Fine particulate matter (PM2.5) impacts Earth’s climate directly through scattering/absorbing solar radiation and indirectly through aerosol-cloud interactions, and is associated with adverse effects on human health. The largest mass fraction of PM2.5 is organic, and is mostly dominated by secondary organic aerosol (SOA) formed from atmospheric oxidation of hydrocarbons. Isoprene (2-methyl-1,3-butadiene, C5H8) is the most abundant non-methane hydrocarbon and is derived from terrestrial vegetation. Although recognized as the single largest source of SOA, the exact manner in which isoprene-derived SOA is formed in the atmosphere remains unclear. Improving our fundamental understanding of isoprene-derived SOA is key to improving existing air quality models, especially in the southeastern U.S. By combining organic synthesis and mass spectrometry with smog chamber, flow tube, and field studies, we demonstrate that reactive epoxides, which include methacrylic acid epoxide (MAE) and isomeric isoprene epoxydiols (IEPOX), produced from the photochemical oxidation of isoprene are key to SOA formation. Anthropogenic pollutants enhance this source of SOA. In the laboratory, reactive uptake of synthetic IEPOX and MAE standards onto acidified sulfate aerosol yields known isoprene-derived SOA tracers that we measure in PM2.5 collected from multiple sites across the southeastern U.S. Notably, IEPOX- and MAE-derived SOA tracers account for a significant mass fraction (10-25%) of fine organic aerosol in this region. Moreover, real-time continuous chemical measurements of fine aerosol made using an Aerodyne Aerosol Chemical Speciation Monitor (ACSM) from summer 2011 through fall 2014 in this region resolved an IEPOX-oxygenated organic aerosol (IEPOX-OOA) factor when applying positive matrix factorization (PMF) to the organic mass spectral time series. This factor (source) profile accounts for upwards of 33-40% of the fine OA mass (depending on location) and is strongly correlated with known IEPOX-derived SOA tracers, and to some extent with sulfate and aerosol acidity. Notably, we see this major source of fine aerosol forming in spring, maxing out in summer, and tailing off in fall. Finally, we have systematically exposed isoprene SOA generated in our smog chambers to human lung cells at the air-liquid interface, and find that isoprene-derived epoxide intermediates and their resultant SOA constituents induce oxidative stress and inflammation-associated gene expression.

Isoprene-derived SOA formation across mulitiple sites in the southeastern U.S.: Implications for air quality and human health

249th National Meeting (2015)

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