MONDAY, Feb. 8, 2016 (HealthDay News) -- Greater exposure to cold viruses may help explain why children with asthma tend to suffer their worst symptoms when their school reopens after a break, a new study suggests.
"The school calendar predicts common cold transmission, and the common cold predicts asthma exacerbations," said senior author Lauren Meyers, a professor of integrative biology and statistics and data sciences at the University of Texas at Austin. "And this study provides a quantitative relationship between those things."
It's been noted that children's asthma symptoms tend to spike when school starts in the fall and after long holidays such as spring break.
Some experts have suggested that environmental factors, such as air quality in schools, might be to blame, but this new study suggests otherwise.
Researchers analyzed 66,000 asthma-related hospitalizations of children in cities across Texas over seven years. They concluded that the spread of cold viruses -- which is heavily influenced by the school year calendar -- was the primary cause of worsening asthma symptoms.
When children aren't in school for an extended time, they're less likely to be exposed to other children with colds and their immunity decreases. When they return to school, there's a sharp increase in their exposure to cold viruses, and their immune systems aren't primed to fight the viruses, the researchers explained.
"This work can improve public health strategies to keep asthmatic children healthy. For example, at the riskiest times of year, doctors could encourage patient adherence to preventative medications, and schools could take measures to reduce cold transmission," Meyers said in a university news release.
The researchers also found that flu virus exposure is the main cause of worsening asthma symptoms among adults.
The study was published Feb. 8 in the journal Proceedings of the National Academy of Sciences.
The U.S. National Heart, Lung, and Blood Institute has more about asthma.
SOURCE: University of Texas at Austin, news release, Feb. 8, 2016
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