summary: Research has shown that ultrafine particles from traffic exhaust significantly alter gene expression in human olfactory mucosa cells.
The first-of-its-kind study combined analysis of diesel fuel emissions and their effects on a human-derived cell model. They found that while the emissions of both renewable and fossil diesel disrupt many cellular functions, renewable diesel has fewer negative effects, especially when equipped with cleaner engine technology.
These findings reveal a potential pathway by which environmental pollutants affect the brain via the olfactory system.
Important facts:
- This study showed that exposure to ultrafine particles from traffic exhaust alters gene expression related to inflammation, xenobiotic metabolism, and olfactory signaling.
- The combination of renewable diesel and clean engine technology resulted in fewer changes in cellular function compared to fossil diesel.
- This study provides evidence that ultrafine particles can mediate adverse effects on the brain via the olfactory pathway and highlights the need to monitor and regulate their release.
sauce: University of Eastern Finland
Exposure to ultrafine particles from road traffic accidents alters the expression of many genes in human olfactory mucosa cells, a new study shows.
The study, led by the University of Eastern Finland, is the first to combine the analysis of emissions from different diesel fuels and exhaust aftertreatment systems with the investigation of their effects in a human-derived olfactory mucosa cell model.
The survey results are Total environmental science.
While particle emissions from road traffic have been regulated in the EU for decades, emissions of ultrafine particles less than 100 nanometers in diameter are still unmonitored and unregulated.
The human olfactory mucosa is a tissue that is directly exposed to the environment and in direct contact with the brain.
“The olfactory system is known to mediate the effects of environmental pollutants on the brain and contribute to the development of brain diseases. However, the precise signaling pathways by which these effects are mediated remain unclear.” said Laura Mussaro, first author and postdoctoral researcher in Kanninen’s lab at the University of Eastern Finland.
In this study, we investigated the molecular-level changes that occur in human olfactory mucosa cells when exposed to various traffic-derived emissions. The researchers investigated the effects of light emission on gene expression: what changes it causes and what mechanisms it activates.
The researchers also investigated whether fossil fuels and renewable diesel fuels cause different impacts, and how modern aftertreatment devices such as particulate filters affect emissions.
The olfactory mucosa cells used in this study were collected from voluntary donors in collaboration with Kuopio University Hospital. This interdisciplinary research combines clinical medicine, genetic research, molecular biology, environmental toxicology, and aerosol physics.
Effects on inflammatory response and xenobiotic metabolism
The particle samples used in the exposure study were collected by VTT Technical Research Center in Finland and analyzed and characterized by VTT and the University of Tampere.
Samples were collected from the exhaust gases of heavy-engine vehicles running on paraffinic renewable diesel and regular fossil diesel. The third sample combines the same renewable diesel with clean engine technology compliant with Euro 6d temperature standards.
All emissions contained ultrafine particles. Additionally, emissions from both renewable and fossil diesel contained large amounts of polycyclic aromatic hydrocarbons (PAHs) and reactive nitrogen compounds. However, when renewable diesel is combined with clean engine technology, emissions are almost non-existent.
Exposure to ultrafine particles altered the function of human olfactory mucosa cells and caused different adverse effects in different fuels and engines. Furthermore, molecular-level analyzes have revealed perturbations in the myriad systems that regulate cellular function.
Exposure to emissions from both renewable and fossil diesel significantly altered the expression of genes related to inflammatory responses, xenobiotic metabolism, olfactory signaling, and olfactory mucosal integrity. However, renewable diesel had less negative effects than fossil diesel.
Emissions from renewable diesel run on cleaner engine technology caused negligible changes in cell function, demonstrating the efficiency of the engine aftertreatment device.
This finding suggests that PAHs may interfere with the inflammatory response and xenobiotic metabolism of human olfactory mucosal cells, and that ultrafine particles may mediate adverse effects on the brain via the olfactory pathway. It supports research.
This study provides important insights into the adverse effects of ultrafine particles in a human-derived cell model of the olfactory mucosa and provides the basis for possible measures to reduce and prevent toxicological hazards.
Funding: This research forms part of the TUBE project funded by the European Union’s Horizon 2020 program. The research was also funded by the Kuopio Regional Respiratory Foundation, the Finnish Brain Foundation, the Iljo Jánsson Foundation, and the Paiwicki and Sakari Solberg Foundation.
About this olfactory and neuroscience research news
author: Maji Voore
sauce: University of Eastern Finland
contact: Maji Vuore – University of Eastern Finland
image: Image credited to Neuroscience News
Original research: Open access.
“Exhaust gases from modern engines cause different effects on human olfactory mucosa cells depending on fuel and aftertreatmentWritten by Laura Mussaro et al. Total environmental science
abstract
Exhaust gases from modern engines cause different effects on human olfactory mucosa cells depending on fuel and aftertreatment
Ultrafine particles (UFPs) with a diameter of 0.1 μm or less are a source of air pollution, primarily derived from traffic emissions, but their health effects are still poorly understood.
The olfactory mucosa (OM) is located at the top of the nasal cavity and is directly exposed to both the environment and the brain. Although increasing evidence suggests that pollutant particles affect the brain through the sense of smell, the precise cellular mechanisms by which the OM responds to air pollutants remain poorly understood.
Here we show that the response of primary human OM cells changes when exposed to UFPs, and that different fuels and engines cause different adverse effects.
We used UFPs collected from the exhaust gases of large engines using renewable diesel (A0) and fossil diesel (A20), and from the exhaust gases of modern diesel vehicles using renewable diesel (Euro6), and used OM We compared the health effects on cells using the following methods. Assess cellular processes at the functional and transcriptomic level.
Quantification revealed that all samples were UFPs, with the majority of particles being 0.1 μm or less in aerodynamic diameter. Exposure to A0 and A20 caused substantial changes in processes related to inflammatory responses, xenobiotic metabolism, olfactory signaling, and epithelial integrity. Euro6 produced only minimal changes, demonstrating the effectiveness of the aftertreatment device.
Additionally, A0 induced less pronounced effects on OM cells when compared to A20, suggesting that renewable diesel induces fewer negative effects on OM cells.
Previous studies and these results suggest that PAHs may interfere with inflammatory processes and xenobiotic metabolism in the OM, and that UFPs may mediate deleterious effects on the brain via the olfactory pathway. Suggests.
This study provides important information regarding the adverse effects of human-based UFP. in vitro Therefore, new insights are gained to form the basis of mitigation and preventive measures against toxic disorders that may be caused by UFP exposure.
