Why can some people remain relatively healthy in polluted areas and why others don't? The severity of the injury depends on the genetic make-up of the affected individual, as researchers from Duke University Medical Center found out.
The culprit
They identified how nanoparticles from diesel exhaust damage lung airway cells, a finding that could lead to new therapies for people susceptible to airway disease.
The work was published recently on-line in the journal Environmental Health Perspectives.
Diesel exhaust particles, a major part of urban smog, consist of a carbon core coated with organic chemicals and metals. The Duke team showed that the particle core delivers these organic chemicals onto brush-like surfaces called cilia, which clear mucus from the airway lining.
Contact with these chemicals then triggers a “signalling cascade,” as the cells respond.
In some patients, who have a single “letter” difference in their DNA, a circuit called the TRPV4 ion channel signals more strongly in response to the pollutants.
Previous research showed that this gene variant makes humans more liable to develop chronic-obstructive disease (COPD), and the current study provides an explanation for this observation, according to a Duke University press release.
Most affected
About 75 per cent of people have the version of the gene MMP-1 that leads to greater production of the molecule MMP-1 mediator, which destroys lung tissue.
This genetic make-up allows for a turbo-charged production of MMP-1, which damages airways and lungs at multiple levels.
A more fortunate 25 per cent of people escape this high level of production of MMP-1, which may be reflected in the fact that certain individuals can better manage the effects of air pollution without grave airway damage.
