Objective:To investigate the effects of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood coagulation in adults.Methods:A total of 73 adult volunteers were recruited in a cohort study and had four clinical visits from November 2014 to January 2016. Blood samples were obtained and used to measure biomarkers of blood thrombogenicity, including soluble CD40 Ligand (sCD40L), soluble P-selection (sCD62P) and Fibrinogen (FIB). White blood cell (WBC), 8-Hydroxy-2′-Deoxyguanosine (8-OHdG), matrix metalloproteinase-2 (MMP-2) and HDL cholesterol efflux capacity (HDL-CEC) were also determined. Daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) were measured throughout the study period, and positive matrix factorization (PMF) approach was used to identity PAHs sources. Linear mixed-effect models including single-pollutant model, two-pollutant model and stratification analysis were constructed to estimate the effects of exposure to ambient fine particulate matter-bound PAHs on blood thrombogenicity in adults after adjusting for potential confounders.Results:The mean age of participants was (23.3±5.4) years. During the study period, the median level of PM 2.5-bound PAHs was (55.29±74.99) ng/m 3. Six sources of PM 2.5-bound PAHs were identified by PMF, with traffic sources contributing more than 50%. The linear mixed-effect model showed that PAHs exposure had a significant effect on elevated blood thrombogenicity. Significant elevations in sCD40L, sCD62P and FIB associated with per IQR increase (60.33 ng/m 3) in exposure to PAHs were 14.36% (95% CI:6.94%-22.28%), 9.33% (95% CI: 1.71%-17.51%) and 2.07% (95% CI:0.44%-2.07%) at prior 5 days, respectively. Blood thrombogenicity levels were significantly and positively correlated with source-specific PAHs, especially gasoline vehicle emissions, diesel vehicle emission and coal burning at prior 1 or 5 days. Stronger associations between PAHs and increased blood thrombogenicity were found in participants with high plaque vulnerability, reduced HDL function, and high levels of inflammation and oxidative stress. Conclusion:Acute exposure to ambient fine particulate matter-bound PAHs, especially PAHs from traffic sources may promote blood thrombogenicity in adults, and PAHs have stronger effects on participants with reduced vascular function and high levels of inflammation and oxidative stress.

Objective:To investigate the effects of exposure to ambient fine particulate matter-bound polycyclic aromatic hydrocarbons on blood coagulation in adults.Methods:A total of 73 adult volunteers were recruited in a cohort study and had four clinical visits from November 2014 to January 2016. Blood samples were obtained and used to measure biomarkers of blood thrombogenicity, including soluble CD40 Ligand (sCD40L), soluble P-selection (sCD62P) and Fibrinogen (FIB). White blood cell (WBC), 8-Hydroxy-2′-Deoxyguanosine (8-OHdG), matrix metalloproteinase-2 (MMP-2) and HDL cholesterol efflux capacity (HDL-CEC) were also determined. Daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) were measured throughout the study period, and positive matrix factorization (PMF) approach was used to identity PAHs sources. Linear mixed-effect models including single-pollutant model, two-pollutant model and stratification analysis were constructed to estimate the effects of exposure to ambient fine particulate matter-bound PAHs on blood thrombogenicity in adults after adjusting for potential confounders.Results:The mean age of participants was (23.3±5.4) years. During the study period, the median level of PM 2.5-bound PAHs was (55.29±74.99) ng/m 3. Six sources of PM 2.5-bound PAHs were identified by PMF, with traffic sources contributing more than 50%. The linear mixed-effect model showed that PAHs exposure had a significant effect on elevated blood thrombogenicity. Significant elevations in sCD40L, sCD62P and FIB associated with per IQR increase (60.33 ng/m 3) in exposure to PAHs were 14.36% (95% CI:6.94%-22.28%), 9.33% (95% CI: 1.71%-17.51%) and 2.07% (95% CI:0.44%-2.07%) at prior 5 days, respectively. Blood thrombogenicity levels were significantly and positively correlated with source-specific PAHs, especially gasoline vehicle emissions, diesel vehicle emission and coal burning at prior 1 or 5 days. Stronger associations between PAHs and increased blood thrombogenicity were found in participants with high plaque vulnerability, reduced HDL function, and high levels of inflammation and oxidative stress. Conclusion:Acute exposure to ambient fine particulate matter-bound PAHs, especially PAHs from traffic sources may promote blood thrombogenicity in adults, and PAHs have stronger effects on participants with reduced vascular function and high levels of inflammation and oxidative stress.

The condition of patients with severe traumatic brain injury (sTBI) complicated by corona virus 2019 disease (COVID-19) is complex. sTBI can significantly increase the probability of COVID-19 developing into severe or critical stage, while COVID-19 can also increase the surgical risk of sTBI and the severity of postoperative lung lesions. There are many contradictions in the treatment process, which brings difficulties to the clinical treatment of such patients. Up to now, there are few clinical studies and therapeutic norms relevant to sTBI complicated by COVID-19. In order to standardize the clinical treatment of such patients, Critical Care Medicine Branch of China International Exchange and Promotive Association for Medical and Healthcare and Editorial Board of Chinese Journal of Trauma organized relevant experts to formulate the Chinese expert consensus on clinical treatment of adult patients with severe traumatic brain injury complicated by corona virus infection 2019 ( version 2023) based on the joint prevention and control mechanism scheme of the State Council and domestic and foreign literatures on sTBI and COVID-19 in the past 3 years of the international epidemic. Fifteen recommendations focused on emergency treatment, emergency surgery and comprehensive management were put forward to provide a guidance for the diagnosis and treatment of sTBI complicated by COVID-19.