景德镇瓷厂工人死因分析

目的 探索危害陶瓷工人健康的主要疾患及职业有害因素对工人寿命的影响.方法 采用流行病学队列研究方法,对景德镇3个瓷厂1972年到1974年在册且工作一年以上所有陶瓷工人建立队列,随访至2003年底.队列中对死者均查询死因,陶工尘肺由当地疾病控制中心诊断小组确诊,肺癌均收集医院诊断病例.以全国城市居民年龄别死亡率为参照计算标化死亡比(SMR).结果 队列成员共4957名,随访至2003年底,共计130 783.6人年,死亡1636人,死亡率为1250.9/10万,累计死亡率为33.1%.影响陶瓷工人寿命的主要疾病按累计死亡率从高到低排序分别是:恶性肿瘤、心血管疾病、呼吸系统疾病、传染性疾病.与全国平均水平比较,陶瓷工人全死因死亡率基本持平,标化死亡比为1.01,死亡率明显升高的疾病有呼吸系统疾病(SMR=1.30)、陶工尘肺(SMR=36.35)、传染性疾病(SMR=5.08)和肺结核(SMR=4.06).陶瓷粉尘对工人寿命的影响十分明显,接尘工人多种疾病的死亡率均高于非接尘组,除陶工尘肺外,接尘组肺癌(RR=1.9,95%CI:1.2～3.1)、呼吸系统疾病(RR=2.4,95%CI:1.8～3.2)、肺结核(RR=1.6,95%CI:1.2～2.1)明显高于非接尘组,差异有统计学意义.研究还发现全死因、肠癌、肺癌、呼吸系统疾病、肺结核危险度均随接尘严重程度而明显增加,呈现接触一反应关系.结论 陶瓷行业主要职业危害为粉尘,卫生工作重点应是控尘和预防肺结核.     

某矿区接尘工人30年恶性肿瘤发病情况调查

目的调查某矿区接尘工人３０年恶性肿瘤的发病情况。方法采用回顾性队列研究，对该矿区１６７１１名接尘工人和７５９８名非接尘工人恶性肿瘤的发病情况进行调查。结果接尘组中肺癌居首，对非接尘组的标化发病比为２．６４８；接尘工人比非接尘工人恶性肿瘤发病率明显增高；４０岁以上接尘工人中，高接尘工龄段肺癌发病率显著高于低接尘工龄段；湿式作业工人肺癌发病率显著低于干式作业工人。结论接尘工人的恶性肿瘤（特别是肺癌）高发，粉尘可能是致病的重要危险因素之一。     

铁矿工人队列死因研究

目的 探索危害铁矿作业工人健康的主要疾患及职业有害因素对工人寿命的影响.方法 用流行病学队列研究方法,对武钢大冶铁矿7 469名职工从1972年开始随访30余年,以全国城市居民年龄别死亡率为参照,用标化死亡比（SMR）作为统计指标,并计算95%可信区间.结果 自1972年至2003年底,共计199 108.0人年,死亡1 752人,累积死亡率为23.5%.影响铁矿工人寿命的主要疾病按累积死亡率从高到低排序分别是：肿瘤（7.8%）、脑血管疾病（3.9%）、心血管系疾病（3.4%）和呼吸系疾病（2.9%）,恶性肿瘤以肺癌和肝癌最多,分别占总死亡数的10%和7.4%.全死因SMR为1.06,高于全国平均水平.死亡率明显升高的疾病有鼻咽癌、肝癌、肺癌、尘肺和意外事故,SMR分别为1.84、1.51、1.83、14.94和1.25.队列中接尘工人与非接尘工人比较,接尘工人全死因、胃癌、肺癌、呼吸系统疾病、心血管疾病和意外事故的累积死亡率明显升高（相对危险度分别为1.35、1.83、1.61、2.27、1.34和1.69）.结论 以粉尘为主的职业有害因素明显影响铁矿工人健康和寿命.     

锡矿作业工人粉尘接触和队列死因分析

[目的]评价混合性粉尘接触对锡矿作业工人健康的影响及累积粉尘接触与主要引起工人死亡疾病的关系。[方法]建立广西4个锡矿1972~1974年在册且工作一年以上工人的研究队列,以全国城市居民年龄别死亡率为参照,标化死亡比(SMR)作为统计指标。[结果]队列共计7837人,至1994年底,共计165156.7人年,死亡1094人。影响锡矿工人健康的主要疾病按累积死亡率从高到低排序分别是:肿瘤(5.3%)、脑血管疾病(2.4%)、心血管系统疾病(1.9%)和呼吸系统疾病(1.7%),这4种疾病引起的死亡占总数的80.7%,恶性肿瘤以肺癌和肝癌最多,分别占总死亡数的12.6%和10.9%。全死因标化死亡比(SMR=0.94)接近全国平均水平,而鼻咽癌、肝癌、肺癌、白血病、尘肺和脑血管疾病的SMR较高,分别为3.41、1.97、2.49、2.31、33.89和1.15。队列中接尘工人4629名,研究发现矿尘接触导致死亡率上升,与粉尘接触存在明确剂量反应关系的疾病主要是尘肺、肺癌和肺结核。[结论]混合性粉尘明显影响工人健康,累积粉尘接触与肺癌死亡存在剂量-反应关系,可能与粉尘中高含量的砷和游离二氧化硅有关。     

金属矿尘接触与肺癌发病的危险度定量评价

本文对大厂矿长坡锡矿1960～1974年井下接尘的工人进行了一次回顾性定群研究。研究队列共1113人,贡献人年26780。观察期间死于肺癌45人,与全国、上海人口比较,SMR分别为2184和519。以累计接尘量作定量评价的结果表明,工人吸入的矿尘与肺癌发病呈明显的剂量—反应关系。用对数线性模型拟合接尘量与吸烟量对肺癌发病的作用,发现接尘量与吸烟量同时引入模型后拟合优度最佳。控制吸烟因素后,不同累计接尘量水平对肺癌发病的相对危险度逐次为4.18、5.20、13.01、16.07;控制接尘量后,不同吸烟量的相对危险度分别为1.74、4.19,接尘量与吸烟量及肺癌发病危险度都呈现剂量—反应关系,表明接尘和吸烟同时为肺癌发病的危险因子。     

肿瘤坏死因子的基因多态性与陶工尘肺和肺结核的关系

目的 探讨肿瘤坏死因子-α(TNF-α)基因多态性在陶工尘肺(以下简称:尘肺)和肺结核发病遗传易感性中的作用及其与累积接尘量(CTE)的交互作用.方法 研究对象选自景德镇市陶瓷工人,收集职业史和工厂历年粉尘监测资料,陶工尘肺和肺结核由当地疾病控制中心诊断小组确诊.采集每个研究对象的外周静脉血,提取DNA,应用实时定量PCR技术检测TNF-α基因-308位点多态性.结果 研究对象902人,其中接尘598人,诊断尘肺157人.研究表明TNF-α-308位点G/A A/A基因型携带者发生尘肺的危险性是G/G基因型的1.9倍,95%CI=0.7～5.1.分层分析发现,高累积接尘量[≥180 mg/(m3·a)]、男性、吸烟者G/A A/A基因型携带者发生尘肺的危险性分别是G/G基因型的1.8(0.8～4.4)、2.4(1.1～5.3)和2.4(1.0～5.6)倍.对吸烟指数进一步分层后发现当吸烟指数>20包/a时,G/A A/A基因型携带者发生尘肺的危险性是G/G基因型的3.4倍(95%CI=1.3～8.8).当3种因素同时存在时,G/A A/A基因型携带者发生尘肺的危险性是G/G基因型的8.8倍.TNF-α-308位点G/G基因型携带者发生肺结核的危险性是G/A A/A基因型的1.6倍,95ZCI:0.7～3.5.结论 TNF-α-308位点的基因多态性在尘肺的发病遗传易感性中不起主要作用.TNF-α-308位点的基因多态性在尘肺的发病过程中与累积接尘量、性别和吸烟之间存在交互作用,累积接尘量超过180 mg/(m3·a)、男性或大量吸烟时,G/A A/A基因型携带者发生尘肺的危险性较G/G基因型显著增加.     

接触粉尘的石英剂量——反应与其危害程度分级研究

本文是根据回顾性调查资料分析，尘肺发病严重程度与生产性粉尘浓度大小及其尘中游离ＳｉＯ＿２含量高低和反映劳动强度与其接尘时间的肺总通气量多少，后三者之积的石英剂量－矽肺发病关系密切。从而拟订以工人接尘２０～３０年，控制尘肺患病率的危害程度分级方案（称方案）为基准，其应用是以现时的石英剂量归纳其方案某档次中，预测预报粉尘危害程度。方法简捷，科学性强，为修改标准（ＧＢ５８１７－８６）提出依据。     

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.     

硅藻土粉尘对接尘工人的危害

利用现场劳动卫生学、职业流行病学方法及接尘工人健康检查, 对硅藻土粉尘对接尘工人的健康危害进行了调查, 发现其可对接尘工人身体产生危害, 甚至发生尘肺。     

瓷厂和钨矿生产性粉尘生物学效应的研究

目的 通过体外细胞实验测定瓷厂和钨矿作业点生产性粉尘的毒性等生物学效应,为评价粉尘的危害作用提供依据.方法 以豚鼠的肺泡巨噬细胞(AM)为作用细胞,以标准石英作为对照,应用肺泡灌洗的方法获得AM后,加入15、30、60、120μg/106个细胞浓度标准石英、瓷厂及钨矿作业点的呼吸性粉尘颗粒培养,测定细胞的乳酸脱氢酶(LDH)活力、细胞活力(MTT)、活性氧释放量和肿瘤坏死因子-α(TNF-α)的释放量.结果 瓷厂和钨矿的生产性粉尘均能诱导豚鼠AM培养液中LDH活力升高,诱导豚鼠AM释放活性氧和TNF-α量升高,并随粉尘浓度升高呈现明显的剂量一反应关系.瓷厂和钨矿粉尘与豚鼠AM共培养后导致AM活力下降,随着生产性粉尘的浓度增加而降低.钨矿粉尘引起LDH活力升高以及诱导豚鼠AM释放TNF-α能力强于瓷厂粉尘,在120μg/106个细胞浓度组,赣州钨矿粉尘诱导的TNF-α水平为(5.2±2.0)ng/ml,景德镇瓷厂粉尘诱导的TNF-α水平为(3.3±1.6)ng/ml,均高于标准石英(2.8±0.5)ng/ml.与钨矿尘肺患病和死亡率均高于瓷厂相印证.结论 不同来源的生产性粉尘具有不同的生物学效应结果,实验测定粉尘的生物学效应为区分生产性粉尘危害作用提供了基础数据.     

煤矿矿工尘肺与肺癌死亡Poisson回归分析

目的 探讨尘肺与肺癌的关系。方法 对涟邵矿务局3140例尘肺矿工进行回顾性队列分析,计算主要死因的标化死亡比（SMR）,对尘肺与肺癌的关系进行Poisson回归分析。结果 尘肺矿工全死因与肺癌均高于对照人数,其中肺癌高于湖南省人群5倍;Poisson回归分析表明尘肺矿工肺癌与对照组的差别主要在25－44岁组。结论 支持尘肺与肺癌的相关关系。     

Exposures to silica mixed dust and cohort mortality study in tin mines: exposure-response analysis and risk assessment of lung cancer

BACKGROUND: Mineral dusts that contain crystalline silica have been associated directly or indirectly with the development of pneumoconiosis or silicosis, non-malignant respiratory diseases, lung cancer, and other diseases. The health impacts on workers with silica mixed dust exposure in tin mines and dose-response relationships between cumulative dust exposure and the mortality from lung cancer are investigated. METHODS: A cohort of 7,837 workers registered in the employment records in 4 Chinese tin mines between 1972 and 1974 was identified for this study and the mortality follow-up was traced through 1994. Of the cohort, the cause of death was ascertained for 1,061 (97%) of the 1,094 deceased workers. Standardized mortality ratios (SMRs) were calculated for all workers, non-exposed workers, and dust-exposed workers with different exposure levels, silicotics, and non-silicotics based on Chinese national rates. RESULTS: The mortality from all causes in four tin mines was nearly the same as the national mortality. Malignant neoplasm, cerebrovascular disease, and cardiovascular disease accounted for 68.6% of all deaths. Mortality excess from lung cancer, liver cancer, all malignant diseases, and non-malignant respiratory diseases was observed among dust-exposed workers; a 50-fold excess of pneumoconiosis was observed. There was an upward trend for SMRs of lung cancer was noted from no exposure to low, medium, and high exposure levels (SMRs=1.29, 2.65, 2.66, 3.33). The shape of the exposure-response curve for risk of lung cancer at high exposure levels was inconsistent in these four mines. CONCLUSIONS: The findings indicated a positive dose-response relation between exposure to cumulative dust and the mortality of lung cancer. High arsenic content in dust particles, together with crystalline silica, may play an important role in causing increased mortality from lung cancer.     

Long-term mortality in miners with coal workers' pneumoconiosis in The Netherlands: a pilot study

In order to investigate whether the prolonged exposure to coal mine dust increases the cancer risk for coal miners, a pilot study in a selected cohort of 334 Dutch miners with coal workers' pneumoconiosis (CWP), followed from 1956 until 1983, was conducted. In total, 165 miners had died (49.4%); for 162 (98.2%) the cause of death was traced. In comparison to the general Dutch male population, total mortality in the cohort was statistically significantly increased (SMR: 153). This was in general due to the significantly higher than expected cancer mortality (SMR: 163), cancer of stomach and small intestine (SMR: 401) and nonmalignant respiratory disease (SMR: 426). The lung cancer mortality was within the expected range.     

Lung cancer mortality and airways obstruction among metal miners exposed to silica and low levels of radon daughters

Starting from a cross-sectional survey in 1973, the mortality of two cohorts of Sardinian metal miners was followed through December 31, 1988. In mine A, the quartz concentration in respirable dust ranged between 0.2% and 2.0% and the exposure to radon daughters averaged 0.13 working level (WL), with the highest estimated cumulative exposure around 80–120 WLM. In mine B, the silica content was much higher (6.5–29%), but exposure to radon daughters was significantly lower than in mine A. More than 98% of the overall work force in 1973 (1,741 miners) entered the cohort, providing 25,842.5 person-years. Smoking, occupational history, chest radiographs, and lung function tests were available for the cohort members at admission. Mortality for all causes was slightly lower than expected. A significant excess for nonmalignant chronic respiratory diseases was noticed in both mines. Twenty-four subjects died of lung cancer, 17 from mine A (SMR: 128; 95% confidence interval [CI]: 75–205) and 7 from mine B (SMR: 85; 95% CI: 34–175). The SMR for lung cancer was highest among the underground workers from mine A (SMR: 148; 95% CI: 74–265), with a significant upward trend by duration of employment in underground jobs. Mine B underground miners showed lung cancer SMRs close to 100 without a significant trend by duration of employment. Among underground miners with spirometric airways obstruction in 1973, those from mine A showed the highest risk (SMR: 316; 95% CI: 116–687). The relationship did not change after adjusting for age and smoking. Based on the present findings, crystalline silica per se does not appear to affect lung cancer mortality. A slight association between lung cancer mortality and exposure to radon daughters, though within relatively low levels, may be considered for underground miners from mine A. Impaired pulmonary function may be an independent predictor of lung cancer and an important risk factor enhancing the residence time of inhaled carcinogens, i.e., alpha particles or PAHs, by impairing their bronchial and alveolar clearance. © 1994 Wiley-Liss, Inc.     

吸烟在云锡矿工肺癌发病中的作用

本文以1975-1984年为时段,对云南锡业公司所属六个单位工人进行了吸烟情况的调查分析。结果表明,吸烟者的肺癌发病率是非吸烟者的3.65倍。吸烟者的SMR为29.41;非吸烟者为8.42。无论吸烟程度如何,其发病、死亡都是有井下史者高于无井下史者。吸烟与职业性因素的复合作用是:吸烟+井下>单纯井下>单纯吸烟>非吸烟无井下史者。     

Nested case-control study of lung cancer in four Chinese tin mines

Objectives: To evaluate the relation between occupational dust exposure and lung cancer in tin mines. This is an update of a previous study of miners with high exposure to dust at four tin mines in southern China.

Methods: A nested case-control study of 130 male lung cancer cases and 627 controls was initiated from a cohort study of 7855 subjects employed at least 1 year between 1972 and 1974 in four tin mines in China. Three of the tin mines were in Dachang and one was in Limu. Cumulative total exposure to dust and cumulative exposure to arsenic were calculated for each person based on industrial hygiene records. Measurements of arsenic, polycyclic aromatic hydrocarbons (PAHs), and radon in the work sites were also evaluated. Odds ratios (ORs), standard statistic analysis and logistic regression were used for analyses.

Results: Increased risk of lung cancer was related to cumulative exposure to dust, duration of exposure, cumulative exposure to arsenic, and tobacco smoking. The risk ratios for low, medium, and high cumulative exposure to dust were 2.1 (95% confidence interval (95% CI) 1.1 to 3.8), 1.7 (95% CI 0.9 to 3.1), and 2.8 (95% CI 1.6 to 5.0) respectively after adjustment for smoking. The risk for lung cancer among workers with short, medium, and long exposure to dust were 1.9 (95% CI 1.0 to 3.5), 2.3 (95% CI 1.3 to 4.1), and 2.3 (95% CI 1.2 to 4.2) respectively after adjusting for smoking. Several sets of risk factors for lung cancer were compared, and the best predictive model included tobacco smoking (OR=1.6, 95% CI 1.1 to 2.4) and cumulative exposure to arsenic (ORs for different groups from low to high exposure were 2.1 (95% CI 1.1 to 3.9); 2.1 (95% CI 1.1 to 3.9); 1.8 (95% CI 1.0 to 3.6); and 3.6 (95% CI 1.8 5 to 7.3)). No excess of lung cancer was found among silicotic subjects in the Limu tin mine although there was a high prevelance of silicosis. Exposures to radon were low in the four tin mines and no carcinogenic PAHs were detected.

Conclusions: These findings provide little support for the hypothesis that respirable crystalline silica induces lung cancer. Ore dust in work sites acts as a carrier, the exposure to arsenic and tobacco smoking play a more important part in carcinogenesis of lung cancer in tin miners. Silicosis seems not to be related to the increased risk of lung cancer.

     

痰液细胞图像分析法筛检锡矿接尘工人肺癌的方法学评价

目的 评价痰液细胞图像分析对锡矿接尘工人肺癌的筛检试验,分析影响锡矿肺癌高危人群发病的危险因素.方法 1998年用单纯随机抽样的方法选取广西某锡矿队列中45岁以上的男性接尘矿工345人为研究对象,采用全自动细胞图像分析法用经验指标(痰液)对研究对象进行肺癌筛检,其后追访该人群至2006年.以临床确诊为金标准,用筛检试验方法评价痰液细胞图像分析对锡矿接尘工人肺癌的筛检效能及最佳工作点.结果 追访期间,共确诊11例肺癌病例;除年龄和职业接触外,吸烟是锡矿高龄接尘工人肺癌发病的危险因素(P=0.0384),调整混杂因素后,高吸烟组的相对危险度为18.21(2.15～154.39).细胞图像分析法经验筛检指标的灵敏度、特异度和正确指数分别为27.3%、83.5%、10.8%;经拟合受试者工作特征(ROC)曲线,C2.5(DNA指数介于1.25～2.50之间所占百分比)以1.70%为最佳工作点,痰液细胞图像系统检测的灵敏度、特异度、一致率、阳性预测值、阴性预测值和正确指数分别为72.7%、62.3%、62.6%、6.0%、98.6%、35.0%.结论 吸烟是高龄接尘工人肺癌的危险因素;使用痰液细胞图像分析法,将指标C2.5的筛检值调整为1.70%,有助于早期发现锡矿高危人群中的可疑肺癌患者.     

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.