Long-Term Exposure to PM2.5 and Cognitive Decline: A Longitudinal Population-Based Study

2021 ◽  
pp. 1-9
Author(s):  
Giulia Grande ◽  
Jing Wu ◽  
Petter L.S. Ljungman ◽  
Massimo Stafoggia ◽  
Tom Bellander ◽  
...  

Background: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. Objectives: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. Methods: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5μm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25%fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. Results: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2–3.2) per interquartile range difference up to mean PM2.5 level (8.6μg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74–1.06). The presence of cerebrovascular diseases further increased such risk by 6%. Conclusion: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.

Author(s):  
Giulia Grande ◽  
Jing Wu ◽  
Petter L.S. Ljungman ◽  
Massimo Stafoggia ◽  
Tom Bellander ◽  
...  

Background: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. Objectives: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. Methods: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5 μm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25% fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. Results: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2–3.2) per interquartile range difference up to mean PM2.5 level (8.6 μg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74–1.06). The presence of cerebrovascular diseases further increased such risk by 6%. Conclusion: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S119-S119 ◽  
Author(s):  
Debora Rizzuto ◽  
Giulia Grande ◽  
Petter Ljungman ◽  
Tom Bellander

Abstract Aim: We aimed to investigate the association between long-term air pollution and cognitive decline and dementia, and to clarify the role of CVD on the studied association. Methods: We examined 3150 dementia-free 60+ year-olds in the Swedish National study on Aging and Care in Kungsholmen, Stockholm for up to 13 years, during which 363 persons developed dementia. Outdoor air pollution levels at the home address were assessed yearly for all participants, using a dispersion model for nitrogen oxides (NOX), mainly emitted from road traffic. Mixed-effect linear regression models were used to quantify the association between air pollution and cognitive decline (with the Mini Mental State Examination). The risk of dementia, in keeping with the Diagnostic and Statistical Manual of Mental Disorders IV edition, was estimated using competing-risks models, considering death as competing event, and considering an exposure window 0-5 years before a year at risk. Stratified analyses by CVD were also performed. Results: Higher levels of traffic-related residential air pollution were associated with steeper cognitive decline over the follow-up period. After controlling for potential confounders, higher levels of air pollution were associated with increased risk of dementia (HR: 1.13, 95%CI: 1.05-1.22, for an µg/m3 unit increase NOX). The stratified analyses showed that the presence of CVD enhanced the effect of air pollution on dementia risk. Conclusion: Long-term exposure to traffic-related air pollution was associated with a higher risk of dementia. Cardiovascular disease might have played a role in this association.


Author(s):  
Alireza Khajavi ◽  
Seyed Saeed Tamehri Zadeh ◽  
Fereidoun Azizi ◽  
Robert D. Brook ◽  
Hengameh Abdi ◽  
...  

Author(s):  
Chao Zhang ◽  
Zhenyu Quan ◽  
Qincheng Wu ◽  
Zhezhen Jin ◽  
Joseph Lee ◽  
...  

Background: Air pollution in large Chinese cities has led to recent studies that highlighted the relationship between particulate matters (PM) and elevated risk of cardio-cerebrovascular mortality. However, it is unclear as to whether: (1) The same adverse relations exist in cities with relatively low levels of air pollution; and (2) the relationship between the two are similar across ethnic groups. Methods: We collected data of PM2.5 (PM with an aerodynamic diameter ≤ 2.5 µm) and PM10 (aerodynamic diameter ≤ 10 µm) in the Yanbian Korean Autonomous Prefecture between 1 January 2015 and 31 December 2016. Using a time-stratified case-crossover design, we investigated whether levels of particulate pollutants influence the risk of cardio-cerebrovascular disease mortality among ethnic Korean vs. ethnic Han residents residing in the Yanbian Korean Autonomous Prefecture. Results: Under the single air pollutant model, the odds ratios (ORs) of cardio-cerebrovascular disease were 1.025 (1.024–1.026) for each 10 μg/m3 increase in PM2.5 at lag0 day, 1.012 (1.011–1.013) for each 10 μg/m3 increase in PM10 at lag1 day. In the multi-pollutant model adjusted by PM10, SO2, and NO2, the ORs of cardio-cerebrovascular disease were 1.150 (1.145–1.155) for ethnic Koreans and 1.154 (1.149–1.158) for ethnic Hans for each 10 μg/m3 increase in PM2.5. In the multi-pollutant model adjusted by PM2.5, SO2, and NO2, the ORs of cardio-cerebrovascular disease were 1.050 (1.047–1.053) for ethnic Koreans and 1.041 (1.039–1.043) for ethnic Hans for each 10 μg/m3 increase in PM10. Conclusion: This study showed that PM2.5 and PM10 were associated with increased risks of acute death events in residential cardio-cerebrovascular disease in Yanbian, China.


PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e52755 ◽  
Author(s):  
Hélène Amieva ◽  
Céline Meillon ◽  
Catherine Helmer ◽  
Pascale Barberger-Gateau ◽  
Jean François Dartigues

2019 ◽  
Vol 50 (1) ◽  
pp. 3-13 ◽  
Author(s):  
Jonas K. Olofsson ◽  
Maria Larsson ◽  
Catalina Roa ◽  
Donald A. Wilson ◽  
Erika Jonsson Laukka

AbstractOlfactory identification impairment might indicate future cognitive decline in elderly individuals. An unresolved question is to what extent this effect is dependent on the ApoE-ε4, a genotype associated with risk of Alzheimer’s Disease (AD). Given the current concern about reproducibility in empirical research, we assessed this issue in a large sample (n = 1637) of older adults (60 – 96 years) from the population-based longitudinal Swedish National Study on Aging and Care in Kungsholmen (SNAC-K). A hierarchical regression analysis was carried out to determine if a low score on an odor identification test, and the presence of ApoE-ε4, would predict the magnitude of a prospective 6-year change in the Mini-Mental State Examination (MMSE) after controlling for demographic, health-related, and cognitive variables. We found that overall, lower odor identification performance was predictive of cognitive decline, and, as hypothesized, we found that the effect was most pronounced among ApoE-ε4 carriers. Our results from this high-powered sample suggest that in elderly carriers of the ApoE-ε4 allele, odor identification impairment provides an indication of future cognitive decline, which has relevance for the prognosis of AD.


2014 ◽  
Vol 2014 (1) ◽  
pp. 1500
Author(s):  
Ikenna Eze* ◽  
Emmanuel Schaffner ◽  
Evelyn Fischer ◽  
Tamara Schikowski ◽  
Martin Adam ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document