Introduction
This topic covers occupational intoxication with non-organic manganese compounds, known as manganism. It addresses the sources and chemical forms of exposure, how manganese is absorbed and distributed, the early behavioural and later extrapyramidal (parkinsonian-type) stages, the lung effects, the laboratory and clinical diagnosis, treatment, and the role of medical expertise in deciding fitness for work.
Etiology and sources of exposure
Manganese is an essential trace element, but excess exposure damages the nervous system. The main hazard is inhalation of dust and fumes containing manganese. The risk is highest in mining, ore processing, ferromanganese and steel production, electrolytic production of manganese metal and alloys, welding, and in electrical and chemical industries, including battery and ceramic manufacture.
Pathogenesis
- Route: inhalation of fine particles is the main route; fine particles reach the alveoli and are absorbed. Gastrointestinal absorption is smaller.
- Distribution: manganese is taken up by the liver, kidneys and bone, and is also carried by transferrin.
- Excretion: the main elimination route is biliary, through the liver into bile and faeces. Impaired liver function therefore increases body burden.
- Blood-brain barrier: manganese crosses the barrier and accumulates selectively in the globus pallidus and striatum (and to a lesser degree the substantia nigra). Accumulation is slow and cumulative, so symptoms often appear after long exposure.
- Mechanisms: oxidative stress, mitochondrial dysfunction, disturbed glutamate and GABA signalling, and astrocyte injury in the basal ganglia. The damage is mainly to the pallidal and striatal circuits, with relative sparing of the dopaminergic neurons that are lost in idiopathic Parkinson disease.