| Summary: | Parkinson’s disease is a chronic degenerative illness, the ultimate causes of which remain largely unknown. This thesis aims to test a new etiological hypothesis: that whole body vibration exposure may be associated with Parkinson’s disease. The thesis comprises three studies relevant to a test of this hypothesis. The first study concerns the methods by which cases of Parkinson’s disease can be defined at a population level and the prevalence of Parkinson’s disease in British Columbia. Levodopa (a drug typically used for Parkinson’s treatment) was increasingly used by people without a Parkinson’s diagnosis between 1996 and 2005, with non-Parkinson’s users outnumbering physician diagnosed cases among women and those under the age of 65 in 2005. These changes in levodopa use could mean that relying on use of levodopa to define Parkinson’s disease cases will be less efficient.
The second study developed a method for retrospectively assessing occupational whole body vibration from a detailed interview conducted in a case control sample. I combined self-reported exposure with estimates of vibration intensity (acceleration) derived from the literature to construct metrics of exposure. I concluded that three of the metrics (duration, most intense equipment exposure, and a dose calculation that combined intensity and duration in a cumulative measure after raising vibration acceleration values to the fourth power) captured sufficiently different aspects of occupational exposure for individual tests of their associations with Parkinson’s disease.
The third study tested these associations using logistic regression. The metrics were categorized to enable the detection of nonlinear effects. Ever being occupationally exposed to whole body vibration was inversely associated with Parkinson’s disease, as was the lowest category of most intense equipment exposure. However, the highest values of most intense equipment exposure were associated with increased odds of Parkinson’s disease. Effects were strongest when exposures that occurred more recently than 20 years prior to diagnosis were excluded. A protective effect of low intensity vibration could be due to correlation with a confounding protective factor such as physical activity, while an increased risk associated with high intensity exposures could be due to mechanical stress imposed by the repetitive shocks incurred.
|
|---|
