Isoprene-Derived Secondary Organic Aerosol Induces the Expression of MicroRNAs Associated with Inflammatory/Oxidative Stress Response in Lung Cells

Exposure to fine particulate matter (PM2.5), of which
secondary organic aerosol (SOA) is a major constituent, is linked
to adverse health outcomes, including cardiovascular disease, lung
cancer, and preterm birth. Atmospheric oxidation of isoprene, the
most abundant nonmethane hydrocarbon emitted into Earth’s atmosphere
primarily from vegetation, contributes to SOA formation. Isoprene-derived
SOA has previously been found to alter inflammatory/oxidative stress
genes. MicroRNAs (miRNAs) are epigenetic regulators that serve as
post-transcriptional modifiers and key mediators of gene expression.
To assess whether isoprene-derived SOA alters miRNA expression, BEAS-2B
lung cells were exposed to laboratory-generated isoprene-derived SOA
constituents derived from the acid-driven multiphase chemistry of
authentic methacrylic acid epoxide (MAE) or isomeric isoprene epoxydiols
(IEPOX) with acidic sulfate aerosol particles. These IEPOX- and MAE-derived
SOA constituents have been shown to be measured in large quantities
within PM2.5 collected from isoprene-rich areas affected
by acidic sulfate aerosol particles derived from human activities.
A total of 29 miRNAs were identified as differentially expressed when
exposed to IEPOX-derived SOA and 2 when exposed to MAE-derived SOA,
a number of which are inflammatory/oxidative stress associated. These
results suggest that miRNAs may modulate the inflammatory/oxidative
stress response to SOA exposure, thereby advancing the understanding
of airway cell epigenetic response to SOA.