A new study has uncovered how air pollution disrupts the lungs’ self-cleaning system, increasing the risk of respiratory infections. It also identifies a potential treatment to help restore lung function.
According to New Atlas, air pollution is widely known to be harmful to human health, particularly to the lungs. However, until now, the molecular mechanisms behind this damage were not well understood.
A Potential Treatment
A recent study conducted by researchers at the Immunology Frontier Research Center (IFReC) at Osaka University—published in Clinical Investigation—revealed how air pollution affects the airways and proposed a potential therapeutic solution.
Rich Findings
Lead researcher Dr. Noriko Shinjyu of IFReC described the findings as “rich in insights,” revealing that fine particulate matter (PM2.5) negatively impacts the mucociliary clearance process—a key defense mechanism in the respiratory system.
This process works by trapping pollutants in sticky mucus, which is then transported out of the airways by tiny hair-like structures called cilia.
The Role of Ciliated Cells
Ciliated cells are specialized lung cells lined with structures resembling tiny hairs—cilia. According to Shinjyu, cilia play a crucial role in clearing mucus from the airways. Each ciliated cell in the airway contains between 200 and 300 cilia, significantly increasing its surface area—hundreds of times more than ordinary cells. This makes them a primary point of contact with airborne pollutants.
PM2.5 Particles
PM2.5—fine particles with a diameter of 2.5 micrometers or smaller—originate from both natural and human-made sources, such as car exhaust, coal-fired power plants, and industrial facilities. Many of these pollutants produce reactive oxygen species, leading to oxidative stress that can damage cells and tissues.
Fatty Acid Oxidation
The researchers found that pollutants cause the oxidation of polyunsaturated fatty acids (PUFAs) in the membranes of ciliated cells. This process results in the formation of reactive molecules called lipid peroxide-derived aldehydes within the airways. These aldehydes alter the structure of the cells, causing dysfunction and damage that can impair the cilia. Once damaged, the cells and their cilia become less effective at clearing debris from the lungs, raising the risk of infection.
Restoring Normal Function
To explore how to reverse this cellular damage, the team studied a gene responsible for producing an enzyme called aldehyde dehydrogenase (ALDH1A1), which helps break down harmful aldehydes.
Yasutaka Okabe, a co-author of the study and associate professor at IFReC with a focus on airway homeostasis, explained:
“ALDH1A1 is a crucial enzyme in protecting against aldehyde toxicity.”
In experiments involving lab mice that lacked the ALDH1A1 gene, the animals showed impaired cilia formation and function, along with elevated levels of aldehydes.
Severe Lung Infections
The mice without ALDH1A1 were significantly more susceptible to severe lung infections when exposed to PM2.5 particles. However, when researchers administered a drug that boosted ALDH1A1 levels, the ciliary function of the mice was restored.
“Our findings show that aldehyde metabolism plays a critical role in maintaining cilia resilience and highlight its therapeutic potential in alleviating air pollution-related respiratory disorders,” the researchers said.
Future Research
Future studies will explore how aldehyde metabolism may impact other respiratory diseases—including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis—which have also been linked to PM2.5 exposure.
