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Table 3 Individual studies reporting the association between environmental risk factors in air and dementia

From: Environmental risk factors for dementia: a systematic review



Sample description





Chang et al., 2014 [28]

CO and NO2

Comprehensive National Health Insurance database in Taiwan – people aged ≥50 years.

29537 (NO2 29547) men and women of whom 1718 (1720) developed dementia

Retrospective cohort study: Cox PH models.

Yearly average CO concentrations based on location of clinic attended. Dementia diagnoses were extracted from electronic health records.

Highest vs lowest quartile of CO and NO2 was associated with an increased risk of dementia incidence (multivariable adjusted HR, 95 % CI: 1.54, 1.34-1.77; 1.61, 1.39-1.85). Similar effects in men and women.


Oudin et al., 2015 [27]

Traffic-related air pollution (NOx)

Participants from the Betula study, randomly sampled from the general population residing in the Umeå municipality

1,806 healthy men and women of whom 302 developed dementia

Prospective cohort study: Cox PH models.

Mean nitrogen oxide levels based on baseline residence and dementia outcome after 15 years.

Highest:lowest quartile of NOx revealed an increased risk of incident dementia (adjusted HR, 95 % CI 1.60, 1.02-2.10). Similar results were observed in AD and VaD.


Chen et al., 2013 [29]

Environmental Tobacco Smoke

Community dwelling adults aged ≥50 years living in rural or urban areas of five provinces of China.

5921 men and women of whom 626 had severe (O3-5) and 869 moderate (O1-2) dementia

Cross-sectional study. Smoking status and ETS exposure (at home, work, and other places) defined by self-report. Dementia was diagnosed using the GMS-AGECAT algorithm.

Multivariable-adjusted RR (95 % CI) for exposure to ETS 0.96 (0.84, 1.09) for moderate dementia and 1.29 (1.05, 1.59) for severe dementia. Risk of severe dementia increased with increasing duration and cumulative dose, particularly in never smokers.


Jung et al. 2015 [33]

PM2.5 and O3

Individuals from Taiwan entered into the longitudinal health insurance database 2000 (LHID2000) aged ≥65 in 2001.

95,690 men and women of whom 1399 developed AD.

Prospective cohort study: Cox PH models.

PM2.5 and O3 levels recorded at 70 Taiwan Environmental Protection Agency monitoring stations from 2000 to 2010. These data were controlled for secondary pollutants (CO, NO2 and SO2). AD was identified when this was recorded at least twice on the insurance database, based on a physician diagnosis.

Baseline O3 was associated with an increased risk of incident AD (multivariable-adjusted HR per interquartile range, 95 % CI: 1.06, 1.00-1.12) but baseline PM2.5 was not (1.03, 0.95-1.11). Change in both O3 and PM2.5 was associated with increased AD risk (3.12, 2.92-3.33; 2.38, 2.21-2.56). This remained after additionally adjusting for secondary pollutants.


Wu et al., 2015 [34]

PM10 and O3

249 AD patients, 125 VaD patients (clinically diagnosed from hospital clinics) and 497 controls (from the elderly health check-up program), all ≥60 years in Taiwan.

374 cases; 497 controls

Cross-sectional study (case–control): multiple regression. 12-year PM10 and 14-year ozone exposure were estimated from spatiotemporal models based on residential location.

Highest vs lowest tertile of PM10 and ozone exposure was associated with increased AD risk (adjusted OR, 95 % CI: 4.17, 2.31-7.54; 2.00, 1.14-3.50). Similar results were found for VaD.


  1. AD = Alzheimer’s dementia, CO carbon monoxide, ETS environmental tobacco smoke, GMS-AGECAT the Automated Geriatric Examination for Computer Assisted Taxonomy algorithm used with the Geriatric Mental State interview (O = “organic” diagnosis from the AGECAT algorithm, levels 1–5), HR hazard ratio, NO 2 nitrogen dioxide, O 3 ozone, OR odds ratio, PH proportional hazards, PM x particulate matter up to x micrometres in size, VaD vascular dementia