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The occurrences of impaired lung function during childhood could substantially influence the health states of the respiratory system in adults. So, the effects of air pollution and green spaces on impaired lung function in children were investigated in this study. The lung function of each student was tested every year from 2015 to 2017 and the method of case-control study was applied. 2087 students aged from 9 to 11 years old of primary schools in Tianjin were ultimately included in this study. The method of propensity score matching (PSM) was performed to minimize the confounding bias and the conditional logistic regression model was carried out to evaluate the effects of indoor and outdoor environmental risk factors on the occurrences of impaired lung function in children. For every interquartile range (IQR) increase in the mixture of six air pollutants at the lag1, lag2, and lag3 periods, the risks of getting impaired lung function were increased by 53.4%, 34.7%, and 16.9%, respectively. The protective effect of greenness at lag2 period (odds ratios (OR)) = 0.022 (95% confidence interval (CI): 0.008-0.035)) was stronger than that at lag1and lag3 periods, respectively. Separate and combined effects of most air pollutants at different lag periods exerted hazardous effects on the lung function of students. Exposure to greenness had protective effects on the lung health of children.

To investigate the health effects of fine particulate matter (≤ 2.5 μm in aerodynamic diameter; PM2.5)-bound heavy metals and polycyclic aromatic hydrocarbons (PAHs) before and after the implementation of the Urban Natural Gas Heating Project (UNGHP), the lifetime cancer risks, hazard quotients (HQs) of heavy metals and PAHs were calculated. Seven kinds of heavy metals (Al, As, Cd, Cr, Mn, Ni and Se) and 12 kinds of PAHs including acenaphthylene (ANY), acenaphthene (ANA), fluoranthene (FLT), pyrene (PYR), chrysene (CHR), benz[a]anthracene (BaA), benzo[b]fluoranthene (BbF), benzo[k]fluoranthene (BkF), benzo[a]pyrene (BaP), dibenz[a,h]anthracene (DBA), benzo[ghi]perylene (BPE) and indeno[1,2,3-cd]pyrene (IPY) were analyzed and used for the health risk assessments. It was found that HQ of Mn fell from 1.09 in the coal-burning period to 0.72 in the gas-burning period in the suburban area. And lifetime cancer risks of PAHs fell from 35.7 × 10–6 in the coal-burning period to 17.22 × 10–6 in the gas-burning period in the urban area. It could be concluded that, during the gas-burning period, downward trends were observed for the lifetime cancer risks and HQs of most kinds of heavy metals and PAHs in all regions of Tianjin compared to those during the coal-burning period. The UNGHP was effective, and we should also take other measures to control the pollution.

Background Isolated distal deep vein thrombosis (IDDVT), a disease frequently detected in hospitalized patients, can progress to proximal deep vein thrombosis (PDVT) and pulmonary embolism (PE). Here, we evaluated the effects of anticoagulation in hospitalized IDDVT patients. Methods We conducted a retrospective study in our hospital and enrolled hospitalized IDDVT patients diagnosed by compression ultrasonography (CUS) from January to December 2020. Participants were divided into anticoagulation (AC) and non-anticoagulation (non-AC) groups. After propensity score matching (PSM), multivariate Cox regression analyses were performed to assess whether anticoagulation was associated with PDVT/PE, and all-cause mortality. Results A total of 426 IDDVT inpatients with CUS follow-up were screened from 1502 distal DVT patients and finally enrolled. The median age was 67 years with 51.4% males and 15.5% cancer patients. The median follow-up was 11.6 months. There were 288 and 138 patients treated with or without anticoagulants, respectively. Patients in the non-AC group had less body mass index and more comorbidities. Patients in the AC group were treated with rivaroxaban or dabigatran (52.1%), low molecular weight heparin (42.7%), and warfarin (5.2%). The PSM generated 111 pairs of well-matched IDDVT patients with or without anticoagulation. The Kaplan–Meier analysis demonstrated that neither the incidence of PDVT/PE (5.4% vs. 2.7%, log-rank p = 0.313) nor all-cause mortality (27.9% vs. 18.9%, log-rank p = 0.098) was significant different between groups. Anticoagulation was not associated with PDVT/PE and all-cause mortality in the multivariable Cox regression analyses using the matched cohorts. The main risk factors for all-cause mortality were age, malignancy history, BMI, sepsis, heart failure, and white blood cell (WBC) count. Conclusions In hospitalized IDDVT patients, the thrombosis extension rate to PDVT/PE was low. Anticoagulation did not reduce the incidence of thrombosis extension of IDDVT and was not associated with all-cause mortality.

As the pollution of fine particulate matter (≤ 2.5 μg/m3 in aerodynamic diameter; PM2.5) and ozone (O3) is becoming more and more serious in developing countries, we, hereby, investigated the effects of PM2.5, constituents of PM2.5 and O3 on the lung function of children in Tianjin, China. The lung functions of 198 pupils from nine primary schools in Tianjin were examined (repeated five times) during the months of October to December in 2016, 2017 and 2018, respectively. And the mixed-effect models were used to evaluate the effects of air pollutants. A 10 μg/m3 increase in PM2.5 and O3-8h might lead to reductions of forced vital capacity (FVC) in 1.03% (− 1.87 to − 0.19%) and 21.09% (− 25.54 to − 16.58%), respectively, while a 10 ng/m3 increment in ANY might account for the 166.44% (− 221.32 to − 112.31%) decreases in FVC. PM2.5 and O3-8h might be more harmful to the lung functions of female students and participants with PS exposure at home. And the main sources of pollution resulting in the decrease in pulmonary function might be traffic pollution and coal combustion.

With the development of the industrialization level in China, high concentrations of fine particulate matter (≤ 2.5 μg/m3 in aerodynamic diameter (PM2.5)) could have a great impact on the health of the population. Our study is to quantify the health benefits on cardiocerebrovascular disease of reducing exposure to PM2.5 in Tianjin, China. We obtained the data on cardiovascular disease (CVD), ischemic heart disease (IHD), and cerebrovascular disease (CD) mortalities to quantify the association between CVD, CD, and IHD mortalities and PM2.5 and calculate health and economic benefits when the annual average concentration of PM2.5 was reduced to National Ambient Air Quality Standard (NAAQS) and World Health Organization (WHO) guidelines by using our concentration response (C-R) functions. There were 435.22 (95% CI 253.86 to 616.57) all-cause, 130.22 (95% CI 66.34 to194.09) IHD, and 204.07 (95% CI 111.66 to 296.47) CD deaths attributed to PM2.5 and the economic benefits obtained by preventing all-cause, IHD, and CD mortalities were equivalent to be 2.79%, 0.83%, and 1.31% of Baodi’s GDP in Tianjin in 2017, respectively. PM2.5 concentration was positive with all-cause, IHD, and CD mortalities in rural, suburban, and urban area of Tianjin, China. Meanwhile, the number of avoidable deaths and economic cost of reducing PM2.5 concentrations to NAAQS and WHO guidelines was highest in the rural area.

The proinflammatory factor high mobility group box protein 1 (HMGB1) has been implicated as an important mediator of many chronic inflammatory diseases, including asthma. Human bronchial epithelial cells (HBECs) play a central role in the pathogenesis of asthma. However, the effects of HMGB1 on HBECs and the underlying mechanisms remain unknown. Here, we investigated receptor expression and proinflammatory cytokine production by primary cultures of HBECs stimulated by HMGB1. We then examined the effects of specific receptor blockade and inhibition of p38 MAPK, ERK1/2, or PI3-K on HMGB1-induced expression of proinflammatory cytokines. HMGB1 increased the expression and secretion of TNF-α, TSLP, MMP-9, and VEGF in a dose- and time-dependent manner. HMGB1 also induced elevated expression of RAGE protein. Secretion of TNF-α, VEGF, MMP-9, and TSLP was significantly decreased by RAGE blockade and p38 MAPK pathway inhibition, while a less pronounced effect was mediated by ERK1/2 inhibition. These observations suggest that HMGB1 binds RAGE and promotes activities of p38 MAPK and ERK1/2 pathways in HBECs. This then enhances the expression of TNF-α, VEGF, MMP-9, and TSLP, which are the important inflammatory factors in asthma. These results demonstrate that HMGB1 enhances the inflammatory responses of HBECs, which are involved in the modulation of inflammatory processes in asthma.

The pro-inflammation factor high-mobility group box protein 1 (HMGB1) has been implicated in the pathogenesis of asthma. In this study, we used a murine model of chronic asthma to evaluate the effects of HMGB1 on airway remodeling. Female BALB/c mice were randomly divided into four groups: control, ovalbumin (OVA) asthmatic, OVA+isotype antibody and OVA+anti-HMGB1 antibody. Anti-HMGB1 antibody therapy was started on day 21 and was administered three times per week for 6 weeks before intranasal challenge with OVA. In this mouse model, HMGB1 expression is significantly elevated. The anti-HMGB1 antibody group exhibited decreased levels of immunoglobulin E (IgE) and inflammatory mediators and reduced inflammatory cell accumulation, airway hyperresponsiveness (AHR), mucus synthesis, smooth muscle thickness and lung collagen content compared with the OVA groups. Treatment with HMGB1 increased proliferation, migration, collagen secretion and α-smooth muscle actin (SMA) expression in MRC-5 cells. Treatment with the HMGB1/IL-1β complex significantly increased the expression and secretion of transforming growth factor (TGF-β1), matrix metalloproteinase (MMP)-9 and vascular endothelial growth factor (VEGF). Altogether, these results suggest that blocking HMGB1 activity may reverse airway remodeling by suppressing airway inflammation and modulating lung fibroblast phenotype and activation.