Background: Upper respiratory tract viral infections cause asthma exacerbations in children. However, the impact of natural colds on children with asthma in the community, particularly in the high-risk urban environment, is less well defined. Objective: We hypothesized that children with high-symptom upper respiratory viral infections have reduced airway function and greater respiratory tract inflammation than children with virus-positive low-symptom illnesses or virus-negative upper respiratory tract symptoms. Methods: We studied 53 children with asthma from Detroit, Michigan, during scheduled surveillance periods and self-reported respiratory illnesses for 1 year. Symptom score, spirometry, fraction of exhaled nitric oxide (FeNO), and nasal aspirate biomarkers, and viral nucleic acid and rhinovirus (RV) copy number were assessed. Results: Of 658 aspirates collected, 22.9% of surveillance samples and 33.7% of respiratory illnesses were virus-positive. Compared with the virus-negative asymptomatic condition, children with severe colds (symptom score ≥5) showed reduced forced expiratory flow at 25% to 75% of the pulmonary volume (FEF25%-75%), higher nasal messenger RNA expression of C-X-C motif chemokine ligand (CXCL)-10 and melanoma differentiation-associated protein 5, and higher protein abundance of CXCL8, CXCL10 and C-C motif chemokine ligands (CCL)-2, CCL4, CCL20, and CCL24. Children with mild (symptom score, 1-4) and asymptomatic infections showed normal airway function and fewer biomarker elevations. Virus-negative cold-like illnesses demonstrated increased FeNO, minimal biomarker elevation, and normal airflow. The RV copy number was associated with nasal chemokine levels but not symptom score. Conclusion: Urban children with asthma with high-symptom respiratory viral infections have reduced FEF25%-75% and more elevations of nasal biomarkers than children with mild or symptomatic infections, or virus-negative illnesses.
Bibliographical noteFunding Information:
Funding Sources: This work was supported by National Institutes of Health grants ES016769 (TCL), ES014677 (TGR), HL081420 (MBH) and AI114220 (TCL and MBH), and Environmental Protection Agency grant EPA-G2008-STAR-B1 (SAB).
Community Action Against Asthma (CAAA) is a community-based participatory research partnership that consists of the following organizations: Arab American Center for Community and Social Services, Community Health and Social Services Center Inc., Detroit Hispanic Development Corporation, Detroiters Working for Environmental Justice, Eastside Community Network, Friends of Parkside, Southwest Detroit Environmental Vision, and faculty from the University of Michigan School of Medicine and the School of Public Health and a community asthma activist. CAAA is an affiliated partnership of the Detroit Community-Academic Urban Research Center. The authors thank Henry Ford Health System Epidemiology Lab for their collaboration, including initial processing and storage of nasal aspirate samples, Ricardo de Majo for database design and technical assistance with encrypted data transfer, Lucas Carlton for quality assessment of spirometry, Laprisha Berry Vaughn and Sonya Grant for their contributions to project management and staff supervision, and Irme Cuadros Tracy for her assistance with data management and quality control. Supplementary data related to this article can be found at https://doi.org/10.1016/j.anai.2018.10.021.
© 2018 Elsevier Ltd