Benjamin Aretz1, Fanny Janssen2, Judith M Vonk3, Michael T Heneka4, H Marike Boezen3, Gabriele Doblhammer5. 1. Institute of Sociology and Demography, University of Rostock, Rostock, Germany; Population Research Centre, Faculty of Spatial Sciences, University of Groningen, Groningen, the Netherlands. Electronic address: benjamin.aretz@uni-rostock.de. 2. Population Research Centre, Faculty of Spatial Sciences, University of Groningen, Groningen, the Netherlands; Netherlands Interdisciplinary Demographic Institute - KNAW/University of Groningen, The Hague, the Netherlands. 3. Department of Epidemiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands; Groningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, University Medical Center Groningen, Groningen, the Netherlands. 4. Department of Neurodegenerative Diseases and Gerontopsychiatry, University of Bonn, Bonn, Germany; Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA; German Center for Neurodegenerative Diseases, Bonn, Germany. 5. Institute of Sociology and Demography, University of Rostock, Rostock, Germany; German Center for Neurodegenerative Diseases, Bonn, Germany.
Abstract
BACKGROUND: Exposure to fine particulate matter and black carbon is related to cognitive impairment and poor lung function, but less is known about the routes taken by different types of air pollutants to affect cognition. OBJECTIVES: We tested two possible routes of fine particulate matter (PM2.5) and black carbon (BC) in impairing cognition, and evaluated their importance: a direct route over the olfactory nerve or the blood stream, and an indirect route over the lung. METHODS: We used longitudinal observational data for 49,705 people aged 18+ from 2006 to 2015 from the Dutch Lifelines cohort study. By linking current home addresses to air pollution exposure data from ELAPSE in 2010, long-term average exposure to PM2.5 and BC was assessed. Lung function was measured by spirometry and Global Initiative (GLI) z-scores of forced expiratory volume in 1s (FEV1) and forced vital capacity (FVC) were calculated. Cognitive performance was measured by cognitive processing time (CPT) assessed by the Cogstate Brief Battery. Linear structural equation modeling was performed to test direct/indirect associations. RESULTS: Higher exposure to PM2.5 but not BC was related to higher CPT and slower cognitive processing speed [Total Effect PM2.5: FEV1 model = 8.31 × 10-3 (95% CI: 5.71 × 10-3, 10.91 × 10-3), FVC model = 8.30 × 10-3 (95% CI: 5.69 × 10-3, 10.90 × 10-3)]. The direct association of PM2.5 constituted more than 97% of the total effect. Mediation by lung function was low for PM2.5 with a mediated proportion of 1.32% (FEV1) and 2.05% (FVC), but higher for BC (7.01% and 13.82% respectively). DISCUSSION: Our results emphasise the importance of the lung acting as a mediator in the relationship between both exposure to PM2.5 and BC, and cognitive performance. However, higher exposure to PM2.5 was mainly directly associated with worse cognitive performance, which emphasises the health-relevance of fine particles due to their ability to reach vital organs directly.
BACKGROUND: Exposure to fine particulate matter and black carbon is related to cognitive impairment and poor lung function, but less is known about the routes taken by different types of air pollutants to affect cognition. OBJECTIVES: We tested two possible routes of fine particulate matter (PM2.5) and black carbon (BC) in impairing cognition, and evaluated their importance: a direct route over the olfactory nerve or the blood stream, and an indirect route over the lung. METHODS: We used longitudinal observational data for 49,705 people aged 18+ from 2006 to 2015 from the Dutch Lifelines cohort study. By linking current home addresses to air pollution exposure data from ELAPSE in 2010, long-term average exposure to PM2.5 and BC was assessed. Lung function was measured by spirometry and Global Initiative (GLI) z-scores of forced expiratory volume in 1s (FEV1) and forced vital capacity (FVC) were calculated. Cognitive performance was measured by cognitive processing time (CPT) assessed by the Cogstate Brief Battery. Linear structural equation modeling was performed to test direct/indirect associations. RESULTS: Higher exposure to PM2.5 but not BC was related to higher CPT and slower cognitive processing speed [Total Effect PM2.5: FEV1 model = 8.31 × 10-3 (95% CI: 5.71 × 10-3, 10.91 × 10-3), FVC model = 8.30 × 10-3 (95% CI: 5.69 × 10-3, 10.90 × 10-3)]. The direct association of PM2.5 constituted more than 97% of the total effect. Mediation by lung function was low for PM2.5 with a mediated proportion of 1.32% (FEV1) and 2.05% (FVC), but higher for BC (7.01% and 13.82% respectively). DISCUSSION: Our results emphasise the importance of the lung acting as a mediator in the relationship between both exposure to PM2.5 and BC, and cognitive performance. However, higher exposure to PM2.5 was mainly directly associated with worse cognitive performance, which emphasises the health-relevance of fine particles due to their ability to reach vital organs directly.
Authors: Stephanie E Cleland; Lauren H Wyatt; Linda Wei; Naman Paul; Marc L Serre; J Jason West; Sarah B Henderson; Ana G Rappold Journal: Environ Health Perspect Date: 2022-06-14 Impact factor: 11.035
Authors: Ji Hyun Kim; Hae Dong Woo; Sunho Choi; Dae Sub Song; Jung Hyun Lee; Kyoungho Lee Journal: Int J Environ Res Public Health Date: 2022-09-14 Impact factor: 4.614