Role of air pollution in development of asthma among children with a history of bronchiolitis in infancy

Background: Few studies have identified potential modifiable risk factors for the development of asthma among infants who experience bronchiolitis. Air pollution has been associated with child asthma development and may be particularly important for this high-risk group. Objectives We assessed the role of early life air pollution on asthma and wheeze among children age 4-6 years with a history of bronchiolitis in the first year of life. Methods Participants were drawn from the ECHO PATHWAYS consortium, a pooled longitudinal pregnancy cohort (N=2684 mother-child dyads) from six cities across the United States. Child participants whose caregiver reported physician-diagnosed bronchiolitis in the first year of life (asked at the age 4-6 year follow up visit) were eligible for this analysis. The International Study of Asthma and Allergies in Childhood survey (ISAAC) was also administered at this visit. Air pollution exposure from age 1 to 4 was estimated from validated spatiotemporal models of fine particulate matter (PM2.5), nitrogen dioxide (NO2) and ozone (O3). Current wheeze and current asthma were derived from the ISAAC responses. We used Poisson regression with robust standard errors and models were adjusted for child, maternal, and home environmental factors. Effect modification by child sex and maternal asthma status were assessed with interaction models. Results Caregivers of 224 children reported bronchiolitis in the child’s infancy. Mean age at asthma assessment was 4.7 (SD 0.9) years. Mean (SD) pollutant concentrations were 8.64 µg/m3 (1.78), 8.36 ppb (2.85), and 26.41 ppb (2.62) for PM2.5, NO2, and O3, respectively. Relative risk ratios for current wheeze and current asthma per 2-ppb higher postnatal O3 were 1.32 (95% CI: 1.01-1.71) and 1.41 (1.09-1.83), respectively. NO2 was inversely associated with current wheeze and current asthma and the effect estimate for PM2.5 was null. NO2 and PM2.5 showed statistically significant interaction by maternal asthma, with evidence suggestive of inverse associations only among children without a history of maternal asthma. No effect modification by maternal asthma status was observed for O3 nor for any pollutant by child sex. Conclusion Modestly higher exposure to postnatal ozone concentrations may further the risk of asthma among the vulnerable subpopulation of infants who experience bronchiolitis. The role of other common air pollutants may differ among children without a genetic predisposition based on maternal history of asthma.