Long-term exposure to air pollution and the incidence of Parkinson's disease: A nested case-control study

• Published in: PloS one Vol. 12; no. 8; p. e0182834
• Main Authors: Chen, Chiu-Ying, Hung, Hui-Jung, Chang, Kuang-Hsi, Hsu, Chung Y, Muo, Chih-Hsin, Tsai, Chon-Haw, Wu, Trong-Neng
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 15-08-2017; Public Library of Science (PLoS)
• Subjects: Adult; Adults; Age; Aged; Aged, 80 and over; Air monitoring; Air pollution; Air Pollution - adverse effects; Air pollution effects; Analysis; Case-Control Studies; Chemical compounds; Chronic exposure; Dementia disorders; Diabetes; Diabetes mellitus; Disease control; Engineering and Technology; Environmental Exposure; Environmental monitoring; Environmental protection; Exposure; Female; Health risk assessment; Health risks; Humans; Hypertension; Incidence; Insurance; Male; Medical diagnosis; Medical records; Medicine and Health Sciences; Mental depression; Metal compounds; Methane; Middle Aged; Movement disorders; Neurodegeneration; Neurodegenerative diseases; Nitrogen dioxide; Outdoor air quality; Parkinson disease; Parkinson Disease - epidemiology; Parkinson Disease - etiology; Parkinson's disease; Particulate emissions; Particulate matter; Particulate Matter - toxicity; Pollution; Pollution effects; Pollution monitoring; Prevalence studies (Epidemiology); Regression analysis; Regression models; Risk factors; Sleep; Sleep disorders; Stations; Stroke; Sulfur dioxide; Taiwan - epidemiology; Taiwan
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0182834

Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson's disease (PD), but this relationship is inconclusive as large-scale prospective studies are limited and the results are inconsistent. Therefore, the purpose of this study was to ascertain the adverse health effects of air pollution exposure in a nationwide population using a longitudinal approach.
We conducted a nested case-control study using the National Health Insurance Research Dataset (NHIRD), which consisted of 1,000,000 beneficiaries in the National Health Insurance Program (NHI) in the year 2000 and their medical records from 1995 to 2013 and using public data on air pollution concentrations from monitoring stations across Taiwan released from the Environmental Protection Administration to identify people with ages ≥ 40 years living in areas with monitoring stations during 1995-1999 as study subjects. Then, we excluded subjects with PD, dementia, stroke and diabetes diagnosed before Jan. 1, 2000 and obtained 54,524 subjects to follow until Dec. 31, 2013. In this observational period, 1060 newly diagnosed PD cases were identified. 4240 controls were randomly selected from those without PD using a matching strategy for age, sex, the year of PD diagnosis and the year of entering the NHI program at a ratio of 1:4. Ten elements of air pollution were examined, and multiple logistic regression models were used to measure their risks in subsequent PD development.
The incidence of PD in adults aged ≥ 40 years was 1.9%, and the median duration for disease onset was 8.45 years. None of the chemical compounds (SO2, O3, CO, NOx, NO, NO2, THC, CH4, or NMHC) significantly affected the incidence of PD except for particulate matter. PM10 exposure showed significant effects on the likelihood of PD development (T3 level: > 65μg/m3 versus T1 level: ≤ 54μg/m3; OR = 1.35, 95% CI = 1.12-1.62, 0.001 ≤ P < 0.01). In addition, comorbid conditions such as dementia (ORs = 3.53-3.93, Ps < 0.001), stroke (ORs = 2.99-3.01, Ps < 0.001), depression (ORs = 2.51-2.64, Ps < 0.001), head injury (ORs = 1.24-1.29, 0.001 ≤ Ps < 0.01 or 0.01 ≤ Ps < 0.05), sleep disorder (OR = 1.23-1.26, 0.001 ≤ Ps < 0.01), and hypertension (ORs = 1.18-1.19, 0.01 ≤ Ps < 0.05) also significantly increased the risk for PD development.
Although PM10 plays a significant role in PD development, the associated chemical/metal compounds that are capable of inducing adverse biological mechanisms still warrant further exploration. Because of a link between comorbid conditions and PM exposure, research on the causal relationship between long-term exposure to PM and the development of PD should be considered with caution because other possible modifiers or mediators, comorbid diseases in particular, may be involved.