Schlatter C
Institute of Toxicology, ETH, Schwerzenbach, Switzerland.
Med Lav. 1992 Sep-Oct;83(5):470-4.
About 2.5 mg of aluminium is absorbed daily with food; it then undergoes minimal absorption via the gastrointestinal tract (0.1%) and total excretion of the absorbed dose via the kidneys. The concentrations of aluminium in blood of non-exposed subjects with normal renal function are extremely low (1-3 micrograms/L). Until the beginning of the 1970's aluminium was considered to be of little toxicological interest, but in 1972 a neurological syndrome due to aluminium intoxication was described in dialysis patients in the UK and in 1973 Canadian research workers speculated on the role of aluminium in Alzheimer's disease (senile or presenile dementia), even though this does not at present have wide support. Al intoxication in dialysis patients can be prevented if the Al concentration in the dialysis solution is kept below 10 micrograms/L. No cases have been reported of systemic intoxication due to aluminium in occupationally exposed subjects. Al in plasma values of 5-15 micrograms/L have been reported in exposed workers, which are 10 times lower than the values observed in dialysis patients with encephalopathic symptoms. However, rare cases of occupational pulmonary fibrosis have been reported where an etiopathological role of aluminium was suspected. Nevertheless, it has been demonstrated that the alumina used in primary aluminium production lacks any fibrogenic potential.
人体每天随食物摄入约2.5毫克铝；随后，铝通过胃肠道的吸收极少（0.1%），并通过肾脏将吸收的剂量全部排出体外。肾功能正常的未接触铝的受试者血液中的铝浓度极低（1 - 3微克/升）。直到20世纪70年代初，铝一直被认为在毒理学方面没有太大研究价值，但1972年英国报道了透析患者因铝中毒出现的一种神经综合征，1973年加拿大研究人员推测铝在阿尔茨海默病（老年性或早老性痴呆）中所起的作用，尽管目前这一观点并未得到广泛支持。如果透析液中的铝浓度保持在10微克/升以下，可预防透析患者的铝中毒。职业接触铝的人群中尚未有因铝导致全身中毒的病例报告。据报道，接触铝的工人血浆铝值为5 - 15微克/升，这比有脑病症状的透析患者所观察到的值低10倍。然而，曾有罕见的职业性肺纤维化病例报告，怀疑铝在其病因学中起作用。不过，已证实原铝生产中使用的氧化铝没有任何致纤维化潜力。
