Exposure to ultrafine particles from traffic alters the expression of several genes in human olfactory mucosa cells, according to a new study. The study, led by the University of Eastern Finland, is the first to combine an analysis of emissions from different diesel fuels and exhaust aftertreatment systems with an examination of their effects in a human cellular model of the olfactory mucosa. The findings were published in Science of the Total Environment.
Particulate emissions from road traffic have been regulated in the EU for decades, but emissions of ultra-fine particles less than 100 nanometers in size are not yet monitored or restricted.
The human olfactory mucosa is a tissue that is directly exposed to the environment and in direct contact with the brain.
“The olfactory system has been found to mediate the effects of environmental pollutants on the brain, thereby contributing to the pathogenesis of brain diseases. However, the exact signaling pathways through which the effects are mediated remain unknown,” says first author PhD Researcher Laura. Mussalo of the Kanninen Laboratory at the University of Eastern Finland.
The study investigated molecular-level changes that occur in human olfactory mucosa cells when exposed to different traffic-derived emissions. The researchers looked at the effects of the emissions on gene expression, that is, what kind of changes the emissions cause and what kind of mechanisms they activate. The researchers also looked at whether fossil and renewable diesel fuels cause different effects and how modern aftertreatment devices, such as particulate filters, affect emissions.
The olfactory mucosa cells used in the study were obtained from volunteer donors, collected in collaboration with Kuopio University Hospital. The interdisciplinary study combined clinical medicine, gene research, molecular biology, environmental toxicology and aerosol physics.
Effects on the inflammatory response and xenobiotic metabolism
The particulate samples used in the exposure studies were collected by the VTT Technical Research Center of Finland and analyzed and characterized by VTT and the University of Tampere. The samples were collected from the exhaust of a heavy-duty vehicle with an engine running on paraffinic renewable diesel and regular mineral diesel. The third sample was a combination of the same renewable diesel technology and a cleaner Euro 6d-temp compliant engine.
All emissions contained extremely fine particles. In addition, both renewable and fossil diesel emissions contained a significant amount of polycyclic aromatic hydrocarbons (PAHs) and reactive nitrogen compounds. However, renewable diesel combined with cleaner engine technology produced very few emissions.
Exposure to ultrafine particles altered the function of human olfactory mucosa cells, and different fuels and engines caused different adverse effects. In addition, molecular-level analysis has revealed disruption in countless systems that regulate cell function. Exposure to both renewable energy and fossil diesel emissions significantly altered the expression of genes related to the inflammatory response, xenobiotic metabolism, olfactory signaling, and olfactory mucosal integrity. However, renewable diesel caused fewer negative impacts than fossil diesel. Emissions from renewable diesels operating with cleaner engine technology caused only negligible changes in cell operation, demonstrating the effectiveness of the engine aftertreatment devices.
The findings support previous studies suggesting that PAHs may disrupt the inflammatory response and xenobiotic metabolism in human olfactory mucosa cells and that ultrafine particles may cause adverse effects in the brain via the olfactory pathway. The study offers important insight into the adverse effects of ultrafine particles in a human model of olfactory mucosa cells, providing a basis for possible measures to mitigate and prevent toxicological risks.
The study is part of the TUBE project, which is funded by the European Union’s Horizon 2020 programme. The study has also received funding from the Kuopio Area Respiratory Foundation, the Finland Brain Foundation, the Yrjö Jahnsson Foundation and the Päivikki and Sakari Sohlberg Foundation.