C25-05 Indoor Pm2.5 Exposure and Nasal Mucosal Cytokine Profiles in Asthmatic Children With and Without Respiratory Viral Infection

Abstract Rationale Data increasingly support the association between fine particulate matter (PM2.5) exposure and upper respiratory viral infection (URI), which is the predominant trigger of asthma exacerbations in children with asthma. Although the underlying mechanisms are still unclear, indoor PM2.5 exposure may modify innate immune pathways in uninfected and/or infected children, possibly contributing to differences in susceptibility to infection and/or in mounting an immune response once infected. Methods To examine the relationships between indoor PM2.5 exposure and biomarkers of innate immunity in children aged 6-17 years with and without URI, we collected nasal swabs and nasal epithelial lining fluid (NELF) from children with persistent asthma enrolled in the Texas Home Assessment of Asthma and Lung Exposures study. URI was defined as a positive nasal swab test for rhinovirus, respiratory syncytial virus, and or influenza nucleic acids using qPCR, regardless of symptoms. NELF was tested for cytokines using the Human Cytokine 29-Plex Kit (Meso Scale Discovery). PM2.5 concentrations were measured in the child’s bedroom using gravimetric sampling methods over ∼5 consecutive days. Using Spearman’s rank correlation coefficients (r), we explored relationships between cytokine concentrations (pg/mL) and PM2.5 concentrations (µg/m3) in three strata: 1) children without URI; 2) children with URI and no cold symptoms in the past two weeks; and 3) children with URI and cold symptoms. Results 73 children (66% male, 56% Hispanic/Latinx, 64% public insurance) were included; 33 (45%) had URI. Among those with URI, 9 (27%) reported cold symptoms. Median (IQR) indoor PM2.5 concentrations were 9.35 µg/m3 (4.52-15.2). In children without URI or without cold symptoms, PM2.5 and cytokine concentrations were weakly correlated (r = -0.3 - 0.3). In contrast, among children with both URI and cold symptoms, PM2.5 and proinflammatory cytokine concentrations were significantly negatively correlated (IFN-γ r=-0.9, p=0.005, IL-2 r=-0.8, p=0.017, IL-6 r=-0.8, p=0.025, Figure), as were PM2.5 and chemokine concentrations, which serve a critical role in recruiting immune cells to the site of infection for pathogen clearance, (Eotaxin r=-0.8, p=0.021 and MCP-1 r=-0.9, p=0.003). Conclusions Asthmatic children with symptomatic URI (but not those without URI or with asymptomatic URI) who are exposed to higher levels of indoor PM2.5 may have reduced proinflammatory and chemokine concentrations typically involved in viral defense. Further research is needed to better understand the clinical implications of these specific cytokine reductions in children with asthma. Figure. Correlations between PM2.5 and IFN-γ concentrations in children with asthma stratified by URI and cold symptoms. This abstract is funded by: Dell Medical School University of Texas at Austin