Connecting the Oxidative Potential of Secondary Organic Aerosols with Reactive Oxygen Species in Exposed Lung Cells.

It has been hypothesized that the cytotoxicity of secondary organic aerosols (SOA) is mediated through the formation of reactive oxygen species (ROS) in the exposed cells. Here, lung epithelial cells (A549) residing at the air-liquid interface were exposed to proxies of anthropogenic and biogenic SOA that were photochemically aged under varying nitrogen oxide (NOx) concentrations in an oxidation flow reactor. The total organic peroxides and ROS radical content in the SOA were quantified by the iodometric spectrophotometric method and by continuous-wave electron paramagnetic resonance. The effect of the exposure was evaluated by measuring cell viability and cellular ROS production following the exposure. The results demonstrate that SOA that aged in the absence of NOx contained more ROS than fresh SOA and were more toxic toward the cells, while varying NOx conditions had no significant influence on levels of the ROS content in fresh SOA and their toxicity. Analysis of ROS in the exposed cells using flow cytometry showed a similar trend with the total ROS content in the SOA. This study provides a first and direct observation of such association.

Aqueous and organic extract of PM2.5 collected in different seasons and cities of Japan differently affect respiratory and immune systems.

Particulate matter with diameters <2.5 µm (i.e., PM2.5) has multiple natural and anthropological sources. The association between PM2.5 and the exacerbation of respiratory allergy and asthma has been well studied, but the components of PM2.5 that are responsible for allergies have not yet been determined. Here, we elucidated the effects of aqueous and organic extract of PM2.5 collected during four seasons in November 2014-December 2015 in two cities (Kawasaki, an industrial area and Fukuoka, an urban area affected by transboundary pollution matter) of Japan on respiratory health. Ambient PM2.5 was collected by high-volume air samplers and extracted into water soluble and lipid soluble components. Human airway epithelial cells, murine bone marrow-derived antigen-presenting cells (APC) and splenocytes were exposed to PM2.5 extracts. We measured the cell viability and release of interleukin (IL)-6 and IL-8 from airway epithelial cells, the DEC205 and CD86 expressions on APCs and cell proliferation, and TCR and CD19 expression on splenocytes. The water-soluble or aqueous extracts, especially those from Kawasaki in fall, had a greater cytotoxic effect than the lipid-soluble or organic extracts in airway epithelial cells, but they caused almost no pro-inflammatory response. Extract of fall, especially the aqueous extract from Fukuoka, increased the DEC205 and CD86 expressions on APC. Moreover, aqueous extracts of fall, summer, and spring from Fukuoka significantly increased proliferation of splenocytes. Organic extract of spring and summer from Kawasaki significantly elevated the TCR expression, and organic extract of summer from Kawasaki decreased the CD19 expression. These results suggest that PM2.5 extract samples are responsible for cytotoxicity in airway epithelial cells and for activating APCs and T-cells, which can contribute to the exacerbation of respiratory diseases such as asthma. These effects can differ by PM2.5 components, collection areas and seasons.

Synergic effects of 9,10-phenanthrenequinone and cadmium on pro-inflammatory responses in airway epithelial cells.

We investigated the synergic effects of components of particulate matter with aerodynamic diameters ≤2.5µm (PM2.5) on airway inflammation. Co-exposure to cadmium (Cd) and 9,10-phenanthrenequinone (9,10-PQ) additively/synergistically increased pro-inflammatory responses in airway epithelial cells, whereas co-exposure to Cd and phenanthrene resulted in no acceleration. These results suggest that the combination of metal and a quinone derivative can contribute to the exacerbation of respiratory diseases by PM2.5.