminium
    welders Nielsen et al (1993) reported a significantly increased
    incidence of pharyngitis. Interestingly, employees exposed to
    aluminium/aluminium oxide for less than 2´ years were more likely to
    experience this symptom, possibly reflecting 'healthy worker'
    selection or the development of tolerance.

    Chronic exposure to stamped aluminium powder (aluminium flake),
    produced by grinding hard unmelted aluminium, may cause
    pneumoconiosis. Initial symptoms include dyspnoea and cough although
    in some patients the first clue to respiratory disease is the finding
    of widespread miliary nodules on chest X-ray (Sjögren et al, 1996a). A
    honeycomb pattern is observed on lung biopsy and lung function tests
    show a restrictive pattern (Jederlinic et al, 1990). Patients may
    develop progressive exertional dyspnoea terminating in respiratory
    failure or corpulmonale (Mitchell, 1959; Mitchell et al, 1961; Sjögren
    et al, 1996a). Spontaneous regression is rare and should prompt
    reconsideration of the diagnosis (Sjögren et al, 1996a).

    Aluminium oxide-induced pulmonary fibrosis may be associated with
    generalized debility and weight loss (Schwarz et al, 1994).

    Schwarz et al (1994) described a 51 year-old sand-blaster who
    presented with an eight month history of cough and dyspnoea. Chest
    X-ray showed diffuse bilateral reticulonodular opacities in the mid
    and lower zones and bronchoalveolar lavage (BAL) fluid analysis
    revealed a marked eosinophilia (61.6 per cent). Transbronchial biopsy
    was consistent with interstitial pneumonia (with a giant-cell
    infiltrate and dust-laden macrophages). Mineralogic assessment
    identified large amounts of aluminium silicate and "hard metal". There
    was symptomatic and radiological improvement and partial resolution of
    BAL eosinophilia (to ten per cent) following removal from exposure and
    three months oral steroid therapy (prednisolone 40mg daily). The
    authors proposed a multifactorial aetiology in this case involving
    aluminium, 'hard metal' and iron exposure plus idiopathic

    In a controlled study of 14 potroom workers exposed to aluminium oxide
    for a mean period of 12.9 ± (SD) 9 years, analysis of bronchoalveolar
    lavage fluid demonstrated a mild alveolitis (as indicated by altered
    macrophage activity and increased alveolar capillary permeability) but
    no evidence of restrictive lung disease (Eklund et al, 1989).

    Occupational asthma has been reported in aluminium-smelter (potroom)
    workers (Kongerud et al, 1990; Saric and Marelja, 1991; Kongerud et
    al, 1992; Desjardins et al, 1994) but these individuals are exposed to
    several other allergens including fluorides and sulphur dioxide
    (Kongerud and Samuelsen, 1991; Sœyseth and Kongerud, 1992; Kongerud et
    al, 1992; Kongerud et al, 1994) which makes it difficult to identify a
    specific aetiological agent.

    Neuropsychiatric toxicity

    There is increasing speculation that Alzheimer's disease may be linked
    aetiologically to the accumulation of aluminium in the brain but this
    remains a highly contentious issue (Ebrahim, 1989; Petit, 1989; Murray
    et al, 1991; Crapper McLachlan, 1994; Munoz, 1994).

    Animal studies have demonstrated the ability of aluminium to induce
    the formation of neurofibrillary tangles (Klatzo et al, 1965), impair
    the learning ability of rats, and increase brain acetylcholinesterase
    activity in a similar way to that seen in Alzheimer's disease
    (Bilkei-Gorzó, 1993).

    Other workers have shown elevated aluminium concentrations in brain
    tissue from patients with Alzheimer's disease (Crapper et al, 1973)
    and laser microprobe studies have demonstrated aluminium accumulation
    in the neurofibrillary tangles of these patients (Good et al, 1992).

    There is conflicting evidence as to whether neuropsychiatric sequelae
    result from chronic aluminium oxide exposure. Gibbs (1981) reported no
    increased mortality from Alzheimer's disease in over 5000 men employed
    at an aluminium plant. Clinical examination of 23 workers in an
    aluminium factory found no neurological signs or symptoms although
    another man who had worked in the same plant for 13´ years died from
    rapidly progressive encephalopathy (McLaughlin et al, 1962). Autopsy
    showed no identifiable cause of death or histological abnormality in
    the brain but the brain aluminium content was reported to be 20 times
    higher than normal.

    Rifat et al (1990) found that although there was no increased
    incidence of neurological diagnoses in miners exposed between 1944 and
    1979 to a mixture of powdered aluminium and aluminium oxide, exposed
    workers performed significantly less well on cognitive testing than
    unexposed controls; the likelihood of impairment increased with
    duration of exposure.

    Bast-Pettersen et al (1994) performed neuropsychological tests on 38
    men who had worked for at least ten years in an aluminium production
    plant. Potroom workers had significantly raised urine aluminium
    concentrations compared to controls; the serum aluminium concentration
    was normal in all groups. Potroom workers also had a significantly
    increased incidence of subclinical tremor compared to controls with
    some evidence of impaired visuospatial organization.

    In another controlled study of 38 aluminium welders with a median
    exposure of 7065 hours, a significant dose-related deterioration in
    certain motor function tests (for example tapping with the non-
    dominant hand) was observed (Sjögren et al, 1996b). Aluminium exposed
    workers had urine aluminium concentrations (spot samples)
    approximately seven times higher than controls.

    Several uncontrolled studies (Sjögren et al, 1990; White et al, 1992;
    Hänninen et al, 1994) have reported subtle memory defects in aluminium
    workers. Hänninen et al (1994) demonstrated a negative association
    between short-term memory loss, learning and attention, and the urine
    aluminium concentration. White et al (1992) also found clinical
    evidence of incoordination in 84 per cent of the 25 workers examined.

    Sjögren et al (1994 and 1996a) described a 78 year-old man with a 47
    year history of aluminium pneumoconiosis, mild extrapyramidal
    impairment and moderate dementia. His cerebrospinal fluid aluminium
    concentration was markedly raised to 259µg/L (normal <10µg/L) without
    a rise in the serum and urine aluminium concentrations and with no
    evidence of cerebrovascular disease.


    Controlled studies among aluminium workers suggest that chronic
    aluminium/aluminium oxide exposure with an increased body aluminium
    burden may be associated with neurocognitive dysfunction but not an
    increased mortality. There is insufficient evidence, however, to
    implicate occupational aluminium oxide exposure in the aetiology of
    Alzheimer's disease.

    Bone toxicity

    Schmid et al (1995) observed increased plasma and urine aluminium
    concentrations (mean 9.7µg/L and 115.8µg/L respectively) among 32
    aluminium production plant workers (corresponding values among 29
    controls were 4.3µg/L and 15.5µg/L respectively). There was however no
    significant difference in lumbar spine bone mineral content (as
    measured by photon absorptiometry) between the two groups. The authors
    concluded that occupational aluminium/aluminium oxide exposure did not
    adversely effect bone density (Schmid et al, 1995).


    Dermal exposure

    Dermal manifestations following topical aluminium oxide are rare. If
    suspected treatment is supportive with removal from exposure.


    Patients with suspected occupational pulmonary toxicity should be
    removed from exposure, treated symptomatically and undergo a full
    assessment of respiratory function.

    Asthmatic symptoms respond to conventional measures although Saric and
    Marelja (1991) demonstrated persistent bronchial hyperresponsiveness
    among potroom workers with occupational asthma (n=30) several years
    (mean 3.7) following a change of occupation.

    Partial resolution of radiographic chest X-ray opacities has been
    reported following systemic corticosteroid therapy in an aluminium
    exposed worker with pulmonary fibrosis (Schwarz et al, 1994) but this
    is unusual.


    Desferrioxamine (deferoxamine)

    Desferrioxamine forms a stable complex with aluminium and in animal
    studies it mobilises aluminium primarily from bone with subsequent
    urinary elimination of the chelate (Gómez et al, 1994; Yokel, 1994).
    It is absorbed poorly from the gastrointestinal tract and parenteral
    therapy is necessary. Theoretically 100mg desferrioxamine can bind
    4.1mg aluminium (Winship, 1993).

    The desferrioxamine chelate is dialyzable and all published clinical
    studies of aluminium chelation using desferrioxamine involve patients
    with renal failure undergoing haemodialysis (Sulkova et al, 1991) or,
    less commonly, peritoneal dialysis (O'Brien et al, 1987) or
    haemofiltration (Sulkova et al, 1991). This is discussed in detail in
    the aluminium sulphate monograph.

    Sulkova et al (1991) suggested that desferrioxamine-induced aluminium
    clearance is greater following haemofiltration (mean serum aluminium
    concentration reduction 66 per cent for 36 filtrations, each a 60 per
    cent body weight volume exchange) than haemodialysis (mean serum
    aluminium concentration reduction 41 per cent for 28 five hour

    Available clinical evidence suggests desferrioxamine therapy can
    improve aluminium-induced encephalopathy in chronic haemodialysis
    patients (Day and Ackrill, 1993) and parenteral desferrioxamine
    therapy may slow the rate of cognitive deterioration in patients with
    Alzheimer's disease (Crapper McLachlan et al, 1991; Crapper McLachlan
    et al, 1993) but there are no data relating to desferrioxamine therapy
    following aluminium oxide exposure. If aluminium-induced
    neurocognitive impairment is confirmed desferrioxamine therapy may
    have a role.

    Desferrioxamine and charcoal haemoperfusion

    Chang and Barre (1983) compared aluminium clearance by desferrioxamine
    plus charcoal haemoperfusion with desferrioxamine plus haemodialysis
    in 17 patients with chronic renal failure who were stable on standard
    haemodialysis. Neither method enhanced aluminium clearance without
    desferrioxamine but forty-eight hours after intravenous
    desferrioxamine charcoal haemoperfusion produced more effective

    aluminium clearance (mean 65.3 ± (SD) 11.2 mL/min; n=6) than
    haemodialysis (mean 44.6 ± (SD) 13.7mL/min; n=4). The authors proposed
    haemoperfusion plus desferrioxamine as an effective method of rapid
    aluminium elimination in aluminium intoxicated patients to be used in
    series with haemodialysis in patients with renal failure. There are no
    data involving patients with aluminium oxide toxicity.


    In patients exposed to aluminium oxide desferrioxamine therapy could
    be considered in those with neurocognitive abnormalities associated
    with a confirmed increased body aluminium burden but there are no
    clinical data to support this.

    Treatment protocol for desferrioxamine

    This is based on experience with aluminium intoxicated haemodialysis
    patients and is usually a once weekly intravenous does of 40-80mg/kg.
    The dose can be reduced to 20-60mg/kg (as indicated by response and
    adverse effects) if treatment is to be continued for several months
    (Domingo, 1989). Canavese et al (1989) have suggested the therapeutic
    effectiveness of desferrioxamine may be exhausted after some two years
    therapy even if aluminium bone deposits persist after this time.

    Adverse effects of desferrioxamine

    Side-effects of long-term treatment with desferrioxamine include
    hypotension, gastrointestinal upset, porphyria cutanea tarda-like
    lesions, transient visual disturbances (McCarthy et al, 1990),
    posterior cataracts, ototoxicity (Domingo, 1989) and an increased
    potential for septicaemia, especially Yersinia sepsis (Boyce et al,

    Some dialysis patients with aluminium encephalopathy develop worsening
    of neurological symptoms within hours of desferrioxamine treatment
    which may be due to desferrioxamine alone or in combination with a
    rising plasma aluminium concentration (McCauley and Sorkin, 1989).

    There are several reports of desferrioxamine-associated systemic
    fungal infection (mucormycosis) in dialysis patients (Goodill and
    Abuelo, 1987; Windus et al, 1987). An international registry of this
    potentially fatal complication has been established (Boelaert et al,
    1991) although a causal link between desferrioxamine and fungal
    infection in these patients has not been confirmed (Vlasveld and van
    Asbeck, 1991).

    Other chelating agents

    The practical problems of desferrioxamine administration and its side
    effects have prompted a search for an alternative aluminium chelator
    although as yet none has been confirmed (Domingo, 1989; Main and Ward,
    1992; Yokel, 1994). Uncontrolled clinical studies with d-penicillamine
    and dimercaprol in dialysis encephalopathy were unsuccessful (Yokel,

    1994) and although in animal studies parenteral citric acid is
    effective (Domingo et al, 1988), evidence in man that oral citrate
    enhances gastrointestinal aluminium absorption means the problems of
    parenteral administration persist.

    Rats treated with intraperitoneal aluminium (as the chloride) 2mg/kg
    daily, four days per week for four weeks, followed by 40mg/kg
    intraperitoneal ethylenediamine-N,N'-di(2-hydroxyphenyl acetic acid)
    (EDDHA) showed significantly increased (p<0.05) urine aluminium
    excretion but no reduction in tissue aluminium concentrations (Graff
    et al, 1995).

    In a recent clinical trial Kontoghiorghes et al (1994) demonstrated
    that the administration of oral 1,2-dimethyl-3-hydroxypyrid-4-one in a
    dose of 40-60 mg/kg to six haemodialysis patients resulted in rapid
    aluminium mobilization. The plasma aluminium concentration peaked at
    one hour post chelation therapy and returned to baseline in most cases
    within seven hours. The aluminium chelate was readily dialysable
    during both haemodialysis and continuous ambulatory peritoneal


    Sulkova et al (1991) reported no aluminium elimination during four
    haemodialyses without prior desferrioxamine administration.

    Peritoneal dialysis

    Aluminium is removed in small amounts by peritoneal dialysis (O'Brien
    et al, 1987) and elimination is enhanced by desferrioxamine. In a 32
    year-old man with aluminium osteodystrophy O'Brien et al (1987)
    reported an aluminium clearance of 2.5mL/min with continuous
    ambulatory peritoneal dialysis (CAPD) alone. CAPD plus intravenous
    desferrioxamine (six grams once a week) gave an aluminium clearance of
    4.2mL/min compared to a clearance of 3.1mL/min when the same
    cumulative desferrioxamine dose was given into the peritoneal cavity.


    During four haemofiltrations (each with a 60 per cent body weight
    volume exchange) Sulkova et al (1991) reported a mean 15 per cent fall
    in the serum aluminium concentration compared to a mean 66 per cent
    reduction (36 haemofiltrations) in patients pre-treated with
    desferrioxamine (see above).


    Chang and Barre (1983) demonstrated that haemoperfusion enhances
    aluminium elimination only in the presence of desferrioxamine.
    Protein(transferrin)-bound aluminium is not dialyzable (Day and
    Ackrill, 1993).

    Enhancing elimination: Conclusions and recommendations

    There is currently insufficient data to advocate chelation therapy or
    extracorporal methods of enhancing elimination in aluminium oxide
    poisoning. Most cases involve pulmonary complications following
    inhalational exposure and should be managed conventionally. The role
    of chelating agents in the management of neuropsychiatric sequelae
    remains to be determined.


    Monitoring airborne aluminium concentrations and periodic assessment
    of respiratory function are important surveillance measures in the
    aluminium industry. Aluminium toxicity should be particularly sought
    in those who develop unexplained respiratory or neuropsychiatric

    Measurement of blood and urine aluminium concentrations are of some
    value but close attention must be paid to avoiding sample
    contamination and consideration given to the potential effect of
    aluminium-containing medications (House, 1992). Grouped data are
    preferable to individual results. The interpretation of urine
    aluminium concentrations is complicated by the fact that the kinetics
    of urine aluminium excretion varies depending on the form of aluminium
    involved (Pierre et al, 1995).

    Aluminium is evenly distributed between plasma and blood cells so that
    plasma and whole blood aluminium concentrations have similar value in
    assessing toxicity (van der Voet and de Wolff, 1985).

    Thirteen workers exposed to aluminium flake ('atomised' aluminium
    solid) had significantly higher mean urine (203.6µg/L) and blood
    (12.4µg/L) aluminium concentrations compared to controls (median urine
    and blood concentrations 2.4µg/L and less than 2.7µg/L respectively)
    although the higher values in exposed workers were not related to
    duration of exposure time (Ljunggren et al, 1991). In the same study
    the mean urine and blood aluminium concentrations among ten retired
    workers were 20.0µg/L and 3.0µg/L respectively.

    Gitelman et al (1995) observed a strong association between grouped
    urine aluminium concentrations and airborne occupational exposure but
    emphasised that individual measurements were not reliable.

    In a study comparing 84 aluminium smelter workers with 48 controls,
    significantly higher mean urine aluminium concentrations were observed
    in workers exposed to airborne aluminium concentrations higher than
    0.35mg/m3 (TLV = 10mg/m3) (Röllin et al, 1996). Urine aluminium
    monitoring was not useful at lower aluminium exposures, probably
    because a smaller proportion of the total airborne metal was in the
    respirable fraction. Serum aluminium concentrations were less valuable
    than urinary aluminium as a biological indicator of exposure.

    Estimation of the aluminium content of cerebrospinal fluid may be
    important in the investigation of aluminium-related dementia (Sjögren
    et al, 1994; Sjögren et al, 1996a). Hair analysis is a poor indicator
    of aluminium exposure (Wilhelm et al, 1989).


    Preterm infants have a limited ability to excrete aluminium.


    Occupational exposure standard

    Long term exposure limit (8 hour TWA reference period) total inhalable
    dust 10 mg/m3, respirable dust 5mg/m3 (Health and Safety
    Executive, 1995).



    Workers involved in aluminium production may be at increased risk of
    developing lung cancer but mortality figures are difficult to
    interpret, especially when comprehensive occupational and smoking
    histories are not available (Andersen et al, 1982). Moreover, these
    workers are exposed to a number of established carcinogens including
    asbestos, chromium and polycyclic aromatic hydrocarbons (Dufresne et
    al, 1996).

    Higher than expected mortality from other cancers, including
    lymphoreticular and genitourinary malignancies have also been reported
    (Gibbs, 1981; Rockette and Arena, 1983) but again concomitant exposure
    to polycyclic aromatic hydrocarbons is likely to be involved
    (Thériault et al, 1984; Spinelli et al, 1991).

    In 521 workers exposed to aluminium oxide in an abrasive manufacturing
    plant and followed up between 1958 and 1983 Edling et al (1987) found
    no significantly increased cancer morbidity or mortality.




     Bacillus subtilis H17 (rec+), M45 (rec-) negative DNA damage
    (DOSE, 1992).

    Fish toxicity


    EEC Directive on Drinking Water Quality 80/778/EEC

    Aluminium: Guide level 0.05mg/L, maximum admissible concentration
    0.2g/L (DOSE, 1992).

    WHO Guidelines for Drinking Water Quality

    No health-based guideline value is recommended (WHO,1993).


    SM Bradberry BSc MB MRCP
    ST Beer BSc

    National Poisons Information Service (Birmingham Centre),
    West Midlands Poisons Unit,
    City Hospital NHS Trust,
    Dudley Road,
    B18 7QH

    This monograph was produced by the staff of the Birmingham Centre of
    the National Poisons Information Service in the United Kingdom. The
    work was commissioned and funded by the UK Departments of Health, and
    was designed as a source of detailed information for use by poisons
    information centres.

    Date of last revision


    Alfrey AC.
    Aluminum metabolism in uremia.
    Neurotoxicology 1980; 1: 43-53.

    Andersen A, Dahlberg BE, Magnus K, Wannag A.
    Risk of cancer in the Norwegian aluminium industry.
    Int J Cancer 1982; 29: 295-8.

    Bast-Pettersen R, Drablos PA, Goffeng LO, Thomassen Y, Torres CG.
    Neuropsychological deficit among elderly workers in aluminum
    Am J Ind Med 1994; 25: 649-62.

    Berland Y, Charbit M, Henry JF, Toga M, Cano JP, Olmer M.
    Aluminium overload of parathyroid glands in haemodialysed patients
    with hyperparathyroidism: effect on bone remodelling.
    Nephrol Dial Tansplant 1988; 3: 417-22.

    Bilkei-Gorzó A.
    Neurotoxic effect of enteral aluminium.
    Food Chem Toxicol 1993; 31: 357-61.

    Birchall JD, Chappell JS.
    Aluminium, chemical physiology, and Alzheimer's disease.
    Lancet 1988; 2: 1008-10.

    Boelaert JR, Fenves AZ, Coburn JW.
    Deferoxamine therapy and mucormycosis in dialysis patients: report of
    an international registry.
    Am J Kidney Dis 1991; 18: 660-7.

    Boyce N, Wood C, Holdsworth S, Thomson NM, Atkins RC.
    Life-threatening sepsis complicating heavy metal chelation therapy
    with desferrioxamine.
    Aust N Z J Med 1985; 15: 654-5.

    Canavese C, Pacitti A, Segoloni G, Thea A, D'Amicone M, Stratta P,
    Rossi P, Sabbioni E, Pietra R, Constantini S.
    Clinical and histological results of long-term management of aluminium
    overloading in uraemic patients with desferrioxamine.
    J Trace Elem Electrolytes Health Dis 1989; 3: 17-23.

    Chang TMS, Barre P.
    Effect of desferrioxamine on removal of aluminium and iron by coated
    charcoal haemoperfusion and haemodialysis.
    Lancet 1983; 2: 1051-3.

    Crapper DR, Krishnan SS, Dalton AJ.
    Brain aluminum distribution in Alzheimer's disease and experimental
    neurofibrillary degeneration.
    Science 1973; 180: 511-3.

    Crapper McLachlan DR.
    Aluminum and Alzheimer's disease. Response.
    Can Med Assoc J 1994; 151: 268-9.

    Crapper McLachlan DR, Dalton AJ, Kruck TPA, Bell MY, Smith WL, Kalow
    W, Andrews DF.
    Intramuscular desferrioxamine in patients with Alzheimer's disease.
    Lancet 1991; 337: 1304-8.

    Crapper McLachlan DR, Smith WL, Kruck TP.
    Desferrioxamine and Alzheimer's disease: video home behavior
    assessment of clinical course and measures of brain aluminum.
    Ther Drug Monit 1993; 15: 602-7.

    CSDS/Chemical Safety Data Sheets. Vol 2.
    Cambridge: Royal Society of Chemistry, 1989.

    Day JP, Ackrill P.
    The chemistry of desferrioxamine chelation for aluminum overload in
    renal dialysis patients.
    Ther Drug Monit 1993; 15: 598-601.

    Desjardins A, Bergeron JP, Ghezzo H, Cartier A, Malo JL.
    Aluminium potroom asthma confirmed by monitoring of forced expiratory
    volume in one second.
    Am J Respir Crit Care Med 1994; 150: 1714-7.

    Dinman BD.
    Aluminum in the lung: the pyropowder conundrum.
    J Occup Med 1987; 29: 869-76.

    Domingo JL.
    The use of chelating agents in the treatment of aluminum overload.
    Clin Toxicol 1989; 27: 355-67.

    Domingo JL, Gómez M, Llobet JM, Corbella J.
    Comparative effects of several chelating agents on the toxicity,
    distribution and excretion of aluminium.
    Hum Toxicol 1988; 7: 259-62.

    DOSE/Dictionary of substances and their effects. Vol 1.
    Cambridge: Royal Society of Chemistry, 1992.

    Dufresne A, Loosereewanich P, Armstrong B, Thériault G, Bégin R.
    Inorganic particles in the lungs of five aluminium smelter workers
    with pleuro-pulmonary cancer.
    Am Ind Hygiene Assoc J 1996; 57: 370-5.

    Ebrahim S.
    Aluminium and Alzheimer's disease.
    Lancet: 1989; 1: 267.

    Edling C, Järvholm B, Andersson L, Axelson O.
    Mortality and cancer incidence among workers in an abrasive
    manufacturing industry.
    Br J Ind Med 1987; 44: 57-9.

    Eklund A, Arns R, Blaschke E, Hed J, Hjertquist S-O, Larsson K,
    Löwgren H, Nyström J, Sköld CM, Tornling G.
    Characteristics of alveolar cells and soluble components in
    bronchoalveolar lavage fluid from non-smoking aluminium potroom
    Br J Ind Med 1989; 46: 782-6.

    Elinder C-G, Ahrengart L, Lidums V, Pettersson E, Sjögren B.
    Evidence of aluminium accumulation in aluminium welders.
    Br J Ind Med 1991; 48: 735-8.

    Erasmus RT, Savory J, Wills MR, Herman MM.
    Aluminum neurotoxicity in experimental animals.
    Ther Drug Monit 1993; 15: 588-92.

    Exley C, Birchall JD.
    The cellular toxicity of aluminium.
    J Theor Biol 1992; 159: 83-98.

    Firling CE, Severson AR, Hill TA.
    Aluminum effects on blood chemistry and long bone development in the
    chick embryo.
    Arch Toxicol 1994; 68: 541-7.

    Gibbs GW.
    Mortality experience in Eastern Canada.
    In: Hughes JP, ed. Health protection in primary aluminium production.
    Vol 2. 2nd ed. London: London International Primary Aluminium
    Institute, 1981; 56-69.

    Gitelman HJ, Alderman FR, Kurs-Lasky M, Rockette HE.
    Serum and urinary aluminium levels of workers in the aluminium
    Ann Occup Hyg 1995; 39: 181-91.

    Gómez M, Domingo JL, del Castillo D, Llobet JM, Corbella J.
    Comparative aluminium mobilizing actions of several chelators in
    aluminium-loaded uraemic rats.
    Hum Exp Toxicol 1994; 13: 135-9.

    Good PF, Perl DP, Bierer LM, Schmeidler J.
    Selective accumulation of aluminum and iron in the neurofibrillary
    tangles of Alzheimer's disease: a laser microprobe (LAMMA) study.
    Ann Neurol 1992; 31: 286-92.

    Goodill JJ, Abuelo JG.
    Mucormycosis - a new risk of deferoxamine therapy in dialysis patients
    with aluminum or iron overload?
    N Engl J Med 1987; 31: 54.

    Graff L, Muller G, Burnel D.
    In vitro and in vivo evaluation of potential aluminium chelators.
    Vet Hum Toxicol 1995; 37: 455-61.

    Hänninen H, Matikainen E, Kovala T, Valkonen S, Riihimäki V.
    Internal load of aluminum and the central nervous system function of
    aluminum welders.
    Scand J Work Environ Health 1994; 20: 279-85.

    Haug A, Shi B, Vitorello V.
    Aluminum interaction with phosphoinositide-associated signal
    Arch Toxicol 1994; 68: 1-7.

    Health and Safety Executive.
    EH40/95. Occupational exposure limits 1995.
    Sudbury: Heath and Safety Executive, 1995.

    House RA.
    Factors affecting plasma aluminium concentrations in nonexposed
    J Occup Med 1992; 34: 1013-7.

    Jederlinic PJ, Abraham JL, Churg A, Himmelstein JS, Epler GR, Gaensler
    Pulmonary fibrosis in aluminum oxide workers. Investigation of nine
    workers, with pathologic examination and microanalysis in three of
    Am Rev Respir Dis 1990; 142: 1179-84.

    Joshi JG, Dhar M, Clauberg M, Chauthaiwale V.
    Iron and aluminum homeostasis in neural disorders.
    Environ Health Perspect 1994; 102: 207-13.

    Klatzo I, Wisniewski H, Streicher E.
    Experimental production of neurofibrillary degeneration. I. Light
    microscopic observations.
    J Neuropathol Exp Neurol 1965; 24: 187-99.

    Kongerud J, Gronnesby JK, Magnus P.
    Respiratory symptoms and lung function of aluminum potroom workers.
    Scand J Work Environ Health 1990; 16: 270-7.

    Kongerud J, Samuelsen SO.
    A longitudinal study of respiratory symptoms in aluminum potroom
    Am Rev Respir Dis 1991; 144: 10-6.

    Kongerud J, Sœyseth V, Burge S.
    Serial measurements of peak expiratory flow and responsiveness to
    methacholine in the diagnosis of aluminium potroom asthma.
    Thorax 1992; 47: 292-7.

    Kongerud J, Boe J, Sœyseth V, Naalsund A, Magnus P.
    Aluminium potroom asthma: the Norwegian experience.
    Eur Resp J 1994; 7: 165-72.

    Kontoghiorghes GJ, Barr J, Baillod RA.
    Studies of aluminium, mobilization in renal dialysis patients using
    the oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one.
    Arzneimittelforschung 1994; 44: 522-6.

    Kotovirta M-L, Salo OP, Visa-Tolvanen K.
    Contact sensitivity to aluminium.
    Contact Dermatitis 1984; 11: 135.

    Ljunggren KG, Lidums V, Sjögren B.
    Blood and urine concentrations of aluminium among workers exposed to
    aluminium flake powders.
    Br J Ind Med 1991; 48: 106-9.

    Main J, Ward MK.
    Potentiation of aluminium absorption by effervescent analgesic tablets
    in a haemodialysis patient.
    Br Med J 1992; 304: 1686.

    McCarthy JT, Milliner DS, Johnson WJ.
    Clinical experience with desferrioxamine in dialysis patients with
    aluminium toxicity.
    Q J Med 1990; 275: 257-76.

    McCauley J, Sorkin MI.
    Exacerbation of aluminium encephalopathy after treatment with
    Nephrol Dial Transplant 1989; 4: 110-4.

    McLaughlin AIG, Kazantzis G, King E, Teare D, Porter RJ, Owen R.
    Pulmonary fibrosis and encephalopathy associated with the inhalation
    of aluminium dust.
    Br J Ind Med 1962; 19: 253-63.

    Mitchell J.
    Pulmonary fibrosis in an aluminium worker.
    Br J Ind Med 1959; 16: 123-5.

    Mitchell J, Manning GB, Molyneux M, Lane RE.
    Pulmonary fibrosis in workers exposed to finely powdered aluminium.
    Br J Ind Med 1961; 18: 10-20.

    Munoz DG.
    Aluminum and Alzheimer's disease.
    Can Med Assoc J 1994; 151: 268.

    Murray JC, Tanner CM, Sprague SM.
    Aluminum neurotoxicity: a re-evaluation.
    Clin Neuropharmacol 1991; 14: 179-85.

    Nielsen J, Dahlqvist M, Welinder H, Thomassen Y, Alexandersson R,
    Skerfving S.
    Small airways function in aluminium and stainless steel welders.
    Int Arch Occup Environ Health 1993; 65: 101-5.

    O'Brien AA, McParland C, Keogh JA.
    The use of intravenous and intraperitoneal desferrioxamine in
    aluminium osteomalacia.
    Nephrol Dial Transplant 1987; 2: 117-9.

    Petit TL.
    Issues in aluminum neurotoxicology.
    Comments Toxicol 1989; 3: 225-38.

    Pierre F, Baruthio F, Diebold F, Biette P.
    Effect of different exposure compounds on urinary kinetics of
    aluminium and fluoride in industrially exposed workers.
    Occup Environ Med 1995; 52: 396-403.

    Rifat SL, Eastwood MR, Crapper McLachlan DR, Corey PN.
    Effect of exposure of miners to aluminium powder.
    Lancet 1990; 336: 1162-5.

    Rockette HE, Arena VC.
    Mortality studies of aluminum reduction plant workers: potroom and
    carbon department.
    J Occup Med 1983; 25: 549-57.

    Röllin HB, Theodorou P, Kilroe-Smith TA.
    The effect of exposure to aluminium on concentrations of essential
    metals in serum of foundry workers.
    Br J Ind Med 1991; 48: 243-6.

    Röllin HB, Theodorou P, Cantrell AC.
    Biological indicators of exposure to total and respirable aluminium
    dust fractions in a primary aluminium smelter.
    Occup Environ Med 1996; 53: 417-21.

    RTECS/Registry of Toxic Effects of Chemical Substances.
    In: Tomes plus. Environmental Health and Safety Series I. Vol 27.
    National Institute for Occupational Safety and Health (NIOSH), 1996.

    Saric M, Marelja J.
    Bronchial hyperreactivity in potroom workers and prognosis after
    stopping exposure.
    Br J Ind Med 1991; 48: 653-5.

    Schmid K, Angerer J, Letzel S, Sturm G, Lehnert G.
    Use of bone mineral content determination by X-ray absorptiometry in
    the evaluation of osteodystrophy among workers exposed to aluminium
    Sci Total Environ 1995; 163: 147-51.

    Schwarz YA, Kivity S, Fischbein A, Ribak Y, Fireman E, Struhar D,
    Topilsky M, Greif J.
    Eosinophilic lung reaction to aluminium and hard metal.
    Chest 1994; 105: 1261-3.

    Sjögren B, Gustavsson P, Hogstedt C.
    Neuropsychiatric symptoms among welders exposed to neurotoxic metals.
    Br J Ind Med 1990; 47: 704-7.

    Sjögren B, Ljunggren KG, Almkvist O, Frech W, Basun H.
    Aluminosis and dementia.
    Lancet 1994; 344: 1154.

    Sjögren B, Ljunggren KG, Almkvist O, Frech W, Basun H.
    A follow-up study of five cases of aluminosis.
    Int Arch Occup Environ Health 1996a; 68: 161-4.

    Sjögren B, Iregren A, Frech W, Hagman M, Johansson L, Tesarz M,
    Wennberg A.
    Effects on the nervous system among welders exposed to aluminium and
    Occup Environ Med 1996b; 53: 32-40.

    Sœyseth V, Kongerud J.
    Prevalence of respiratory disorders among aluminium potroom workers in
    relation to exposure to fluoride.
    Br J Ind Med 1992; 49: 125-30.

    Spinelli JJ, Band PR, Svirchev LM, Gallagher RP.
    Mortality and cancer incidence in aluminum reduction plant workers.
    J Occup Med 1991; 33: 1150-5.

    Strong MJ.
    Aluminum neurotoxicity: an experimental approach to the induction of
    neurofilamentous inclusions.
    J Neurol Sci 1994; 124: 20-6.

    Sulkova S, Laurincova Z, Valek A.
    Haemofiltration or haemodialysis in aluminium elimination?
    Nephrol Dial Transplant 1991; 6: 3-5.

    Thériault G, Cordier S, Harvey R.
    Skin telangiectases in workers at an aluminum plant.
    New Engl J Med 1980; 303: 1278-81.

    Thériault G, Cordier S, Tremblay C, Gingras S.
    Bladder cancer in the aluminium industry.
    Lancet 1984; 1: 947-50.

    van der Voet GB and de Wolff FA.
    Distribution of aluminium between plasma and erythrocytes.
    Human Toxicol 1985; 4: 643-8.

    Visser WJ, Van de Vyver FL.
    Aluminium-induced osteomalacia in severe chronic renal failure (SCRF).
    Clin Nephrol 1985; 24: 30-6.

    Vlasveld LT, van Asbeck BS.
    Treatment with deferoxamine: a real risk factor for mucormycosis?
    Nephron 1991; 57: 487-8.

    White DM, Longstreth WT, Rosenstock L, Claypoole KHJ, Brodkin CA,
    Townes BD.
    Neurologic syndrome in 25 workers from an aluminum smelting plant.
    Arch Intern Med 1992; 152: 1443-8.

    Wilhelm M, Passlick J, Busch T, Szydlik M, Ohnesorge FK.
    Scalp hair as an indicator of aluminium exposure: comparison to bone
    and plasma.
    Human Toxicol 1989; 8: 5-9.

    Windus DW, Stokes TJ, Julian BA, Fenves AZ.
    Fatal Rhizopus infections in hemodialysis patients receiving
    Ann Intern Med 1987; 107: 678-80.

    Winship KA.
    Toxicity of aluminium: a historical review, Part 1.
    Adverse Drug React Toxicol Rev 1992; 11: 123-41.

    Winship KA.
    Toxicity of aluminium: a historical review, Part 2.
    Adverse Drug React Toxicol Rev 1993; 12: 177-211.

    Yokel RA.
    Aluminum chelation: chemistry, clinical, and experimental studies and
    the search for alternatives to desferrioxamine.
    J Toxicol Environ Health 1994; 41: 131-74.

    See Also:
       Toxicological Abbreviations