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。     

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。     

吸入含矽粉尘和煤尘在大鼠肺中滞留的比较研究

以大鼠动式吸入染尘方法吸入含矽尘和煤尘２周。用甲酸消化法测定大鼠肺和纵膈淋巴结中的粉尘含量。结果发现在染尘结束后的第３天，煤尘组大鼠肺中的粉尘含量高于矽尘组；９０天后则矽尘组大鼠肺中的粉尘含量高于煤尘组。提示含矽粉尘在肺中滞留较煤尘持久，因而可对肺产生较为严重的损伤。结果也同时证实淋巴系统是肺内粉尘转移的一条重要途径。     

矽肺大鼠模型肺组织超声影像学改变初步探讨

选取22只SPF级SD大鼠，随机分为正常组5只，17只大鼠经气管非暴露式灌注矽尘混悬液双肺染尘，建立矽肺模型。染尘1个月后对正常组（未染尘）和模型组大鼠进行肺组织及胸膜线超声观察。结果显示，与正常组比较，模型组大鼠9只（52.9%）肺组织见低回声团；模型组大鼠17只（100.0%）胸膜线厚度较染尘前明显增加，14只（82.4%）胸膜线模糊、不规则且连续性中断。提示染矽尘大鼠肺组织及胸膜线的超声影像学变化可为矽肺病病程进展提供参考依据。     

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     

不同变质期煤尘致病作用的实验研究

1942年Hartasiett提出了煤品位学说[1]，认为煤的变质程度越高其致病性越强。国内外不少流行病学调查的结果也显示不同煤矿煤工尘肺患病率的差异与煤变质程度的高低有关，煤变质程度越高，尘肺患病率也越高。但广西几个主要煤矿的煤工尘肺患病率差异却与煤的变质程度高低无关[2，3]。为查明原因，我们采集了4个不同煤矿的新鲜煤样进行了实验研究。1材料与方法1．1实验动物Wistar健康大鼠84只，雌雄各半，体重180～200g，随机分为6组，即石英尘组（阳性对照）、生理盐水组（阴性对照）、无烟煤组、烟煤组Ⅰ组、烟煤Ⅱ组及褐煤组，每组大鼠14…     

高浓度矽尘接触对大鼠氧化应激的作用研究

目的探讨大鼠高浓度矽尘接触过程中是否存在氧化应激反应。方法选40只SPF级Wistar雄性大鼠随机分为4组,即高剂量染尘组（1 000mg/m^3）、中剂量染尘组（500mg/m^3）、低剂量染尘组（100mg/m^3）和对照组,选用自然动式染尘装置每天染尘2h。染尘49d后处死大鼠,测定肺组织匀浆超氧化物歧化酶（SOD）、总抗氧化能力（T-AOC）活性及丙二醛（MDA）、还原性谷胱甘肽（GSH）含量。结果长时间、高浓度矽尘接触降低大鼠肺组织的SOD（30.25±0.49）U/ml、T-AOC活性（7.93±0.74）kU/L和GSH（2.34±0.96）g/L含量,同时MDA（5.65±0.13）nmol/ml水平升高,与对照组比较,差异有统计学意义（P〈0.01）。结论大鼠高浓度矽尘接触过程早期炎症反应发生可能与机体氧化应急有关。     

石英染尘大鼠早期肺灌洗液细胞中羟脯氨酸等指标变化

对不同剂量（５、１０、２０、４０ｍｇ）石英粉尘染尘两周大鼠肺灌洗液细胞中羟脯氨酸等指标变化进行研究。结果表明，各染尘组肺灌洗液中细胞分类、细胞中羟脯氨酸及总脂、上清液中总脂、总蛋白、乳酸脱氢酶、铜蓝蛋白及全肺胶原含量均出现明显变化。进一步分析表明，以肺灌洗液细胞中羟脯氨酸与全肺胶原之间的相关性最好（γ＝０．８３４），说明该指标能较好地反映染尘早期全肺胶原含量的增加。     

淡泉水对染尘大鼠脂质过氧化和超氧化物歧化酶活力的影响

目的：探讨淡泉水对染尘大鼠体内脂质过氧化物（LPO）和超氧化物歧化酶（SOD）的影响。方法：大鼠经气管注入石英粉尘后,饮淡泉水8周后,处死动物取肺、肝、脑组织测定LPO含量,取全血测SOD活力。取肺测定胶原蛋白和称肺重量。结果：染尘＋饮淡泉水组的肺、肝、脑组织LPO、肺胶原蛋白含量、肺重量明显低于染尘对照组（P＜0．05－P＜0．01）。血中SOD活力明显高于染尘对照组（P＜0．05）。结论：结果表明,该淡泉水能在一定程度上提高SOD活力。对SiO2引起的大鼠体内LPO的升高有一定的抑制作用。     

Pulmonary Effects of Tobacco and Related Substances

Pulmonary burdens of quartz dust and bituminous coal dust, respectively, were imposed upon rats and hamsters by inhalation and intratracheal injection before and after production of papain- induced emphysema. Quantitation was performed of the pulmonary content of silica, hydroxyproline, and lipids of the animals burdened with quartz dust and of the pulmonary dust content only of the animals burdened with coal dust. There were statistically significant reductions in mean silica content as well as mean coal dust content of emphysematous lungs in all four groups of hamsters. In rats, whereas the mean pulmonary dust content was lower in emphysematous animals than in nonemphysematous controls, this difference was statistically significant in only two of the four groups. Improved dust clearance is believed to be a major factor in the reduction of dust content of emphysematous lungs.     

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.     

The response of rat alveolar macrophages to chronic inhalation of coal dust and/or diesel exhaust

The use of diesel-powered equipment in underground mines has raised questions regarding possible synergistic effects of coal dust and diesel emissions. Therefore, the effects of chronic exposure of rats to coal dust and/or diesel exhaust on various properties of alveolar macrophages were investigated. Inhalation exposure of rats was 7 hr/day, 5 days/week for 2 years. Exposure groups were: filtered air controls, 2 mg/m3 coal dust, 2 mg/m3 diesel particulate, and 1 mg/m3 coal dust plus 1 mg/m3 diesel exhaust. Exposure to coal dust and/or diesel exhaust had little effect on oxygen consumption, membrane integrity, lysosomal enzyme activity, or protein content of alveolar macrophages. However, exposure to coal dust increased macrophage yield, enhanced chemiluminescence, and increased the activity of the cell membrane (i.e., increased cellular spreading and surface ruffling). In contrast, diesel emissions depressed chemiluminescence and decreased the ruffling of the cell membrane. Therefore, the data suggest that exposure to coal dust and/or diesel exhaust does not affect the viability of alveolar macrophages. However, coal dust may activate alveolar macrophages while diesel emissions may depress the phagocytic activity of these cells. The combination of exposures to coal dust and diesel exhaust results in a phagocytic activity which is an average of the effects of separate exposures.     

The protective role of zinc in the toxic action of coal dust upon mouse macrophages.

Macrophages from mice were cultured at 37 degrees C with 1640 medium containing 10% bovine serum. The macrophage suspension was made from 50 Swiss mice and was cultured in the following groups: control group; coal dust group (with added coal dust particles (10 micrograms/ml) smaller than 4 microns diameter); subdivided zinc-coal dust group (as coal dust group with zinc added in three different concentrations--namely, 10 ppm, 30 ppm, and 60 ppm). Cells were examined by light microscopy. Obvious differences were found in the rate of cell deaths between the coal dust group and the zinc-coal dust group after culture for 48 hours. The cell membranes were ruptured after culturing with coal dust, and the presence of zinc appeared in some degree to protect cell membranes from damage caused by the dust. Staining the cells with Gomori's modified method, showed that acid phosphatase particles in the zinc-coal dust group were more numerous than in the coal dust group. The results indicate that the trace element zinc may play an important part in protecting against the cytotoxic action of coal dust.     

煤矿工煤肺患病率、煤尘实验研究及其影响因素的分析

本文选择了均属烟煤的大同煤矿和汾西煤矿为研究对象。比较了两矿煤肺的患病率,并取煤尘进行溶血试验,细胞毒性实验及大鼠染尘实验,均表明大同煤较汾西煤的致纤维化作用强。大同媒中多种金属元素(Ni、Pb、Cu、Co)及挥发份均非常显著地高于汾西煤。为此将两种煤去掉挥发份后,再进行实验,结果表明,处理后的两种煤均较未处理的煤对细胞的毒性减低。认为挥发份在煤尘致纤维化作用中有一定影响,但并不是唯一的因素。