The specific mechanisms involved in associations between air pollution and respiratory illness without viral infection are not understood, especially compared with those of respiratory viruses and asthma exacerbation.
A recent investigation revealed associations between outdoor air pollution in urban areas and non-viral asthma exacerbations, as well as specific inflammatory pathways in the airways of children with asthma.
The prevalence and severity of asthma increased with the rise of urbanization, and according to the study, children in low-income urban centers have the highest rates of asthma. While the relationship has been observed in previous literature, the mechanisms involved are not understood, especially in comparison to those that facilitate the relationship between respiratory viruses and asthma exacerbation.
In the study, Matthew Altman, MD, Systems Immunology Division, Benaroya Research Institute, and investigators, focused on asthma exacerbations without the presence of respiratory virus, but the team also aimed to examine regional air pollutant concentrations, respiratory illnesses, lung function, and upper airway transcriptional signatures in children with asthma.
The retrospective analysis evaluated data from the MUPPITS1 cohort from 2017, which enrolled 208 children aged 6-17 years from urban areas across 9 cities. The participating patients had exacerbation-prone asthma and were recruited between October 2015-October 2016, then their respiratory status was monitored. The final visit of the investigation took place in January 2017.
Investigators then validated their findings with the ICATA cohort, which recuited 419 patients with persistent allergic asthma, aged 6-20 years, that lived in urban areas across 8 US cities. Enrollment occurred from October 2006-March 2008, with the final visit dated December 2009.
For this assessment, investigators included patients who reported respiratory illness within the MUPPITS1 study duration. Patient data from the ICATA cohort were included if they had nasal samples collected at the time of respiratory illness or a scheduled visit.
Air quality index values and air pollutant concentrations for PM2.5, PM10, O3, NO2, SO2, CO, and Pb from the US Environmental Protection Agency spanning the years of both cohorts, were used to match values and concentrations of each illness for each participant. Then, investigators utilized an amalgamation of generalized additive models, case crossover analyses, and generalized linear mixed-effects models in order to identify associations between regional air pollutant concentrations and respiratory illnesses and asthma exacerbations, pulmonary function, and upper airway transcriptional signatures.
The data demonstrated a rise in air quality index values, that resulted from increased PM2.5, O3 concentrations, showed a significant association with decreased pulmonary functions and the presence of asthma exacerbations without viral infection. The analysis consisted of 168 patients from MUPPITS1 (98 males; 70 females), and 189 patients from ICATA (115 males; 74 females).
Evidence of altered gene expression in coordinated inflammatory pathways was significantly linked to individual pollutants. This observation related to PM2·5 with increased epithelial induction of tissue kallikreins, mucus hypersecretion, barrier functions and O3 with increased type-2 inflammation, the team reported.
"Our findings suggest that air pollution is an important independent risk factor for asthma exacerbations in children living in urban areas and is potentially linked to exacerbations through specific inflammatory pathways in the airway," investigators wrote. "Further investigation of these potential mechanistic pathways could inform asthma prevention and management approaches."
The study "Associations between outdoor air pollutants and non-viral asthma exacerbations and airway inflammatory responses in children and adolescents living in urban areas in the USA: a retrospective secondary analysis" was published in The Lancet Planetary Health.
This article was published by our sister publication HCP Live.