The New England Journal of Medicine

Our medical research library holds 57 studies published in The New England Journal of Medicine (1965–2024). 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. 6 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 9 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: Massachusetts Medical Society
• Published: 1928 to the present, United States
• Language: English
• ISSN: 0028-4793 (print), 1533-4406 (electronic)
• Continues: Boston Medical and Surgical Journal
• Its record in the NLM Catalog

2020s

• Pleural Plaques from Secondhand Asbestos Exposure. S. Chillag, R.S. Morehead. 2024;391(23):2255. Case report PubMed · Publisher

2010s

• A Most Reckless Proposal - A Plan to Continue Asbestos Use in the United States. P.J. Landrigan, R.A. Lemen. 2019;381(7):598-600. Historical article PubMed · Publisher

  Summary

  In this Perspective article, the authors, both former senior officials of the National Institute for Occupational Safety and Health, discussed U.S. regulation of asbestos. They stated that nearly 40,000 Americans die each year from asbestos-related diseases, and that U.S. asbestos use fell by more than 99%, from more than 650,000 metric tons in 1963 to roughly 750 metric tons in 2018. They noted that asbestos has never been permanently banned in the United States. Permitted uses include chlorine and caustic soda production in chloralkali plants, sheet gaskets, oil-field brake blocks, and aftermarket brakes for trucks and buses. They described the 1991 court decision that overturned the Environmental Protection Agency's 1989 ban attempt. They also described the stalled review of asbestos under the 2016 Frank R. Lautenberg Chemical Safety for the 21st Century Act. The authors argued that the EPA's significant new use rule, which took effect on June 24, 2019, created loopholes. In their view, it permitted continued use, mining and importation of asbestos, and set out a process for industries to propose new uses. They feared that another generation of workers would be exposed. They concluded that the Alan Reinstein Ban Asbestos Now Act of 2019, introduced on March 7, which would ban the import, manufacture, processing and distribution of all asbestos, deserved to be enacted.

  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.

• Fibulin-3 as a biomarker for pleural mesothelioma. K. Hollevoet, E. Sharon. 2013;368(2):189. Letter · Comment PubMed · Publisher · Free full text

  Summary

  In this letter, the authors commented on a study by Pass et al. that had reported fibulin-3 as a new soluble biomarker for malignant mesothelioma. They noted that the diagnostic accuracy of plasma fibulin-3 levels in the Detroit and New York cohorts (area under the receiver-operating-characteristic curve [AUC], 0.99) exceeded that of any previously reported marker. In the external validation cohort, however, accuracy fell to an AUC of 0.87. The authors suggested this decrease was probably due to differences in the study population, although the study had shown no association between plasma fibulin-3 levels and common patient characteristics. They called for research to identify the factors that affect plasma fibulin-3 levels. They pointed out that the AUC of 0.87 was similar to values previously reported for serum mesothelin, which they described as the standard biomarker for mesothelioma (AUC, 0.72 to 0.93). They added that data from matched analyses comparing or combining fibulin-3 with mesothelin were lacking. They concluded that future validation efforts should continue to focus on the performance of fibulin-3 in early-stage disease and should maintain the high standards of the study by Pass et al. In the accompanying reply, Pass and Goparaju reported a post hoc analysis of 29 patients with mesothelioma and 41 patients exposed to asbestos from their Detroit cohort. It showed an AUC of 0.74 for soluble mesothelin-related peptides and 1.0 for fibulin-3.

  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.

• Fibulin-3 as a biomarker for pleural mesothelioma. H.I. Pass, C. Goparaju. 2013;368(2):190. Letter · Comment PubMed · Publisher

  Summary

  In this reply, Pass and Goparaju responded to two letters, one from Hollevoet and Sharon and one from Lamote and colleagues, about their earlier report on fibulin-3 as a blood and effusion biomarker for pleural mesothelioma. They agreed that well-designed prospective studies were needed, both for further diagnostic validation and to explore the preclinical efficacy of fibulin-3. They questioned whether soluble mesothelin-related peptides were really a "standard" biomarker for mesothelioma. They noted that their blinded validation study, which showed an area under the curve (AUC) of 0.87, was one of the only blinded validation studies in mesothelioma. They wrote that many biomarkers fail validation because of differences in patient characteristics such as glomerular filtration rate and body-mass index, poor procedures for harvesting, processing and storing samples, and inappropriate controls. They said this experience had led them to prefer plasma over serum. They reported a post hoc analysis of matched samples from their Detroit cohort: 29 patients with mesothelioma and 41 people exposed to asbestos. In this analysis the AUC was 0.74 for serum soluble mesothelin-related peptides and 1.0 for plasma fibulin-3. Citing other studies, they reported that the AUC for mesothelin-related peptides fell to 0.69 when patients with non-mesothelioma metastases were the comparison group, against 0.94 for fibulin-3. They agreed that blinded validation of other markers, alone and combined with fibulin-3, was lacking. They added that preliminary observations suggested the fibulin-3 level in pleural effusions was an independent prognostic factor.

  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.

• Fibulin-3 as a biomarker for pleural mesothelioma. K. Lamote, P. Baas, J.P. van Meerbeeck. 2013;368(2):189-90. Letter · Comment PubMed · Publisher

• Fibulin-3 as a blood and effusion biomarker for pleural mesothelioma. H.I. Pass, S.M. Levin, M.R. Harbut, et al. 2012;367(15):1417-27. PubMed · Publisher · Free full text

  Abstract

  Background: New biomarkers are needed to detect pleural mesothelioma at an earlier stage and to individualize treatment strategies. We investigated whether fibulin-3 in plasma and pleural effusions could meet sensitivity and specificity criteria for a robust biomarker.

  Methods: We measured fibulin-3 levels in plasma (from 92 patients with mesothelioma, 136 asbestos-exposed persons without cancer, 93 patients with effusions not due to mesothelioma, and 43 healthy controls), effusions (from 74 patients with mesothelioma, 39 with benign effusions, and 54 with malignant effusions not due to mesothelioma), or both. A blinded validation was subsequently performed. Tumor tissue was examined for fibulin-3 by immunohistochemical analysis, and levels of fibulin-3 in plasma and effusions were measured with an enzyme-linked immunosorbent assay.

  Results: Plasma fibulin-3 levels did not vary according to age, sex, duration of asbestos exposure, or degree of radiographic changes and were significantly higher in patients with pleural mesothelioma (105±7 ng per milliliter in the Detroit cohort and 113±8 ng per milliliter in the New York cohort) than in asbestos-exposed persons without mesothelioma (14±1 ng per milliliter and 24±1 ng per milliliter, respectively; P<0.001). Effusion fibulin-3 levels were significantly higher in patients with pleural mesothelioma (694±37 ng per milliliter in the Detroit cohort and 636±92 ng per milliliter in the New York cohort) than in patients with effusions not due to mesothelioma (212±25 and 151±23 ng per milliliter, respectively; P<0.001). Fibulin-3 preferentially stained tumor cells in 26 of 26 samples. In an overall comparison of patients with and those without mesothelioma, the receiver-operating-characteristic curve for plasma fibulin-3 levels had a sensitivity of 96.7% and a specificity of 95.5% at a cutoff value of 52.8 ng of fibulin-3 per milliliter. In a comparison of patients with early-stage mesothelioma with asbestos-exposed persons, the sensitivity was 100% and the specificity was 94.1% at a cutoff value of 46.0 ng of fibulin-3 per milliliter. Blinded validation revealed an area under the curve of 0.87 for plasma specimens from 96 asbestos-exposed persons as compared with 48 patients with mesothelioma.

  Conclusions: Plasma fibulin-3 levels can distinguish healthy persons with exposure to asbestos from patients with mesothelioma. In conjunction with effusion fibulin-3 levels, plasma fibulin-3 levels can further differentiate mesothelioma effusions from other malignant and benign effusions. (Funded by the Early Detection Research Network, National Institutes of Health, and others.).

2000s

• The legacy of World Trade Center dust. J.M. Samet, A.S. Geyh, M.J. Utell. 2007;356(22):2233-6. PubMed · Publisher

  Summary

  In this Perspective article, published more than 5 years after the World Trade Center disaster of September 11, 2001, the authors reviewed evidence on the health risks of inhaling dust from the collapse of the twin towers, the fires, and the cleanup. Air was not sampled immediately after the collapse. Settled dust contained combustion-related carcinogens, building materials, and some asbestos. Most Environmental Protection Agency samples had asbestos content below the clearance threshold used for schools. The authors judged that some site workers probably inhaled asbestos fibers. They judged that exposure among nearby residents and workers was probably too low to cause asbestosis or a measurable rise in lung cancer risk, although it might slightly increase mesothelioma risk, which would not become evident for decades. Firefighters developed "World Trade Center cough." Those on site the first morning had three times the bronchial hyperreactivity of later arrivals. In the year after the disaster, firefighters lost about 320 ml in forced expiratory volume in 1 second, compared with an expected 30 ml. Residents within 1.5 km of the site reported more respiratory symptoms than people in a control area. The authors concluded that uncertainty about exposure will not be reduced. They stated that cancer risks will not be apparent for decades. They said prospective studies, including the World Trade Center Health Registry of more than 71,000 registrants, will be needed, though some questions may never be answered.

  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 serum osteopontin. A. Hiraki, K. Aoe, H. Ueoka. 2006;354(3):304-5; author reply 304-5. Comment · Letter PubMed

• Asbestos exposure and serum osteopontin. A.W. O'Regan, D. Serlin, J.S. Berman. 2006;354(3):304-5; author reply 304-5. Comment · Letter PubMed · Publisher

  Summary

  This item is published correspondence about a study by Pass et al. on serum osteopontin levels in asbestos-exposed workers and in patients with pleural mesothelioma. O'Regan, Serlin and Berman questioned osteopontin's usefulness as a tumor marker. They noted that osteopontin is expressed in numerous benign inflammatory and fibrotic lung diseases. They also noted that levels similar to those seen with lung carcinoma occur in tuberculosis, interstitial lung diseases and cardiac disease, which pose diagnostic difficulties in patients with asbestos-related pleural disease. They suggested that future studies might define osteopontin variants with higher diagnostic potential, but concluded that until then its specificity was too low for use as a screening tool for mesothelioma. In an accompanying letter, Hiraki, Aoe and Ueoka reported pleural-fluid osteopontin in 9 patients with pleural mesothelioma and 27 with various nonmalignant diseases. Mean levels were 22,692 versus 9575 ng per milliliter (P<0.001), and the area under the ROC curve was 0.885. At a cutoff of 11,436 ng per milliliter, sensitivity was 100 percent and specificity 77.8 percent. In reply, Pass and colleagues stressed studying an appropriate high-risk asbestos-exposed cohort prospectively. They said a National Cancer Institute validation study would address specificity, and that the Hiraki data needed comparison with effusions from asbestos-exposed people without cancer.

  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.

• Advances in malignant mesothelioma. B.W. Robinson, R.A. Lake. 2005;353(15):1591-603. Review PubMed · Publisher

  Summary

  This review article summarized advances in the understanding, diagnosis and management of malignant mesothelioma over the preceding 5 to 10 years. The authors described the tumor as an aggressive cancer of serosal surfaces such as the pleura and peritoneum. Its incidence was increasing worldwide, probably as a result of widespread exposure to asbestos. They reviewed the clinical features and the causes of the disease. They named asbestos as the principal carcinogen and noted continuing debate about whether chrysotile causes mesothelioma, as well as a possible but unproved role for simian virus 40. They also reviewed the epidemiology, including predicted peak years of incidence and estimated compensation costs of up to $200 billion in the United States and $80 billion in Europe over the next 40 years. They outlined four processes by which asbestos may affect the pleura and the biologic features of mesothelioma cells. The diagnostic sections covered cytology, immunohistochemistry, imaging and serum markers. Serum mesothelin-related protein was elevated in 84 percent of patients with mesothelioma and in less than 2 percent of patients with other pulmonary or pleural diseases. Median survival from diagnosis was 12 months. In a phase 3 study of 448 patients, pemetrexed plus cisplatin gave a longer median survival than cisplatin alone (12.1 vs. 9.3 months). The authors also reviewed surgery, radiotherapy, immunotherapy, gene therapy and palliation. They concluded that the rising incidence and compensation costs gave strong moral and economic reasons for urgent, focused research.

  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, pleural mesothelioma, and serum osteopontin levels. H.I. Pass, D. Lott, F. Lonardo, et al. 2005;353(15):1564-73. PubMed · Publisher

  Abstract

  Background: We investigated the presence of osteopontin in pleural mesothelioma and determined serum osteopontin levels in three populations: subjects without cancer who were exposed to asbestos, subjects without cancer who were not exposed to asbestos, and patients with pleural mesothelioma who were exposed to asbestos.

  Methods: A group of 69 subjects with asbestos-related nonmalignant pulmonary disease were compared with 45 subjects without exposure to asbestos and 76 patients with surgically staged pleural mesothelioma. Tumor tissue was examined for osteopontin by immunohistochemical analysis, and serum osteopontin levels were measured by an enzyme-linked immunosorbent assay.

  Results: There were no significant differences in mean (+/-SE) serum osteopontin levels between age-matched subjects with exposure to asbestos and subjects without exposure to asbestos (30+/-3 ng per milliliter and 20+/-4 ng per milliliter, respectively; P=0.06). In the group with exposure to asbestos, elevated serum osteopontin levels were associated with pulmonary plaques and fibrosis (56+/-13 ng per milliliter) but not with normal radiographic findings (21+/-5 ng per milliliter), plaques alone (23+/-3 ng per milliliter), or fibrosis alone (32+/-7 ng per milliliter) (P=0.004). Serum osteopontin levels were significantly higher in the group with pleural mesothelioma than in the group with exposure to asbestos (133+/-10 ng per milliliter vs. 30+/-3 ng per milliliter, P<0.001). Immunohistochemical analysis revealed osteopontin staining of the tumor cells in 36 of 38 samples of pleural mesothelioma. An analysis of serum osteopontin levels comparing the receiver-operating-characteristic curve in the group exposed to asbestos with that of the group with mesothelioma had a sensitivity of 77.6 percent and a specificity of 85.5 percent at a cutoff value of 48.3 ng of osteopontin per milliliter. Subgroup analysis comparing patients with stage I mesothelioma with subjects with exposure to asbestos revealed a sensitivity of 84.6 percent and a specificity of 88.4 percent at a cutoff value of 62.4 ng of osteopontin per milliliter.

  Conclusions: Serum osteopontin levels can be used to distinguish persons with exposure to asbestos who do not have cancer from those with exposure to asbestos who have pleural mesothelioma.

  Copyright 2005 Massachusetts Medical Society.

• Serum osteopontin levels--is it time to screen asbestos-exposed workers for pleural mesothelioma?. M.R. Cullen. 2005;353(15):1617-8. Comment · Editorial PubMed · Publisher

  Summary

  In this editorial, the author commented on a study by Pass et al., published in the same issue, of serum osteopontin levels as a marker of pleural mesothelioma in asbestos-exposed people. He noted that 2500 to 3000 mesothelioma cases occurred annually in the United States, that mean survival after diagnosis remained 6 to 10 months, and that there was no well-validated blood test. He described the osteopontin test as appearing reliable and straightforward. Its sensitivity and specificity allowed mesothelioma to be identified among workers with similar asbestos exposure, many with asbestosis or benign pleural lesions, and its results were better than or rivalled other available tests. He argued that its diagnostic value still had to be assessed in other asbestos-related conditions, such as diffuse pleural thickening, lung cancer with pleural involvement and rounded atelectasis. On screening, he cited unpublished data on 4060 heavily exposed men in the Beta-Carotene and Retinol Efficacy Trial. Over 12 to 19 years, their cumulative mesothelioma risk was 0.9 percent (38 cases), compared with 6.9 percent for lung cancer (282 cases). At such risk levels, he wrote, the test's predictive value would be very low. It was also unknown whether early detection changed outcome. He concluded that surveillance should focus on lung cancer and other more treatable asbestos-related cancers, while the findings offered a faint glimmer of hope. The author reported being medical director of Alcoa.

  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.

• Clinical problem-solving. Red snapper or crab?. P.B. Cornia, B.A. Lipsky, G. Dhaliwal, et al. 2004;350(14):1443-8. Case report PubMed · Publisher

• Cough and bronchial responsiveness in firefighters at the World Trade Center site. J.H. Lange. 2003;348(1):76-7; author reply 76-7. Comment · Letter PubMed

1990s

• Asbestos--still a carcinogen. P.J. Landrigan. 1998;338(22):1618-9. Comment · Editorial PubMed · Publisher

  Summary

  In this editorial, the author commented on a study by Camus et al., in the same journal issue, of nonoccupational asbestos exposure among women in the asbestos-mining townships of Quebec. He summarized evidence that all commercial forms of asbestos, including chrysotile, cause lung cancer, mesothelioma and other asbestos-related diseases. He also described how asbestos in buildings is managed in place under the 1986 Asbestos Hazard Emergency Response Act. Camus et al. had found no excess lung cancer mortality among the women. They also found that excess lung cancer deaths were at least 10 times fewer than an EPA risk-assessment model predicted, that the pleural cancer death rate was more than seven times that in nonmining areas (relative risk 7.63), and that asbestosis mortality was substantially increased. The author weighed possible explanations: a threshold or flatter dose-response at low doses, which he called speculative; overestimated past exposure; and exposure to chrysotile only. He judged it most plausible that many airborne particles in mining areas were too large to reach the lungs, so that light-microscopy counts overstated alveolar exposure. He concluded that the population's highly atypical exposure made the study an inappropriate basis for revising US building regulations. He also concluded that the pleural cancer excess confirmed chrysotile as a potent carcinogen, and that claims that chrysotile can be used safely in developing nations are contrary to fact and extremely dangerous.

  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.

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. B.W. Case. 1998;339(14):1001; author reply 1002. Comment · Letter PubMed

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. H. Demiroglu. 1998;339(14):999-1000; author reply 1001-2. Comment · Letter PubMed

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. R.W. Morgan, M. Goodman. 1998;339(14):1001; author reply 1002. Comment · Letter PubMed

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. A. Churg. 1998;339(14):999; author reply 1001-2. Comment · Letter PubMed · Publisher

  Summary

  In a letter to the editor, Churg responded to a study by Camus et al. of lung cancer risk among women with nonoccupational exposure to chrysotile asbestos in Quebec's mining regions. He argued that the study's standardized mortality ratios for mesothelioma and asbestosis may have been seriously confounded by hidden exposure to the amphibole asbestos types amosite and crocidolite. His laboratory had analyzed many lung specimens obtained at autopsy from chrysotile workers in the Thetford Mines region and from residents who never worked in the mines or mills. As a rule, only chrysotile and tremolite had been found. However, three women from the region who had died of mesothelioma between 1983 and 1988, and who had not worked in the mines or mills, had elevated amosite and crocidolite levels of 100,000, 1,000,000 and 4,300,000 fibers per gram of dry lung. The laboratory's maximal background level was 10,000. These levels were within the range seen in mesothelioma cases among amphibole-exposed workers. The second and third women had levels typical of amphibole-associated asbestosis and had asbestosis at autopsy. Both had worked in an asbestos-bag-repair operation, the probable source of their exposure. The first woman's source was uncertain but was not ambient air. Churg concluded that the cases were probably counted by Camus et al. and that the mesothelioma risk from nonoccupational chrysotile exposure in that population was lower than reported. An editor's note stated that he had served as an expert witness in asbestos litigation. In their reply, Camus and Siemiatycki called his suggestion a possibility to be explored in ongoing research.

  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.

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. M. Camus, J. Siemiatycki, B. Meek. 1998;338(22):1565-71. PubMed · Publisher

  Abstract

  Background: Heavy industrial exposure to asbestos causes lung cancer and mesothelioma, but it remains unknown whether much lower environmental exposure to asbestos also causes these cancers. Nevertheless, regulatory agencies, including the Environmental Protection Agency (EPA), have assessed the risk of lung cancer by extrapolating known risks from past industrial exposure to asbestos to today's much lower environmental asbestos levels (roughly 100,000 times lower). We also tested the EPA's model for predicting the risk of asbestos-induced lung cancer in a population of women with relatively high levels of nonoccupational exposure to asbestos.

  Methods: Mortality among women in 2 chrysotile-asbestos-mining areas of the province of Quebec was compared with mortality among women in 60 control areas, and age-standardized mortality ratios were derived. With the help of an expert panel, we estimated past exposure to asbestos among women in the mining areas and used these data with the EPA's model to predict the relative risk of lung cancer. We then compared this prediction with the observed mortality ratios.

  Results: On the basis of the estimated exposure in the asbestos-mining areas, a relative risk of death due to lung cancer of 2.1 was predicted by the EPA's model, amounting to about 75 excess deaths from lung cancer in this population. By contrast, we calculated a standardized mortality ratio of 1.0 and a standardized proportionate mortality ratio of 1.1 (P> 0.05), suggesting that there were between 0 and 6.5 excess deaths from lung cancer among the women with nonoccupational exposure to asbestos. Seven deaths from pleural cancer were observed (relative risk=7.63; P<0.05).

  Conclusions: We found no measurable excess risk of death due to lung cancer among women in two chrysotile-asbestos-mining regions. The EPA's model overestimated the risk of asbestos-induced lung cancer by at least a factor of 10.

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. A.M. Langer. 1998;339(14):1000-1; author reply 1002. Comment · Letter PubMed

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. E. Costas, A. Garrido, V.J. Goyanes. 1998;339(14):1000; author reply 1001-2. Comment · Letter PubMed

• Nonoccupational exposure to chrysotile asbestos and the risk of lung cancer. R.K. Sokas. 1998;339(14):1000; author reply 1001-2. Comment · Letter PubMed

• Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. G.S. Omenn, G.E. Goodman, M.D. Thornquist, et al. 1996;334(18):1150-5. Randomized trial PubMed · Publisher

  Abstract

  Background: Lung cancer and cardiovascular disease are major causes of death in the United States. It has been proposed that carotenoids and retinoids are agents that may prevent these disorders.

  Methods: We conducted a multicenter, randomized, double-blind, placebo-controlled primary prevention trial -- the Beta Carotene and Retinol Efficacy Trial -- involving a total of 18,314 smokers, former smokers, and workers exposed to asbestos. The effects of a combination of 30 mg of beta carotene per day and 25,000 IU of retinol (vitamin A) in the form of retinyl palmitate per day on the primary end point, the incidence of lung cancer, were compared with those of placebo.

  Results: A total of 388 new cases of lung cancer were diagnosed during the 73,135 person-years of follow-up (mean length of follow-up, 4.0 years). The active-treatment group had a relative risk of lung cancer of 1.28 (95 percent confidence interval, 1.04 to 1.57; P=0.02), as compared with the placebo group. There were no statistically significant differences in the risks of other types of cancer. In the active-treatment group, the relative risk of death from any cause was 1.17 (95 percent confidence interval, 1.03 to 1.33); of death from lung cancer, 1.46 (95 percent confidence interval, 1.07 to 2.00); and of death from cardiovascular disease, 1.26 (95 percent confidence interval, 0.99 to 1.61). On the basis of these findings, the randomized trial was stopped 21 months earlier than planned; follow-up will continue for another 5 years.

  Conclusions: After an average of four years of supplementation, the combination of beta carotene and vitamin A had no benefit and may have had an adverse effect on the incidence of lung cancer and on the risk of death from lung cancer, cardiovascular disease, and any cause in smokers and workers exposed to asbestos.

• Asbestos-related diseases. D.G. Kern, D.C. Christiani, K.T. Kelsey, et al. 1991;324(3):195-7. Comment · Letter PubMed · Publisher

• Asbestos-related diseases. 1990;322(2):129-31. Comment · Letter PubMed · Publisher

• Case 28-1989: pulmonary infiltrates and an axillary mass. E.P. Gabor. 1990;322(2):131. Comment · Letter PubMed · Publisher

1980s

• Asbestos-associated diseases in a cohort of cigarette-filter workers. J.A. Talcott, W.A. Thurber, A.F. Kantor, et al. 1989;321(18):1220-3. PubMed · Publisher

  Abstract

  To estimate the effects on health of occupational exposure to crocidolite, a highly toxic form of asbestos, we studied a cohort of 33 men who worked in 1953 in a Massachusetts factory that manufactured cigarette filters containing crocidolite fibers from 1951 to 1957. Twenty-eight of the men have died, as compared with 8.3 deaths expected. This increased mortality was attributable to asbestos-associated diseases. Fifteen deaths were caused by cancer, as compared with 1.8 expected (relative risk, 8.2; 95 percent confidence interval, 4.6 to 13.4), including eight from lung cancer, five from malignant mesothelioma, and two from other types of cancer. There were seven deaths from nonmalignant respiratory disease, as compared with 0.5 expected (relative risk, 14.7; 95 percent confidence interval, 5.9 to 30.3), of which five were due primarily to asbestosis. In contrast, the mortality rates from cardiovascular diseases and all other causes were not increased. Four of the five living workers have pulmonary asbestosis; three of them have recently diagnosed cancers, including two additional lung cancers. We conclude that the extremely high morbidity and mortality in these workers were caused by intense exposure to crocidolite asbestos fibers.

• Asbestos-related diseases. B.T. Mossman, J.B. Gee. 1989;320(26):1721-30. Review PubMed · Publisher

• Malignant mesothelioma. A cluster in a native American pueblo. R.J. Driscoll, W.J. Mulligan, D. Schultz, et al. 1988;318(22):1437-8. PubMed · Publisher

• Asbestos in play sand. A.M. Langer, R.P. Nolan. 1987;316(14):882. Letter PubMed · Publisher

• Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 4-1987. A 50-year-old man with recurrent pleuropulmonary abnormalities. 1987;316(4):198-208. Case report PubMed · Publisher

• Asbestos in play sand. M. Germine. 1986;315(14):891. Letter PubMed · Publisher

• Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 32-1986. A 74-year-old man with increasing dyspnea. 1986;315(7):437-49. Case report PubMed · Publisher

• Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 27-1982. Pleural thickening in a man with rheumatoid arthritis and exposure to asbestos. 1982;307(2):104-12. Case report PubMed · Publisher

• Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 35-1982. A 29-year-old Puerto Rican man with a miliary pulmonary pattern on radiologic examination. 1982;307(10):605-14. Case report PubMed · Publisher

• Exposure to asbestos and human disease. M.R. Becklake. 1982;306(24):1480-2. Editorial PubMed · Publisher

• Pathogenesis of asbestos-associated diseases. M.E. Meeks. 1982;307(24):1526-7. Letter PubMed

• The pathogenesis of asbestos-associated diseases. J.E. Craighead, B.T. Mossman. 1982;306(24):1446-55. Review PubMed · Publisher

• Pericardial mesothelioma after exposure to asbestos. V.L. Roggli. 1981;304(17):1045. Case report · Letter PubMed · Publisher

• Current concepts: malignant mesothelioma. K.H. Antman. 1980;303(4):200-2. Review PubMed · Publisher

1970s

• Asbestos in schools -- a public health problem. C.M. Spooner. 1979;301(14):782-3. PubMed · Publisher

• Lung cancer after employment in shipyards during World War II. W.J. Blot, J.M. Harrington, A. Toledo, et al. 1978;299(12):620-4. PubMed · Publisher

  Abstract

  A case-control study, undertaken to identify reasons for the exceptionally high rate of lung cancer among male residents of coastal Georgia, revealed a significantly increased risk associated with employment in area shipyards during World War II. The summary relative-risk estimate, adjusted for smoking, other occupations, age, race and county of residence was 1.6 (95 per cent confidence limits = 1.1 to 2.3). A synergistic relation was found between shipyard employment and cigarette smoking. These findings suggest that asbestos and possible other shipyard exposures during wartime employment account for part of the excess mortality from lung cancer in certain coastal areas of the United States.

• Lung cancer in shipyard workers: a plea for prevention. E.L. Wynder. 1978;299(12):651-2. Editorial PubMed · Publisher

• Talc in drugs. M.J. Nicar, D.A. Norman. 1978;299(10):556-7. Letter PubMed · Publisher

• Hazards from asbestos - more problems for hospital staffs. J. Lister. 1976;295(9):490-1. PubMed · Publisher

• "Nonspecific" interstitial pulmonary fibrosis. Association with asbestos fibers detected by electron microscopy. A. Miller, A.M. Langer, A.S. Teirstein, et al. 1975;292(2):91-3. PubMed · Publisher

• Letter: Submicroscopical asbestos fibers and disease. 1975;292(22):1194-6. PubMed

• Letter: Conjugal malignant mesothelioma. G.A. Lillington, R.W. Jamplis, J.R. Differding. 1974;291(11):583-4. PubMed · Publisher

• Malignant mesothelial tumors - histologic type and asbestos exposure. D. Magner, A.D. McDonald. 1972;287(11):570-1. PubMed

• Action on asbestos. B. Gee, A. Bouhuys. 1971;285(23):1317-8. PubMed · Publisher

• Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 14-1971. 1971;284(14):778-86. Case report PubMed · Publisher

• Effects of low concentrations of asbestos. Clinical, environmental, radiologic and epidemiologic observations in shipyard pipe coverers and controls. R.L. Murphy, B.G. Ferris, W.A. Burgess, et al. 1971;285(23):1271-8. PubMed · Publisher

1960s

• Asbestos or ferruginous bodies. E.A. Gaensler, W.W. Addington. 1969;280(9):488-92. Review PubMed · Publisher
• Asbestos bodies in peritoneum. B. Castleman. 1968;278(11):630. PubMed
• Asbestos bodies in peritoneum. H. Levine. 1968;278(11):630. PubMed · Publisher
• Relation between exposure to asbestos and mesothelioma. I.J. Selikoff, J. Churg, E.C. Hammond. 1965;272:560-5. PubMed · Publisher

Browse every journal in the library or the library by type of article, or return to medical research.