MiR-582-3p participates in the regulation of biological behaviors of A549 cells by ambient PM2.5 exposure.

Ambient fine particulate matter (PM2.5) is one of the main environmental air pollutants that is closely related to the development of lung cancer, but the mechanisms are unclear. In this study, A549 cells were exposed to ambient PM2.5 to investigate the alterations of biological behaviors, and the possible role of miR-582-3p in the effects was further explored. The findings showed that PM2.5 exposure could significantly enhance the biological behaviors of A549 cells, and promote their epithelial-mesenchymal transition (EMT) transformation, especially at relatively low doses. Over-activation of Wnt/ß-catenin signaling pathway and increased expression of miR-582-3p were also found in A549 cells after PM2.5 exposure. After the knockdown of miR-582-3p in A549 cells, the effects of PM2.5 on malignant biological behavior changes, EMT, and the activation of Wnt/ß-catenin signaling pathway were all significantly alleviated. Furthermore, the inhibition of Wnt/ß-catenin signaling pathway also inhibited the EMT process of A549 cells, which was rescued by the overexpression of miR-582-3p. Therefore, this study showed that ambient PM2.5 can upregulate the expression of miR-582-3p, consequently activate the Wnt/ß-catenin signaling pathway, and thereby enhance EMT transformation and promote the malignant biological behaviors of A549 cells. These findings provide evidence for further research into the mechanisms by which exposure to PM2.5 in the environment promotes lung cancer.

Association between preconceptional air pollution exposure and medical purposes for selective termination of pregnancy.

BACKGROUND: Exposure to air pollutants is associated with adverse pregnancy outcomes. But evidence on the effects of preconceptional air pollution exposure on the risk of termination of pregnancy (TOP) caused by pregnancy losses and congenital malformations is lacking. METHODS: The distributed lag nonlinear model (DLNM) was used to evaluate the impact of short-term air pollutants exposure on the risk of TOP. Stratified analyses by age (<35 years old, ≥ 35 years old) and season (warm season, cold season) were further conducted. Relative risk (RR) and 95 % confidential interval (95 % CI) were calculated for per interquartile range (IQR) increment in air pollutants during the study period. RESULTS: PM2.5, PM10, and O3 exposure were significantly associated with elevated risk of TOP. The risk of TOP was associated with PM2.5 exposure from lag11 to lag15 in the single-pollutant model, and the strongest association was observed at lag13 (RR = 1.021, 95%CI:1.002-1.040). PM10 exposure from lag10 to lag15 was associated with increased TOP risk, with the corresponding peak association being at lag13 (RR = 1.020, 95%CI: 1.004-1.037). For O3, the single-day lag association appeared to be statistically significant from lag26 to lag27, with the highest RR of TOP cases being at lag27 (RR = 1.044, 95%CI: 1.005-1.084). Similar results were observed for pregnancy losses (PL). However, no significantly association between air pollution exposure and the risk of congenital malformations (CM) was found in this study. Stratified analyses showed that pregnant women with more advanced ages were more susceptible to PM2.5, PM10, and O3 exposure. The effect of PM2.5 exposure was statistically significant in cold season subgroups. CONCLUSION: The findings suggest that exposure to PM2.5, PM10, and O3 before pregnancy are associated with the risk of TOP in Lu'an, China, reflecting the significance of preconceptional environmental exposure in the development of adverse pregnancy outcomes.

Associations between air pollution exposure and birth defects: a time series analysis.

Air pollution is a serious environmental problem in China. Birth defects are particularly vulnerable to outdoor air pollution. Our study was to evaluate the association between short-term exposure to air pollutants and the risk of birth defects. Daily data including the air pollutants, meteorological characteristics, and birth records were obtained in Hefei, China, during January 2013 to December 2016. The findings showed that PM2.5, PM10, SO2, NO2, and O3 exposures were positively correlated with the risk of birth defects. Maternal exposure to PM2.5 and SO2 during the 4th to 13th gestational weeks was observed to have a significant association with the risk of birth defects, with the maximum effect in the 7th or 8th week for PM2.5 and the maximum effect in the 7th week for SO2. The positively significant exposure windows were the 4th to 14th weeks for PM10, the 4th to 12th weeks for NO2, and the 26th to 35th weeks for O3, respectively. The strongest associations were observed in the 8th week for PM10, the 7th week for NO2, and in the 31st or 32nd week for O3. The findings of this study demonstrate that air pollutants increase the risk of birth defects among women during pregnancy in Hefei, China, which provide evidence for improving the health of pregnant women and neonates in developing countries, and uncovered potential opportunities to reduce or prevent birth defects by proactive measures during pregnancy.

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 between weekly air pollution exposure and congenital heart disease.

BACKGROUND: The topic of congenital heart diseases (CHDs) has attracted more and more attentions. Accumulating evidence suggests that exposure to air pollutants during pregnancy is associated with CHDs, yet the results are inconsistent and study about weekly exposure is few. Our study evaluated the association between weekly air pollution and CHDs in Hefei, China. MATERIALS AND METHODS: Daily CHDs admission data were obtained from eight hospitals in Hefei from October 2015 to September 2017. Meteorological data and air quality were collected from China Meteorological Data Network. Distributed lag nonlinear model (DLNM) considering both the lag effect of exposure factors and the nonlinear relationship of exposure-reaction was used to assess the effect of weekly air pollutants exposure on CHDs admission. RESULTS: During the study period, totally 47,046 cases of perinatal infants were recruited, and the incidence of CHDs was 9.71 per thousand. The findings showed PM2.5, PM10, SO2 and NO2 significantly increased the risk of CHDs. Each 10 µg/m3 increase in PM2.5 during gestational weeks 20-26 increased the risk of CHDs. The susceptibility windows of PM10 (weeks 0-2 and weeks 25-29 of pregnancy), SO2 (weeks 8-16 and weeks 29-38) and NO2 (week 40), while the strongest effects of these 4 pollutants on CHDs were observed in week 22 (RR = 1.034, 95% CI: 1.007-1.062), week 0 (RR = 1.081, 95% CI: 1.02-1.146), week 37 (RR = 1.528, 95% CI: 1.085-2.153) and week 40 (RR = 1.171, 95% CI: 1.006-1.364), respectively. CONCLUSIONS: Air pollutants (SO2, NO2, PM10, and PM2.5) exposure could increase the risk of CHDs, while the most crucial susceptibility windows for the exposure were mainly in the second and third trimesters. Boys seemed to be more sensitive to air pollution. Our study contributes to the knowledge of the association between maternal exposure to air pollution and CHDs, but the associations need to be verified by further studies.

Toxicity of cooking oil fume derived particulate matter: Vitamin D3 protects tubule formation activation in human umbilical vein endothelial cells.

Cooking oil fumes-derived PM2.5 (COFs-derived PM2.5) is the main source of indoor pollution. Exposure to COFs-derived PM2.5 can cause oxidative stress and affect angiogenesis. Here we investigated the roles of vitamin D3 (VD3) in protecting tubule formation injury induced by COFs-derived PM2.5, and the roles of ROS/NLRP3/VEGF signaling pathway in the effects. Human umbilical vein endothelial cells (HUVECs) were exposed to 0 (1‰ DMSO), 1000 nmol/l VD3, 100 µg/ml PM2.5, and 1000 nmol/l VD3 + 100 µg/ml PM2.5, respectively. Cell viability and tube formation, as well as protein and mRNA levels were measured. The results showed that exposure of COFs-derived PM2.5 dose-and time-dependently reduced the viability of HUVECs, increased the levels of mitochondrial and intracellular ROS, and changed the mitochondrial membrane potential level. While co-incubation with VD3 rescued these adverse effects. Both Western blot and real-time PCR (RT-PCR) showed that the expressions of NLRP3, caspase-1, Interleukin (IL)-1ß, and IL-18 in COFs-derived PM2.5 exposure group increased significantly, which could be effectively decreased by co-incubation with VD3. COFs-derived PM2.5 exposure could also reduce the expression of VEGF, while co-incubating HUVECs with VD3 evidently up-regulated the protein level of VEGF in HUVECs. In addition, COFs-derived PM2.5 could also inhibit the tube formation of HUVECs in vitro, which could be effectively rescued by the co-incubation of VD3. Our study proved that COFs-derived PM2.5 could damage the tubule formation of HUVECs in vitro, which could be effectively rescue by co-incubation with VD3, in which processes the ROS/NLRP3/VEGF signaling pathway played a crucial role. It provides a new theoretical basis for further study on the toxicity of PM2.5 to umbilical cord blood vessels.

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.