Immunotoxicity of aluminum

Aluminum (Al) is present in the daily life of all humans. With the incidence of Al contamination increased in recent years, the toxicity of Al on the immune function has attracted more attention. Even with this increased attention, the mechanism of Al immunotoxicity still remains unclear. The mechanism of Al immunotoxicity reviewed herein focused on the effects of Al on the splenic trace elements, the status of α-naphthyl acetate esterase (ANAE) cells, cytokines, complement and immunoglobulins, as well as macrophages. The studies in the literature showed that Al decreased splenic iron (Fe) and zinc (Zn) levels, but the effects of Al on splenic copper (Cu) level was ambiguous and controversial. Al exposure inhibited levels of ANAE(+) cells, the production of interleukin (IL)-2 and the functions of macrophages. With respect to other key cytokines, studies showed that Al suppressed the production of tumor necrosis factor (TNF)-α in vitro; effects of Al on TNF-α formation in vivo were less overt. Al exposure reduced complement 3 (C3) level, but effects of Al exposure on complement 4 (C4) level were not as clear-cut. Lastly, the effects of Al exposure on the IgG, IgM and IgA levels were conflicting. Taken in totality, the results of several studies in the literature demonstrated that Al could impart adverse effects on immune function.