Long-term exposure to air pollution and the incidence of Parkinson’s disease: A nested case-control study
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 t...
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| Published in | PloS one Vol. 12; no. 8; p. e0182834 |
|---|---|
| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Public Library of Science
15.08.2017
Public Library of Science (PLoS) |
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| Online Access | Get full text |
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| Abstract | 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. |
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| AbstractList | Background 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. Materials and methods 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 [greater than or equal to] 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. Results The incidence of PD in adults aged [greater than or equal to] 40 years was 1.9%, and the median duration for disease onset was 8.45 years. None of the chemical compounds (SO.sub.2, O.sub.3, CO, NO.sub.x, NO, NO.sub.2, THC, CH.sub.4, or NMHC) significantly affected the incidence of PD except for particulate matter. PM.sub.10 exposure showed significant effects on the likelihood of PD development (T3 level: > 65[mu]g/m.sup.3 versus T1 level: [less than or equal to] 54[mu]g/m.sup.3 ; OR = 1.35, 95% CI = 1.12-1.62, 0.001 [less than or equal to] 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 [less than or equal to] Ps < 0.01 or 0.01 [less than or equal to] Ps < 0.05), sleep disorder (OR = 1.23-1.26, 0.001 [less than or equal to] Ps < 0.01), and hypertension (ORs = 1.18-1.19, 0.01 [less than or equal to] Ps < 0.05) also significantly increased the risk for PD development. Conclusions Although PM.sub.10 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. 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.BACKGROUNDPrevious 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.MATERIALS AND METHODSWe 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.RESULTSThe 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.CONCLUSIONSAlthough 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. 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. 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 [greater than or equal to] 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 [greater than or equal to] 40 years was 1.9%, and the median duration for disease onset was 8.45 years. None of the chemical compounds (SO.sub.2, O.sub.3, CO, NO.sub.x, NO, NO.sub.2, THC, CH.sub.4, or NMHC) significantly affected the incidence of PD except for particulate matter. PM.sub.10 exposure showed significant effects on the likelihood of PD development (T3 level: > 65[mu]g/m.sup.3 versus T1 level: [less than or equal to] 54[mu]g/m.sup.3 ; OR = 1.35, 95% CI = 1.12-1.62, 0.001 [less than or equal to] 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 [less than or equal to] Ps < 0.01 or 0.01 [less than or equal to] Ps < 0.05), sleep disorder (OR = 1.23-1.26, 0.001 [less than or equal to] Ps < 0.01), and hypertension (ORs = 1.18-1.19, 0.01 [less than or equal to] Ps < 0.05) also significantly increased the risk for PD development. Although PM.sub.10 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. 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. Background 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. Materials and methods 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. Results 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 (SO 2 , O 3 , CO, NO x , NO, NO 2 , THC, CH 4 , or NMHC) significantly affected the incidence of PD except for particulate matter. PM 10 exposure showed significant effects on the likelihood of PD development (T3 level: > 65μg/m 3 versus T1 level: ≤ 54μg/m 3 ; 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. Conclusions Although PM 10 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. Background 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. Materials and methods 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. Results 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. Conclusions 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. |
| Audience | Academic |
| Author | Tsai, Chon-Haw Wu, Trong-Neng Chen, Chiu-Ying Chang, Kuang-Hsi Hung, Hui-Jung Hsu, Chung Y. Muo, Chih-Hsin |
| AuthorAffiliation | Liverpool School of Tropical Medicine, UNITED KINGDOM 6 Department of Healthcare Administration, Asia University, Taichung, Taiwan 3 Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan 1 Department of Public Health, China Medical University, Taichung, Taiwan 2 Graduate Institute of Clinical Medical Science, College of Medicine, China Medical University, Taichung, Taiwan 4 School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan 5 Department of Neurology, China Medical University Hospital, Taichung, Taiwan |
| AuthorAffiliation_xml | – name: Liverpool School of Tropical Medicine, UNITED KINGDOM – name: 4 School of Medicine, College of Medicine, China Medical University, Taichung, Taiwan – name: 1 Department of Public Health, China Medical University, Taichung, Taiwan – name: 2 Graduate Institute of Clinical Medical Science, College of Medicine, China Medical University, Taichung, Taiwan – name: 3 Management Office for Health Data, China Medical University Hospital, Taichung, Taiwan – name: 5 Department of Neurology, China Medical University Hospital, Taichung, Taiwan – name: 6 Department of Healthcare Administration, Asia University, Taichung, Taiwan |
| Author_xml | – sequence: 1 givenname: Chiu-Ying surname: Chen fullname: Chen, Chiu-Ying – sequence: 2 givenname: Hui-Jung surname: Hung fullname: Hung, Hui-Jung – sequence: 3 givenname: Kuang-Hsi surname: Chang fullname: Chang, Kuang-Hsi – sequence: 4 givenname: Chung Y. surname: Hsu fullname: Hsu, Chung Y. – sequence: 5 givenname: Chih-Hsin surname: Muo fullname: Muo, Chih-Hsin – sequence: 6 givenname: Chon-Haw surname: Tsai fullname: Tsai, Chon-Haw – sequence: 7 givenname: Trong-Neng orcidid: 0000-0001-5227-4597 surname: Wu fullname: Wu, Trong-Neng |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28809934$$D View this record in MEDLINE/PubMed |
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| Snippet | Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson's disease (PD), but this... Background Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson's disease (PD),... Background Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson’s disease (PD),... Background Previous studies revealed that chronic exposure to air pollution can significantly increase the risk of the development of Parkinson’s disease (PD),... |
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| Title | Long-term exposure to air pollution and the incidence of Parkinson’s disease: A nested case-control study |
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