By Jane Lewis
A large study of workers from welding worksites has concluded that exposure to manganese (Mn)-containing fumes may cause a dose-dependent progression of parkinsonian symptoms, especially limb rigidity and upper limb bradykinesia.
‘This study adds to previous observations about parkinsonism in those people working as welders who are exposed to Mn “toxicity”,’ commented Professor Simon Lewis, neurologist at the Royal Prince Alfred Hospital, Sydney, and Professor of Cognitive Neuroscience at the University of Sydney.
‘However, it should be appreciated that this does not necessarily mean that Mn is a cause for idiopathic Parkinson’s disease. Rather, it provides insight into the relationships between neurotoxins that can drive a neurodegenerative process,’ he told Medicine Today.
Published in the journal Neurology, the US longitudinal cohort study included 886 welding-exposed workers examined by neurologists at baseline, with 398 of them followed up for up to 9.9 years. Progression of parkinsonism was measured as annual change in Unified Parkinson Disease Rating Scale motor subsection part 3 (UPDRS3), and cumulative Mn exposure (mg Mn/m3-year) was estimated from detailed work histories.
Progression of parkinsonism was found to increase with cumulative Mn exposure in a dose-dependent manner (annual change in UPDRS3 was 0.24 for each mg Mn/m3-year of exposure), despite estimated Mn concentrations being ‘near some regulatory thresholds,’ the authors reported. They described the rates of progression as ‘clinically meaningful’ and noted that progression was largely due to upper limb bradykinesia and limb rigidity, with some speech and facial expression abnormalities also apparent.
‘This study emphasises the need for stringent workplace monitoring of manganese exposures and the greater use of personal protective equipment and ventilation, as well as more systematic worker assessments in occupations such as welding,’ commented Professor Lewis.
The author of an accompanying editorial said the study had ‘many strengths,’ but also ‘a few limitations that should be considered before applying these findings to the diagnosis of manganese-parkinsonism in a clinical setting,’ including the inability to exclude the potential role of other neurotoxic chemicals in symptom progression.
Neurol 2017; 88: 1-8.
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