Ambient air pollution, covert cerebrovascular disease and cognition: results from the ISSYS study

Abstract

Air pollution; Cerebrovascular disorders; Cognitive impairment

Contaminación del aire; Trastornos cerebrovasculares; Deterioro cognitivo

Contaminació de l'aire; Trastorns cerebrovasculars; Deteriorament cognitiu

Background and purpose Although air pollution (AP) has been associated with stroke and dementia, data regarding its relationship with covert cerebrovascular disease (cCVD) and cognition over time are sparse. The aim of this study was to explore these relationships. Methods A prospective population-based study of 976 stroke-free and non-demented individuals living in Barcelona, Spain, was conducted during 2010–2016. A land use regression model was used to estimate the exposure of each participant to AP: NOx, NO2, PM2.5, PM10, PMcoarse and PM2.5 absorbance. Cognitive function and cCVD were assessed at baseline (n = 976) and 4 years after (n = 317). Multivariate-adjusted models were developed. Results At baseline, 99 participants (10.1%) had covert brain infarcts and 91 (9.3%) had extensive periventricular white matter hyperintensities (WMHs). Marked subcortical WMH progression was seen in 19.7%; the incidence of other covert cerebrovascular lessons ranged between 5% and 6% each. PM2.5 was related to higher odds of having a covert brain infarct (odds ratio [OR] 2.21; 95% confidence interval [CI] 1.06–4.60). PM2.5 absorbance was related to higher odds of having extensive subcortical WMHs (OR 1.72; 95% CI 1.13–2.60), whereas NO2 was related to higher odds of having extensive subcortical (OR 1.66; 95% CI 1.17–2.35) or periventricular (OR 1.96; 95% CI 1.10–3.50) WMHs and to higher odds of developing marked subcortical WMH progression (OR 1.40; 95% CI 1.05–1.90). NOx was related to incident cerebral microbleeds (OR 1.36; 95% CI 1.04–1.79). There was no association between AP and cognition. Conclusions Air pollutant predicts the presence and accumulation of cCVD. Its impact on cognitive impairment remains to be determined.

This work was supported by the Instituto de Salud Carlos III (grant numbers PI14/1535, PI19/00217, INT20/00084, CM20/00218 and CM22/00226) co-financed by the European Regional Development Fund. The Neurovascular Research Laboratory receives funds from the Spanish Research Stroke Network (RD/16/0019/0021 and RICORS-ICTUS-Enfermedades Vasculares Cerebrales, RD21/0006/0007). MCT is funded by a Ramón y Cajal Fellowship (RYC-2017-01892) from the Spanish Ministry of Science, Innovation and Universities and co-funded by the European Social Fund. ISGlobal acknowledges support from the Spanish Ministry of Science and Innovation through the ‘Centro de Excelencia Severo Ochoa 2019–2023’ Programme (CEX2018-000806-S) and support from the Generalitat de Catalunya through the CERCA Programme.