Study Links Ultrafine Air Pollution Particles to Epigenetic Changes in Human Cells

A recent study led by the University of Eastern Finland has demonstrated that exposure to ultrafine particles (UFPs) from air pollution can alter gene transcription in human cells through epigenetic mechanisms. The research, published in Environment International, focused on the impact of these changes on cellular survival.

UFPs, primarily originating from traffic emissions, are the smallest particles contributing to air pollution and are increasingly recognized as a health concern. They have been implicated in neurodegenerative diseases, including Alzheimer’s disease (AD). Although air pollution’s influence on gene transcription via mechanisms such as DNA methylation and microRNAs is known, the specific role of UFPs has been less explored.

The research team, led by Professor Katja Kanninen, utilized a human-based in vitro model of the olfactory mucosa-tissue located at the top of the nasal cavity and in direct contact with the brain. This model was developed from cells donated by volunteers in collaboration with Kuopio University Hospital. The olfactory mucosa is particularly susceptible to UFP deposition, and disturbances in olfactory function are among the earliest signs of AD.

According to first author Laura Mussalo, “The association between air pollution and AD is well established, however, the understanding of the molecular mechanisms of how air pollutants are involved in AD pathobiology remain obscure. This study deep dives into one signaling pathway connected to AD to understand these complex interactions of how environmental stressors shape our bodily responses.”

The study investigated how UFPs affect gene regulation in olfactory mucosa cells, focusing on the PI3K/AKT signalling pathway, which is crucial for cellular growth and survival and is known to be altered in AD. The researchers found that UFPs impair this pathway through a complex network involving DNA methylation and microRNAs. While many genes related to cell cycle and apoptosis were affected, significant cell death was not observed, suggesting possible adaptation mechanisms. Notably, cells from individuals with AD showed increased vulnerability to UFP exposure compared to healthy controls.