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.