Gene Expression Profiling in Human Lung Cells Exposed to Isoprene-Derived Secondary Organic Aerosol

Secondary organic aerosol (SOA) derived from the photochemical oxidation of isoprene contributes a substantial mass fraction to atmospheric fine particulate matter (PM_2.5). The formation of isoprene SOA is influenced largely by anthropogenic emissions through multiphase chemistry of its multigenerational oxidation products. Considering the abundance of isoprene SOA in the troposphere, understanding mechanisms of adverse health effects through inhalation exposure is critical to mitigating its potential impact on public health. In this study, we assessed the effects of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air–liquid interface exposure. Gene expression profiling of 84 oxidative stress and 249 inflammation-associated human genes was performed. Our results show that the expression levels of 29 genes were significantly altered upon isoprene SOA exposure under noncytotoxic conditions (<i>p</i> < 0.05), with the majority (22/29) of genes passing a false discovery rate threshold of 0.3. The most significantly affected genes belong to the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) transcription factor network. The Nrf2 function is confirmed through a reporter cell line. Together with detailed characterization of SOA constituents, this study reveals the impact of isoprene SOA exposure on lung responses and highlights the importance of further understanding its potential health outcomes

Isoprene-Derived Secondary Organic Aerosol Induces the Expression of Oxidative Stress Response Genes in Human Lung Cells

Atmospheric oxidation of isoprene in the presence of acidic sulfate aerosol leads to secondary organic aerosol (SOA) that substantially contributes to the mass of outdoor fine particulate matter (PM_2.5). The potential adverse health effects resulting from exposure to this PM type are largely unknown. Isoprene-derived epoxides, isoprene epoxydiols (IEPOX) and methacrylic acid epoxide (MAE), have recently been identified as key gaseous intermediates leading to isoprene SOA formation through acid-catalyzed multiphase chemistry. Altered expression of oxidative stress-associated genes was assessed from exposure to laboratory-generated IEPOX- and MAE-derived SOA in an <i>in vitro</i> model of human airway epithelial cells (BEAS-2B). Exposure to SOA filter extracts is associated with an increased level of expression of oxidative stress response genes in human lung cells under noncytotoxic conditions, with MAE-derived SOA extracts showing greater potency than IEPOX-derived SOA extracts. Our findings highlight the importance of future work aimed at linking PM source, composition, exposure biomarkers, and health outcomes