It has already been established that air pollution exacerbates the hallmark symptoms of asthma, including coughing, wheezing, shortness of breath, and chest tightness. Now new research headed by two local academics has found that traffic-related air pollution (TrAP), in particular, can lead to the development of asthma in children who are genetically susceptible to the chronic condition.

Michael Brauer, a professor in UBC’s school of population and public health, and Chris Carlsten, UBC associate professor of medicine and chair in occupational and environmental lung disease, worked with a team of researchers for their study. They looked at the effects of vehicle pollution in subjects from a large database of Canadian and European children to analyze the gene-environment interactions in the development of asthma. The findings could ultimately help reduce the negative health impacts of TrAP and even introduce evidence-based guidelines for pollution reduction and land development.

“There’s been a lot of studies that show if you already have asthma and if you’re exposed to higher levels of air pollution, it makes your asthma symptoms worse,” Brauer says in a phone interview. “But does air pollution cause new cases of asthma? That’s been unclear. Most of the prior research suggested that if you compared Vancouver to Toronto to Edmonton, there’s really no link between the level of air pollution and the likelihood for developing asthma.”

There seemed to be something specific about traffic pollution that made it a trigger, however. Not all kids who grow up near high-traffic areas will go on to develop asthma, of course. But if the researchers could establish whether children with specific genetic mutations were at higher risk of developing asthma in vehicle-polluted environments, it would bolster their theory that this pollution can, in fact, lead to the inflammatory lung disease.

“If you bring in genetics, then you can show that that relationship holds for kids that have a certain genetic profile, and that makes the case that it’s a true causal link,” Brauer says.

Brauer and Carlsten collaborated with investigators from the Allergy, Genes, and Environment Network (AllerGen)—a national research group established in 2004 by Industry Canada—from across the country. These included people at SFU, the University of Manitoba, and the University of Alberta, as well as national and international partner organizations, such as the Centre for Allergy Research at Sweden’s Karolinska Institutet, the University of Bristol, and the University of Düsseldorf. With funding from AllerGen, the researchers conducted what has become known as the Traffic pollution, Asthma, and Genetics (TAG) study, which was published last year in the journal Environmental Health Perspectives.

In the largest study of its kind, researchers zeroed in on 10 variants of four genes: gluathione S-transferase pi (GSTP1); the tumour necrosis factor, or TNF, gene; and two from a class of proteins called toll-like receptors, TLR2 and TLR4, that appear to play a role in mobilizing the immune system against invading bacteria.

They then combined data from more than 15,000 children enrolled in six birth cohorts in Canada and Europe. They recorded the distance of each child’s home address from busy roads, the degree of exposure to TrAP, the presence of any of the 10 identified genetic variants, the presence of other common risk factors for asthma and allergies, and whether the child had developed asthma or allergies by age eight. They obtained complete data sets for more than 5,100 subjects.

The results of the analysis showed that children with specific genetic profiles had a significantly higher risk of developing asthma in high-TrAP environments. In fact, TrAP-exposed children with one variant of the GSTP1 gene had double the expected risk. A variant of the TNF gene also increased the risk of TrAP-related asthma.

“This brings us closer to understanding the mechanism of action of traffic pollution in vulnerable people,” Brauer says.

According to the Asthma Society of Canada, about 2.74 million people in this country are affected by the disease. Other risk factors include family history of asthma or allergy (such as allergic rhinitis); exposure to high levels of an antigen such as house dust mites in infancy; exposure to tobacco smoke or chemical irritants in the workplace; allergic triggers such as mould, pollen, and animal dander; and nonallergic triggers such as certain drugs (including beta blockers), chemicals, fumes, odours, viral respiratory infections, cold air, and strenuous exercise. Aside from medication, environmental control is an essential part of managing the illness.

Without looking at people’s genetic vulnerabilities, Brauer says, it may be harder for researchers and health professionals to identify the effects of pollution and subsequently develop effective preventive measures.

“It’s our job to protect the most vulnerable people in our society,” Brauer says. “When we know we’re protecting them, we know we’re protecting the population as a whole.

“Maybe we need to now set a lower level of exposure [to TrAP] because we know these people exist in the population,” he adds, noting that another possible outcome could be the decision to build a new school farther away from a busy road than initially planned.

“Those are the kinds of ways I could see this information being used,” Brauer says. “We can use environmental information to argue for tighter policies.”