Specific Pollutants Linked to Asthma Attacks in Urban Children

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Air emissions at a manufacturing complex in Toronto, Canada. Credit: UN Photo/Kibae Park

Key points:

  • Researchers have linked ozone and fine particulate matter to increased asthma attacked in with asthma attacks in children and adolescents living in low-income urban areas.
  • Over a 6 month period, asthma attacks had a non-viral cause in nearly 30% of children—2 to 3x the proportion seen in non-urban children.
  • The study is one of the first to link specific outdoor air pollutants in particular urban locations to distinct changes in the airways during asthma attacks.

A study by the National Institutes of Health has associated moderate levels of two outdoor air pollutants—ozone and fine particulate matter—with asthma attacks in children and adolescents living in low-income urban areas.

The study draws a link between exposure to the two pollutants and molecular changes in the children’s airways during non-viral asthma attacks, suggesting potential mechanisms for those attacks.

The observational study is one of the first to link elevated levels of specific outdoor air pollutants in particular urban locations to distinct changes in the airways during asthma attacks not triggered by respiratory viruses, according to the research team.

For the study, published in Lancet Planetary Health, researchers examined the relationship between air pollutant levels and asthma attacks occurring in the absence of a respiratory virus among 208 children ages 6 to 17 years who had attack-prone asthma and lived in low-income neighborhoods in one of nine U.S. cities.

Then the researchers validated the associations they found between air pollutant levels and non-viral asthma attacks in an independent cohort of 189 children ages 6 to 20 years with persistent asthma who also lived in low-income neighborhoods in four U.S. cities.

Following the children for approximately 6 months, the researchers found that asthma attacks had a non-viral cause in nearly 30% of children—2 to 3x the proportion seen in non-urban children.

The investigators linked changes in the expression of specific sets of genes that play a role in airway inflammation to elevated levels of these two pollutants by analyzing nasal cell samples obtained from the children during respiratory illnesses. Some of the identified gene-expression patterns suggest that unique biological pathways may be involved in non-viral asthma attacks, the NIH team says.

 

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