University of Utah researchers have received a five-year, $3 million grant from the National Institute of Environmental Health Sciences to study how variations in pollutant-sensing genes in the lungs could influence air pollution effects on children who have asthma. The researchers believe that the newly funded effort could possibly lead to the development of personalized medical interventions capable of treating or even preventing the disease.
Although Salt Lake City, the largest city in Utahm is surrounded by stunning mountainous landscapes, it has one of the worst air pollution problems in the winter with the phenomenon known as the “inversion layer.” It especially impacts the youth. About 6% of Utah children younger than 18 have asthma, reports the Utah Department of Health. Asthma, a chronic lung disease causing inflammation of the airways and difficulty breathing, is responsible for 2,800 emergency visits, 780 hospitalizations and up to 30 deaths among Utah children annually. Nationally the disease afflicts about 8% of children and accounts for more than 625,000 emergency room visits and hospital stays each year, reports the Centers for Disease Control and Prevention.
The Study and Tracker
The University of Utah (locally known as “the U”) will deploy a team of pediatricians, computer scientists, engineers, epidemiologists, nursing researchers, pharmacologists, and toxicologists to recruit about 500 children and follow them for several years. They will use the “e-Asthma Tracker,” an app developed by University of Utah team members, to assess children’s symptoms on a weekly basis. Data from the asthma tracker surveys allows treating physicians to track an individual’s symptom control and make timely recommendations to stabilize worsening asthma. This asthma tracker will produce data that will be compared to local air pollution and integrated with genetic data to help determine what types of pollutants affect individual children with the disease over time.
The team will center their attention on genetic variations in what they call “particle sensor” genes. These genes encode transient receptor potential channels (TRPs), which when activated lead to airway/lung irritation and inflammation.
What are TRPs?
Ion channels located on the membranes of epithelial and sensory cells, they are activated in the presence of select stimuli, such as heat, cold, and pungent foods or spices like chili pepper, wasabi or horseradish. People may react differently to them.
Discussion to Date
The evidence thus far collected by University of Utah team members leads them to suspect that there is a similar range of tolerance/intolerance for air pollutants. They believe the key to addressing asthma lies in a person’s TRP genes. For example, different TRPs are also activated by a variety of inhaled pollutants like cigarette and wood smoke, vehicle exhaust, and even certain dusts. Theoretically, the more active some of the TRPs are, the greater the response to a specific pollutant. If this is true, then the more a child is exposed to that pollutant, he or she could be more likely to develop airway inflammation or have an asthma attack.
The Implications: Precision or “Individualized” Therapies
Well, this could lead to the development of individualized treatments for children with asthma that could ultimately suppress the activity of TRPs. Moreover, this information can be used for individual risk stratification for those at high risk for asthma.
Christopher Reilly, PhD, professor of pharmacology and toxicology, University of Utah College of Pharmacy
Call to Action: A number of other investigators are involved—we include a link to the source for review.