3例除锈工铁尘肺病理分析

本文报告3例船体除锈工铁尘肺尸检材料。病理诊断均为Ⅰ期尘斑型生肺,病理表现与电焊工尘肺类似,呼吸性细支气管壁及其肺泡群、血管、支气管周围组织粉尘沉着及粉尘纤维灶,无尘性融合病灶,肺间质尘性改变较电焊工尘肺为轻。肺元素分析表明肺内铁、锰含量明显高于非尘肺组,但肺锰含量又低于电焊工尘肺组。肺游离SiO_2含量比矽肺和矽酸盐肺低10倍。肺灰化片偏光镜检查未见矽粒。作者认为肺内铁尘长期沉积可引起尘肺改变,在病变上逊于电焊工尘肺的严重程度,此可能与粉尘中锰的含量较低有关。     

某锑矿井下锤工尸检1例分析报告

死者安某，男３５岁，某锑矿井下锤工，接尘工龄１２年，生前诊断为“Ⅱ期矽肺合并肺结核”，死于右心衰竭，经尸检作病理检查和锑及游离二氧化硅含量分析，发现尸检结果与生前诊断相符，各主要器官及矽结节，肺门淋巴结中含有锑，矽结节和肺门淋巴结合有游离二氧化硅。     

煤工尘肺肺动脉病变的定量分析

[目的]研究煤工尘肺(CWP)肺细小动脉病变与肺心病的关系.[方法]取48例矿工尸检肺组织和12例非矿工手术标本进行了病理观察.对外径＜200μm的细小动脉在光镜观察的基础上用德国Kontron公司IBAS/Ⅱ图象分析仪进行测试.[结果]尘肺组细小动脉壁增厚与对照组相比EA/TA、WA/TA、WD/TD三项比值,Ⅰ期尘肺差异有显著性(P＜0.05),ⅡⅢ期差异有非常显著性(P＜0.01),ⅡⅢ期与Ⅰ期相比60～200μm小动脉差异有显著性(P＜0.05)说明CWP肺血管病变范围随尘肺病变加重而加重,CWP肺细小动脉壁尘细胞沉积及尘性纤维化是造成肺血管硬化使其顺应性降低的主要原因之一.与年龄因素相比,尘肺细小的动脉病变与粉尘破坏作用有更大关系.吸烟也不足以掩盖粉尘对血管这的损伤作用.[结论]尘性气管炎和尘斑气肿是导致煤工尘肺肺动脉高压的主要原发疾病.     

四川省自贡市极薄煤层煤矿煤工尘肺流行病学及影像学特点

目的探讨四川省自贡市极薄煤层煤矿煤工尘肺流行病学及影像学特点,为极薄煤层煤矿煤工尘肺防治提供基础性依据。方法对自贡市2004-2011年诊断资料完整的672例煤工尘肺采取回顾性调查研究;采用分层抽样,对15家煤矿企业的总粉尘浓度和游离二氧化硅含量进行现场检测;并用Spss20.0进行统计分析。结果 672例煤工尘肺来源于荣县和富顺县。发病工种主要为采煤工,占总数的69.05%。Ⅰ、Ⅱ、Ⅲ期煤工尘肺平均发病工龄分别为16.43年、16.98年和18.37年。606例煤工尘肺胸片影像表现以圆形小阴影为主,其中q影431例,占总数的71.12%。15家企业106个岗位的8 h时间加权平均浓度均超过国家职业卫生限值,88.89%的粉尘的游离二氧化硅含量大于10%。结论自贡市煤工尘肺的防治重点为荣县和富顺县的采煤工,其胸片影像以小阴影q影为主。     

五种职业性尘肺肺组织内尘量测定及尘粒的电镜能谱分析

本研究是取病理诊断为Ⅱ期的五种尘肺即矽肺、石棉肺、电焊工尘肺、水泥尘肺、煤工尘肺各2例的尸检肺组织用化学法测定其肺内总含尘量及二氧化硅,硅酸盐及碳尘含量,另取上述肺组织经脱水、环氧树酯包埋制成超薄切片,电镜观察,能谱分析(EDXA),兹报告于后。方法五种尘肺患者的接尘史在11-24年,操作环境的粉尘浓度在4.65-77.43mg/m~3。各例肺组织均取右肺中叶、各为2gm,用分析纯浓硝酸予以消化,     

几种煤矿岩尘与大鼠肺胶原蛋白含量关系的分析

煤矿尘肺是我国目前煤矿重要职业病之一,粉尘中游离二氧化硅含量是尘肺发病的一个重要的因素,粉尘中游离二氧化硅的含量与尘肺纤维化的严重程度成正比,而肺胶原蛋白含量的多少与肺纤维化程度有密切的关系。到目前为止,有关煤矿岩尘与大鼠肺胶原蛋白含量的关系分析资料报道甚少。为此,我们对几个有代表性的煤矿岩尘进行了动物实验研究,旨在分析煤矿岩尘中游离二氧化硅含量与大鼠肺胶原蛋白含量的相关性。为探讨煤矿尘肺发病的影响因素提供依据。     

19例煤工尘肺合并结核的病理观察

肺结核是煤工尘肺较常见而严重的合并症,尤其在晚期煤工尘肺中合并结核是引起煤矿工人死亡的重要原因之一。对象与方法在1980～1989年搜集的122例煤工尸检肺中,被确诊为煤工尘肺合并结核的有19例,占尸解总数的15.57%。其中掘进工6例,采煤工1例,混合工11例,煤矿地面石工1例。粉尘作业工龄4～40年,平均21.1年。本组19例煤工尘肺合并结核生前尘肺诊断:Ⅲ期1例,Ⅰ期2例,0~ 及0期各为8例。     

五例电焊工尘肺病理分析

本文报告了五例船厂电焊工尘肺尸检材料,其中三例为尘斑型,二例结节型。病理特点为呼吸性细支气管壁及其肺泡群、血管及支气管周旁组织出现粉尘和粉尘纤维灶及结节,同时还有肺间质的尘性纤维化。肺组织元素分析证明肺内铁、锰含量明显高于其他尘肺或非尘肺组肺内含量的200～50倍,而游离SiO_2含量低10倍,肺显微灰化片偏光镜检也未见矽粒.作者认为肺内铁、锰的存在可能是引起肺纤维化的因素,游离SiO_2在发病中不起直接作用。     

自贡市极薄煤层煤矿煤工尘肺X射线影像分析

目的了解极簿煤层煤矿工作场所职业卫生状况并探讨其与煤工尘肺X射线影像特征的关系。方法对15家煤矿井下、地面作业岗位开展职业病危害因素检测,对确诊的672例煤工尘肺病例的X射线胸片进行影像表现的统计分析。结果采煤、掘进、地面卸煤(岩石)岗位游离二氧化硅含量最低5.9%,最高58.4%,平均含量大于10%。极薄煤层煤矿工人工作场所接触的粉尘应为煤矽混合尘,工作场所粉尘浓度最低1.05 mg/m3,最高16.04 mg/m3。所测定的104份煤矿井下、地面工作场所粉尘样品浓度平均值均超过了国家职业卫生标准的限值。672份煤工尘肺X射线胸片表现形态为圆形小阴影的病例占90.18%。以圆形小阴影为主的X线胸片中q型占71.12%,p型25.41%r,型3.47%。Ш期煤工尘肺均表现为大阴影。Ⅰ期煤工尘肺小阴影主要分布于中下肺区的占67.33%;Ⅱ期煤工尘肺小阴影主要分布于上中下肺区的95.80%。Ш期煤工尘肺大阴影主要分布于上肺区和上中肺区。结论自贡市煤矿工人接触的粉尘为煤矽混合尘,煤工尘肺病患者X线影像形态大小以q型为主。     

氧化铁尘肺肺组织元素含量及病理分析

氧化铁尘肺肺组织元素含量及病理分析郑超，张磊，钱智勇，戴岩，常莹华，吴国新，李林随着钢铁工业的发展，接触氧化铁尘的工人不断增加。氧化铁是否导致尘肺发生，各家看法不同，有关铁尘肺尸检肺组织元素分析报道甚少。为此，本文对有代表性的９例废钢铁汽割工、冶炼工...     

Association between lymph node silicosis and lung silicosis in 4,384 German uranium miners with lung cancer

This study investigates the association between lymph node-only and lung silicosis in uranium miners with lung cancer and exposure to quartz dust. Tissue slides of 4,384 German uranium miners with lung cancer were retrieved from an autopsy archive and reviewed by 3 pathologists regarding silicosis in the lungs and lymph nodes. Cumulative exposure to quartz dust was assessed with a quantitative job-exposure matrix. The occurrence of silicosis by site was investigated with regression models for exposure to quartz dust. Miners with lung silicosis had highest cumulative quartz exposure, followed by lymph node-only silicosis and no silicosis. At a cumulative quartz exposure of 40 mg/m(3) × years, the probability of lung silicosis was above 90% and the likelihood of lymph node-only silicosis and no silicosis do not differ anymore. The results support that lymph node silicosis can precede lung silicosis, at least in a proportion of subjects developing silicosis, and that lung silicosis strongly depends on the cumulative quartz dose.     

Silicosis screening in surface coal miners--Pennsylvania, 1996-1997

Silicosis is an occupational respiratory disease caused by inhaling respirable crystalline silica dust. Silicosis is irreversible, often progressive (even after exposure has ceased), and potentially fatal. Exposure to silica dust occurs in many occupations, including mining (1). During 1996-1997, surface coal miners at eight sites in Pennsylvania were screened to estimate the prevalence of silicosis, to identify risk factors for silicosis, and to refer miners with a possible diagnosis of silicosis or other conditions for medical evaluation and treatment. This report summarizes the results of the screening, which indicated that an increased prevalence of and risk for silicosis is associated with miners' age and years of drilling experience, and provides recommendations for preventing silicosis among miners.     

Risk of silicosis in cohorts of Chinese tin and tungsten miners, and pottery workers (I): an epidemiological study

BACKGROUND: Epidemiological evaluations of the risk of silicosis in relation to exposure to crystalline silica have raised the question of whether different types of silica dust exposures vary with respect to their ability to cause silicosis. The aim of this study is to compare the risk of silicosis among cohorts of silica dust-exposed Chinese tin miners, tungsten miners, and pottery workers and to assess whether gravimetric measurements of respirable silica dust sufficiently determine the risk of silicosis or whether other factors of exposure may play a significant role. METHODS: Cohorts were selected from 20 Chinese mines and potteries. Inclusion criteria were starting employment after January 1, 1950 and being employed for at least 1 year during 1960-1974 in one of the selected workplaces. Radiological follow-up for silicosis onset was from January 1, 1950 through December 31, 1994. Silicosis was assessed according to the Chinese radiological criteria for diagnosis of pneumoconiosis (as suspect, Stage I, II, or III). Exposure-response relationships were estimated for silicosis of Stage I or higher. Silica dust exposure was estimated in terms of cumulative total dust exposure, calculated from a workplace, job title, and calendar year exposure matrix, and individual occupational histories. Cumulative total dust exposure was converted in two steps into cumulative respirable dust exposure and cumulative respirable silica dust exposure using conversion factors estimated from side-by-side measurements conducted in 1988-89. RESULTS: The male cohorts included 4,028 tin miners, 14,427 tungsten miners, and 4,547 pottery workers who had similar onset of employment and duration of follow-up. For a given exposure level, the risk of silicosis was higher for the tin and tungsten than the pottery workers. CONCLUSION: The observed differences in the risk of silicosis among the three cohorts suggest that silica dust characteristics, in addition to cumulative respirable silica dust exposure, may affect the risk of silicosis.     

Respiratory outcomes among South African coal miners at autopsy

BACKGROUND: Studies of dose-response relationships between respiratory outcomes at autopsy and coal dust exposure are limited. The Pathology Automation System (PATHAUT) database of South African miners, is one of the largest autopsy databases of occupational lung disease. This study described the prevalence of respiratory outcomes among South African coal miners at autopsy, and determined whether dose response relationships existed between emphysema and exposure. METHODS: Autopsies conducted from 1975 to 1997 on coal miners with exclusive coal mining exposure and having exposure duration information (n = 3,167) were analyzed from PATHAUT. Logistic regression was used to determine relationships between exposure and outcomes, controlling for race, smoking and age on a subset for whom smoking history was available (n = 725). RESULTS: The mean duration of exposure was 11.0 years. Most were black miners (75.3%) with significant differences in the mean ages of black and white miners (37.9 and 55.3 years, respectively). Only 22.9% of cases had information on smoking. The prevalence of silicosis, tuberculosis (TB), coal workers' pneumoconiosis (CWP), and moderate and marked emphysema were 10.7%, 5.2%, 7.3%, and 6.4%, respectively. All diseases, except TB, were associated with exposure duration. Black miners had 8.3 and 1.2 fold greater risks for TB and CWP, respectively, than white miners. White miners had an increased risk of 1.4 and 5.4 for silicosis and moderate to marked emphysema, respectively. In models unadjusted for age, and including smoking, moderate to marked emphysema was strongly associated with exposure duration (OR = 3.4; 95% CI = 1.9-5.9 for highest tercile of exposure duration). Exposure-related risk estimates were reduced when age was introduced into the model. However, age and duration of exposure were highly correlated, (r = 0.68) suggesting a dilution of the exposure effect by age. CONCLUSIONS: There were significant dose related associations of disease, including emphysema, with coal dust exposure.     

Case-control study of silicosis, silica exposure, and lung cancer in white South African gold miners

A case-control study was undertaken to assess the association between lung cancer and silicosis or silica dust exposure in white South African gold miners. Cases and controls were identified from deaths reported to the Gold Miners Provident Fund for the period January, 1979-October, 1983. Two controls were matched to each case by year of birth (+/- 2 years) and by smoking (+/- 5 cigarettes or equivalents per day) assessed 10 years (+/- 2 years) prior to death. One hundred thirty-three matched triplets were identified. The results showed no overall association between lung cancer and radiological silicosis (OR = 1.08, p = 0.92). Autopsy data indicated no overall associations between lung cancer and silicosis of the lung parenchyma (OR = 1.49, p = 0.11), the pleura (OR = 0.72, p = 0.30), or the hilar glands (OR = 0.85, p = 0.72). A trend toward increased severity of silicosis of the parenchyma was evident; however, this was not statistically significant (p = 0.08). Odds ratios for lung cancer and silicosis were higher at lower levels of cumulative silica dust exposure (ORs = 2.43, 1.72, 1.35 and 0.62 for lung cancer and autopsy silicosis of the parenchyma for the lowest, second, third, and highest quartiles of dust exposure, respectively; all p greater than 0.05). Cases did not differ from controls for total silica dust exposure, length of exposure, weighted average intensity of exposure, or number of shifts at high dust (all p greater than 0.20). The data do not support the hypothesis of a carcinogenic role for silica dust and no statistically significant associations were found between lung cancer and silicosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

肺癌病因研究中接尘量计算的真实性评价

为评价肺癌病例对照研究中接尘剂量估算方法的真实性,对广西锡矿病因研究对象进行了重新计算。广西锡矿队列发现男性肺癌死者１３０例,配对照６２７例。共７５７人。其中接法工人５７２名,发现各期矽肺共２４３例,根据在斩工业卫生监测资料估算所有接尘工人的累积总粉尘接触量,再计算不同接尘水平下矽肺的发病率。结果显示,随接尘水平上升,矽肺发病率升高,两者存在明显的接触剂量反应关系。完全符合矽肺发病特点。从而间接证     

Exposure to silica and silicosis among tin miners in China: exposure-response analyses and risk assessment

OBJECTIVES—To investigate the risk of silicosis among tin miners and to investigate the relation between silicosis and cumulative exposure to dust (Chinese total dust and respirable crystalline silica dust).
METHODS—A cohort study of 3010 miners exposed to silica dust and employed for at least 1 year during 1960-5 in any of four Chinese tin mines was conducted. Historical total dust data from China were used to create a job exposure matrix for facility, job title, and calendar year. The total dust exposure data from China were converted to estimates of exposure to respirable crystalline silica for comparison with findings from other epidemiological studies of silicosis. Each worker''s work history was abstracted from the complete employment records in mine files. Diagnoses of silicosis were based on 1986 Chinese pneumoconiosis Roentgen diagnostic criteria, which classified silicosis as stages I-III—similar to an International Labour Organisation (ILO) classification of 1/1 or greater.
RESULTS—There were 1015 (33.7%) miners identified with silicosis, who had a mean age of 48.3 years, with a mean of 21.3 years after first exposure (equivalent to 11.0 net years in a dusty job). Among those who had silicosis, 684 miners (67.4%) developed silicosis after exposure ended (a mean of 3.7 years after). The risk of silicosis was strongly related to cumulative exposure to silica dust and was well fitted by the Weibull distribution, with the risk of silicosis less than 0.1% when the Chinese measure of cumulative exposure to total dust (CTD) was under 10 mg/m³-years (or 0.36 mg/m³-years of respirable crystalline silica), increasing to 68.7% when CTD exposure was 150 mg/m³-years (or 5.4 mg/m³-years of respirable crystalline silica). Latency period was not correlated to the risk of silicosis or cumulative dose of exposure. This study predicts about a 36% cumulative risk of silicosis for a 45 year lifetime exposure to these tin mine dusts at the CTD exposure standard of 2 mg/m³, and a 55% risk at 45 years exposure to the current United States Occupational Safety and Health Administration and Mine Safety and Health Administration standards of 0.1 mg/m³ 100% respirable crystalline silica dust.
CONCLUSIONS—A clear exposure-response relation was detected for silicosis in Chinese tin miners. The study results were similar to most, but not all, findings from other large scale exposure-response studies.


     

Silica exposure and silicosis among Ontario hardrock miners: III. Analysis and risk estimates

An epidemiological investigation was undertaken to determine the relationship between silicosis in hardrock miners in Ontario and cumulative exposure to silica (free crystalline silica--alpha quartz) dust. This report describes the analytic method and presents the risk estimates.     

Emphysema and airway obstruction in non-smoking South African gold miners with long exposure to silica dust.

OBJECTIVE--Occupational exposure to silica dust is associated with significant impairment of lung function. The present study investigates which pathological changes in the lung are associated with impairment of lung function in silica dust exposed workers who were life-long non-smokers. METHODS--242 South African white gold miners who were lifelong non-smokers and who had a necropsy at death were studied. The pathological features identified at necropsy were the degree and type of emphysema, the presence of airway disease, and the degree of silicosis in the lung parenchyma and pleura. These features were related to lung function tests done a few years before death, to type of impairment (obstructive or restrictive), and to cumulative silica dust exposure. RESULTS--The degree of emphysema found at necropsy was not associated with a statistically significant impairment of lung function or with dust exposure. The degree of silicosis in the lung parenchyma and the large airways disease (based on mucus gland hyperplasia) were associated with a statistically significant impairment of lung function. The large airway disease was, however, not positively associated with dust exposure or silicosis. In miners with a moderate or a higher degree of limitation of airflow the main findings were silicosis, heart disease, and obesity. The presence of small airways disease could not be established from the necropsy material. CONCLUSION--The results indicate that the level of exposure to silica dust to which these miners were exposed, without a confounding effect of tobacco smoking, is not associated with a degree of emphysema that would cause a statistically significant impairment of lung function. Silicosis of the lung parenchyma was associated with loss of lung function. Other factors that may play a part in impairment of lung function in these miners are obesity and heart disease.