Growing epidemiological evidence suggests that air pollution may increase the risk of cognitive decline and neurodegenerative disease. A hallmark of neurodegeneration and an important diagnostic biomarker is volume reduction of a key brain structure, the hippocampus. We aimed to investigate the possibility that outdoor air nitrogen dioxide (NO2) and particulate matter with diameter ≤2.5 μm (PM2.5) and ≤10 μm (PM10) adversely affect hippocampal volume, through a meta-analysis. We considered studies that assessed the relation between outdoor air pollution and hippocampal volume by structural magnetic resonance imaging in adults and children, searching in Pubmed and Scopus databases from inception through July 13, 2021. For inclusion, studies had to report the correlation coefficient along with its standard error or 95% confidence interval (CI) between air pollutant exposure and hippocampal volume, to use standard space for neuroimages, and to consider at least age, sex and intracranial volume as covariates or effect modifiers. We meta-analyzed the data with a random-effects model, considering separately adult and child populations. We retrieved four eligible studies in adults and two in children. In adults, the pooled summary β regression coefficients of the association of PM2.5, PM10 and NO2 with hippocampal volume showed respectively a stronger association (summary β −7.59, 95% CI −14.08 to −1.11), a weaker association (summary β −2.02, 95% CI −4.50 to 0.47), and no association (summary β −0.44, 95% CI −1.27 to 0.40). The two studies available for children, both carried out in preadolescents, did not show an association between PM2.5 and hippocampal volume. The inverse association between PM2.5 and hippocampal volume in adults appeared to be stronger at higher mean PM2.5 levels. Our results suggest that outdoor PM2.5 and less strongly PM10 could adversely affect hippocampal volume in adults, a phenomenon that may explain why air pollution has been related to memory loss, cognitive decline, and dementia.
Bibliographical noteFunding Information:
Drs Balboni, Filippini, and Vinceti were supported by grant ‘Dipartimenti di Eccellenza 2018–2022” to the UNIMORE Department of Biomedical, Metabolic and Neural Sciences from the Italian Ministry of Education, University and Research . Dr. Vinceti was supported by grant ‘ UNIMORE FAR 2019 Interdisciplinare Linea FCRMO - Fondazione Cassa di Risparmio di Modena ’ and Dr. Filippini was supported by grant ‘ UNIMORE FAR IMPULSO 2020 ’ (no. 494/2020 ) from the University of Modena and Reggio Emilia .
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