PCDD/Fs from a large-scale municipal solid waste incinerator under transient operations: Insight formation pathways and optimal reduction strategies.

Polychlorinated dibenzo-p-dioxin and dibenzofurans (PCDD/Fs) emissions from the transient operation of municipal solid waste incinerators can reach up to 690 ng/Nm3, as measured in this study. To control the extreme emissions to meet the national standard, the formation pathways of PCDD/F were investigated under transient operations (cold start-up, hot start-up, and after start-up) and normal operations. Compared with normal operations, transient operations facilitate the formation of low-chlorinated congeners rather than highly chlorinated congeners. Statistically, for transient operations, strong correlations were found among tetrachlorodibenzo-p-dioxin or tetrachlorodibenzofuran isomers. An abundant carbon matrix is an important carbon source for PCDD formation. Moreover, the comprehensive study revealed that the oxidation of deposited soot is the main source of PCDD/F emissions, relative to de novo synthesis, chlorobenzene-route synthesis, chlorophenol-route synthesis, and chlorination of dibenzo-p-dioxin/dibenzofuran. In addition, the optimal start-up procedure was constructed by analyzing main formation pathways and operating conditions. The relationship between the international toxic quantity (I-TEQ) values (CI-TEQ) and the reaction time can be assigned as CI-TEQ = 11.72t-0.65 (R2 = 0.97) for the circulating fluidized bed. The relationship of CI-TEQ = 4.61t-0.59 (R2 = 0.85) was also proven on the dataset with a grate furnace. Then, the optimal feeding rate of activated carbon was further proposed by the relationship between the reaction time and I-TEQ, and the semi-empirical equation for PCDD/Fs adsorption. Finally, the PCDD/Fs emissions can be reduced to 0.1 ng I-TEQ/Nm3 under transient operations according to the time since start-up.

Distribution of ACE2, CD147, cyclophilins, CD26 and other SARS-CoV-2 associated molecules in human tissues and immune cells in health and disease

BackgroundMorbidity and mortality from COVID-19 caused by novel coronavirus SARS-CoV-2 is accelerating worldwide and novel clinical presentations of COVID-19 are often reported. The range of human cells and tissues targeted by SARS-CoV-2, its potential receptors and associated regulating factors are still largely unknown. The aim of our study was to analyze the expression of known and potential SARS-CoV-2 receptors and related molecules in the extensive collection of primary human cells and tissues from healthy subjects of different age and from patients with risk factors and known comorbidities of COVID-19. MethodsWe performed RNA sequencing and explored available RNA-Seq databases to study gene expression and co-expression of ACE2, CD147 (BSG), CD26 (DPP4) and their direct and indirect molecular partners in primary human bronchial epithelial cells, bronchial and skin biopsies, bronchoalveolar lavage fluid, whole blood, peripheral blood mononuclear cells (PBMCs), monocytes, neutrophils, DCs, NK cells, ILC1, ILC2, ILC3, CD4+ and CD8+ T cells, B cells and plasmablasts. We analyzed the material from healthy children and adults, and from adults in relation to their disease or COVID-19 risk factor status. ResultsACE2 and TMPRSS2 were coexpressed at the epithelial sites of the lung and skin, whereas CD147 (BSG), cyclophilins (PPIA and PPIB), CD26 (DPP4) and related molecules were expressed in both, epithelium and in immune cells. We also observed a distinct age-related expression profile of these genes in the PBMCs and T cells from healthy children and adults. Asthma, COPD, hypertension, smoking, obesity, and male gender status generally led to the higher expression of ACE2- and CD147-related genes in the bronchial biopsy, BAL or blood. Additionally, CD147-related genes correlated positively with age and BMI. Interestingly, we also observed higher expression of ACE2- and CD147-related genes in the lesional skin of patients with atopic dermatitis. ConclusionsOur data suggest different receptor repertoire potentially involved in the SARS-CoV-2 infection at the epithelial barriers and in the immune cells. Altered expression of these receptors related with age, gender, obesity and smoking, as well as with the disease status might contribute to COVID-19 morbidity and severity patterns.