转化生长因子-β1基因509C/T多态性在宁夏煤工尘肺人群中的分布

[目的]探讨转化生长因子-β1（TGF-β1）基因509C/T多态性在宁夏汉族煤工尘肺（coal worker’s pneumoconiosis,CWP）人群中的分布情况。[方法]从宁夏某煤业集团所属煤矿已确诊的病例中随机抽取110名煤工尘肺病例（煤工尘肺组）、110名煤尘接触者（煤尘接触组）和110名当地不接尘的正常居民（非煤尘接触组）为研究对象,采集静脉血,使用聚合酶链反应-限制片段长度多态性（PCR-RFLP）分析TGF-β1基因509CT位点多态性。[结果]煤工尘肺组、煤尘接触组及非煤尘接触组平均年龄分别为（48.30±13.16）岁、（43.86±4.20）岁、（41.73±5.45）岁。煤工尘肺组和煤尘接触组工龄分别为（17.40±7.84）年和（16.95±6.10）年。工种构成：主掘进工在煤工尘肺组和煤尘接触组中分别占48.2%和49.1%。煤工尘肺组和煤尘接触组及非煤尘接触组中吸烟烟龄分别为（10.48±10.12）年、（11.34±10.48）年、（12.65±11.53）年;接尘工龄、工种构成、吸烟烟龄均无差别,均P〉0.05。TGF-β1基因509C/T位点多态性在煤工尘肺组、煤尘接触组及非煤尘接触组中所占比例分别为51.8%、30.9%、25.5%;等位基因频率T在煤工尘肺组、煤尘接触组及非煤尘接触组中所占比例分别为40.90%、23.20%、19.10%;煤工尘肺组与煤尘接触组比较,TGF-β1基因中CT基因型差异有统计学意义（P〈0.01）。煤工尘肺组不同期别人群的等位基因频率差异有统计学意义（P〈0.01）。[结论]TGF-β1-509C/T位点多态性在宁夏地区煤工尘肺者中的分布可能不同。     

IL-12B＋1188A／C基因多态性与宁夏汉族煤工尘肺易感性研究

[目的]探讨白介素-12B（interleukin-12B,IL-12B）基因3＇UTR区1188A／C位点多态性与宁夏汉族煤工尘肺（coal worker’s pneumoconiosis,CWP）易感性的关系。[方法]采用聚合酶链反应-限制片段长度多态性（PCR—RFLP）法对120例CWP患者和120例煤尘接触组IL-12B基因1188A／C位点多态性进行分型,对等位基因及基因型分布进行统计学分析。[结果]煤工尘肺组与煤尘接触组在接尘工龄、工种构成、吸烟烟龄差异无统计学意义（P〉0．05）.对年龄进行标化后,分析发现IL-12B 1188A／C位点在煤工尘肺组和煤尘接触组中检出三种基因型爿爿、AC、CC型,这三种基因型在尘肺组和接触组间分布差异无统计学意义（P〉0．05）;等位基因C在煤工尘肺组和煤尘接触组中所占比例分别为45．8％和36．7％,差异有统计学意义（P〈0．05）,在接尘工龄、工种和是否吸烟中的分布无差异（P〉0．05）.[结论]IL-12B 1188A／C位点C等位基因可能是宁夏汉族煤工尘肺的易感基因之一。     

转化生长因子β1基因多态性对煤工尘肺遗传易感性的影响

目的：探讨转化生长因子β1（TGF-β1）基因-509位点多态性对煤工尘肺遗传易感性的影响。方法：以110例汉族煤工尘肺患者和110例汉族煤尘接触者为研究对象，进行问卷调查，采集其外周静脉血提取DNA并应用PCR-RFLP技术检测其TGF-β1基因-509位点多态性。结果：煤工尘肺患者中TGF-β1基因-509位点为C／T及T／F基因型的占81．8％，C／C基因型占18．2％；而煤尘接触者中则分别为53．6％和46．4％，两组之间差异有统计学意义（P〈0．05）。调整接尘工龄后，C／T及T/T基因型罹患煤工尘肺危险度是C／C基因型的3．308倍（P〈0．05）。logistic回归分析结果显示TGF-β1基因-509位点基因型、接尘工龄、吸烟3个因素均对罹患煤工尘肺有影响。结论：TGF-β1基因-509位点C／T及T/T基因型可能比C／C基因型者易于罹患煤工尘肺，接尘工龄、吸烟亦是煤工尘肺重要的影响因素。     

肿瘤坏死因子-α及其Ⅱ型受体基因多态性与煤工尘肺

目的　探讨肿瘤坏死因子 α(TNF α)及其Ⅱ型受体 (TNFRⅡ )基因多态性在煤工尘肺发病遗传易感性中的作用及其与煤工尘肺纤维化程度的联系。方法　选择 2 34例汉族煤工尘肺患者和4 4 0例煤尘接触者为研究对象 ,拍摄高仟伏X射线后前位胸片 ,按尘肺病诊断标准进行诊断和分期 ;采集研究对象的外周静脉血 ,应用多聚酶链反应 -限制片段长度多态性 (PCR RFLP)技术检测其TNF α及TNFRⅡ基因多态性。结果　TNF α - 30 8位点G A A A基因型和TNFRⅡ 196位点T G G G基因型分布频率在成组或 1∶1配对分析中 ,煤工尘肺患者和煤尘接触者两组间差异均无显著性 (P >0 .0 5 )。G A A A基因型频率在Ⅲ期煤工尘肺患者中为 2 0 .0 0 % ,高于煤尘接触者 (10 .91% )、Ⅰ期(10 .34% )和Ⅱ期煤工尘肺患者 (7.5 0 % ) ;1∶1配对后 ,G A A A基因型携带者发展成Ⅲ期煤工尘肺的危险性是G G基因型的 3倍 (95 %CI:0 .35～ 2 5 .84 )。结论　TNF α和TNFRⅡ基因多态性在汉族煤工尘肺发病的遗传易感性中不起主要作用。TNF α基因多态性可能与煤工尘肺纤维化严重程度相关。     

肿瘤坏死因子-α及其Ⅱ型受体基因多态性与煤工尘肺的遗传易感性

[目的]探讨肿瘤坏死因子-α（TNF-α）基因-308位点、肿瘤坏死因子Ⅱ型受体（TNFRⅡ）基因196位点的基因多态性与煤工尘肺病遗传易感性的关系。[方法]采用病例对照研究方法，选择接尘工龄大于1年，无免疫系统疾病史，除尘肺患者外，对照组接触工人无肺部疾病史，以问卷调查和现场体检方式收集职业接触史、既往病史、家族史和尘肺诊断史，采集每个研究对象静脉血3ml，采用盐析法从外周静脉血的有核细胞中提取DNA。按文献报道的合成序列引物、采用PCR扩增反应和RFLP技术分析TNF-α和TNFRⅡ。[结果]TNF-α308位点G／A＋A／A基因型和TNFRⅡ196位点T／G＋G／G基因型分布频率在成组或1：1配对分析中，煤工尘肺患者和煤尘接触者两组间差异均无显著性（P〉0．05）。G／A＋A／A基因型频率在Ⅲ期煤工尘肺患者中为20．00％，高于煤尘接触者（10．91％）、Ⅰ期（10．34％）和Ⅱ期煤工尘肺患者（7．50％）；1：1配对后G／A＋A／A基因型携带者发展成Ⅲ期煤工尘肺的危险性是G／G基因型的3倍（95％CI：0．35～25．84）。[结论]TNF-α基因．308位点和TNFRⅡ基因196位点多态性在中国汉族煤工尘肺发病的遗传易感因素中不起主要作用。TNF-α基因-308位点多态性可能与煤工尘肺重度纤维化相关联，值得进一步研究证实；TNFRⅡ基因196位点与煤工尘肺纤维化程度无关。     

肿瘤坏死因子-α及其Ⅱ型受体基因多态性与矽肺

目的 探讨肿瘤坏死因子-α(TNF-α)及其Ⅱ型受体(TNFR Ⅱ)基因多态性在矽肺发病遗传易感性中的作用及其与二氧化硅暴露的交互作用。方法 选择259例矽肺患者和341例矽尘接触者(对照)为研究对象,对其职业史、尘肺病史、既往病史等进行问卷调查;拍摄其高仟伏X射线后前位胸片,根据尘肺病诊断标准进行诊断和分期;采集每个研究对象的外周静脉血,应用聚合酶链反应-限制性片断长度多态性(PCR-RFLP)技术检测其TNF-α及TNFR Ⅱ基因多态性。结果 在成组或1:1配对分析中,矽肺患者和矽尘接触者两组间TNF-α基因-308位点G/A A/A基因型和TNFRⅡ196位点T/G G/G基因型分布频率的差异均无统计学意义(P>0.05)。当接尘工龄<15年时,G/A A/A基因型携带者发生矽肺的危险性是G/G基因型的6.74倍,95％CI:1.01-44.99。结论TNF-α和TNFRⅡ基因多态性在汉族人群矽肺发病的遗传易感性中不起主要作用。TNF-α基因-308位点基因多态性在矽肺发病过程中与接尘工龄存在交互作用,当累积接尘量较低时,G/A A/A基因型携带者发生矽肺的危险性较G/G基因型明显增加。     

转化生长因子-β及肿瘤坏死因子基因多态性与煤工尘肺的关系

目的 探讨转化生长因子-β(TGF-B)和肿瘤坏死因子-α(TNF-α)基因多态性与煤工尘肺发生的关系.方法 选择234名汉族男性煤工尘肺患者为病例组,440名接触煤尘无尘肺及其他肺部疾病者为对照组,采集外周静脉血,采用聚酶链反应-限制性片段长度多态性(PCR-RFLP)技术检测TGF-β(+869)位点和TNF-α(-238)位点基因多态性.结果 煤工尘肺病例组TGF-β(+869)位点基因型、等位基因分布频率与对照组比较,差异均无统计学意义(P>0.05).TNF-α(-238)位点为G/A基因型者患Ⅰ期煤工尘肺的危险度是G/G基因型的1.74倍(95%CI:1.01～3.01,P<0.05),调整年龄、接尘工龄和工种后为1.58倍(95%CI:0.89～2.78,P>0.05).I期煤工尘肺患者G、A等位基因频率分别为93.10%和6.90%,对照组G、A等位基因频率分别为95.80%和4.20%,两组比较,X2=3.828,P=0.05.结论 TNF-α(-238)位点和TGF-β(+869)位点的多态性对煤工尘肺的发生不起主要作用.     

白细胞介素-1基因多态性与尘肺易感性的关系

目的 探讨白细胞介素-1（IL-1）基因多态性与尘肺易感性的关系.方法 以80例Ⅰ期矽肺和45例Ⅰ期煤工尘肺为病例,以与病例年龄相差小于5岁、同性别、同民族、同一工作地点、开始接尘时间和累积接尘工龄相差不超过2年的非尘肺接尘工人为对照,进行1：1配对.采集静脉血,用酚-氯仿法抽提DNA,采用聚合酶链反应限制性片段长度多态性（PCR-RFLP）和PCR方法检测IL-1α（-889）、IL-1β（-511）、IL-1 Ra（＋2018）和IL-1Ra数目可变的串联重复序列4个基因位点的基因型,并进行单因素、多因素分析.结果 两组IL-1α（-889）1/2＋2/2基因型的携带率的差异有统计学意义（P＜0.01）,病例组与对照组IL-1α（-889）等位基因2的频率分别为57.6%和40.8%,差异有统计学意义（P＜0.01）,多因素分析表明,IL-1α（-889）突变基因型及等位基因2为尘肺的危险因素.病例组与对照组之间IL-1β（-511）1/2＋2/2基因型、IL-1 Ra（＋2018）1/2＋2/2基因型和IL-1Ra VNTR1/2＋2/2基因型携带率的差异均无统计学意义（P＞0.05）,病例组与对照组IL-1β（-511）、IL-1 Ra（＋2018）和IL-1 Ra VNTR等位基因2的频率差异无统计学意义（P＞0.05）.矽肺组和煤工尘肺组间4个等位基因及基因型分布频率差异均无统计学意义（P＞0.05）.结论 IL-1α（-889）基因多态性与尘肺患病有关,携带IL-1α（-889）等位基因2的接尘者患尘肺的危险性增加,未发现IL-1β（-511）、IL-1Ra（＋2018）及IL-1 Ra VNTR基因多态性与尘肺发病有关联.     

肿瘤坏死因子-a及其Ⅱ型受体基因多态性与矽肺

目的探讨肿瘤坏死因子-a(TNF-a)及其Ⅱ型受体(TNFRⅡ)基因多态性在矽肺发病遗传易感性中的作用及其与二氧化硅暴露的交互作用.方法选择259例矽肺患者和341例矽尘接触者(对照)为研究对象,对其职业史、尘肺病史、既往病史等进行问卷调查;拍摄其高仟伏X射线后前位胸片,根据尘肺病诊断标准进行诊断和分期;采集每个研究对象的外周静脉血,应用聚合酶链反应-限制性片断长度多态性(PCR-RFLP)技术检测其TNF-a及TNFRⅡ基因多态性.结果在成组或11配对分析中,矽肺患者和矽尘接触者两组间TNF-a基因-308位点G/A+A/A基因型和TNFRⅡ196位点T/G+G/G基因型分布频率的差异均无统计学意义(P＞0.05).当接尘工龄＜15年时,G/A+A/A基因型携带者发生矽肺的危险性是G/G基因型的6.74倍,95%CI1.01～44.99.结论TNF-α和TNFRⅡ基因多态性在汉族人群矽肺发病的遗传易感性中不起主要作用.TNF-α基因-308位点基因多态性在矽肺发病过程中与接尘工龄存在交互作用,当累积接尘量较低时,G/A+A/A基因型携带者发生矽肺的危险性较G/G基因型明显增加.     

白细胞介素-8基因多态性与尘肺易感性研究

目的分析白细胞介素-8基因多态性与尘肺易感性的关系,探讨粉尘接触人群易感生物标志物。方法采用整群病例对照研究方法,以2568名接触煤矿粉尘和1265名接触矽尘工人为调查对象,均拍摄后前位胸大片,由专家组按照GBZ70—2009尘肺病诊断标准盲法诊断,以确诊的壹期男性尘肺患者为病例组,共213例,其中矽肺101例,煤工尘肺112例。从受检的接尘工人中选择与病例发病年龄相似、同一工作场所无尘肺的汉族男性接尘工人251名为对照组。采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)和PCR方法检测白细胞介素-8(IL-8)4个位点基因型。结果病例组和对照组平均年龄分别为(54.9±9.4)岁和(54.8±6.3)岁,累积接尘工龄分别为(29.3±6.1)a和(29.5±4.9)a。两组年龄、累积接尘工龄比较,差异均无统计学意义(P>0.05);IL-8Met31Arg位点GG、GT和TT基因型频率病例组分别为0%、14.1%和85.9%,对照组分别为0.4%、3.6%和96.0%,差异有统计学意义(χ2=17.25,P<0.05);-251A/T位点AA、AT和TT基因型频率病例组分别为39.0%、48.8%和12.2%,对照组分别为17.9%、17.9%和64.2%,差异有统计学意义(χ2=19.19,P<0.05);病例组781C/T位点TT基因型频率(21.6%)高于对照组(13.9%),差异有统计学意义(χ2=4.68,P<0.05);病例组和对照组RA+860位点基因型分布比较,差异无统计学意义(P>0.05)。结论携带IL-8Met31Arg位点GT基因型和781C/T位点TT基因型的接尘工人患尘肺的危险性增加,而携带IL-8-251A/T位点TT基因型接尘工人患尘肺危险性降低;未证实RA+860位点的基因多态性与尘肺易感性有关。     

白细胞介素-6基因-174C/G和-634C/G多态性与尘肺易感性的Meta分析

目的探索白细胞介素-6(interleukin-6,IL-6)基因-174C/G和-634C/G多态性与尘肺易感性的关系。方法以尘肺、白细胞介素-6及多态性为关键词,检索中文数据库Sinomed、万方医学、中国知网和维普;以pneumoconiosis、interleukin-6及polymorphism为关键词,检索英文数据库Pubmed、Embase、Cochrane Library和Web of Science。采用Revman Manager 5.2软件进行效应值的合并和文献质量评价。结果共纳入7篇文献(9组病例-对照研究),包括IL-6基因-174C/G位点病例660例,对照848例;IL-6基因-634C/G位点病例344例,对照362例。Meta分析结果表明,IL-6基因-174C/G位点多态性与尘肺易感性之间无关联(CC对CG+GG,OR=1.05(95%CI 0.76～1.45), CG对GG+CC,OR=0.79(95%CI 0.40～1.55), C对G,OR=0.95(95%CI 0.80～1.14))。IL-6基因-634 C/G多态性位点与尘肺发病之间有关联...     

白细胞介素-8基因多态性与矽肺易感性研究

目的 探讨白细胞介素(IL)-8基因多态性与矽肺易感性的关系.方法 选择确诊的101例矽肺患者为病例组,以接触同性质粉尘、首次诊断年龄相近的非矽肺的接尘工人为对照(121例).采集外周静脉血,盐析法提取DNA,应用聚合酶链-限制性片段长度多态性(PCR-RFLP)技术检测IL-8(Met31Arg、781C/T、-251A/T、RA+860)4个位点的基因型和等位基因频率并进行分析.结果 两组对象的首次诊断年龄、累积接尘工龄、吸烟率的差异均无统计学意义(P＞0.10).病例组IL-8(Met31Arg)GT基因型的分布频率为12.87%,对照组为2.48%,差异有统计学意义(P＜0.05),病例组和对照组携带等位基因G的频率分别为6.44%和2.07%,差异有统计学意义(P＜0.05).病例组IL-8(-251A/T)从基因型的分布频率为9.90%,对照组为25.62%,差异有统计学意义(P＜0.05).病例组IL-8(781C/T)基因型CC、CT、TT的分布频率分别为38.61%、40.59%、20.79%,与对照组(46.28%、40.50%、13.22%)相比,差异无统计学意义(P＞0.05).病例组IL-8(RA+860)基因型GG、GC、CC的分布频率分别为75.25%、21.78%、2.97%,与对照组(80.17%、14.88%、4.96%)相比,差异无统计学意义(P＞0.05).结论 IL-8的Met31Arg位点和一251MT位点的基因多态性与矽肺易感性有关,携带IL-8(Met31Arg)GT基因型的接尘工人患矽肺的危险性增加;携带IL-8(-251)从基因型的接尘工人患矽肺的危险性降低.未发现IL-8(781C/T和RA+860)位点的基因多态性与矽肺易感性有关.

Abstract：

Objective To explore the relationship between the polymorphisms of interleukin-8(IL-8)and the silicosis susceptibility. Methods The case group consisted of 101 male patients with stage I silicosis diagnosed by the Pneumoconiosis Diagnosis Expert Panel according to the Chinese National Diagnosis Criteria of Pneumoconiosis (GBZ 70-2009). The control group consisted of 121 workers without silicosis exposed to same dusts. The cases and the controls had the same dust exposure history. The peripheral venous blood was drawn from each subject. DNA was extracted from leucocytes by the salting method. The polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) techniques and PCR were used to examine polymorphism of IL-8(Met31Arg, 781C/T,-251A/T and RA+860). Results There were no the differences of age, cumulative exposure time and smoking between the cases and the controls (P＞0.05). The frequencies of IL-8 (Met31Arg) GT genotypes in cases and controls were 12.87% and 2.48%, respectively, there was significant difference (P＜0.05).The frequencies of allele G in cases and controls were 6.44% and 2.07%, respectively, there was significant difference (P＜0.05). The frequencies of IL-8 (-251A/T) AA genotypes in cases and controls were 9.90% and 25.64%, respectively, there was significant difference (P＜0.05). The frequencies of IL-8 (781C/T) CC, CT, TT genotypes in cases and controls were 38.61%,40.59%,20.79% and 46.28%,40.50%, 13.22%, respectively, there zwas no significant difference (P＞0.05). The frequencies of IL-8 (RA+860) GG, GC and CC genotypes in cases and controls were 75.25%, 21.78%, 2.97%, 80.17%, 14.88%, 4.96%, respectively, there was no significant difference (P＞0.05). Conclusions IL-8 (Met31 Arg and -251A/T) genetic polymorphisms might play a role in the development of silicosis. The risk of pneumoconiosis in workers carrying (Met31 Arg) genotype GT is likely to increase.The risk of pneumoconiosis in workers carrying IL-8 (-251A/T) AA genotype is likely to decrease. The relationship between IL-8 781C/T and RA+860 genes polymorphisms and silicosis is not found.     

煤工尘肺患者血清中基质金属蛋白酶-9及其抑制因子水平的变化

目的 探讨煤工尘肺患者血清中基质金属蛋白酶(MMP-9)及基质金属蛋白酶抑制剂(TIMP-9)水平的变化及意义.方法 采用双抗体夹心ELISA法检测188例煤工尘肺(煤肺组53例,煤矽肺组67例,矽肺组68例)、57例0期(0~+期组)、64例接尘对照组和50例健康对照组血清中MMP-9及TIMP-9含量;分析血清中MMP-9和TIMP-9水平在各煤工尘肺组及各对照组间的变化,以及二者的相关性;并根据煤工尘肺期别、是否有并发症以及接尘年限等因素进行分析.结果 煤肺组血清中MMP-9水平为17.16 ng/ml、煤矽肺组为15.14ng/ml,矽肺组为17.50 ng/ml,与健康对照组比较,差异均有统计学意义(P<0.05)与接尘对照组、0~+组比较,均呈降低趋势,其中矽肺组及煤矽肺组差异有统计学意义(P<0.05).3组煤工尘肺患者血清中MMP-9水平比较,差异无统计学意义(P>0.05);煤肺组、煤矽肺组和矽肺组血清中TIMP-9水平分别为(330.00±108.42),(312.044±120.09),(366.81±135.50)ng/ml,均低于健康对照组,其中矽肺组和煤肺组血清中TIMP-9水平较接尘对照组、1~+组明显增高,差异有统计学意义(P<0.05),3组煤工尘肺组间比较,矽肺组血清中TIMP-9水平较煤矽肺组升高,差异有统计学意义(P<0.05).3组煤工尘肺患者血清中MMP-9和TIMP-9水平按不同的疾病分期、是否有并发症以及接尘年限进行分析,差异均无统计学意义(P>0.05);矽肺组血清中TIMP-9水平与年龄呈正相关(r=0.249,P<0.05),血清中MMP-9和TIMP-9水平在接尘对照组中呈正相关(r=0.294,P<0.05),其他组中未发现相关性.结论 血清中MMP-9与TIMP-9水平变化与粉尘对机体的损害程度有关,MMP-9与TIMP-9共同参与了煤工尘肺的病理生理过程;动态观察0~+期及健康煤矿工人血清中MMP-9和TIMP-9水平,可为煤工尘肺的预防及早期诊断提供参考.     

凋亡相关基因FAS-1377和FAS-670及其配体FASL-844位点基因多态性与中国汉族煤工尘肺的关系

目的探讨FAS／FASL基因多态性在煤工尘肺患者发病遗传易感性中的作用及其与煤工尘肺纤维化程度的联系。方法选择340例汉族煤工尘肺为观察对象，312例汉族煤尘接触者为对照组，应用多聚酶链反应-限制片段多态性（PCR—RFLP）技术检测FAS-1377G〉A、FAS-670A〉G位点及FASL-844T〉C位点的基因多态性。结果煤工尘肺组FAS．1377、FAS-670及FASL-844各基因及等位基因分布频率与对照组比较，差异无统计学意义（乃0．05）。以接尘工龄／〉25年为对照，工龄〈25年的煤工尘肺患者FAS-1377GA／AA型者发生尘肺的危险性是GG型的1．463倍（P=0．098，95％CI：0．932～2．298）；FAS-670AG型发生尘肺的危险性是GG型者的1．494倍（P=0．098，95％C／：0．928～2．404）：FASL-844TT型和TC型发生尘肺的危险性分别是CC型的5,455倍（P=0．039，95％CI：1,088-27．358）及1,338倍（P=0．098，95％CI：0．852-2．101）。接尘工龄〈25年FASL-844基因分布频率和工龄≥25年比较，差异有统计学意义（P〈0．05），FASL-844Tr型发生煤工尘肺的危险性是CC／TC型的4．810倍（P=O．054，95％CI：0．971-23．833）；接尘工龄≥25年为对照，工龄〈25年组FASL-844TT／CT＋FAS-1377GA型发生煤工尘肺的危险性是FASL-844CC＋FAS-1377GG型的1．810倍；FASL-844TT／CT＋FAS．670AG型是FASL-844CC＋FAS-670AA型的2．117倍；FASL-8TT／CT＋FAS-1377GA／AA＋FAS-670AG／GG型发生煤工尘肺的危险性是FASL-844CC＋FAS-1377GG＋FAS-670AA型的2．043倍。结论FAS．1377G〉A、FAS-670A〉G及FASL-844T〉C3个位点的基因多态性在中国汉族煤工尘肺发病的遗传易感性中不起主要作用，但这3个多态性位点及位点的联合作用对病变的发展有影响。     

Respiratory impairments due to dust exposure: A comparative study among workers exposed to silica,asbestos, and coalmine dust

We conducted a comparative study of pulmonary dysfunction among workers who were exposed to silica, asbestos, or coalmine dust. The results showed that all three groups of dust-exposed workers, even those without radiographic signs of pneumoconiosis, had decreased spirometric parameters and diffusing capacity (DLco) in both nonsmokers and smokers. Pulmonary function was further decreased when pneumoconioses were present in the three groups. In accord with increasing radiographic categories, pulmonary function in the workers' pneumoconiosis (CWP), it changed relatively little. Workers with mild to moderate (radiographic category I–II) silicosis or asbestosis showed similarly decreased DLco, but those with silicosis showed lower FEV₁/FVC than those with asbestosis. The workers with CWP also showed a lower FEV₁/FVC than those with asbestosis. The major impairment patterns for silica workers, asbestos workers, and coal miners were mixed, restrictive and mixed, and obstructive, respectively. Smoking obviously increased the prevalence of obstruction for all the groups. We conclude from the present study that all the three dusts cause functional abnormalities that precede radiographic changes of pneumoconiosis. We should pay more attention to respiratory impairment in the initial stage of silicosis and CWP. Am. J. Ind. Med. 31:495–502, 1997. © 1997 Wiley-Liss, Inc.     

Pneumoconiosis and advanced occupational lung disease among surface coal miners--16 states, 2010-2011

Coal workers' pneumoconiosis (CWP) is a chronic occupational lung disease caused by long-term inhalation of dust, which triggers inflammation of the alveoli, eventually resulting in irreversible lung damage. CWP ranges in severity from simple to advanced; the most severe form is progressive massive fibrosis (PMF). Advanced CWP is debilitating and often fatal. To prevent CWP, the Coal Mine Health and Safety Act of 1969 established the current federal exposure limit for respirable dust in underground and surface coal mines. The Act also established a surveillance system for assessing prevalence of pneumoconiosis among underground coal miners, but this surveillance does not extend to surface coal miners. With enforcement of the exposure limit, the prevalence of CWP among underground coal miners declined from 11.2% during 1970-1974 to 2.0% during 1995-1999, before increasing unexpectedly in the last decade, particularly in Central Appalachia. Exposure to respirable dust is thought to be less in surface than underground coal miners. Although they comprise 48% of the coal mining workforce, surface coal miners have not been studied since 2002. To assess the prevalence, severity, and geographic distribution of pneumoconiosis among current surface coal miners, CDC obtained chest radiographs of 2,328 miners during 2010-2011 through the Coal Workers' Health Surveillance Program of the National Institute for Occupational Safety and Health (NIOSH). Forty-six (2.0%) of 2,257 miners with >1 year of surface mining experience had CWP, including 37 who had never worked underground. Twelve (0.5%) had PMF, including nine who had never worked underground. A high proportion of the radiographs suggested silicosis, a disease caused by inhalation of crystalline silica. Surface coal mine operators should monitor worker exposures closely to ensure that both respirable dust and silica are below recommended levels to prevent CWP. Clinicians should be aware of the risk for advanced pneumoconiosis among surface coal miners, in addition to underground coal miners, to facilitate prompt disease identification and intervention.     

24 years of pneumoconiosis mortality surveillance in Australia

Asbestosis, silicosis and Coal Worker's Pneumoconiosis (CWP) represent three of the most important occupationally-related dust diseases in Australia. To gain a clear picture of pneumoconiosis trends over time, a 24-yr retrospective analysis of national mortality data was performed for the period 1979 to 2002. Over 1,000 pneumoconiosis-related fatalities occurred during this time, 56% of which were caused by asbestosis, 38% by silicosis and 6% by CWP. Between 1979 and 1981, silicosis accounted for 60% of all pneumoconiosis-related fatalities in Australia, followed by asbestosis (31%). By 2002 however, asbestosis was causing 78% of all fatalities, while silicosis accounted for only 19%. Asbestos-related mortality increased three-fold between 1979 and 2002, with a clear excess risk demonstrated among males. On the other hand, mortality rates for silicosis and CWP declined significantly during the same time period. Overall, this study suggests that pneumoconiosis, particularly asbestosis, continues to be an important occupational disease in Australia. Although progress has been made in reducing deaths due to occupational silicosis and CWP, asbestosis rates continue to rise, reflecting the long latency between dust exposure and clinical disease. Countries which continue to use asbestos products in the workplace should note the tragic legacy of this material within contemporary Australia.     

Silicosis and coal workers' pneumoconiosis

Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; d) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.     

Changing patterns of pneumoconiosis mortality--United States, 1968-2000

Pneumoconioses are caused by the inhalation and deposition of mineral dusts in the lungs, resulting in pulmonary fibrosis and other parenchymal changes. Many persons with early pneumoconiosis are asymptomatic, but advanced disease often is accompanied by disability and premature death. Known pneumoconioses include coal workers' pneumoconiosis (CWP), silicosis, asbestosis, mixed dust pneumoconiosis, graphitosis, and talcosis. No effective treatment for these diseases is available. This report describes the temporal patterns of pneumoconiosis mortality during 1968-2000, which indicates an overall decrease in pneumoconiosis mortality. However, asbestosis increased steadily and is now the most frequently recorded pneumoconiosis on death certificates. Increased awareness of this trend is needed among health-care providers, employers, workers, and public health agencies.