Abstract
Recent evidence suggests that products of indoor ozone chemistry contribute to cardiovascular pathophysiology. A hypothetical exposure pathway is the formation of reactive oxygen species (ROS) on indoor surfaces, and subsequent partitioning of ROS to respirable particulate matter (PM). For this pathway to be relevant, the ozone-initiated surface yield of ROS should be large enough to contribute substantially to total ROS intake by PM. Here, we exposed a model indoor surface film comprising a mixture of skin and cooking oil lipids to ozone and measured the yield of condensed-phase ROS using a colorimetric method sensitive primarily to hydroperoxides and calibrated with hydrogen peroxide. Approximately 46% of the ozone that was consumed in the reaction formed ROS on a molar basis. Approximately half of the ROS formed is persistent for at least several hours on the surface. ROS continued to form in the absence of ozone, suggesting that a mechanism other than ozonation continues to oxidize the lipids, such as autoxidation. The yields observed here are well above that necessary to contribute to the ROS airborne concentrations observed in field studies.
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