The instrument used to determine the rate of change over the follow-up period, the UPDRS3, rates motor signs on a scale of 0 to 4, with 0 being absent and 4 being very severe. Because individuals with absent or very mild signs at baseline might be expected to show little or no progression over the follow-up period, i.e., to remain non-symptomatic, those groups with higher percentages of such members would be expected to show the lowest rates of progression. Conversely, those groups with more members with greater initial levels of impairment might be expected to show higher rates of progression. The findings therefore could primarily reflect the initial level of impairment of each of the groups at baseline.
To determine the role of the baseline scores on the UPDRS3 on the results, the baseline score on this instrument should have been controlled or the findings stratified by initial scores on the UPDRS3. Using non-linear outcomes like the UPDRS3 score to assess linear slopes of change is questionable.
If the findings reflect initial differences in the mean scores of welders, welder helpers, and non-welding workers, they would suggest that welders are at higher risk of parkinsonian signs. However, it is important to keep in mind that the welders in this study represent a volunteer sample with a participation rate of about 50 percent. If the welders who chose not to participate in the study did so because they had a lower rate of symptomatology than those who did, the initial level of parkinsonian signs in “welders” would be overestimated. The non-welding comparison group selected by the union without input from the investigators could well have been selected on the basis of good health and lack of parkinsonian features, assuring a low mean UPDRS score at baseline and low rate of progression at follow-up. The role of selection bias in producing the differences in baseline performance on the UPDRS3 in this study needs to be considered.
This study by Racette and colleagues revealing a dose-response relationship between exposure to manganese containing welding fumes and parkinsonism makes important contributions to the fields of neurotoxicology and industrial hygiene. It is, however, important to recognize that while these findings provide additional support for the role of manganese in parkinsonism, these data do not indicate that manganese causes idiopathic PD per se. That said, it is nevertheless scientifically plausible that the changes in neurological function observed in this study could exacerbate those due to idiopathic PD in workers exposed to welding fumes. Stabilization or even improvement in neurological function is expected to occur with cessation of exposure in those subjects with manganese-induced parkinsonism, whereas symptoms would be expected to continue to progress despite cessation of exposure in those patients with idiopathic PD.
Comments
University of South Florida
The instrument used to determine the rate of change over the follow-up period, the UPDRS3, rates motor signs on a scale of 0 to 4, with 0 being absent and 4 being very severe. Because individuals with absent or very mild signs at baseline might be expected to show little or no progression over the follow-up period, i.e., to remain non-symptomatic, those groups with higher percentages of such members would be expected to show the lowest rates of progression. Conversely, those groups with more members with greater initial levels of impairment might be expected to show higher rates of progression. The findings therefore could primarily reflect the initial level of impairment of each of the groups at baseline.
To determine the role of the baseline scores on the UPDRS3 on the results, the baseline score on this instrument should have been controlled or the findings stratified by initial scores on the UPDRS3. Using non-linear outcomes like the UPDRS3 score to assess linear slopes of change is questionable.
If the findings reflect initial differences in the mean scores of welders, welder helpers, and non-welding workers, they would suggest that welders are at higher risk of parkinsonian signs. However, it is important to keep in mind that the welders in this study represent a volunteer sample with a participation rate of about 50 percent. If the welders who chose not to participate in the study did so because they had a lower rate of symptomatology than those who did, the initial level of parkinsonian signs in “welders” would be overestimated. The non-welding comparison group selected by the union without input from the investigators could well have been selected on the basis of good health and lack of parkinsonian features, assuring a low mean UPDRS score at baseline and low rate of progression at follow-up. The role of selection bias in producing the differences in baseline performance on the UPDRS3 in this study needs to be considered.
View all comments by James MortimerBoston University Chobanian & Avedisian School of Medicine
This study by Racette and colleagues revealing a dose-response relationship between exposure to manganese containing welding fumes and parkinsonism makes important contributions to the fields of neurotoxicology and industrial hygiene. It is, however, important to recognize that while these findings provide additional support for the role of manganese in parkinsonism, these data do not indicate that manganese causes idiopathic PD per se. That said, it is nevertheless scientifically plausible that the changes in neurological function observed in this study could exacerbate those due to idiopathic PD in workers exposed to welding fumes. Stabilization or even improvement in neurological function is expected to occur with cessation of exposure in those subjects with manganese-induced parkinsonism, whereas symptoms would be expected to continue to progress despite cessation of exposure in those patients with idiopathic PD.
View all comments by Marcia RatnerMake a Comment
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