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Analysis of ferruginous bodies in bronchoalveolar lavage from foundry workers. 铸造工人支气管肺泡灌洗液中含铁体的分析。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1032
R F Dodson, M O'Sullivan, C J Corn, J G Garcia, J M Stocks, D E Griffith

Classical ferruginous bodies in tissue samples are considered to be markers of past exposure to asbestos. Recent studies have shown that the presence of ferruginous bodies in bronchoalveolar lavage (BAL) fluid correlates with past exposure to asbestos and offers a more sensitive reference than occupational history. Lavage samples from five subjects who had worked in foundries were evaluated by light microscopy for the presence of ferruginous bodies and by transmission electron microscopy for both characterisation of the uncoated fibre burden and analysis of the cores of the ferruginous bodies. All samples at lower magnification (light microscopy (200 x)) contained ferruginous bodies that were externally consistent with asbestos bodies. At higher magnification (400 x), a separate population from this group could be identified by the presence of a thin black ribbon. Transmission electron microscopy of the core materials of ferruginous bodies and comparable uncoated particulates supported the reliability of higher magnification light microscopy for distinguishing most of those non-asbestos cores; however, a population of transparent non-asbestos cored ferruginous bodies were also shown to exist.

组织样本中的典型含铁体被认为是过去接触石棉的标志。最近的研究表明,支气管肺泡灌洗液(BAL)中含铁小体的存在与既往石棉暴露有关,并提供比职业史更敏感的参考。在铸造厂工作的五名受试者的冲洗样品通过光学显微镜评估含铁体的存在,并通过透射电子显微镜评估未涂层纤维负荷的特征和分析含铁体的核心。在较低倍率(光学显微镜(200倍))下,所有样品都含有铁质体,其外部与石棉体一致。在更高的放大倍数(400倍)下,可以通过一条细黑带的存在来识别从这个群体中分离出来的一个单独的种群。对含铁体和类似的未包覆颗粒的核心材料进行透射电子显微镜观察,证明了高倍光学显微镜在区分大多数非石棉核心材料时的可靠性;然而,一群透明的非石棉包芯含铁体也被证明存在。
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引用次数: 17
Study of occupational lung cancer in asbestos factories in China. 中国石棉工厂职业性肺癌的研究。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1039
H Zhu, Z Wang

A retrospective cohort study (1972-81) of occupational cancers in asbestos (chrysotile) factories has been previously published. In this paper the results of continued tracing and interviewing of members of this cohort from 1982 to 1986 is reported. The cohort included 5893 persons (45,974 person-years for men and 39,445 person-years for women). Malignant tumours played a large part in causes of death (36.9%). There were 183 cancers and 67 lung cancers among 496 deaths. The mortality due to lung cancer had a tendency to increase. By comparison with a control group, the RR of lung cancer was 5.32 (p < 0.01), and the SRR of lung cancer was 4.2 (p < 0.01), significantly higher than those of a control group. Among 148 cases of death from asbestosis there were 33 cases complicated with lung cancer (22.3%). The dose-response relations between exposure to asbestos and incidence of asbestosis and lung cancer were also studied in one asbestos factory. There was a positive correlation. A synergistic effect was found between cigarette smoking and lung cancer. Preventive and control measures and exposure limits for asbestos dust in the air of workplaces were recommended.

一项关于石棉(温石棉)工厂职业性癌症的回顾性队列研究(1972-81)此前已发表。本文报告了1982年至1986年对该队列成员的持续追踪和访谈结果。该队列包括5893人(男性45,974人/年,女性39,445人/年)。恶性肿瘤在死亡原因中占很大比例(36.9%)。在496例死亡中,有183例癌症和67例肺癌。肺癌死亡率有上升趋势。与对照组比较,肺癌的RR为5.32 (p < 0.01),肺癌的SRR为4.2 (p < 0.01),均显著高于对照组。148例石棉肺死亡中有33例合并肺癌(22.3%)。还在一家石棉工厂研究了石棉暴露与石棉沉滞和肺癌发病率之间的剂量-反应关系。有正相关。在吸烟和肺癌之间发现了协同效应。建议了工作场所空气中石棉粉尘的预防和控制措施和接触限值。
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引用次数: 17
Pulmonary effects of exposure to fine fibreglass: irregular opacities and small airways obstruction. 接触细玻璃纤维对肺部的影响:不规则混浊和小气道阻塞。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1054
W Weiss
Sir,-Kilburn et al (1992;49: 714-20) published a cross sectional prevalence study of workers exposed to fibreglass in an appliance manufacturing plant by means of chest x ray films and spirometry. They concluded that fibreglass used for insulating purposes seems to produce human disease similar to asbestosis. Because of the well known interobserver error in the reading of chest films, it is essential as a matter of good science that the investigation includes "blind" concurrent readings of films from unexposed controls similar to the exposed group in all respects except for the exposure being studied. Kilburn et al neglected to include such a procedure. The use of the standard films for pneumoconiosis is no substitute for proper controls as it tells us nothing about under or over-reading by the investigators. The reading of control films intermixed with films of the exposed group without knowledge by the readers as to which group each film belongs to might have shown no differences if there was matching by at least age, sex, and smoking habits. Smoking habits should include type of tobacco use and degree as well as duration of smoking. Kilburn et al did not include any adjustment for degree of cigarette smoking in their adjustment of their spirographic results and there is no evidence of adjustment for smoking habits with regard to the readings of the chest films in their study. Consequently, their conclusion is not warranted because their method was seriously flawed. In addition, I agree with the other points made by Rossiter. ' The reply by Kilburn et al contains a section labelled "No fibrosis from cigarette smoking alone" which is full of error. They claimed that I used minifilms (70 mm) in a 1972 paper and deny the existence of Rossiter's reference No 5 to my 1991 paper in the British J'ournal of Industial Medicine!2 My original studies of this subject were done with minifilms and were reported in the 1960s but subsequent studies were done with the use of large films, all without my knowledge of smoking habits, and these later reports entailed the use of the 1980 International Labour Office standard films and classification. These reports were confirmatory of the early findings. Kilburn et al are apparently unaware of my papers published in 19843 and 1988.4 These include extensive reviews of relevant publications. Perhaps they have simply ignored this body of work? It is interesting to note that Kilburn5 (Rossiter's reference No 6) in 1981 not only denied the validity of my earlier reports on the relation between cigarette smoking and radiological abnormalities suggestive of mild diffuse pulmonary fibrosis but also castigated my publications since 1971 on the increased frequency of asbestosis in smokers compared with non-smokers. Yet in 1986 he published a study,6 the only reference in his response to Rossiter' in which his own data confirmed this phenomenon. Neither in 1986 nor now has he referred to his 1981 error in denying
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引用次数: 6
Contact allergens in registered cleaning agents for industrial and household use. 工业和家庭使用的注册清洁剂中的接触过敏原。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1043
M A Flyvholm

Cleaning work is a common cause of both irritant and allergic contact dermatitis. Cleaning agents for industrial and household use are registered in the Danish Product Register Data Base (PROBAS) according to a special notification rule issued by the Danish Environmental Protection Agency. About 2350 registered washing and cleaning agents containing about 1250 different chemical substances were marketed in Denmark in February 1992. The occurrence of 49 contact allergens in 16 different product types within washing and cleaning agents were listed. Preservatives and surface active agents made up the main part of contact allergens. Isothiazolinones and formaldehyde releasers were the most commonly registered preservatives, and coconut diethanolamide the most commonly registered surface active agent. The major product types registered as containing contact allergens were general cleaners, skin cleaners, hair shampoos, and floor polishes.

清洁工作是引起刺激性和过敏性接触性皮炎的常见原因。工业和家庭用清洗剂根据丹麦环境保护局发布的特别通知规则在丹麦产品登记数据库(PROBAS)中登记。1992年2月,在丹麦销售了约2350种已注册的洗涤和清洁剂,其中含有约1250种不同的化学物质。列出了在16种不同产品类型的洗涤和清洁剂中发生的49种接触性过敏原。接触性过敏原主要由防腐剂和表面活性剂组成。异噻唑啉酮类和甲醛释放剂是最常见的防腐剂,椰子二乙醇酰胺是最常见的表面活性剂。登记为含有接触性过敏原的主要产品类型是普通清洁剂、皮肤清洁剂、洗发香波和地板抛光剂。
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引用次数: 44
Coal mining, emphysema, and compensation revisited. 煤矿开采,肺气肿,和补偿重新审视。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1051
W K Morgan
Seaton, in his editorial, relied mainly on three publications to support his thesis that coal mining may lead to disabling impairment in the absence of progressive massive fibrosis and cigarette smoking.2It is well established that the category of simple coal workers' pneumoconiosis is linearly related to the coal content of the lungs.5 6 In this context Ruckley et al have shown that the extent of emphysema found at postmortem increases with the amount of coal present in the lung and also with lifetime dust exposure.4 If this is so, and there seems little doubt that it is, then increasing category of simple coal workers' pneumoconiosis and its associated emphysema should be associated with a significant decrease in the forced expiratory volume in one second (FEV1). Thus it should follow that the more dust present in the lungs, the more emphysema, and the worse the lung function. This is not the case, there being no difference in lung function in those with and without simple coal workers' pneumoconiosis.7 8 Further evidence in support of the hypothesis is said to come from an examination of the lungs of a group of 95 non-smoking miners, which showed a clear inverse relation between the extent of the emphysema and the FEV1.' The evidence for this statement is said to be contained in a technical report,4 which was not available to us at the time Gee and I questioned the validity of certain conclusions in Seaton's editorial.9 The report has since become available to us, but nowhere in the report is there any evidence to support the claim that there is an inverse relation between emphysema and the FEV, in non-smoking miners. Of the lungs obtained from the 95 non-smoking miners only 40 (42%) showed the presence of emphysema, centriacinar, panacinar or both. In this connection, the study showed that panacinar emphysema was entirely unrelated to dust exposure.4 Of the 40 subjects whose lungs showed emphysema, only 33 (35%) had centriacinar emphysema, of whom 23 also had progressive massive fibrosis, an acknowledged cause of centriacinar emphysema. This left only 10 subjects whose lungs showed centriacinar emphysema in the absence of progressive massive fibrosis. Of these 10, eight had fibrotic nodulessimple coal workers' pneumoconiosis-whereas the other two did not. The authors concluded that because there were only two non-smoking subjects who had emphysema in the absence of coal workers' pneumoconiosis, no conclusions could be drawn as to the effect of dust in the induction of emphysema in those
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引用次数: 5
Semen quality in welders exposed to radiant heat. 曝露在辐射热下的焊工精液质量。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1055-b
L W Raymond
Sir,-We read with interest the article by Pisati et al (1993;50:60-4) regarding outcome according to persistence or cessation of exposure to toluene diisocyanate. In a recent analysis of asthma compensation claims in Ontario, we have also found (data submitted for publication), as have some of the other reports referenced by Pisati et al, that duration of symptoms before leaving exposure and initial pulmonary function measures were important predictors of outcome. In explaining the poor state of group A who were still exposed, is it possible that Pisati et al could further sort out the role of continued exposure to toluene diisocyanate v the initial circumstances such as long duration of exposure and long duration of symptoms before diagnosis? In particular, among the nonimproved subjects within group B (subgroup III) who were no longer exposed, the baseline PDI5 of 424 was similar to that among group A who were still exposed (425). Moreover, as the authors point out, subgroup III had a long mean duration of exposure (15-9 years), and mean duration of symptoms before diagnosis (5 4 years), again similar to those among group A (25 and 6-3 years, respectively). The baseline FEV, was somewhat lower, however, among group A than subgroup III (86-8% v 94%). The authors indicated that it was not possible to analyse group A in this way (because no subjects recovered). Whereas removal from exposure is probably the only effective way of preventing deterioration, it would be of interest if the authors could look at subgroups or examine the relative importance of duration of exposure and symptoms before diagnosis v persistent exposure as predictors of outcome in comparing group A and subgroup III, as they were similar at baseline. GARY M LISS Ontanro Ministry of Labour SUSAN M TARLO The Gage Research Institute, Toronto, Ontanro, Canada
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引用次数: 3
Ethylene oxide: an assessment of the epidemiological evidence on carcinogenicity. 环氧乙烷:对致癌性的流行病学证据的评估。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.971
R E Shore, M J Gardner, B Pannett

Mortality from cancer among workers exposed to ethylene oxide (EtO) has been studied in 10 distinct cohorts that include about 29,800 workers and 2540 deaths. This paper presents a review and meta-analysis of these studies, primarily for leukaemia, non-Hodgkin's lymphoma, stomach cancer, pancreatic cancer, and cancer of the brain and nervous system. The magnitude and consistency of the standardised mortality ratios (SMRs) were evaluated for the individual and combined studies, as well as trends by intensity or frequency of exposure, by duration of exposure, and by latency (time since first exposure). Exposures to other workplace chemicals were examined as possible confounder variables. Three small studies by Hogstedt initially suggested an association between EtO and leukaemia, but in seven subsequent studies the SMRs for leukaemia have been much lower. For the combined studies the SMR = 1.06 (95% confidence interval (95% CI) 0.73-1.48). There was a slight suggestion of a trend by duration of exposure (p = 0.19) and a suggested increase with longer latency (p = 0.07), but there was no overall trend in risk of leukaemia by intensity or frequency of exposure; nor did a cumulative exposure analysis in the largest study indicate a quantitative association. There was also an indication that in two studies with increased risks the workers had been exposed to other potential carcinogens. For non-Hodgkin's lymphoma there was a suggestive risk overall (SMR = 1.35, 95% CI 0.93-1.90). Breakdowns by exposure intensity or frequency, exposure duration, or latency did not indicate an association, but a positive trend by cumulative exposure (p = 0.05) was seen in the largest study. There was a suggested increase in the overall SMR for stomach cancer (SMR = 1.28, 95% CI 0.98-1.65 (CI 0.73-2.26 when heterogeneity among the risk estimates was taken into account)), but analyses by intensity or duration of exposure or cumulative exposure did not support a causal association for stomach cancer. The overall SMRs and exposure-response analyses did not indicate a risk from EtO for pancreatic cancer (SMR = 0.98), brain and nervous system cancer (SMR = 0.89), or total cancer (SMR = 0.94). Although the current data do not provide consistent and convincing evidence that EtO causes leukaemia or non-Hodgkin's lymphoma, the issues are not resolved and await further studies of exposed populations.

对接触环氧乙烷(EtO)的工人的癌症死亡率进行了10个不同队列的研究,其中包括约29,800名工人和2540名死亡人员。本文对这些研究进行综述和荟萃分析,主要针对白血病、非霍奇金淋巴瘤、胃癌、胰腺癌以及脑癌和神经系统癌。评估了单独研究和联合研究的标准化死亡率(smr)的幅度和一致性,以及暴露强度或频率、暴露持续时间和潜伏期(自首次暴露以来的时间)的趋势。暴露于其他工作场所化学物质作为可能的混杂变量进行了检查。Hogstedt的三个小型研究最初提出了EtO与白血病之间的联系,但在随后的七项研究中,白血病的smr要低得多。对于联合研究,SMR = 1.06(95%置信区间(95% CI) 0.73-1.48)。暴露时间有轻微的趋势(p = 0.19),暴露时间越长,白血病风险越高(p = 0.07),但暴露强度或暴露频率对白血病风险没有总体趋势;在最大规模的研究中,累积暴露分析也没有显示出定量关联。还有迹象表明,在两项风险增加的研究中,工人暴露于其他潜在的致癌物中。对于非霍奇金淋巴瘤,总体上存在提示风险(SMR = 1.35, 95% CI 0.93-1.90)。暴露强度或频率、暴露持续时间或潜伏期的分析没有显示出相关性,但在最大的研究中,累积暴露显示出正趋势(p = 0.05)。研究表明,胃癌的总体SMR增加(SMR = 1.28, 95% CI 0.98-1.65(考虑到风险估计的异质性,CI 0.73-2.26)),但暴露强度或持续时间或累积暴露的分析不支持胃癌的因果关系。总体SMR和暴露反应分析没有显示EtO对胰腺癌(SMR = 0.98)、脑和神经系统癌(SMR = 0.89)或总癌(SMR = 0.94)的风险。虽然目前的数据没有提供一致和令人信服的证据,证明EtO会导致白血病或非霍奇金淋巴瘤,但这些问题尚未解决,需要对暴露人群进行进一步的研究。
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引用次数: 105
Mortality of iron miners in Lorraine (France): relations between lung function and respiratory symptoms and subsequent mortality. 洛林(法国)铁矿工人的死亡率:肺功能和呼吸症状与随后死亡率之间的关系。
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1017
N Chau, L Benamghar, Q T Pham, D Teculescu, E Rebstock, J M Mur

An increased mortality from lung and stomach cancer was found in previous studies on Lorraine iron miners. A detailed analysis, however, was not possible due to the lack of data for survivors. In this study the cohort included 1178 workers selected at random from all the 5300 working miners aged between 35 and 55 at the start of the follow up period, which ranged from 1975 to 1985. Occupational exposures and tobacco consumption, lung function tests, and respiratory symptoms were assessed for each subject in 1975, 1980, and 1985. This study confirmed the excess of lung cancer (standardised mortality ratio (SMR) = 389, p < 0.001) and of stomach cancer (SMR = 273, p < 0.05). There was no excess of lung cancer in non-smokers and moderate smokers (< 20 pack-years) or the miners who worked only at the surface or underground for less than 20 years. A significant excess (SMR = 349, p < 0.001) was found in moderate smokers when they worked underground for between 20 and 29 years. Heavy smokers (over 30 pack-years) or subjects who worked underground for more than 30 years experienced a high risk: SMR = 478 (p < 0.001) for moderate smokers who worked underground for over 30 years; 588 (p < 0.001) for heavy smokers who worked underground for between 20 and 29 years; and 877 (p < 0.001) for heavy smokers who worked underground for over 30 years. This showed an interaction between smoking and occupational exposure. The excess mortality from lung cancer was because there were some subjects who died young (from 45 years old). Comparison with the results of a previous study showed that additional hazards produced by diesel engines and explosives increased the mortality from lung cancer. The SMR was higher than 400 (p < 0.001) from 45 years old instead of from 56 years. A relation was found between a decrease in vital capacity (VC), forced expiratory volume in one second (FEV1) and of FEV1/VC and mortality from all causes and from lung cancer in heavy smokers or men who had worked underground for more than 20 years. Respiratory symptoms were related to mortality from lung cancer among smokers (moderate and heavy) who worked underground for more than 20 years. It is considered that the risk of lung cancer in the Lorraine iron miners was mainly due to dust, diesel engines, and explosives although the role of low exposure to radon daughters could not be totally excluded.

先前对洛林铁矿工人的研究发现,肺癌和胃癌的死亡率增加。然而,由于缺乏幸存者的数据,无法进行详细的分析。在这项研究中,队列包括从5300名年龄在35岁至55岁之间的矿工中随机选择的1178名工人,随访期从1975年到1985年。在1975年、1980年和1985年对每个受试者的职业暴露和烟草消费、肺功能检查和呼吸症状进行了评估。本研究证实肺癌(标准化死亡率(SMR) = 389, p < 0.001)和胃癌(SMR = 273, p < 0.05)的发生率过高。在不吸烟者和中度吸烟者(< 20包年)或只在地面或地下工作不到20年的矿工中没有过量的肺癌。在地下工作20 - 29年的中度吸烟者中发现了显著的过量(SMR = 349, p < 0.001)。重度吸烟者(超过30包年)或在地下工作超过30年的受试者有较高的风险:中度吸烟者在地下工作超过30年的SMR = 478 (p < 0.001);在地下工作20至29年的重度吸烟者的588 (p < 0.001);在地下工作超过30年的重度吸烟者为877例(p < 0.001)。这显示了吸烟和职业暴露之间的相互作用。肺癌的高死亡率是因为有一些受试者死于年轻(45岁以上)。与先前的研究结果比较表明,柴油发动机和爆炸物产生的额外危害增加了肺癌的死亡率。45岁的SMR高于56岁的400 (p < 0.001)。在重度吸烟者或地下工作超过20年的男性中,肺活量(VC)、每秒用力呼气量(FEV1)和FEV1/VC的降低与各种原因死亡率和肺癌死亡率之间存在相关性。在地下工作超过20年的吸烟者(中度和重度)中,呼吸道症状与肺癌死亡率有关。尽管不能完全排除氡子体低暴露的作用,但人们认为洛林铁矿工人患肺癌的风险主要是由于粉尘、柴油发动机和爆炸物。
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引用次数: 39
Hazards of deep-sea fishing. 1971. 深海捕鱼的危害。1971.
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.27
R S Schilling
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引用次数: 0
Author's reply 作者的回复
Pub Date : 1993-11-01 DOI: 10.1136/oem.50.11.1055-a
N. Aghakhani
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引用次数: 0
期刊
British Journal of Industrial Medicine
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