Objectives: This study investigates the association between short-term exposure to air pollutants and panic attacks requiring emergency department (ED) visits. Methods: We identified 1926 patients who visited EDs in Seoul with panic attacks as the primary cause during the period from 2008 to 2014. We estimated short-term exposure to particles <2.5 μm (PM2.5), particles <10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO). We applied a time-stratified case-crossover study design and conducted a conditional logistic regression analysis to assess the association between air pollutants levels and ED visits due to panic attacks. Results: Increasing O3 concentration was significantly associated with an increased risk of panic attacks requiring ED visits (odds ratio: 1.15; 95% confidence interval: 1.04–1.27) on the same day of exposure. This association was robust to the sensitivity analysis using two pollutant models. Conclusion Our results show that short-term exposure to elevated O3 concentration is associated with the exacerbation of panic attacks. This finding strongly suggests the detrimental effects of O3 on major public health problems and provides insights for further research to investigate the causal associations between air pollution and poor mental health.

Objectives: This study investigates the association between short-term exposure to air pollutants and panic attacks requiring emergency department (ED) visits. Methods: We identified 1926 patients who visited EDs in Seoul with panic attacks as the primary cause during the period from 2008 to 2014. We estimated short-term exposure to particles <2.5 μm (PM2.5), particles <10 μm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), ozone (O3), and carbon monoxide (CO). We applied a time-stratified case-crossover study design and conducted a conditional logistic regression analysis to assess the association between air pollutants levels and ED visits due to panic attacks. Results: Increasing O3 concentration was significantly associated with an increased risk of panic attacks requiring ED visits (odds ratio: 1.15; 95% confidence interval: 1.04–1.27) on the same day of exposure. This association was robust to the sensitivity analysis using two pollutant models. Conclusion Our results show that short-term exposure to elevated O3 concentration is associated with the exacerbation of panic attacks. This finding strongly suggests the detrimental effects of O3 on major public health problems and provides insights for further research to investigate the causal associations between air pollution and poor mental health.

PURPOSE: This study evaluated the extent of damage due to hypothermia in the mature and immature brain. METHODS: Hippocampal tissue cultures at 7 and 14 days in vitro (DIV) were used to represent the immature and mature brain, respectively. The cultures were exposed at 25degrees C for 0, 10, 30, and 60 minutes (n=30 in each subgroup). Propidium iodide fluorescent images were captured 24 and 48 hours after hypothermic injury. Damaged areas of the cornu ammonis 1 (CA1), CA3, and dentate gyrus (DG) were measured using image analysis. RESULTS: At 7 DIV, the tissues exposed to cold injury for 60 minutes showed increased damage in CA1 (P<0.001) and CA3 (P=0.005) compared to the control group at 48 hours. Increased damage to DG was observed at 24 (P=0.008) and 48 hours (P=0.011). The 14 DIV tissues did not demonstrate any significant differences compared with the control group, except for the tissues exposed for 30 minutes in which DG showed less damage at 48 hours than the control group (P=0.048). In tissues at 7 DIV, CA1 (P=0.040) and DG (P=0.013) showed differences in the duration of cold exposure. CONCLUSION: The immature brain is more vulnerable to hypothermic injury than the mature brain.
Animals ; Brain ; Dentate Gyrus ; Hippocampus ; Hypothermia, Induced* ; Neurons* ; Propidium ; Rats*