Ilias S. Frydas1,2,3, Marianthi Kermenidou1,2, Konstantinos Papageorgiou3, Ioannis Grivas3, Dimosthenis A. Sarigiannis1,2,4, and Spyridon Kritas3

Author information

1Environmental Engineering Laboratory, Department of Chemical Engineering, Aristotle University of Thessaloniki, Greece
 2HERACLES Research Center on the Exposome and Health – Center for Interdisciplinary Research and Innovation, Aristotle University of Thessaloniki, Greece
3Laboratory of Microbiology and Infectious Diseases, Department of Veterinary Medicine, Aristotle University of Thessaloniki
4Environmental Health Engineering Chair, Science, Technology and Society Department, University School for Advanced Study (IUSS), Pavia, Italy

Abstract

During the last years plastic waste has significantly increased in the aquatic environment and in the atmosphere. Microplastics are plastic fragments which originate from multiple sources such as the textile industry and households. Further fragmentation of microplastics results in nanoplastics (NPs, <1000 nm) formation, and in their respective distribution in the environment. In addition, atmospheric pollution has significantly increased in urban environments due to particulate matter (PM) concentration. Acute and chronic exposure to PM air pollution is linked to an increased risk of cardiovascular and metabolic diseases. The current synergistic and antagonistic effects of mixtures of NPs, PM and airborne pathogens on the environment and in human health as of date have not been well understood, and instead they remain a cause for general concern. In this work, the synergistic effect of NPs, PM and airborne viruses has been evaluated in the context of cytotoxicity, primary immune responses and cell viability. In brief, primary porcine alveolar lung macrophages were treated and exposed for 24 and 48 h with different concentrations of NPs, PM and pseudorabies virus, under the same conditions. Culture supernatants were collected and cells were subjected in pcr and different assays to measure changes in cell viability, cytopathic effect, virus replication and transcriptional expression of cytokines. Results showed significantly reduced cell viability and increased cytopathic effect in alveolar macrophages for the synergistic exposure groups of virus/PM and virus/NPs compared to the control group. Moreover, increased expression of TNFα, IL6 and IL4, but decreased expression of   IFNγ and GM-CSF were observed for the same synergistic exposure groups, suggesting different mechanisms by which NPs, PM and airborne respiratory viruses regulate inflammatory responses in mammalian cells. Our results confirm the increased health burden concerning the simultaneous exposure to human pathogens and environmental factors, and show a differential immunological response after synergistic treatment of cells to mixtures of viruses, NPs and PM.

Publication type

Editorial

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