Inflammation and the coagulation cascade are considered to be the potential mechanisms of ambient particulate matter (PM) exposure-induced adverse cardiovascular events. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-8 (IL-8), and fibrinogen are arguably the four most commonly assayed markers to reflect the relationships of PM with inflammation and blood coagulation. This review summarized and quantitatively analyzed the existing studies reporting short- and long-term associations of PM 2.5 (PM with an aerodynamic diameter ≤2.5 μm)/PM 10 (PM with an aerodynamic diameter≤10 μm) with important inflammation and blood coagulation markers (TNF-α, IL-6, IL-8, fibrinogen). We reviewed relevant studies published up to July 2020, using three English databases (PubMed, Web of Science, Embase) and two Chinese databases (Wang-Fang, China National Knowledge Infrastructure). The OHAT tool, with some modification, was applied to evaluate risk of bias. Meta-analyses were conducted with random-effects models for calculating the pooled estimate of markers. To assess the potential effect modifiers and the source of heterogeneity, we conducted subgroup analyses and meta-regression analyses where appropriate. The assessment and correction of publication bias were based on Begg’s and Egger’s test and “trim-and-fill” analysis. We identified 44 eligible studies. For short-term PM exposure, the percent change of a 10 μg/m 3 PM 2.5 increase on TNF-α and fibrinogen was 3.51% (95% confidence interval (CI): 1.21%, 5.81%) and 0.54% (95% confidence interval (CI): 0.21%, 0.86%) respectively. We also found a significant short-term association between PM 10 and fibrinogen (percent change = 0.17%, 95% CI: 0.04%, 0.29%). Overall analysis showed that long-term associations of fibrinogen with PM 2.5 and PM 10 were not significant. Subgroup analysis showed that long-term associations of fibrinogen with PM 2.5 and PM 10 were significant only found in studies conducted in Asia. Our findings support significant short-term associations of PM with TNF-α and fibrinogen. Future epidemiological studies should address the role long-term PM exposure plays in inflammation and blood coagulation markers level change.

Background Decreased heart rate variability (HRV) is a predictor of autonomic system dysfunction, and is considered as a potential mechanism of increased risk of cardiovascular disease (CVD) induced by exposure to particulate matter less than 2.5 μm in diameter (PM2.5). Previous studies have suggested that exposure to PM2.5 may lead to decreased HRV levels, but the results remain inconsistent. Methods An updated systematic review and meta-analysis of panel studies till November 1, 2019 was conducted to evaluate the acute effect of exposure to ambient PM2.5 on HRV. We searched electronic databases (PubMed, Web of Science, and Embase) to identify panel studies reporting the associations between exposure to PM2.5 and the four indicators of HRV (standard deviation of all normal-to-normal intervals (SDNN), root mean square of successive differences in adjacent normal-to-normal intervals (rMSSD), high frequency power (HF), and low frequency power (LF)). Random-effects model was used to calculate the pooled effect estimates. Results A total of 33 panel studies were included in our meta-analysis, with 16 studies conducted in North America, 12 studies in Asia, and 5 studies in Europe. The pooled results showed a 10 μg/m3 increase in PM2.5 exposure which was significantly associated with a − 0.92% change in SDNN (95% confidence intervals (95%CI) − 1.26%, − 0.59%), − 1.47% change in rMSSD (95%CI − 2.17%, − 0.77%), − 2.17% change in HF (95%CI − 3.24%, − 1.10%), and − 1.52% change in LF (95%CI − 2.50%, − 0.54%), respectively. Overall, subgroup analysis suggested that short-term exposure to PM2.5 was associated with lower HRV levels in Asians, healthy population, and those aged ≥ 40 years. Conclusion Short-term exposure to PM2.5 was associated with decreased HRV levels. Future studies are warranted to clarity the exact mechanism of exposure to PM2.5 on the cardiovascular system through disturbance of autonomic nervous function.

Leukemia is one of the most common cancers. We conducted this study to comprehensively analyze the temporal trends of leukemia mortality during 2003–2017 and project the trends until 2030. We extracted national-level data on annual leukemia mortality from China Health Statistics Yearbooks (2003–2017). We applied the Joinpoint regression model to assess leukemia mortality trends in urban and rural China by sex during 2003–2017. We also produced sex-specific leukemia mortality using the adjusted Global Burden Disease (GBD) 2016 projection model. In urban areas, age-standardized leukemia mortality decreased significantly among females during 2003–2017 (APC = −0.9%; 95% CI: −1.7, −0.1%). In rural areas, significant decreases of age-standardized leukemia mortality were both found among males (APC = −1.7%; 95% CI: −2.9, −0.5%) and females (APC = −1.6%; 95% CI: −2.6, −0.7%) from 2008 to 2017. Rural-urban and sex disparities of leukemia mortality will continue to exist until the year 2030. According to projection, the leukemia mortality rates of males and rural populations are higher than that of females and urban populations. In 2030, leukemia mortality is projected to decrease to 3.03/100,000 and 3.33/100,000 among the males in urban and rural areas, respectively. In females, leukemia mortality will decrease to 1.87/100,000 and 2.26/100,000 among urban and rural areas, respectively. Our study suggests that more precautionary measures to reduce leukemia mortality are need, and more attention should be paid to rural residents and males in primary prevention of leukemia in China.

Ferroptosis refers to a novel modality of regulated cell death characterized by excessive iron accumulation and overwhelming lipid peroxidation, which takes an important part in multiple pathological processes associated with cell death. Considering the crucial roles of the liver in iron and lipid metabolism and its predisposition to oxidative insults, more and more studies have been conducted to explore the relationship between ferroptosis and various liver disorders, including non-alcoholic fatty liver disease (NAFLD). With increased morbidity and high mortality rates, NAFLD has currently emerged as a global public health issue. However, the etiology of NAFLD is not fully understood. In recent years, an accumulating body of evidence have suggested that ferroptosis plays a pivotal role in the pathogenesis of NAFLD, but the precise mechanisms underlying how ferroptosis affects NAFLD still remain obscure. Here, we summarize the molecular mechanisms of ferroptosis and its complicated regulation systems, delineate the different effects that ferroptosis exerts in different stages of NAFLD, and discuss some potential effective therapies targeting ferroptosis for NAFLD treatment, which putatively points out a novel direction for NAFLD treatment.