Researchers from the University of Eastern Finland have identified that traffic emissions may disrupt our sense of smell. They observed that traffic-related ultrafine particles change gene expression in human olfactory mucosa cells. The olfactory mucosa, a specialized tissue situated in the upper nasal cavity, is integral to our sense of smell.
While road traffic particle emissions are regulated in the EU, ultrafine particles smaller than 100 nanometres are not monitored or restricted. The human olfactory mucosa, in direct contact with the brain, is exposed to these particles.
The Unseen Impact on Our Olfactory Senses
This study is the first to analyze emissions from different diesel fuels and exhaust after-treatment systems. It also examines their effects on a human-derived cell model of the olfactory mucosa.
The study thoroughly investigated how emissions affect gene expression and compared the impacts of fossil and renewable diesel fuels. It also assessed the influence of modern after-treatment technologies, such as particle filters, on emissions.
The study found disruptions in cell-regulation systems due to emissions from fossil and renewable diesel. Renewable diesel had fewer negative impacts, and cleaner engine technology minimized changes in cell operation.
The study confirms the brain’s vulnerability to ultrafine particles via the olfactory pathway and highlights the disruptive impact of polycyclic aromatic hydrocarbons on olfactory mucosa cells. It suggests potential mitigation strategies based on insights from human-cell-derived models. Despite regulations, road traffic emissions remain a persistent issue.
