08. 08. 2024
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Scientists from the Department of Toxicology and Molecular Epidemiology have co-authored a new international study published in the high-impact journal Redox Biology (open in a new window) (IF 10.7), in which they investigated the toxic effects of ultrafine particulates from automotive traffic emissions on mitochondrial function in olfactory mucosal cells.
There is growing scientific evidence that air pollution may play a significant role in the development of Alzheimer’s disease (AD) and other neurodegenerative diseases. Ultrafine particulates (UFPs) are among the primary and most risky components of air pollution. These are mainly produced by the burning of fuel in internal combustion engines, especially diesel engines. A significant proportion of UFPs is also produced by tyre and brake wear. The danger of these particles comes mainly from their small size, which allows them to penetrate the human body, including the brain, causing inflammation, oxidative stress and other pathological processes. In addition, they have a relatively large surface area, which allows them to bind other harmful substances (e.g. organic compounds or heavy metals).
Experts from the prestigious Lancet Commission on Pollution and Health have classified air pollution as a modifiable risk factor for dementia. For example, the accumulation of black carbon particles in the brains of AD patients has recently been proven. Ultrafine particles (UFPs; diameter ≤100 nm) derived mainly from traffic emissions, are considered especially harmful due to their small size and ability to cross bodily membranes, potentially even reaching the brain. The connection of UFPs to AD-related changes in the brain, such as increased amyloid-beta levels, perturbed redox balance, inflammation, neurotoxicity, and cognitive decline, have been described in animal models. However, the exact mechanisms by which UFPs contribute to cellular and molecular changes in the human brain have not yet been clarified. For this purpose, the researchers used an in vitro model consisting of olfactory mucosa cells obtained by biopsy from AD patients and a control group of healthy individuals. The olfactory mucosa cells, which are located on the roof of the nasal cavity, are exposed to toxic substances from the environment with every breath and are in direct contact with the central nervous system via the olfactory nerve. The aim of the study was to understand how exposure to UFPs from different sources of traffic emissions affects the function of these cells and how the response differs depending on whether the cells originate from healthy individuals or AD patients.
The actual research was preceded by Ethics Committee approval, and in addition, for individuals with significant cognitive impairment, consent from a family member or other representative of the donor (AD patient). Biopsies were obtained at the Department of Otorhinolaryngology, Kuopio University Hospital. Furthermore, for the purpose of the study, UFP samples were collected from the exhaust of a heavy-duty diesel engine (HDE) without exhaust after-treatment systems and from the engine of a diesel passenger car with modern exhaust after-treatment technology according to the Euro 6 standard. Both engines were operated with renewable and petroleum diesel.