Impact of Secondary Organic Aerosol on the Respiratory Viral Infection in Vitro

Abstract

Inhalation of viable airborne pathogens often leads to respiratory infections. Among the different factors that affect the survival of airborne pathogens, specific aerosol composition, such as secondary organic aerosol (SOA), may impact the severity of respiratory infection by stimulating host cell apoptotic responses. Here, we studied the in vitro effects of SOA (biogenic and anthropogenic) on respiratory infection of the human influenza A virus (H1N1). Viral gene copies in the human bronchial epithelial cell line (BEAS-2B) and human fetal lung fibroflast cell line (MRC-5) treated with SOA were measured to be significantly different from the control group. A maximum enhancement of 56%, 77%, and 45% in H1N1 replication was observed for BEAS-2B cells exposed to different doses of α-pinene SOA, toluene SOA, and naphthalene SOA, respectively. SOA from various precursors impacted viral replication differently, indicating the importance of emission source and composition. For BEAS-2B cells, anthropogenic SOA (toluene and naphthalene) significantly suppressed viral replication at low doses (1 μg mL^–1 and 5 μg mL^–1) and enhanced viral replication at higher doses. Interplay among the source, composition, oxidative stress, host cell apoptosis, and respiratory viral infection highlights the importance of having air pollution mitigation strategies out of a public health perspective.