瓷厂及钨矿生产性粉尘对血管内皮细胞的损伤效应

目的 评价瓷厂和钨矿生产性粉尘对血管内皮细胞的直接损伤作用,探讨粉尘引发心血管疾病的机制.方法 以人脐静脉内皮细胞(HUVEC)株HUV-EC-C为作用细胞,以瓷厂、钨矿作业点收集的生产性粉尘为实验粉尘,以中国标准石英为对照,将粉尘配制成25、50、100、200、400μg/ml浓度与HUVEC共培养24 h,测定细胞乳酸脱氢酶(LDH)活力、细胞的活力噻唑蓝(MTT)、一氧化氮(NO)和肿瘤坏死因子-α(TNF-α)的释放量.结果 瓷厂和钨矿作业点的生产性粉尘均能使HUVEC细胞培养液中LDH活力升高,释放NO及TNF-α水平升高,并随粉尘浓度升高呈现明确的剂量-反应关系.瓷厂和钨矿作业点生产性粉尘均能导致HUVEC细胞活力下降,呈剂量-反应关系.石英粉尘诱导HUVEC培养液中LDH活力升高的能力明显高于瓷厂和钨矿的生产性粉尘,差异有统计学意义(P＜0.05).瓷厂和钨矿生产性粉尘诱导HUVEC细胞活力下降及释放NO的能力相近且与标准石英相当.在较低剂量组(25、50、100μg/ml)时,瓷厂和钨矿生产性粉尘诱导TNF-α的释放量与标准石英相当,差异无统计学意义(P＞0.05),而在较高剂量组(200、400 μg/ml)时,标准石英诱导TNF-α的释放量明显高于瓷厂和钨矿生产性粉尘,差异有统计学意义(P＜0.05).结论 不同来源的生产性粉尘及标准石英均能损伤血管内皮细胞,诱导TNF-α释放,引起不同程度的生物学效应.     

纳米颗粒致人血管内皮细胞损伤的比较

目的 比较3种不同类型的颗粒对血管内皮细胞的毒性效应,探讨颗粒成分和粒径对其心血管的毒性效应.方法 选择纳米二氧化硅(nano-SiO2)、纳米二氧化钛(nano-TiO2)和标准石英作为染尘颗粒,其中nano-TiO2和标准石英分别作为nano-SiO2的成分对照和粒径对照.将剂量为5.0、10.0、20.0、40.0 μg/ml的3种颗粒分别作用于人脐静脉内皮细胞,以不含颗粒物的DMEM培养液为对照组,24 h后收集培养液上清,测定乳酸脱氢酶(LDH)、总超氧化物歧化酶(SOD)活力、NO、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)释放量.结果 与0μg/ml剂量组比较,各剂量nano-SiO2染尘组和10.0、20.0、40.0 μg/ml nano-TiO2染尘组及标准石英染尘组的LDH活力明显升高,差异均有统计学意义(P＜0.01).与0 μg/ml剂量组比较,5.0、10.0、20.0 μg/ml nano-SiO2染尘组和40.0 μg/ml nano-TiO2染尘组及20.0、40.0 μg/ml标准石英染尘组的SOD活力明显增加,40.0μml nano-SiO2染尘组的SOD活力明显降低,差异均有统计学意义(P＜0.05,P＜0.01).与0μg/ml剂量组比较,10.0、20.0、40.0 μg/mlnano-SiO2染尘组和各剂量nano-TiO2染尘组及40.0 μg/ml标准石英染尘组的TNF-α释放量明显增加,差异均有统计学意义(P＜0.01).与0μg/ml剂量组比较,10.0、20.0、40.0 μg/mlnano-SiO2染尘组和20.0、40.0μg/ml nano-TiO2染尘组及40.0 μg/ml标准石英染尘组的IL-6释放量明显增加,差异有统计学意义(P＜0.01).5.0、10.0、20.0、40.0 μg/ml nano-SiO2染尘组的LDH活力明显高于标准石英染尘组,10.0、20.0、40.0 μg/ml nano-TiO2染尘组LDH活力明显低于标准石英染尘组,差异均有统计学意义(P＜0.05).5.0、10.0、20.0μg/ml nano-SiO2染尘组SOD活力明显高于标准石英染尘组,40.0 μg/ml nano-SiO2染尘组和20.0 μg/ml nano-TiO2染尘组SOD活力明显低于标准石英染尘组,差异均有统计学意义(P＜0.01).5.0、10.0、20.0、40.0 μg/ml nano-SiO2染尘组和5.0、10.0μg/ml nano-TiO2染尘组的TNF-α释放量均明显高于标准石英染尘组,差异均有统计学意义(P＜0.01).5.0、10.0、20.0、40.0μg/ml nano-SiO2染尘组和20.0、40.0 μg/ml nano-TiO2染尘组的IL-6释放量明显高于标准石英染尘组,差异有统计学意义(P＜0.05).结论 3种颗粒都能够对细胞产生一定的毒性效应,其中以nano-SiO2的作用最强,nano-TiO2和标准石英的细胞毒性表现不一.颗粒物毒性与其成分和粒径有关.     

氧化苦参碱对石英作用肺泡巨噬细胞保护效应的初步研究

目的 探讨氧化苦参碱对石英作用肺泡巨噬细胞（AM）的保护效应。方法 用支气管肺灌洗方法收集大鼠AM并培养,用小鼠胸腺细胞增殖法和双抗夹心法分别测定AM培养上清液中的白细胞介素-1（IL-1）、肿瘤坏死因子α（TNF-α）的含量;用2,4二硝基苯肼比色法测定AM培养上清液中乳酸脱氢酶（LDH）的含量;用TBA比色法测定AM脂质过氧化终产物丙二醛（MDA）的含量。结果 氧化苦参碱为200～1600μg／ml时可以降低石英对AM的作用,AMTNF-α的表达水平随氧化苦参碱剂量的增加而从20．11ng／ml下降到9．44ng／ml,且差异有显著性。当浓度达到3200μg／ml时．药效略减弱;IL-1的表达水平也随氧化苦参碱剂量的增加而使其液闪计数cpm值从3051．67降低到1603．35,尤其是在800～l600μg／ml时有明显下降;对MDA和LDH也显示了随药物剂量的增加而趋于下降,但药效相对较弱。结论 氧化苦参碱能抑制石英诱导AM分泌TNF-α和IL-1,同时还具有抗石英对巨噬细胞的氧化作用和保护巨噬细胞膜的功能。     

内毒素对外周T淋巴细胞凋亡及TNF-α的影响

目的:通过观察不同浓度内毒素(LPS)对外周血中T淋巴细胞凋亡和肿瘤坏死因子(TNF-α)的影响以探讨两者之间的关系.方法:健康志愿者全血加入RPMII640培养液以1:1稀释,加入不同浓度LPS,5%CO2培养箱培养4 h,分离淋巴细胞流式细胞术检测CD4+T淋巴细胞凋亡并以放免法测定TNF-α浓度.结果:不同浓度LPS均能诱导TNF-α的释放,LPS浓度＞10 ng/ml时TNF-α释放达到浓度平台.淋巴细胞凋亡率随LPS浓度增高而增加,浓度为50-100μg/ml时,各组淋巴细胞凋亡率迅速增加(P＜0.01).结论:炎症因子并不是引起淋巴细胞凋亡的决定因素,LPS诱导淋巴细胞凋亡可能存在炎症因子以外的其他途径.高浓度LPS对淋巴细胞凋亡存在直接作用,其机制值得进一步探讨.     

纳米SiO_2致内皮细胞毒性作用剂量效应和时间效应

目的观察纳米二氧化硅颗粒(纳米SiO_2)对人脐静脉内皮细胞的毒性作用及其剂量和时间效应。方法将不同质量浓度(0、5、10、20、40mg/L)纳米SiO_2颗粒作用于人脐静脉内皮细胞,在不同时间点(6、12、24、48h)检测细胞培养液上清中乳酸脱氢酶(LDH)活性、总超氧化物歧化酶(SOD)活力、肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)的释放量。结果细胞培养液上清中LDH活性、TNF-α释放量和IL-6释放量呈浓度和时间依赖性增加。染尘6、12h,SOD活力随染尘浓度的增加而增加,染尘24h则先增后减,染尘48h则随染尘浓度的增加而减少;随着作用时间的延长,所有染尘浓度组SOD活力先增后减。结论纳米SiO_2颗粒能够诱导HUVECs发生膜损伤、氧化损伤和炎症反应,且存在剂量和时间效应。     

外向钾通道在纳米SiO2致内皮细胞毒性中的作用

目的探讨电压依赖性外向钾通道(voltage-dependent potassium channel,Kv)在纳米二氧化硅(SiO2)致血管内皮细胞毒性中的作用,以验证钾外流与纳米SiO2致细胞炎性反应的关系。方法以人脐静脉内皮细胞(HUVECs)正常培养为阴性对照组,单独加入20μg/ml纳米SiO2为阳性对照组,在20μg/ml纳米SiO2基础上添加不同剂量的Kv通道阻断剂氯化四乙胺(TEA-Cl)或4-氨基吡啶(4-AP)为实验组,检测各组细胞存活率、乳酸脱氢酶(LDH)活力、肿瘤坏死因子(TNF-α)以及白介素-6(IL-6)释放量。用全细胞膜片钳电生理测定正常HUVECs及染不同浓度纳米SiO2时Kv电流变化,验证纳米SiO2对血管内皮细胞Kv的影响。结果与阴性对照(正常细胞组)比较,纳米SiO2(阳性对照组)导致内皮细胞存活率明显降低,LDH活力、TNF-α和IL-6释放量明显增加。与阳性对照组比较,加入钾通道阻断剂TEA-Cl或4-AP后,细胞存活率明显升高,但高剂量阻断剂组反而降低。钾通道阻断剂也导致LDH活力降低,但在最高剂量时甚至达到阳性对照水平。只有高剂量TEA-Cl使TNF-α释放量明显减少,而4-AP自低到高剂量使TNF-α释放量逐渐降低,呈剂量-效应关系。TEA-Cl和4-AP均可明显降低纳米SiO2诱导IL-6释放量。膜片钳电生理实验中,内皮细胞Kv电流表现延迟整流特性,4-AP对该电流的抑制作用明显。与阴性对照(正常细胞组)比较,纳米SiO2导致外向钾电流明显增大,激活曲线左移,斜率因子降低(P<0.05),表明Kv活性增加,通道开放速率明显增高。结论纳米SiO2可引起细胞炎性反应,Kv开放引起的钾外流增加在该毒性效应中可能起着活化细胞、激活炎性体的早期信号作用。     

结缔组织生长因子对石英粉尘诱导人支气管上皮细胞释放IL-17A的影响

目的探讨结缔组织生长因子(CTGF)对石英粉尘诱导人支气管上皮细胞(16HBE)表达白介素17A(IL-17A)水平的影响。方法采用0、12.5、25、50、100μg/ml石英粉尘染毒人支气管上皮细胞(16HBE)24、48 h,采用CCK-8法测定细胞存活率,以荧光定量PCR方法检测细胞内CTGF mRNA相对表达水平;用CTGF siRNA干扰16HBE细胞12 h后,加入0、25、50μg/ml石英粉尘染毒48 h,并设同样剂量石英粉尘染毒的16HBE细胞为对照组,收集细胞上清液,采用酶联免疫吸附法(ELISA)检测细胞上清液中IL-17A的含量。结果与24 h染尘组比较,石英粉尘染毒16HBE细胞48 h后细胞毒性作用更明显,其细胞存活率随石英粉尘浓度的增加逐渐降低(P0.05);同时细胞内CTGF mRNA相对表达水平和细胞分泌IL-17A的水平均显著升高(P0.05),且呈剂量-效应关系,50μg/ml染毒组细胞内表达CTGF mRNA和分泌IL-17A的水平达到最高;与同样剂量石英粉尘染毒的16HBE细胞相比,25、50μg/ml石英粉尘诱导CTGF siRNA干扰组细胞分泌IL-17A的水平显著降低,差异具有统计学意义(P0.05)。结论抑制CTGF可显著降低石英粉尘诱导16HBE细胞表达IL-17A的水平,提示CTGF可能参与调节石英粉尘致肺部炎性及纤维化的反应过程。     

长春市冬季大气PM2.5对RAW264.7细胞毒性机制研究

目的研究长春市冬季大气PM_(2.5)对小鼠单核巨噬细胞白血病细胞(RAW264.7细胞)的毒性作用。方法采用2016年11月16日至2017年3月18日期间基于空气质量指数的五级及以上雾霾天气采集的长春市大气PM_(2.5)对RAW264.7细胞进行体外染毒,终浓度分别为0、50、100、200、400μg/ml。以四甲基偶氮唑盐比色法(MTT)检测细胞活力,用酶标仪测定胞内活性氧(ROS)、乳酸脱氢酶(LDH)释放量及Ca~(2+)浓度,并用流式细胞仪测定细胞凋亡率,用ELISA法检测肿瘤坏死因子(TNF-α)和白细胞介素-6(IL-6)含量。结果 PM_(2.5)染毒浓度为100、200、400μg/ml时,RAW264.7细胞存活率明显低于对照组,LDH、ROS水平和Ca~(2+)浓度明显高于对照组,TNF-α和IL-6含量明显高于对照组,细胞凋亡率亦随染毒浓度的增加而升高,差异均有统计学意义(P0.05)。结论长春市冬季重污染大气PM_(2.5)可使RAW264.7细胞产生炎症损伤和氧化应激,进而引起细胞凋亡。     

茶多酚对脂多糖诱导的支气管上皮细胞损伤的保护作用及其机制

目的 探讨茶多酚在脂多糖诱导的人支气管上皮细胞损伤中的保护作用及其机制。方法 培养人支气管上皮细胞16HBE,给予不同浓度的脂多糖(1,25,50,100 μg/ml)和茶多酚(100,200,400,800 g/ml)作用。MTT检测细胞的生长,流式细胞术检测细胞凋亡,western blot检测细胞核内和总NFκB的蛋白表达,ELISA检测IL-6,IL-13和TNF-α的含量,试剂盒检测MDA,SOD和LDH的水平。结果 与对照组相比,LPS组的细胞生长显著降低;细胞凋亡显著升高;IL-6,IL-13和TNF-α的含量升高;核内和NFκB总蛋白上升;MDA和LDH含量增加,SOD的活性降低,而茶多酚处理抑制以上LPS诱导的16HBE损伤。结论 茶多酚可以通过抑制氧化应激缓解脂多糖诱导的人支气管上皮细胞损伤。     

瓷厂与锡矿及钨矿石英粉尘表面铝硅酸盐包裹的测定和分析

目的 探讨石英粉尘表面铝硅酸盐包裹的测定方法和包裹对粉尘致病作用的影响.方法 应用呼吸性粉尘采样器以2 L/min采集江西钨矿、瓷厂和广西锡矿粉尘,用扫描电镜-能散X线分光计（SEM-EDS）以5 keV和20 keV电压照射测定呼吸性粉尘颗粒中各元素成分的含量,计算不同电子伏特照射下粉尘颗粒中硅与铝的比值.结果 7个瓷厂、3个锡矿和3个钨矿的47个粉尘样本共计3 982个粉尘颗粒,瓷厂样本的89%（24/27）与锡矿样本的27%（3/11）和钨矿样本的56%（5/9）存在明确的铝硅酸盐包裹,与对照样本比较,差异有统计学意义（P＜0.01）.瓷厂粉尘颗粒的45%、锡矿的18%和钨矿的13%存在表面铝硅酸盐包裹.瓷厂粉尘与钨矿和锡矿粉尘表面铝硅酸盐含量的差异有统计学意义（P＜0.01）,高铝硅酸盐含量的粉尘颗粒在瓷厂、锡矿和钨矿样本中的比率分别为22%、7%和10%.结论 瓷厂工作场所粉尘颗粒表面夹杂铝硅酸盐含量高于钨矿和锡矿的粉尘,粉尘颗粒表面成分的分析对解释不同厂矿尘肺发病的差异有一定作用.     

陶瓷厂和钨矿生产性粉尘中11种元素比较分析

目的探讨陶瓷厂和钨矿生产性粉尘中多种元素含量的差异以及其对粉尘毒性和致病作用的可能影响。方法收集厂矿粉尘各50g，用火焰原子吸收光谱法检测陶瓷厂和钨矿粉尘样品中铜、锌、铅、镉、镍、铁、锰、钙、镁9种元素的含量，用石墨炉原子吸收光谱法检测样品中铝元素的含量，用原子荧光光谱法检测样品中砷元素的含量。结果陶瓷厂和钨矿粉尘样品中铝、砷、镉、铁、锰、铅元素含量的差异有统计学意义（P〈0．05），陶瓷厂粉尘中铝元素的平均含量为104688．71μg/g，大于钨矿粉尘中的平均含量64883．17μg／g；陶瓷厂粉尘中砷、镉、铁、锰、铅元素的平均含量分别为31．04、2．27、4473．23、369．67、96．86μg/g，而钨矿的分别为80．32、20．64、28619．06、1596．93、333．02μg／g，均高于陶瓷厂。结论陶瓷厂和钨矿粉尘中多种元素的含量有明显的差异，元素含量的不同，可能会影响粉尘的生物学效应活性，对粉尘的致病作用有一定的影响。     

陶瓷矿山粉尘细胞毒性研究与评价

本文应用体外细胞培养方法,研究了景德镇所属九个陶瓷矿山粉尘对细胞的毒性作用,采用细胞存活率、乳酸脱氢酶和细胞内钾含量三项指标进行观察。结果表明,各种粉尘对肺泡巨噬细胞均有不同程度的毒性。用定量的方法综合三项指标危害指数比较了不同陶瓷矿山粉尘的毒性作用。本研究对陶瓷矿山粉尘危害分级管理提供了理论及实际应用依据。     

早期煤工尘肺支气管肺泡灌洗液中SP-A及TNF-α含量的变化

目的　探讨煤尘职业接触者和早期煤工尘肺患者支气管肺泡灌洗液(BALF)中细胞因子含量改变的特点及意义。方法　采煤工23人,按X线胸片诊断为煤尘接触组(接尘组)、煤工尘肺0+和Ⅰ期组;健康农民7人为对照组。经纤支镜做支气管肺泡灌洗,收集BALF,用酶联免疫吸附法(ELISA)测定肺泡表面活性蛋白-A(SP-A)及肿瘤坏死因子(TNF-α)含量。结果　接尘组BALF中SP-A含量为(6528.2±1872.0)ng/ml,TNF-α含量为(8.23±1.61)U/ml,均明显高于对照组［(1050.1±912.2)ng/ml及(5.17±0.89)U/ml］,差异有显著性(P<0.01);且随煤工尘肺期别进展,SP-A及TNF-α含量降低,SP-A及TNF-α含量变化与煤工尘肺病变严重性之间呈负相关(前者r=-0.64,P<0.01;后者r=-0.45,P<0.05)。结论　BALF中SP-A和TNF-α含量升高可能是煤尘接触的效应指标。     

金属矿山和瓷厂的粉尘及有害因素

本文为研究金属矿工和瓷厂作业工人的肺癌病因,对4类金属矿(钨、锡,铜、铁)和9个瓷厂作业环境的粉尘,30种化学元素、放射性氡子体、γ射线和17种多环芳烃(PAH)等有害因素作了现场测定,并对各厂矿的历史测尘资料进行了整理分析。结果发现粉尘浓度早期以钨矿为最高。自70年代开始,钨矿降为最低。但游离SiO_2含量以钨矿最高,瓷厂次之,铁矿最低。瓷厂粉尘分散度比矿尘低。元素结果表明,砷、镉以锡矿最高:铁、镍以铁矿最高,这些被认为致癌物和可疑致癌物元素,可能成为矿工的致癌因素之一。井下氡子体仅铜矿超标,故铜矿工肺癌高发可能受氡暴露的影响。PAH 以井下使用柴油铲运机的锡矿、铜矿、铁矿为最高。但因其接触时间不长,其致癌作用还需进一步观察。     

Estimating historical respirable crystalline silica exposures for Chinese pottery workers and iron/copper, tin, and tungsten miners.

Collaborative studies of Chinese workers, using over four decades of dust monitoring data, are being conducted by the National Institute for Occupational Safety and Health (NIOSH) and Tongji Medical University in China. The goal of these projects is to establish exposure-response relationships for the development of diseases such as silicosis or lung cancer in cohorts of pottery and mine workers. It is necessary to convert Chinese dust measurements to respirable silica measurements in order to make results from the Chinese data comparable to other results in the literature.This article describes the development of conversion factors and estimates of historical respirable crystalline silica exposure for Chinese workers. Ambient total dust concentrations (n>17000) and crystalline silica concentrations (n=347) in bulk dust were first gathered from historical industrial hygiene records. Analysis of the silica content in historical bulk samples revealed no trend from 1950 up to the present. During 1988-1989, side-by-side airborne dust samples (n=143 pairs) were collected using nylon cyclones and traditional Chinese samplers in 20 metal mines and nine pottery factories in China. These data were used to establish conversion factors between respirable crystalline silica concentrations and Chinese total dust concentrations. Based on the analysis of the available evidence, conversion factors derived from the 1988-1989 sampling campaign are assumed to apply to other time periods in this paper. The conversion factors were estimated to be 0.0143 for iron/copper, 0.0355 for pottery factories, 0.0429 for tin mines, and 0.0861 for tungsten mines. Conversion factors for individual facilities within each industry were also calculated. Analysis of variance revealed that mean conversion factors are significantly different among facilities within the iron/copper industry and within the pottery industry. The relative merits of using facility-specific conversion factors, industry-wide conversion factors, or a weighted average of the two are discussed. The exposure matrix of the historical Chinese total dust concentrations was multiplied by these conversion factors to obtain an exposure matrix of historical respirable crystalline silica concentrations.     

Risk of silicosis in cohorts of Chinese tin and tungsten miners and pottery workers (II): Workplace-specific silica particle surface composition

BACKGROUND: It is hypothesized that surface occlusion by alumino-silicate affects the toxic activity of silica particles in respirable dust. In conjunction with an epidemiological investigation of silicosis disease risk in Chinese tin and tungsten mine and pottery workplaces, we analyzed respirable silica dusts using a multiple-voltage scanning electron microscopy-energy dispersive X-ray spectroscopy (MVSEM-EDS). METHODS: Forty-seven samples of respirable sized dust were collected on filters from 13 worksites and were analyzed by MVSEM-EDS using high (20 keV) and low (5 keV) electron beam accelerating voltages. Changes in the silicon-to-aluminum X-ray line intensity ratio between the two voltages are compared particle-by-particle with the 90th percentile value of the same measurements for a ground glass homogeneous control sample. This provides an index that distinguishes a silica particle that is homogeneously aluminum-contaminated from a clay-coated silica particle. RESULTS: The average sample percentages of respirable-sized silica particles alumino-silicate occlusion were: 45% for potteries, 18% for tin mines, and 13% for tungsten mines. The difference between the pottery and the metal mine worksites accounted for one third of an overall chi-square statistic for differences in change in measured silicon fraction between the samples. CONCLUSION: The companion epidemiological study found lower silicosis risk per unit cumulative respirable silica dust exposure for pottery workers compared to metal miners. Using these surface analysis results resolves differences in risk when exposure is normalized to cumulative respirable surface-available silica dust.     

A nested case-control study of lung cancer among silica exposed workers in China.

In an attempt to assess whether silica induces lung cancer, a nested case-control study of 316 male lung cancer cases and 1352 controls was carried out among pottery workers and tungsten, copper-iron, and tin miners from five provinces in south central China. Exposure to dust and silica for each study subject was evaluated quantitatively by cumulative exposure measures based on historical industrial hygiene records. Measurements on confounders such as inorganic arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon were also collected from the worksites. Information on cigarette smoking was obtained by interviews of the subjects or their next of kin. A significant trend of increasing risk of lung cancer with exposure to silica was found for tin miners, but not for miners working in tungsten or copper-iron mines. Concomitant and highly correlated exposures to arsenic and PAHs among tin miners were also found. Risk of lung cancer among pottery workers was related to exposure to silica, although the dose-response gradient was not significant. Risks of lung cancer were significantly increased among silicotic subjects in iron-copper and tin mines, but not in pottery factories or tungsten mines. The results of this study provide only limited support for an aetiological association between silica and lung cancer.     

A nested case-control study of lung cancer among silica exposed workers in China.

In an attempt to assess whether silica induces lung cancer, a nested case-control study of 316 male lung cancer cases and 1352 controls was carried out among pottery workers and tungsten, copper-iron, and tin miners from five provinces in south central China. Exposure to dust and silica for each study subject was evaluated quantitatively by cumulative exposure measures based on historical industrial hygiene records. Measurements on confounders such as inorganic arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon were also collected from the worksites. Information on cigarette smoking was obtained by interviews of the subjects or their next of kin. A significant trend of increasing risk of lung cancer with exposure to silica was found for tin miners, but not for miners working in tungsten or copper-iron mines. Concomitant and highly correlated exposures to arsenic and PAHs among tin miners were also found. Risk of lung cancer among pottery workers was related to exposure to silica, although the dose-response gradient was not significant. Risks of lung cancer were significantly increased among silicotic subjects in iron-copper and tin mines, but not in pottery factories or tungsten mines. The results of this study provide only limited support for an aetiological association between silica and lung cancer.