车间空气中岩棉粉尘卫生标准的研究

为制订车间空气中岩粉尘卫生标准，对岩棉制品厂进行了劳动卫生学调查及岩棉粉尘对大鼠肺致纤维化作用实验。调查结果显示了工人作业场所空气中粉尘污染明显，时间加权平均浓度为２．０４－１２．５３ｍｇ／ｍ＾３。实验结果表明了岩棉粉尘对大鼠轻度致纤维作用。长期接触高浓度，岩棉粉尘对人呼吸器官可能靠成影响，有引起肺纤维化的可能。根据本研究结果和参考国外卫生标准，建议车间空气中岩棉粉尘卫生标准（时间加权平均浓度）为     

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。     

硼矿粉尘对大鼠肺致纤维化的实验研究

将硼矿粉尘对大鼠气管内染尘，实验分７组：硼镁石组、熟料、井下降尘、围岩、石英特尘及盐水对照组。各组染尘剂量每只５０ｍｇ，生料Ⅱ组１００ｍｇ，观察３￣２１个月。定期解剖、肺及肺门淋巴结作病理检查，并测定肺干重及全肺胶原蛋白含量。结果表明，硼矿各类粉尘仅能引起肺轻度纤维化，以细胞性结节为主，井下降尘组稍重，生料组与熟料组次之，围岩组最轻。     

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。     

尼龙六六盐粉尘对大鼠肺致纤维化实验研究

目的 研究尼龙六六盐粉尘对大鼠肺的致纤维化作用。方法 采用大鼠被动式粉尘吸入法染尘。以肺组织形态学改变为观察指标。并参考支气管肺泡灌洗（BAL）的实验结果。结果 实验组大鼠肺病理切片上可见轻度的网织纤维增生和少量胶原纤维，石英粉尘对照组可见明显的纤维化，两者差异有显著性，BAL实验组的各项指标实验组均高于正常对照组。低于石英粉尘组。结论 尼龙六六盐粉尘对大鼠肺有轻度的致纤维化作用。     

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。     

车间空气中聚丙烯腈纤维粉尘卫生标准的研制

目的　探讨聚丙烯腈纤维粉尘的致病作用 ,制订车间空气中聚丙烯腈纤维粉尘卫生标准。方法　大鼠经气管注入粉尘 80mg ,分别于染尘后的 12、18个月剖检 ,观察肺部病理改变。发现聚丙烯腈纤维粉尘可致肺组织轻度纤维化改变。对 10 3名平均接尘工龄 5 4年 (1～ 14 6年 )接尘女工的健康状况进行了调查分析。结果　呼吸系统症状检出率、胸部X线异常改变和肺通气功能损伤程度 ,接尘组均明显高于对照组 (P <0 0 1)。结论　聚丙烯腈纤维粉尘对人体有一定的致病作用。提出车间空气中聚丙烯腈纤维粉尘最高容许浓度为 4mg/m3,时间加权平均容许浓度为 2mg/m3。     

碳纤维及其复合材料粉尘对大鼠肺灌洗液的影响

本文采用毒性和致纤维化作用弱的TiO_2和SAFFIL纤维粉尘以及生理盐水为阴性对照,采用石英和温石棉粉尘为阳性对照,探讨了碳纤维和碳纤维复合材料粉尘对大鼠肺灌洗液的影响。结果表明,这两种粉尘的毒性均明显低于石英和温石棉尘,而接近于TiO_2和SAFFIL纤维粉尘。本研究为制订这两种粉尘的卫生标准提供了实验室依据。     

含铁粉尘致大鼠肺纤维化的病理观察

本实验选用三种含铁粉尘(纯氧化铁尘、电焊烟尘及铁锈尘),给大鼠气管内注入染尘,动物于染尘后1、3、6和9个月分别处死,在光镜和透射电镜下观察不同粉尘的致肺纤维化能力。结果表明,纯氧化铁尘可引起肺轻度纤维组织增生,电焊烟尘和铁锈尘的致肺纤维化能力较纯氧化铁尘明显,但远较石英尘为弱。作者认为含铁粉尘能引起轻度的肺纤维化,而粉尘中的锰、铬等金属成分的存在可能增强了其致纤维化能力。     

矿渣粉尘对大鼠肺脏致纤维化作用的实验研究

作者用矿渣粉尘对大鼠肺脏致纤维化作用进行了研究,结果表明,矿渣组动物的死亡率、金肺干湿重量和肺胶原蛋白含量等,均明显地高于空白对照组,动物染尘6个月,肺组织有大小不等的尘性纤维灶,G.S和V.G染色灶内均有较多的网状纤维和较明显的胶原纤维。作者认为,矿渣粉尘对大鼠肺脏有较明显的致纤维化作用。     

羊毛尘和皮毛作业混合尘致肺纤维化的实验研究

将羊毛尘50mg、80mg和皮毛作业混合尘50mg,经大鼠气管注入染尘。测定肺干重、全肺胶原蛋白含量,观察了病理改变。表明:羊毛尘组最初为异物炎性反应和肉芽肿损害,24个月发现肺间质轻度纤维化和纤维细胞灶,有较多的网织纤维和少量纤细胶原纤维。皮毛作业混合尘组早期为尘细胞结节;中期尘细胞结节群集;晚期以纤维细胞结节为主,少量细胞纤维性结节。作者认为,羊毛尘、皮毛混合尘可引起不同程度肺纤维化。     

棕榈尘生物学作用的实验研究

本文研究了纯棕尘、现场棕尘及纯棕尘+石英尘对体外家兔肺灌洗巨噬细胞的毒性及致大白鼠肺部纤维化的作用。结果表明,各实验组均具有明显的细胞毒性,可引起细胞膜受损、细胞崩解死亡,其中又以现场棕尘毒性最大。体内实验表明,棕尘各实验组均可引起肺间质纤维化,其病变进展速度与游离二氧化硅含量有关。棕尘所致的气道损伤,比石英出现早而严重。     

黄麻粉尘致肺纤维化的实验研究

以黄麻粉尘（游离ＳｉＯ２含量分别为９．３２％、４、４％、０．９８％）８０ｍｇ经气管注入大白鼠肺内，于染尘后１、３、６、１２个月时处死动物，进行病理学观察及肺胶原蛋白含量测定。染尘早期，肺内为细胞性反应和肺间质肺炎样改变。染尘晚期，含游离ＳｉＯ２９．３２％的黄麻粉尘可引起细胞纤维性结节，含游离ＳｉＯ２４．４０％的黄麻粉尘可引起细支气管旁轻度纤维增生，含游离ＳｉＯ２０．９８％的黄麻粉尘仅见细胞性结节。     

职业接触岩棉对肺通气功能及呼吸系统症状的影响

目的探讨职业性接触岩棉对肺通气功能及呼吸系统症状的影响。方法选择70名岩棉生产和加工人员作为接触组,51名空气分离企业的劳动者作为对照组。进行现场职业卫生学调查,对所有调查对象进行肺通气功能健康检查和呼吸系统症状问卷调查。结果接触组中所有岗位每班接触的纤维浓度均<1f/ml,生产线操作工和深加工班操作工每班接触的总粉尘浓度>3mg/m3。接触组FVC%和FEV1.0/FVC%均数低于对照组,差异有统计学意义(P<0.05);接触组中3个不同接触工龄组FVC%、FEV1.0%和FEV1.0/FVC%均数比较,差异均无统计学意义(P>0.05)。限制性通气功能障碍是岩棉致肺通气功能损害的主要类型,与接触工龄呈线性趋势关系(P<0.05),与吸烟未显示有关联性(P>0.05),吸烟与岩棉未显示具有联合作用(P>0.05)。接触组与对照组呼吸系统症状比较,差异均无统计学意义(P>0.05)。结论长期接触低纤维浓度水平的岩棉,仍能够损害劳动者的肺通气功能,应控制其总粉尘浓度的接触水平。     

氧化镁粉尘对肺部损害的实验研究

用不同剂量(100mg,50mg)镁尘注入大鼠肺内,在光镜及扫描电子显微镜下观察了染尘动物肺内的病理改变和立体超微结构的病变特点。结果发现,该粉尘可引起粉尘灶,Ⅰ型肺泡上皮细胞损伤,Ⅱ型细胞的增生,肺泡结构的破坏,肺气肿,呼吸道炎症和肺间质纤维化。100mg剂量组的病理变化比50mg组更为明显。作者认为,镁矿尘不是惰性粉尘,并提出应注意镁矿尘的职业危害以保护工人健康。     

苏州市工业园区电炉企业生产性粉尘危害调查

目的调查分析电炉厂生产性粉尘对作业工人健康的危害情况。方法对苏州工业园区32家电炉厂作业场所进行劳动卫生学调查,并对1800名作业工人进行职业性体检。结果电炉厂的粉尘种类主要是电焊烟尘和岩棉尘（总尘、下同）,其中电焊烟尘时间加权平均容许浓度（PC-TWA）为0.68～64.07 mg/m^3,超标率12.5%,超限倍数0.2～16.0。岩棉粉尘PC-TWA为1.05～12.53 mg/m^3,超标率26.6%,超限倍数0.3～4.3。作业工人体检1800人（接尘工人1067人,非接尘工人733人）,尘肺0^＋检出人数2人,检出率1.1‰;职业禁忌证14例（肺结核12例、肺气肿2例）,检出率7.8‰;肺部异常阴影2例,检出率1.1‰。肺功能测试结果分为接尘组和非接尘组,结果接触粉尘可导致肺通气功能和小气道功能指标下降,接尘工龄长肺功能值异常率高,接尘工人的肺功能障碍的发生率高于非接尘工人。结论电炉厂存在比较严重的粉尘职业危害,接尘工人的肺功能已受到一定程度的损害,有关部门应重点做好通风防尘工作和个人卫生防护;做好从业人员健康监护,保障作业工人的健康。     

Wool and grain dusts stimulate TNF secretion by alveolar macrophages in vitro.

OBJECTIVE: The aim of the study was to investigate the ability of two organic dusts, wool and grain, and their soluble leachates to stimulate secretion of tumour necrosis factor (TNF) by rat alveolar macrophages with special reference to the role of lipopolysaccharide (LPS). METHODS: Rat alveolar macrophages were isolated by bronchoalveolar lavage (BAL) and treated in vitro with whole dust, dust leachates, and a standard LPS preparation. TNF production was measured in supernatants with the L929 cell line bioassay. RESULTS: Both wool and grain dust samples were capable of stimulating TNF release from rat alveolar macrophages in a dose-dependent manner. The standard LPS preparation caused a dose-dependent secretion of TNF. Leachates prepared from the dusts contained LPS and also caused TNF release but leachable LPS could not account for the TNF release and it was clear that non-LPS leachable activity was present in the grain dust and that wool dust particles themselves were capable of causing release of TNF. The role of LPS in wool dust leachates was further investigated by treating peritoneal macrophages from two strains of mice, LPS responders (C3H) and LPS non-responders (C3H/HEJ), with LPS. The non-responder mouse macrophages produced very low concentrations of TNF in response to the wool dust leachates compared with the responders. CONCLUSIONS: LPS and other unidentified leachable substances present on the surface of grain dust, and to a lesser extent on wool dust, are a trigger for TNF release by lung macrophages. Wool dust particles themselves stimulate TNF. TNF release from macrophages could contribute to enhancement of inflammatory responses and symptoms of bronchitis and breathlessness in workers exposed to organic dusts such as wool and grain.     

Injurious effects of wool and grain dusts on alveolar epithelial cells and macrophages in vitro.

Epidemiological studies of workers in wool textile mills have shown a direct relation between the concentration of wool dust in the air and respiratory symptoms. Injurious effects of wool dust on the bronchial epithelium could be important in causing inflammation and irritation. A pulmonary epithelial cell line in vitro was therefore used to study the toxic effects of wool dust. Cells of the A549 epithelial cell line were labelled with 51Cr and treated with whole wool dusts and extracts of wool, after which injury was assessed. Also, the effects of grain dust, which also causes a form of airway obstruction, were studied. The epithelial injury was assessed by measuring 51Cr release from cells as an indication of lysis, and by monitoring cells which had detached from the substratum. No significant injury to A549 cells was caused by culture with any of the dusts collected from the air but surface "ledge" dust caused significant lysis at some doses. Quartz, used as a toxic control dust, caused significant lysis at the highest concentration of 100 micrograms/well. To determine whether any injurious material was soluble the dusts were incubated in saline and extracts collected. No extracts caused significant injury to epithelial cells. A similar lack of toxicity was found when 51Cr labelled control alveolar macrophages were targets for injury. Significant release of radiolabel was evident when macrophages were exposed to quartz at concentrations of 10 and 20 micrograms/well, there being no significant injury with either wool or grain dusts. These data suggest that neither wool nor grain dust produce direct injury to epithelial cells, and further studies are necessary to explain inflammation leading to respiratory symptoms in wool and grain workers.     

Injurious effects of wool and grain dusts on alveolar epithelial cells and macrophages in vitro

Epidemiological studies of workers in wool textile mills have shown a direct relation between the concentration of wool dust in the air and respiratory symptoms. Injurious effects of wool dust on the bronchial epithelium could be important in causing inflammation and irritation. A pulmonary epithelial cell line in vitro was therefore used to study the toxic effects of wool dust. Cells of the A549 epithelial cell line were labelled with 51Cr and treated with whole wool dusts and extracts of wool, after which injury was assessed. Also, the effects of grain dust, which also causes a form of airway obstruction, were studied. The epithelial injury was assessed by measuring 51Cr release from cells as an indication of lysis, and by monitoring cells which had detached from the substratum. No significant injury to A549 cells was caused by culture with any of the dusts collected from the air but surface "ledge" dust caused significant lysis at some doses. Quartz, used as a toxic control dust, caused significant lysis at the highest concentration of 100 micrograms/well. To determine whether any injurious material was soluble the dusts were incubated in saline and extracts collected. No extracts caused significant injury to epithelial cells. A similar lack of toxicity was found when 51Cr labelled control alveolar macrophages were targets for injury. Significant release of radiolabel was evident when macrophages were exposed to quartz at concentrations of 10 and 20 micrograms/well, there being no significant injury with either wool or grain dusts. These data suggest that neither wool nor grain dust produce direct injury to epithelial cells, and further studies are necessary to explain inflammation leading to respiratory symptoms in wool and grain workers.     

钇稀土粉尘的生物学作用及其车间卫生标准的研究

本文从钇稀土生产矿的劳动卫生、职业流行病学调查及动物体内、外实验研究了钇稀土粉尘的生物学作用,并对钇稀土生产车间空气粉尘卫生标准进行探讨。作业场所粉尘浓度在1.3—25.9mg/m~3,25名接尘工人中X线O~+检出率为16%,平均接尘工龄为8.8年。接尘组工人的肺功能及化验检查某些指标改变较对照组有显著差异,经动物体内外实验研究,钇组稀土粉尘显示的致肺纤维化作用和细胞毒性大于铈组粉尘但显著低于石英粉尘,根据本研究结果提出了生产车间钇组稀土粉尘卫生标准为3mg/m~3的建议值。