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dc.contributor.authorAretz, Benjamin
dc.contributor.authorJanssen, Fanny
dc.contributor.authorVonk, Judith M.
dc.contributor.authorHeneka, Michael T
dc.contributor.authorBoezen, H. Marike
dc.contributor.authorDoblhammer, Gabriele
dc.date2022-08-11T08:08:25.000
dc.date.accessioned2022-08-23T15:54:53Z
dc.date.available2022-08-23T15:54:53Z
dc.date.issued2020-10-15
dc.date.submitted2020-12-03
dc.identifier.citation<p>medRxiv 2020.10.14.20212506; doi: https://doi.org/10.1101/2020.10.14.20212506. <a href="https://doi.org/10.1101/2020.10.14.20212506" target="_blank" title="preprint in medRxiv">Link to preprint on medRxiv.</a></p>
dc.identifier.doi10.1101/2020.10.14.20212506
dc.identifier.urihttp://hdl.handle.net/20.500.14038/29638
dc.description<p>This article is a preprint. Preprints are preliminary reports of work that have not been certified by peer review.</p>
dc.description.abstractBackground 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 31232 people aged 18+ from 2006 to 2015 from the Dutch Lifelines cohort study. By linking current and past home addresses to air pollution exposure data from ELAPSE, long-term average exposure (≥ ten years) to PM2.5 and BC was calculated. Lung function was assessed 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 the direct/indirect associations. Results Higher exposure to PM2.5 but not BC was directly related to higher CPT and thus slower cognitive processing speed [18.33 (×10−3) SD above the mean (95% CI: 6.84, 29.81)]. 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 1.78% (FEV1) and 2.62% (FVC), but higher for BC (28.49% and 46.22% respectively). Discussion Our results emphasize 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 emphasizes the health-relevance of fine particles due to their ability to reach vital organs directly.
dc.language.isoen_US
dc.relationNow published in Environmental Research doi: 10.1016/j.envres.2021.111533
dc.rightsThe copyright holder for this preprint is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectOccupational and Environmental Health
dc.subjectfine particulate matter
dc.subjectlung function
dc.subjectcognition
dc.subjectEnvironmental Public Health
dc.subjectOccupational Health and Industrial Hygiene
dc.titleLong-Term Exposure to Fine Particulate Matter, Lung Function and Cognitive Performance: A Prospective Dutch Cohort Study on the Underlying Routes [preprint]
dc.typePreprint
dc.source.journaltitlemedRxiv
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2853&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/1854
dc.identifier.contextkey20389333
refterms.dateFOA2022-08-23T15:54:54Z
html.description.abstract<p><p id="x-x-x-x-x-p-2">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. <p id="x-x-x-x-x-p-3">Objectives We tested two possible routes of fine particulate matter (PM<sub>2.5</sub>) 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. <p id="x-x-x-x-x-p-4">Methods We used longitudinal observational data for 31232 people aged 18+ from 2006 to 2015 from the Dutch Lifelines cohort study. By linking current and past home addresses to air pollution exposure data from ELAPSE, long-term average exposure (≥ ten years) to PM<sub>2.5</sub> and BC was calculated. Lung function was assessed by spirometry and Global Initiative (GLI) z-scores of forced expiratory volume in 1s (FEV<sub>1</sub>) 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 the direct/indirect associations. <p id="x-x-x-x-x-p-5">Results Higher exposure to PM<sub>2.5</sub> but not BC was directly related to higher CPT and thus slower cognitive processing speed [18.33 (×10<sup>−3</sup>) SD above the mean (95% CI: 6.84, 29.81)]. The direct association of PM<sub>2.5</sub> constituted more than 97% of the total effect. Mediation by lung function was low for PM<sub>2.5</sub> with a mediated proportion of 1.78% (FEV<sub>1</sub>) and 2.62% (FVC), but higher for BC (28.49% and 46.22% respectively). <p id="x-x-x-x-x-p-6">Discussion Our results emphasize the importance of the lung acting as a mediator in the relationship between both exposure to PM<sub>2.5</sub> and BC, and cognitive performance. However, higher exposure to PM<sub>2.5</sub> was mainly directly associated with worse cognitive performance, which emphasizes the health-relevance of fine particles due to their ability to reach vital organs directly.</p>
dc.identifier.submissionpathfaculty_pubs/1854
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology


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The copyright holder for this preprint is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
Except where otherwise noted, this item's license is described as The copyright holder for this preprint is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.