Manganese, malformations and motor disorders: findings in a manganese-exposed population
Kilburn, C.J.
Neurotoxicology 8(3): 421-429
1987
ISSN/ISBN: 0161-813X PMID: 3658240 Document Number: 4322
A more accurate assessment of the relative risks of stillbirth and congenital malformation on Groote Eylandt awaits completion of the examination of the control group. Even then, because the etiology of these misfortunes are incompletely understood and matching for risk factors so difficult, it is unlikely that the influence of living in a manganese rich environment will be observed in isolation. Small numbers also make interpretation of incidence rates of various congenital malformations nearly impossible. A "cleaner" look at this area is probably best provided by laboratory studies such as those of Webster, described in this issue. Is it possible to assign a probability as to the role manganese plays in the neurological disorders on Groote Eylandt? The arguments implicating manganese include: Is it a well documented neurotoxin; there are increasing data associating increased levels of manganese in the spinal cord and motor neurone disease; increased blood and hair levels of manganese have been demonstrated in Aborigines living on Groote Eylandt; factors exist on Groote Eylandt which are known to potentiate the absorption and toxicity of manganese intrauterine and neonatal exposure, iron deficiency and low protein diet; and the association, in the Western Pacific region, between foci of neurological disease and manganese rich ecologies. In defense of manganese, it must be said that the neurological disorders on Groote Eylandt are not the same as those described in manganese miners (though the pattern of exposure also differs), nor those described in the Western Pacific foci. Electrophysiological studies have not yet been extensively pursued to confirm the clinical diagnosis of motor neurone disease and no postmortem studies have been performed to identify the pathological mechanisms or to assay manganese concentration. The genealogical enquiries provide no answers. Restriction of neurological dysfunction to two pedigrees suggests a familial or polygenic influence, but does not rule out an environmental trigger. The available evidence can only implicate manganese by association. Further information is needed before the true role of manganese is defined with any clarity. The results of more extensive blood sampling of affected and non-affected individuals is eagerly awaited. Electrophysiological studies are required. Most important, perhaps, are postmortem studies to identify the pathological basis of these disorders and to examine trace metal concentration in brain, spinal cord and other tissues. The accumulation of postmortem material is necessarily a slow process. Until then, at least with respect to the Groote Eylandt disorders, manganese must remain an "element of doubt".
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