The short-term effect of PM2.5/O3 on daily mortality from 2013 to 2018 in Hefei, China.

This research intends to explore the short-term impacts of PM2.5/O3 on daily death in Hefei from 2013 to 2018. Data on daily death of Hefei residents, meteorological factors, and air pollutants were collected from Jan 1, 2013, to Dec 31, 2018. The correlation between PM2.5/O3 and daily death in Hefei during the research period was studied by time series analysis. From 2013 to 2018, there were 61,683 non-accidental deaths, including 27,431 cardiovascular deaths, 5587 respiratory deaths, 20,921 malignant tumor deaths, and 1674 diabetes deaths, in Hefei. Annual mean concentrations of PM2.5, PM10, NO2, SO2, CO, and O3 in Hefei were 66.18, 92.37, 39.75, 15.39, 930, and 79.08 µg m-3, respectively. An increase of 10 µg m-3 in PM2.5 was related with 0.53% (95% CI 0.31-0.75%), 0.93% (95% CI 0.60-1.26%), 0.90% and (95% CI 0.23-1.57%) increase in non-accidental, cardiovascular and respiratory diseases mortality, respectively. The association between ozone and mortality was not significant. In cold seasons, PM2.5 had a stronger effect on the deaths resulting from non-accidental, cardiovascular, and respiratory diseases. The effect of O3 on deaths was not significantly different between the cold season and the warm season. Women and the elders (over 65 years) were at high risk of being affected by PM2.5/O3. Short-term exposure to PM2.5 was positively correlated with increased deaths due to non-accidental, cardiovascular and respiratory diseases in Hefei. Females and elders were more vulnerable to PM2.5/O3 exposure. No significant associations were observed between ozone and deaths from non-accidental, cardiovascular, respiratory, malignant tumors, and diabetes diseases.

Associations of ambient PM2.5 and O3 with cardiovascular mortality: a time-series study in Hefei, China.

China is among the countries with the worst air quality throughout the world. As PM2.5 was not included in the national air quality monitoring network before January 2013 in China, no study has investigated the associations of ambient PM2.5 and O3 with cardiovascular mortality in Hefei, China. In this time-series analysis, Poisson regression in generalized additive model was adopted to assess the associations between the air pollutants and cardiovascular mortality during the 2013-2015 in Hefei, China. The findings showed that the daily average level of PM2.5 and O3 was 77.8 µg/m3 and 60.1 µg/m3 in the study period, respectively. PM2.5 and O3 exposure tended to increase cardiovascular mortality, but the associations were statistically insignificant. Further stratified analyses by seasons showed that with every 10 µg/m3 increase of PM2.5 in the cold season (October-March), the risk of cardiovascular death increased by 0.22% (95% CI 0.05%, 0.39%); while every 10 µg/m3 increase of O3 in the warm season (April-September), the risk of cardiovascular death increased by 1.29% (95% CI 0.26%, 2.33%) on Lag0. Interestingly, stratified analysis by gender showed that the associations of PM2.5, but not O3 exposure, could significantly increase cardiovascular mortality in females, but not males. The findings of this study especially underscored the adverse associations of PM2.5 and O3 exposure with females in specific seasons. More studies are needed to verify our findings and further investigate the underlying mechanisms. Graphical Abstract.

Effects of cooking oil fume derived fine particulate matter on blood vessel formation through the VEGF/VEGFR2/MEK1/2/ERK1/2/mTOR pathway in human umbilical vein endothelial cells.

In China, cooking oil fume derived fine particulate matter (COF-derived PM2.5) is a principal source of indoor air pollution. Here, we investigated cytotoxicity of COF-derived PM2.5, as well as the roles of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR cascade in the inhibitory effects of COF-derived PM2.5, on angiogenesis in human umbilical vein endothelial cells (HUVECs). After exposure to COF-derived PM2.5, cell viability and tube formation, as well as protein and mRNA levels of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR in HUVECs were measured. Cell viability and number of tubes reduced dose-dependently after COF-derived PM2.5 and SU5416 treatment. In addition, SU5416 and VEGF significantly affected tube formation. The protein and mRNA levels of VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR all tended to reduce with the increase of COF-derived PM2.5 concentrations. These findings demonstrate that VEGF, VEGFR2, MEK1/2, ERK1/2, and mTOR play key roles in COF-derived PM2.5 induced inhibition of angiogenesis in HUVECs.

The effects of cooking oil fumes-derived PM2.5 on blood vessel formation through ROS-mediated NLRP3 inflammasome pathway in human umbilical vein endothelial cells.

BACKGROUND: Cooking oil fumes (COFs), a main pollutant in kitchen air, is a major risk to human health. In our previous research, exposure to COFs-derived PM2.5 could cause umbilical vascular endothelial dysfunction, leading to decreased fetal weight. Here, to test the role of ROS-mediated NLRP3 inflammasome pathway in blood vessel formation of human umbilical vein endothelial cells (HUVECs) caused by COFs-derived PM2.5, the cells were exposed to COFs-derived PM2.5 at different concentrations with and without N-acetyl-L-cysteine (NAC). METHODS: MTT assay was used to determine HUVECs viability. Intracellular ROS and mitochondrial ROS levels were assessed with DCFH-DA and MitoSOX™ assay. The levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway and VEGF were measured by western blot and real-time PCR (RT-PCR). Tube formation in HUVECs was detected by tube formation assay. RESULTS: The results revealed that COFs-derived PM2.5 exposure reduced HUVECs viability, increased the intracellular and mitochondrial ROS levels in cells, and up-regulated the levels of proteins and mRNA involved in NLRP3 inflammasome signaling pathway. However, the protein and mRNA expression of VEGF were reduced with the increasing exposure concentrations. In addition, COFs-derived PM2.5 also affected the tube formation. However, co-incubation with NAC effectively rescued the damages caused by COFs-derived PM2.5 exposure. CONCLUSIONS: This study proved that COFs-derived PM2.5 could significantly reduce HUVECs viability, induce the overproduction of ROS, lead to inflammation and inhibit VEGF expression, thus affect angiogenesis of HUVECs in vitro. It was revealed that the impact caused by COFs-derived PM2.5 on blood vessel formation through a ROS-mediated NLRP3 inflammasome pathway.

The short-term effects of air pollution on respiratory diseases and lung cancer mortality in Hefei: A time-series analysis.

Accumulating evidence has shown the effects of air pollution on respiratory disease and lung cancer mortality, but the evidence is still inconclusive to date. We conducted a time-series analysis, which included 10388 subjects, to assess the short-term effects of air pollution on respiratory disease and lung cancer mortality in Hefei, China, from 2009 to 2015. The mean concentrations of pollutants (PM10, NO2 and SO2) were 106.35, 30.40, and 20.66 µg/m3, respectively, during the study period. An increase of 10 µg/m3 in SO2, NO2, and PM10 was associated with 7.69% (95%CI: 3.41%-12.15%), 4.38% (95%CI: 1.33%-7.53%), and 1.55% (95%CI: 0.80%-2.30%) increase of respiratory diseases mortality, respectively. In contrast, lung cancer mortality was only significantly associated with SO2 level. Subgroup analyses showed that female in respiratory disease patients were more sensitive to air pollution than male. Studies about seasonality of pollutants on respiratory and lung cancer mortality were inconsistent. Further analyses with multiple-pollutant model showed that the effects of pollutants were generally decreased after the other pollutants were adjusted, except the effects of SO2 on lung cancer. These findings demonstrated that air pollution could evidently increase the respiratory disease and lung cancer mortality.

Association between air pollution and cardiovascular mortality in Hefei, China: A time-series analysis.

In recent years, air pollution has become an alarming problem in China. However, evidence on the effects of air pollution on cardiovascular mortality is still not conclusive to date. This research aimed to assess the short-term effects of air pollution on cardiovascular morbidity in Hefei, China. Data of air pollution, cardiovascular mortality, and meteorological characteristics in Hefei between 2010 and 2015 were collected. Time-series analysis in generalized additive model was applied to evaluate the association between air pollution and daily cardiovascular mortality. During the study period, the annual average concentration of PM10, SO2, and NO2 was 105.91, 20.58, and 30.93 µg/m3, respectively. 21,816 people (including 11,876 man, and 14,494 people over 75 years of age) died of cardiovascular diseases. In single pollutant model, the effects of multi-day exposure were greater than single-day exposure of the air pollution. For every increase of 10 µg/m3 in SO2, NO2, and PM10 levels, CVD mortality increased by 5.26% (95%CI: 3.31%-7.23%), 2.71% (95%CI: 1.23%-4.22%), and 0.68% (95%CI: 0.33%-1.04%) at a lag03, respectively. The multi-pollutant models showed that PM10 and SO2 remained associated with CVD mortality, although the effect estimates attenuated. However, the effect of NO2 on CVD mortality decreased to statistically insignificant. Subgroup analyses further showed that women were more vulnerable than man upon air pollution exposure. These findings showed that air pollution could significantly increase the CVD mortality.