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Dr Swati Y Bhave, Adjunct Professor in Adolescent Medicine; Dr D Y Patil Medical College, & Dr D Y Patil Vidyapeeth, Pune; Sr. consultant, Adolescent Pediatrics & Head-In-charge of Adolescent Wellness Clinic, Jehangir Hospital Pune 12 January 2023
Exposure to even moderate levels of PM2.5 and ozone could trigger an acute asthma exacerbation among children living in densely-populated low-income urban areas even in the absence of a viral respiratory infection, suggests a study published in The Lancet Planetary Health.1
The current study examined if ambient air pollution was associated with the risk of asthma exacerbations occurring in children with asthma without viral infection. For this they retrospectively analysed data of 168 children from the Mechanisms Underlying Asthma Exacerbations Prevented and Persistent with Immune-based Therapy (MUPPITS1) cohort, aged 6-17 years, lived in low-income neighborhoods across 9 cities in the US. The associations between air pollutant levels and non-viral asthma attacks were validated in 189 children from the Inner-City Anti-immunoglobulin (IgE) Therapy for Asthma (ICATA) cohort, aged 6–20 years, with persistent allergic asthma living in low-income areas in four US cities.
The respiratory illnesses were classified as viral (V+) or nonviral (V–) and whether they were associated with exacerbation (Ex+) or not (Ex–). The study participants were followed up for around 6 months or two episodes of respiratory illnesses, whichever occurred first. Each respiratory illness was matched with AQI and various air pollutants in the respective cities on the dates close to the acute event.
A total of 336 respiratory events were recorded in the MUPPITS1 cohort; 143 were Ex+ and 193 were without exacerbations (Ex-). AQI values were found to be significantly higher in the 9 days before and after the onset of respiratory symptoms in children with Ex+ respiratory events vs the Ex- events. Nearly 34% of respiratory events were non-viral in origin; this included almost 30% of the Ex+ events. Exposure to increased AQI values during the 9 days before and after the illness was higher among children with nonviral respiratory illness and exacerbation (V- and Ex+) vs those in the V+/Ex+, V+/Ex–and V–/Ex– groups. The exposure to ozone, NO2 and PM2.5 was also higher among V–/Ex+ group. A significant inverse association was also observed with FEV1% and FEV1/FVC in the V–/Ex+ group.
PM2.5 levels were associated with increased epithelial induction of tissue kallikreins, mucus hypersecretion and barrier functions, while ozone levels were associated with increased eosinophilic or type-2 inflammation and reduced lung function. The association between higher AQI and V–/Ex+ events was particularly evident during the spring and summer.
Among the participants from the ICATA trial, there were 100 episodes of asthma exacerbations; 47 were non-viral (V-) and 53 were viral (V+). In this study too, patients in the V–/Ex+ group had high exposure to increased AQI, ozone and PM2.5 levels vs other groups. A noteworthy observation was the association of asthma exacerbations with only moderate increase in levels of these pollutants.
In this study, nearly 30% of children with acute asthma exacerbations had a non-viral etiology suggesting air pollution as an independent risk factor for asthma exacerbations in children living in cities. Even in the absence of respiratory viral infections which are the commonest cause of asthma exacerbations in children and adolescents, air pollutants, specifically ozone and fine particulate matter, could trigger an acute asthma attack via inflammatory pathways in the airway. This study also suggests possible mechanisms by which pollutants increase risk of exacerbations. It adds to the growing evidence of the adverse impact of air pollution on human health and provides further impetus to develop innovative strategies to reduce air pollution.
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