不同品位煤尘细胞毒性作用的实验研究

本文报道用广西不同品位煤尘与家兔肺巨噬细胞（ＰＡＭ）进行体外培养，观察了各时点的细胞培养液中乳酸脱氢酶（ＬＤＨ）及酸性磷酸酶（ＡＣＰ）相对含量的变化，结果表明各孵育时点内烟煤尘组的这两种酶含量开始明显增高，而后增长缓慢，褐煤尘组则与之相反，而无烟煤尘组的两种酶含量始终较低，显示了煤尘的细胞毒性大小与煤尘的品位高低不一致。作者认为煤尘中ＳｉＯ２含量及表面性质是影响其毒性的重要因素。     

3种煤尘细胞毒性与其成纤维细胞效应的关系

采用ＳＥＭ／ＥＤＸＳ和ＸＰＤ检测不同变质期３种煤尘的化学元素和矿物成分．将不同浓度的煤尘作用于大鼠肺泡巨噬细胞（ＡＭ），测定粉尘－ＡＭ上清液中ＰＧＥ２、ＭＤＡ、ＬＤＨ含量和细胞存活率。将煤尘和标准石英作用过的粉尘－ＡＭ上清液，再作用于成纤维细胞。选用３Ｈ－ＴｄＲ同位素掺入法、ＭＴＴ法和放射自显影法，检测２ＢＳ细胞的增殖能力；对二甲氨基苯甲酸法测定２ＢＳ细胞胶原合成；在透射电镜下，观察２ＢＳ细胞超微结构变化．并测算其粗面内质网的扩张程度．结果显示：３种煤尘细胞毒性大小顺序Ａ＞Ｍ＞Ｆ，并不与其致纤维化效应强弱的顺序（Ｆ＞Ａ＞Ｍ）相一致。这可能与其矿物成分有关。     

较低剂量石英粉尘所致大鼠肺脏的早期变化

目的研究较低剂量的石英对肺组织损伤的特点。方法对大鼠采用较低剂量的石英和石棉粉尘（每只１０ｍｇ）染尘后，测定两种粉尘在两个月内所致大鼠支气管肺泡灌洗液中细胞总数、蛋白含量、总脂含量和乳酸脱氢酶（ＬＤＨ）活性等毒性指标以及全肺胶原含量的变化，并观察肺组织的病理改变。结果石英可引起灌洗液中细胞总数、蛋白质含量、总脂含量和ＬＤＨ活性持续升高，全肺胶原含量持续增加；而石棉只引起细胞总数和ＬＤＨ在染尘后１０天的一过性升高，全肺胶原含量虽也逐渐增加，但不如石英明显。结论较低剂量的石英具有很强的肺毒性和致纤维化能力。     

钒钛磁铁矿尘对家兔肺泡巨噬细胞毒作用的体外研究

目的探讨钒钛磁铁矿尘（钒钛尘）对肺泡巨噬细胞的毒性作用及程度。方法运用体外细胞培养及卵壳膜盖片透射电镜法来比较钒钛尘、五氧化二钒（Ｖ２Ｏ５）、二氧化钛（ＴｉＯ２）和石英（ＳｉＯ２）在不同时间、剂量作用下对肺泡巨噬细胞存活率、形态和功能的影响及培养液中乳酸脱氢酶（ＬＤＨ）和酸性磷酸酶（ＡＣＰ）的活性变化。结果４种粉尘均可使肺泡巨噬细胞存活率下降，ＬＤＨ和ＡＣＰ活性升高，形态和功能发生变化。但程度因粉尘种类而异。结论钒钛尘对肺泡巨噬细胞的毒性作用低于Ｖ２Ｏ５和ＳｉＯ２，但高于ＴｉＯ２。ＴｉＯ２对肺泡巨噬细胞亦有轻微的毒性作用     

烟草尘致大鼠肺脏损伤的实验研究

Ｗｉｓｔａｒ大鼠随机分成３组。烟草尘组每只大鼠经气管注入４０ｍｇ经消毒的烟草尘，设置石英尘和生理盐水两个对照组。结果显示烟草尘组大鼠体重在染尘早期低于生理盐水对照组，全肺干重、全肺湿重、全肺胶原、血清铜蓝蛋白活性、血浆Ｄ－Ｄｉｍｅｒ含量均高于生理盐水对照组，但显著低于石英对照组。提示烟草尘对肺脏有一定毒作用和轻度致纤维化作用     

沙漠尘对鼠肺急性影响的研究

通过肺灌洗分析的方法，研究沙漠尘急性毒作用。结果提示：沙漠尘组ＡＫＰ、ＡＣＰ、和ＬＤＨ活性，ＮＡ含量和巨噬细胞及白细胞百分含量随集尘剂量的增加而升高。６０ｍｇ／ｋｇ时ＬＤＨ、ＡＣＰ、ＡＫＰ和巨噬细胞及白细胞百分含量显著升高。３０ｍｇ／ｋｇ石英组各项指标均显著高于６０ｍｇ／ｋｇ沙漠尘组。结果说明：沙漠尘对肺部存在一定的急性毒作用，但明显弱于石英尘。     

淮北煤矿煤尘的急性肺部反应实验研究

目的：为评价煤尘对肺细胞的损伤，提供呼吸毒理学依据。方法：测定了淮北煤矿各个矿区煤样的游离二氧化硅含量。采用一次性气管内注入染尘方式，分析了大鼠支气管肺泡灌洗液（ＢＡＬＦ）中细胞成份与生化指标的变化，比较了不同矿区煤样标本对肺细胞毒性和病理改变，用全自动图象分析仪和数字模板画图仪进行了肺巨噬细胞内煤尘负荷的形态计量分析。结果：①淮北矿务局九个矿区煤样标本的游离ＳｉＯ２含量平均为６．３３％；②ＢＡＬＦ中细胞成份及生化指标的改变与煤尘含游离ＳｉＯ２量有剂量－效应关系；③对每一巨噬细胞内尘含量的形态计量分析表明，随着染尘剂量的增加，含尘巨噬细胞总数的百分率随之上升，巨噬细胞的表面积也随之增加，呈剂量－效应关系。结论：本研究中煤尘引起大鼠病理组织上可见急性肺损伤的呼吸性尘的阈剂量为１５ｍｇ／ｋｇ，未见明显急性损伤呼吸性尘的阈下剂量为７．５ｍｇ／ｋｇ，据此推算，引起人急性肺毒性反应的呼吸性尘阈浓度为４０．３６ｍｇ／ｍ３（相当于总尘空气浓度为１２１．０８ｍｇ／ｍ３）。     

褐煤粉尘对呼吸系统的危害

本文调查了一个褐煤矿和402名井下工人,结果:煤尘中游离二氧化硅含量为2.4～6.6%;粉尘浓度平均为4.7～12.0mg/m~3;检出煤尘肺1人,观察对象14人,慢性支气管炎患病率为20.4%。实验结果:褐煤尘所致尘肺的特点是纤维化程度很轻,进展缓慢,以纤维性煤尘细胞灶为主,并伴有局灶性肺气肿的尘肺。     

二硫化碳对体内脂质逆向转运过程影响的实验研究

本文报道了不同剂量ＣＳ２染毒后和同剂量ＣＳ２染毒不同时间后大鼠血清中高密度脂蛋白胆固醇（ＨＤＬ－Ｃ）及其亚组分（ＨＤＬ２－Ｃ，ＨＤＬ３－Ｃ）含量变化的研究。结果表明：染毒结束时，各染毒组（１２０、２４０、３６０ｍｇ／ｋｇ）与对照组比较，ＨＤＬ－Ｃ及ＨＤＬ２－Ｃ、ＨＤＬ３－Ｃ均未见显著性差异（Ｐ＞０．０５）。随染毒时间的延长（从０→２１天→４９天），染毒组（３６０、１２０ｍｇ／ｋｇ）血清中（与对照组比较）ＨＤＬ－Ｃ及其亚组浓度也未见显著性改变。表明：在本实验条件下，ＣＳ２对脂质的逆向转运过程无明显的毒性作用，对这一过程中主要的环节（包括重要代谢酶类）无明显影响。提示：肝外组织脂质合成增加且逆向转运并未加速而致脂质堆积，可能是ＣＳ２导致脂质代谢障碍，乃致心血管毒性作用的机制之一。     

支气管肺泡灌洗术排尘治疗矽肺的实验研究

通过观察染尘后不同时间矽肺大鼠支气管肺泡灌洗液（ＢＡＬＦ）中ＳｉＯ２含量、细胞总数、ＬＤＨ活性．蛋白和脂质过氧化物（ＬＰＯ）含量，结合矽肺病理变化情况，对支气管肺泡灌洗术（ＢＡＬ）治疗矽肺的可能性及有关机制进行初步探讨。实验结果表明：当染尘后不同时期ＢＡＬＦ中细胞总数、ＬＤＨ活性、总蛋白及ＬＰＯ含量均高于相应对照组，且差别有显著或非常显著意义（Ｐ＜０．０５或Ｐ＜０．０１）。随着染尘时间延长，ＢＡＬＦ中ＬＤＨ含量、细胞总数、ＬＤＨ活性和总蛋白含量呈下降趋势，而矽肺病变则逐渐加剧。提示：ＢＡＬ可以通过排出肺内部分粉尘、细胞和非细胞成份，对减少肺内纤维化机会，延缓矽肺病变的发生发展将有积极作用。且以早期或急性矽肺施行ＢＡＬ为宜。     

煤尘引起肺组织反应的超微结构观察

从超微结构方面研究了动物模型中三个煤种的煤尘与肺巨噬细胞的相互作用及其作用下的肺组织反应。煤尘在肺巨噬细胞中发生了诸如粉尘粒子边缘模糊,呈云雾状,电子密度不均,半壁消融等改变,但各煤种反应强度不一。巨噬细胞保持完好,细胞器增生,出现模一层结构,褐煤尘组肺组织自始至终出现显著的Ⅱ型细胞反应。煤尘同样能引起浆细胞反应及一些胶原纤维增生。吞噬了煤尘的退化的肺巨噬细胞有向纤维细胞转化的倾向。     

不同矿区煤尘细胞毒性与金属元素关系的研究

本文对不同矿区的煤尘分别进行了SiO_2和金属元素的测定,并研究了它们对大鼠肺巨噬细胞存活率、吞噬率、坏变率和溶酶体膜的影响。综合分析结果表明,各煤尘对细胞有一定的毒性。煤尘细胞毒性大小与SiO_2的含量不完全一致。煤尘中金属元素对细胞毒性有一定影响,含镍元素高的细胞毒性大。含锌和钛元素高的细胞毒性小。     

煤尘细胞毒性与金属元素含量的关系

煤尘对肺巨噬细胞具有一定毒性,使细胞存活率降低。煤尘中金属元素含量较低。经相关分析,八个煤矿煤尘的细胞存活率与各矿煤尘中的26种金属元素含量和游离SiO_2含量相关不显著。     

Contrasting bronchoalveolar leukocyte responses in rats inhaling coal mine dust, quartz, or titanium dioxide: effects of coal rank, airborne mass concentration, and cessation of exposure

The aim of this study was to determine the bronchoalveolar leukocyte response to airborne coal mine dust; quartz and titanium dioxide were used as positive and negative controls, respectively. Groups of rats were exposed to airborne mass concentrations of 10 and 50 mg/m3 of the dusts for 7 hr/day, 5 days/week and their bronchoalveolar space was lavaged at time points between 2 and 75 days of exposure, to assess the leukocyte response. This study revealed time-dependent and airborne mass concentration-dependent recruitment of neutrophils and macrophages into the bronchoalveolar region with coal mine dust inhalation but no real difference in the magnitude of the response between coal mine dusts from collieries mining coal of different rank and quartz content although the maximum quartz content in the dusts used was 6%. The inflammatory response was much less than that produced by quartz, at similar airborne mass concentrations, and more than that produced by titanium dioxide which was, in general, a poor inflammogen in the rat lung. Groups of rats were exposed to the airborne dusts for 32 or 75 days, then removed from the exposure chambers, and allowed to recover by breathing room air for a further 64 days. During this recovery period there was marked progression of the leukocyte response with quartz and persistence of the response with coal mine dust. Chronic recruitment of leukocytes to the lungs of individuals inhaling coal mine dust is likely to be an important factor in the development of coal workers' pneumoconiosis.     

石英粉尘粒径与肺损伤作用关系的实验研究

目的　比较不同粒径石英粉尘对肺的损伤作用。方法　分别用微米级石英粉尘 (粒径 <5 μm)和纳米级石英粉尘 ,粒径 (10± 5 )nm ,经气管对雌性Wistar大鼠一次染尘 (2 0mg/只 ) ,于染尘后第 30d和第 6 0d测定动物全肺湿重和肺羟脯氨酸含量。结果　染尘后第 6 0d微米组大鼠全肺湿重显著高于正常对照组 ,而纳米组者显著低于微米组 ,与正常对照组无显著性差异。染尘后第 30 ,6 0d微米组大鼠肺羟脯氨酸含量比正常对照显著增高 ,纳米组者则显著低于微米组而与正常对照组无显著性差异。结论　石英粉尘粒径由微米级降低至纳米级后 ,其肺损伤作用减弱     

Fibres in Lower Silesia hard coal mines respirable dusts

The paper describes the presence of fibres in respirable coal dust in high rank coal mines in Lower Silesia. The amount of fibres in dust particles is about 1.5% (by count). Testing by the incineration test, the lack of atomic number contrast in electron back-scattering imaging in SEM and X-ray microanalysis allow the fibres to be identified as coal. The authors suggest the possible role of coal fibres in the increased fibrogenic activity of the dusts in coal mines in Lower Silesia.     

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。     

Assessment of respirable dust and its free silica contents in different Indian coalmines

Assessment of respirable dust, personal exposures of miners and free silica contents in dust were undertaken to find out the associated risk of coal workers' pneumoconiosis in 9 coal mines of Eastern India during 1988-91. Mine Research Establishment (MRE), 113A Gravimetric Dust Sampler (GDS) and personal samplers (AFC 123), Cassella, London, approved by Director General of Mines Safety (DGMS) were used respectively for monitoring of mine air dust and personal exposures of miners. Fourier Transform Infra-red (FTIR) Spectroscopy determined free silica in respirable dusts. Thermal Conditions like Wet Bulb Globe Temperature (WBGT) index, humidity and wind velocity were also recorded during monitoring. The dust levels in the face return air of both, Board & Pillar (B&P) and Long Wall (LW) mining were found above the permissible level recommended by DGMS, Govt. of India. The drilling, blasting and loading are the major dusty operations in B&P method. Exposures of driller and loader were varied between, 0.81-9.48 mg/m3 and 0.05-9.84 mg/m3 respectively in B&P mining, whereas exposures of DOSCO loader, Shearer operator and Power Support Face Worker were varied between 2.65-9.11 mg/m3, 0.22-10.00 mg/m3 and 0.12-9.32 mg/m3 respectively in LW mining. In open cast mining, compressor and driller operators are the major exposed groups. The percentage silica in respirable dusts found below 5% in all most all the workers except among query loaders and drillers of open cast mines.     

Alveolitis caused by exposure to coal mine dusts: production of interleukin-1 and immunomodulation by bronchoalveolar leukocytes

Two kinds of coal mine dust, low rank with high quartz (bituminous) and high rank with low quartz (anthracite), were assayed for ability to induce alveolitis and to stimulate interleukin-1 release from normal alveolar macrophages in vitro. Dust-elicited bronchoalveolar leukocytes were also assessed for their effects on macrophage-depleted splenocyte mitogenesis and their ability to produce interleukin-1. Quartz and titanium dioxide were used for comparison as toxic and inert dusts, respectively. Both coal mine dusts caused substantial release of interleukin-1 from normal alveolar macrophages in vitro and the levels were higher than those caused by quartz. Bituminous coal mine dust provoked acute but rapidly subsiding macrophage/neutrophil alveolitis which was greater than that provoked by titanium dioxide; anthracite caused less alveolitis than titanium dioxide and quartz caused large scale, persistent alveolitis. Whole bronchoalveolar leukocytes, including polymorphonuclear neutrophils, elicited by exposure to dust, were less inhibitory to lymphocyte mitogenesis than normal alveolar macrophages and bituminous coal mine dust-induced neutrophils were augmentary to lymphocyte mitogenesis; macrophages from inflamed lungs were, on the whole, inhibitory to lymphocyte mitogenesis. Alveolar macrophages from bituminous coal mine dust- or titanium dioxide-exposed lungs showed increased ability to release interleukin-1 on stimulation in vitro. These findings suggest that bronchoalveolar leukocytes elicited by coal mine dust could modulate immunity by means of interleukin-1 release and enhancement of lymphocyte proliferation.