Background: Exposure to air pollution is associated with chronic obstructive pulmonary disease (COPD). However, findings on the effects of air pollution on lung function and systemic inflammation in Chinese COPD patients are inconsistent and scarce. This study aims to evaluate the effects of ambient air pollution on lung function parameters and serum cytokine levels in a COPD cohort in Beijing, China. Methods: We enrolled COPD participants on a rolling basis from December 2015 to September 2017 in Beijing, China. Follow-ups were performed every 3 months for each participant. Serum levels of 20 cytokines were detected every 6 months. Hourly ambient pollutant levels over the same periods were obtained from 35 monitoring stations across Beijing. Geocoded residential addresses of the participants were used to estimate daily mean pollution exposures. A linear mixed-effect model was applied to explore the effects of air pollutants on health in the first-year of follow-up. Results: A total of 84 COPD patients were enrolled at baseline. Of those, 75 COPD patients completed the first-year of follow-up. We found adverse cumulative effects of particulate matter less than 2.5 μm in aerodynamic diameter (PM_2.5), nitrogen dioxide (NO₂), sulfur dioxide (SO₂) and carbon monoxide (CO) on the forced vital capacity % predicted (FVC % pred) in patients with COPD. Further analyses illustrated that among COPD patients, air pollution exposure was associated with reduced levels of serum eotaxin, interleukin 4 (IL-4) and IL-13 and was correlated with increased serum IL-2, IL-12, IL-17A, interferon γ (IFNγ), monocyte displacing protein 1 (MCP-1) and soluble CD40 ligand (sCD40L). Conclusion: Acute exposures to PM_2.5, NO₂, SO₂ and CO were associated with a reduction in FVC % pred in COPD patients. Furthermore, short-term exposure to air pollutants increased systemic inflammation in COPD patients; this may be attributed to increased Th1 and Th17 cytokines and decreased Th2 cytokines.

The prevalence of cardiovascular disease has been increasing worldwide. As a common pathogenic risk factor, dyslipidemia played a great role in the incidence and progress of these diseases. We investigated to achieve accurate and up-to-date information on the prevalence of dyslipidemia and its associations with other lipid-related diseases in rural North China. Using a complex, multistage, probability sampling design, we conducted a large-scale cross-sectional study of 8528 rural participants aged over 18 years in Shandong Province. Prevalence and characteristics of dyslipidemia were demonstrated. The odds ratios between dyslipidemia types and lipid-related diseases were further analyzed by logistic regression. Among the overall population, 45.8 % suffered from dyslipidemia. The prevalence of lipid abnormality (including high and very high levels) was 18.6, 12.7, 9.8 and 12.7 % for total cholesterol (TC), high-density lipoprotein (HDL), and low-density lipoprotein (LDL) cholesterol and triglycerides (TG), respectively. Among all participants with dyslipidemia, 23.9 % were aware, only 11.5 % were treated, 10.0 % were controlled. For subjects with dyslipidemia, the risk for non-alcoholic fatty liver disease (NAFLD) was highest with a 3.3-fold over that of non-dyslipidmia (OR = 3.30, P < 0.001); followed by hyperuricemia and diabetes mellitus (DM), while with 2-fold increase (OR = 1.99, P < 0.001; OR = 1.92, P < 0.001); with only 1.5-fold risk for atherosclerosis (AS) (OR = 1.47, P < 0.001). The presence of high cholesterol was mainly associated with AS, while abnormal TG was correlated with NAFLD and DM. Dyslipidemia has become a serious public health issue in rural North China. The rapid increase of high TC and incremental risk of high TG may contribute to the epidemic of AS, NAFLD and DM. It is imperative to develop individualized prevention and treatment guidelines according to dyslipidemia phenotypes.

Lymphangioleiomyomatosis (LAM) is a rare lung disease and the mammalian target of the rapamycin (mTOR) inhibitors has been used as an effective therapy. Here we conducted a systematic review and meta-analysis with the aims to quantify the efficacy and safety of mTOR inhibitors in LAM patients. The following databases were searched for clinical trials regarding LAM patients treated with mTOR inhibitors until December 2017: Pubmed, Embase, Cochrane Library and OVID medicine. Random effect models were used for the quantitative analysis. Nine eligible studies were included in our systematic review, 7 of which were used for the meta-analysis. In LAM patients, mTOR inhibitors improved forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) significantly, with the weighted mean difference (WMD) 0.15 L (95%CI: 0.08 to 0.22, P < 0.01, I2 = 0%) and 0.22 L (95%: 0.11 to 0.32, P < 0.01, I2 = 0%) respectively. There was no significant change in neither the diffusing capacity for carbon monoxide (WMD: 0.51 ml/mm Hg/min, 95%CI: -0.48 to 1.49, P = 0.31, I2 = 0%) nor 6-min walking distance (WMD: 5.29 m, 95%CI: -18.01 to 28.59, P = 0.66, I2 = 1%). The weighted partial response rate was 0.68 (95%CI: 0.53 to 0.84, P < 0.01, I2 = 72%) for renal angiomylipoma. The cumulative incidence rates of common safety events were 50, 40, 23, 20 and 19% for oral mucositis, hyperlipidemia, headache, bone marrow suppression, and diarrhea, respectively. And most events were low grade and tolerant. In LAM patients, there are improvements of FEV1 and FVC after the application of mTOR inhibitors and over a half achieved the shrinkage of renal angiomyolipoma. PROSPERO registration number: CRD42018085470. Registered 22 January 2018.

Background: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease with high morbidity and mortality worldwide. Observational studies have shown correlations between common extrapulmonary comorbidities and COPD, but the existence of correlations does not necessarily prove a causal association. Therefore, causal relationships between diseases need to be explored by means of causal inference methods. Materials and Methods: Genetic correlation and two-sample Mendelian randomization (MR) analysis were explored to assess the causal relationship between exposures and outcomes with the genome-wide association studies (GWAS) dataset. Different sensitivity analyses were conducted to verify the robustness and consistency of results. Results: The linkage disequilibrium score regression showed that cardiovascular disease (CVD), hypertension (HTN) and type 2 diabetes mellitus (T2DM) were significantly genetically associated with COPD. T2DM and HTN were found to have a positive causal effect on COPD. The odds ratio (OR) of T2DM on COPD was 1.111 (95% CI, 1.063– 1.160; P< 0.0001) and that of HTN on COPD was 1.125 (95% CI, 1.084– 1.167; P < 0.0001). Similar results were verified by different MR methods. Furthermore, COPD had a positive causal effect on T2DM (OR 1.152 (95% CI, 1.064– 1.246; P=0.0005)). Conclusion: Our findings provided evidence for the causal association between HTN, T2DM and COPD, which would render new insights into the pathogenesis, prevention and intervention for COPD.