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BACKGROUND@#Air pollutants and their pathogenic effects differ among regions and seasons. We aimed to explore the relationship between fine particulate matter (PM2.5), sulfur dioxide (SO2), and ozone-8 hours (O3-8h) concentrations in heating and non-heating seasons and the associated death risk due to cardiovascular diseases (CDs), respiratory diseases (RDs), and malignant tumors.@*METHODS@#Data were collected in Shenyang, China, from April 2013 to March 2016. We analyzed the correlation or lagged effect of atmospheric pollutant concentration, meteorological conditions, and death risk due to disorders of the circulatory system, respiratory system, and malignant tumor in heating and non-heating seasons. We also used multivariate models to analyze the association of air pollutants during holidays with the death risk due to the evaluated diseases while considering the presence or absence of meteorological factors.@*RESULTS@#An increase in the daily average SO2 concentration by 10 μg/m increased the death risk by CDs, which reached a maximum of 2.0% (95% confidence interval [CI]: 1.3%-2.7%) on lagging day 4 during the non-heating season and 0.2% (95% CI: 0.1%-0.4%) on lagging day 3 during the heating season. The risk of death caused by RDs peaked on lagging day 1 by 0.8% (95% CI: 0.4%-1.2%) during the heating season. An increase in O3-8h concentration by 10 μg/m increased the risk of RD-related death on lagging day 2 by 1.0% (95% CI: 0.4%-1.7%) during the non-heating season, which was significantly higher than the 0.1% (95% CI: 0-0.9%) increase during the heating season. Further, an increase in the daily average PM2.5 concentration by 10 μg/m increased the risk of death caused by RDs by 0.3% and 0.8% during heating and non-heating seasons, respectively, which peaked on lagging day 0. However, air pollution was not significantly associated with the risk of death caused by malignant tumors.@*CONCLUSION@#Short-term exposure to PM2.5, SO2, and O3 during the non-heating season resulted in higher risks of CD-related death, followed by RD-related death.
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Background@#Air pollutants and their pathogenic effects differ among regions and seasons. We aimed to explore the relationship between fine particulate matter (PM2.5), sulfur dioxide (SO2), and ozone-8 hours (O3-8h) concentrations in heating and non-heating seasons and the associated death risk due to cardiovascular diseases (CDs), respiratory diseases (RDs), and malignant tumors.@*Methods@#Data were collected in Shenyang, China, from April 2013 to March 2016. We analyzed the correlation or lagged effect of atmospheric pollutant concentration, meteorological conditions, and death risk due to disorders of the circulatory system, respiratory system, and malignant tumor in heating and non-heating seasons. We also used multivariate models to analyze the association of air pollutants during holidays with the death risk due to the evaluated diseases while considering the presence or absence of meteorological factors.@*Results@#An increase in the daily average SO2 concentration by 10 μg/m3 increased the death risk by CDs, which reached a maximum of 2.0% (95% confidence interval [CI]: 1.3%–2.7%) on lagging day 4 during the non-heating season and 0.2% (95% CI: 0.1%-0.4%) on lagging day 3 during the heating season. The risk of death caused by RDs peaked on lagging day 1 by 0.8% (95% CI: 0.4%–1.2%) during the heating season. An increase in O3-8h concentration by 10 μg/m3 increased the risk of RD-related death on lagging day 2 by 1.0% (95% CI: 0.4%–1.7%) during the non-heating season, which was significantly higher than the 0.1% (95% CI: 0–0.9%) increase during the heating season. Further, an increase in the daily average PM2.5 concentration by 10 μg/m3 increased the risk of death caused by RDs by 0.3% and 0.8% during heating and non-heating seasons, respectively, which peaked on lagging day 0. However, air pollution was not significantly associated with the risk of death caused by malignant tumors.@*Conclusion@#Short-term exposure to PM2.5, SO2, and O3 during the non-heating season resulted in higher risks of CD-related death, followed by RD-related death.
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<p><b>OBJECTIVE</b>To study endothelial damage by observing changes of circulating endothelial cells (CECs) in blood, coagulation and fibrinolysis index in patients with acute respiratory distress syndrome.</p><p><b>METHODS</b>CECs were separated by isopycnic centrifugation method in 14 patients with acute lung injury (ALI), 7 patients with acute respiratory distress syndrome (ARDS), 10 intensive care unit (ICU) controls, and 15 healthy controls. Plasma prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FG), fibrin degradation products (FDP), and D-dimer were examined simultaneously. Acute physiology and chronic health evaluation (APACHE) II and lung injury score (LIS) were recorded to evaluate severity of illness and lung injury.</p><p><b>RESULTS</b>(1) The number of CECs in ALI (10.4 +/- 2.3) and ARDS groups (16.1 +/- 2.7) was higher than that in the healthy (1.9 +/- 0.5) (P < 0.01). In both ALI and ARDS, the number of CECs correlated with APACHE II (r = 0.55, P < 0.05 and r = 0.62, P < 0.05, respectively) and LIS (r = 0.60, P < 0.05 and r = 0.53, P < 0.05, respectively). CEC number was negatively correlated with PaO2 in ALI and ARDS (r = -0.49, P < 0.05 and r = -0.64, P < 0.05, respectively). (2) The level of FDP and D-dimer were higher in ALI and ARDS patients than that in ICU and healthy control groups (P < 0.05). The level of FG in ARDS group was significantly higher than in the ICU and healthy control groups (P < 0.05). But in ALI group, the level of FG was significantly higher than only healthy control group (P < 0.05).</p><p><b>CONCLUSIONS</b>Endothelial cell damage occurs in ARDS patients, which may play a major role in the pathophysiology of ARDS. Changes of endothelial cell activation and damage markers, such as CECs, plasma coagulation and fibrinolysis index, to some extent reflect severity of illness and lung injury in ARDS.</p>