石灰石型砂预防矽肺效果评价

1970年戚墅堰机车车辆厂铸钢车间开始成功地以石灰石砂代替石英砂为型砂,当时简称70砂。十余年来,戚机厂及上钢三厂坚持及完善了这项技术,并成功地预防了矽肺的发病,具体情况调查报告如下:     

石灰石砂造型10年防止矽肺病效果

上海第三钢铁厂铸钢车间1958年正式成立,年产钢约7万吨,铸钢件约2万吨。起初生产环境的粉尘浓度很高,以清砂为例,1961年之前平均437.2mg/m~3,1962～1980年平均为53.8～169.6mg/m~3,远远超过了国家的允许标准,造成矽肺患病率达15.4％,清砂工高达77.5％,发病工龄平均仅5.2年。 该车间1972年学习了铁道部戚墅堰机车辆厂先进经验,采用石灰石砂(含游离SiO_2仅2％左右)代替石英砂(含游离SiO_296.4％)造型,1974年推广使用,现已10年余,石灰石砂     

上钢三厂两个不同铸造车间粉尘危害的比较

上钢三厂铸造车间于1949年成立,1958年分成铸钢、铸铁两个车间。铸钢造型从1972年起“70砂”(石灰石砂)代替石英砂。本文对不同粉尘所致尘肺的情况进行比较。     

眼外伤职业眼病杂志征订通知

矽肺是机械俦造业中职业危害较严重的一种疾病。虽然采用水瀑清砂、震动落砂、水力清砂、抛丸清砂新工艺和通风除尘设施等，但矽肺发病尚未得到有效的控制。为掌握矽肺发病的发展趋势，给预防矽肺提供资料，1986年对俦造分厂清理工段的矽肺发病情况进行调查，词查对象工龄3年以上，从事清砂、清理气割、开箱、回火等工种者计181人，鉴于矽肺发病的控制是以预防为主，为此调查中还就个人使用劳防用品、吸烟情况作了调查和分析。     

18家玻璃灯具厂尘肺患病调查

富阳市某镇,从１９９３年开始生产玻璃灯具,现有玻璃灯具生产企业１８家,从业人员１４００余人。为了解职工劳动条件,掌握矽肺发病情况,我们于１９９６年对某镇玻璃灯具业进行了劳动卫生学调查,现将结果报告如下。 基本情况 该镇现有玻璃灯具厂１８家,均属个体企业。首家企业创办于１９８３年,主要产品为各种型号的照明玻璃灯罩。其主要工艺流程为： 配料（石英砂、砷灰等）→烧制→吹制→磨砂→包装喷吵包装部份产品根据用户要求,磨砂后用石英砂抛制、打磨。 调查结果 １．工种与矽肺发病情况：１９９６年５月,富阳市卫生防疫站…     

某矿晚发型矽肺病例调查

[目的]了解某矿接尘工人晚发型矽肺的患病情况，为更好地做好健康监护工作提供科学依据。[方法]2000年12月对某矿现有矽肺病人进行回顾性调查。[结果]245名矽肺患者中，离尘后发病的107例，占43．67％。其中，现有Ⅰ期病人86例，Ⅱ期病人19例，Ⅲ期病人2例；接尘工龄平均19．78年(4．7～42年)，发病至脱尘时间平均8．27年(1～32．4年)；初次诊断矽肺时(发病)年龄平均50．79岁，其中45～59岁占81．31％；运搬、手锤、风钻、爆破、支柱等矿山坑内作业工种合计占88．77％，20世纪50～60年代开始接尘的占81．31％；肺结核合并率为13．08％。[结论]该矿接尘工人离尘后发生矽肺的较多，大都从事主要工种，接尘工人离尘后应定期安排健康检查。     

全国石灰石砂铸钢技术研讨会在常州举行

在最近结束的“全国石灰石砂铸钢技术研讨会”上,全国一百二十多位专家、教授和工程技术人员一致认为,要进一步把这项我国独创的、具有很好经济效益和社会效益的技术在全国更大范围内推广. 过去,世界各国一直沿用石英砂作为铸钢用型砂,采用这种砂,作业场地的矽尘严重,     

矽肺合并冷凝集素综合征引起雷诺氏现象1例

矽肺合并冷凝集素综合征引起雷诺氏现象１例胡一本，李全路，黄绣球陆某，男，６４岁，于１９９８年８月入院，系缝纫机厂造型浇铸工，工龄２９年，接触石英砂、陶土、红煤粉。粉尘浓度超标达２０～３０倍。同工种的期５０多名工人中已有２人患矽肺。患者于１９８６年５月...     

70砂模浇钢时急性中毒事故原因探讨─—附9例急性中毒报告

７０砂模浇钢时急性中毒事故原因探讨─—附９例急性中毒报告上海市职业病医院（２００００３）周泽深，唐春元上海市第三钢铁厂江淑梅石灰石砂（７０砂）因游离二氧化硅（ＳｉＯ２）含量明显低于石英砂，１９７２年开始，上海某钢铁厂用其代替石英砂作为造型材料。自用７...     

铸钢车间30年矽肺发病情况探析

本厂铸钢车间，从1963～1992年30年来，工龄满一年以上，有接触矽尘工人1277人,其中矽肺患者84例,患病率为6．58%。各工种间，患病率差异较大。清理与配料工种患病率最高，因此，在治理尘害时，仍应从清理、配料二个工种为重点。矽肺患者的发病工龄与发病年龄随着粉尘浓度得到控制，逐渐延长。可见，积极落实防尘措施，是可以控制或连缓矽肺发病的．但该车间另有观察对象97例,检出率7．66%，从历年累计资料看，在五年内有55．88％的观察对象确诊为矽肺I期。照此推测，今后10年内可能有部分观察对象被确诊为矽肺，故应进一步加强防尘工作。本车间有17例晚发矽肺病例。据分析，脱尘后15年内被诊断矽肺者占82．35%、故脱尘或退体后仍要定期给予胸部摄片检查,同时为安全可靠起见,追踪时间最好为15年以上。     

深圳某小型宝石加工厂矽肺的调查分析

目的 调查小型宝石加工厂矽肺的发病情况。方法对深圳某小型宝石加工厂接尘工人进行矽肺横断面调查。结果该厂工作场所矽尘短时间接触平均浓度（STEL）为3．9mg／m^3，游离SiO2含量平均为92．5％。矽肺检出率为11．54％（9／78），发病年龄（22．58±2．92）岁，接尘工龄为（3．53±1．37）年。患者X射线胸片表现以圆形小阴影“q”影为主。矽肺并发肺结核率11．11％。矽肺患者VC、FVC、FEVL0，、FEVL0／FVC和MVV值明显低于其他接尘工人（P〈0．01）。结论 小型宝石加工厂工人接触矽尘水平高，矽肺发病严重，须采取针对性措施，减少工人接触，减缓病程进展。     

4例石英喷砂工矽肺的调查分析

[目的]了解石英喷砂工矽肺的发病情况。[方法]采用职业健康体检。[结果]发现4例矽肺患者,均为男性,发病早,年龄24～42岁,接尘工龄4～12年,平均7年,4例均合并支气管炎,2例合并肺气肿,1例合并肺大泡。现场连续跟踪一个班岗位工人粉尘浓度为220.101mg/m3,游离二氧化硅含量92.1%,粉尘分散度5μm以下占91.3%。[结论]发病工龄短,进展快,一次发病人数多都是近年少见,提醒我们必须加强对相应企业的监督力度。     

2013年上海市奉贤区铸造企业作业场所空气中矽尘浓度检测结果

目的了解上海市奉贤区铸造企业在生产环境中所产生矽尘的职业危害和分布规律,为改善作业环境,保护作业人员健康,提供科学依据。方法对产生矽尘企业进行职业卫生学调查,按国家有关标准和规范对作业工人进行个体采样,并检测生产环境空气中的时间加权平均浓度（CTWA）。结果对63名作业工人进行个体采样,男性55人,女性8人;年龄最小为23岁,最大58岁,平均年龄40.4岁。矽尘浓度范围0.2~9.0 mg/m3,平均浓度为（2.27±1.95）mg/m3,中位数为1.60 mg/m3。矽尘浓度检测合格率为23.8%。各工种在空气中矽尘浓度检测合格率差异无统计学意义（χ2=6.226,P〉0.05）。不同接尘工龄矽尘浓度检测合格率差异有统计学意义（χ2=9.078,P〈0.05）。结论应重点加强对35~49岁组和接尘工龄1~9 a组职业卫生健康监护,进一步加强生产工艺改革和通风排毒防护措施、改善作业环境,有效控制矽肺职业病的发生。     

Change of exposure response over time and long-term risk of silicosis among a cohort of Chinese pottery workers

An analysis was conducted on a cohort of Chinese pottery workers to estimate the exposure-response relationship between respirable crystalline silica dust exposure and the incidence of radiographically diagnosed silicosis, and to estimate the long-term risk of developing silicosis until the age of 65. The cohort comprised 3,250 employees with a median follow-up duration of around 37 years. Incident cases of silicosis were identified via silicosis registries (Chinese X-ray stage I, similar to International Labor Organisation classification scheme profusion category 1/1). Individual exposure to respirable crystalline silica dust was estimated based on over 100,000 historical dust measurements. The association between dust exposure, incidence and long-time risk of silicosis was quantified by Poisson regression analysis adjusted for age and smoking. The risk of silicosis depended not only on the cumulative respirable crystalline silica dust exposures, but also on the time-dependent respirable crystalline silica dust exposure pattern (long-term average concentration, highest annual concentration ever experienced and time since first exposure). A long-term "excess" risk of silicosis of approximately 1.5/1,000 was estimated among workers with all annual respirable crystalline silica dust concentration estimates less than 0.1 mg/m(3), using the German measurement strategy. This study indicates the importance of proper consideration of exposure information in risk quantification in epidemiological studies.     

宝石加工工人矽肺的流行病学调查

目的　调查宝石加工作业环境的粉尘危害及宝石加工工人的矽肺发病特征。方法　对某宝石加工厂接尘作业工人进行矽肺横断面流行病学调查。结果　该厂生产环境粉尘浓度平均为2 .3mg/m3 ,游离SiO2 含量平均为 94 .6 4 %。该厂 10 2 7例接尘作业工人中 ,诊断各期矽肺 4 7例 ,患病率为 4 .5 8% ,发病年龄为 (2 7.0 4± 3.2 5 )岁 ,接尘工龄为 (4.6 7± 1.17)年。患者X线胸片表现以q影为主。患者肺结核并发率为 10 .6 4 % ;肺气肿并发为 4 4 .6 8% ;自发性气胸发生率为 10 .6 4 %。结论　宝石粉尘对工人健康危害极大。宝石加工工人矽肺发病率高 ,发病年龄小 ,接尘工龄短 ,并发症多 ,致病残程度较重 ,预后较差。     

某大型人造宝石厂矽肺患病情况调查分析

目的调查某大型人造宝石加工厂工人矽肺的发病特征。方法对某大型人造宝石加工厂接尘工人进行矽肺横断面流行病学调查。结果该厂作业场所52个矽尘浓度检测点中36个超过卫生标准,最高超标9倍,矽尘浓度平均为3.2mg/m3,游离SiO2含量为51.5%。该厂矽肺发病率为4.65%(79/1700),发病年龄21￣35岁,接尘工龄为3￣13年。作业场所无任何防尘措施,工人未配备个人防护用品。结论大批工人暴露于无任何防护的接尘作业,必然会导致尘肺病人的群体性暴发,必须进行技改,防止作业场所的粉尘浓度超过卫生标准。     

矽肺患者血清中SOD和GSH-Px水平观察

目的观察矽尘接触者和矽肺患者血清中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）水平,探讨SOD、GSH-Px在矽肺发生发展中的作用。方法采用酶联免疫吸附法和化学比色法对100名不接触粉尘的对照人群,200名接触矽尘1 a以上的接尘工人,32名矽尘作业观察对象及130例矽肺患者,检测其血清SOD、GSH-Px水平。结果接尘组和矽肺组SOD水平明显低于正常对照组,矽肺组SOD水平与对照组比较,差异有统计学意义（P〈0.05）;GSH-Px水平矽肺组明显高于正常对照组和接尘组,差异有统计学意义（P〈0.01）,且矽肺期别愈高GSH-Px亦随之升高。结论血清中SOD、GSH-Px水平与矽肺发病有明显相关关系,并与矽肺的严重程度也有关,提示机体氧化和抗氧化系统的失衡与矽肺的发生发展有关。     

An old threat in a new setting: High prevalence of silicosis among jewelry workers

BACKGROUND: Silicosis is caused by inhaling free crystalline silica. Few case reports have addressed the risk of silicosis in the jewelry trade where chalk molds containing a high percentage of silica are used in casting. We conducted a cross-sectional study involving 100 goldsmiths exposed to silica. METHODS: All workers replied to a questionnaire and underwent a clinical examination, pulmonary function tests, a chest X-ray and a high-resolution CT scan. RESULTS: High-resolution CT visualized signs of silicosis in 23 cases, confirmed by standard chest X-rays in 10. In the 23 workers with CT evidence of silicosis Total Lung Capacity, FEV1 and the Lung Diffusing Capacity did not differ from the workers without the disease. Pulmonary function tests did not correlate with silica exposure. CONCLUSION: In this study we demonstrate that use of chalk molds in casting in jewelry causes silicosis. The composition of the dust could be responsible of the high prevalence observed.     

Silicosis in the 1980's

At the request of the Mine Safety and Health Administration (MSHA), the National Institute for Occupational Safety and Health (NIOSH) recently investigated the health of workers at two silica flour mills. Both mills have a long history of failure to maintain workplace concentrations of dust containing free silica below the MSHA exposure standard. Thirty-seven percent of sixty-one workers and ex-workers with one or more years of silica dust exposure had chest radiographic evidence of silicosis. Because of the high prevalence of silicosis in workers at these two silica flour producers, MSHA silica dust measurements were reviewed for twenty-five other active U.S. silica flour producers. Eighty-nine percent of the work force in these 27 silica flour producers are employed at workplaces where more than twenty-five percent of the dust samples reviewed were above the exposure standard. Fifty-three percent of all samples were above the MSHA standard. No significant decline in silica dust levels occurred during the period (1974-1979) covered by the data supplied by MSHA. Based on the NIOSH study and MSHA data, it is apparent that the risk of silicosis is very high among workers in this industry. Prevention of this disease will require a concerted effort of government enforcement agencies, workers and management.     

Risk of pulmonary tuberculosis relative to silicosis and exposure to silica dust in South African gold miners [published erratum appears in Occup Environ Med 1999 Mar;56(3):215-6]

OBJECTIVES: To investigate the following questions. (1) Is silica dust on its own, without the presence of silicosis, associated with an increased risk of pulmonary tuberculosis (PTB) in workers exposed to silica dust? (2) In the absence of silicosis is the excess risk dose related? (3) What is the predominant chronological sequence between the development of PTB and the development of silicosis after the end of exposure to dust? METHODS: A cohort of 2255 white South African gold miners has been followed up from 1968 to 1971, when they were 45-55 years of age, to 31 December 1995 for the incidence of PTB. During the follow up 1592 (71%) men died. Of these, 1296 (81%) had a necropsy done at the National Centre for Occupational Health (NCOH) to determine the presence of silicosis and PTB. The incidence of PTB in the cohort was studied relative to cumulative exposure to dust and the onset of silicosis. For the miners with necropsy, the incidence for PTB was studied relative to the severity of silicosis found at necropsy. RESULTS: There were 115 subjects who developed PTB. The total person- years of follow up was 39,319. For the whole cohort, the factors associated with increased risk of PTB were cumulative exposure to dust (mg/m3.y) (the adjusted rate ratio (RR) 1.07; (95% confidence interval (95% CI) 1.04 to 1.10)), silicosis diagnosed radiologically (3.96 (2.59 to 6.06)), and tobacco pack-years (1.02 (1.01 to 1.03)). The RR (95% CI) for PTB increased with increasing quartiles of cumulative exposure to dust 1.0, 1.51 (0.78 to 2.91), 2.35 (1.28 to 4.32), and 3.22 (1.75 to 5.90). In miners who did not have radiologically diagnosed silicosis (n = 1934, PTB = 74), the adjusted RR (95% CI) for PTB and cumulative exposure to dust was 1.10 (1.06 to 1.13), and increased with quartiles of cumulative exposure to dust as 1.00, 1.46 (0.70 to 3.03), 2.67 (1.37 to 5.23), and 4.01 (2.04 to 7.88). For the subjects who had a necropsy (n = 1296, PTB = 70), the adjusted RR (95% CI) for PTB increased with the severity of silicosis found at necropsy; 1.0 for no silicosis, 1.88 (0.97 to 3.64) for negligible, 2.69 (1.35 to 5.37) for slight, and 2.30 (1.16 to 4.58) for moderate or marked silicosis. For subjects who had a necropsy and no silicosis (n = 577, PTB = 18), the adjusted RR (95% CI) increased slightly with quartiles of cumulative dust 1.0, 1.11 (0.31 to 4.00), 1.42 (0.43 to 4.72), and 1.38 (0.33 to 5.62). CONCLUSION: Exposure to silica dust is a risk factor for the development of PTB in the absence of silicosis, even after exposure to silica dust ends. The risk of PTB increases with the presence of silicosis, and in miners without radiological silicosis, with quartiles of exposure to dust. The severity of silicosis diagnosed at necropsy was associated with increasing risk of PTB and even < 5 nodules--that is, undetectable radiologically--was associated with an increased risk of PTB. The diagnosis of PTB was on average 7.6 years after the end of exposure to dust, at around 60 years of age. The onset of radiological silicosis preceded the diagnosis of PTB in 90.2% of the cases with PTB who had silicosis. The results have implications for medical surveillance of workers exposed to silica dust after the end of exposure.