It’s well known that exposure to air pollution increases the likelihood and health problems linked to cardiorespiratory diseases. Air pollutants consist of a mixture of gases and particulate matter such as secondary organic aerosols (SOA). SOA are formed through the oxidation of natural sources like plants and trees, as well as from industry emissions like naphthalene.

In the SOCAAR Seminar held on February 3, Jackie Ye, a PhD candidate at the University of Toronto’s Department of Chemical Engineering & Applied Chemistry, and Sepehr Salehi of the University Health Network’s Department of Medicine, presented an experimental model used to evaluate the health effects of chronic exposure to gaseous pollutants and particulate matter at “real-life” levels.

The experiments were conducted with healthy mice that were chronically exposed to different concentrations of naphthalene, ozone, and NO3. The lung functions of these mice were subsequently measured by assessing the lung resistance to methacholine. Methacholine is a chemical that causes the airway to narrow and is commonly used to diagnose asthma in human patients.

Mice that were exposed to naphthalene SOA on a daily basis showed increases in the airway responsiveness to methacholine, as well as increasing lung resistance with exposures to higher naphthalene concentrations. The addition of ozone didn’t affect the airway responsiveness to methacholine in the mice. Furthermore, exposure to the SOA or gaseous pollutants didn’t affect the total leukocyte count in the bronchoalveolar lavage fluid or lung tissue. The researchers believe the increased airway response was not associated with airway inflammation, which is typically observed with asthma. The researchers has future plans to investigate the chronic exposure of SOA and gaseous pollutants on already diseased mice, such as those with asthma or cystic fibrosis.