Background: Several studies have suggested the potential protective role of β2-adrenoreceptor agonist (β2AR-agonist) on the development of Parkinson's disease (PD). However, those could not reflect a different epidemiologic background in eastern countries. We explored β2AR-agonist's effect on PD development by controlling for smoking.
Materials and methods: We used the Korean national sample cohort data (from 2002 to 2013) containing 1,025,340 participants (2.2% of the whole population). The subjects over 60 years were included. PD was defined based on the ICD-10 code, which should be diagnosed by neurologists. Atypical Parkinsonisms or ataxic disorders were excluded. We made Set 1 (from 2003 to 2007) and Set 2 (from 2003 to 2008) based on the exposure period for the sensitivity analysis. We observed whether PD had developed during the follow-up periods in each subset.
Results: The PD (Set 1, n = 742; Set 2, n = 699) and non-PD group (Set 1, n = 57,645; Set 2, n = 66,586) were collected. Old age, Medicaid, and asthma were risk factors, whereas smoking was a significant protective factor for PD development. The proportion of β2AR-agonist use was significantly higher in the PD group than in the non-PD group (Set 1, 3.6% vs. 2.4%; Set 2, 4.1% vs. 2.6%). β2AR-agonist use still was a risk factor in developing PD from the multiple logistic regression analysis.
Conclusions: β2-AR-agonist looked like a risk factor rather than a protective factor for PD development. Well-controlled studies reflecting various epidemiologic backgrounds are required to confirm the role of β2AR-agonist.
Keywords: Parkinson's disease; smoking; β2-adrenoreceptor agonist.