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High Resolution Image Download MS PowerPoint Slide Air pollution is associated with mortality and morbidity worldwide. The health effects are primarily associated with the inhalation of particulate matter (PM), which can lead to oxidative stress through the excessive production of reactive oxygen species (ROS) in the respiratory, cardiovascular, and neurological systems. The influence of PM size and gaseous oxidants on the production of ROS in the lung is understudied, as most studies to date have focused on assessing this aspect broadly in fine or coarse PM. In this work, we used a kinetic model of redox chemistry in the lung epithelial lining fluid (KM-SUB-ELF) to study the production of ROS (including hydroxyl radical; • OH) from the inhalation of size-resolved PM (spanning eight size bins between 0.18 and 10 μm), ozone (O 3 ), and nitrogen dioxide (NO 2 ) at three sites located at different distances from roadways in Toronto. The highest ROS production was found at the site located next to a major highway, with particulate pollutants being the primary contributor. The total ROS production peaked in the PM accumulation mode at all sites (up to 41% associated with submicrometer PM), following closely the size distribution of trace metals, especially Cu. The • OH production was more site-specific; it peaked in the accumulation mode with highway traffic emissions, and in quasi-ultrafine (<0.18 μm) mode in areas with moderate traffic, following the trends of soluble Fe and PM (up to 60% associated with submicron PM). ROS production in the lung was also induced by gaseous oxidants. Ozone played the dominant role, particularly at sites with moderate traffic but high O 3 levels where up to 52% of ROS and 14% of • OH produced in the lung were attributed to inhaled O 3 . The results highlight the importance of traffic emissions, submicrometer PM, and gaseous oxidants in deriving the health effects of air pollutants in urban environments.
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Shahpoury et al. (2026) studied this question.
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