Study On Acute Toxicological Effects And Mechanism Of Ambient Air TSP,PM_2.5and PM_2.5in Printing Room On Mice

Background and Aims:According to the survey,modern people spend about 80%of their time indoors.People's health was affected by the quality of indoor air directly.Sick building syndrome(SBS)has evolved into one of the most common indoor hygiene problems we face.Sick building syndrome is a combination of a variety of non-specific factors,including the main factor and the guest factor.The main factors are the ventilation system problems and various volatile pollution sources indoors.Syndrome of sexual symptoms,mainly manifested as eye,nose,and throat skin discomfort,cough,fatigue,chest tightness,headache,etc.At present,printers are widely used in our study and life,and gradually become one of the sources of indoor air pollution,and constitute an incentive for SBS.There were many cases of printer-related occupational diseases,and even as early as 1979,it was reported that post office staff had itchy eyes and erythematic due to long-term use of wet toner.With the increase of the occupational exposure time related to the printer,it may cause more serious diseases such as pneumoconiosis,thrombosis,and carbon nano particle peritoneal deposition.The purpose of this study was to explore the damage effect of particulate matter in the printing room on the lung tissue of mice,and to reveal its formation mechanism,in order to further understand the impact of particulate matter on human health.Therefore,this article established two models of lung injury in ambient air and printing room air particles in mice and lung injury in PM2.5 mice with different concentrations in the printing room.The results are as follows:Conclusion one:1.Ambient air TSP,PM2.5 and printing room PM2.5 all cause damage to the lung of mice.Among them,the damage caused by the single-source printing room PM2.5 is between the mixed source ambient air TSP and PM2.5,and the damage caused by printing room PM2.5 cannot be ignored.2.Ambient air TSP,PM2.5 and printing room PM2.5 can cause oxidative stress in the lung of mice,resulting in decreased SOD activity and increased MDA content in the lung of mice.Compared with different particle sizes,the oxidative stress response of the lung of mice caused by ambient air PM2.5 is greater than that of ambient air TSP.Compared to the same particle size,the oxidative stress response in the lung of mice caused by the mixed source of ambient air PM2.5 is slightly larger than the single source PM2.5 in the printing room,but the oxidative stress damage caused by the printing room PM2.5 cannot be ignored.3.Ambient air TSP,PM2.5 and print room PM2.5 can increase the secretion of pro-inflammatory factors IL-1?,IL-6,TNF-? and the secretion of anti-inflammatory factor IL-2,resulting in inflammation.Compared with different particle sizes,the inflammatory response caused by ambient air PM2.5 is greater than that of ambient air TSP.Compared to the same particle size,the inflammatory response caused by ambient air PM2.5 is slightly larger than that of print room PM2.5,but the inflammatory reaction caused by PM2.5 in the printing room deserves attention.4.Ambient air TSP,PM2.5,and print room PM2.5 may cause inflammation,fibrosis,apoptosis and other damages in the lungs of mice by regulating the expression of COX2,p-p65/p65,TGF-?1,and Bax/Bcl-2.Compared different particle sizes,the inflammatory,fibrotic,and apoptosis damage caused by ambient air PM2.5 is greater than that of ambient air TSP.Compared to the same particle size,The inflammation,fibrosis,and apoptosis damage caused by ambient air PM2.5 is slightly larger than the PM2.5 in the printing room.The damage caused by the PM2.5 in the printing room cannot be underestimated.5.Ambient air TSP,PM2.5 and print room PM2.5 can cause the lung flora to deviate from normal,resulting in a decrease in the abundance of beneficial microorganisms Deinococcus,Adlercreutzia,Gordonia,and harmful microorganisms Gluconacetobacter,Acidovorax increased in abundance.Conclusion two:1.The lung tissue damage caused by PM2.5 at different concentrations in the printing room showed a concentration-dependent trend.With the increase in the concentration of PM2.5 in the printing room,the lung damage in mice became more and more serious,while the lung damage caused by PM2.5 in the low concentration printing room on mouse was not obvious.2.High-concentration printing room PM2.5 could significantly down-regulate SOD activity,and up-regulate MDA content,resulting in lung oxidative damage.Low concentration printing room PM2.5 had little effect on the SOD activity and MDA content in the lungs of mice.3.Print room PM2.5 with different concentrations increased the secretion of pro-inflammatory factors IL-1?,IL-6 and TNF-? in a concentration-dependent manner,and at the same time,reduced the secretion of IL-2.4.PM2.5 in the printing room may cause inflammation,fibrosis,apoptosis and other damage to the lungs of mice by regulating the expression levels of proteins such as COX2,p-p65/p65,TGF-?1,and Bax/Bcl-2 in a concentration dependency.5.Printroom PM2.5 increased the abundance of harmful microorganisms such as Burkholderia,Betaproteobacteria,and Coriobacteriia,and increases the risk of host disease,showing a concentration-dependent trend.