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Aim We explored the feasibility of a long‐term but low‐frequency psychological preventive intervention in a high school setting. Background High school students may experience depression; psychological interventions to improve social and cognitive skills may be useful to decrease such depression. A long‐term but low‐frequency intervention may be feasible in this setting because of its minimal time demands and lack of need for specialist human resources Design We conducted a single‐arm longitudinal descriptive study with an intervention applied six times over 2 years in one high school. Method We conducted a psychological preventive intervention with 94 high school students in one school for 2 years (April 2014 to March 2016). This intervention aimed to improve social and cognitive skills. We measured social skills, cognitive distortion, and depression five times during the 2‐year period, through a self‐report scale. Results/Findings Scores for maintaining relationship skills tended to increase over the 2 years. However, depression did not decrease over the intervention period. Conclusion Although our research did not include control conditions and the intervention did not decrease depression, the six‐session programme for high school adolescents improved an aspect of social skills that is a preventive factor against depression.

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Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon in the air, triggers pulmonary inflammation. This study focused on BaP-induced inflammation in the alveolar epithelium. A549 cells were stimulated with BaP for four days. BaP treatment markedly increased NLRP1 expression but slightly decreased NLRP3. Furthermore, aryl hydrocarbon receptor (AhR) knockdown displayed no increase in BaP-induced NLRP1 expression. Similar results were also observed by blocking reactive oxygen species (ROS), which is mediated through AhR, suggesting that the AhR-ROS axis operates in BaP-induced NLRP1 expression. p53 involvement in ROS-mediated NLRP1 induction has also been implied. When we confirmed inflammasome activation in cells treated with BaP for four days, while BaP transiently activated NLRP3, it predominantly activated the NLRP1 inflammasome. These findings have led to the conclusion that BaP could be a potential ligand for the NLRP1 inflammasome persistently observed in the lung epithelium. Our study may provide additional evidence for the sustained pulmonary inflammation caused by environmental air pollution.