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Background: There is a well-documented empirical relationship between lipoprotein (a) [Lp(a)] and cardiovascular disease (CVD); however, causal evidence, especially from the Chinese population, is lacking. Therefore, this study aims to estimate the causal association between variants in genes affecting Lp(a) concentrations and CVD in people of Han Chinese ethnicity. Methods: Two-sample Mendelian randomization analysis was used to assess the causal effect of Lp(a) concentrations on the risk of CVD. Summary statistics for Lp(a) variants were obtained from 1256 individuals in the Cohort Study on Chronic Disease of Communities Natural Population in Beijing, Tianjin and Hebei. Data on associations between single-nucleotide polymorphisms (SNPs) and CVD were obtained from recently published genome-wide association studies. Results: Thirteen SNPs associated with Lp(a) levels in the Han Chinese population were used as instrumental variables. Genetically elevated Lp(a) was inversely associated with the risk of atrial fibrillation [odds ratio (OR), 0.94; 95% confidence interval (95%CI), 0.901–0.987; P = 0.012)], the risk of arrhythmia (OR, 0.96; 95%CI, 0.941–0.990; P = 0.005), the left ventricular mass index (OR, 0.97; 95%CI, 0.949–1.000; P = 0.048), and the left ventricular internal dimension in diastole (OR, 0.97; 95%CI, 0.950–0.997; P = 0.028) according to the inverse-variance weighted method. No significant association was observed for congestive heart failure (OR, 0.99; 95% CI, 0.950–1.038; P = 0.766), ischemic stroke (OR, 1.01; 95%CI, 0.981–1.046; P = 0.422), and left ventricular internal dimension in systole (OR, 0.98; 95%CI, 0.960–1.009; P = 0.214). Conclusions: This study provided evidence that genetically elevated Lp(a) was inversely associated with atrial fibrillation, arrhythmia, the left ventricular mass index and the left ventricular internal dimension in diastole, but not with congestive heart failure, ischemic stroke, and the left ventricular internal dimension in systole in the Han Chinese population. Further research is needed to identify the mechanism underlying these results and determine whether genetically elevated Lp(a) increases the risk of coronary heart disease or other CVD subtypes. [ABSTRACT FROM AUTHOR]

Background Large-scale epidemiological surveys focusing on characteristic differences in psychological and physical health conditions in Chinese adults are lacking. Objective To investigate the association of noncommunicable chronic diseases (NCDs) with depression, anxiety and stress in the Chinese general population. Methods A total of 13784 participants were recruited from the baseline survey of the Cohort Study on Chronic Disease of Communities Natural Population in Beijing, Tianjin and Hebei (CHCN-BTH) from 2017 to 2019. Sociodemographic characteristics, lifestyle and NCDs were assessed via questionnaire. Stress, anxiety and depression were assessed by the Depression-Anxiety-Stress Scale (DASS-21). The relationship of NCDs with psychological symptoms was determined through logistic regression analysis. Results Multivariate logistic regression analysis revealed that the prevalence of stress (OR = 1.640; 95% CI: 1.381-1.949), anxiety (OR = 1.654; 95% CI: 1.490-1.837) and depression (OR = 1.460; 95% CI: 1.286-1.658) symptoms were all significantly higher in patients with NCDs. Multimorbidities were associated with a higher risk of stress (OR = 2.310; 95% CI: 1.820-2.931), anxiety (OR = 2.119; 95% CI: 1.844-2.436) and depression (OR = 2.785; 95% CI: 1.499-2.126) than single NCDs. A course of disease within 1 year or more than 5 years also was associated with a higher risk. Limitations The cross-sectional design could not examine the causal link between psychological symptoms and NCDs. Conclusion Psychological symptoms were more prevalent among individuals with NCDs in the Chinese general population. This study suggests that more attention should be paid to the mental health problems of patients with NCDs. [ABSTRACT FROM AUTHOR]

• Benefits of indoor air filtration during air pollution wave is unclear. • Exploring the effects of PM 2.5 on both inflammation and DNA methylation (DNAm). • Air filtration attenuated PM 2.5 's adverse effects by changing cytokines and DNAm. Benefits of indoor air filtration in heavily polluted areas are not fully understood. This study aims to examine whether short-term air filtration intervention could attenuate the hazards from acute exposure to fine particulate matter (PM 2.5), and investigate the potential impact on inflammatory cytokines and DNA methylation. A randomized, double-blind crossover trial of true or sham indoor air filtration was conducted among 29 healthy young adults in Beijing, China. Each episode covered a typical air pollution wave, and 38 cytokines and DNAm of 20 genes were measured at 3 time points: pre-smog, during smog, and post-smog. Linear mixed-effect models were used to evaluate the associations. The indoor PM 2.5 concentration with true filtration was 67.8 % lower than sham filtration (13.8 μg/m3 vs. 42.8 μg/m3). Air filtration was significantly associated with the decreases in 9 cytokines, from 6.61 % to 21.24 %. PM 2.5 exposure was significantly associated with elevated levels of 9 cytokines and changed methylation at 7 CpG sites. Notably, PM 2.5 was significantly associated with GM-CSF, sCD40L, MCP-1, and FGF-2, as well as methylation in corresponding genes, but no mediation effect was observed. This trial suggested that indoor air filtration might attenuate the adverse effects of PM 2.5 exposure through changing cytokines and DNAm. [ABSTRACT FROM AUTHOR]

• Long-term air pollutant exposures may contribute to cardiac conduction abnormalities. • PM 2.5 may be the most stable pollutant reflecting the associations. • People with specific characteristics are more susceptible to the adverse effects. Evidence regarding the effects of long-term and high-level ambient air pollution exposure on cardiac conduction systems remains sparse. To investigate the associations of long-term exposure to air pollution and cardiac conduction abnormalities in Chinese adults and explore the susceptibility characteristics. In 2017, a total of 27,047 participants aged 18–80 years were recruited from the baseline survey of the Cohort Study on Chronic Disease of Communities Natural Population in Beijing, Tianjin and Hebei (CHCN-BTH). The three year (2014–2016) average pollutant concentrations were assessed by a spatial statistical model for PM 2.5 and air monitoring stations for PM 10 , SO 2 , NO 2 , O 3 and CO. Residential proximity to a roadway was calculated by neighborhood analysis. Associations were estimated by two-level generalized linear mixed models. Stratified analyses related to demographic characteristics, health behaviors, and cardiometabolic risk factors were performed. Two-pollutant models were used to evaluate the possible role of single pollutants. We detected significant associations of long-term air pollutant exposure with increased heart rate (HR), QRS and QTc, such that an interquartile range increase in PM 2.5 was associated with 3.63% (95% CI: 3.07%, 4.19%), 1.21% (95% CI: 0.83%, 1.60%), and 0.13% (95% CI: 0.07%, 0.18%) changes in HR, QRS and QTc, respectively. Compared to the other pollutants, the estimates of PM 2.5 remained the most stable across all two-pollutant models. Similarly, significant associations were observed between living closer to a major roadway and higher HR, QRS and QTc. Stratified analyses showed generally greater association estimates in older people, males, smokers, alcohol drinkers, and those with obesity, hypertension and diabetes. Long-term exposure to ambient air pollution was associated with cardiac conduction abnormalities in Chinese adults, especially in older people, males, smokers, alcohol drinkers, and those with cardiometabolic risk factors. PM 2.5 may be the most stable pollutant to reflect the associations. [ABSTRACT FROM AUTHOR]

Previous studies have mainly focused on the associations between particulate matters and infant mortality. However, evidence regarding the associations between gaseous pollutants and mortality among children aged <5 years remains sparse. The aim of this study was to investigate the associations between ambient air pollution and death among children aged <5 years in Beijing, China, and explore the impact of age, gender and specific causes of death on these associations. Concentrations of ambient air pollution and the number of deaths among children aged <5 years in Beijing from January 2014 to September 2016 were extracted from authoritative electronic databases. The associations were estimated for a single-month lag from the current month up to the previous 5 months (lag0-lag5) and moving averages of the current and previous months (lag01-lag05) using generalized additive Poisson regression (adjusted for time trends, season, meteorological variables and holidays). Subgroup analyses related to age, gender and specific diseases were performed. Two-pollutant models were used to evaluate the possible role of single pollutants. Sulfur dioxide (SO 2), nitrogen dioxide (NO 2) and carbon monoxide (CO) demonstrated the strongest associations with death among children aged <5 years at lag0, and the estimates decreased or even turned negative with the increasing lag periods. For an interquartile range increase in SO 2 , NO 2 and CO at lag0, the odds ratios (OR) were 1.332 (95% CI 1.152-1.539), 1.383 (95% CI 1.113-1.718) and 1.273 (95% CI 1.028-1.575). However, CO lost significance after adjusting for SO 2 and NO 2 , and PM 2.5 gained significance (OR 1.548, 95% CI 1.061-2.258) after adjusting for PM 10. The ORs for SO 2 and NO 2 remained the most stable across all two-pollutant models. The associations for children aged 1–5 years were stronger than those reported for infants at lag0 but lower at the other lag months. The pollutant associations were stronger for congenital heart disease-related death than overall and pneumonia-related death. We did not find significant differences in terms of gender. Exposure to air pollution may increase the incidence of death among children aged <5 years. SO 2 and NO 2 may be the most stable pollutants reflecting associations between air pollution and death, deserving further attention. Children with congenital heart diseases are more susceptible to air pollution. Therefore, it is urgent to implement the clean air targets established by WHO and reduce the exposure of children to air pollution. • Exposure to ambient air pollution may account for increased deaths among children aged <5 years in Beijing, China. • SO 2 and NO 2 may be the most stable pollutants reflecting the associations of death, deserving further attention. • Children with congenital heart diseases are more susceptible to air pollution. [ABSTRACT FROM AUTHOR]