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The only data from which one can estimate the percentage of aluminium absorbed from inhalation exposure is from exposures in the occupational environment. As the percentage of aluminium estimated to be absorbed during inhalation exposure is greater than from oral aluminium intake, it seems unlikely that absorption from the GI tract accounts for the absorption of all inhaled aluminium.


The absorption of aluminium from the lung can be estimated from a few studies of occupational aluminium exposure. Daily urinary aluminium excretion by 12 aluminium welders, whose lung aluminium burden may have been approaching a steady state, averaged 0.1 mg. Daily aluminium deposition into their lungs was estimated to be 4.2 mg. This would suggest absorption of ~ 2.4% of the aluminium (Sjögren et al., 1997). Results from workers exposed to ~ 0.2 to 0.5 mg soluble Al/m3 in the air (particle size not described) suggest ~ 2% absorption (Pierre et al., 1995). Fractional absorption was similar in the workers in a second study (Gitelman et al., 1995) who were exposed to a similar air aluminium concentration containing 25% respirable (< 10 μm diameter) aluminium. The estimate of26Al absorption from inhalation of26Al oxide particles which had a MMAD of 1.2 μm by two subjects was 1.9% (Priest, 2004).



The human whole body aluminium burden has been estimated to be 30 to 50 mg (ATSDR, 1999). One hr after ingestion of26Al citrate by one volunteer, 99% of the aluminium was in plasma (80% with transferrin (Tf) and 4% in a low molecular weight fraction) and the remaining 1% was in erythrocytes. The distribution of aluminium in blood taken 880 days after26Al citrate injection was 86% in plasma and 14% associated with erythrocytes (Day et al., 1994). The volume of distribution (Vd) of aluminium is initially consistent with the blood volume, and then increases with time. As bone is a major site of aluminium storage, prolonged urinary aluminium excretion may reflect a prolonged t1⁄2of aluminium in bone. A t1⁄2of 7 years was estimated in one human who had received an i.v. injection of26Al citrate 3.2 years earlier (Priest et al., 1995). An updated estimate in this individual, based on whole-body monitoring collected up to 3000 days after the injection, suggests the t1⁄2is ~ 50 years (Priest, 2004). This prolonged whole-body t1⁄2may largely reflect the t1⁄2of aluminium inbone.



The t1⁄2of aluminium elimination positively correlated with the duration of exposure (Ljunggren et al., 1991). Elimination t1⁄2s of hours, weeks and years were seen after termination of short-term inhalation exposure, < 1 year exposure and upon retirement, respectively (Ljunggren et al., 1991). These results are consistent with more than one compartment of aluminium storage. This kinetic behaviour might result from retention of aluminium in a depot from which it is slowly eliminated. This depot is probably bone which stores ~ 58% of the human aluminium body burden. Multiple phases of elimination were seen in a study in which one human received i.v.26Al citrate suggesting multiple compartments of aluminium distribution. About 85 to 90% of the aluminium was eliminated in < 24 h. Four percent of the injected26Al remained after 3.2 years (Priest et al., 1995) and ~ 2% after 9.2 years (Priest, 2004). Calculations based on results up to 14 years after the injection suggested at least three components of the aluminium elimination with t1⁄2of 1.4, 40 and 1727 days, and a retention t1⁄2of ~ 50 years (Priest, 2004). This unusual kinetic behaviour might result from retention of an aluminium species other than that administered, creating a depot, probably in bone, from which the aluminium is slowly eliminated.