Airborne transmission of the Delta variant of SARS-CoV-2 in an auditorium.

The Delta variant of SARS-CoV-2 has inflicted heavy burdens on healthcare systems globally, although direct evidence on the quantity of exhaled viral shedding from Delta cases is lacking. The literature remains inconclusive on whether existing public health guidance, based on earlier evidence of COVID-19, should respond differently to more infectious viral strains. This paper describes a study on an outbreak of the Delta variant of COVID-19 in an auditorium, where one person contracted the virus from three asymptomatic index cases sitting in a different row. Field inspections were conducted on the configuration of seating, building and ventilation systems. Numerical simulation was conducted to retrospectively assess the exhaled viral emission, decay, airborne dispersion, with a modified Wells-Riley equation used to calculate the inhalation exposure and disease infection risks at the seat level. Results support the airborne disease transmission. The viral emission rate for Delta cases was estimated at 31 quanta per hour, 30 times higher than those of the original variant. The high quantity of viral plume exhaled by delta cases can create a high risk zone nearby, which, for a mixing ventilation system, cannot be easily mitigated by raising mixing rates or introducing fresh air supply. Such risks can be reduced by wearing an N95 respirator, less so for social distancing. A displacement ventilation system, through which the air is supplied at the floor and returned from the ceiling, can reduce risks compared with a mixing system. The study has implications for ventilation guidelines and hygiene practices in light of more infectious viral strains of COVID-19.

Long-Term Formaldehyde Emissions from Medium-Density Fiberboard in a Full-Scale Experimental Room: Emission Characteristics and the Effects of Temperature and Humidity.

We studied formaldehyde emissions from the medium-density fiberboard (MDF) in a full-scale experimental room to approximate emissions in actual buildings. Detailed indoor formaldehyde concentrations and temperature and humidity data were obtained for about 29 months. Temperature, relative humidity (RH), and absolute humidity (AH) ranged over -10.9-31.4 °C, 46.5-83.6%, and 1.1-23.1 g/kgair, respectively. Annual cyclical seasonal variations were observed for indoor formaldehyde concentrations and emission rates, exhibiting entirely different characteristics than those in an environmental chamber under constant environmental conditions. The maximum concentration occurred in summer rather than at initial introduction of the material. The concentrations in summer could be a few up to 20 times higher than that in winter, depending on the indoor temperature and humidity conditions. Concentrations decreased by 20-65% in corresponding months of the second year. Indoor formaldehyde concentrations were positively correlated with temperature and AH but were poorly correlated with RH. The combined effects of temperature and AH on formaldehyde emissions from MDF in actual buildings were verified. These detailed long-term experimental results could be used with environmental chamber measurement data to scale up and validate emission models from chambers held at constant conditions to actual buildings.

An Occupational Dimethylacetamide Poisoning Incident Responded Efficiently in Health Emergency Response Network - Zhuhai City, Guangdong Province, China, August 2023.

What is already known about this topic?: Dimethylacetamide (DMA), a colorless liquid with low toxicity, is commonly used as a solvent in the production of synthetic materials, petroleum processing, and pharmaceutical manufacture. In comparison to substances of higher toxicity, occupational exposure to DMA presents a deceptive risk due to its insidious and subacute progression, increasing the likelihood of escalating into major incidents. What is added by this report?: In August 2023, an incident of occupational DMA poisoning involving six cases was reported at a spandex manufacturing factory in Zhuhai City, Guangdong Province, China, following post-fire management activities. All affected individuals were employees of an equipment maintenance company tasked with cleaning polymerizers. With the coordinated efforts of the health institutions in Guangdong Health Emergency Response Network for Poisoning Emergencies (HERNPE), the situation was promptly identified and addressed. What are the implications for public health practice?: HERNPE serves as an effective framework for enhancing the integration of health institutions across various levels, facilitating a coordinated response that combines clinical services with public health initiatives. By leveraging the leadership of national centers, HERNPE plays a crucial role in the early detection, prevention, and management of large-scale health events.

Anti-inflammatory protein TSG-6 secreted by BMSCs attenuates silica-induced acute pulmonary inflammation by inhibiting NLRP3 inflammasome signaling in macrophages.

Silicosis is a severe occupational lung disease caused by inhalation of silica particles. Unfortunately, there are currently limited treatment options available for silicosis. Recent advances have indicated that bone marrow mesenchymal stem cells (BMSCs) have a therapeutic effect on silicosis, but their efficacy and underlying mechanisms remain largely unknown. In this study, we focused on the early phase of silica-induced lung injury to investigate the therapeutic effect of BMSCs. Our findings demonstrated that BMSCs attenuated silica-induced acute pulmonary inflammation by inhibiting NLRP3 inflammasome pathways in lung macrophages. To further understand the mechanisms involved, we utilized RNA sequencing to analyze the transcriptomes of BMSCs co-cultured with silica-stimulated bone marrow-derived macrophages (BMDMs). The results clued tumor necrosis factor-stimulated gene 6 (TSG-6) might be a potentially key paracrine secretion factor released from BMSCs, which exerts a protective effect. Furthermore, the anti-inflammatory and inflammasome pathway inhibition effects of BMSCs were attenuated when TSG-6 expression was silenced, both in vivo and in vitro. Additionally, treatment with exogenous recombinant mouse TSG-6 (rmTSG-6) demonstrated similar effects to BMSCs in attenuating silica-induced inflammation. Overall, our findings suggested that BMSCs can regulate the activation of inflammasome in macrophages by secreting TSG-6, thereby protecting against silica-induced acute pulmonary inflammation both in vivo and in vitro.

Apelin Prevents and Alleviates Crystalline Silica-induced Pulmonary Fibrosis via Inhibiting Transforming Growth Factor Beta 1-triggered Fibroblast Activation.

Silicosis is a common and ultimately fatal occupational disease, yet the limited therapeutic option remains the major clinical challenge. Apelin, an endogenous ligand of the G-protein-coupled receptor (APJ), is abundantly expressed in diverse organs. The apelin-APJ axis helps to control pathological and physiological processes in lung. The role of apelin in the pathological process and its possible therapeutic effects on silicosis have not been elucidated. In this study, we found that lung expression and circulating levels of apelin were markedly decreased in silicosis patients and silica-induced fibrotic mice and associated with the severity. Furthermore, in vivo data demonstrated that pre-treatment from day 3 and post-treatment from day 15 with apelin could both alleviate silica-induced pulmonary fibrosis in mice. Besides, apelin inhibited pulmonary fibroblast activation via transforming growth factor beta 1 (TGF-ß1) signaling. Our study suggested that apelin could prevent and reverse silica-induced pulmonary fibrosis by inhibiting the fibroblast activation through TGF-ß1 signaling pathway, thus providing a new potential therapeutic strategy for silicosis and other pulmonary fibrosis.

Clinical analysis of 43 cases of chronic benzene poisoning.

Benzene can result in bone marrow suppression. Chronic benzene poisoning (CBP) can be found among workers with excessive benzene exposure. CBP could give the appearance of different types of disorders such as leukopenia, agranulocytosis, anemia, pancytopenia, aplastic anemia (AA), myelodysplastic syndrome (MDS), and leukemia. This paper describes 43 CBP cases with the patients' ages ranging from 18 to 36 years (average: 23 years). Among them, 13 (30%) were male and 30 (70%) were female. Their job titles were furniture maker, shoemaker, industrial painter and metal shop worker. Their work durations ranged from 1.5 to 72 months (average: 14 months). Benzene levels in these workplaces exceeded 30 mg/m3. Ten of the 43 cases (23%) were diagnosed as mild cases of CBP, another 10 (23%) were moderate, and 23 (53%) were severe. Treatment for CBP included the following: cessation of benzene exposure, general supportive therapy, antibiotics, vitamins, corticosteroids, androgens, colony-stimulating factors (G-CSF, GM-CSF), blood component therapy, and traditional Chinese medicine. Thirty-three (77%) of the cases recovered completely, nine (21%) cases improved, and one (2%) died. In general, prognosis of CBP cases is optimistic when appropriate treatment is given. However, a few of the benzene-induced AA cases showed no response to treatment, which raises questions about the traditional view of the pathogenesis of the illness. Furthermore, only a part of the population with the same level of benzene exposure would suffer from the disease. Still, CBP cases with the same benzene exposure level exhibited different extents of severity of the illness. This evidence suggests strongly the existence of individual susceptibility. Detection of the biological markers regarding the individual susceptibility would be valuable for screening workers who are not suitable to be exposed to benzene.

iTRAQ-based proteomic profiling of human serum reveals down-regulation of platelet basic protein and apolipoprotein B100 in patients with hematotoxicity induced by chronic occupational benzene exposure.

Benzene is an important industrial chemical and an environmental contaminant, but the pathogenesis of hematotoxicity induced by chronic occupational benzene exposure (HCOBE) remains to be elucidated. To gain an insight into the molecular mechanisms and developmental biomarkers for HCOBE, isobaric tags for relative and absolute quantitation (iTRAQ) combined with two-dimensional liquid chromatography-tandem mass spectrometry (2D-LC-MS/MS) were utilized. Identification and quantitation of differentially expressed proteins between HCOBE cases and healthy control were thus made. Expressions of selected proteins were confirmed by western blot and further validated by ELISA. A total of 159 unique proteins were identified (≥95% confidence), and relative expression data were obtained for 141 of these in 3 iTRAQ experiments, with fifty proteins found to be in common among 3 iTRAQ experiments. Plasminogen (PLG) was found to be significantly up-regulated, whereas platelet basic protein (PBP) and apolipoprotein B100 (APOB100) were significantly down-regulated in the serum of HCOBE cases. Additionally, the altered proteins were associated with the molecular functions of binding, catalytic activity, enzyme regulator activity and transporter activity, and involved in biological processes of apoptosis, developmental and immune system process, as well as response to stimulus. Furthermore, differential expressions of PLG, PBP and APOB100 were confirmed by western blot, and the clinical relevance of PBP and APOB100 with HCOBE was validated by ELISA. Overall, our results showed that lowered expression of PBP and APOB100 proteins served as potential biomarkers of HCOBE, and may play roles in the benzene-induced immunosuppressive effects and disorders in lipid metabolism.