Association between air pollution and risk of vascular dementia: A multipollutant analysis in Taiwan

Chung Yi Li, Chien Hsin Li, Santi Martini, Wen Hsuan Hou

Research output: Contribution to journalArticle

Abstract

Evidence regarding the association of specific air pollutants with vascular dementia (VaD) risk is limited. In this nested case–control study, we enrolled 831 adults aged >65 years with VaD (International Classification of Diseases, Ninth Revision, Clinical Modification code 290.4x) newly diagnosed during 2005–2013; 3324 controls were age-, sex-, and VaD diagnosis year–matched with the study patients. Both patients with VaD and controls were selected from among a cohort of one million beneficiaries of Taiwan's National Health Insurance program, all of whom were registered in 2005. Exposure to the mean daily air pollutant concentration, derived from 76 fixed air quality monitoring stations, in 3, 5, and 7 years before VaD diagnosis was assessed using the spatial analysis method (i.e., ordinary kriging) on ArcGIS. A logistic regression model was used to calculate covariate-adjusted odds ratios (ORs) of VaD in relation to specific air pollutants. After potential confounders and other air pollutants were controlled for, high concentrations of coarse particulate matter (10 µm or less in diameter) and carbon monoxide (CO) were sporadically associated with higher OR of VaD. The most prominent association was observed for nitrogen dioxide (NO2) exposure within 5 and 7 years before diagnosis. Compared with the <25th percentile of NO2 exposure, the 25th–50th, 50th–75th, and >75th percentiles of NO2 exposure significantly increased ORs (95% confidence intervals): 1.62 (1.28–2.23), 1.61 (1.11–2.33), and 2.22 (1.35–3.65) within 5 years before diagnosis, respectively, and 1.59 (1.20–2.11), 1.65 (1.15–2.37), and 2.05 (1.28–3.28) within 7 years before diagnosis, respectively. We found that higher NO2 exposure in the past was significantly associated with an elevated risk of VaD. Although less consistent, higher exposure to CO was also associated with a higher risk of VaD. Most NO2 in cities originates from motor vehicle exhaust; other sources of NO2 are petrol and metal refining, electricity generation from coal-fired power stations, other manufacturing industries, and food processing. Future studies should investigate associations of VaD with specific sources of NO2.

Original languageEnglish
Article number105233
JournalEnvironment International
Volume133
DOIs
Publication statusPublished - 2019 Dec

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atmospheric pollution
carbon monoxide
health insurance
food processing
coal-fired power plant
electricity generation
nitrogen dioxide
kriging
spatial analysis
confidence interval
particulate matter
logistics
manufacturing
analysis
exposure
air pollutant
industry
metal

All Science Journal Classification (ASJC) codes

  • Environmental Science(all)

Cite this

@article{5a17b095cfe94aff8288d8063c78045e,
title = "Association between air pollution and risk of vascular dementia: A multipollutant analysis in Taiwan",
abstract = "Evidence regarding the association of specific air pollutants with vascular dementia (VaD) risk is limited. In this nested case–control study, we enrolled 831 adults aged >65 years with VaD (International Classification of Diseases, Ninth Revision, Clinical Modification code 290.4x) newly diagnosed during 2005–2013; 3324 controls were age-, sex-, and VaD diagnosis year–matched with the study patients. Both patients with VaD and controls were selected from among a cohort of one million beneficiaries of Taiwan's National Health Insurance program, all of whom were registered in 2005. Exposure to the mean daily air pollutant concentration, derived from 76 fixed air quality monitoring stations, in 3, 5, and 7 years before VaD diagnosis was assessed using the spatial analysis method (i.e., ordinary kriging) on ArcGIS. A logistic regression model was used to calculate covariate-adjusted odds ratios (ORs) of VaD in relation to specific air pollutants. After potential confounders and other air pollutants were controlled for, high concentrations of coarse particulate matter (10 µm or less in diameter) and carbon monoxide (CO) were sporadically associated with higher OR of VaD. The most prominent association was observed for nitrogen dioxide (NO2) exposure within 5 and 7 years before diagnosis. Compared with the <25th percentile of NO2 exposure, the 25th–50th, 50th–75th, and >75th percentiles of NO2 exposure significantly increased ORs (95{\%} confidence intervals): 1.62 (1.28–2.23), 1.61 (1.11–2.33), and 2.22 (1.35–3.65) within 5 years before diagnosis, respectively, and 1.59 (1.20–2.11), 1.65 (1.15–2.37), and 2.05 (1.28–3.28) within 7 years before diagnosis, respectively. We found that higher NO2 exposure in the past was significantly associated with an elevated risk of VaD. Although less consistent, higher exposure to CO was also associated with a higher risk of VaD. Most NO2 in cities originates from motor vehicle exhaust; other sources of NO2 are petrol and metal refining, electricity generation from coal-fired power stations, other manufacturing industries, and food processing. Future studies should investigate associations of VaD with specific sources of NO2.",
author = "Li, {Chung Yi} and Li, {Chien Hsin} and Santi Martini and Hou, {Wen Hsuan}",
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Association between air pollution and risk of vascular dementia : A multipollutant analysis in Taiwan. / Li, Chung Yi; Li, Chien Hsin; Martini, Santi; Hou, Wen Hsuan.

In: Environment International, Vol. 133, 105233, 12.2019.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Association between air pollution and risk of vascular dementia

T2 - A multipollutant analysis in Taiwan

AU - Li, Chung Yi

AU - Li, Chien Hsin

AU - Martini, Santi

AU - Hou, Wen Hsuan

PY - 2019/12

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N2 - Evidence regarding the association of specific air pollutants with vascular dementia (VaD) risk is limited. In this nested case–control study, we enrolled 831 adults aged >65 years with VaD (International Classification of Diseases, Ninth Revision, Clinical Modification code 290.4x) newly diagnosed during 2005–2013; 3324 controls were age-, sex-, and VaD diagnosis year–matched with the study patients. Both patients with VaD and controls were selected from among a cohort of one million beneficiaries of Taiwan's National Health Insurance program, all of whom were registered in 2005. Exposure to the mean daily air pollutant concentration, derived from 76 fixed air quality monitoring stations, in 3, 5, and 7 years before VaD diagnosis was assessed using the spatial analysis method (i.e., ordinary kriging) on ArcGIS. A logistic regression model was used to calculate covariate-adjusted odds ratios (ORs) of VaD in relation to specific air pollutants. After potential confounders and other air pollutants were controlled for, high concentrations of coarse particulate matter (10 µm or less in diameter) and carbon monoxide (CO) were sporadically associated with higher OR of VaD. The most prominent association was observed for nitrogen dioxide (NO2) exposure within 5 and 7 years before diagnosis. Compared with the <25th percentile of NO2 exposure, the 25th–50th, 50th–75th, and >75th percentiles of NO2 exposure significantly increased ORs (95% confidence intervals): 1.62 (1.28–2.23), 1.61 (1.11–2.33), and 2.22 (1.35–3.65) within 5 years before diagnosis, respectively, and 1.59 (1.20–2.11), 1.65 (1.15–2.37), and 2.05 (1.28–3.28) within 7 years before diagnosis, respectively. We found that higher NO2 exposure in the past was significantly associated with an elevated risk of VaD. Although less consistent, higher exposure to CO was also associated with a higher risk of VaD. Most NO2 in cities originates from motor vehicle exhaust; other sources of NO2 are petrol and metal refining, electricity generation from coal-fired power stations, other manufacturing industries, and food processing. Future studies should investigate associations of VaD with specific sources of NO2.

AB - Evidence regarding the association of specific air pollutants with vascular dementia (VaD) risk is limited. In this nested case–control study, we enrolled 831 adults aged >65 years with VaD (International Classification of Diseases, Ninth Revision, Clinical Modification code 290.4x) newly diagnosed during 2005–2013; 3324 controls were age-, sex-, and VaD diagnosis year–matched with the study patients. Both patients with VaD and controls were selected from among a cohort of one million beneficiaries of Taiwan's National Health Insurance program, all of whom were registered in 2005. Exposure to the mean daily air pollutant concentration, derived from 76 fixed air quality monitoring stations, in 3, 5, and 7 years before VaD diagnosis was assessed using the spatial analysis method (i.e., ordinary kriging) on ArcGIS. A logistic regression model was used to calculate covariate-adjusted odds ratios (ORs) of VaD in relation to specific air pollutants. After potential confounders and other air pollutants were controlled for, high concentrations of coarse particulate matter (10 µm or less in diameter) and carbon monoxide (CO) were sporadically associated with higher OR of VaD. The most prominent association was observed for nitrogen dioxide (NO2) exposure within 5 and 7 years before diagnosis. Compared with the <25th percentile of NO2 exposure, the 25th–50th, 50th–75th, and >75th percentiles of NO2 exposure significantly increased ORs (95% confidence intervals): 1.62 (1.28–2.23), 1.61 (1.11–2.33), and 2.22 (1.35–3.65) within 5 years before diagnosis, respectively, and 1.59 (1.20–2.11), 1.65 (1.15–2.37), and 2.05 (1.28–3.28) within 7 years before diagnosis, respectively. We found that higher NO2 exposure in the past was significantly associated with an elevated risk of VaD. Although less consistent, higher exposure to CO was also associated with a higher risk of VaD. Most NO2 in cities originates from motor vehicle exhaust; other sources of NO2 are petrol and metal refining, electricity generation from coal-fired power stations, other manufacturing industries, and food processing. Future studies should investigate associations of VaD with specific sources of NO2.

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