PM2.5大气污染物致大鼠呼吸系统病理学变化

目的 探讨大气污染物对大鼠气管的病理学改变.方法 通过制备大气混合污染物的动物模型,即实验大鼠气管注入大气可吸入颗粒物( PM2.5)混悬液及动态吸入SO2、NO2、CO的空气混合气,观测染毒不同时期大鼠气管和肺泡的超微结构变化.结果 大鼠气管扫描电镜观察可见,随着染尘染毒剂量的增高,气管上皮纤毛粘连、紊乱;PM25对大鼠肺组织的损害比对气管上皮的损害严重得多,中剂量PM25染尘染毒30 d,可使肺纤维增生,肺泡腔变小,高剂量PM2.5染尘染毒30 d,可使肺泡上皮细胞脱落溶解,大鼠气管和肺组织透射电镜观察可见,中剂量染尘染毒后1d使肺泡上皮排列不规则;7 d肺泡上皮紧密连接消失;30 d肺泡上皮细胞溶解脱落.结论 大气污染物可引起大鼠气管纤毛的摆动功能减弱及丧失,导致其排出功能障碍.     

铅染毒大鼠肾组织病理学观察

铅染毒大鼠肾组织病理学观察白银公司劳动卫生研究所（７３０９００）魏肖莹本项研究的目的是通过观察不同剂量染毒后，急、慢性铅中毒所造成的实验动物肾组织病理学改变，探讨铅毒性肾损害的剂量效应关系。１材料和方法１．１化学纯醋酸铅［Ｐｂ（ＣＨ３ＣＯＯ）２］，用...     

大剂量N-乙酰半胱氨酸对染尘大鼠肺组织的影响

目的 观察大剂量N-乙酰半胱氨酸(NAC)对矽肺形成过程中炎症和纤维化反应的影响.方法 将Wisar大鼠随机分为模型组、干预组、对照组,每组32只.模型组和干预组以二氧化硅结晶体诱发染尘大鼠模型,干预组以大剂量NAC进行干预.分别在染尘后的第3、7、14、28天处死8只大鼠.对大鼠肺组织进行HE染色及Masson染色,观察肺组织病理变化.用酶联免疫法(EusA)测定肺泡灌洗液中肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)的含量.结果 NAC干预组病理观察显示,肺泡炎症和纤维化程度均较模型组明显减轻.与模型组(13.84±1.61、9.23±0.87、11.23±1.25、9.56±0.76)比较,第3、7、14、28天十预组肺脏系数(9.30±0.78、6.29±0.74、7.63±0.88、6.06±1.16)均明显降低.差异有统计学意义(P＜0.01.与对照组相比,各时间点模型组肺泡灌洗液中TNF-α和IL-8含量均明显升高,差异有统计学意义(P＜0.01);与模型组相比,各时间点干预组的TNF-α和IL-8含量均明显降低,差异有统计学意义(P＜0.01).结论 早期大剂量NAC干预能够明显减轻染尘大鼠的肺组织炎症,降低肺泡灌洗液中TNF-α和IL-8含量,抑制和延缓肺纤维化的发生.

Abstract：

Objective To explore the effects of high-dose N-acetylcysteine on the lung tissues of rats exposed to silica. Methods Ninety-six Wistar rats were randomly divided into model group, intervention group and control group (32 rats for each group). The rats of model group and intervention group were exposed to silica by intratracheal infusion of silica dust suspension. The rats in the intervention group were orally given high dose N-acetylcysteine. In 3,7,14,28 days after exposure, eight rats in each group were sacrificed, respectively and the lung samples were collected. The pathological changes of lung were evaluated by HE and Masson staining methods. The levels of TNF-α and IL-8 in the BALF were detected by ELISA. Results Compared with the control group, the alveolitis and pulmonary fibrosis in the intervention group were significantly reduced. In 3,7,14,28 days after exposure, the lung/body coefficients in the intervention group were 9.30±0.78, 6.29±0.74,7.63±0.88,6.06+1.16 respectively, which were significantly lower than those (13.84±1.61,9.23±0.87, 11.23±1.25,9.56±0.76, P＜0.01 )in the model group (P＜0.01). At the different time points, the levels of TNF-α and IL-8 in the BALF in the intervention group were significantly higher than those in the control group (P＜0.01), but were significantly lower than those in the model group (P＜0.01). Conclusion The intervention with high dose N-acetylcysteine can significantly reduce the alveolitis and the TNF-α and IL-8 levels in the BALF, therefore, inhibit and delay the development of pulmonary fibrosis of rats exposed to silicon dioxide.     

PM2.5短期暴露与儿童青少年血压的关联

目的 研究PM2.5短期暴露与儿童青少年血压的关联,为综合保护儿童青少年的健康提供科学依据.方法 选择参加2017-2018学年某市中小学生健康体检中人口学特征和血压等资料完整且无心脏等重要脏器疾病史的144 813名初一和高一年级学生为研究对象.从各学校附近的空气质量和气象监测站获取PM2.5等污染物及气象要素数据,...     

PM2.5染尘大鼠海马中铅铝锰含量及神经递质的变化

为探讨吸入大气PM2.5的大鼠海马组织和全血中铅、铝、锰含量变化及血清和海马中神经递质一氧化氮(NO)和一氧化氮合酶(NOS)的变化,将SPF级雄性大鼠32只随机分为对照组、PM2.5低剂量组(5 mg/kg)、PM2.5中剂量组(10 mg/kg)、PM2.5高剂量组(20 mg/kg),每组8只,经气管注入PM2.5混悬液,每周1次,连续12周。测定大脑海马组织和全血中铅、铝、锰含量及血清、海马中NO含量和NOS活力。结果显示,随着染毒剂量的增加,大鼠海马中铅含量逐渐升高,中、高剂量组海马中锰含量和高剂量组海马中铝含量高于对照组,高剂量组血清NO含量和各染毒组海马组织中NO含量低于对照组,高剂量组海马组织中NOS活力低于对照组,差异均有统计学意义(P0.05)。提示PM2.5可使大鼠海马中铅、铝、锰含量升高,海马NO含量和NOS活力降低。     

大鼠吸入氯气亚急性毒性的病理学观察

本文对反复接触氯气9周后大鼠的气管、支气管及肺进行了组织学观察,将结果报告如下。材料和方法染毒用氯气由北京化工二厂提供,纯度为99.9%。染毒期间氯气浓度测定采用甲基橙法     

雷帕霉素对染尘大鼠肺组织胶原蛋白表达的影响

目的探讨雷帕霉素对染矽尘大鼠肺组织胶原蛋白表达的影响。方法对50只SPF级健康雄性大鼠建立肺纤维化模型,随机分为模型组和雷帕霉素组,两组均一次性气管灌注二氧化硅(250 mg/kg);同时,分别腹腔注射生理盐水和雷帕霉毒[2μg/(kg·d)],均隔天给药,持续28 d,分别于第7、14、28、60、90天,用酶联免疫法测定血清中肿瘤坏死因子α(TNF-α)、转化生长因子β(TGF-β)含量,用Massson染色观察大鼠肺组织病理组织学变化,用q RT-PCR法测定肺组织中Ⅰ型和Ⅲ型胶原m RNA含量。结果大鼠肺组织Massson染色结果显示,雷帕霉素组大鼠肺纤维化较模型组严重。随着时间的延长,模型组大鼠血清中TNF-α和TGF-β逐渐升高,差异有统计学意义(P0.05)。雷帕霉素组大鼠血清中TNF-α和TGF-β随着时间的延长而升高,在60 d时降低,90 d时再次升高;除60 d外,其他时间均高于模型组(P0.05)。随着时间的延长,模型组大鼠肺组织Ⅰ、Ⅲ型胶原m RNA逐渐升高,且差异有统计学意义(P0.05)。雷帕霉素组大鼠肺组织Ⅰ、Ⅲ型胶原m RNA表达随各时间点呈降低-升高波动趋势,其中Ⅰ型胶原m RNA表达在除60 d外的各时间点均高于模型组,Ⅲ型胶原m RNA表达在7、28、90 d高于模型组,差异有统计学意义(P0.05)。结论雷帕霉素后期给药可能通过抑制m TOR信号通路而加重染尘大鼠的肺组织纤维化程度。     

维生素C对PM2.5悬浊液诱导的大鼠肺组织炎性损伤的缓解作用

目的探索维生素C(VC)对PM2.5诱导的肺脏炎性损伤的缓解作用及其分子机制。方法 32只雄性SD大鼠随机分为:空白对照(control group, CON)、阴性对照(negative group, NEG)、PM2.5染毒(PM 2.5 exposure group,PM2.5)和VC干预(vitamin C group,VC)共4组。CON组无任何处理,NEG组采用生理盐水气管滴注和灌胃,PM2.5组采用PM2.5悬浊液气管滴注同时生理盐水灌胃,VC组采用PM2.5悬浊液气管滴注同时VC灌胃。动物饲养与干预共21d,每日进行灌胃,气管滴注于D8、D10、D12进行。大鼠处死后采集肺脏和血清,HE染色及酶学试剂盒评估肺脏组织炎性损伤和氧化应激状态,同时使用Western blot和ELISA法检测NLRP3炎症小体信号通路中关键蛋白的表达水平。结果肺组织HE染色表明CON组与NEG组未出现明显的炎性损伤,而PM2.5组肺脏炎性损伤显著,VC组炎性液体渗出和炎细胞浸润较PM2.5组明显减轻。同时,与PM2.5组相比,VC组肺脏中ROS和MDA含量降低而SOD、GSH-Px活力增强。...     

芥子气对雄性大鼠生殖器官影响的病理学观察

芥子气直接损伤组织细胞,引起局部皮肤、眼和呼吸道黏膜的炎症、坏死,大剂量时可致全身吸收中毒.我们曾观察到芥子气中毒对雄性大鼠生殖系统有明显影响,其血生化分析表明血清FSH水平显著升高.本文通过电子显微镜进一步观察了芥子气中毒后雄性大鼠生殖器官的微观病理学变化.     

肺灌注PM2.5对高血压大鼠心血管系统的炎性作用

目的 观察大气细颗粒物对机体心血管系统的炎性作用,探寻其可能作用机制.方法 在上海市某非工业区采集大气PM2.5,选取雄性自发性高血压(spontantously hypertensive,SH)和Wsitar Kyoto(WKY)大鼠各24只作为实验对象,设低、中、高3个剂量组和1个对照组,染毒剂量分别是1.6、8.0、40.0mg/kg,采用气管滴注法进行PM2.5染毒,观察不同染毒剂量组、不同机体内血清高敏C-反应蛋白(high sensitive C-reaction protein,hsCRP)的水平,同时检测心肌白细胞介素1-β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和MIP-2细胞因子的mRNA表达水平,了解机体肺灌注PM2.5后心血管系统的炎性反应,从而探索PM2.5对心血管系统的毒性效应及其可能机制.结果 大鼠PM2.5染毒后,WKY和SH大鼠各染毒组血清hsCRP水平与对照组比较,差异均有统计学意义,且随染毒剂量增加而增加,即存在剂量-反应关系.同时在相同染毒剂量下,WKY和SH大鼠hsCRP水平差异有统计学意义.此外,心肌组织中IL-1β、IL-6、TNF-α和MIP-2的mRNA表达水平总体上随染毒剂量增加有增加趋势,同时相同染毒剂量时,在SH大鼠体内上述各细胞因子的mRNA表达较WKY大鼠高.PM2.5对SH大鼠的心血管系统的炎性反应可能大于对WKY大鼠的作用.结论 PM2.5引起WKY和SH大鼠心血管系统出现明显的炎性反应,且对SH大鼠的作用更为明显,提示PM2.5对机体心血管系统有一定的损伤作用.     

正己烷染毒对大鼠视网膜病理形态学和超微结构的影响

目的 研究正己烷染毒对大鼠视网膜组织的损伤.方法 将32只雄性SD大鼠随机分成对照组和正己烷染毒组.对照组:8只,吸人空气;染毒组:24只,采取静式吸入染毒方式,正己烷浓度为35.2 g/m3,每组6只,分别染毒1、3、7、14 d后处死大鼠.采用光学显微镜和透射电子显微镜观察正已烷对视网膜组织病理学和超微结构的影响.结果 对照组大鼠视网膜组织结构层次清楚,染色均匀,细胞形态规整.染毒组大鼠正己烷染毒7 d和14d时视网膜出现明显变性,并随染毒时间延长损伤加重.染毒14d,大鼠光感受器外节失去正常的膜盘结构,部分膜盘溶解;内节线粒体肿胀甚至消失.外核层细胞水肿,核内染色质浓缩.内核层水平细胞、双极细胞和无长突细胞出现明显变性.节细胞胞质水肿,细胞器明显减少.外丛状层、内丛状层和神经纤维层神经突起水肿,突触内微丝和小泡减少.结论 正己烷可造成大鼠视网膜组织的明显损害,将导致眼底病的发生.     

接尘工人经支气管肺活检的病理分析

目的 探讨经纤维支气管镜肺活检肺组织标本病理学改变在尘肺诊断中的价值.方法 2011年5月至2011年9月在我院经支气管肺活检(TBLB)取得肺组织标本的职业性粉尘接触者35例,同期经胸腔镜或开胸肺叶切除取得的肺组织标本的无粉尘接触史的患者27例,进行肺组织纤维组织增生、类结节、粉尘沉积和晶粒偏光等病理指标对比.结果 接尘组中度粉尘沉着6例(17.1％),与对照组(0)相比,差异有统计学意义(P＜0.05).接尘组肺组织纤维化增生28例(80.0％),明显高于对照组(11例,40.7％),差异有统计学意义(P＜0.05).接尘组有6例发现晶粒偏光阳性,6例发现类结节,对照组病例无晶粒偏光阳性或类结节改变.结论 TBLB病理检查能取得接触粉尘引起肺内相关改变的依据,在尘肺病的诊断中有一定的应用价值.     

Biologic monitoring of workers exposed to silver

Summary Air-lead levels (PbA) and biological indices were studied in three ceramic factories (185 workers altogether). A difference in the pattern of lead exposure was found in the largest factory (A) and the other two smaller factories (B and C). PbA never exceeded 67 g/m³ in factory A, but reached values as high as 378 g/m³ in factory B. 19% of PbB values were higher than 40 g/100 ml in factory A, 63% in factory B and 35% in factory C. As was expected, a closer analysis of the jobs confirmed a higher exposure level in people directly in contact with lead glazes (glazers and kiln operators). In factories B and C, however, there was also a significant lead uptake in selection and maintenance staff, who worked in areas at some distance from the glazing lines. This may be due in part to pollution spread over all departments, but also to the lack of hygiene and washing facilities whose importance is stressed for effective prevention. Biological monitoring is suggested as being useful for all workers, whatever the lead-air level, bearing in mind the possibility of lead intake orally through soiling.     

交通污染相关PM_(2.5)亚急性染毒对大鼠免疫功能的影响

目的建立交通污染相关PM_(2.5)大鼠亚急性染毒模型,研究其对大鼠肺泡巨噬细胞吞噬功能、体液免疫和细胞免疫功能的影响。方法将24只雄性SD大鼠随机分为4组,即对照组(生理盐水组)及低、中、高剂量PM_(2.5)染毒组(剂量分别为1.5、6、24 mg/kg)。采用气管内滴注PM_(2.5)混悬液的方式对大鼠进行染毒,隔天染毒1次,共染毒6次。采用中性红比色法测定肺泡巨噬细胞吞噬功能,MTT法检测T淋巴细胞增殖功能,ELISA法测定血清中IgG、IgM、IgA水平。结果大鼠肺泡巨噬细胞的吞噬功能随着染毒剂量的增加而下降,24 mg/kg PM_(2.5)染毒组大鼠的肺泡巨噬细胞吸光度(OD值)低于1.5 mg/kg PM_(2.5)组,差异有统计学意义(P0.05)。大鼠脾脏T淋巴细胞增殖功能随着染毒剂量的增加而下降,各剂量PM_(2.5)染毒组大鼠刺激指数(SI)均低于对照组,差异有统计学意义(P0.05)。大鼠血清IgG、IgM、IgA水平随着染毒剂量的增加而降低,6、24 mg/ml PM_(2.5)染毒组大鼠血清IgG水平低于对照组,1.5、6、24 mg/ml PM_(2.5)染毒组血清IgM、IgA水平低于对照组,差异均有统计学意义(P0.05)。结论交通污染相关PM_(2.5)可能抑制大鼠的肺泡巨噬细胞吞噬功能、细胞免疫功能和体液免疫功能。     

Evaluation of cytokine expression in BEAS cells exposed to fine particulate matter (PM2.5) from specialized indoor environments

Fine particles were collected in three indoor environments and an outdoor reference site. Samples were acid and aqueous extracted for metal analyses and cytokine expression study using a BEAS-2B line. Results revealed that the average PM(2.5) concentration indoors was 5.8 μg/m(3) while outside, it was 9.4 μg/m(3). The airborne metal concentrations in indoor air ranged from 0.01 ng/m(3) (Cd) to 620 ng/m(3) (Al). All metals analyzed were higher indoors when compared to outdoor (I/O ratio) indicating a contribution from the workplace. Some metals were more efficiently extracted (e.g., Ni, V, As) in the aqueous phase than others (e.g., Fe and Al). Toxicological assays showed that the aqueous extracts at 20% induced IL-6 and subsequently inhibited it at a higher concentration (50%); both IL-8 and MCP-1 were inhibited at 20 and 50%. As, Ni and V concentrations seem to be the most important metals associated with the cytokine induction/inhibition response probably due to the higher bioavailability.     

不同出行方式PM_(2.5)个体暴露水平的比较研究

目的在不同浓度大气PM_(2.5)水平下,比较不同出行方式的PM_(2.5)个体暴露水平,并进一步比较地铁站不同位置的PM_(2.5)浓度,以期为城市居民选择适宜的出行方式提供科学依据。方法于2015年12月30日至2016年1月4日,选择北京市城区的某条路线作为研究地点,使用便携式PM_(2.5)监测仪同时测量步行、乘坐公交车和地铁3种出行方式的PM_(2.5)个体暴露水平;对地铁站台、安检处和地铁车厢内的PM_(2.5)浓度进行同步监测并比较。结果在同一研究时期,步行、乘坐公交车和地铁测得的PM_(2.5)个体暴露浓度均值分别为219.34、209.61、167.56μg/m3。当大气PM_(2.5)浓度较低时(≤60μg/m3),乘坐地铁的PM_(2.5)个体暴露水平高于步行和乘坐公交车;当大气PM_(2.5)浓度较高时(100μg/m3),乘坐地铁的个体PM_(2.5)暴露水平明显低于步行和公交车,差异均有统计学意义(P0.05)。监测期间地铁站台、安检处和车厢内的PM_(2.5)浓度均值分别为196.90、170.20、136.82μg/m3。结论在不同的大气PM_(2.5)污染水平下,不同出行方式的人群PM_(2.5)个体暴露水平不同。     

2010年北京市归因于大气PM2.5污染的过早死亡研究

目的 评估大气PM2.5长期暴露导致的过早死亡,为科学制定政策保护人群健康提供科学依据.方法 收集卫星遥感反演的北京市2010年的PM2.5浓度数据、人口数据、基线死亡率等基础数据,利用GIS空间统计工具将网格化的PM2.5污染数据转换为区县尺度数据,基于WHO的经典全球疾病负担评估模型和PM25全暴露范围RR函数表,评估北京市各区县归因于大气PM2.5污染的过早死亡,并探讨其空间分布特征及分疾病种类的特点.结果 2010年北京市各区县的大气PM25年均浓度均超过GB 3095-2012《环境空气质量标准》二级浓度限值(35 μg/m3);北京市归因于大气PM:5污染的过早死亡数为16 527人,归因死亡率为0.843‰,中心城区和东南部郊区的过早死亡风险较高,过早死亡数最多的为朝阳区(5 648人,归因死亡率为1.542‰)和海淀区(4 21 1人,归因死亡率为1.284‰),过早死亡数最少的为西北部郊区.结论北京市2010年归因于大气PM2.5污染的过早死亡人数较多,应引起相关部门的重视;在制定政策减少归因于大气PM2.5污染的过早死亡时,应重点关注人口密集的中心城区和发展较快的东南部郊区,并基于各区县过早死亡的疾病分布特点开展针对性的宣教和防控.     

Assessing personal travel exposure to on-road PM2.5 using cellphone positioning data and mobile sensors

PM_2.5 pollution imposes substantial health risks on urban residents. Previous studies mainly focused on assessing peoples' exposures at static locations, such as homes or workplaces. There has been a scarcity of research that quantifies the dynamic PM_2.5 exposures of people when they travel in cities. To address this gap, we use cellphone positioning data and PM_2.5 concentration data collected from smart sensors along roads in Guangzhou, China, to assess personal travel exposure to on-road PM_2.5. First, we extract the trips of cellphone users from their trajectories and use the shortest path algorithm to calculate their travel routes on the road network. Second, the travel exposure of each user is estimated by associating their movement patterns with PM_2.5 concentrations on roads. The result shows that most users’ average travel exposures per hour fall within the range of 20 ug/m³ to 75 ug/m³. Travel exposure varies across users, and 54.0% of users experience low travel exposure throughout the day, 25.5% of users experience high travel exposure in the evening, and 20.5% of users experience high travel exposure in the afternoon. Furthermore, the impacts of on-road PM_2.5 on urban populations are uneven across roads. More attention should be given to roads with high PM_2.5 concentrations and traffic flows in each period, such as Huan Shi Middle Road in the morning, Inner Ring Road in the afternoon, and Xinjiao Middle Road in the evening. The findings in this study can contribute to a more in-depth understanding of the relationship between air pollution and the travel activities of urban populations.