Secondary Organic Aerosol Formation from Atmospheric Oxidation of Isoprene: Implications for Air Quality, Climate and Public Health, by Jason Surratt, UNC Chapel Hill
Jointly sponsored by the Department of Chemistry and Biochemistry, CIRES, and the Environmental Program
Secondary Organic Aerosol Formation from Atmospheric Oxidation of Isoprene: Implications for Air Quality, Climate and Public Health
"Atmospheric fine particulate matter (PM 2.5 ) plays a key role in climate and is associated with adverse effects on air quality and human health. The largest mass fraction of PM 2.5 is organic, which is mostly derived from secondary organic aerosol (SOA) formed by the atmospheric oxidation of hydrocarbons. Atmospheric oxidation of isoprene (2-methyl- 1,3-butadiene), the most abundant non-methane hydrocarbon emitted into the atmosphere, is now recognized as one of the largest contributors to PM 2.5 . Despite its abundance, the exact manner in which isoprene- derived SOA is formed has been recently examined through the combination of synthetic organic and analytical chemistry with flow reactor, smog chamber, and field studies. Through these recent studies, we have identified reactive epoxides and hydroperoxides produced from the atmospheric oxidation of isoprene under low-nitric oxide (NO) conditions that are crucial to the formation of ambient SOA. Notably, certain isoprene-derived SOA constituents have been recently observed in cloud water samples and shown to contribute to light-absorbing aerosol, indicating that isoprene-derived SOA may be important for aerosol climate effects. We have found that anthropogenic pollutants, such as acidic sulfate aerosol, significantly enhance isoprene SOA. This is of great public health importance since isoprene is primarily emitted from terrestrial vegetation, and thus, is not controllable, whereas anthropogenic emissions are controllable. Whether SOA derived from this source contributes to the adverse health effects induced by exposure to ambient PM 2.5 reported in epidemiological studies is largely unknown. Using an in vitro model of human airway epithelial cells (BEAS-2B), we have also evaluated the potential early biological effects induced by exposure to isoprene-derived epoxides and hydroperoxides and their resultant SOA constituents. Exposure induced cytotoxicity and expression of oxidative stress and inflammation-associated genes have been assessed. Our initial findings suggest that isoprene-derived epoxides, hydroperoxides and the resultant SOA constituents induce altered oxidative stress and inflammation-associated gene expression in human lung cells under non-cytotoxic conditions. These recent findings highlight the importance of future work aimed at linking PM 2.5 source, composition, exposure biomarkers and health outcomes."