14 August 2006
ByAppeared in BioNews 371
Researchers believe they have discovered why chronic exposure to passive smoking can cause some young people to go on to develop serious chest problems like asthma, while others are not as badly affected. They have warned that children who inherit a common gene defect face a heightened risk from passive smoking.
The team, from the University of Dundee Medical School, studied 600 children and young people with asthma. They checked airway peak flows, using a blowing test. The team identified gene defects that increase the risk of developing asthma, and worsen lung function in patients with asthma, when exposed to tobacco smoke in the environment. These findings are published in the journal Paediatrics.
The genes that they studied help the body produce an enzyme called glutathione-S-transferase (GST), which is particularly effective in detoxifying inhaled tobacco smoke within the lungs. However, the genes that produce GST are subject to two common defects, one of which is present in around 50 per cent of the population with the other occurring in around 12 per cent of the population. The research team found that children who had either of the two defects were more susceptible to asthma associated with environmental tobacco smoke, compared to those with intact GST genes. They also found that teenagers with asthma had 15 per cent lower peak flows if they had one of the GST gene defects and were exposed to tobacco smoke, compared to asthmatic teenagers with intact genes.
Dr Somnath Mukhopadhyay, one of the researchers, said: 'There is a risk that these children and teenagers, naturally unaware of their susceptible status resulting from this gene defect, could be undergoing a silent, long-standing decline in lung function over the years'. The two defects in the GST genes defined a high-risk population of young Scottish asthmatics in whom tobacco smoke was particularly harmful. Dr Mukhopadhyay added: 'What I worry about is people smoking more and more in the home and you could potentially have a vulnerable population who are perhaps getting a higher dose of cigarette smoke'.
These new findings follow a study in 2004 where researchers at the Children's University in Munich found that children of smokers, who had also inherited an altered version of the glutathione S transferase (GST) gene, were five times more likely to develop asthma, compared to children who did not have the gene variation. At present there is no screening for the gene defects. The researchers of the latest study suggest early identification of these gene defects, with concurrent strategies targeted at the protection of the high-risk population, may be effective in the long term in reducing the prevalence of asthma in Scotland.