Summary: A new study shows that ultrafine particles from traffic emissions markedly change gene expression in human olfactory mucosa cells, indicating a plausible route for air pollution to affect the brain.
This first-of-its-kind investigation linked detailed emission analysis from different diesel fuels and after-treatment systems with experiments on human-derived olfactory mucosa cells. Researchers found that both fossil and renewable diesel exhausts altered numerous cellular pathways, but renewable diesel—particularly when paired with modern, cleaner engine technology—produced fewer harmful effects.
The findings provide important insight into how ultrafine particles (UFPs) from traffic can influence inflammation, xenobiotic metabolism, and olfactory signaling in a tissue that is directly exposed to the environment and connected to the brain.
Key facts:
- Exposure to ultrafine traffic particles changed expression of genes involved in inflammatory response, xenobiotic metabolism, olfactory signaling, and epithelial integrity.
- Renewable diesel produced fewer adverse cellular changes than fossil diesel; emissions were lowest when renewable diesel was combined with Euro 6d-temp level after-treatment technology.
- Results support the idea that UFPs may reach and affect the brain via the olfactory pathway, highlighting the need to monitor and regulate ultrafine traffic emissions.
Source: University of Eastern Finland
Overview
Led by the University of Eastern Finland, the study is the first to combine exhaust characterization from different diesel fuels and after-treatment systems with functional and transcriptomic analysis of primary human olfactory mucosa (OM) cells. The work was multidisciplinary, drawing on clinical sampling, molecular biology, environmental toxicology, aerosol physics, and gene expression analysis.
The study’s findings appear in Science of the Total Environment. Despite long-standing vehicle emission regulations in the EU, ultrafine particles—defined as particles with aerodynamic diameters ≤0.1 µm—are not yet routinely monitored or regulated. These UFPs are a major component of traffic-derived ambient air pollution and are suspected contributors to neurological and respiratory health effects.
Why the olfactory mucosa matters
The olfactory mucosa lines the roof of the nasal cavity, is directly exposed to inhaled air, and provides a potential direct route to the brain via olfactory neurons. Previous research suggests airborne pollutants can influence brain health through this pathway, but the molecular mechanisms remain unclear. This study investigated how OM cells respond at the molecular level to real-world traffic-derived particles.
Methods and samples
Primary human OM cells were collected from voluntary donors in cooperation with Kuopio University Hospital. Particle samples for cell exposures were gathered by the VTT Technical Research Centre of Finland and characterized by VTT and Tampere University. Samples came from exhausts of a heavy-duty engine operated on paraffinic renewable diesel (A0) and on conventional fossil diesel (A20), plus a modern vehicle run on renewable diesel with Euro 6d-temp compliant after-treatment technology (Euro6).
All samples were confirmed to contain ultrafine particles, and emissions from both renewable and fossil diesel contained polycyclic aromatic hydrocarbons (PAHs) and reactive nitrogen compounds. The Euro6 configuration produced very low emissions, demonstrating the effectiveness of contemporary after-treatment systems.
Main results
Exposure to UFPs altered cellular functions in OM cells, with notable changes in gene expression profiles. Both A0 (renewable diesel) and A20 (fossil diesel) triggered substantial alterations in pathways tied to inflammatory response, xenobiotic metabolism, olfactory signaling, and epithelial integrity. Compared with A20, A0 generally induced less pronounced disturbances. The Euro6 sample caused only negligible changes, underscoring the mitigation potential of advanced engine and exhaust treatment technologies.
Molecular analyses support earlier work linking PAHs to disruption of inflammatory processes and xenobiotic metabolism in nasal tissues. The constellation of results strengthens the hypothesis that UFPs can mediate adverse effects on the brain via the olfactory route.
Implications
This study provides human-relevant in vitro evidence that ultrafine traffic particles modulate gene networks in olfactory mucosa cells, with fuel type and after-treatment technology determining the severity of effects. Findings suggest that switching to low-emission fuels and deploying effective after-treatment systems can reduce cellular harm and potentially lower neurological risks associated with traffic-derived UFP exposure. The work also supports calls for monitoring and regulating ultrafine particles as part of air quality policy.
Funding The research is part of the TUBE project funded by the EU Horizon 2020 programme and received additional support from the Kuopio Area Respiratory Foundation, the Finnish Brain Foundation, the Yrjö Jahnsson Foundation, and the Päivikki and Sakari Sohlberg Foundation.
About this olfaction and neuroscience research news
Author: Maj Vuorre
Source: University of Eastern Finland
Contact: Maj Vuorre – University of Eastern Finland
Image: Image credited to Neuroscience News
Original research: Open access. Title: “Emissions from modern engines induce distinct effects in human olfactory mucosa cells, depending on fuel and aftertreatment” by Laura Mussalo et al., published in Science of The Total Environment.
Abstract (condensed)
Ultrafine particles (≤0.1 µm), mainly from traffic exhaust, are poorly characterized for health effects despite being pervasive in ambient air. The olfactory mucosa, positioned at the roof of the nasal cavity, is directly exposed to inhaled pollutants and provides a potential pathway to the brain. This study shows that primary human OM cells respond to UFP exposure with altered functional and transcriptomic profiles. UFPs collected from heavy-duty engine exhausts run on renewable and fossil diesel produced significant changes in inflammatory and xenobiotic pathways, while particles from a modern engine with effective after-treatment produced minimal changes. Renewable diesel generally had milder effects than fossil diesel. These results offer mechanistic insight into how traffic-derived UFPs may impact olfactory tissues and potentially the brain, and they support mitigation efforts through fuel choices and advanced emission controls.