Pulmonary Health Effects Of Wintertime Particulate Matter From China And California In Mice

Fine particulate matter(PM2.5)has become more popular for global attention which is due to its potential toxicity causing multiple human diseases.Epidemiological studies show a strong association between PM2.5 air pollution and adverse cardiopulmonary effects,since PM2.5 can pass through the upper airway and deposit into lung,and it will lead to an increase in the morbidity and mortality of various respiratory diseases.PM2.5 toxicity has been linked to physicochemical composition and exposure scenario.In the present study,wintertime PM2.5 samples were obtained from three different geographical regions:Sacramento,California,USA;Jinan,Shandong,China;and Taiyuan,Shanxi,China(PMca,PMSD,and PMsx,respectively)with high atmospheric PM2.5 emissions.Firstly,PM2.5 chemical composition analysis were performed.And then PM2.5 extract samples were oropharyngeally administered to different groups of BALB/C mice,at equal mass concentrations[0(water vehicle control only)or 20?g/50 ?L],on five different occasions over a two-week period,for a cumulative PM dose of 0 or 100 ?g/mouse.Mice were necropsied on Days 1,2 and 4 after the final exposure,bronchoalveolar lavage fluid(BALF),histopathology,quantitative polymerase chain reaction tests(qPCR),and enzyme-linked immunosorbent assays(ELISA)were evaluated for pulmonary effects of different PM2.5.The results are shown below:(1)The main components of three PM2.5 samples were organic,and the proportion of organic in PMSD was 57%.However,PMCA was more oxidized with 45.3%oxygen in the organics.And the main components of the inorganics were sulfate and nitrate.The sulfate proportion of PMsx is 26%,which is about 13 and 2 times higher than PMCA and PMSD,respectively.While nitrate was more abundant in PMCA,which was about 2 and 3 times than PMSD and PMsx.Also,metal analysis demonstrated that Cu,Mg and Pb in PMsx was much higher than PMCA and PMSD.Additionally,the concentration of K,Ca,Zn,Fe,and Niwas similar in all three PM2.5 samples.(2)BALF and histopathology demonstrated that,at post-OPA Days land 2,PMsx had more neutrophil numbers versus control,PMCA and PMSD.By Day 4,all the groups PM2.5 exhibited more severe bronchiolitis and alveolitis than controls.And PMsx showed the highest bronchiolar and alveolar inflammation scores among three PM2.5 samples,which is 2.3 and 2.4.Also neutrophilic influxes into the peribronchiolar and alveolar regions of the lungs that were not observed in other groups confirmed inflammation scores.(3)The qPCR results showed that,at post-OPA day 1 IL-1? and TNF-?mRNA expression of all three PM2.5 group increased significantly versus control,and PMsx led a significant elevation of CXCL-1 compared to control group.At Day 2,compared to control,only PMsx induced TNF-? mRNA expression.By Day 4,PMCA and PMsx induced IL-1? expression;only PMsx significantly increased the TNF-? mRNA level;otherwise,CXCL-1 in all three PM2.5 groups were significantly higher relative to control,and PMsx was even higher than PMCA and PMSD.(4)The results of ELISA indicated that,in all three PM groups,IL-1?,TNF-? and CXCL-1 protein levels were not significantly different from control at post-OPA day 1.At day 2,only PMsx induced an increase of TNF-? and CXCL-1 protein level compared to control.By day 4,IL-1? and TNF-? protein levels in all three PM2.5 groups were higher than control;PMSD showed a significance increase in CXCL-1 protein expression versus control,while PMsx had even higher CXCL-1 protein level than PMCA and control.Cumulative findings from the present study suggested that,at post OPA Daysl,2 and 4,higher sulfate in PMsx which caused by coal burning and abundant metal of Cu and Pb may have contributed to greater pulmonary inflammatory responses in mice.In addition,compared to Days 1 and 2,all PM2.5 groups caused more severe pulmonary effects at Day 4.Therefore,we could find a time-lag effect of PM-induced lung injury,but the peak of inflammatory response hasn't been estimated.The above results can provide more scientific basis for PM2.5 toxicity and lay a foundation for the future research.