New research reveals how the smallest air pollutants can harm our sense of smell and potentially contribute to Alzheimer’s disease. A team led by scientists at the University of Eastern Finland has uncovered how ultrafine particles from vehicle exhaust interfere with vital cellular processes in the nose.
Microscopic Menace: How Ultrafine Particles Affect Our Cells
Ultrafine particles (UFPs) are the tiniest components of air pollution, measuring less than 100 nanometers across. Despite their small size, these particles can have outsized effects on human health. The new study, published in the journal Redox Biology, shows that UFPs from traffic can penetrate deep into cells of the olfactory mucosa – the tissue responsible for our sense of smell.
Once inside these cells, the particles wreak havoc on mitochondria, often called the powerhouses of the cell. Mitochondria generate energy for cellular functions, but exposure to UFPs disrupts this process. The researchers found that UFPs impair oxidative phosphorylation, the main way mitochondria produce energy. This leads to decreased ATP levels, essentially reducing the cell’s available energy.
Laura Mussalo, the study’s lead author, explains: “Dysfunction of mitochondria plays a key role in the development and progression of neurodegenerative diseases such as Alzheimer’s disease, and mitochondria are known to be especially vulnerable to environmental toxicants.”
A Direct Path to the Brain: Why Olfactory Cells Matter
The olfactory mucosa is unique because it’s directly exposed to the environment and connects to the brain. This makes it a potential entry point for pollutants to affect brain health. Interestingly, one of the earliest symptoms of Alzheimer’s disease is an impaired sense of smell, highlighting the importance of this tissue in neurological health.
The researchers used a sophisticated model of human olfactory mucosa cells, collected from both healthy volunteers and individuals with Alzheimer’s disease. This allowed them to compare how UFPs affected cells in different states of neurological health.
Their findings showed that cells from people with Alzheimer’s disease responded slightly differently to UFP exposure compared to healthy cells. This suggests that individuals with Alzheimer’s might be more vulnerable to the harmful effects of air pollution.
Why it matters: This research provides crucial evidence linking air pollution to cellular changes that could contribute to neurodegenerative diseases. By understanding these mechanisms, we may be able to develop better strategies to protect brain health and reduce the risk of conditions like Alzheimer’s disease.
The study also compared the effects of different fuel types and engine technologies. Encouragingly, they found that modern aftertreatment devices, such as particulate filters, significantly reduced the harmful effects of exhaust on cells. This underscores the importance of continued improvements in vehicle emissions technology.
As we continue to grapple with the health impacts of air pollution, studies like this provide valuable insights into the microscopic processes that can lead to major health problems. By shedding light on how even the tiniest particles can disrupt our cells, this research may help shape future policies to protect public health and reduce the burden of neurodegenerative diseases.
