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Determining the toxicological effects of indoor air pollution on both a healthy and an inflammatory-comprised model of the alveolar epithelial barrier in vitro

Kirsty Meldrum, Stephen Evans Orcid Logo, Michael Burgum, Shareen Doak Orcid Logo, Martin Clift Orcid Logo

Particle and Fibre Toxicology, Volume: 21, Issue: 1

Swansea University Authors: Kirsty Meldrum, Stephen Evans Orcid Logo, Michael Burgum, Shareen Doak Orcid Logo, Martin Clift Orcid Logo

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Abstract

Exposure to indoor air pollutants (IAP) has increased recently, with people spending more time indoors (i.e. homes, offices, schools and transportation). Increased exposures of IAP on a healthy population are poorly understood, and those with allergic respiratory conditions even less so. The objecti...

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Published in: Particle and Fibre Toxicology
ISSN: 1743-8977
Published: Springer Science and Business Media LLC 2024
Online Access: Check full text

URI: https://cronfa.swan.ac.uk/Record/cronfa66993
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Abstract: Exposure to indoor air pollutants (IAP) has increased recently, with people spending more time indoors (i.e. homes, offices, schools and transportation). Increased exposures of IAP on a healthy population are poorly understood, and those with allergic respiratory conditions even less so. The objective of this study, therefore, was to implement a well-characterised in vitro model of the human alveolar epithelial barrier (A549 + PMA differentiated THP-1 incubated with and without IL-13, IL-5 and IL-4) to determine the effects of a standardised indoor particulate (NIST 2583) on both a healthy lung model and one modelling a type-II (stimulated with IL-13, IL-5 and IL-4) inflammatory response(such as asthma). Using concentrations from the literature, and an environmentally appropriate exposure we investigated 232, 464 and 608ng/cm2 of NIST 2583 respectively. Membrane integrity (blue dextran), viability (trypan blue), genotoxicity (micronucleus (Mn) assay) and (pro-)/(anti-)inflammatory effects (IL-6, IL-8, IL-33, IL-10) were then assessed 24 h post exposure to both models. Models were exposed using a physiologically relevant aerosolisation method (VitroCell Cloud 12 exposure system). No changes in Mn frequency or membrane integrity in either model were noted when exposed to any of the tested concentrations of NIST 2583. A significant decrease (p < 0.05) in cell viability at the highest concentration was observed in the healthy model. Whilst cell viability in the “inflamed” model was decreased at the lower concentrations (significantly (p < 0.05) after 464ng/cm2). A significant reduction (p < 0.05) in IL-10 and a significant increase in IL-33 was seen after 24 h exposure to NIST 2583 (464, 608ng/cm2) in the “inflamed” model. Collectively, the results indicate the potential for IAP to cause the onset of a type II response as well as exacerbating pre-existing allergic conditions. Furthermore, the data imposes the importance of considering unhealthy individuals when investigating the potential health effects of IAP. It also highlights that even in a healthy population these particles have the potential to induce this type II response and initiate an immune response following exposure to IAP.
Keywords: Indoor air pollution, In vitro, Particulate matter, Inhalation, Lung, Disease model, Healthy
College: Faculty of Medicine, Health and Life Sciences
Funders: This study was funded and supported by the United Kingdom Environmental Mutagen Society (UKEMS) (UKEMS Small Grants Scheme for Feasibility awarded to KM), the UKRI (NERC) funded ’RESPIRE’ study (Grant No. NE/W002264/1)
Issue: 1