https://www.sciencedirect.com/science/article/pii/S0013935125016512?via%3Dihub
Gerrit Bredeck a1, Tina Wahle a, Angela A.M. Kämpfer a, Jochen Dobner a, A. John F. Boere b, Paul Fokkens b, Evert Duistermaat b, Tim Spannbrucker a, Andrea Rossi a, Flemming R. Cassee bc, Roel P.F. Schins ad
a IUF – Leibniz Research Institute for Environmental Medicine, Auf’m Hennekamp 50, 40225 Düsseldorf, Germany
b Centre for Sustainability, Environment and Health, National Institute for Public Health and the Environment, PO box 1, Bilthoven, 3720, the Netherlands
c Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, the Netherlands
d Department of Pharmacology and Toxicology, Research Institute for Nutrition and Translational Research in Metabolism (NUTRIM), Maastricht University, Maastricht, the Netherlands
Abstract
In this new study, traffic-derived air pollution (TDAP) is investigated regarding its potential health effects linked to respiratory diseases via oxidative stress and inflammation.
The responses are investigated using a human lung co-culture model (bronchial epithelial cells and alveolar macrophages from three donors) exposed to TDAP from a high-traffic street in Düsseldorf over three days.
TDAP was enriched from 8–42 μg/cm² to 54–143 μg/cm² using aerosol concentration enrichment system.
Aerosol exposure slightly upregulated interleukin 6 in one co-culture but showed minimal overall effects, preventing day-specific response analysis. Donor variability was observed in four genes. Transcriptomic analysis suggested TDAP-induced changes in lung disease-related genes, but qRT-PCR did not confirm this.
As conclusion, higher TDAP concentrations, repeated exposures, and larger donor panels are needed for robust results, with minimized airflow background effects to improve model reliability.
