Objectives Manganese exposure leads to diffuse cerebral metal deposition with the highest concentration in the globus pallidus associated with increased T1-weighted MRI signal. T1 signal intensity in extra-pallidal basal ganglia (caudate and putamen) has not been studied in occupationally exposed workers. Diffusion weighted imaging is a non-invasive measure of neuronal damage and may provide a quantification of neurotoxicity associated with welding and manganese exposure. This study investigated extra-pallidal T1 basal ganglia signal intensity as a marker of manganese exposure and basal ganglia diffusion weighted imaging abnormalities as a potential marker of neurotoxicity.
Methods A 3T MR case:control imaging study was performed on 18 welders and 18 age- and gender-matched controls. Basal ganglia regions of interest were identified for each subject. T1-weighted intensity indices and apparent diffusion coefficients were generated for each region.
Results All regional indices were higher in welders than controls (p≤0.05). Combined basal ganglia (ρ=0.610), caudate (ρ=0.645), anterior (ρ=0.595) and posterior putamen (ρ=0.511) indices were more correlated with exposure than pallidal (ρ=0.484) index. Welder apparent diffusion coefficient values were lower than controls for globus pallidus (p=0.03) and anterior putamen (p=0.004).
Conclusions Welders demonstrated elevated T1 indices throughout the basal ganglia. Combined basal ganglia, caudate and putamen indices were more correlated with exposure than pallidal index suggesting more inclusive basal ganglia sampling results in better exposure markers. Elevated indices were associated with diffusion weighted abnormalities in the pallidum and anterior putamen suggesting neurotoxicity in these regions.
- exposure assessment
- neurobehavioural effects
- cell biology
- mortality studies
- coal dust
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Funding This study was sponsored by the following: Michael J. Fox Foundation, NIH grants: R01 ES013743, K24 ES017765, KL2 RR024994, P42ES04696, 5T32NS007205-27, RO1 NS41509, RO1 NS058714, the Clinical Science Translational Award NCRR UL1 RR024992, the Neuroscience Blueprint grant NS057105, the American Parkinson's Disease Association (APDA) Advanced Research Center at Washington University, the Greater St. Louis Chapter of the APDA, the McDonnell Center for Higher Brain Function and the Barnes-Jewish Hospital Foundation (Elliot Stein Family Fund and Jack Buck Fund for PD Research).
Competing interests The authors of this paper have received research support from the American Parkinson's Disease Association, Merck, Chiltern, TEVA, Eisai, Medivation, Neurogen, Huntington Disease Society of American, the Michael J. Fox Foundation, McDonnell Center, Bander Foundation, the Barnes Jewish Hospital Foundation, NIH and the Department of Defense.
Patient consent Obtained.
Ethics approval Ethics approval was provided by Washington University School of Medicine Human Research Protection Office.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement The authors have full access to all the data and have the right to publish any and all data separate and apart from any sponsor. Data have not been shared beyond the authors listed and are presented in aggregate to protect individual-subject confidentiality.
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