Diurnal trends in redox characteristics of water-soluble and -insoluble PM components.
Densely populated cities with a compact urban built environment have concerns over health risks derived from high levels of airborne particulate matter (PM) exposure. Understanding the association between PM and reactive oxygen species (ROS) is an important step towards unravelling the mechanisms behind. This study investigated the role of time-integrated PM sampling on cellular toxicity mechanism on a diurnal scale. The sampling took place in a highly urbanized part of Hong Kong at two contrast roadside and background sites, with simultaneous solid-PM and semi-volatile-PM (SV-PM) collection in both summer and winter seasons. A sampling day consisted three sampling intervals of 6 h each - 04:00-10:00, 12:00-18:00 and 20:00-02:00 h, representing morning rush hours, afternoon and night periods, respectively. Water and organic extracts of PM were prepared, with and without filtration, and exposed to RAW264.7 and A549  cell lines on a dose and time-dependent manner. Solid-PM and SV-PM contribution to total PM2.5 mass concentration was 9:1, with much higher SV-PM fraction at roadside over urban background (p < 0.001, n = 36). Also, the SV-PM mass concentration increased by 10-20% during 20:00-02:00 h compared to morning and afternoon sampling periods. Organic PM extract was observed to cause 23-29% higher cell death compared to water-soluble PM, which is complemented with increased ROS production in both cell lines. The cellular damage caused by oxidative stress, determined from increased HO-1 and TNF-α expression in RAW264.7 was higher compared to the A549, which demonstrated the greater induction of toxicity from organic PM extract over soluble PM. Similarly, the SV-PM induced greater than 2-fold cellular ROS generation on PM mass basis compared to solid-PM. Lack of phagocytic action in A549 compared to RAW264.7 suggested novel toxicity routes for water-soluble and organic PM that can be expected to occur during human PM inhalation-bronchi-alveolar exposure.