Chronic manganese poisoning Clearance of tissue manganese concentrations with persistence of the neurological picture

INTEREST IN chronic manganese poisoning was evoked by some clinical similarities to parkinsonism and to Wilson’s disease.’ An earlier study of Chilean ex-miners with neurological consequences of this poisoning showed that the clinical picture prevailing in Chile resembled that reported from other parts of the world.’ Furthermore, it was shown that the rate of loss of artificial radiomanganese (54Mn) from the whole body of healthy, working manganese miners was accelerated, whereas it was normal in patients with chronic manganese poisoning. By examining the blood and plasma clearances as well as the disappearance of 54Mn from individual segments of the body, the present study investigated whether the rapidly excreted metal was located in a single major pool or in a system if interconnecting pools. The data favored the latter alternative; healthy, working miners had accelerated tissue turnovers of radiomanganese in contrast to the poisoned ex-miners who had normal turnovers. Earlier work on animals had shown that accelerated turnovers are sometimes due to elevated tissue concentrations of natural manganese (5sMn) .?-4 Therefore, it was suspected that the healthy miners conformed to this laboratory precedent, whereas the diseased ex-miners did not. Direct evidence was needed to decide whether the treatment of Wilson’s disease with metal binding agents5 constitutes a model for treating chronic manganese poisoning. Thus, the concentrations of 55Mn were also determined in selected tissues from healthy miners and patients with chronic poisoning.