Abstract
Abstract. Reactive oxygen species (ROS) present on or generated by particulate matter (PM) have been implicated in PM-induced health effects. Methodologies to quantify ROS concentrations vary widely, both in detection and collection methods. However, there is currently an increasing emphasis on rapid collection and measurement due to observations of short half-life ROS. To address this problem, this paper details the design and characterization of a novel instrument for the measurement of PM-bound ROS named the Particle Into Nitroxide Quencher (PINQ). This instrument combines the 9,10-bis (phenylethynyl) anthracene-nitroxide (BPEAnit) ROS assay in conjunction with a purpose-built aerosol collection device, the insoluble aerosol collector (IAC). The IAC continuously collects PM regardless of size or chemistry directly into a liquid sample with a collection efficiency of > 0.97 and a cut-off size of < 20 nm. The sampling time resolution of the PINQ is 1 min, with a limit of detection (LOD) of 0.08 nmol m−3 in equivalent BPEAnit-Me concentration per volume of air. This high sample time resolution and sensitivity is achieved due to a combination of the highly concentrated IAC liquid sample, minimized liquid sample volume, and the rapid reaction and stability of the BPEAnit probe.
Highlights
The World Health Organization (WHO) found air pollution was responsible for more than 7 million premature deaths in 2012
The collection efficiency of the insoluble aerosol collector (IAC) for both fine (PM2.5) and ultrafine (PM0.1) particles was investigated through the comparison of mass concentration of ammonium sulfate collected with the IAC and those collected onto membrane filters
The IAC investigation was initially focused on mass collection efficiency in order to directly measure the fraction of aerosol collected into the sample liquid
Summary
The World Health Organization (WHO) found air pollution was responsible for more than 7 million premature deaths in 2012. Studies have shown a link between exposure to PM in diesel exhaust and an increased lung cancer risk (Silverman et al, 2012). A key mechanism used to explain these adverse health effects is oxidative stress (Ayres et al, 2008; Li et al, 2002). The ultrafine particle ranges have been shown to be hazardous in this respect. Their ability to penetrate deeper into tissues than their larger counterparts allows them to collect inside mito-
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