Scientists have shown how diesel fumes trigger respiratory reflexes which could potentially worsen underlying conditions, such as asthma.

The study, led by researchers at Imperial College London, is the first to demonstrate a mechanism by which diesel exhaust particles, a major component of air pollution in European cities, directly affect the lungs to initiate symptoms such as a tightening of the airways and cough.

Previous research has shown a strong association between urban air pollution and respiratory symptoms such as coughing, wheezing and shortness of breath, but the underlying mechanism has been unclear.

In the latest study, published in the Journal of Allergy and Clinical Immunology, an international team has shown that by–products from burning diesel fuel – called polycyclic aromatic hydrocarbons (PAHs) – directly stimulate nerves in the lungs, causing a reflex response in the airways.

The findings may provide a key link between exposure to air pollution on city streets and respiratory symptoms which can lead to hospitalisation for people at higher risk, such as the very young, the elderly, and those with respiratory diseases.

Working with researchers from King’s College London and University of British Columbia, Professor Belvisi’s team used commercially available diesel exhaust and generator diesel which mimics ‘real–world’ urban environment conditions to test the effects of exposure in a guinea pig model and animal nerve tissue. The effects were also tested on human tissue, using sections of vagus nerve from donor lung tissue that was surplus to transplant requirement.

The researchers found that when the tissue had been exposed to PAH’s, sensory nerves responsible for the reflex events and initiating common respiratory symptoms, such as coughing and wheezing, were stimulated. The evidence suggests that when these organic compounds are inhaled, they interact with receptors in the airways to cause oxidative stress. This stress then cascades and opens ion channels, tipping the electrochemical balance and causing the nerves to ‘fire’.

These findings were further supported using nerve tissue from mice lacking the functioning ion channel (called TRPA1), in which this change to the electrochemical balance in the nerves, and subsequent symptoms, was not seen.

“Our work shows that particles from diesel exhaust can activate these ion channels, stimulating the nerves in the lungs. This may be responsible for the respiratory symptoms we see following exposure to urban air pollution,” explained Professor Belvisi.