Summary: study reveals that ultrafine particles from traffic emissions significantly alter gene expression in human olfactory mucosa cells.
This first-of-its-kind study combined analyses of diesel fuel emissions and their effects on a human-derived cell model. It found that both renewable and fossil diesel emissions disrupt numerous cellular functions, but renewable diesel, especially with cleaner engine technology, causes fewer adverse effects.
These findings shed light on the potential pathway for environmental pollutants to affect the brain through the olfactory system.
- The study showed that exposure to ultrafine particles from traffic emissions alters gene expression related to inflammation, xenobiotic metabolism, and olfactory signaling.
- Renewable diesel combined with cleaner engine technology resulted in fewer cell function alterations compared to fossil diesel.
- The research provides evidence that ultrafine particles may mediate adverse brain effects via the olfactory pathway, underscoring the need for monitoring and regulating these emissions.
Source: University of Eastern Finland
Exposure to ultrafine particles from traffic 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 an analysis of emissions from different diesel fuels and exhaust after-treatment systems with an examination of their effects in a human-derived cell model of the olfactory mucosa.
The findings were published in Science of the Total Environment.
Particle emissions from road traffic have been regulated in the EU for decades, but emissions of ultrafine particles with a diameter less than 100 nanometres in size aren’t monitored or restricted yet.
The human olfactory mucosa is a tissue 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, thus contributing to the pathogenesis of brain diseases. However, the exact signalling pathways through which the effects are mediated remain unknown,” says first author, Doctoral Researcher Laura Mussalo of the Kanninen Lab at the University of Eastern Finland.
The study explored molecular-level changes occurring in human olfactory mucosa cells when exposed to different emissions derived from traffic. The researchers examined the effects of emissions on gene expression, i.e., what kind of alterations emissions cause, and what kind of mechanisms they activate.
The researchers also examined whether fossil and renewable diesel fuels cause different effects, and how modern after-treatment devices, such as particulate filters, affect emissions.
The olfactory mucosa cells used in the study were obtained from voluntary donors, collected in collaboration with Kuopio University Hospital. The multidisciplinary study combined clinical medicine, gene research, molecular biology, environmental toxicology and aerosol physics.
Effects on inflammatory response and xenobiotic metabolism
The particle samples used in the exposure studies were collected by VTT Technical Research Centre of Finland, and they were analysed and characterised by VTT and Tampere University.
The samples were collected from exhausts of a heavy-duty-engine vehicle run on paraffinic renewable diesel and on regular fossil diesel. The third sample was a combination of the same renewable diesel and cleaner engine technology complying with the Euro 6d-temp standard.
All emissions contained ultrafine particles. In addition, emissions from both renewable and fossil diesel contained a significant amount of polycyclic aromatic hydrocarbons (PAHs) and reactive nitrogen compounds. However, renewable diesel combined with cleaner engine technology produced very little emissions.
Exposure to ultrafine particles altered human olfactory mucosa cell function, and different fuels and engines caused different adverse effects. Furthermore, molecular-level analysis revealed disturbance in countless systems that regulate cell function.
Exposure to emissions from both renewable and fossil diesel significantly altered the expression of genes associated with inflammatory response, xenobiotic metabolism, olfactory signalling and olfactory mucosa integrity. However, renewable diesel caused less adverse effects than fossil diesel.
Emissions from renewable diesel run on cleaner engine technology caused only negligible alterations in cell function, demonstrating the efficiency of engine after-treatment devices.
The findings back earlier studies suggesting that PAHs may disturb the inflammatory response and xenobiotic metabolism in human olfactory mucosa cells, and that ultrafine particles may mediate adverse effects to the brain via the olfactory pathway.
The study offers important insight into the adverse effects of ultrafine particles in a human-derived cell model of the olfactory mucosa, providing a basis for possible measures to mitigate and prevent toxicological hazards.
Funding: The study constitutes part of TUBE project, which is funded by the Horizon 2020 programme of the European Union. The study has also received funding from the Kuopio Area Respiratory Foundation, the Finnish Brain Foundation, Yrjö Jahnsson Foundation, and Päivikki and Sakari Sohlberg Foundation.
About this olfaction and neuroscience research news
Original Research: Open access.
“Emissions from modern engines induce distinct effects in human olfactory mucosa cells, depending on fuel and aftertreatment” by Laura Mussalo et al. Science of The Total Environment
Emissions from modern engines induce distinct effects in human olfactory mucosa cells, depending on fuel and aftertreatment
Ultrafine particles (UFP) with a diameter of ≤0.1 μm, are contributors to ambient air pollution and derived mainly from traffic emissions, yet their health effects remain poorly characterized.
The olfactory mucosa (OM) is located at the rooftop of the nasal cavity and directly exposed to both the environment and the brain. Mounting evidence suggests that pollutant particles affect the brain through the olfactory tract, however, the exact cellular mechanisms of how the OM responds to air pollutants remain poorly known.
Here we show that the responses of primary human OM cells are altered upon exposure to UFPs and that different fuels and engines elicit different adverse effects.
We used UFPs collected from exhausts of a heavy-duty-engine run with renewable diesel (A0) and fossil diesel (A20), and from a modern diesel vehicle run with renewable diesel (Euro6) and compared their health effects on the OM cells by assessing cellular processes on the functional and transcriptomic levels.
Quantification revealed all samples as UFPs with the majority of particles being ≤0.1 μm by an aerodynamic diameter. Exposure to A0 and A20 induced substantial alterations in processes associated with inflammatory response, xenobiotic metabolism, olfactory signaling, and epithelial integrity. Euro6 caused only negligible changes, demonstrating the efficacy of aftertreatment devices.
Furthermore, when compared to A20, A0 elicited less pronounced effects on OM cells, suggesting renewable diesel induces less adverse effects in OM cells.
Prior studies and these results suggest that PAHs may disturb the inflammatory process and xenobiotic metabolism in the OM and that UFPs might mediate harmful effects on the brain through the olfactory route.
This study provides important information on the adverse effects of UFPs in a human-based in vitro model, therefore providing new insight to form the basis for mitigation and preventive actions against the possible toxicological impairments caused by UFP exposure.