British Journal of Industrial Medicine最新文献

{"title":"Analysis of ferruginous bodies in bronchoalveolar lavage from foundry workers.","authors":"R F Dodson,&nbsp;M O'Sullivan,&nbsp;C J Corn,&nbsp;J G Garcia,&nbsp;J M Stocks,&nbsp;D E Griffith","doi":"10.1136/oem.50.11.1032","DOIUrl":"https://doi.org/10.1136/oem.50.11.1032","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1032-8"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Study of occupational lung cancer in asbestos factories in China.","authors":"H Zhu,&nbsp;Z Wang","doi":"10.1136/oem.50.11.1039","DOIUrl":"https://doi.org/10.1136/oem.50.11.1039","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1039-42"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary effects of exposure to fine fibreglass: irregular opacities and small airways obstruction.","authors":"W Weiss","doi":"10.1136/oem.50.11.1054","DOIUrl":"https://doi.org/10.1136/oem.50.11.1054","url":null,"abstract":"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","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1054"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contact allergens in registered cleaning agents for industrial and household use.","authors":"M A Flyvholm","doi":"10.1136/oem.50.11.1043","DOIUrl":"https://doi.org/10.1136/oem.50.11.1043","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1043-50"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coal mining, emphysema, and compensation revisited.","authors":"W K Morgan","doi":"10.1136/oem.50.11.1051","DOIUrl":"https://doi.org/10.1136/oem.50.11.1051","url":null,"abstract":"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","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1051-3"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267947","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semen quality in welders exposed to radiant heat.","authors":"L W Raymond","doi":"10.1136/oem.50.11.1055-b","DOIUrl":"https://doi.org/10.1136/oem.50.11.1055-b","url":null,"abstract":"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","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1055-6"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1055-b","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ethylene oxide: an assessment of the epidemiological evidence on carcinogenicity.","authors":"R E Shore,&nbsp;M J Gardner,&nbsp;B Pannett","doi":"10.1136/oem.50.11.971","DOIUrl":"https://doi.org/10.1136/oem.50.11.971","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"971-97"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.971","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19268633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mortality of iron miners in Lorraine (France): relations between lung function and respiratory symptoms and subsequent mortality.","authors":"N Chau,&nbsp;L Benamghar,&nbsp;Q T Pham,&nbsp;D Teculescu,&nbsp;E Rebstock,&nbsp;J M Mur","doi":"10.1136/oem.50.11.1017","DOIUrl":"https://doi.org/10.1136/oem.50.11.1017","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"1017-31"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.1017","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hazards of deep-sea fishing. 1971.","authors":"R S Schilling","doi":"10.1136/oem.50.11.27","DOIUrl":"https://doi.org/10.1136/oem.50.11.27","url":null,"abstract":"","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"50 11","pages":"27-35"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/oem.50.11.27","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19267950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author's reply","authors":"N. Aghakhani","doi":"10.1136/oem.50.11.1055-a","DOIUrl":"https://doi.org/10.1136/oem.50.11.1055-a","url":null,"abstract":"","PeriodicalId":9254,"journal":{"name":"British Journal of Industrial Medicine","volume":"132 1","pages":"1055 - 1055"},"PeriodicalIF":0.0,"publicationDate":"1993-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73953644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}