含矽粉尘的不同负荷吸入方式对大鼠肺中粉尘滞留和肺灌洗液中磷脂的影响

用甲酸法测定大鼠肺和纵膈淋巴结中的粉尘含量；用高效液相色谱法检测肺泡灌洗液中的磷脂。结果发现在染尘总剂量相同时，短时间以冲击量吸入含矽粉尘（冲击组）的大鼠肺中粉尘的含量在染尘结束后的第３天高于其它组；总磷脂的含量在第３天、第１０天也明显高于对照组。提示短时间突然吸入大量含矽粉尘可对肺产生较为严重的损伤     

红茶菌制剂对染尘大鼠肺干重及游离二氧化硅含量的影响

目的通过给予含与不含中草药的红茶菌制剂进行喷雾治疗,研究其对染尘大鼠全肺干重及肺游离二氧化硅含量的影响。方法取SD大鼠24只,随机分为红茶菌复合制剂组、红茶菌单纯制剂组、阳性对照组、阴性对照组(不染尘)。用标准石英粉尘配成的矽尘混悬液注入大鼠气管,复制矽肺动物模型。染尘后第4天开始对2个红茶菌制剂组进行喷雾给药,给药4周后处死动物,进行全肺干重及肺游离二氧化硅含量测定。结果红茶菌单纯制剂组全肺干重和游离二氧化硅含量均为最高,与阳性对照组比较差异无统计学意义(P0.05);红茶菌复合制剂组肺游离二氧化硅含量值低于其他各染矽尘组,差异有统计学意义(P0.05)。结论红茶菌复合制剂组能促进二氧化硅粉尘从大鼠肺部组织排出,具有一定的生物排尘功能。红茶菌单纯制剂对大鼠的排尘效果不明显。     

石棉矿精选车间自然吸入染尘家犬肺病理观察

本文报导家犬于新康石棉矿精选车间自然吸入石棉等飘尘3年所致肺部病变。实验选用家犬13只分为:(1)自然吸入染尘组(6只);(2)气管内注入染尘组(3只);(3)空白对照组(4只)。其结果与人体石棉肺病变相比较。实验结果看出各组间肺内粉尘分布和尘性病变均有差异。自然吸入染尘组、粉尘相对均匀地分布于两肺各叶的外周带,随接尘时间延长,肺内粉尘量增多,往往呈全肺弥漫分布。气管内注入染尘组,粉尘在肺内分布极不均匀,尘粒多集中在双肺下叶,常造成呼吸细支气管腔甚至部分细小支气管腔尘性阻塞,而肺间质内仅有微量粉尘存在。空白对照组仅有微量粉尘沉着于呼吸细支气管壁和相应的肺泡壁内。各组动物肺内均未见石棉小体形成。粉尘所致肺病变,自然吸入染尘组以弥漫性纤维化占优势。而气管内注入柒尘组则以小结节形成更为突出。因此自然吸入柒尘组的粉尘分布以及尘性病变看来更接近于人体石棉肺的发生、发展规律。根椐部分自然吸入染尘动物肺组织消化滤物及肺内尘灶原位X线能谱分析,证实在肺纤维化中石棉尘起主导作用(其他矽酸盐矿尘如高岭石……可能也起一定作用)。     

不同品位煤尘对大鼠肺冲洗液中脂质含量的影响

目的 观察不同品位煤尘对大鼠肺冲洗液中脂质含量的影响。方法 实验分为９组，染尘时间分别为３０、９０、１８０和３６０天。结果 各煤尘组大鼠肺冲洗液中脂质含量高于同期对照组，但又都低于同期石英组。煤尘组间的差异与煤变质程度的高低无关，与煤尘中游离二氧化矽含量高低有关。结论 煤尘的致病性强弱与煤尘中ＳｉＯ２含量高低有关。     

自然吸入煤尘大鼠肺病变的观察

大鼠自然吸入煤尘的慢性染尘方式，所致病变分布均匀，动态地观察肺内煤尘性病变的发生发展过程。吸入到肺泡内的煤尘被肺世噬细胞吞噬，多在终末细支管及呼吸性细支气管周围或其所属的肺泡腔积聚或填充。随时间延长，发展成煤尘细胞灶，煤细胞性结节以及融合结节。煤尘致纤维化作用弱，１２月组见少数纤维细胞性结节，与矽尘性实验动物所示的纤维性结节有显著差别。     

蔺草染土尘对染尘早期大鼠肺损伤的实验观察

目的研究蔺草染土尘对染尘早期大鼠肺脏的致纤维化作用。方法采用非暴露式气管注入技术对SD雄性大鼠进行染尘（50mg/只），于染尘后3、6个月取大鼠肺组织做病理观察。结果染尘组病理观察可见，肺泡Ⅱ型细胞增生、脱落，病灶内粉尘沉着，尘细胞、成纤维细胞聚集，可见Ⅰ，Ⅱ级矽结节和少量胶原纤维性变。结论蔺草染土尘对染尘早期大鼠肺部有轻度致纤维化作用。     

广西不同煤质和围岩粉尘对大鼠肺纤维化病变的研究

目的：探讨不同煤种煤尘致病性的特点，确定影响煤尘致病性的主要因素。方法：采用广西烟煤、无烟煤和褐煤不同煤种粉尘制作大鼠尘肺模型，从生化指标来探讨不同的煤种粉尘与尘肺的发病关系。结果：染尘大鼠肺冲洗液中酸性磷酸酶、乳酸脱氢酶，肺组织中脂质过氧化物、胶原蛋白含量均为石英组最高，其次依次是烟煤组、无烟煤组、褐煤组，最低为正常对照组，结果差异有显著性（P＜0．01）。结论：围岩煤尘具有一定的致病性，但较石英弱，其致病性强弱与煤质优劣无关，与围岩煤尘中游离二氧化矽的含量高低有一定关系。     

沙漠尘致大鼠肺纤维化的实验研究

本实验采用某沙漠地区沙漠尘给大鼠气管内注入染尘。实验分石英、沙漠尘高剂量组（分别５０ｍｇ／只）和低剂量组（分别２５ｍｇ／只）及空白对照组。大鼠染尘后１、３、６、９和１２个月分别处死，测定肺重及全肺胶原蛋白、总脂和类脂含量，并作病理组织学检查。结果表明：沙漠尘对肺重及组织生化指标有一定的作用，且粉尘在肺组织中长期沉积，并引起以异物巨细胞为主的反应，与石英尘相比，未见明显矽结节纤维化改变。作者认为，沙漠尘致纤维化能力弱。     

低浓度晶体石英粉尘与矽肺发病关系及其最高容许浓度

用雄性Wistar大白鼠经动式吸入低农度(1mg/m~3)晶体石英粉尘历时一年另三个月。结果发现实验组动物全肺胶原蛋白含量均高于对照组(P<0.001),且随染尘时间的延长而增长。病理组织学观察有矽尘反应性慢性支气管炎,肺硬化和细胞纤维性矽结节等矽肺的早期变化。实验结束,石英尘在鼠肺组织中的平均沉积量为0.91863mg,占粉尘总吸入量的3.92%。该报告表明,我国现行石英粉尘MAC宜不超过1mg/m~8是可行的,但从长远看仍有一定危险性。至于修改已有的标准需进一步作流行病学调查。     

煤尘及煤矽混合性粉尘所致大白鼠肺脏的形态学变化

本文从病理形态学角度来观察了煤尘及煤矽混合性粉尘对大白鼠肺脏的影响。结果含矽低的煤尘不引起明显纤维化,有轻度致炎作甩,能引起一系列机体变化;而煤矽混合性粉尘是煤尘和矽尘所致病变的联合,兼有矽尘和煤尘的形态学变化。     

不同变质期煤尘致病作用的实验研究

在广西四个不同煤矿矿井下回采工作面采集新鲜无烟煤、烟煤及褐煤,制成煤尘后对Wistar大鼠进行非暴露式一次染尘。染尘45天及90天宰杀大鼠进行实验研究。结果:大鼠肺冲洗液中脂质含量、鼠肺干、湿重及全肺胶原含量,石英组(阳性对照)大于煤尘组,煤尘组大于生理盐水组(阴性对照),差异有显著性意义(P<0.01);煤尘组间的差异与其变质程度的高低无关。提示石英尘的致病性比煤尘强,煤尘致病性的强弱与其变质程度的高低无相关关系。     

不同变质期煤尘致病作用的实验研究

在广西四个不同煤矿矿井下回采工作面采集新鲜无烟煤、烟煤及褐煤，制成煤尘后对Ｗｉｓｔａｒ大鼠进行非暴露式一次染尘。染尘４５天及９０天时宰杀大鼠进行实验研究。结果：大鼠肺冲洗液中脂质含量、鼠肺干、湿重及全肺胶原含量，石英组（阳性对照）大于煤尘组，煤尘组大于生理盐水组（阴性对照），差异有显著性意义（Ｐ＜０．０１）；煤尘组间的差异与其变质程度的高低无关。提示石英尘的致病性比煤尘强，煤尘致病性的强弱与其变质程度的高低无相关关系。     

Lung dust and lung iron contents of coal workers in different coalfields in Great Britain

Bergman, I., and Casswell, C. (1972).Brit. J. industr. Med.,29, 160-168. Lung dust and lung iron contents of coal workers in different coalfields in Great Britain. Lung dust analyses from seven coalfields are studied and it is found that the average dust composition varies significantly with the rank of coal. The higher the rank, the higher the coal percentage and the lower the quartz percentage of the lung dust. This holds for all coalfields except in Scotland, where the lung dust contains mainly soot instead of coal.

Samples of airborne dust collected at the coalface in different coalfields show a similar but small variability of composition with rank of coal, and the results from Scotland are in good agreement with the results from other coalfields.

The amount of iron in simple pneumoconiosis lungs is related to their mineral and coal contents and to the factor `years underground'. The strongest relationship is with coal and mineral for coalface workers from England. For pit accident cases (all simple pneumoconiosis) mineral is important as well as years underground, while for simple pneumoconiosis cases from Scotland, years underground is the most important factor.

     

Lung oxidative response after acute coal dust exposure

Coal dust exposure can induce an acute alveolar and interstitial inflammation that can lead to chronic pulmonary diseases. The objective of this study was to describe the acute and later effects of acute coal dust exposure in lung parenchyma and the involvement of reactive oxygen species in coal dust effects. Forty-eight male Wistar rats (200-250 mg) were separated into four groups: 48 h, 7 days, 30 days, and 60 days after coal dust instillation. Gross mineral coal dust (3 mg/0.5 mL saline) was administered directly in the lungs of the treatment group by intratracheal instillation. Control animals received only saline solution (0.5 mL). Lipid peroxidation was determined by the quantity of thiobarbituric acid-reactive species (TBARS), oxidative damage to protein was obtained by the determination of carbonyl groups, the total radical-trapping antioxidant parameter (TRAP) was estimated by luminol chemoluminescence emission, catalase activity was measured by the rate of decrease in hydrogen peroxide, and superoxide dismutase activity was assayed by the inhibition of adrenaline autooxidation. Histological evaluation of coal dust-treated rats demonstrated an inflammatory infiltration after 48 h of the exposure. Initially, this was a cellular infiltration suggestive of lymphocyte infiltration with lymphoid hyperplasia that remained until 7 days after induction. This initial response was followed by a chronic inflammatory infiltration characterized by aggregates of macrophages 30 days after induction. This inflammatory response tended to resolve 60 days after induction, being similar to that of control animals. During both the acute and chronic phases of lung inflammation we observed a decrease in the TRAP in the lung of coal dust-exposed animals compared to that in control animals. We also observed an activation of superoxide dismutase 60 days after coal dust exposition. TBARS were increased 60 days after coal dust exposure and protein carbonyl groups increased at all times after coal dust exposure (48 h, 7 days, 30 days, and 60 days). These data suggested a biphasic inflammatory response and the involvement of oxidative damage in coal dust-induced lung damage.     

Dust exposure, dust recovered from the lung, and associated pathology in a group of British coalminers

The relation between dust exposure, retained lung dust, and pneumoconiosis have been examined in 430 dead coalminers who had participated in a large scale epidemiological survey of respiratory health. The men were divided into three groups depending on the presence of particular lesions in their lungs. Lungs containing no fibrotic lesions in excess of 1 mm were included in the "M" group, those with fibrotic lesions of between 1 mm and 9 mm in diameter were included in the "F" group, and those with any lesion 10 mm or more were categorised as having progressive massive fibrosis (PMF). The men were further divided into four groups according to the rank of coal mined at the colliery of employment. The mean weight of lung dust increased over the pathological range (M----F----PMF) regardless of the rank of coal mined. The men with PMF had not received unusually high exposures to dust in life but were found to have accumulated more dust in their lungs per unit of dust exposure than men without PMF, providing further evidence for differences in the patterns of deposition or clearance, or both, of dust in these men compared with those who do not develop PMF. For men who had mined the higher rank coals there was no difference in the composition of the lung dust between the pathological groups. Lungs from men mining low rank coal, however, showed a striking increase in the proportion of ash over the pathological groups (M, F, and PMF). In men who had mined low rank coal the proportion of ash in the airborne dust to which they had been exposed and in the dust retained in their lungs was, as expected, greater than in men who had worked with higher rank coals. For the same men, and particularly associated with the presence of some dust related fibrosis, the proportion of ash in retained dust was higher than that in the dust to which the men were exposed suggesting the occurrence of selective deposition or retention of the mineral components of dust in this group.     

Dust exposure, dust recovered from the lung, and associated pathology in a group of British coalminers.

The relation between dust exposure, retained lung dust, and pneumoconiosis have been examined in 430 dead coalminers who had participated in a large scale epidemiological survey of respiratory health. The men were divided into three groups depending on the presence of particular lesions in their lungs. Lungs containing no fibrotic lesions in excess of 1 mm were included in the "M" group, those with fibrotic lesions of between 1 mm and 9 mm in diameter were included in the "F" group, and those with any lesion 10 mm or more were categorised as having progressive massive fibrosis (PMF). The men were further divided into four groups according to the rank of coal mined at the colliery of employment. The mean weight of lung dust increased over the pathological range (M----F----PMF) regardless of the rank of coal mined. The men with PMF had not received unusually high exposures to dust in life but were found to have accumulated more dust in their lungs per unit of dust exposure than men without PMF, providing further evidence for differences in the patterns of deposition or clearance, or both, of dust in these men compared with those who do not develop PMF. For men who had mined the higher rank coals there was no difference in the composition of the lung dust between the pathological groups. Lungs from men mining low rank coal, however, showed a striking increase in the proportion of ash over the pathological groups (M, F, and PMF). In men who had mined low rank coal the proportion of ash in the airborne dust to which they had been exposed and in the dust retained in their lungs was, as expected, greater than in men who had worked with higher rank coals. For the same men, and particularly associated with the presence of some dust related fibrosis, the proportion of ash in retained dust was higher than that in the dust to which the men were exposed suggesting the occurrence of selective deposition or retention of the mineral components of dust in this group.     

探讨尘肺病分类的合理性

粉尘不同,诊断的尘肺病种类不同。我国现有尘肺病13种分别对应不同的粉尘或工种。ILO（国际劳工组织）的专家们普遍认为区分致纤维化矿物粉尘如二氧化硅和石棉和非致纤维化矿物粉尘如云母和石墨是重要的。我国的专家持不同的观念,认为吸入并贮留在肺内的任何粉尘均能引起异物反应,长期贮留在肺内的异物均可以导致非特异性的纤维性增生。从各种尘肺的病理特点以及普通型间质性肺炎的病理改变中发现,二氧化硅和石棉所致肺问质纤维化最具特点。二氧化硅可以致肺组织内形成同心圆排列的玻璃样变。石棉粉尘主要的病理改变是导致胸膜斑的形成。其他各种粉尘多是在肺内引起多发性粉尘灶,可能是这些粉尘在局部潴留而形成继发性纤维化。将矿物性粉尘区分为致纤维化和非致纤维化2个大类,并设定合理的开放性目录,为职业病诊断提供便利。国际癌症组织（IARC）将石棉和石英列为人类已知的致癌物,致纤维化粉尘的概念突出了游离二氧化硅和石棉的危害。癌症比肺间质纤维化更具有致死性;致纤维化粉尘比非致纤维化粉尘更具侵入性。     

铀矿尘致大鼠肺纤维化中转化生长因子β1的表达

目的探讨铀矿尘诱导肺组织纤维化过程转化生长因子-β1(TGF-β1)在肺组织中的表达以及TGF-β1含量的变化。方法36只大鼠随机等分为铀矿尘组和对照组。采用一次性非暴露式气管内滴注染尘方法,铀矿尘组每只大鼠气管内滴注20mg/ml的粉尘悬液1ml,对照组气管内滴注生理盐水1ml,分别于处理后第14、30d及60d每组随机处死6只取样,观察肺组织病理形态改变以及肺组织中TGF-β1的表达,测定肺匀浆和血浆中TGF-β1含量的改变。结果铀矿尘组在染尘后第14d时肺组织主要表现为炎症改变,第30d时出现纤维增生同时TGF-β1表达增强,第60d时表现为大量的纤维增生并伴有TGF-β1强表达。肺匀浆和血浆中TGF-β1含量在第14d时高于对照组,第30d及60d时肺匀浆和血浆中TGF-β1含量显著高于对照组(P0.01)。结论铀矿尘诱导肺组织纤维化过程中存在TGF-β1高表达,肺匀浆和血浆中TGF-β1含量明显增加。     

某煤业集团煤工尘肺病人肺通气功能分析

目的了解某煤业集团煤工尘肺病人和接尘非煤工尘肺病人肺通气功能损伤情况,探讨煤工尘肺病人不同工种、工龄、分期之间肺通气功能损伤的差异。方法选取某煤业集团确诊的煤工尘肺病人555名。另外选取该煤业集团555名接尘的非煤工尘肺病人和207名非接尘工人作为对照。采用统一的体检表格,由专业医师进行统一体检,并逐一填写表格。肺功能测定仪器为北京产AS.507型肺量计,进行肺通气功能指标测定。运用卡方检验、单因素方差分析、相关分析进行统计学处理。结果尘肺病人组肺功能异常率高于接尘非尘肺病人组和不接尘健康工人组,差异有统计学意义(χ2=193.319,P<0.001);采用单因素方差分析,三组人群各指标的比较结果显示,尘肺病人组的FEV1.0相对值和FEV1.0%低于接尘非尘肺病人组和不接尘工人组,尘肺病人组和接尘非病人组的FVC相对值均低于不接尘工人组。555名尘肺病人包括不吸烟108人、戒烟427人和吸烟20人,其肺功能异常率分别是67.6%、74.5%和90.0%(χ2=4.381,P=0.036<0.05),不吸烟组和吸烟组的FVC相对值均低于戒烟组,戒烟组的FEV1.0%明显低于不吸烟组。FEV1.0相对值在各组之间差异无统计学意义。各工种之间FVC相对值、FEV1.0相对值,FEV1.0%比较,差异均无统计学意义;各工龄组之间差异亦无统计学意义。各期别尘肺病人FVC相对值、FEV1.0相对值比较,差异无统计学意义,但贰期、叁期尘肺病人FEV1.0%高于壹期尘肺病人。结论接尘非煤工尘肺病人与煤工尘肺病人肺通气功能均有损伤,煤工尘肺病人肺通气功能损伤重于接尘非煤工尘肺病人,说明肺通气功能可以作为监测煤工尘肺的早期敏感动态观察指标。吸烟是影响肺通气功能的一个重要因素,吸烟加剧煤工尘肺病人肺通气功能的损伤程度。