Lancet

Our medical research library holds 97 studies published in Lancet (1960–2016). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 16 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 26 studies PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: Elsevier
• Published: 1823 to the present, England
• Language: English
• ISSN: 0140-6736 (print), 1474-547X (electronic)
• Its record in the NLM Catalog

2010s

• A new standard for malignant pleural mesothelioma. M.G. Zauderer. 2016;387(10026):1352-1354. Comment PubMed · Publisher · Free full text

• Bevacizumab for newly diagnosed pleural mesothelioma in the Mesothelioma Avastin Cisplatin Pemetrexed Study (MAPS): a randomised, controlled, open-label, phase 3 trial. G. Zalcman, J. Mazieres, J. Margery, et al. 2016;387(10026):1405-1414. Randomized trial PubMed · Publisher

  Abstract

  Background: Malignant pleural mesothelioma is an aggressive cancer with poor prognosis, linked to occupational asbestos exposure. Vascular endothelial growth factor is a key mitogen for malignant pleural mesothelioma cells, therefore targeting of vascular endothelial growth factor might prove effective. We aimed to assess the effect on survival of bevacizumab when added to the present standard of care, cisplatin plus pemetrexed, as first-line treatment of advanced malignant pleural mesothelioma.

  Methods: In this randomised, controlled, open-label, phase 3 trial, we recruited patients aged 18-75 years with unresectable malignant pleural mesothelioma who had not received previous chemotherapy, had an Eastern Cooperative Oncology Group performance status of 0-2, had no substantial cardiovascular comorbidity, were not amenable to curative surgery, had at least one evaluable (pleural effusion) or measurable (pleural tumour solid thickening) lesion with CT, and a life expectancy of >12 weeks from 73 hospitals in France. Exclusion criteria were presence of central nervous system metastases, use of antiaggregant treatments (aspirin ≥325 mg per day, clopidogrel, ticlopidine, or dipyridamole), anti-vitamin K drugs at a curative dose, treatment with low-molecular-weight heparin at a curative dose, and treatment with non-steroidal anti-inflammatory drugs. We randomly allocated patients (1:1; minimisation method used [random factor of 0·8]; patients stratified by histology [epithelioid vs sarcomatoid or mixed histology subtypes], performance status score [0-1 vs 2], study centre, or smoking status [never smokers vs smokers]) to receive intravenously 500 mg/m(2) pemetrexed plus 75 mg/m(2) cisplatin with (PCB) or without (PC) 15 mg/kg bevacizumab in 21 day cycles for up to six cycles, until progression or toxic effects. The primary outcome was overall survival (OS) in the intention-to treat population. Treatment was open label. This IFCT-GFPC-0701 trial is registered with ClinicalTrials.gov, number NCT00651456.

  Findings: From Feb 13, 2008, to Jan 5, 2014, we randomly assigned 448 patients to treatment (223 [50%] to PCB and 225 [50%] to PC). OS was significantly longer with PCB (median 18·8 months [95% CI 15·9-22·6]) than with PC (16·1 months [14·0-17·9]; hazard ratio 0·77 [0·62-0·95]; p=0·0167). Overall, 158 (71%) of 222 patients given PCB and 139 (62%) of 224 patients given PC had grade 3-4 adverse events. We noted more grade 3 or higher hypertension (51 [23%] of 222 vs 0) and thrombotic events (13 [6%] of 222 vs 2 [1%] of 224) with PCB than with PC.

  Interpretation: Addition of bevacizumab to pemetrexed plus cisplatin significantly improved OS in malignant pleural mesothelioma at the cost of expected manageable toxic effects, therefore it should be considered as a suitable treatment for the disease.

  Funding: Intergroupe Francophone de Cancérologie Thoracique (IFCT).

  Copyright © 2016 Elsevier Ltd. All rights reserved.

• IARC in the dock over ties with asbestos industry. D. Holmes. 2013;381(9864):359-61. News PubMed · Publisher

  Summary

  This news report in The Lancet's World Report section described criticism of the International Agency for Research on Cancer (IARC), an arm of WHO, over alleged ties with the asbestos industry. In late 2012, IARC accepted an invitation from the Russian Scientific Research Institute of Occupational Health (SRIOH), a joint organiser, to send one of its scientists, Valerie McCormack, to present data at a conference in Kiev, Ukraine, entitled Chrysotile Asbestos: Risk Assessment and Management. The Italian Minister of Health and others had urged IARC not to attend. The report stated that the presentation used a 2000 estimate by Hodgson and Darnton of the relative mesothelioma risk of chrysotile, amosite and crocidolite (1:100:500). It omitted the same authors' 2009 revision (1:10:50). The report also described objections to IARC's collaboration with SRIOH on a historical cohort study of cancer mortality among chrysotile workers in Asbest, Russia, led by Evgeny Kovalevskiy. These objections came in a letter from Richard Lemen, Arthur Frank and Barry Castleman, who described him as a leading promoter of chrysotile use. An IARC spokesperson, Nicolas Gaudin, said the conference was an opportunity to emphasise the dangers of asbestos and that IARC was not associated with the conference resolution. He also said the Asbest study was not a condition of Russia's resumed financial contributions. The report placed these events before the April 2013 Rotterdam Convention meeting, which would again consider listing chrysotile in Annex III. Canada had dropped its opposition, and Russia would for the first time have the power to veto. Campaigners argued that the Kiev conference and the IARC collaboration supported Russia's opposition to the listing.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Canadian hypocrisy regarding chrysotile. J. Bridle, J. Hoskins. 2011;377(9767):720. Letter · Comment PubMed · Publisher

• Canada accused of hypocrisy over asbestos exports. T. Kirby. 2010;376(9757):1973-4. News PubMed · Publisher

• Health experts concerned over India's asbestos industry. T. Burki. 2010;375(9715):626-7. News PubMed · Publisher

  Summary

  This news report from The Lancet's World Report section described health experts' concerns about the growth of asbestos use in India. It drew on published figures and interviews with experts from WHO, Drexel University (USA), the Occupational Health and Safety Centre in Mumbai, the Ban Asbestos Network of India, a Canadian member of parliament who was a former asbestos miner, and an environmental consultant. The report stated that India's asbestos use rose from roughly 125 000 metric tonnes in 2000 to about 300 000 in 2007. Nearly all of it was mixed with cement to make roofing sheets. The asbestos-cement industry was growing by about 10% a year and employed more than 100 000 people. Import tariffs fell from 78% in the mid-1990s to 15% by 2004. About 7 million tonnes had been built into buildings since 1960. Experts described several problems: poor recording of death and disease, little occupational health training among doctors, misdiagnosis of asbestosis as tuberculosis or bronchitis, and minimal protection for workers, including India's roughly 60 000 ship breakers. The report set the Canadian-government-funded Chrysotile Institute's claim that chrysotile can be used safely against WHO's position that all types of asbestos are carcinogenic. Experts expected much more death and disease. They said workers who are already ill must be compensated, and that the final aim was an outright ban.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

2000s

• Active symptom control with or without chemotherapy in the treatment of patients with malignant pleural mesothelioma (MS01): a multicentre randomised trial. M.F. Muers, R.J. Stephens, P. Fisher, et al. 2008;371(9625):1685-94. Randomized trial PubMed · Publisher · Free full text

  Abstract

  Background: Malignant pleural mesothelioma is almost always fatal, and few treatment options are available. Although active symptom control (ASC) has been recommended for the management of this disease, no consensus exists for the role of chemotherapy. We investigated whether the addition of chemotherapy to ASC improved survival and quality of life.

  Methods: 409 patients with malignant pleural mesothelioma, from 76 centres in the UK and two in Australia, were randomly assigned to ASC alone (treatment could include steroids, analgesic drugs, bronchodilators, palliative radiotherapy [n=136]); to ASC plus MVP (four cycles of mitomycin 6 mg/m2, vinblastine 6 mg/m2, and cisplatin 50 mg/m2 every 3 weeks [n=137]); or to ASC plus vinorelbine (one injection of vinorelbine 30 mg/m2 every week for 12 weeks [n=136]). Randomisation was done by minimisation, with stratification for WHO performance status, histology, and centre. Follow-up was every 3 weeks to 21 weeks after randomisation, and every 8 weeks thereafter. Because of slow accrual, the two chemotherapy groups were combined and compared with ASC alone for the primary outcome of overall survival. Analysis was by intention to treat. This study is registered, number ISRCTN54469112.

  Findings: At the time of analysis, 393 (96%) patients had died (ASC 132 [97%], ASC plus MVP 132 [96%], ASC plus vinorelbine 129 [95%]). Compared with ASC alone, we noted a small, non-significant survival benefit for ASC plus chemotherapy (hazard ratio [HR] 0.89 [95% CI 0.72-1.10]; p=0.29). Median survival was 7.6 months in the ASC alone group and 8.5 months in the ASC plus chemotherapy group. Exploratory analyses suggested a survival advantage for ASC plus vinorelbine compared with ASC alone (HR 0.80 [0.63-1.02]; p=0.08), with a median survival of 9.5 months. There was no evidence of a survival benefit with ASC plus MVP (HR 0.99 [0.78-1.27]; p=0.95). We observed no between-group differences in four predefined quality-of-life subscales (physical functioning, pain, dyspnoea, and global health status) at any of the assessments in the first 6 months.

  Interpretation: The addition of chemotherapy to ASC offers no significant benefits in terms of overall survival or quality of life. However, exploratory analyses suggested that vinorelbine merits further investigation.

• Asbestos-related disease--a preventable burden. 2008;372(9654):1927. Editorial PubMed · Publisher

  Summary

  This Lancet editorial discussed a ruling by the High Court of England and Wales on Nov 21, 2008. The ruling allowed patients with mesothelioma to claim compensation from the insurers of the companies that employed them when they were exposed to asbestos. Before the ruling, liability lay with the employer at the time the disease presented, often 25–40 years after exposure. The editorial stated that all forms of asbestos are carcinogenic and that mesothelioma has no known cure, with a median survival of 9–12 months from presentation. It cited estimates that 125 million people are at risk from asbestos and that about 90 000 asbestos-related deaths occur worldwide each year. It also cited a figure of 2000 asbestos deaths a year in the UK, expected to peak between 2011 and 2015. It warned that a similar epidemic is likely in developing countries where asbestos is still widely used. It reported that 43 countries have national bans. It noted that Canada, Russia, Pakistan and India opposed adding chrysotile to the Prior Informed Consent list of the Rotterdam Convention. It criticised Canada for exporting 98% of its asbestos to developing countries while limiting its use at home. The editorial concluded that all countries should follow WHO's advice that the only way to eliminate asbestos-related disease is to stop using all types of asbestos worldwide.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Belgium: historical champion in asbestos consumption. T.S. Nawrot, G. Van Kersschaever, E. Van Eycken, et al. 2007;369(9574):1692. Comment · Letter PubMed · Publisher

  Summary

  This letter responded to an ecological analysis by Lin and colleagues, published in The Lancet on March 10, 2007, that related asbestos consumption in the 1960s to mesothelioma and asbestosis in the early 2000s. Belgium had not been included in that analysis because recent national mortality statistics were lacking. The authors pointed out that Belgium and Luxembourg consumed an average of 53 790 tons of asbestos a year during 1960–70, for a total population of about ten million. They stated that none of the countries Lin and colleagues analysed had a per capita consumption as high. Using cancer mortality data for the Flemish region (about six million inhabitants), they reported 116 mesothelioma deaths in 2000, 143 in 2001, 122 in 2002, 111 in 2003 and 137 in 2004. This gave a yearly average of 126, of whom 106 were men. That corresponded to a crude mortality of about 35 per million men per year, or 20 per million men when standardised as in Lin and colleagues' study. The Belgian Fund for Occupational Diseases recognised 203 asbestosis deaths (197 men) between 2000 and 2004. This gave an asbestosis mortality of about eight per million men per year, which the authors stated was higher than in any of the 33 countries in Lin and colleagues' study. A figure reproduced the original ecological plot with Belgium added.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Ecological association between asbestos-related diseases and historical asbestos consumption: an international analysis. R.T. Lin, K. Takahashi, A. Karjalainen, et al. 2007;369(9564):844-849. Historical article PubMed · Publisher

  Abstract

  Background: The potential for a global epidemic of asbestos-related diseases is a growing concern. Our aim was to assess the ecological association between national death rates from diseases associated with asbestos and historical consumption of asbestos.

  Methods: We calculated, for all countries with data, yearly age-adjusted mortality rates by sex (deaths per million population per year) for each disease associated with asbestos (pleural, peritoneal, and all mesothelioma, and asbestosis) in 2000-04 and mean per head asbestos consumption (kg per person per year) in 1960-69. We regressed death rates for the specified diseases against historical asbestos consumption, weighted by the size of sex-specific national populations.

  Findings: Historical asbestos consumption was a significant predictor of death for all mesothelioma in both sexes (adjusted R2=0.74, p<0.0001, 2.4-fold [95% CI 2.0-2.9] mortality increase was predicted per unit consumption increase for men; 0.58, p<0.0001, and 1.6-fold [1.4-1.9] mortality increase was predicted for women); for pleural mesothelioma in men (0.29, p=0.0015, 1.8-fold [1.3-2.5]); for peritoneal mesothelioma in both sexes (0.54, p<0.0001, 2.2-fold [1.6-2.9] for men, 0.35, p=0.0008, and 1.4-fold for women [1.2-1.6]); and for asbestosis in men (0.79, p<0.0001, 2.7-fold [2.2-3.4]). Linear regression lines consistently had intercepts near zero.

  Interpretation: Within the constraints of an ecological study, clear and plausible associations were shown between deaths from the studied diseases and historical asbestos consumption, especially for all mesothelioma in both sexes and asbestosis in men. Our data strongly support the recommendation that all countries should move towards eliminating use of asbestos.

• The fallout from asbestos. G.R. Wagner. 2007;369(9566):973-4. Comment PubMed · Publisher

  Summary

  In this Comment, the author discussed an ecological study by Lin and colleagues that analysed the experience of 33 countries. That study showed that national asbestos consumption was followed, after a latent period of 30–40 years, by a proportional number of deaths from mesothelioma and asbestosis. The author noted that other known outcomes of asbestos exposure were not counted: lung cancer, laryngeal tumours and perhaps malignant disorders of the gastrointestinal tract. He described the study's ability to detect the relation with crude national measures of exposure and response as surprising. He observed that the richest countries, which historically used the most asbestos, were now paying the greatest mortality and economic price and were dealing with compensation, citing the UK and the USA. He summarised international action. The European Union had banned asbestos and started a programme to prevent exposure, the International Labour Organization had endorsed a ban in 2006, and at least 40 countries had forbidden or severely restricted new use. He noted that so-called safe use of chrysotile was still promoted and that countries with the least developed worker health protection tended to have the least restrictive policies. He stressed hazards across the whole life cycle of asbestos, including maintenance, renovation, demolition, ship dismantling and waste disposal. He concluded that countries with little historical use could help avoid a future epidemic of asbestos-related deaths by deciding soon to restrict or eliminate asbestos importation and use.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Malignant mesothelioma. B.W. Robinson, A.W. Musk, R.A. Lake. 2005;366(9483):397-408. Review PubMed · Publisher

  Abstract

  Malignant mesothelioma is an aggressive, treatment-resistant tumour, which is increasing in frequency throughout the world. Although the main risk factor is asbestos exposure, a virus, simian virus 40 (SV40), could have a role. Mesothelioma has an unusual molecular pathology with loss of tumour suppressor genes being the predominant pattern of lesions, especially the P16INK4A, and P14ARF, and NF2 genes, rather than the more common p53 and Rb tumour suppressor genes. Cytopathology of mesothelioma effusions or fine-needle aspirations are often sufficient to establish a diagnosis, but histopathology is also often required. Patients typically present with breathlessness and chest pain with pleural effusions. Median survival is now 12 months from diagnosis. Palliative chemotherapy is beneficial for mesothelioma patients with high performance status. The role of aggressive surgery remains controversial and growth factor receptor blockade is still unproven. Gene therapy and immunotherapy are used on an experimental basis only. Patterns identified from microarray studies could be useful for diagnosis as well as prognostication.

• Asbestos exposure as a risk factor for retroperitoneal fibrosis. T. Uibu, P. Oksa, A. Auvinen, et al. 2004;363(9419):1422-6. PubMed · Publisher

  Abstract

  Background: Retroperitoneal fibrosis (RPF) is an uncommon disease with unknown causation in most cases. The pathognomonic finding is a fibrous mass covering the abdominal aorta and the ureters. Our aim was to clarify the possible role of asbestos exposure in the development of RPF. The hypothesis was based on the ability of asbestos to cause fibrosis in pulmonary and pleural tissue.

  Methods: We undertook a case-control study of 43 patients with the disease (86% of eligible cases) treated in three university hospital districts of Finland in 1990-2001. For every patient, five population-based controls were selected, matched by age, sex, and central hospital district. We assessed asbestos exposure and medical history using a postal questionnaire and a personal interview. Of the 215 eligible controls, 179 (83%) participated in the study.

  Findings: The age-standardised incidence of RPF was 0.10 (95% CI 0.07-0.14) per 100?000 person-years. The disease was strongly associated with asbestos exposure. The odds ratio (OR) was 5.54 (1.64-18.65) for less than 10 fibre-years of asbestos exposure and 8.84 (2.03-38.50) for 10 or more fibre-years, the attributable fraction being 82% and 89%, respectively. Other risk factors were previous use of ergot derivates (OR 9.92 [1.63-60.26]), abdominal aortic aneurysm (OR 6.73 [0.81-56.08]), and smoking for more than 20 pack-years (OR 4.73 [1.28-17.41]).

  Interpretation: Our results show that occupational asbestos exposure is an important causal factor for RPF. For patients with work-related asbestos exposure, RPF should be considered an occupational disease.

• Evidence against a role for SV40 infection in human mesotheliomas and high risk of false-positive PCR results owing to presence of SV40 sequences in common laboratory plasmids. F. López-Ríos, P.B. Illei, V. Rusch, et al. 2004;364(9440):1157-66. PubMed · Publisher

  Abstract

  Background: PCR-based evidence of infection by simian virus 40 (SV40) has been reported in varying proportions of pleural mesotheliomas and other tumours, but data are conflicting and reproducibility limited. During a study of SV40 in relation to homozygous deletion of CDKN2A in mesotheliomas, we became concerned by inconsistent results and therefore used several independent techniques to investigate SV40 in these tumours.

  Methods: High-quality DNA and RNA were extracted from 71 frozen mesothelioma samples. DNA PCR was done with four sets of primers for the SV40 T-antigen gene. RNA transcripts were examined by RT-PCR.

  Findings: The first two primer sets for DNA PCR gave positive results in proportions similar to those reported in positive studies (56-62%) but there were unusual reproducibility difficulties. These primers were in a region of the T-antigen gene (nucleotides 4100-4713) that is present in many common laboratory plasmids. In assays with PCR primers not included within that region, only four cases (6%) showed products but these were too faint to suggest clonal infection. Further PCR assays confirmed that the SV40 sequences in the tumour samples had a deletion found only in plasmids, not in native functional SV40. Review of previous studies showed a similar pattern of discrepancies between SV40 T-antigen DNA PCR results obtained with primers within and beyond the region 4100-4713. All 71 mesotheliomas were negative for T-antigen transcripts by RT-PCR, and lacked T-antigen-positive tumour cells by immunohistochemistry.

  Interpretation: Our data based on three independent experimental approaches do not support a significant role for SV40 in human mesotheliomas. The risk of false-positive results due to contamination by common laboratory plasmids containing SV40 sequences has been underestimated. Studies of SV40 based on PCR methods require careful primer design to reduce this risk.

  Relevance To Practice: This paper presents several lines of evidence against the proposed link between SV40 infection and human mesotheliomas. Studies reporting a high prevalence of SV40 DNA in human tumours have been based on molecular assays prone to false-positive results. Because SV40 appears unlikely to have a major role, if any, in human mesotheliomas, clinicians should continue to consider asbestos exposure as the most likely and most thoroughly established aetiological factor in individuals with this cancer.

• Mesothelin-family proteins and diagnosis of mesothelioma. B.W. Robinson, J. Creaney, R. Lake, et al. 2003;362(9396):1612-6. PubMed · Publisher

  Abstract

  Background: Mesothelioma is a highly aggressive tumour for which there are no reliable serum tumour markers. Identification of such a marker would be useful in diagnosis of mesothelioma and for monitoring responses to treatment and screening at-risk individuals.

  Methods: We assayed serum concentrations of soluble mesothelin-related proteins (SMR) using a double determinant (sandwich) ELISA in a blinded study of serum samples from 44 patients with histologically proven mesothelioma; 68 matched healthy controls, 40 of whom had been exposed to asbestos; and 160 patients with other inflammatory or malignant lung and pleural diseases.

  Findings: 37 (84%) of 44 patients with mesothelioma had raised concentrations of SMR at a serum dilution of 1/80, compared with three (2%) of 160 patients with other cancers or other inflammatory lung or pleural diseases, and with none of 28 controls who had not been exposed to asbestos. SMR concentrations correlated with tumour size and increased during tumour progression. Seven of the 40 asbestos-exposed individuals had increased serum concentrations of SMR; three of those seven developed mesothelioma and one developed lung carcinoma within 1-5 years. None of the 33 asbestos-exposed participants whose serum samples had normal concentrations of SMR and who were followed up over 8 years developed mesothelioma.

  Interpretation: Determination of SMR in serum could be a useful marker for diagnosis of mesothelioma and to monitor disease progression. It might also prove helpful for screening asbestos-exposed individuals for early evidence of mesothelioma.

• Indian groups demand ban on asbestos. D.C. Sharma. 2002;359(9315):1414. PubMed · Publisher

1990s

• Asbestos--the legacy lives on. D. Bonn. 1999;353(9161):1336. News PubMed · Publisher

• Chrysotile asbestos: enough is enough. M.R. Cullen. 1998;351(9113):1377-8. PubMed · Publisher

  Summary

  In this commentary, the author discussed four recent papers by J C McDonald, A D McDonald, F D K Liddell and collaborators on cancer risks among Quebec chrysotile miners and millers. He summarised their finding that virtually all of the mesothelioma and lung cancer risk at the several mines and two large milling centres appeared to come from exposure in the regions most heavily contaminated with tremolite. The dose-response relation was very shallow, and there was no excess of other cancers such as larynx, stomach and colon. The investigators had inferred that pure chrysotile had minimal, if any, potential to cause mesothelioma, that it was much less carcinogenic than the amphiboles, and that it could be used commercially with very little health risk under appropriate exposure controls. The author argued that discrepancies in existing data precluded ready acceptance of these conclusions. He stated that chrysotile had nowhere proven free of mesothelioma risk, and that the difference from amphiboles was perhaps only three-fold. He added that chrysotile products probably remained the world's leading cause of mesothelioma because of their wider use, and that the very high lung cancer rates in chrysotile textile workers could not be explained by tremolite. He acknowledged that a predicted 'third wave' from low-level exposure had shown little evidence of materialising. He concluded that, because safer substitutes exist, putting more asbestos into the environment or relaxing exposure controls would be foolhardy.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Hazards of white asbestos. H. Demiruglu. 1998;352(9124):322-3. Comment · Letter PubMed · Publisher

• Hazards of white asbestos. A.J. Dalton. 1998;352(9124):322. Letter · Comment PubMed · Publisher

• Asbestosis and silicosis. G.R. Wagner. 1997;349(9061):1311-5. Review PubMed · Publisher

  Abstract

  Interstitial fibrosis resulting from workplace exposure to asbestos and crystalline silica persists throughout the world despite knowledge of the causes and effective means for prevention. Asbestosis and silicosis occurrence is predictable among people overexposed to dusts in various industries and occupations such as mining, construction, manufacturing, and building maintenance. Asbestosis and silicosis are incurable and may be progressive even after dust exposure has ceased, therefore early recognition and supportive interventions are important. Although current disease is a result of past exposures, effective control of current workplace exposures is the only way to prevent continued occurrence of these potentially debilitating diseases. Physicians can contribute to this effort through accurate diagnosis and disease reporting.

• Asbestos and idiopathic retroperitoneal fibrosis. J.C. Boulard, T. Hanslik, L.M. Doleris, et al. 1995;345(8961):1379. Case report · Letter PubMed · Publisher

  Summary

  In this letter, the authors noted that retroperitoneal fibrosis had previously been reported alongside diffuse pleural thickening in one asbestos-exposed patient. They described two more men previously exposed to asbestos who had retroperitoneal fibrosis with evidence of pleural involvement. The first, a 51-year-old man who had worked for 25 years in road building, was admitted with acute renal failure. Abdominal echography and magnetic resonance imaging showed retroperitoneal fibrosis blocking both ureters. He refused biopsy. Steroid therapy relieved the ureteral obstruction immediately and his kidney function returned to normal. His chest radiographs showed bilateral calcified pleural plaques on the diaphragm, which the authors described as typical of asbestos exposure. The second, a 54-year-old man, had maintained the boiler of a thermal power station in the car industry and had been exposed to asbestos for 20 years. He presented with renal failure due to retroperitoneal fibrosis. His chest radiographs showed chronic pleural thickening on one side, and his kidney function improved with steroid therapy. In neither man did the authors find any of the usual causes of retroperitoneal fibrosis, such as tumour, injury, aneurysm, infection, radiation or medicines. They cited necropsy findings of asbestos bodies in most organs, including retroperitoneal organs, and the link between asbestos and peritoneal mesothelioma. They suggested that asbestos might cause retroperitoneal fibrosis and proposed that the search for its cause should include systematic inquiry into asbestos exposure.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos: a risk too far?. W. Weiss. 1995;346(8970):305; author reply 306. Comment · Letter PubMed

• Asbestos: a risk too far?. H. Weill, J.M. Hughes, R.N. Jones. 1995;346(8970):304; author reply 306. Letter · Comment PubMed

• Asbestos: a risk too far?. E.S. Johnson. 1995;346(8970):304-5; author reply 306. Comment · Letter PubMed

• Asbestos: a risk too far?. K. Browne. 1995;346(8970):305-6. Comment · Letter PubMed

• Continuing increase in mesothelioma mortality in Britain. J. Peto, J.T. Hodgson, F.E. Matthews, et al. 1995;345(8949):535-9. PubMed · Publisher

  Abstract

  Mesothelioma is closely related to exposure to asbestos, and mesothelioma mortality can be taken as an index of past exposure to asbestos in the population. We analysed mesothelioma mortality since 1968 to assess the current state of the mesothelioma epidemic, and to predict its future course. We found that rates of mesothelioma in men formed a clear pattern defined by age and date of birth. Rates rose steeply with age showing a very similar pattern in all five-year birth cohorts. By date of birth, rates increased from mid-1893 to mid-1948, and then fell. Relative to the 1943-48 cohort, the risk for the 1948-53 cohort is 0.79 and for the 1953-58 cohort 0.48. Despite these falls, if the age profile of rates for these cohorts follows the pattern of past cohorts, their predicted lifetime mesothelioma risks will be 1.3%, 1.0%, and 0.6%. Combining projections for all cohorts results in a peak of annual male mesothelioma deaths in about the year 2020 of between 2700 and 3300 deaths. If diagnostic trend is responsible for a 20% growth in recorded cases every 5 years--an extreme but arguable case--and if this trend has now ceased, the peak of annual male deaths will be reduced to 1300, reached around the year 2010. Analysis of occupations recorded on death certificates indicate that building workers, especially plumbers and gas fitters, carpenters and electricians are the largest high-risk group. These data indicate that mesothelioma deaths will continue to increase for at least 15 and more likely 25 years. For the worst affected cohorts--men born in the 1940s--mesothelioma may account for around 1% of all deaths. Asbestos exposure at work in construction and building maintenance will account for a large proportion of these deaths, and it is important that such workers should be aware of the risks and take appropriate precautions.

• Is lung cancer associated with asbestos exposure when there are no small opacities on the chest radiograph?. P. Wilkinson, D.M. Hansell, J. Janssens, et al. 1995;345(8957):1074-8. PubMed · Publisher

  Abstract

  This study was designed to test the hypothesis that the risk of lung cancer from asbestos exposure is confined to persons with radiographic evidence of pulmonary fibrosis. Occupational and smoking histories were obtained from 271 patients with a confirmed diagnosis of primary lung cancer and 678 referents (279 with other respiratory disease and 399 with cardiac disease). Histories were reviewed blind to assess the timing, duration, and probability of exposure to asbestos. To allow for a lag between asbestos exposure and the development of lung cancer, subjects were classified by the time they had spent in an occupation entailing definite or probable exposure more than 15 years before diagnosis. The presence and extent of fibrosis was assessed blindly from chest radiographs by three readers and scored for small opacities with the ILO 1989 International Classification of Radiographs of the Pneumoconioses. 93 (34.3%) cases had worked in an occupation with definite or probable asbestos exposure compared with 176 (25.8%) referents (crude odds ratio for lung cancer 1.49, 95% CI 1.09-2.04). After adjustment for age, sex, smoking history, and area of referral, the odds ratio (95% CI) was 2.03 (1.00-4.13) in the subgroup of 211 with a median ILO score for small parenchymal opacities of 1/0 or more, and 1.56 (1.02-2.39) in the 738 with a score of 0/1 or less (ie, those without radiological evidence of pulmonary fibrosis). These results suggest that asbestos is associated with lung cancer even in the absence of radiologically apparent pulmonary fibrosis.

• Mesothelioma. H. De Vos Irvine. 1995;345(8959):1233. Comment · Letter PubMed

• Mesothelioma. R.A. Damhuis, H.T. Planteydt. 1995;345(8959):1233-4. Letter · Comment PubMed

• Mesothelioma. H. Weill, J.M. Hughes. 1995;345(8959):1234. Letter · Comment PubMed

• Malignant pleural mesothelioma associated with exposure to tremolite. D. Luce, P. Brochard, P. Quénel, et al. 1994;344(8939-8940):1777. Letter PubMed · Publisher

  Summary

  The authors reported preliminary results of an investigation into the high frequency of malignant pleural mesothelioma (MPM) in New Caledonia, which occupational asbestos exposure could not explain. They examined the 28 histologically confirmed MPM cases diagnosed there between 1984 and 1993: 13 men and 15 women, with a mean age at diagnosis of 56.7 years and 3 under 40. Only 2 had been occupationally exposed to asbestos, and 23 were Melanesian (45% of the population). The excess was restricted to some areas, where crude annual incidence could reach 3 cases per 10000 inhabitants. In these areas a friable local rock was used as whitewash for house walls. Analytical transmission electron microscopy showed that rock and whitewash samples consisted primarily of asbestiform tremolite. Air sampling in two villages found no tremolite fibres in the general atmosphere. High concentrations were found in road dust clouds from a car (59 and 669 fibres per L), during whitewash preparation (558 fibres per L), and while whitewashed houses were swept (up to 78000 fibres per L). Tremolite fibres were detected in bronchoalveolar lavage fluid from 2 of 3 MPM cases and in parenchymal tissue from 6 of 8 patients with bronchial cancer. The authors concluded that environmental exposure to tremolite, mainly from the whitewash, is a cause of the high MPM incidence, and said preventive measures were in progress.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Environmental asbestos. K. Browne. 1991;338(8772):949. Comment · Letter PubMed · Publisher

• Malignant mesothelioma after exposure to asbestos in dental practice. A.S. Reid, B.E. Causton, J.S. Jones, et al. 1991;338(8768):696. Case report · Letter PubMed · Publisher

  Summary

  In this letter, the authors reported malignant mesothelioma in a dentist and discussed asbestos exposure in dental practice. A 60-year-old retired dentist presented with recurrent left pleural effusions. Histology of tissue from a left pleurectomy confirmed malignant mesothelioma. He developed paraplegia and died 10 months after presentation. Post-mortem examination showed a mixed-type mesothelioma that had extended into the pericardial cavity, chest wall and paravertebral tissue. Mineral analysis found 0.7 x 10^6 crocidolite fibres per gram of dry lung. The authors described this as lower than expected with longstanding occupational exposure but higher than in the general population. No chrysotile fibres were found. The authors described how, until the mid-1970s, asbestos paper was used to line casting rings and crucibles for metal fillings and dentures, and chrysotile powder served as a binder in periodontal dressings. They cited measurements of 21 to 27 fibres per ml of air released when moulds were dismantled. They noted that dental undergraduates commonly cast at least 40 sets of dentures. The Health and Safety Executive found no other source of the patient's exposure to asbestos and no previous reports of mesothelioma in dental personnel. The authors concluded that this first reported case illustrated another potential occupational association between asbestos exposure and mesothelioma.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Mesothelioma and non-occupational environmental exposure to asbestos. C. Magnani, G. Borgo, G.P. Betta, et al. 1991;338(8758):50. Letter PubMed · Publisher

  Summary

  This letter asked whether pleural mesothelioma occurred in excess among residents of Casale Monferrato, north-west Italy, apart from occupational exposure. The town, with about 40 000 people, was the site of the largest Italian asbestos-cement plant, which operated from 1907 to 1985. In an earlier mortality study of the plant's workers for 1964-86, the authors had found 864 deaths against 710 expected, including 117 from lung cancer, 43 from pleural cancer and 89 from asbestosis. For this report, the authors searched the records of the local hospital and four other large hospitals for histological diagnoses of pleural mesothelioma among residents of the local health unit. The area was divided into three zones: Casale Monferrato itself, adjacent towns, and other towns and villages. They found 89 residents with a histological diagnosis during 1980-89. Linkage with employee rosters showed that 26 had worked at the plant, and 3 were wives of workers. The remaining 60 cases were used to calculate rates, which were compared with rates from the Varese Province cancer registry for 1976-87. The authors reported an impressive excess of pleural mesothelioma in both men and women that was not attributable to work at the plant. The numbers were small, but rates appeared to fall with distance from Casale Monferrato. They discussed possible biases and concluded that a cancer risk from asbestos may arise in the general, non-occupational environment.

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• Asbestos and the Romans. K. Browne, R. Murray. 1990;336(8712):445. Historical article · Letter PubMed · Publisher

1980s

• Asbestos-contaminated nappies and familial mesothelioma. F.P. Li, M.G. Dreyfus, K.H. Antman. 1989;1(8643):909-10. Letter PubMed · Publisher

  Summary

  The authors described a family cluster of mesothelioma linked to household asbestos exposure. Cotton cloth sacks that had carried moulded asbestos insulation were made into diapers (nappies) for the children of an asbestos worker, an insulator. The oldest child died of mesothelioma at age 32 years. Her 29-year-old sister had been similarly exposed but remained unaffected. The mother, who had laundered the diapers and her husband's work clothes, died of mesothelioma at age 49. A maternal uncle, who had lived in the contaminated household as a teenager and worked briefly as an insulator, developed mesothelioma at age 43. The father died with asbestosis and cirrhosis of the liver at age 53. The authors noted that mesothelioma usually develops in older men three or four decades after they become asbestos workers. These long intervals suggested that the proband was exposed in childhood and her mother and uncle in early adulthood. The two women had no occupational contact with asbestos and had probably been exposed at home. The authors concluded that the diapers appeared to have been one source of exposure, which emphasised the hazard of recycling asbestos-contaminated textiles. They recommended that employers arrange educational programmes and monitor security measures to prevent removal of asbestos-contaminated materials from the worksite.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Iron, asbestos, and carcinogenicity. E.D. Weinberg. 1989;1(8651):1399-400. Letter PubMed · Publisher

  Summary

  In this letter, the author argued that the iron content of asbestos may help explain why some asbestos types are more carcinogenic than others. He noted that iron overload increases the risk of neoplasia, that iron is an essential nutrient for cancer cells and impairs inflammatory defence mechanisms, and that overload can arise from the diet, enhanced iron absorption, parenteral iron or blood, cigarette smoke, or occupational sources such as iron ore mining and milling, welding, and painting with iron-containing substances. Citing published work, he stated that the amphibole varieties crocidolite and amosite are strongly carcinogenic, while the serpentine type chrysotile is far less dangerous, and that carcinogenicity has been correlated in part with the physical characteristics of the fibres. He proposed that chemical composition also plays a part: crocidolite and amosite contain approximately 27% and 31% iron, compared with about 0.3% for chrysotile. Asbestos that contains or is contaminated with iron catalyses the generation of hydroxyl radicals, which increase DNA strand breakage and lipid membrane peroxidation; these activities are prevented by the chelator desferrioxamine. Noting that over 95% of asbestos mined worldwide is chrysotile, he suggested that eliminating industrial use of crocidolite, amosite, and chrysotile contaminated with iron or iron-containing tremolite could strikingly reduce asbestos-related cancer. He added that even then, dust control and discouraging cigarette smoking by asbestos workers and their families would remain prudent.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Benign asbestos pleural effusions. 1988;1(8595):1145-6. Editorial PubMed

• Asbestos exposure and carcinoma of penis. E. Raffn, B. Korsgaard. 1987;2(8572):1394. Letter PubMed · Publisher

• Association of Metsovo lung and pleural mesothelioma with exposure to tremolite-containing whitewash. A.M. Langer, R.P. Nolan, S.H. Constantopoulos, et al. 1987;1(8539):965-7. PubMed · Publisher

  Abstract

  Pleural thickening, bilateral pleural hyalinised plaques, and restrictive lung function are found among inhabitants of four small villages in northwestern Greece. Transbronchial biopsy samples from patients with disease contained tremolite fibres. Malignant pleural mesothelioma has now been reported in these villages and accounts for approximately 1% of the total mortality from 1981 to 1985. The principal whitewash once used in this area is predominantly asbestiform tremolite. The fibre is identical in every respect to fibres found in the lung tissues of people with Metsovo lung. The membrane activity of this tremolite is greater than that of the commercially used asbestiform amphiboles amosite and crocidolite. This measure of cytotoxicity lends further support to the hypothesis that this fibre is the agent of Metsovo lung and mesothelioma.

• Mesothelioma in manufacturers of asbestos-containing cigarette filters. J. Talcott, W. Thurber, E. Gaensler, et al. 1987;1(8529):392. Letter PubMed · Publisher

• Pleural effects of tremolite in north-west Greece. T. Bazas. 1987;1(8548):1490-1. Letter PubMed · Publisher

• Regional findings in Metsovo lung. S.H. Constantopoulos, A.M. Langer, N. Saratzis, et al. 1987;2(8556):452-3. Letter PubMed · Publisher

  Summary

  In this letter, the authors reported further findings on 'Metsovo lung', the pleural calcification seen among inhabitants of Metsovo and three adjacent villages in northwest Greece. They had previously linked it to inhaling asbestiform tremolite fibre from a soil widely used before 1950 for interior whitewashing, and had found a high incidence of malignant pleural mesothelioma in the same area. Chest X-rays of more than 800 people from Metsovo showed evidence of pleural disease on 46% of films. No sex or occupational factor was found, and prevalence increased with age: 81% of adults over 70 had calcified pleural plaques. Because chest X-ray is insensitive to early disease, computerised tomography was performed on 16 X-ray-negative subjects born in Metsovo before 1940, and all scans showed pleural calcification. Of some 500 Metsovites who had emigrated since 1970 to Trikala, in Thessaly, where the geology precludes environmental exposure to asbestiform fibre, 71 had chest X-rays and 50 (70%) showed pleural calcification. Its age distribution and prevalence were identical to those in Metsovo. The authors compared this with mesothelioma among Turkish emigrants in Sweden exposed early in life to erionite in Karain. They had found four more affected areas in northwest Greece, where investigations were under way. They expected clusters across Balkan states and concluded that Metsovo lung appeared more widespread than previously thought.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Early-onset, asbestos-associated mesothelioma?. C.L. Berry, T.J. Jones. 1986;1(8489):1094. Letter PubMed · Publisher

• Malignant pleural mesothelioma five years after domestic exposure to blue asbestos. S.J. Booth, E.J. Weaver. 1986;1(8478):435. Case report · Letter PubMed · Publisher

  Summary

  In this letter, the authors reported the case of a 28-year-old man with advanced malignant pleural mesothelioma, seen at the Department of Cardiothoracic Surgery, London Hospital. They noted that the latent period between asbestos exposure and mesothelioma is usually said to be 20-60 years (average 35-40 years). The man presented with a 1-year history of weight loss, with 6 months of night sweats and general malaise. His erythrocyte sedimentation rate was 128 mm/h. Chest X-ray and computerised tomography showed multiple pleural nodules. Five years earlier, while renovating his house, he had knocked down a wall partition packed with blue asbestos. He had been heavily exposed to the dust over a 72-hour period and had not worn a face mask. A pleuropneumonectomy was performed. The tumour showed focal cellular positivity for cytokeratin, negative immunoperoxidase staining for carcinoembryonic antigen, cytoplasmic tonofilaments and poorly formed microvilli. These features supported a diagnosis of malignant mesothelioma of the mixed type, containing both spindle and pleomorphic cells. The patient died before external beam radiotherapy could be started, and no necropsy was done. The authors believed this to be the youngest reported case. They considered there was sufficient evidence to suggest that the tumour was initiated by the short period of domestic blue asbestos exposure. They concluded that the case highlighted the need for extreme care during exposure to dust environments.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Mesothelioma shortly after brief exposure to asbestos. P. Elmes, K. Browne. 1986;1(8483):746. Letter PubMed · Publisher

  Summary

  This letter responded to a report by Booth and Weaver (Lancet, Feb 22, p 435) of mesothelioma in a young man. Booth and Weaver had attributed it to a short period of domestic blue asbestos exposure during demolition of a wall partition. Elmes and Browne asked whether the presence of asbestos had been established. Even assuming asbestos exposure, they doubted this cause because the latent period was short and the exposure brief. They stated that in published studies of industrial workers, no case among many hundreds of mesotheliomas had a latent period of less than 13 years. In Baris' series of 185 cases from rural Anatolia, attributed mainly to erionite, continuous exposure from infancy required a latent period at least twice as long. They cited direct and indirect evidence that common environmental or domestic exposures rarely if ever cause mesothelioma. They also noted earlier young cases, including 23 (0.5%) below age 26 in a review of 4710 published cases and 12 of 509 (2.4%) below age 30 in a South African review. They put the incidence in unexposed people at about 1 per million per year. Series from Britain and North America found cases with no identifiable asbestos exposure, and series from Los Angeles and France suggested that unexposed cases had a younger mean age. They concluded that the case was probably in this unexposed category and asked for a lung fibre burden estimate. In a reply, Booth stated that asbestos was improbable but not impossible as the cause.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Predicting the risks from asbestos. 1986;1(8487):954. Editorial PubMed

• Tobacco and asbestos litigation. T.R. Goffe. 1986;2(8510):811-2. Letter PubMed · Publisher

• Tobacco and asbestos litigation. K. Anderson, F. Moran. 1986;2(8514):1038. Letter PubMed · Publisher

• Early peritoneal mesothelioma: a treatable malignancy. K.H. Antman, R.T. Osteen, K.L. Klegar, et al. 1985;2(8462):977-81. PubMed · Publisher

  Abstract

  37 patients with malignant peritoneal mesothelioma were studied to assess the efficacy of combined therapy. 14 patients presented after 1982. Of 6 patients treated intensively, all remain alive with no evidence of disease by computed tomographic scan at 9-36 months. Of 8 patients treated palliatively, 5 are dead. (5 had stable disease, 1 has progressed despite all treatment, and 2 were not treated.) Survival of the intensively treated group is significantly better than that of other stage I patients in this series. Patients under 40 had a significantly better survival rate than older patients.

• Asbestos and the pathologist. 1984;1(8371):262. Editorial PubMed

• Long fibre asbestos in a chrysotile textile worker. A. Churg, R.A. Harley. 1984;1(8381):845. Letter PubMed · Publisher

  Summary

  The authors addressed epidemiological evidence that workers using processed chrysotile, for example in the textile industry, may have more asbestosis and lung carcinoma than chrysotile miners with comparable dust exposure, possibly because of differences in fibre size. They carried out a mineralogical study of the lung of a long-term worker at an asbestos textile plant in South Carolina who had died of asbestosis. Formalin-fixed post-mortem lung tissue was dissolved in bleach, and the mineral particles were collected and analysed. Fibre sizes were compared with those found in a group of Quebec chrysotile industry workers. In the textile worker, 47% of chrysotile fibres were longer than 5 µm, compared with 15% in the chrysotile miners. For tremolite group amphiboles (tremolite, actinolite and anthophyllite, which are natural components of the chrysotile ore body) the figures were 18% and 6%. The authors described a marked shift towards longer chrysotile fibres in the textile worker and a less pronounced but probably significant shift for the tremolite group. They noted general agreement that long fibres are associated with disease. On that basis they concluded that their findings offered an explanation for the differences in disease incidence between textile and mining groups. They also noted that long tremolite fibres, which were found in this lung, have considerable potential for inducing mesothelioma, whereas the carcinogenic potential of chrysotile fibres in man is in dispute.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos and non-Hodgkin's lymphoma. 1983;1(8317):189-90. Case report · Letter PubMed

• Asbestos exposure and non-Hodgkin's lymphoma. H. Olsson, L. Brandt. 1983;1(8324):588. Letter PubMed · Publisher

  Summary

  In this letter, the authors responded to a case-control study by Ross and colleagues that had reported a relation between asbestos exposure and histiocytic lymphomas primary to the oral cavity and gastrointestinal tract. Using a standardised questionnaire and personal interviews, the authors had obtained occupational histories from school age to diagnosis for a consecutive series of 169 men with recently diagnosed non-Hodgkin's lymphoma admitted to their hospital in Lund, southern Sweden, in 1979-82. Lymphomas were classified according to Rappaport, and all patients were clinically staged. Eleven patients had histiocytic lymphoma in the oral cavity or gastrointestinal tract without signs of systemic disease, and six more had such lymphomas there and at other sites. The authors stated that none of these 17 had been occupationally exposed to asbestos for 6 months or more. They reported that 3 of the 11 (27%) with lymphoma primary to these sites may have been exposed to asbestos in some prior occupation. This compared with 7 of 39 (18%) with histiocytic lymphoma presenting elsewhere, a difference that was not significant (p>0.30). The authors concluded that their data did not support the reported relation. They suggested that the discrepancy might reflect differing exposure criteria or regional differences in environmental hazards between Los Angeles and southern Sweden, and called for further epidemiological studies in various parts of the world.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos-like fibres of biogenic silica in sugar cane. R.H. Newman. 1983;2(8354):857. Letter PubMed · Publisher

  Summary

  In this letter, the author asked whether sugar cane leaf contains fibres that resemble asbestos. He noted that asbestos dust is linked to pulmonary fibrosis, bronchogenic carcinoma and mesothelioma, and that fibre size and shape are thought to govern carcinogenicity. He also noted that plant silica has been linked to bronchiolitis obliterans and to oesophageal cancer in parts of Africa, north-east Iran and northern China. Sugar cane fields may be set on fire before harvest, which creates large quantities of airborne plant residue. The author examined leaf from immature and one-year-old sugar cane from Trinidad. The leaf was either ashed by heating to red heat or digested in concentrated nitric acid. Residues were examined by scanning electron microscopy, and their elemental composition was determined by energy-dispersive X-ray analysis. The residues contained silica structures from the epidermis, mesophyll, prickle hairs and hypoderm, and were composed almost entirely of silicon. From 5 g of nitric acid digest of mature leaf, 150 hypoderm fibres were obtained. They were 0.85 µm in diameter and 10-300 µm long, with a modal length of 200 µm. Biogenic silica made up 5-7% (as printed in the extracted text) of the weight of mature dried leaf. The author concluded that these dimensions are similar to those of asbestos and may have implications for carcinogenesis among sugar cane workers.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos: further steps towards reducing the risks. 1983;2(8349):563. PubMed

• Exposure to asbestos versus organic fibrous dusts. G.D. Clarke, R.H. Newman, C.H. O'Neill, et al. 1983;2(8364):1423-4. Letter PubMed · Publisher

• Man-made mineral fibres--a safe alternative to asbestos?. 1983;2(8359):1125. Editorial PubMed

• Standards for asbestos exposure. N. Stack. 1983;2(8364):1424. Letter PubMed · Publisher

• Trends in mortality of diffuse malignant mesothelioma of pleura. V.E. Archer, W.N. Rom. 1983;2(8341):112-3. Letter PubMed · Publisher

  Summary

  In this letter the authors asked whether the rise in world asbestos use, from about 1 million to 5 million tons between 1950 and 1975, had been followed by an increase in diffuse malignant mesothelioma of the pleura (DMMP). They used a National Cancer Institute compilation of United States cancer deaths to construct age- and sex-specific mortality curves for malignant neoplasms of the pleura. They omitted 1950-57, when DMMP was not separated from other lung and chest neoplasms. They analysed 1958-67 (code 162.2) and 1968-77 (code 163.0) separately because the coding was not comparable, and they gave 90% confidence limits for selected points. No significant secular trends were found. For 1958-67 there was no indication of a change in any age group. For 1968-77 there was a non-significant suggestion that, in both sexes, rates fell among people under 60 and rose among those aged 60-74. Below age 45, rates were comparable between the sexes. Above age 45, rates for males were about twice those for females, which the authors attributed to occupational differences such as insulating and plumbing work. They concluded that by 1978 the increased use of asbestos had produced at most a small increase in DMMP, apparently limited to people exposed occupationally. They also concluded that the lack of any increase among people under 45 suggested consumer asbestos products had been largely innocuous. They called for further study of trends in the 1980s to allow for the 20-40 year latent period.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos exposure and lymphomas of the gastrointestinal tract and oral cavity. R. Ross, R. Dworsky, P. Nichols, et al. 1982;2(8308):1118-20. PubMed · Publisher

  Abstract

  An epidemiological case-control study of non-Hodgkin's lymphomas revealed an excess of male patients with large-cell lymphomas primary to the gastrointestinal tract and oral cavity who had evidence of substantial exposure to asbestos. Between 1977 and 1981, 28 men with large-cell lymphomas primary to these sites were interviewed about previous environmental exposure. Pathology slides from 26 of these cases were reviewed by haematopathologists, who confirmed each to be non-Hodgkin's lymphoma of large-cell type. Neighbourhood controls were matched to patients for age, race, and sex. 13 matched pairs were discordant for asbestos exposure, and in 12 of these the exposed individual was a lymphoma patient. 10 patients and 1 control also reported a history of malaria.

• Asbestos exposure and malignant lymphoma. N.O. Bengtsson, L. Hardell, M. Eriksson. 1982;2(8313):1463. Letter PubMed · Publisher

• Mesothelioma in a brake repair worker. A.M. Langer, W.T. McCaughey. 1982;2(8307):1101-3. Case report · Letter PubMed · Publisher

  Summary

  This letter described a case of diffuse pleural mesothelioma in a man whose only known asbestos exposure was to chrysotile during brake maintenance and repair. A 55-year-old man was admitted to hospital in October 1980 with right-sided chest pain. Chest X-ray showed a right-sided pleural effusion, and a cytological diagnosis of mesothelioma was confirmed by biopsy and examination of resected tumour. He died in September 1981. Since age 19 he had serviced automobiles, including replacing brake linings, and had worked in used car, tyre and car repair businesses. He had no history of construction, shipyard or other occupational asbestos contact and had never lived near an asbestos-fabricating plant. Necropsy showed an epithelial type diffuse malignant mesothelioma, with slight interstitial fibrosis and anthracosis of the lung. No typical asbestos bodies were seen in tissue, and only one was found after ashing. Lung tissue (6310 mg) was digested and the residue examined by electron microscopy. Electron diffraction confirmed chrysotile fibrils, including fibrils longer than 5 µm. No amphibole fibres were found. The authors noted that brake repair work, particularly bevelling, refurbishing and refitting brake pads, can release unaltered chrysotile fibre. They stated that analytical electron microscopy may be essential for diagnosis in chrysotile-exposed people. They also stated that, given the large number of workers involved, more cases may be seen in the future.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Mysterious pleural effusions. 1982;1(8283):1226. Editorial PubMed

• Amosite asbestos and mesothelioma. 1981;2(8260-61):1397-8. Editorial PubMed

• Asbestos in water. 1981;2(8238):132. Editorial PubMed

• Asbestos in water. R. Murray, K. Browne. 1981;2(8243):415. Letter PubMed · Publisher

• Malignant mesothelioma and radiological chest abnormalities in two villages in Central Turkey. An epidemiological and environmental investigation. Y.I. Baris, R. Saracci, L. Simonato, et al. 1981;1(8227):984-7. PubMed · Publisher

  Abstract

  A comparative epidemiological and environmental study in two neighbouring villages, Karain and Karlin, in Central Turkey showed an excess adult mortality, shortening of life expectancy, and an excess of pleural radiological abnormalities in Karain. This supports an earlier report of an endemic of pleural mesothelioma in the village. Concentrations of airborne respirable fibres were uniformly very low in Karlik and higher in some of the air samples from Karain, the fibres being similar in composition to those of erionite-a mineral of the zeolite family and the major contributor to the Karain clouds. This is compatible with the hypothesis of a causal association between endemic mesothelioma and inhalation of erionite fibres, but the fibre concentrations in all samples are so low as to leave in question the aetiological role of erionite. In addition to their local importance these results may have relevance for the wider scientific and public-health issue of long-term inhalation of mineral fibres at low concentrations.

• Mesothelioma in a factory using amosite and chrysotile asbestos. E.D. Acheson, C. Bennett, M.J. Gardner, et al. 1981;2(8260-61):1403-6. PubMed · Publisher

  Abstract

  5 deaths have been certified as due to mesothelioma (4 pleural and 1 peritoneal) in men who worked at a London factory where insulation board has been manufactured since 1946 from a mixture of amosite and chrysotile asbestos. It seems reasonable to relate 4 of these cases to work at the factory. Amosite has been the fibre predominantly in use and seems likely to be the cause of the tumours.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Possible synergism between chrysotile and amphibole asbestos. E.D. Acheson, M.J. Gardner. 1980;1(8170):706. Letter PubMed

1970s

• Age and latency in mesothelioma. G. McDonald, A. McDonald. 1979;2(8151):1074. Letter PubMed · Publisher

• Asbestos and health. 1979;2(8148):887. Editorial PubMed

• Cosmetic talc and ovarian cancer. D.L. Longo, R.C. Young. 1979;2(8150):1011-2. Letter PubMed · Publisher

• Cosmetic talc and ovarian cancer. D.L. Longo, R.C. Young. 1979;2(8138):349-51. PubMed · Publisher

  Abstract

  The causes of ovarian cancer are unknown. The increased incidence in industrialised countries suggests an environmental influence. Epidemiological, experimental, and clinical data seem to link asbestos and talc with ovarian cancer. Direct passage of talc or asbestos-contaminated talc through the female reproductive tract to the ovarian surface may play an ætiological role. Further systematic evaluation of talc and asbestos as ovarian carcinogens is needed.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Isolation of diatoms and asbestos bodies from lungs by subtilisin-A. A.A. Watson, J.S. Oliver. 1979;2(8148):913-4. Letter PubMed · Publisher

• Latency period for mesothelioma. A. Chovil, C. Stewart. 1979;2(8147):853. Letter PubMed · Publisher

  Summary

  In this letter, the authors questioned the impression given by some textbooks and papers that asbestos-related mesothelioma develops in old age, a very long time after exposure. They described the cases of mesothelioma attributable to occupational asbestos exposure that the Workmen's Compensation Board of Ontario, Canada, had compensated since 1970. Claims had been accepted for 26 cases that occurred between 1958 and 1978. Most of the workers had been in industries with high potential exposures, mainly to chrysotile fibres. Age at diagnosis (or death) ranged from 37 to 78 years, with a mean of 56.0 years. Latency, defined as the period from first known exposure to diagnosis, ranged from 6 to 44 years, with a mean of 26.9 years. The authors noted that they could not rule out additional earlier non-occupational exposure. Nineteen of the cases were pleural in origin and 7 were peritoneal. The authors stated that their series was small but did not fit the textbook picture. They noted that Elmes and Simpson had suggested that latency for this tumour may be a function of dose, and that this may account for their observations.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos on Maryland's roads. A.M. Langer, A.N. Rohl, I.J. Selikoff. 1978;1(8076):1263-4. Letter PubMed · Publisher

• Non-occupational exposure to asbestos and malignant mesothelioma in females. N.J. Vianna, A.K. Polan. 1978;1(8073):1061-3. PubMed · Publisher

  Abstract

  A study of the occupational histories of 52 females with malignant mesothelioma and certain of their relatives, carried out to measure the risk of this disorder attributable to indirect asbestos exposure, showed that a significantly greater number of husbands and fathers of cases than of controls worked in asbestos-related industries, and the relative risk for this factor was 10. The frequency of parental cancer, especially gastrointestinal malignancy, was also significantly greater for cases than for their controls. This raises the possibility of a genetic predisposition to malignant mesothelioma.

• Non-occupational exposure to asbestos and malignant mesothelioma. S.F. McCullagh. 1978;2(8088):521-2. Letter PubMed · Publisher

• Non-occupational exposure to asbestos. S.F. McCullagh. 1978;2(8094):844. Letter PubMed · Publisher

• Proposals on asbestos. 1978;1(8076):1243. Editorial PubMed

• The hygiene standard for chrysotile asbestos. J. Peto. 1978;1(8062):484-9. PubMed · Publisher

  Abstract

  Previous studies, including the analysis on which the current 2 fibres/cm3 hygiene standard is based, may have underestimated the risk of morbidity or mortality following exposure to low levels of asbestos dust. Accurate dose-response data at levels below 2 fibres/cm3 are unlikely to be available for the foreseeable future, and the biologically plausible assumption that excess cancer mortality is approximately proportional to dust level should be provisionally accepted. It may be reasonable, however, to postulate a safe threshold for mortality from asbestosis. If excess mortality from asbestos-related disease is proportional to dust level for each cause, approximately 10% of male asbestos workers might, under certain assumptions, eventually die of asbestos-induced disease after 50 years' exposure at 2 fibres/cm3. Peritoneal mesothelioma is usually due to crocidolite (blue asbestos) or other amphiboles, but exposure to chrysotile (white asbestos) alone may lead to a substantial risk of pleural mesothelioma. These predictions are based on rather small numbers in a single factory, and further studies in other working environments are required. Fibre counts based on optical microscopy are likely to be less relevant than total counts by electron microscopy, and excess mortality is virtually confined to men first exposed more than 20 years ago, when little or no accurate data on dust levels were collected.

• Asbestos. 1977;2(8050):1211-2. Editorial PubMed

• Community exposure to asbestos. D. Davies. 1977;2(8044):924. Letter PubMed · Publisher

• Asbestos and cancer of head and neck. P.M. Stell, T. McGill. 1973;1(7804):678. PubMed · Publisher

  Summary

  This letter reported a hospital-based comparison of workplace asbestos exposure among patients with head and neck cancer. The authors, at the Ear, Nose and Throat Infirmary of the University of Liverpool, questioned 100 male patients with carcinoma of the head and neck about their exposure to asbestos. They also collected data from 100 controls, matched for age and sex, who were attending the hospital for various non-malignant diseases. No dates for the study were given. In all, 22 of the cancer patients had been exposed to asbestos at work, compared with 2 of the controls. The occupations with asbestos exposure most often reported were unloading raw asbestos on the docks, scaling boilers, and insulating pipes with asbestos. The latent interval between the start of exposure and the development of carcinoma was 31 years, and the average period of exposure was 24 years. The authors reported that the difference between patients and controls for the whole group was statistically highly significant (χ2 = 16.6, n = 1). They stated that their table, which broke the results down by cancer site, suggested that asbestos exposure was most likely to be important in laryngeal carcinoma. They reported that a more detailed study of this group was being undertaken.

  PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

• Asbestos and cancer of head and neck. S. Holmes. 1973;1(7807):839. PubMed · Publisher

• Asbestos and laryngeal carcinoma. P.M. Stell, T. McGill. 1973;2(7826):416-7. PubMed · Publisher

  Abstract

  One hundred male patients with squamous carcinoma of the larynx and one hundred matched controls with various non-malignant diseases were questioned about their exposure to asbestos. Thirty-one patients and three controls had experienced an important degree of exposure to asbestos. The difference between the two groups was statistically highly significant. The average latent interval between first exposure and development of laryngeal carcinoma was 30 years, and the average duration of exposure was 27 years.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Asbestos leads to lung cancer leads to mesothelioma. 1973;1(7807):815-6. PubMed

• Fibroblast anchorage in carcinogenesis by fibres. N.G. Maroudas, C.H. O'Neill, M.F. Stanton. 1973;1(7807):807-9. PubMed · Publisher

  Abstract

  A correlation is drawn between the lengths of asbestos and other mineral fibres which will induce mesothelioma in the rat, and the lengths of glass fibres which will induce growth of fibroblasts in culture. Particles smaller than 20 µ in length induce neither growth in vitro nor mesothelioma in vivo. It is postulated that fibres induce two basic types of cellular reaction, according to length—anchorage-dependent growth (40-320 µ) and phagocytosis (below 20 µ). The resultant hyperplasia, in mesenchymal or reticuloendothelial tissue, leads to mesothelioma or histiocytic lymphoma, respectively.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Combined effect of asbestos exposure and smoking on mortality from lung cancer in factory workers. G. Berry, M.L. Newhouse, M. Turok. 1972;2(7775):476-8. PubMed · Publisher

1960s

• Dangers of asbestos. 1968;1(7532):32-3. PubMed
• Detection o asbestos in asbestos bodies. P.R. Peacock. 1968;1(7552):1153-4. PubMed · Publisher
• Pleural mesothelioma in an asbestos worker. 1968;1(7540):469. PubMed
• Control of the asbestos hazard. 1967;1(7503):1311-2. PubMed
• Health hazards of asbestos. 1966;1(7436):530-1. PubMed
• Asbestosis and abdominal neoplasms. E.E. Keal. 1960;2(7162):1211-6. PubMed · Publisher

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