Annals of the New York Academy of Sciences

About the journal

Publisher: New York Academy of Sciences
Published: 1877 to the present, United States
Language: English
ISSN: 0077-8923 (print), 1749-6632 (electronic)
Its record in the NLM Catalog

2020s

A critique of Occupational Safety and Health Administration's halfmask respirator assigned protection factor. M. Nicas. 2024;1536(1):5-12. PubMed · Publisher

Abstract

Halfmask air-purifying respirators are used by millions of workers to reduce inhaling air contaminants, both chemical (e.g., asbestos, styrene) and biological (e.g., SARS-CoV-2, Mycobacterium tuberculosis). In 2006, the federal Occupational Safety and Health Administration (OSHA) promulgated a standard that gave halfmask respirators an assigned protection factor (APF) of 10. This signified that OSHA assumes a fit-tested and trained wearer will experience a 10% maximum total inward leakage of contaminated air into the facepiece. To derive APF = 10, OSHA analyzed data from 16 workplace studies of the efficacy of halfmask respirators worn against particulate contaminants. In this commentary, I contend that, in considering the data, OSHA made several errors that overstated halfmask respirator efficacy. The errors were (i) failing to properly account for within-wearer and between-wearer variability in respirator efficacy; (ii) ignoring the effect of particle deposition in the respiratory tract; (iii) aggregating unbalanced data within and between studies, and effectively double-counting the data in some studies; and (iv) ignoring the effect that particle size exerts in penetrating respirator facepiece leak paths. The net result is that OSHA's APF = 10 can lead to excessive toxicant exposure for many workers.

© 2024 The New York Academy of Sciences.

2010s

Adenosine diphosphate regulates MMP2 and MMP9 activity in malignant mesothelioma cells. A. Muscella, L.G. Cossa, C. Vetrugno, et al. 2018;1431(1):72-84. PubMed · Publisher

Abstract

Although an association between cancer progression and matrix metalloproteinase (MMP) 2 and MPP9 expression has been known, the expression, nuclear localization, and physiologically controlled activation of these two MMPs have not been investigated in malignant mesothelioma cells. We examined the expression and intracellular localization of MMP2/9 in ZL55 malignant mesothelioma cells, as well as their regulation by ADP. Using real-time PCR, we showed that activation of the P2Y1 receptor by ADP increased the expression of MMP2/9 mRNAs; MMP2/9 collected from conditioned media also showed an increase in activity; and ADP induced the nuclear localization of MMP2/9. The effects of ADP on transcription of the MMPs were due to activation of c-Src, Akt, and NF-κB, while ERK1/2 phosphorylation was needed for the increase in enzymatic activity and the regulation of nuclear import. We also showed that the nuclear localization of MMP2/9 induced by ADP causes the cleavage and inactivation of poly-ADP-ribose polymerase-1. These findings may help to elucidate the mechanisms regulating MMP2/9 activation in ZL55 human epithelioid mesothelioma cells, and perhaps other cells. Therapeutic approaches that promote ADP accumulation in a tumor environment may constitute an effective means to induce anticancer activity.

© 2018 New York Academy of Sciences.
Inflammation precedes the development of human malignant mesotheliomas in a SCID mouse xenograft model. J.M. Hillegass, A. Shukla, S.A. Lathrop, et al. 2010;1203:7-14. PubMed · Publisher · Free full text

Abstract

Asbestos fibers cause chronic inflammation that may be critical to the development of malignant mesothelioma (MM). Two human MM cell lines (Hmeso, PPM Mill) were used in a SCID mouse xenograft model to assess time-dependent patterns of inflammation and tumor formation. After intraperitoneal (IP) injection of MM cells, mice were euthanized at 7, 14, and 30 days, and peritoneal lavage fluid (PLF) was examined for immune cell profiles and human and mouse cytokines. Increases in human MM-derived IL-6, IL-8, bFGF, and VEGF were observed in mice at 7 days postinjection of either MM line, and a striking neutrophilia was observed at all time points. Free-floating tumor spheroids developed in mice at 14 days, and both spheroids and adherent MM tumor masses occurred in all mice at 30 days. Results suggest that inflammation and cytokine production precede and may be critical to the development of MMs.
The role of iNOS-mediated DNA damage in infection- and asbestos-induced carcinogenesis. Y. Hiraku, S. Kawanishi, T. Ichinose, et al. 2010;1203:15-22. Review PubMed · Publisher

Abstract

Chronic inflammation contributes to a substantial part of environmental carcinogenesis. Various infectious diseases and physical, chemical, and immunological factors participate in inflammation-related carcinogenesis. Under inflammatory conditions, reactive oxygen and nitrogen species are generated from inflammatory and epithelial cells, and resulting DNA damage may participate in carcinogenesis. 8-Nitroguanine is a mutagenic DNA lesion formed during chronic inflammation. We performed immunohistochemical analysis, and demonstrated that 8-nitroguanine was formed at the sites of carcinogenesis in animal models and patients with various cancer-prone infectious and inflammatory diseases, caused by parasites, viruses, and asbestos exposure. In asbestos-exposed mice, 8-nitroguanine was formed in bronchial epithelial cells, and it is noteworthy that crocidolite induced significantly more intense 8-nitroguanine formation than chrysotile, inconsistent with their carcinogenic potentials. On the basis of these findings, we have proposed that 8-nitroguanine could be a potential biomarker to evaluate the risk of inflammation-related carcinogenesis.

2000s

Mesothelioma and environmental exposure. C. Varga, K. Szendi. 2008;1138:73-6. PubMed · Publisher

Abstract

A novel animal model was developed to study the direct exposure of mesothelial cells to crocidolite and chrysotile asbestos fibers. Chemically pure and pretreated Union Internationale Centre le Cancer (UICC) samples were implanted into a peritoneal envelope (Kertai's fold) of Wistar rats. Following the 12-month exposure, lack of mesothelioma induction was detected in all groups. Results suggest that the mechanism of mesothelioma formation is not a consequence of peritoneal physical exposure to the fibers.
Adverse health effects of fluoro-edenitic fibers: epidemiological evidence and public health priorities. C. Bruno, P. Comba, A. Zona. 2006;1076:778-83. PubMed · Publisher

Abstract

Subsequent to the detection of a cluster of mesothelioma cases in the Sicilian town of Biancavilla, located at the slopes of Etna volcano, ad hoc epidemiological studies and environmental monitoring suggested an etiological role of an asbestiform fiber present in a stone quarry. The fiber was shown to constitute a new mineral species named fluoro-edenite. Fluoro-edenitic fibers were found in the materials extracted from the quarry and used in the local building industry, as well as in soils. Besides the risk of mesothelioma, residents in Biancavilla showed a significantly increased mortality from chronic obstructive pulmonary disease, which was particularly evident among women. In the light of these findings, Biancavilla was defined a site of national interest for environmental reclamation. The first preventive action involved termination of quarrying activity, covering with asphalt of roads previously paved with local soil materials, and removal of sources of dust in the urban area. Concurrent to the implementation of environmental cleanup, some specific "second generation" studies are now being designed and performed, namely morbidity surveys based on hospital discharge cards, monitoring of fibers in sputum and health surveillance in selected population groups. In this frame, special emphasis is given to the issue of communication, both to the general public and to target groups like family doctors, teachers, and media professionals. This experience could represent a useful basis for the elaboration of a strategy to approach similar environmental issues.
Asbestos ban in India: challenges ahead. T.K. Joshi, U.B. Bhuva, P. Katoch. 2006;1076:292-308. PubMed · Publisher

Abstract

Rapidly industrializing India is described by the International Monetary Fund as a young, disciplined, and vibrant economy with a projected growth of 6.7% for 2005. The total workforce of 397 million has only 7% of workers employed in the organized sector with construction, where asbestos exposure is prevalent, employing 4.4%. The domestic production of asbestos declined from 20,111 tons in 1998-1999 to 14,340 tons in 2002-2003. The imports from Russia and Canada increased from 61,474 tons in 1997-1998 to 97,884 tons in 2001-2002. The production of asbestos cement products went up from 0.68 million tons in 1993-1994 to 1.38 million tons in 2002-2003. The asbestos industry has been delicensed since March 2003. The number of asbestos-based units stood at 32, with the western state of Maharashtra having the largest number. According to official figures, the industry employs 8000 workers. The occupational exposure standard is still 2 fibers/mL, worse still, mesothelioma is not recognized as an occupational disease. The latest cancer registry data have no information on mesothelioma. The health and safety legislation does not cover 93% of workers in the unorganized sector where asbestos exposures are extremely high. Workers remain uninformed and untrained in dealing with asbestos exposure. Enforcement agencies are not fully conscious of the risks of asbestos exposure. Industrial hygiene assessment is seldom carried out and pathologists do not receive training in identifying mesothelioma histopathologically. The lack of political will and powerful influence of the asbestos industry are pushing India toward a disaster of unimaginable proportion.
Carcinogens in the construction industry. B. Järvholm. 2006;1076:421-8. PubMed · Publisher

Abstract

The construction industry is a complex work environment. The work sites are temporary and rapidly changing. Asbestos has been widely used in construction industry, but the risks were primarily detected in specialized trades, such as insulation workers and plumbers. Today, the majority of cases related to asbestos exposure will occur in other occupational groups in the construction industry. In a large cohort of Swedish construction workers, insulators and plumbers constituted 37% of all cases of pleural mesothelioma between 1975 and 1984 while they constituted 21% of the cases between 1998 and 2002. It is estimated that 25-40% of all male cases of pleural mesothelioma in Sweden are caused by asbestos exposure in the construction trades. There are many other known carcinogens occurring in the construction industry, including PAHs, diesel exhausts, silica, asphalt fumes, solvents, etc., but it is difficult to estimate exposures and thus the size of the risk. The risk of cancer is less easy to detect with traditional epidemiological methods in the construction industry than in other industrial sectors. It is not sufficient to rely upon broad epidemiological data to estimate the risk of cancer due chemicals in the construction industry. Thus, a strategy to decrease exposure, e.g., to dust, seems a feasible way to reduce the risk.
Diesel exhaust and coal mine dust: lung cancer risk in occupational settings. B. Hoffmann, K.H. Jöckel. 2006;1076:253-65. PubMed · Publisher

Abstract

Conflicting evidence on the carcinogenicity of diesel exhaust (DE) and coal mine dust in occupational settings exist. Exposure measurement in most studies is inferred on the basis of job classifications and may lead to misclassification. Confounding behavioral factors (i.e., smoking) and occupational risk factors (exposure to asbestos, arsenic, radon) need to be considered. We evaluated the epidemiological evidence and current findings of the carcinogenicity of DE and coal mine dust in occupational settings. Pertaining literature was identified through Medline search and recent review articles. Strengths and limitations of recent approaches are discussed. Many epidemiological studies have addressed the question of carcinogenicity in workers exposed to DE, and most showed a low-to-medium increase in the risk of bronchial carcinoma. The pooled relative risk (RR) estimates lie between 1.33 and 1.47, and a consistent rise in risk across various job categories and study designs point to a causal relationship. Data on the carcinogenicity of coal mine dust are less consistent and the potential for confounding by unmeasured risk factors (arsenic, radon, DE) are higher. While silica as one of its components has been evaluated as carcinogenic, there is inadequate evidence for the carcinogenicity of pure coal dust according to the International Agency for Research on Cancer (IARC). There is sufficient evidence for a causal relationship between DE and lung cancer in occupational settings. The evidence for coal mine dust is less convincing, but individual studies show an increase in risk of lung cancer in exposed workers.
Health effects of hazardous waste. S.M. Dearwent, M.M. Mumtaz, G. Godfrey, et al. 2006;1076:439-48. PubMed · Publisher

Abstract

Since 1995, the Agency for Toxic Substances and Disease Registry (ATSDR) has evaluated environmental contaminants and human health risks at nearly 3000 sites. Hazardous substances at these sites include newly emerging problems as well as historically identified threats. ATSDR classifies sites according to the degree of hazard they represent to the public. Less than 1% of the sites investigated are considered urgent public health hazards where chemical or physical hazards are at levels that could cause an immediate threat to life or health. Approximately 20% of sites have a potential for long-term human exposures above acceptable risk levels. At almost 40% of sites, hazardous substances do not represent a public health hazard. Completed exposure pathways for contaminants in air, water, and soil have been reported at approximately 30% of evaluated sites. The most common contaminants of concern at these sites include heavy metals, volatile organic compounds, and polychlorinated biphenyls. This article reviews ATSDR's ongoing work by examining the historic hazard of lead, the contemporary hazard of asbestos, and the emerging issue of perchlorate contamination.
Manufactured uncertainty: protecting public health in the age of contested science and product defense. D. Michaels. 2006;1076:149-62. PubMed · Publisher

Abstract

The strategy of "manufacturing uncertainty" has been used with great success by polluters and manufacturers of dangerous products to oppose public health and environmental regulation. This strategy entails questioning the validity of scientific evidence on which the regulation is based. While this approach is most identified with the tobacco industry, it has been used by producers of asbestos, benzene, beryllium, chromium, diesel exhaust, lead, plastics, and other hazardous products to avoid environmental and occupational health regulation. It is also central to the debate on global warming. The approach is now so common that it is unusual for the science not to be challenged by an industry facing regulation. Manufacturing uncertainty has become a business in itself; numerous technical consulting firms provide a service often called "product defense" or "litigation support." As these names imply, the usual objective of these activities is not to generate knowledge to protect public health but to protect a corporation whose products are alleged to have toxic properties. Evidence in the scientific literature of the funding effect--the close correlation between the results of a study desired by a study's funder and the reported results of that study--suggests that the financial interest of a study's sponsors should be taken into account when considering the study's findings. Similarly, the interpretation of data by scientists with financial conflicts should be seen in this light. Manufacturing uncertainty is antithetical to the public health principle that decisions be made using the best evidence currently available.
Measurements of asbestos burden in tissues. R.F. Dodson, M.A. Atkinson. 2006;1076:281-91. PubMed · Publisher

Abstract

Asbestos inhaled into the lung is recognized as a potential causal agent for the development of diseases in man. The diseases induced by asbestos include lung cancer, fibrosis of the lung (asbestosis), and extrapulmonary tumors including mesothelioma (a tumor of the serosal membrane), as well as fibrosis and other changes in the pleura linings. The cause of these diseases can often be more specifically linked to asbestos exposure once tissue burden of asbestos is established. The asbestos burden in tissue can be defined as the number of asbestos bodies and/or the numbers and types of asbestos fibers found in the tissue. In either of these cases the quality of information is directly dependent on the preparative techniques and instrumentation used in the analysis. The present article will discuss the significance of findings of tissue burden based on both these variables.
The economic costs of health service treatments for asbestos-related mesothelioma deaths. A. Watterson, T. Gorman, C. Malcolm, et al. 2006;1076:871-81. PubMed · Publisher

Abstract

This article explores the complex and neglected picture of occupational and environmental disease healthcare costs specifically relating to asbestos. Diagnosed mesothelioma cases in Scotland in one calendar year were used to investigate the subject in greater depth. Data from UK sources on asbestos disease types recorded in 2000 and their disease treatment costs were obtained. Acute care economic costs of these diseases are estimated. One hundred and twenty diagnosed, recorded, and treated cases of asbestos-related diseases occurred in 2000 in Scotland. Mesothelioma accounted for 100 cases and directly cost Scottish National Health Service hospitals an estimated 942,038 pounds. The estimated UK figure in 2000 was at least 16,014,646 pounds because official figures for diagnosed and recorded deaths from mesothelioma are running at over 1700 a year with rises predicted for 2010 of 2000 deaths. By 2003, 50,000 people in the UK had died from diagnosed and recorded mesothelioma since records began. Earlier disease treatment costs would have been significantly lower than those in 2000 but, at 2000 prices, cost to the UK was roughly 471,019,000 pounds in acute hospital expenditure. Figures for primary care costs, including caregiver costs, are incomplete or unknown. These disease costs are substantial and have some international generalizability. Treatment patterns and costs vary greatly. Many lung cancer cases due to asbestos exposure occur globally for each mesothelioma case. Hence figures provided in this article are certain to be gross underestimates of the total health service and personal economic costs of asbestos illness and treatment in Scotland.
Asbestos fibers contributing to the induction of human malignant mesothelioma. Y. Suzuki, S.R. Yuen. 2002;982:160-76. PubMed · Publisher

Abstract

Unlabelled: To elucidate the features of the asbestos fibers contributing to the induction of human malignant mesothelioma, we used high-resolution analytical electron microscopy to determine the type, number, and dimensions of asbestos fibers in lung and mesothelial tissues in 168 cases of mesothelioma.

Results: 1. Asbestos fibers were present in almost all of the lung and mesothelial tissues from the mesothelioma cases. 2. The most common types of asbestos fibers in lung were either an admixture of chrysotile with amphiboles, amphibole alone, and occasionally chrysotile alone. In mesothelial tissues, most asbestos fibers were chrysotile. 3. In lung, amosite fibers were greatest in number followed by chrysotile, crocidolite, tremolite/actinolite, and anthophyllite. In mesothelial tissues, chrysotile fibers were 30.3 times more common than amphiboles. 4. In some mesothelioma cases, the only asbestos fibers detected in either lung or mesothelial tissue were chrysotile fibers. 5. The average number of asbestos fibers in both lung and mesothelial tissues was two orders of magnitude greater than the number found in the general population. 6. The majority of asbestos fibers in lung and mesothelial tissues were shorter than 5 micro m in length.

Conclusions: 1) Fiber analysis of both lung and mesothelial tissues must be done to determine the types of asbestos fibers associated with the induction of human malignant mesothelioma; 2) short, thin asbestos fibers should be included in the list of fiber types contributing to the induction of human malignant mesothelioma; 3) RESULTS support the induction of human malignant mesothelioma by chrysotile.
Product liability forecasting for asbestos-related personal injury claims: a multidisciplinary approach. E. Stallard. 2001;954:223-44. Review PubMed · Publisher

Abstract

This paper focuses on three aspects of forecasting models for asbestos-related disease/injuries relating to the Manville asbestos case: (1) The structure of forecasting models for asbestos-related personal injuries. (2) The epidemiologic evidence supporting the selected model structure and the constraints on the modeling assumptions imposed by that evidence. (3) The range of uncertainty associated with projections based on these forecasting models and issues relating to decision making under uncertainty.

1990s

Sources of uncertainty in dose-response modeling of epidemiological data for cancer risk assessment. L. Stayner, A.J. Bailer, R. Smith, et al. 1999;895:212-22. PubMed · Publisher

Abstract

Epidemiologic data is increasingly being used for dose-response analysis in risk assessment. The Environmental Protection Agency (EPA) and other U.S. agencies have expressed a preference for using epidemiologic data rather than toxicologic data when possible. However, there are a number of important sources of uncertainty in using epidemiologic data for this purpose that need to be clearly recognized and, when possible, quantified. This paper presents a critical review of the major sources of uncertainty in the use of epidemiologic data for cancer risk assessment. These may include: (1) study design issues such as potential confounding and other biases, inadequate sample size, and followup, (2) the choice of the data set, (3) specification of the dose-response model, (4) estimation of exposure and dose, and (5) unrecognized variability in susceptibility. Examples from risk assessments for cadmium, asbestos, and diesel exhaust are used to illustrate the potential magnitude of some of these sources of uncertainty. It is shown that the overall uncertainty from these various sources combined may often result in highly uncertain risk estimates from dose-response modeling of epidemiologic data. For this reason, we believe it is best to present a range of possible risk estimates, which, to the extent possible, reflects the variability and uncertainty inherent in the dose-response evaluation of epidemiologic data.
The contribution of environmental monitoring in the epidemiological assessment of exogenous risk. The experience of ARPA in the Emilia-Romagna Region of Italy. A. Zavatti, P. Lauriola. 1999;895:173-87. PubMed · Publisher

Abstract

The aim of the Emilia Romagna-Region Agency for Prevention and Environment (ARPA) is to define and improve interactions among the various prevention departments of the Emilia-Romagna Local Health Authorities in order to attain better knowledge about the health status of the population by using epidemiology and etiology studies, as well as predictive models. This is the basis for the environmental health risk assessment strategy of ARPA. The priority activity areas for ARPA are: urban areas, environmental and health effects of traffic (atmospheric pollution and noise pollution); industrial areas (Ravenna chemical plants, Modena/Reggio-Emilia ceramic factories and Ferrara chemical plants); high-speed trains; pesticides; asbestos; and pollution of the Adriatic Sea.
The long-lasting legacy of industrial carcinogens: the lesson of asbestos. Irving J. Selikoff Memorial Lecture, 1995. C. Maltoni. 1997;837:570-86. PubMed · Publisher
Interleukin-6- and interleukin-4-related proteins (C-reactive protein and IgE) are prognostic factors of asbestos-related cancer. A. Lange, L. Karabon, J. Tomeczko. 1995;762:435-8. PubMed · Publisher
Asbestos-induced nitric oxide production: synergistic effect with interferon-gamma. G. Thomas, T. Ando, K. Verma, et al. 1994;725:207-12. PubMed · Publisher

Abstract

This study has shown, for the first time, that in vitro exposure of rat AMs to either crocidolite (amphibole) or chrysotile (serpentine) asbestos fibers induces the synthesis not only of the O2*- anion, but also of the nitrogen radical, NO*. Furthermore, this asbestos-related effect is enhanced in the presence of interferon-gamma. NO* has been implicated in several pathologic reactions, such as inflammation and immune complex-mediated cell injury. Additionally, NO* may interact with secondary amines to generate nitrosamines, which are potent carcinogens. Our findings could represent a novel type of asbestos-mediated injury, and we propose that the injurious effects of asbestos might be mediated via the interaction of NO* with O2*-, with the generation of ONOO- and other potent toxic free radicals.
A comparison of asbestos burden in lung parenchyma, lymph nodes, and plaques. R.F. Dodson, M.G. Williams, C.J. Corn, et al. 1991;643:53-60. PubMed · Publisher

Summary

This study examined whether asbestos that reaches the lymph nodes and pleural plaques can be measured, and how that burden compares with the burden in the lung. The authors cited an earlier statement that plaques and pleura are not useful for mineral analysis, and they designed the study to test it. Tissue was collected at autopsy at the General Hospital of Monfalcone, Italy, from eight former shipyard workers (seven men and one woman, aged 58 to 82). Lung tissue, tracheal lymph nodes and pleural plaques were digested. Ferruginous bodies were counted by light microscopy. Uncoated fibers of 0.5 µm or longer were counted, identified and measured by transmission electron microscopy. Lung tissue contained 269 to 853,000 ferruginous bodies per gram dry weight. In three people, ferruginous bodies were more numerous in the nodes than in the lung. None were found in plaques. Uncoated fibers per gram were greater in the nodes than in the lung. For each of the eight people, the highest uncoated fiber count was in an extrapulmonary site: the plaques in two and the nodes in six. Most fibers at all sites were short, but fibers longer than 10 µm were found in both nodes and plaques. Under light microscopy counting rules (fibers longer than 5 µm), none of the chrysotile and only 5% to 10% of amphiboles would have been counted. The longest lung fiber, a 65 µm chrysotile fiber, was 0.03 µm wide. The authors concluded that asbestos reaches both lymph nodes and pleura, and that counting criteria and detection limits must be defined.

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.
A population of children at risk of exposure to asbestos in place. P.J. Landrigan. 1991;643:283-6. PubMed · Publisher

Summary

This paper argued that children are a population at potentially high risk of exposure to asbestos in place in buildings. The author presented two sets of New York data. A statewide survey of schools, mandated by the U.S. Environmental Protection Agency (EPA) under the Asbestos Hazard Emergency Response Act and completed in September 1989, found 252,796,000 square feet of asbestos in public and private school buildings. More than 23 million square feet, about 9%, was deteriorated or friable. All 762 public school districts and 91% of private school districts complied. A 1988 New York City survey of 900 buildings found asbestos in 600, and 13% of all buildings had deteriorated or friable asbestos. The author traced the problem to a failure to heed warnings known since the 1930s, since asbestos use in schools peaked in the 1950s to 1970s. He reprinted portions of an American Academy of Pediatrics statement on risk. He noted that mesothelioma risk rises with roughly the fourth power of time since first exposure, and that children have greater exposure for body weight. He cited an EPA estimate of 1,000 premature deaths over 30 years among 3 million students in 8,500 schools with friable asbestos. He described management options from maintenance to removal and concluded that exposure must be reduced to blunt a third wave of asbestos disease.

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.
Absence of evidence for a significant background incidence of diffuse malignant mesothelioma apart from asbestos exposure. E.J. Mark, T. Yokoi. 1991;643:196-204. Review PubMed · Publisher

Abstract

The incidence of diffuse malignant mesothelioma is rising. Physicians can diagnose a disease only when they know that it exists, so one explanation for the rise in incidence is more widespread appreciation of the clinical and pathological features of the disease. Modern pathology has ascribed specific requirements for the diagnosis of diffuse malignant mesothelioma. A priori one cannot assume that these requirements have increased the likelihood of the diagnosis because the requirements also can serve to exclude the diagnosis depending on the findings. Most cases of diffuse malignant mesothelioma are suspected by macroscopic and routine microscopic techniques that have been available since the last part of the nineteenth century. Although single reported instances of some pulmonary diseases have survived from the nineteenth century, pathologists did not identify enough cases to convincingly establish the existence of diffuse malignant mesothelioma of the pleura as an entity until the 1930s or 1940s. One must conclude that the background level of diffuse malignant mesothelioma in Europe and in the United States prior to 1930 was extremely low. No case was detected at the Massachusetts General Hospital until 1946.
Analysis of asbestos fibers in lung parenchyma, pleural plaques, and mesothelioma tissues of North American insulation workers. N. Kohyama, Y. Suzuki. 1991;643:27-52. PubMed · Publisher

Abstract

Asbestos fibers and ferruginous bodies (FBs) in lung parenchyma, lung cancer tissues, pleural plaques, and pleural and peritoneal mesothelioma tissues from 13 North American insulation workers were analyzed and quantified using an analytical transmission electron microscope and a polarized microscope. Diseases from which these workers suffered included asbestosis, lung cancer, and mesothelioma. They had been occupationally exposed to materials containing chrysotile and amosite; their pathological diagnoses, occupational and cigarette smoking histories, and clinical summaries have been reported. Large numbers of FBs were found in the lungs and small numbers found in extrapulmonary sites. Most of the FBs had cores of amosite fibers. In all instances, lung parenchyma and lung cancer tissues showed chrysotile and amosite fibers in high concentrations (63.1 x 10(6) and 150.2 x 10(6) fibers/g dry tissue as mean values, respectively). Crocidolite fibers were seen in seven of the 13 cases, but in much smaller numbers. Other amphiboles were rarely found. In pleural plaques and in pleural and peritoneal mesothelioma tissues, amosite fibers were markedly fewer in number, whereas chrysotile fibers were seen in similar numbers as in the lungs. No significant differences in the size distribution of asbestos fibers were seen in the different sites. However, the mean widths of chrysotile fibers were thinner than those of amosite fibers. These results strongly suggest that translocation of inhaled asbestos fibers from the lung to other tissues, such as the pleura and the peritoneum, occurs frequently, and that chrysotile may be more actively translocated from the lung, compared to amosite or amphibole asbestos. The likelihood of translocation seems to be strongly related to the thinness of the fibers. Translocated chrysotile fibers may play an important role in the induction of either malignant mesothelioma and/or hyaline plaques, since the asbestos fibers detected in both these sites were mainly chrysotile.
Analysis of the exposure-response relationship for mesothelioma among asbestos-cement factory workers. M.M. Finkelstein. 1991;643:85-9. PubMed · Publisher
Application of pulmonary function tests to the evaluation of asbestosis. A. Miller. 1991;643:145-8. PubMed · Publisher
Asbestos disease at low exposures after long residence times. G.K. Sluis-Cremer. 1991;643:182-93. PubMed · Publisher

Summary

The author reviewed his group's South African studies of crocidolite and amosite miners to examine disease at "low" exposure, defined as an average below 2 fibers/mL or a cumulative exposure below 5 fiber-years/mL, after long residence times (years since onset of exposure). In 807 miners autopsied between 1974 and 1988, no asbestosis was found below 2 fiber-years/mL, although few such men had residence times over 30 years. At 2-5 fiber-years/mL, asbestosis was found in 1 of 32 men with residence times under 15 years and 3 of 24 with 16-30 years. In 1,454 men X-rayed in 1970-1975 and again 2-16 years later, radiological progression from category 0/0 to 1/0 occurred in 12% of those with continued exposure and 10.5% of those whose exposure had stopped. Appreciable progression was seen with under 5 years or under 5 fiber-years/mL of exposure. In a mortality study of 7,317 white miners (1,225 deaths by 1980), the lung cancer SMR was 172.4, and 143.9 in the 1-5 fiber-years/mL group. In a case-referent analysis of autopsied men, asbestosis was the strongest predictor of bronchial cancer. There were 30 mesotheliomas, 20 in crocidolite miners, none with under 3 months' exposure. The author concluded that low industrial exposures with long residence times carry a considerable disease burden, though they remain far above environmental exposures.

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 disease in construction, refinery, and shipyard workers. K.H. Kilburn, R.H. Warshaw. 1991;643:301-12. PubMed · Publisher

Summary

The authors examined how common asbestosis was among construction, shipyard, refinery and production workers, and how shipyard work and cigarette smoking affected it. Workers were recruited through local unions if their first asbestos exposure was at least 15 years earlier and had lasted 5 years. From 1986 to 1989, one mobile medical team examined 8,749 workers. A single reader interpreted chest X-rays using ILO conventions. Asbestosis was defined as irregular opacities of profusion 1/0 or greater with occupational exposure and at least 15 years since first exposure. Pleural abnormalities were counted separately. Workers also had lung function tests and questionnaires. Asbestosis prevalence was 20% to 30% in nine of eleven trades with at least 100 workers. Boilermakers, pipefitters and sheet-metal workers, who handled asbestos directly, had no higher prevalence than bystander trades. Overall prevalence was 27.4% in construction trades and 36.6% in shipyard workers. It was 43.8% in oil refinery, 23.0% in aluminum refining, 21.6% in papermaking, 17.7% in fiberglass and 7.9% in copper smelter workers. In nearly all union groups, workers with shipyard experience had higher prevalence. Half of never-smokers had asbestosis at 75-80 years of age, compared with 60-65 years for current smokers. Mid-expiratory flow fell and air-trapping rose as opacity profusion increased, while total lung capacity did not decrease. The authors concluded that bystander and shipyard exposures cause substantial asbestosis and confound studies of other materials such as fiberglass.

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 fire fighting. S.B. Markowitz, K. Garibaldi, R. Lilis, et al. 1991;643:573-7. PubMed · Publisher

Summary

The authors examined whether long-term New York City fire fighters showed radiographic signs of asbestos-related lung and pleural disease. They invited fire fighters who had been employed by the New York City Fire Department as of December 1963, had worked in a ladder company for at least five years during the 1960s, and had been assigned to firehouses in areas with large office buildings, factories and warehouses, or heavy fire activity. Of 550 invited, 212 (39%) took part. All were male, their mean age was 57, and 72% were still active. Evaluation included occupational, smoking and medical histories, a respiratory symptom questionnaire, physical examination, spirometry, and chest X-rays read by two readers using the 1980 ILO classification. Overall, 42 participants (20%) had pleural thickening and/or small irregular parenchymal opacities. Of 152 fire fighters reporting no asbestos exposure before fire fighting, 20 (13%) had abnormalities, including 13 (9%) with pleural thickening and 8 (6%) with parenchymal opacities. Of 60 with prior exposure, 22 (37%) had abnormalities, including 18 (30%) with pleural thickening and 7 (12%) with parenchymal opacities. The abnormalities were mild. The authors concluded that fire fighters are at risk of asbestos-induced pleural and pulmonary fibrosis independent of other exposure. They noted that 9% pleural thickening exceeded the roughly 2% reported in general population studies. They recommended reducing exposure, using respiratory protection throughout all phases of fires, and providing medical surveillance.

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Asbestos exposure from activities in buildings with asbestos-containing materials. D.L. Keyes, J.R. Millette. 1991;643:509-10. PubMed · Publisher
Asbestos fibers are mutagenic after all: new signs of orthodoxy for a paradoxical group of carcinogens. T.M. Fasy. 1991;643:271-9. Review PubMed · Publisher

Summary

In this review, the author examined whether asbestos fibers can damage DNA and cause mutations, at a time when the prevailing view held that they lacked clear genotoxic potential. He summarized earlier work. There was general agreement that asbestos fibers induced aneuploidy and chromosome breaks. Results on sister chromatid exchanges disagreed. Mammalian cell specific-locus assays had reported little or no mutagenic activity. The author argued that, because a mutation is a heritable change in the genome, aneuploidy counts as mutation, so asbestos fibers should be regarded as mutagens. He contended that the standard specific-locus assays cannot detect large multilocus deletions, because cells that lose neighbouring essential genes do not survive. He outlined possible routes to gene mutation: fibers adhering to, entangling or piercing chromosomes; generation of reactive oxygen species; and chrysotile-mediated uptake and insertion of foreign DNA. He described two newer assays able to detect large deletions, AS52 and AL-J1. He cited an early unpublished report by Waldren that chrysotile caused loss of a marker, and later reports that UICC chrysotile and crocidolite were highly mutagenic in the AL-J1 system. He then discussed how deletion mutations could inactivate tumor-suppressor genes, and argued that asbestos may also act as a tumor promoter. He rejected the view that only initiators are genotoxic as a false dichotomy. He concluded that asbestos oncogenesis may serve as a clarifying model rather than an inexplicable exception.

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Asbestos in place in Metropolitan New York. L.B. Molloy. 1991;643:614-21. PubMed · Publisher
Asbestos in place: a building management perspective. H.G. Irwig, L.C. Oliver, T. Page, et al. 1991;643:589-96. PubMed · Publisher
Asbestos in the lungs of children. A.K. Haque, M.F. Kanz, M.G. Mancuso, et al. 1991;643:419-29. PubMed · Publisher
Asbestos-associated deaths among insulation workers in the United States and Canada, 1967-1987. I.J. Selikoff, H. Seidman. 1991;643:1-14. Review PubMed · Publisher

Summary

After reviewing the history of how asbestos disease was recognized, including among insulation workers, the authors reported 20 years of mortality follow-up of insulators. The cohort comprised 17,800 men enrolled in the insulators' union in the United States and Canada on January 1, 1967. They were followed from 1967 through 1986, giving 301,592.6 person-years of observation. Causes of death were taken from death certificates and were also assigned by "best evidence" after review of clinical, X-ray and pathology material. Mesothelioma was counted only when histopathology was verified by the authors' pathologist. Expected deaths were based on U.S. white male rates. There were 4,951 deaths against 3,453.5 expected. By best evidence there were 1,168 lung cancer deaths (268.66 expected), 173 pleural and 285 peritoneal mesotheliomas, 189 gastrointestinal cancer deaths (135.69 expected) and 427 asbestosis deaths. Cancers of the oropharynx and buccal cavity, larynx, kidney, pancreas (54 observed, 39.52 expected), and gallbladder and bile ducts were also increased. Apparent excesses of brain and liver cancer on death certificates disappeared after review, mainly because metastases had been misdiagnosed as primary tumours. No increase was found for cancer of the urinary bladder, prostate, testis, primary liver or brain, or for melanoma, leukemia or lymphoma. Little or no excess occurred within 15 years of onset of work, and most excess risk appeared 25 to 35 or more years after onset. The authors concluded that each organ appears to have its own neoplastic response to asbestos.

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Asbestos-associated pleural mesothelioma in school teachers: a discussion of four cases. D.E. Lilienfeld. 1991;643:454-58. Case report PubMed · Publisher

Abstract

The causal relationship between malignant mesothelioma and exposure to asbestos is well established. In part as a result of that association, much public attention has focused on asbestos abatement in buildings, such as public schools, in which that asbestos was used as a construction material. The present communication is a report of four cases of malignant mesothelioma in school teachers whose only apparent exposure to asbestos was in the schools in which they taught. The concerns raised by this report are also discussed.
Asbestos-related abnormalities in school maintenance personnel. L.C. Oliver, N.L. Sprince, R. Greene. 1991;643:521-9. PubMed · Publisher
Asbestos-related disease among sheet-metal workers. Preliminary results of the National Sheet Metal Worker Asbestos Disease Screening Program. L.S. Welch, D. Michaels, S. Zoloth. 1991;643:287-95. PubMed · Publisher

Summary

The authors reported preliminary results of a national screening program for asbestos-related disease among sheet-metal workers. Members first employed in the construction sector at least 20 years earlier were invited for a questionnaire, physical examination, spirometry and chest X-ray read using the ILO classification, at 61 clinics in the United States and Canada. Of 26,329 invited, 12,454 (47%) had been examined. This analysis covered 8,288 male United States workers employed only in the building trades. Parenchymal disease was defined as ILO profusion 1/0 or greater. The proportion with pleural changes, parenchymal changes or both rose with years since first exposure, except in the shortest-latency group. Fewer than 1% had profusion 2/1 or higher. Ever-smokers had more parenchymal disease than never-smokers at every latency, and the difference for pleural disease was much smaller. Restrictive lung function was found in 10% and obstructive in 17% (17.6% of smokers, 3% of nonsmokers). Chronic bronchitis affected 22.8% of smokers and 11.7% of nonsmokers. Among men with 20-24 years since first exposure, 13% had pleural and 6% parenchymal disease, rates comparable to the 25-29 year group. The authors concluded that asbestos-related disease was common among sheet-metal workers, although they do not use asbestos directly. They suggested that asbestos already in place in buildings may also be causing disease.

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Asbestos-related disease in custodial and building maintenance workers from a large municipal school district. J.R. Balmes, A. Daponte, J.E. Cone. 1991;643:540-9. PubMed · Publisher

Summary

The authors examined whether occupational exposure to asbestos-containing materials (ACM) in public school buildings was sufficient to cause asbestos-related lung disease in school district workers. California OSHA required a large urban school district to set up a medical surveillance program for about 900 employees judged likely to have been exposed. Between May 1983 and June 1985, 673 participants completed a questionnaire on occupational, medical and smoking history and symptoms, a limited physical examination, spirometry, and chest X-rays. Each X-ray was read by three NIOSH-certified B readers using the 1980 ILO classification. Women and workers reporting asbestos exposure before district employment were excluded, leaving 422 men. Of the 315 men with at least 10 years of district employment, 36 (11.4%) had asbestos-related disease: 18 had parenchymal asbestosis only, 13 had pleural disease only, and 5 had both. Compared with the other 279 men, cases were older, had smoked more, had worked longer, and had lower mean percent predicted FEV1 (91.8 vs 104) and FVC (89.5 vs 100.2). Prevalence rose with length of employment. Current smokers had about twice the risk of never-smokers. Prevalence was 17.0% among plumbers and about 9% among custodial and building maintenance workers. The authors concluded that long-term occupational exposure to ACM in public schools can cause asbestos-related lung disease and that collecting mortality data for these workers should be a research priority.

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Asbestos-related disease in employees of a steel mill and a glass bottle-manufacturing plant. R.S. Kronenberg, J.L. Levin, R.F. Dodson, et al. 1991;643:397-403. PubMed · Publisher
Asbestos-related X-ray changes in refinery workers. K.D. Rosenman. 1991;643:390-6. PubMed · Publisher
Aspects of asbestos exposure in place in the Federal Republic of Germany. H.J. Woitowitz. 1991;643:407-11. PubMed · Publisher
Cancer mortality in merchant seamen. M. Greenberg. 1991;643:321-32. PubMed · Publisher

Abstract

Cancer mortality excess has been reported repeatedly over the past hundred years to occur in merchant seamen. More recently lung cancer has been found to account for some of this excess and the question of the contribution made by cigarette smoking raised. In the one study where there was some information on smoking habit, it did not appear that cigarettes would have accounted for all the excess cancer observed. In other mortality studies, where excess cancer mortality was observed, the other cigarette-linked causes of death were not prominent. In a preliminary mortality analysis of a small population of merchant seamen, two cases of malignant mesothelioma have so far been identified, and in a national mesothelioma register 28 cases have been reported in seamen: both instances constitute abnormal occurrences. The presence of substantial amounts of asbestos-containing materials in naval construction which are continuously subjected to vibration and intermittently disturbed during servicing, and the detection of radiological stigmata consistent with asbestos exposure, add plausibility to the hypothesis that occupational asbestos exposure contributes to the apparent excess cancer mortality in merchant seamen. Methodologic deficiencies in epidemiologic studies reported to date make for uncertainty. Properly designed studies will be needed to quantify disease excess and to identify potentially causal associations. Even in the absence of such data it would be prudent to contain the asbestos currently installed and to promote smoking cessation programs.
Carcinogenicity of chrysotile asbestos: evidence from cohort studies. J.M. Dement. 1991;643:15-23. Review PubMed · Publisher

Summary

This paper reviewed cohort studies with lung cancer exposure-response data, focusing on chrysotile asbestos. It examined explanations proposed for the very steep lung cancer exposure-response seen in chrysotile textile workers: the "amphibole hypothesis" (risk due to tremolite contamination) and the "mineral oil hypothesis." The author reported that differences in lung cancer dose-response between cohorts depended more on industry than on fiber type, and that textile operations had a higher proportion of long airborne fibers. Cited lung tissue analyses found 5.3 fibers/mg chrysotile and 18.4 fibers/mg tremolite in Quebec miners and millers, against 0.63 and 0.38 fibers/mg in South Carolina textile workers. Airborne tremolite was 2.5 times lower in textile operations than in Canadian mines and mills. The author also cited vermiculite workers, who had over 100-fold more airborne tremolite but a less steep lung cancer exposure-response. Preliminary results were presented from a nested case-control study in a South Carolina chrysotile textile cohort of 1,261 white men employed between 1940 and 1965 and followed through 1975. It included 35 lung cancer deaths, with four controls per case. Mineral oil exposure was rated qualitatively in three groups. Across three cumulative asbestos exposure levels, crude odds ratios were 1.00, 2.17 and 5.44, and oil-adjusted odds ratios were 1.00, 2.26 and 4.50. The author concluded that neither mineral oil nor tremolite plausibly explained the textile excess and that a role for long, thin fibers needed further investigation.

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Cigarette smoking, asbestos, and parenchymal opacities revisited. P. Blanc. 1991;643:133-41. Meta-analysis PubMed · Publisher
Comparability of mesothelioma in humans and in experimental animal studies. Y. Suzuki. 1991;643:219-22. Review PubMed · Publisher

Summary

This symposium paper compared malignant mesothelioma in humans with mesothelioma produced in laboratory animals. The author summarized published work and his own laboratory's studies. Animal studies showed that asbestos and other fibrous minerals induced mesothelioma after inhalation or injection into the peritoneal or pleural cavity. Fiber shape, length (>8 µm), diameter (<1.5 µm) and durability mattered more than chemical composition, and amphiboles accumulated in the lung more readily than chrysotile. In humans, asbestos was considered virtually the only cause, with erionite and radiation also suggested. In animals, erionite, fibrous glass, brucite, sepiolite, radiation and several chemicals also induced the tumor. Latency was long in both: 20 years or more in humans, 7 months or longer in mice, 1 year or longer in rats, and 6 years and 2 months or longer in baboons. Human tumors were 65% epithelial, 25% biphasic and 10% fibrous. Mouse tumors after intraperitoneal asbestos or erionite were 1%, 11% and 88%, a difference of unknown cause. Some epidemiologists reported that crocidolite carried greater risk in humans, while in animals all asbestos types induced tumors without notable differences. In tissue from asbestos-insulation workers, pleural plaques and pleural and peritoneal mesothelioma tissue contained almost exclusively chrysotile, although lung fibers were mainly amosite. The author suggested testing Stanton's fiber-size hypothesis with inhalation rather than direct inoculation.

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Comparative dose-response relationships of asbestos fiber types: magnitudes and uncertainties. W.J. Nicholson. 1991;643:74-84. Review PubMed · Publisher

Summary

This conference paper examined whether the cancer-causing potency of chrysotile asbestos differs from that of amphibole asbestos. It responded in detail to a 1990 Science article by Mossman and colleagues, which argued that chrysotile exposure in U.S. schools and other buildings, and in workplaces meeting OSHA standards, was not a health risk. The author reviewed worker mortality studies with exposure-response data, summary results from the U.S. EPA's 1986 Airborne Asbestos Health Assessment Update, rat inhalation experiments by Wagner et al., and air measurements in buildings. In non-mining cohorts, the increase in lung cancer for a 1-year exposure to 1 f/cm3 ranged from 0.5% to 4.3%, irrespective of fiber type. In three predominantly chrysotile textile plants it ranged from 1.0% to 2.6% per f-yr/cm3. Chrysotile mining and milling showed a risk about ten times lower. Ratios of mesothelioma to excess lung cancer were similar for chrysotile, amosite and mixed exposures. Only 100% crocidolite exposures appeared higher, about two to four times that of predominantly chrysotile. Short-term concentrations as high as 18 f/cm3 were cited during routine maintenance in a library. The estimated lifetime risk for a 13-year school exposure at 0.002 f/cm3 was 4-12 asbestos-related cancer deaths per 100,000. The author concluded that chrysotile is as potent a lung carcinogen as other asbestos varieties and carries a substantial mesothelioma risk. He also concluded that building risks are similar to other environmental risks that government agencies regulate.

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Contributions of experimental asbestosis in sheep to the understanding of asbestosis. R. Bégin, A. Cantin, S. Massé, et al. 1991;643:228-38. Review PubMed · Publisher

Summary

This review summarized about 15 years of research by the authors' group in Sherbrooke, Québec, using a sheep model of asbestosis developed in the late 1970s, alongside observations in Québec asbestos miners and millers. Sheep were used because their size and docile nature allow repeated lung function tests, chest radiography, gallium-67 lung scans and bronchoalveolar lavage (BAL). The authors reported that disease in sheep closely resembled human asbestosis, both pathologically and functionally. After high or repeated exposures, an early macrophage-dominated alveolitis preceded radiographic and functional changes. This alveolitis could be detected by gallium-67 scanning and by BAL. In workers without radiographic asbestosis, 50 percent had enhanced gallium uptake. Among long-term workers with an abnormal scan, asbestosis appeared to develop in 75% within 3 to 5 years. The authors described four tissue reactions to asbestos: no-retention, low-retention, high-retention and intermediate. They suggested that the intermediate reaction might explain non-progressive cases of minimal asbestosis. Exposure dose and frequency influenced the intensity and speed of disease. In asbestotic sheep given cyclophosphamide, 80 percent died within a year, with more intense fibrosis. Sheep that developed asbestosis had retained more fibers, particularly fibers longer than 5 µm, and this excess accumulation preceded the alveolitis. The authors concluded that alveolar fiber retention is a major determinant of individual susceptibility and that animal models have significantly improved understanding of the human disease.

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Dangerous and cancer-causing properties of products and chemicals in the oil-refining and petrochemical industries. Part IX: Asbestos exposure and analysis of exposures. M.A. Mehlman. 1991;643:368-89. Review PubMed · Publisher

Summary

This article, part of a series on hazards in the oil-refining and petrochemical industries, examined asbestos exposure in these industries. The author summarized the chemical and physical properties of five types of asbestos, earlier studies of mesothelioma and chest X-ray abnormalities in refinery and petrochemical workers, and historical reports of asbestos hazards. In 1990 a questionnaire was mailed to Oil, Chemical and Atomic Workers local unions representing many companies, including Mobil, Chevron, Shell, Texaco and Exxon. It asked when and on what equipment asbestos was used, how much contact workers had with it during installation, repair or removal, and what protective equipment was used. About 400 bulk samples of materials from a typical refinery were analyzed by polarized light microscopy. The survey found asbestos in boilers, building insulation, compressors, crude columns, furnaces, gaskets, valves, piping, heat exchangers, towers, turbines, tanks and other areas. From 1940 to 1990, 81%, 90% and 90% of workers were exposed during installation, repair and removal of asbestos. Reported use of precautions was 33% for mechanical exhaust, 57% for respirators, 42% for protective clothing, 45% for shielding of the worksite and 38% for waste disposal. Of 398 samples, the types found were chrysotile, amosite (about 30%) and a chrysotile-amosite combination (about 30%). Photographs showed deteriorating asbestos insulation. The author concluded that all types and sizes of asbestos fibers can potentially cause cancer, that there is no safe level of exposure, and that workers and their families are at significant risk of lung cancer and mesothelioma.

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Health effects of tremolite. Now and in the future. B.W. Case. 1991;643:491-504. Review PubMed · Publisher

Abstract

Although tremolite asbestos has been well characterized since 1916, appreciation of its role in disease induction is relatively recent. It has always been understood that the morphology of tremolite is complex, and part of the slowness in recognizing it as a hazard has been definitional in nature. Reduced to simple terms the questions are, when is tremolite "asbestos-like," when is it an innocuous amorphous particle, do these forms occur together, with what confidence can they be separated for regulatory purposes, and what is the spectrum of disease potential for varying exposure? A brake on regulation is partially due to a convergence of opinion of unlikely and unintentional allies: industries producing tremolite-containing materials and some epidemiologists resisting attribution of risk to tremolite on the grounds that its known effects--pleural plaques, asbestosis, lung cancer and mesothelioma--are principally due to chrysotile, which is often contaminated with fibrous tremolite. The latter group concentrate their skepticism on internal-dose biomarker studies associating lung tremolite content with mesothelioma (but not so clearly with lung cancer or asbestosis). They ignore the basic carcinogenic quality of fibrous tremolite, shown in both animal and epidemiological studies. Evidence from the Quebec chrysotile/tremolite mining districts suggests that very low concentrations of tremolite in ambient air can be translated into high concentrations in lung, even in those without occupational exposure. Disease incidence, especially for mesothelioma, seems also to be associated with tremolite air and lung content. The risk associated with tremolite has been demonstrated in Corsica, Cyprus, the United States, and Canada. Of particular importance is an apparent increase in the proportion of mesothelioma risk attributable to tremolite, since the fibers heretofore most responsible for that disease--commercial amphiboles--have been or are being severely regulated or completely eliminated in production and use. Further, amosite and crocidolite, while still a concern, form a small fraction of "asbestos-in-place": most of this material is chrysotile and we do not really know to what degree it is contaminated with tremolite. The available evidence suggests that bulk analysis or airborne fiber analysis will not answer this question, and perhaps only animal bioaccumulation assay is sufficient. Until we know more, it seems prudent for public health to avoid dispersing chrysotile/tremolite into the environment, and, where we can, to regulate all tremolite "fibers" conservatively.
Improved detection of asbestos-related pleural plaques with digital radiography. R. Greene, C.M. Schaefer, L.C. Oliver. 1991;643:90-6. PubMed · Publisher
Limitations in drawing etiologic inferences based on measurement of asbestos fibers from lung tissue. D.B. Baker. 1991;643:61-70. Review PubMed · Publisher

Summary

This paper examined the methodological limitations of using measurements of asbestos fibers and asbestos bodies in lung tissue to estimate past asbestos exposure and to draw inferences about disease causation. The author reviewed published lung fiber burden studies within an epidemiologic framework of selection bias, information bias, confounding and random variation, and then reviewed technical sources of error in preparing and counting tissue specimens. Cited studies showed that fiber concentrations varied several-fold from site to site within a lung. Light microscopy was estimated to visualize only 5% of crocidolite, 26.5% of amosite and 0.14% of chrysotile fibers present in lung tissue. Ratios of amosite fibers to ferruginous bodies ranged from 11:1 to 30,000:1 among 12 former asbestos workers. The author noted that chrysotile tends to be cleared from the lung more rapidly than amphiboles, that laboratories produced markedly different absolute values, and that studies based on few cases had low statistical power. The author concluded that lung fiber burden analyses cannot reliably give quantitative estimates of past exposure or cumulative dose, though they may allow ranking of exposure within cohorts with known high occupational exposure. They cannot be used to estimate past chrysotile exposure or relative exposure to different asbestos types, and absence of chrysotile fibers cannot rule out exposure. Light microscopy and asbestos body counts cannot be used to estimate exposure. Nonsignificant findings should be considered inconclusive rather than negative.

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Mesothelioma among employees with likely contact with in-place asbestos-containing building materials. H.A. Anderson, L.P. Hanrahan, J. Schirmer, et al. 1991;643:550-72. Case report PubMed · Publisher

Abstract

The occurrence of mesothelioma is a sentinel event in occupational and environmental disease. A mesothelioma surveillance system was established utilizing existing computerized Wisconsin vital statistics data maintained since 1959 and a Cancer Reporting System (CRS) established in 1978. Review of the death certificate listing of usual occupation and industry from 487 mesothelioma deaths in Wisconsin from 1959 to 1989 led to the investigation of 41 persons with likely exposure to inplace asbestos-containing building materials (ACBM): 12 school teachers, 10 school maintenance employees, 7 public building maintenance workers, 5 private building maintenance workers, and 7 commercial and factory workers performing maintenance activities. For 10 (34%) of the 29 maintenance workers the only source of asbestos exposure identified was their maintenance work. For five (17%) histories indicated some prior employment in occupations and industries with probable asbestos exposures. Opportunities for indirect occupational exposure were identified for ten who had been employed in the residential construction industry. One maintenance worker was exposed to asbestos in the household and another had neighborhood exposure. For 9 (75%) of the school teachers, the only identifiable potential source of asbestos exposure was derived from in-place ACBM in schools. One teacher had spent a season in the merchant marine aboard an iron ore-hauling ship and 2 had worked in the residential construction industry. Two of the teachers were sisters, and in two instances, two teachers had taught in the same school facility. We conclude that individuals occupationally exposed to in-place ACBM are at risk for the subsequent development of mesothelioma.
Mesothelioma in Swiss railroad workers. J.R. Rüttner. 1991;643:404-6. PubMed · Publisher

Summary

The author updated an earlier report of a cluster of mesotheliomas among Swiss railroad workers who had not themselves handled asbestos, and examined mesothelioma in furniture workers. By the end of 1989 the Zurich Pneumoconiosis Research Group had registered 205 autopsied mesotheliomas: 191 in men and 14 in women, 193 pleural and 12 peritoneal. Qualitative mineralogical lung dust analysis was done in 179 cases, and asbestos was found in 168 (94%). Amphiboles alone were found in 109 cases (61%), chrysotile with amphibole in 52 (29%), chrysotile alone in 7 (4%) and no asbestos in 11 (6%). Forty patients had worked in railway coach construction and repair factories in German-speaking Switzerland. About one-third had direct occupational exposure. In the remaining 26 the tumours were attributed to passive, unnoticed workplace exposure. This exposure was recognised only after autopsy, lung analysis and a detailed search of past occupations, which allowed compensation. Responding to a death-certificate study that linked furniture work to mesothelioma and raised wood dust as a possible cause, the author re-examined 18 mesotheliomas in furniture workers. Asbestos was found in the lungs of 17; six had also worked in railroad factories. The author concluded that death certificates cannot establish asbestos exposure. Each case needs a careful occupational history going back decades, mineralogical lung dust analysis and a correct pathological diagnosis.

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Mesotheliomas among railroad workers in the United States. T.F. Mancuso. 1991;643:333-46. PubMed · Publisher

Summary

This paper described asbestos exposure among U.S. railroad workers, mainly in the steam locomotive era, and the occurrence of mesothelioma among them. Retired machinists described how asbestos lagging was stripped from and applied to locomotive boilers, producing heavy dust throughout railroad shops. About 375 lagging blocks, roughly 6,000 pounds of insulation, were used on a 30-foot boiler. The cohort study used a seniority list from railroad company "A" of machinists and other crafts alive on January 1, 1945, who had been hired before 1935. A subcohort of 181 white male machinists hired in 1920-1929 was followed through 1989, analyzed by individual year of hire. There were 159 deaths, 42 from cancer. Of these, 15 (35%) were histologically confirmed mesotheliomas (14 pleural, one peritoneal) and 11 were lung cancers. Together they made up 61% of cancers, or 1 in every 7 machinists. The interval from first employment to death ranged from 33 to 64 years. The author also compiled 151 mesothelioma deaths among railroad workers from at least 20 companies across the country. He stressed that this was not a national study, and most of these deaths occurred at age 65 or over. He noted that research based on the Railroad Retirement Board omits 4.9 million former workers with under 10 years of service. An appendix cited railroad medical proceedings from 1932-1958 that discussed asbestosis and dust control. The author concluded that an unrecognized epidemic of occupational cancer had occurred among railroad workers, and he called for further studies, including of short-term workers and families.

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Mesotheliomas due to asbestos used in railroads in Italy. C. Maltoni, C. Pinto, A. Mobiglia. 1991;643:347-67. Review PubMed · Publisher

Abstract

The available knowledge of the oncogenic risks of asbestos, the presentation of some data on the uses of asbestos in railroads, with particular regard to the Italian State Railroads (Ferrovie dello Stato = FS), and the identification of groups at risk because of exposure to asbestos used in railroads are briefly reviewed. The available data in the literature on the pathologic effects of such exposure, and in particular on the onset of mesotheliomas among machinists and other railroad workers, are also summarized. Eighty-three cases, in various Italian regions, of mesothelioma (78 pleural, 4, peritoneal, and 1 pericardial) are reported that are related to the exposure to asbestos used in railroads. Twenty-six of these cases (among which 25 were reported in the Emilia-Romagna region) were submitted to a detailed study at the Bologna Institute of Oncology. Forty-nine cases of mesothelioma occurred among FS workers, in particular machinists; 29 cases occurred among machinists of rolling-stock workshops not belonging to the FS; 3 cases occurred among travelling workers of rolling-stock not belonging to the FS; 2 cases were found in members of the family (a daughter and a wife) of FS workers. This series of cases, together with similar data from the literature, proves the existence and gravity of an actual health risk due to asbestos used in the railroads. On the basis of the available data, the following steps are considered necessary: the adoption of preventive measures, the performance of medical oncological surveillance, the promotion of systematic epidemiologic investigations, and, finally, the placement of greater emphasis on basic research, aimed at generating information on the biological events taking place during the incubation period of the tumors. This information, hopefully, could be used to reduce the biological effect of exposure, and therefore for controlling the neoplastic process before onset of the disease in those who, having been exposed, although healthy, are potentially at risk.
Mineral fiber content of lung tissue in patients with environmental exposures: household contacts vs. building occupants. V.L. Roggli, W.E. Longo. 1991;643:511-8. Case report PubMed · Publisher

Abstract

Analysis of tissue mineral fiber content in patients with environmental exposures has seldom been reported in the past. Our studies of six household contacts of asbestos workers indicate that these individuals often have pulmonary asbestos concentrations similar to some occupationally exposed individuals. In contrast, our studies of four occupants of buildings with asbestos-containing materials indicate that these individuals often have pulmonary asbestos burdens indistinguishable from the general nonoccupationally exposed population. However, one such building occupant exposed for many years and who later developed pleural mesothelioma was studied in detail, and it was concluded that her exposure as a teacher's aide in a school building containing acoustical plaster was the likely cause of her mesothelioma.
Mortality experience of family contacts of asbestos factory workers. L. Joubert, H. Seidman, I.J. Selikoff. 1991;643:416-8. PubMed · Publisher

Summary

This short report described deaths among household contacts of workers at UNARCO Industries, an amosite asbestos factory in New Jersey that made thermal insulation from 1941 to 1954. The contacts were people who lived with a worker during his or her employment. The authors believed they were exposed to asbestos dust carried home on the worker's work clothes, hair and shoes. None had personal occupational exposure. The factory employed 1664 workers, who had 4044 household contacts. Of these contacts, 878 were examined (1973-1976 according to the table; the authors stated they had been observing the group since 1975), and 870 (99.1%) were traced through January 1990. Most contacts were first exposed at ages 10 to 15. The worker's length of employment, ranging from one day to 13 years, was used in place of each contact's exposure, whose intensity and duration were not known. Death certificates were obtained for all deaths and coded by the cause on the certificate. There were 115 deaths, of which 43 were from cancer: lung 12, digestive organs 10, non-Hodgkin's lymphoma 7, breast 4, pleural mesothelioma 4, reproductive organs 2, and other 4. The authors reported that 38% of deaths were from cancer, about double the national estimate of about 22%. They urged studies of other groups of family contacts to confirm whether such limited asbestos contact is as dangerous as it appeared.

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Neoplastic findings in experimental asbestos studies and conclusions for fiber carcinogenesis in humans. F. Pott. 1991;643:205-18. Review PubMed · Publisher

Summary

This paper gave a brief overview of animal carcinogenicity studies of asbestos, mainly inhalation experiments in rats, with some results from injection directly into the serous body cavities, and drew conclusions for fiber carcinogenesis in humans. In most chrysotile inhalation experiments, exposure for 35 hours per week for 12 months produced lung tumors in about 20 to 50% of animals. Calidria chrysotile induced no tumors. High tumor rates after crocidolite inhalation were reported in only one study, and the same group could not confirm them. Amosite and tremolite gave tumor rates of 32% and 51%. In data from Davis and colleagues on 'long' and 'short' chrysotile and amosite, no difference was detected between the two fiber types. The author stated that these data did not support the view that lung cancer is most closely associated with fibers longer than 10 µm, but could not disprove it. The rat dose-response differed by a factor of more than 100 from the estimated risk in chrysotile textile workers. About 5,000 µg of 'short' amosite per rat lung was not associated with any lung tumor, whereas about 5% of this mass of 'long' chrysotile was associated with a 55% tumor rate. The author proposed that fibers implanted in the bronchial wall cause lung cancer, which could explain the combined effect of asbestos and cigarette smoke. He concluded that inhalation tests can give false-negative results and that mineral fibers may need to be classified using studies in which fibers are placed directly into a serous cavity.

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Noninvasive detection of early asbestos-related disease of the thorax: algorithmic analysis of radiographic, nuclear, and serologic tests. S.D. Rockoff, A.M. Schwartz. 1991;643:121-32. Review PubMed · Publisher

Abstract

Improved imaging techniques may assist in the diagnosis of early asbestosis, such as could occur from "asbestos in place." These include (1) increased visualization of visceral pleural thickening, (2) high-resolution computed tomography (HRCT), and (3) gallium scanning, combined with evidence of serum markers indicating inflammation-associated pulmonary collagen formation. Combining these imaging and serum test observations with a clinically useful algorithmic approach may permit the diagnosis of "early" asbestosis, which is not now possible from the individual test results or from an unweighted combination of such data.
Observations on the carcinogenicity of asbestos fibers. M.C. Jaurand. 1991;643:258-70. Review PubMed · Publisher

Abstract

This paper summarizes animal experiments and in vitro data carried out to study the oncogenic effects of asbestos fibers on mesothelial cells. An interpretation of the results is made in light of current statements on the carcinogenicity of asbestos fibers. Experimental results appear to show that the carcinogenicity of mineral fibers is a complex, multiparametric phenomenon. Chromosomal mutations and possibly oxygen derivatives are involved in the genesis of the fiber-induced neoplastic process and may be the result of the intrinsic fiber properties, size, and physicochemistry. The role of fiber solubility is discussed; it is suggested that additional experiments are necessary for a better understanding of the importance of solubility in the concept of biopersistence.
Pleural abnormality as a cause of impairment and disability. P. Ernst, J. Bourbeau, M.R. Becklake. 1991;643:157-61. Review PubMed · Publisher
Pleural effects of environmental asbestos pollution in Corsica. J.R. Viallat, C. Boutin, J. Steinbauer, et al. 1991;643:438-43. PubMed · Publisher

Summary

This report described a series of surveys of pleural disease and environmental asbestos in Corsica. Outcrops containing chrysotile and tremolite occur in the island's northeastern area. The surveys followed a 1978 finding of bilateral pleural plaques in 3.8% of control subjects who were not occupationally exposed to asbestos. At a hospital in central Corsica, two experts who did not know the patients' birthplace read chest radiographs of 1,851 patients over 50 years old who were born and living in Corsica. After exclusions, bilateral plaques were found in 3.7% of patients born in the northeast and 1.1% of those born in the northwest (p < 0.05; relative risk 3.3). In 1982, 30 of 92 people over 50 (33%) in exposed villages, with no known occupational exposure, had bilateral plaques. A 1988 survey found plaques in 41% of inhabitants over 50 in Murato, an exposed village, compared with 6% in Vezzani, an unexposed village. Air samples from eight villages were analysed by transmission electron microscopy. Mean tremolite concentrations were 24 ng/m3 in exposed northeastern villages and 0.2 ng/m3 in control villages (p < 0.05). Mean chrysotile concentrations were 15.2 and 0.5 ng/m3, a difference that was not statistically significant. Since 1978 the authors had recorded eight patients with malignant mesothelioma, which they attributed to childhood environmental exposure. Lung mineral analyses showed elevated tremolite and variable chrysotile. The authors concluded that an elevated tremolite lung burden is a marker of environmental exposure in Corsica. They also stated that their data were not sufficient to show that either mineral alone was responsible for the pleural disease.

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Pleural plaques in the general population. G. Hillerdal. 1991;643:430-7. PubMed · Publisher

Summary

The author used pleural plaques to measure the impact of asbestos on the general population of Uppsala county, Sweden, which had a population of 250,782 in 1985. A general health survey invited all inhabitants aged 15 and over every second or third year until June 1985 and included a small-size chest X-ray. The study included all persons found from 1970 to June 1985 with plaques meeting strict radiological criteria: bilateral, at least 5 mm thick and/or calcified, well demarcated, and progressing over 5 years. Referred patients were also included. All were recalled for examination and an exposure history. There were 1,596 men and 79 women, and 1,349 (84.6 percent) were found in the survey. By 1985, plaques were present in 2.7 percent of males over 40. Of the men, 88.4 percent had occupational asbestos exposure, most often in building and construction, 0.8 percent had nonoccupational exposure, and 10.8 percent denied exposure. Of the women, 13.9 percent had occupational exposure, 17.7 percent had mostly domestic exposure, and 68.4 percent denied exposure. Mean latency in 1,096 men was 33.2 years. Finnish-born persons made up 49.4 percent of the women. Finnish men denied exposure more often than Swedish men (28.2 versus 9.5 percent). The author concluded that plaques in men usually reflect occupational exposure, whereas in women exposure is often not found.

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Radiological abnormalities and asbestos exposure among custodians of the New York City Board of Education. S.M. Levin, I.J. Selikoff. 1991;643:530-9. PubMed · Publisher

Abstract

Six hundred sixty custodians employed by the New York City Board of Education underwent examination from 1985 through 1987 for asbestos-related disease and other general medical conditions by the clinical staff of the Division of Environmental and Occupational Medicine of the Mount Sinai School of Medicine of the City University of New York. Two-thirds of the men (no women were examined) were 20 or more years from onset of any custodial work, with 44% having had at least 20 years of employment as custodial workers in New York City Board of Education schools. Twenty-four percent had begun custodial work in buildings 30 or more years earlier. Findings among them were of particular interest since asbestos-related disease might forecast what might be expected among school custodians with less seniority. Since the Board of Education, in selecting custodians for examination, had chosen only custodians currently employed, the study group comprised men still working in the school system. These, then, represented a "survivor population" (4% had retired between the time of enrollment in the study and the date of examination, and only one of the seventeen retirees had left work owing to disability). Although a considerable amount of clinical information was obtained, abnormalities on chest X-ray consistent with asbestos-induced scarring were used as the key index of disease resulting from exposure to asbestos. Since scarring of the lung tissue or lining of the lung or chest wall (pleura) may be present but undetectable on standard chest radiographs (a relatively insensitive diagnostic technique), the prevalence of abnormality on X-ray film represents a conservative estimate of the actual burden of scarring lung disease in the group. Such changes are indicative of previous asbestos exposure, however, and provide evidence of an increased risk of later asbestos-related malignancy. Overall, abnormalities on chest X-ray consistent with asbestos-related scarring were found in 28% of the men examined. The expected relationship of increasing prevalence of radiographic changes with increasing time since onset of exposure in buildings was demonstrated; among those with 35 or more years since beginning custodial work, 39% had abnormal films. This is evidence that custodial workers as a group have had asbestos exposure in the past, as reflected also in the work histories obtained at the time of examination. Eighty-four percent reported that they themselves removed asbestos-containing materials in the course of their work. Eighty-nine percent had been present in the work area during asbestos abatement projects in the schools in more recent years.(ABSTRACT TRUNCATED AT 400 WORDS)
Role of peptide growth factors in asbestos-related human lung cancer. B. Guillemin, Y. Zhang, T.C. Lee, et al. 1991;643:245-57. Review PubMed · Publisher
Should asbestos in buildings be regulated on an environmental or occupational basis?. D.M. Hashimoto, T.A. Brennan, D.C. Christiani. 1991;643:609-13. PubMed · Publisher
Swedish approaches to industry-wide studies: the construction industry. A. Englund. 1991;643:313-5. PubMed · Publisher
The carcinogenicity of chrysotile asbestos. J.S. Harington. 1991;643:465-72. Review PubMed · Publisher

Abstract

In in vitro test systems, chrysotile is markedly toxic, causes chromosomal aberrations, and is capable of inducing morphological and preneoplastic transformation. In carefully designed animal experiments, chrysotile produces lung cancer and mesothelioma as effectively as do the amphiboles tested. Human population studies do not refute these experimental results. Chrysotile asbestos is carcinogenic to humans, especially for the induction of lung cancer and mesothelioma in exposed populations. For cancers of other sites, with the exception of laryngeal and possibly gastrointestinal cancer, the evidence for association with exposure to all forms of asbestos, including chrysotile, is not yet adequate for evaluation.
The clinical relevance of asbestos-induced pleural fibrosis. D.A. Schwartz. 1991;643:169-77. PubMed · Publisher

Abstract

Asbestos-induced pleural fibrosis is the most common radiographic abnormality among asbestos-exposed persons. Circumscribed pleural plaques and diffuse pleural thickening account for more than 90% of the asbestos-induced chest wall abnormalities, and their prevalence is expected to increase for the next 15 to 20 years. Several investigators have recently found that pleural plaques and diffuse pleural thickening independently contribute to the development of restrictive lung function. The work presented in this paper indicates that asbestos-induced pleural fibrosis is also associated with evidence of interstitial lung abnormalities, even among those with normal parenchyma on chest X-ray film. These parenchymal abnormalities include an increased percentage of lymphocytes on bronchoalveolar lavage and an increase in the interstitial changes observed on high-resolution chest computerized tomography (HRCT) scan. However, neither a lymphocytic alveolitis nor an interstitial parenchymal fibrosis influenced the relationship between pleural fibrosis and restrictive lung function. We conclude that asbestos-induced pleural disease contributes to the development of restrictive lung function and identify a group of exposed individuals who are at excess risk of asbestosis.
The costs of imprecision: perspectives in asbestos abatement. N.A. Esmen. 1991;643:582-8. PubMed · Publisher
The effect of asbestos-induced pleural fibrosis on pulmonary function: quantitative evaluation. R. Lilis, A. Miller, J. Godbold, et al. 1991;643:162-8. Review PubMed · Publisher

Summary

The authors proposed an integrative index of pleural fibrosis (INDEX) and used it to examine how asbestos-related pleural fibrosis relates to pulmonary function. The index combined all pleural features recorded under the 1980 ILO International Classification of Radiographs of Pneumoconioses: chest wall pleural fibrosis in profile (extent and width), pleura face on, diaphragmatic plaque and pleural calcification. It was scored for each hemithorax, with a maximum total of 40. INDEX values were calculated for 1,584 asbestos insulation workers with long-term exposure, most for more than 30 years. All were members of a cohort of 17,800 men in the United States and Canada who were examined between July 1981 and November 1983, 30 or more years after starting work. The examination included histories, chest X-rays and spirometry. Pleural fibrosis was present in 1,185 men (75%); 82.3% of these cases were circumscribed and 17.7% diffuse. Years since first exposure was the only variable significantly correlated with the index. High INDEX values (≥12) were more common when interstitial fibrosis was also present (8% versus 1.5%). In multiple regression, the index was significantly associated with lower forced vital capacity (FVC % predicted), independently of the profusion of small opacities, smoking and years since first exposure. In the circumscribed subgroup, the inverse relationship was significant (p < .0001). In the diffuse subgroup, the presence of diffuse fibrosis lowered FVC even at low index values. The authors concluded that extensive circumscribed pleural fibrosis has a negative, restrictive effect on pulmonary function.

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The increasing importance of asbestos-related pleural disease. L. Rosenstock, L.D. Hudson. 1991;643:296-300. PubMed · Publisher
The pathobiology of asbestos-induced lung disease: a proposed role for macrophage-derived growth factors. J.A. Lasky, J.C. Bonner, A.R. Brody. 1991;643:239-44. Review PubMed · Publisher
The Third Wave of Asbestos Disease: Exposure to Asbestos in Place--Public Health Control. Conference. New York, New York, June 7-9, 1990. 1991;643:1-625. PubMed
The third wave of asbestos disease: exposure to asbestos in place. Public health control. Introduction. P.J. Landrigan. 1991;643:xv-xvi. PubMed · Publisher

Summary

This introduction opened the proceedings of a conference on asbestos in place, held in New York on June 6–8, 1990, under the auspices of the Collegium Ramazzini. The author recalled two earlier New York Academy of Sciences reports, Biological Effects of Asbestos (1965) and Health Hazards of Asbestos Exposure, which documented links between asbestos exposure and asbestosis, lung cancer and mesothelioma. He described a first phase of asbestos disease among workers in mining, milling and product manufacture, recognized from the 1920s. A second phase occurred among people who used asbestos products. A potential third phase could affect people repairing, renovating or demolishing ageing buildings containing asbestos, and building users such as school children, office workers and maintenance workers. He stated that epidemiologic studies had shown that all forms of asbestos could cause these diseases, in a positive dose-response relationship with cumulative exposure, and that even short-term or low-level exposures posed risk. He cited an estimate of 30,000 to 50,000 premature deaths in New York State by the end of the century from occupational exposures before 1980. He also cited a projection of about 1,000 cases of mesothelioma and lung cancer over the next 30 years among people exposed to asbestos in school buildings as children. The conference was called to better understand the consequences of low-level exposure. The author argued that carefully reviewed scientific information offered the best basis for meeting this challenge.

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The Veterans Administration's Asbestos Abatement Program. G.W. Schepers. 1991;643:597-608. PubMed · Publisher
Abstract
1. The Veterans Administration has developed a program of asbestos abatement for its more than 1000 buildings, where health care personnel from 173 hospitals and 238 ambulatory care clinics are likely to encounter respirable asbestos. 2. This is a costly program, which has averaged about $25 million annually for the past ten years. 3. The VA has banned the use of new asbestos products containing more than 1% of asbestos in building construction or renovation projects. 4. Industrial hygiene engineering programs have been ordered instituted at all VA medical centers to monitor dust levels in compliance with OSHA and EPA requirements. 5. Health surveillance programs, managed by an environmental health physician at each medical center, have been instituted for all personnel who have been identified to have breathed asbestos fibers in excess of OSHA-EPA threshold limit values. 6. The health care program focuses on the identification of asbestosis and asbestos-related cancer through periodic X-ray films, lung function tests, and electrocardiographic and physical examination screening. 7. The program also stresses cessation of smoking.
Variability in interpretation of radiographs for asbestosis abnormalities: problems and solutions. A.M. Ducatman. 1991;643:108-20. Review PubMed · Publisher

Abstract

Interobserver variation continues to be a substantial problem for interpretation of asbestos-workers' X-rays, despite incremental improvements in the International Labour Office (ILO) classification system. The apparent degree of agreement/variability is affected by the population disease prevalence. For most populations, experts will be able to agree routinely about normal films. Yet designed trials show that selected experts exhibit a two-fold or greater range for perceived prevalence of abnormal profusions. This degree of variability would be adequate for many population studies were it achieved under real-life conditions of interpretation. Unfortunately, the realistic degree of interobserver variability is probably much higher under actual population surveillance conditions. Asbestos population surveillance programs have provided little or no quality assurance for ILO interpretations, so the very high variability suggested by available data are not surprising and are not the fault of the classification. Recommendations include required participation in quality-assurance panels for those who wish to be certified as interpreters, with consistent feedback and the dropping of outliers. If quality-assurance programs are implemented, the classification will achieve its intended epidemiologic purposes.
Variations in the carcinogenicity of tremolite dust samples of differing morphology. J.M. Davis, J. Addison, C. McIntosh, et al. 1991;643:473-90. PubMed · Publisher

Abstract

Six samples of tremolite of different morphological type were prepared as dusts of respirable size and used in intraperitoneal injection studies in rats. Three "asbestiform" tremolites produced mesotheliomas in almost all animals, although with significantly different tumor-induction periods. A brittle type of fibrous tremolite which, when manipulated to prepare "respirable dust," produced a sample with relatively few asbestiform fibers remaining nonetheless produced tumors in 70% of rats. Two samples of nonfibrous tremolite produced respirable dust samples containing numerous elongated fragments with aspect ratios greater than 3:1, which therefore fitted the definition of respirable fibers. Both these samples produced relatively few tumors, although one had more long "fibers" than did the brittle tremolite that produced 70% of tumors. This study has therefore demonstrated that different morphologic forms of tremolite produce dusts with very different carcinogenic potential. Carcinogenicity does not depend simply on the number of elongated particles injected, and we need to develop methods of distinguishing carcinogenic tremolite fibers from relatively innocuous tremolite dusts, with similar numbers of elongated particles of similar aspect ratios.

In plain English

Edinburgh researchers tested six tremolite dust samples of different physical forms in rats. Three were asbestiform tremolites: Californian, Korean, and one supplied by a Swansea laboratory whose country of origin was uncertain. One was a brittle fibrous tremolite from Italy. Two, from Dornie and Shinness in Scotland, were made up mostly of cleavage fragments. Each dust was injected once, at 10 mg, into the abdominal cavity of 33 or 36 rats, which lived out their lives. Peritoneal mesothelioma developed in 36 of 36 rats given California tremolite, 35 of 36 given Swansea, 32 of 33 given Korean, 24 of 36 given Italian, 4 of 33 given Dornie and 2 of 36 given Shinness tremolite. The Italian sample caused far more tumors than the Dornie sample, even though the Italian dose had only about one-third as many fibers longer than 8 micrometers. No single fiber-size measure fully explained the differences. The authors concluded that different forms of tremolite produce dusts with very different carcinogenic potential, and that methods are needed to tell carcinogenic fibers from relatively harmless dusts.

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Decline in death rates among asbestos insulation workers 1967-1986 associated with diminution of work exposure to asbestos. H. Seidman, I.J. Selikoff. 1990;609:300-17; discussion 317-8. PubMed · Publisher

Abstract

We investigated the consequences of a reduction of asbestos exposure among a cohort of asbestos insulation workers in the United States and Canada. By examining data over three time periods during which asbestos exposure declined, we obtained data indicating that reduction in exposure was associated with an observable decrease in mortality, with little time lag, from some asbestos-associated diseases, even among workers previously exposed for 20 or more years.

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1980s

An industrial hygienist's perspective on generic standards. J.S. Lee. 1989;572:93-9; discussion 107-9. PubMed · Publisher

Abstract

OSHA and EPA regulations promulgated to date contain the necessary framework to consider generic standards in the 1990s. Missing in OSHA standards has been the requirement for a competent person to define and manage an occupational health program and the requirement for all employers who have toxic materials with significant exposures to have a basic occupational health program. Certainly we have evolved to a point where every worker significantly exposed to toxic materials has a right to know what that exposure is. Fundamental to generic standards is the need to define what is meant by toxic substance and significant exposure level. It is suggested that NIOSH maintain a list of recognized safe exposure levels that have been recommended by credible organizations including NIOSH. It is suggested that action levels be defined as one-half the lowest recognized safe exposure level. It is proposed that all employers be required to conduct an initial inspection of their workplace, using competent persons, to determine if exposures exceed action levels. This is only one step beyond the requirements of the OSHA Hazard Communication Rule which requires that employers identify and maintain a list of all hazardous materials known to be present in the workplace and to inform workers of the hazards. If exposure levels are found in excess of action levels, then the basic elements of current standards would be required, including regular employee-exposure monitoring, medical surveillance, sanitation, training and education, and a management plan.
Results of recent experimental research on the carcinogenicity of natural and modified asbestos. F. Minardi, C. Maltoni. 1988;534:754-61. PubMed · Publisher

Abstract

Long-term experimental bioassays were carried out on natural asbestos of different types and origin (crocidolite, chrysotile, amosite, antophyllite), on asbestos cement, and on industrially modified chrysotiles. The materials were tested on Sprague-Dawley rats by intraperitoneal and intrapleural injection. The experiments were carried out with highly standardized procedures on all materials to enable comparative evaluation of the results. The data presented confirm that asbestos of different types produces peritoneal and pleural mesotheliomas, show that asbestos cement is also mesotheliomatogenic, and demonstrate that the peritoneum is more responsive than the pleura. Furthermore, evidence is provided that the mesotheliomatogenic effects of different types of asbestos vary with the types and origin of the minerals, and that physical and chemical modifications of the natural chrysotile can lower its carcinogenic effect.
Short-term tests for the evaluation of potential cancer risk of modified asbestos fibers. M.C. Jaurand, A. Renier, A. Gaudichet, et al. 1988;534:741-53. PubMed · Publisher

Summary

The authors used short-term in vitro tests to assess the potential carcinogenic potency of Canadian chrysotile fibers that had been chemically modified by a phosphatation process for industrial purposes. They compared these with unmodified chrysotile. Fiber size was measured by optical and electron microscopy. Durability was assessed by electron microprobe analysis of fibers ingested by rabbit alveolar macrophages. Cytotoxicity, chromosomal aberrations and cell transformation were tested in rat pleural mesothelial cells (RPMC), in some experiments with benzo(a)pyrene added.

The two fiber types had similar size distributions. Fibers meeting Stanton's criteria numbered about 3 x 10^6 per microgram, about 15 percent of all fibers. After 24 hours in macrophages, unleached untreated chrysotile fell to about 30 percent. Mean Mg/Si peak ratios were 0.76 for unmodified and 0.94 for modified fibers, against starting values of 0.89 and 0.91. Modified fibers were less cytotoxic: viability with 10 µg/ml of untreated fibers was similar to that with 20 µg/ml of modified fibers. Unmodified chrysotile significantly increased chromosomal aberrations from 7 to 15 µg/ml. The increase with modified fibers was not statistically significant. Both types significantly altered chromosome number. Both increased the transformation index compared with controls. The index fell as more cells were plated.

The authors concluded that the modified fibers were more stable and less cytotoxic and clastogenic per unit weight. Transforming potency appeared equivalent, but the assay was not sufficiently established. Animal experiments were in progress.

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The release of bombesin-like peptides from small cell lung cancer cells. T.W. Moody, L.Y. Korman. 1988;547:351-9. PubMed · Publisher

Abstract

High levels of BN/GRP are present in classic SCLC and lung carcinoids, whereas BN immunoreactivity is absent in variant SCLC, adenocarcinoma, large cell carcinoma, squamous cell carcinoma, and mesothelioma cell lines. BN-like peptides are secreted from classic SCLC into the tissue culture medium. The secretion rate of BN-like peptides from cell line NCI-H345 was increased 3-fold by VIP (1 microM). Also, VIP increased the cAMP levels in cell line NCI-H345 by an order of magnitude. Therefore, SCLC cells have functional VIP receptors which regulate the secretion of BN-like peptides. Also, SRIF (100 nM) inhibits the VIP-stimulated increase in cAMP levels and secretion rate of BN-like peptides from SCLC cells. Because BN stimulates colony formation, VIP and/or SRIF may be able to alter the growth of SCLC cells. BN-like peptides are secreted from SCLC cells into the plasma. The levels of BN immunoreactivity in the plasma of SCLC patients with extensive disease is 2- to 40-fold greater than that of patients with limited disease. Secretin infusion into patients with extensive disease produces a transient increase (7-fold) in the plasma concentration of BN-like peptides. BN-like peptides are also present in the CSF of SCLC patients. When released from SCLC cells, BN-like peptides may interact with cell surface receptors. [Tyr4]BN binds with high affinity (Kd = 0.5 nM) to a single class of sites (1500/cell) on cell line NCI-H345. The carboxyl terminus of BN or GRP is essential for high-affinity binding activity. BN-like peptides elevate cytosolic Ca2+ levels as a result of increased phosphatidylinositol turnover. The putative BN receptor antagonist [D-Arg1, D-Pro2, D-Trp7,9, Leu11]substance P inhibits high-affinity [Tyr4]BN binding, the ability of BN to elevate cytosolic Ca2+ levels, and colony formation of SCLC cells. Therefore, BN receptor antagonists may serve as useful agents to inhibit the growth of SCLC.
The role of intervention studies in ascertaining the contribution of dietary factors in lung cancer. The Seattle chemoprevention trial of retinoids in asbestos-exposed workers. G.S. Omenn, G.E. Goodman, G.D. Kleinman, et al. 1988;534:575-83. PubMed · Publisher

Summary

This paper described the design of the Seattle chemoprevention trial, which tested whether oral retinoids could reduce lung cancer and mesothelioma in asbestos-exposed workers, and discussed problems of prevention trials. Eligible subjects were aged 45 to 74. They had either at least 15 years since first asbestos exposure and a positive chest X-ray by ILO criteria, or 5 years' work in a high-risk trade in the Pacific Northwest, such as pipefitting, insulating or shipyard work. Subjects were located through workers' compensation systems, the U.S. Navy Asbestos Medical Surveillance program at Bremerton, medical specialists, lawyers and union screening programs. The planned double-blind randomized trial required about 2500 subjects (1250 per arm) receiving 25,000 units of retinol plus 15 mg of beta-carotene daily, or placebo. Subjects completed a 2-month run-in period and were stratified by smoking status, time since first exposure and chest X-ray result. The endpoints were the incidences of lung cancer and mesothelioma. From data reported by Berry and by Selikoff and Hammond, the authors estimated a lung cancer risk of 10 per 1000 person-years in the placebo group. They calculated that, allowing for 20 percent attrition over 5 years, a 40-50 percent reduction could be detected with 80 percent power. All of the first 36 subjects met the run-in compliance criterion. The authors noted that prevention trials differ from treatment trials in endpoints, duration, sample size, dosing strategy and logistics; almost 10 million capsules would be needed. They concluded that drug-based chemoprevention was a useful approach complementing primary prevention, but that its logistic complications and costs needed to be appreciated and streamlined.

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Exposure of sheet-metal workers to asbestos during the construction and renovation of commercial buildings in New York City. A case study in social medicine. E. Drucker, D. Nagin, D. Michaels, et al. 1987;502:230-44. PubMed · Publisher

Abstract

New York City sheet-metal workers have a history of significant exposure to asbestos. Prior to 1972 when the use of sprayed asbestos insulation was banned in New York City, sheet-metal workers involved in building construction were exposed as they worked adjacent to spraying operations. Subsequent to that date, exposure continued as they renovated these same buildings. In 1982 the Occupational Health Program of Montefiore Medical Center and the Albert Einstein College of Medicine initiated a multidimensional asbestos evaluation and intervention program for the sheet-metal industry and union in New York. The long-term goal of the program was to eliminate asbestos exposure through the safe, systematic removal of asbestos in New York City buildings, most likely a legislated solution. In the short term, we attempted to assess and reduce asbestos exposure in the sheet-metal trade by a series of steps consisting of: mortality and morbidity studies; a medical audit of clinical screening services provided to sheet-metal workers; a comprehensive health education program; development of safe work practices; evaluation of personal protective equipment; and investigation into and support of legislative and regulatory solutions to the problem of asbestos contamination of commercial buildings. This intervention can be seen as a case study in the practice of social medicine.
What's wrong with the environment?. R.J. Benoit. 1987;502:1-20. Review PubMed · Publisher
Initial deposition pattern of inhaled minerals and consequent pathogenic events at the alveolar level. A.R. Brody, D.B. Warheit, L.Y. Chang, et al. 1984;428:108-20. Review PubMed · Publisher

Summary

This paper reviewed the authors' recent laboratory findings on the earliest events after mineral dusts are inhaled into the alveolar region of the lung. Rats were exposed briefly (1-3 hr) to chrysotile asbestos, crocidolite asbestos, fiberglass, alpha-quartz or Mt. St. Helens ash, and mice to chrysotile. Scanning electron microscopy showed that, regardless of mineral type, shape or concentration, particles reaching the alveoli were deposited primarily at alveolar duct bifurcations. Chrysotile fibers were taken up by type I epithelial cells during the first hour and reached the interstitium within four days. One month after a one-hour exposure, about 50% of bifurcations contained calcium deposits inside fibroblast-like cells, often with chrysotile fibrils at their centre. Chrysotile bound to sialic acid on red blood cell membranes and altered sodium and potassium flux within 5 minutes. Macrophages gathered at bifurcations within 48 hr of a one-hour chrysotile exposure. Complement-deficient mice and complement-depleted rats had fewer macrophages at these sites, which the authors attributed to a chemotactic factor believed to be C5a. Macrophages washed from exposed rats showed reduced phagocytosis, impaired migration and raised acid phosphatase and lactate dehydrogenase. Morphometry 48 hr after exposure showed that the tissue area of first bifurcations nearly doubled and interstitial macrophage density tripled, and some changes persisted at one month. The authors proposed that these changes represent the earliest anatomic lesion of asbestosis.

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Role of gene and chromosomal mutations in cell transformation. J.C. Barrett, D.G. Thomassen, T.W. Hesterberg. 1983;407:291-300. Review PubMed · Publisher

Abstract

To understand the role of mutagenesis in carcinogenesis fully, we must consider all types of mutations including gene, chromosomal, and gene-number mutations and all changes involved in the progressive development of neoplastic cells. We have found that certain known human carcinogens (i.e., DES and asbestos), which were classified as epigenetic carcinogens based on gene-mutation assays, have mutational activity at the chromosomal level that correlates with their ability to induce cell transformation. This should caution against classification of chemicals as genotoxic or epigenetic without a complete understanding of their mechanism of action. Furthermore, our studies indicate that more than gene-mutation assays is needed for carcinogen testing. In particular, chromosomal changes induced by chemicals, both aberrations and aneuploidy, need to be carefully assessed. In addition, the role of all types of mutation in the overall process of neoplastic transformation needs to be determined. This can only be examined by studying each individual change involved in neoplastic progression. Thus, any attempt to assess a chemical's carcinogenic potential should consider not only all types of mutational changes but both early and late changes involved in neoplastic transformation.
Mortality of brain tumors among asbestos insulation workers in the United States and Canada. H. Seidman, I.J. Selikoff, E.C. Hammond. 1982;381:160-71. PubMed · Publisher

Abstract

Death resulting from brain tumors among workers in the petrochemical industry have called attention to the possibility that these neoplasms may be the result of occupational exposure to carcinogens. We have examined the experience of a cohort of 17,800 insulation workers known to be at significant increased risk of cancer at a number of sites (lung, mesothelioma, gastrointestinal, oral cavity, pharyngeal, larynx, renal) to ascertain whether their asbestos exposure also increased their risk of brain tumors. From 1967 to 1979, there were 24 deaths from primary brain tumors in this cohort, somewhat more than were anticipated (18.0 such deaths were expected based on U.S. general population data, and 20.5 if smoking was taken into account). The excess was not "statistically significant" at the 5% level although this does not rule out the possibility of an etiological association. It was of interest that the observed excess was concentrated (about twice expected) among insulators in the younger ages (those under 50) and during the early period after onset of work (15-24 years), in contrast with age distribution and latency in other asbestos-associated neoplasms. This may have relevance to theoretical concerns about questions of initiation and promotion in the etiology of cancer, particularly with regard to brain tumors.
The investigation of brain tumor occurrence in other occupational groups: introduction. I.J. Selikoff. 1982;381:116-8. PubMed · Publisher

Summary

This short introduction to a conference session on brain tumors in occupational groups addressed why earlier presentations had reached conflicting conclusions, with methodological problems suggested as a possible explanation. To illustrate these difficulties, the author presented mortality data from an earlier study of 17,800 asbestos insulation workers in the United States and Canada, all identified on January 1, 1967, and followed to December 31, 1976 (166,853 man-years of observation). Causes of death were classified both by best available evidence (autopsy, surgical, clinical) and by death certificate alone. Expected deaths were based on U.S. white male rates. About 3,000 men were more than 30 years from onset of exposure. Increased asbestos-associated cancers were readily identified for common sites. However, almost nothing was seen earlier than 20 years from onset: there were 325 deaths before 20 years, compared with 1,946 at 20 or more years. Only 83 of 995 cancers, and 5 of 175 mesotheliomas, occurred before 20 years. For less common cancers, including brain (14 observed by best evidence and 17 by death certificate, against 10.4 expected), the data were not sufficient for confidence. The author concluded that small numbers and inadequate latency make cancer hard to detect, even for a well-defined carcinogen, so continued debate about brain tumors was to be expected.

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1970s

Asbestos abatement in schools: observations and experiences. R.N. Sawyer, E.J. Swoszowski. 1979;330:765-75. PubMed · Publisher
Asbestos contamination in United States schools from use of asbestos surfacing materials. W.J. Nicholson, E.J. Swoszowski, A.N. Rohl, et al. 1979;330:587-96. PubMed · Publisher

Summary

The authors examined the use and condition of asbestos surfacing materials in United States schools and the resulting airborne asbestos levels. In a New Jersey survey, 265 of about 2400 schools had reported nearly three million square feet of what they considered asbestos material in pupil areas. With the state Department of Education, the Mount Sinai Environmental Sciences Laboratory visited 48 schools in 21 districts. Districts were selected randomly, weighted toward those reporting more asbestos use. Sixty-four bulk samples were analysed. Materials were classified as loose friable fibrous spray, moderately dense spray, or plaster or textured paint, and graded for damage. Asbestos was confirmed in 97% of schools that believed their sprayed material contained it, and two-thirds of schools with asbestos surfaces showed visible damage. Four- to eight-hour air samples were taken in ten schools with visible damage in New Jersey, Massachusetts and New York and analysed for chrysotile by electron microscopy. Concentrations ranged from 9 to 1950 ng/m3, averaging 217 ng/m3. Outside air at three schools averaged 14 ng/m3. Ninety-six percent of school samples exceeded 20 ng/m3, whereas 98.5% of 187 ambient samples from 48 US cities were below that level. The authors estimated that two to six million pupils and 100,000 to 300,000 teachers nationally may be in schools with asbestos surfaces. They concluded that visible damage indicates increased air concentrations and that long-term exposure of children above 100 ng/m3 may not be without later risk of asbestos disease.

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Asbestos disease and compensation. R.E. Sweeney, B. Castleman. 1979;330:273-80. Historical article PubMed · Publisher
Asbestos disease in maintenance workers of the chemical industry. R. Lilis, S. Daum, H. Anderson, et al. 1979;330:127-35. PubMed · Publisher

Abstract

In several large groups of workers employed in chemical plants, chest x-ray abnormalities (small irregular opacities and/or pleural changes) of the type known to be induced by asbestos were found in a proportion of those examined. A cross-sectional study of maintenance workers in a large chemical plant was undertaken to evaluate the prevalence of asbestosis; 185 workers were examined. Radiologic evidence of parenchymal interstitial fibrosis was found in 24% of those examined; in 10% of workers, parenchymal fibrosis was the only abnormality. Pleural fibrosis and/or calcification was found in the absence of parenchymal fibrosis in 14% of cases; in another 14% of workers, both parenchymal and pleural abnormalities were detected. The prevalence was significantly higher in those employed 20 or more years. Pleural abnormalities were more prevalent than were parenchymal changes. The increased risk of lung cancer and mesothelioma remains to be studied.
Asbestos disease in United States shipyards. I.J. Selikoff, R. Lilis, W.J. Nicholson. 1979;330:295-311. PubMed · Publisher

Summary

The authors examined whether asbestos-associated disease was a problem among United States shipyard workers. They reviewed wartime records showing that shipyard employment rose from 168,000 in June 1940 to 1,722,500 in December 1943, with high labor turnover. About one in 500 private-shipyard workers was an "asbestos worker," but other trades also had opportunity for exposure. They followed 440 insulation workers in nine shipyard union locals from 1967 through 1976. Of these, 79 died, including 39 from cancer (16.21 expected), 21 from lung cancer (5.73 expected) and 8 from mesothelioma. Asbestosis caused 17.8% of deaths among shipyard insulators and 7.8% among other insulators. The shipyard figure rested on only 13 asbestosis deaths, and mortality otherwise did not differ substantially between the groups. In 1975-1976 the authors examined 1000 volunteer workers at a shipyard in Groton, Connecticut. A panel of five readers classified chest x-rays using the ILO U/C classification. Abnormalities were found in 459 workers (45.9%): 274 of 636 less than 20 years from onset of exposure and 185 of 364 at 20 or more years. Excluding insulators, prevalence rose from 13.9% at 0-9 years from onset to 61.0% at 30 or more years. No trade was free of changes. The authors concluded that past asbestos exposure was common across shipyard trades. They recommended avoiding further exposure, informing exposed workers and developing medical surveillance.

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Asbestos exposure, cigarette smoking and death rates. E.C. Hammond, I.J. Selikoff, H. Seidman. 1979;330:473-90. PubMed · Publisher

Summary

The study examined the combined effects of cigarette smoking and occupational asbestos exposure on death rates. Members of the insulation workers' union in the United States and Canada answered smoking questionnaires in 1966, and 17,800 men alive on January 1, 1967 were traced through December 31, 1976. The analysis was confined to 12,051 men observed 20 or more years after entering the trade (77,391 man-years, 1,946 deaths). Causes of death were coded from death certificates and from the best available medical evidence, including review of histologic slides and x-rays. Expected deaths were based on U.S. white male rates and on age- and smoking-specific rates of 73,763 comparable men from an American Cancer Society prospective study. All-cause mortality ratios were 1.70 and 1.41. Lung cancer ratios ranged from 4.24 to 5.51. Best evidence identified 170 mesothelioma deaths (61 pleural, 109 peritoneal) and 160 asbestosis deaths. Age-standardized lung cancer death rates per 100,000 man-years were 11.3 for unexposed nonsmokers, 58.4 for asbestos-exposed nonsmokers, 122.6 for unexposed smokers and 601.6 for asbestos-exposed smokers. The authors concluded that asbestos and smoking acted synergistically on lung cancer risk. They also concluded that smoking increased asbestosis deaths, that ex-smokers had lower death rates than continuing smokers, and that asbestos increased deaths from colorectal and esophageal cancer.

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Asbestos exposure: factors associated with excess cancer and respiratory disease mortality. V.L. Henderson, P.E. Enterline. 1979;330:117-26. PubMed · Publisher

Abstract

A cohort of 1075 men who completed their working lifetimes with an asbestos company, worked at a facility in the United States, and retired with a company pension during the period 1941--67 was updated for deaths through 1973. The average length of employment was 25 years, and all had been exposed to asbestos dust. Respiratory cancer and pneumoconiosis-pulmonary fibrosis mortalities were examined in relation to cumulative dust exposure and to other factors after taking into account cumulative dust exposure. Men who worked in the production of asbestos cement pipe exhibited a higher risk of respiratory cancer, as did men with some crocidolite asbestos exposure. Because these two groups overlap, we could not be certain that crocidolite asbestos was responsible for the increased risk. Men working in general plant maintenance displayed a striking lack of deaths due to pneumoconiosis-pulmonary fibrosis, as compared with production workers and with maintenance personnel assigned to specific departments. Five mesothelioma deaths were observed at age 65 and over. Three of these deaths occurred during the period 1970--3.
Asbestos in public water supplies: discussion of future problems. J.P. Hills. 1979;330:573-7. PubMed · Publisher
Asbestos in school buildings: results of a nation-wide survey. K.Z. Silver. 1979;330:777-86. PubMed · Publisher
Asbestos law: victims' rights and industry's reaction. K. Asch. 1979;330:255-72. PubMed · Publisher
Asbestos risk among full-time workers in an electricity-generating power station. A. Hirsch, L. Di Menza, A. Carre, et al. 1979;330:137-45. PubMed · Publisher

Abstract

A matched survey of 55 full-time workers probably exposed to asbestos in an electricity-generating power station (exposed group) and of 53 unexposed workers in an automobile plant has been conducted. The asbestos risk in the power station was confirmed by the presence of airborne fibers in the range 0.1--6000 X 10(-9) g/m3 in the air sampled during the survey period and by the presence of FB in the sputa of 32.7% of the workers. The following parameters were significantly related to asbestos exposure in the study group: FB in the sputa, localized rectitude of the diaphragm, pleural thickening, pleural calcification, and the chest pain. Moreover, for all persons studied, gastrointestinal symptoms and recent hoarsening of the voice were significantly related to the number of FB in the sputa.
Asbestos-associated disease in employees of Devonport Dockyard. G. Sheers. 1979;330:281-7. PubMed · Publisher

Summary

This paper described asbestos-associated abnormalities during the 10 years after 1966 in Devonport Dockyard, the largest of the four main UK naval dockyards. About 15,000 men worked there, and past exposure was to chrysotile and, in most cases, also crocidolite and amosite. A 1966 one-in-ten sample showed a prevalence of all asbestos-associated abnormality of 4.5% (pleural 4.2%, pulmonary fibrosis 0.3%). Of 971 men with normal radiographs in 1966 who were re-examined in 1977, 96 had nonmalignant asbestos-related abnormalities: 79 plaques, 11 diffuse pleural fibrosis and six pulmonary fibrosis. Annual attack rates were 8.4 per thousand for pleural abnormalities and 0.5 per thousand for pulmonary fibrosis. Among 256 men with pleural abnormalities followed for over 10 years, 38% of hyaline plaques were unchanged, and 10% overall progressed to pulmonary fibrosis. Acute pleural reactions were seen in 52 cases. Among 410 men with pleural abnormalities there were 75 deaths in 1967-1976, with an excess of cancer deaths, mainly mesothelioma. No excess bronchial carcinoma mortality was demonstrable in men with plaques. Of 103 mesothelioma cases diagnosed in the Plymouth area, 100 were associated with dockyard work or naval service. The author concluded that a dockyard pleural plaque could no longer be assumed to be only a marker of exposure, and that fibrosing disease was now seldom severe. He expected mesothelioma incidence to keep rising into the 1980s.

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Asbestosis among household contacts of asbestos factory workers. H.A. Anderson, R. Lilis, S.M. Daum, et al. 1979;330:387-99. PubMed · Publisher

Summary

The authors studied whether household contacts of asbestos factory workers, with no occupational exposure of their own, had asbestos-associated chest x-ray changes. From 1973 to 1978, over 3,100 household contacts of 1,664 workers at a factory that made amosite asbestos insulation products from 1941 to 1954 were identified, and 771 were examined. The analysis included 679 contacts who had lived with a worker while he was employed and had no personal occupational asbestos or fibrogenic dust exposure. Posteroanterior chest films were read blind by five readers using the 1971 ILO U/C classification and compared with films from 325 controls from the same urban New Jersey community with a similar age and sex distribution. All contacts were more than 20 years from first exposure. Abnormalities were found in 239 (35%) contacts and 15 (5%) controls. These included pleural thickening (19% vs 1%), pleural calcification (8% vs 0) and small opacities (17% vs 3%). Prevalence rose with longer household exposure and with earlier onset of exposure. Wives had the highest prevalence (48%) and daughters the lowest (21%). Dyspnea, rales, cyanosis and clubbing were more common among contacts with abnormal x-rays. Five of slightly over 550 recorded deaths were due to pleural mesothelioma. The authors concluded that household exposure can cause pleuro-pulmonary disease and that pleural changes are a better indicator of environmental exposure than small opacities.

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Based on available data, can we project an acceptable standard for industrial use of asbestos? Absolutely. K. Robock. 1979;330:205-10. PubMed · Publisher
Based on available data, can we project an acceptable standard for industrial use of asbestos? No. A. Englund. 1979;330:219-21. PubMed · Publisher
Based on available data, can we project an acceptable standard for industrial use of asbestos? Perhaps. S. Samuels. 1979;330:215-8. PubMed · Publisher
Based upon available data, can we project an acceptable standard for industrial use of asbestos? Yes. P. Kotin. 1979;330:211-3. PubMed · Publisher
Care of the injured worker: a labor perspective. R.J. Steinfurth. 1979;330:521-3. PubMed · Publisher
Clinical measurement in Quebec chrysotile miners: use for future protection of workers. M.R. Becklake. 1979;330:23-9. PubMed · Publisher

Abstract

There is a relationship between dust exposure, on the one hand, and serious disease and death, on the other, in chrysotile asbestos mine and mill workers of Quebec. Studies in current working populations indicate that prevalence of abnormality increases with increasing exposure. However, the relationship is weak and offers only a partial explanation of between-subject variability. In addition, there is no certain way to detect or predict change. Because of the relative nonspecificity of the health measurements examined and their poor relationship to exposure, control should be based on environmental monitoring, with biologic monitoring considered in a complementary role. This leaves the clinician with the dilemma of how best to advise the worker in whom questionable changes have been detected. At present, there appears little doubt that the decision must remain essentially clinical, based, on one hand, on all available information about the man, his job, and the plant or mine in which he works, from which an estimate of likely outcome must be made, and, on the other hand, on the social and human factors concerned, including the fact that removal from exposure does not necessarily prevent the appearance of abnormality.
Combined effect of asbestos exposure and tobacco smoking on Finnish anthophyllite miners and millers. L.O. Meurman, R. Kiviluoto, M. Hakama. 1979;330:491-5. PubMed · Publisher

Summary

This study examined how asbestos exposure and tobacco smoking combine to affect lung cancer risk among workers at two Finnish anthophyllite asbestos quarries. It updated a 1974 report that lacked direct smoking data on deceased workers. The cohort included all workers employed for 3 months or longer between 1936 and July 1, 1967, a total of 1092. Of these, 1045 were followed until September 1, 1977. In 1967, smoking habits were obtained by interview from 793 employees. Causes of death came from death certificates, hospital records and histologic findings, and were based on autopsy in 80 cases. Expected deaths were derived from Finnish proportional mortality statistics and adjusted for heavier smoking among the asbestos workers.

There were 384 deaths. All 44 lung cancer deaths occurred among males, significantly more than expected. The relative risk rose from 1.7 for deaths before July 1967 to 2.4 for later deaths. In 1967-77, the relative risk of lung cancer was 3.3 among heavily exposed workers and 1.4 with low to moderate exposure. Assuming multiplicative effects, the relative risks were 1 for nonsmokers not exposed to asbestos, 1.6 for nonsmoking asbestos workers, 12 for smokers not exposed to asbestos, and 19 for asbestos workers who smoked. Only one nonsmoking asbestos worker had lung cancer. Of 42 asbestosis cases, seven occurred among nonsmokers. Asbestosis was present in 22 of 28 heavily exposed lung cancer deaths.

The authors found a dose-response relationship and results compatible with both multiplicative and promoter models. They concluded that preventive measures are needed.

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Contribution of electron microscopy to the diagnosis of pleural mesothelioma. P. Stoebner, J.F. Bernaudin, M. Nebut, et al. 1979;330:751-60. PubMed · Publisher

Abstract

The contribution of scanning and electron microscopy to the diagnosis of suspected pleural mesotheliomas has been under investigation. The diagnostic value of the scanning electron microscopy has not been found to be decisive in pleural effusions. By contrast, the transmission electron microscopy was of great value, particularly in lesions or tumors composed mainly of spindle cells. The finding of fibroblastoid mesothelial, or transitional cells, alongside typical mesothelial cells is a clue to the diagnosis of mesotheliomas.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.
Dose-response relationships for asbestos-related disease: implications for hygiene standards. Part II. Mortality. J. Peto. 1979;330:195-203. PubMed · Publisher

Summary

This conference paper argued that, for the purpose of setting hygiene standards, excess cancer risk from asbestos should be assumed to be linearly related to dust level until this is disproved. The author presented this as a pragmatic proposal rather than a scientific statement. He reasoned that threshold models can underestimate low-dose risk by an order of magnitude, and that a standard is not an absolute maximum, because individual exposures vary around the average. Using hypothetical worked examples, he showed how risks observed in exposed cohorts could be scaled to lower dust levels. For bronchial carcinoma, relative risk was assumed to remain constant after exposure. A 10% rise in relative risk would then mean about nine asbestos-induced deaths per 1000 men, given that 9% of male deaths in England and Wales were due to lung cancer. For mesothelioma, incidence data from North American insulation workers fitted three different time models similarly up to 45 years after first exposure. In the example, lifelong risk was about 8% for mesothelioma and 9% for bronchial carcinoma at an average of 20 fibers/cm3, implying about 1.7% at 2 fibers/cm3. The paper also described a method for converting risks between fiber types. Modelled effects of age at first exposure and duration were shown, with gastrointestinal cancer and asbestosis set aside. The author concluded that occupational exposure must be rigorously monitored, but that risk to the general population is likely to be extremely low.

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Dose-response relationships for asbestos-related disease; implications for hygiene standards. Part I. Morbidity. G. Berry, H.C. Lewinsohn. 1979;330:185-94. PubMed · Publisher

Summary

The authors related measured asbestos dust levels to morbidity in an asbestos textile factory in the north of England, extending a study included in the British Occupational Hygiene Society's 1968 report. A total of 392 men met the inclusion criteria: more than 10 years' work in scheduled areas since 1933 by the end of 1972, excluding men who left before June 30, 1966. Of these, 197 were first employed in 1951 or later, and 13 men were later excluded. Most asbestos processed was chrysotile, with some crocidolite up to 1968. Each man's yearly exposure was estimated from his job history and static dust sampling. Measured fiber counts were available from 1961, converted particle counts from 1951 to 1960, and estimated levels before 1951. The authors assessed medical records, chest radiographs read by four readers, and lung function. Crepitations were heard in 22% of men, compared with 6% in the 1966 study. There were 58 cases of possible asbestosis, 47 of them since mid-1966. Their incidence was compatible with a linear relationship with cumulative exposure. Among men first employed after 1950, forced expiratory volume fell by 12.1% and forced vital capacity by 10.6% per 100 fiber-years/cm3. For 40 years' exposure at the UK standard of 2 fibers/cm3, predicted prevalence of possible asbestosis ranged from 4% to 14%, depending on the exposure measure. The authors concluded that there was considerable doubt about the likely consequences of the current hygiene standard.

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Dust control in a conventional asbestos textile factory. H.C. Lewinsohn, C.A. Kennedy, J.E. Day, et al. 1979;330:225-41. PubMed · Publisher

Summary

The authors, from Raybestos-Manhattan, described how the company reduced asbestos dust at its Marshville asbestos textile plant while continuing to make asbestos textiles by conventional methods. They set this against US standards that lowered the permissible limit to 2 fibers/cm3 (8-hour time-weighted average) from July 1976. When the company acquired the plant in 1969, dust counts were barely below 12 f/cc. Raw chrysotile fiber was handled by hand, and many operations had little or no exhaust ventilation. Product and process changes followed between 1969 and 1973. In June 1975 a 'clean system' plan for asbestos textiles costing $12.3 million was approved, of which $2.6 million was for Marshville. The work, completed in July 1977, included closed pneumatic fiber handling with no manual handling of raw asbestos, double-enclosed and exhausted carding machines, and enclosed and exhausted winders. Other measures were wet weaving with resin treatment, a 50,000-square-foot smooth-surfaced addition, fresh make-up air units, and a 110,000 CFM baghouse with bagged waste removal. Work practices, protective equipment, disciplinary enforcement, more clean-up staff, employee education and dust monitoring were also introduced. Mean fiber counts were compared for 1969, 1974 and 1978. The authors reported that all levels were maintained below 1 fiber/ml (8-hour TWA) and stressed the importance of work practices. They noted that such changes over time complicate epidemiological dose-response studies.

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Environmental considerations in surveillance of asbestos miners and millers. G.W. Gibbs, R.S. du Toit. 1979;330:163-78. PubMed · Publisher
Environmental mesothelioma in Turkey. Y.I. Bariş, M. Artvinli, A.A. Sahin. 1979;330:423-32. PubMed · Publisher

Summary

The authors, from the Chest Diseases Division of Hacettepe University, Ankara, summarized their studies of environmental (non-occupational) asbestos-related and fiber-related diseases in rural Turkey. Mass chest photofluorography and radiographic surveys of villages in several regions found endemic calcified pleural plaques (CPP). Rates were 5-10% in some villages near Mihaliççik, 5.2% in two villages near Ilgaz, and close to 25% CPP and/or chronic fibrosing pleuritis (CFP) in Bedirli-Yeşilova. Villages nearby with similar living conditions had few or no cases. Villagers in several areas used soil containing asbestos as white stucco. In the village of Karain (Nevşehir), 11 of 18 deaths in 1974 were from malignant pleural mesothelioma (MPM). Twenty-seven patients were added between January 1975 and May 1978. In Tuzköy, among 312 randomly selected residents over 25 years old, 53 (17%) had CPP and 33 (10.5%) had pleural thickening. There were no asbestos deposits near Karain or Tuzköy. Respirable erionite-type zeolite fibers were found in rock and soil samples from both villages but not in control villages. Such fibers were also found in the lung tissue of a Tuzköy patient with CFP. The authors described 148 MPM cases (92 male, 56 female) and 20 CFP cases, mostly in rural peasants. They concluded that CPP, CFP and MPM may be related to fibers other than asbestos. They also concluded that tumor induction by asbestos in drinking water was highly improbable.

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Fiber dimensions and aspect ratio of crocidolite, chrysotile and amosite particles detected in lung tissue specimens. F.D. Pooley, N. Clark. 1979;330:711-6. PubMed · Publisher

Abstract

Chrysotile, amosite and crocidolite fibers detected in autopsy tissue specimens from cases of mesothelioma and controls have been characterized by particle length, diameter and aspect ratio using a transmission electron microscope. The pooled information from such specimens reveals that the fibers of each mineral type detected in biological material have very different physical characteristics although in all samples fibers less than 5 microns in length are predominant by number while fibers over 25 microns in length are found very infrequently. Chrysotile fibers on average appear as the shortest fibers with the most fine diameter distribution, amosite fibers are on average the longest with the most coarse diameter distribution, crocidolite fibers on average have dimensions which are intermediate between both chrysotile and amosite. The percentage number of fibers of chrysotile, amosite and crocidolite detected with an aspect ratio less than or equal to 10 were 31.7%, 24.2% and 18.5% respectively.
French mesothelioma register. J. Bignon, P. Sebastien, L. Di Menza, et al. 1979;330:455-66. PubMed · Publisher

Abstract

A total of 197 definite cases of mesothelioma (mainly of the pleura) have been reported by pathologists to the French Mesothelioma Register for the period 1965--78. A moderate linear increase in the annual incidence of mesothelioma cases since 1965 was noted. In men and women over the ages of 47 and 41 years, respectively, the annual death rate was higher in those with mesothelioma than in those of the general population. The proportions of mesothelioma patients who had experienced occupational, para-occupational, and unknown asbestos exposures were 77%, 3%, and 20% respectively. The number of cases reported to the register is obviously an underestimate of the true number of mesothelima cases in France, because such cases are not reported to the register systematically. Mesothelioma registers cannot provide information about dose-response relationships; however, with good management of the register, such relationships could be obtained, since a good assessment of dose can be accomplished by biologic monitoring.
Functions of mesothelioma panels. M. Kannerstein, J. Churg, W.T. McCaughey. 1979;330:433-9. PubMed · Publisher

Summary

The authors described the history and functions of mesothelioma pathology reference panels, which were proposed at the 1964 New York Academy of Sciences conference on the biological effects of asbestos. They reported on the United States Mesothelioma Reference Panel registry at Barnert Memorial Hospital Center in Paterson, New Jersey. Over a 10-year period it received about 800 cases. Of these, 517 were graded for certainty of diagnosis, and 419 were considered highly possible to definitely mesothelioma: 253 (60%) pleural, 146 (35%) peritoneal, 15 involving both cavities, 2 pericardial and 3 of the tunica vaginalis. In 168 cases from a 1972 national survey, panel members graded diagnostic certainty on a 0-4 scale, and the panel median was used. Seventy percent were accepted as probable or definite mesothelioma, 13% were rejected and 16% were considered possible. Agreement among members was strong in the probable/definite and rejected categories but poor in the possible group. Majority opinion favored epithelial type in 64% and mixed type in 13%, with no majority in 14%. The Canadian panel, founded in 1968, had reviewed almost 300 cases. The authors concluded that panels have performed a useful function. They suggested that panels could do more with better organization and support, including stimulating case detection, educating pathologists, holding periodic meetings and developing lung asbestos analysis.

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Future problems to be anticipated: demolition, repair, and disposal. R.S. Prust. 1979;330:545-7. PubMed · Publisher
Health hazards of asbestos exposure. 1979;330:1-814. PubMed
Human and experimental data on translocation of asbestos fibers through the respiratory system. J. Bignon, G. Monchaux, P. Sebastien, et al. 1979;330:745-50. PubMed · Publisher

Abstract

The translocation of fibrous dusts through the respiratory system is discussed on the basis of human and experimental data obtained with the transmission electron microscope. Comparison of the characteristics (numerical and mass concentrations, sizes, types) of asbestos fibers retained in different locations of the respiratory system in humans exposed to asbestos has shown that there is no relationship between the numerical concentrations in lung parenchyma and those in parietal pleura. Moreover, almost al fibers encountered in the pleura were ultimate, short fibrils of chrysotile. The animal data are from rats injected intrapleurally with different types of fibers (chrysotile, crocidolite and glass fibers) and sacrificed at different times. There was a progressive increase in the number and mass of fibers translocated into lung parenchyma from the pleural cavity that was particularly obvious after 90 days. After this time, the mean length of fibers, especially chrysotile, increased, indicating that more long fibers are retained in alveolar tissue than short fibers.
Incidence of bronchial carcinoma in shipyard workers with pleural plaques. J.R. Edge. 1979;330:289-94. PubMed · Publisher

Summary

This study asked whether men with pleural plaques have an increased risk of dying from bronchial carcinoma. The subjects were 429 men from Barrow-in-Furness, England, mostly shipyard workers, who had radiologic evidence of pleural plaques and whose first radiographs were taken between 1964 and 1971. They were compared with 429 controls from Carlisle, where there was no known industrial asbestos exposure. Controls were matched by age, sex and date of first radiograph and had no plaques. No one in either group had radiologic pulmonary fibrosis. Most of the men were over 60. Deaths were traced through national and local records. Three subjects and eight controls could not be traced.

There were 127 deaths among the men with plaques (30%) and 74 among the controls (17.2%) (p < 0.001). Bronchial carcinoma caused 19 deaths among the men with plaques and 4 among the controls (p < 0.01). Mesothelioma caused 23 deaths among the men with plaques and none among the controls. Smoking histories were not available. Deaths from ischemic heart disease and chronic bronchitis were similar in the two groups. Men drawn from hospital or clinic sources had a higher proportion of carcinoma deaths, which the author took as a sign of bias. After excluding six men who already had symptoms or suggestive radiographs at entry, the excess (13 versus 4) was of doubtful significance (p < 0.05). In an analysis against national rates, carcinoma deaths after 6 years were twice the expected number. The author concluded that men with pleural plaques carry a twofold risk of bronchial carcinoma and that continued follow-up is needed.

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Indoor asbestos pollution: application of hazard criteria. R.N. Sawyer. 1979;330:579-86. PubMed · Publisher

Abstract

Asbestos contamination of relatively contained environments within structures can occur under many conditions and in association with various activities. Such contamination persists and can potentially expose all structure users. The more significant contamination levels are associated with disturbance of friable asbestos-containing materials, although bonded material is also capable of fiber dissemination under special conditions. Application of occupational government standards for limitation of exposure, both presently in force and proposed or recommended, indicates that levels found in some situations exceed those considered potentially carcinogenic.
Industrial hygiene perspectives in control of asbestos exposure. W. Reitze. 1979;330:223-4. PubMed · Publisher
Industry responsibility for the use of its products. P. Kotin. 1979;330:503-5. PubMed · Publisher
Influence of crystallization habit of minerals on in vitro cytotoxicity. L.D. Palekar, C.M. Spooner, D.L. Coffin. 1979;330:673-86. PubMed · Publisher

Abstract

Four samples of cummingtonite-grunerite series in various crystallization habits were tested in vitro. The cytotoxicity to Chinese hamster ovary cells and hemolysis to sheep erythrocytes were inversely proportional to the structural faults and surface defects of the minerals. At a comparable surface area, asbestiform grunerite (UICC amosite), semi-asbestiform cummingtonite, acicular cummingtonite, and acicular grunerite were found to be cytotoxic and hemolytic in a decreasing order. The influence of particle size on hemolysis and cytotoxicity was observed with acicular grunerite. Although samples of relatively large particle size were found to be inert, samples of smaller particle size were cytotoxic as well as hemolytic. No apparent relationship between surface charge and hemolysis as well as cytotoxicity was observed.
Levels of asbestos air pollution in some environmental situations. P. Sebastien, M.A. Billon, G. Dufour, et al. 1979;330:401-15. PubMed · Publisher

Abstract

Asbestos contamination of the outside aid in Paris and suburbs has been monitored in some environmental situations, namely, "typical" urban sites removed from known sources of asbestos emissions, crossroad locations, the vicinity of a freeway, areas with buildings under construction, and areas around asbestos factories. In the same manner, measurements have been performed inside buildings of various types: those sprayed with asbestos-containing materials, those fitted with asbestos products, and control buildings. Air has been sampled by use of 0.45 micrometer pore size Millipore filters. After low-temperature ashing, ultrasonicated ashes were transferred to carbon film on 200-mesh gold grids examined under an analytic transmission electron microscope. Levels of pollution were expressed in terms of gravimetric concentrations. Inside buildings, when the air was in contact with significant amounts of asbestos-containing materials (spray, sheets), the levels were in the range 0.1--1000 10(-9) g m-3. In the vicinities of asbestos plants, the concentrations were higher: 1000--3000 10(-9) g m-3. Under other circumstances, the levels were of the same order of magnitude: 99% of the values were below 7 X 10(-9) g m-3. The Conseil Supérieur d'Hygiène Publique de France proposed a numerical ambient air quality standard of 50 X 10(-9) g m-3 inside buildings sprayed with asbestos.
Long-term mortality experience of chrysotile miners and millers in Thetford Mines, Quebec. W.J. Nicholson, I.J. Selikoff, H. Seidman, et al. 1979;330:11-21. PubMed · Publisher

Abstract

Among a cohort of 544 men with at least 20 years of employment in chrysotile mining and milling at Thetford Mines, Canada, 16% of the deaths were from lung cancer and 15% from asbestosis. The excess over expected deaths from these causes account for 43 of 178 deaths in the group. The risk of death of asbestosis, at equal times fron onset of exposure, is very similar in miners and millers, factory workmen and insulators. The ratio of observed to expected deaths from lung cancer is similar in the miners and millers and factory workers, but higher in insulators. The risk of death of mesothelioma in miners and millers is decidedly less than the other two groups. The exact causes of the reduced risk in this category are not yet completely clarified.
Lung cancer mortality in the United States: shipyard correlations. W.J. Blot, J.F. Fraumeni. 1979;330:313-5. PubMed · Publisher
Malignant disease and environmental control in an asbestos cement plant. L. Djerassi, G. Kaufmann, M. Bar-Nets. 1979;330:243-53. PubMed · Publisher

Summary

The authors described an asbestos-cement plant (Isasbest) in North Nahariya, Israel, and the mortality of its workforce. The plant began regular production in 1953, mainly of pipes and corrugated sheets, using chrysotile and crocidolite. Since 1953, 3608 workers had been employed, 750 of them currently, and 54.8% had worked less than one year. Dust monitoring began in 1960 with an impinger and later a koniometer, but these measurements were sporadic and unreliable. Asbestos fiber counts were introduced in 1972, and 70 work stations were monitored with personal samplers. Fibers from work clothing were detected at a laundry almost 40 km away. In 1967, after a high incidence of malignant disease became evident, crushing of crude asbestos was stopped and asbestos was delivered in dust-proof bags. Among 53 deaths in the cohort, there were two bronchial carcinomas and one laryngeal carcinoma, three stomach and two colon cancers, four kidney, two brain, one leukemia and one mesothelioma. The mesothelioma occurred in a man with four to six months' exposure and was judged probably unrelated to the plant. Malignant disease caused 30% of deaths, compared with an average of 16.1% among Israeli males and 22.1% at a Haifa power station. The cancer share fell from 41% (1960-66) to 18.8% (1972-78). The authors said the numbers were too small for statistical evaluation and, given the long latency of asbestos-related cancer, did not necessarily show environmental improvement.

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Mesothelioma incidence in a Dutch shipyard. J. Stumphius. 1979;330:317-22. PubMed · Publisher

Abstract

On Walcheren Island (the Netherlands), 25 cases of mesothelioma were diagnosed from 1962 to 1968. In 22 cases, there had been an occupational association with Royal Schelde, the shipyard in Vlissingen. A relationship with exposure to asbestos, frequently used in shipbuilding in the past, could be demonstrated. Further observations showed the expected increase of mesothelioma cases in Royal Schelde workers. In 1974, the number of cases totaled 42; in 1978, the number rose to 57. In addition, five more recent cases have not yet been confirmed histologically, but the clinical symptoms are unmistakable. In seven of 12 mesothelioma cases on Walcheren Island that had no association with Royal Schelde, asbestos exposure in the occupational history could also be traced. Finally, a few facts are mentioned about the recent Dutch Asbestos Act.
Mesothelioma on the coast of Brittany, France. M. de Lajartre, A.Y. de Lajartre. 1979;330:323-32. PubMed · Publisher

Summary

The authors described 70 cases of diffuse pleural mesothelioma seen between 1956 and April 1978 in the Nantes–St. Nazaire region of Brittany, France, where asbestos was widely used in shipyards. Diagnosis rested on clinical course and histology, mostly from surgical biopsy. Fifty-four patients had thoracotomy, nine were autopsied and 10 had pleural needle biopsy. The number of cases rose from four in 1956–1964 to 14 in 1964–1970 and 51 in 1970–1978. Mean age at diagnosis was 57 years (range 22–83), and 67 patients were men. The usual presentation was recurring pleural effusion (90% of cases). Hyaluronic acid was found in the pleural fluid in 13 of 15 tests. Fifty-five tumours were epithelial and 15 were mixed. Mean duration of illness was 15 months, and eight patients were still alive. Metastases were found in 14 of 62 deceased subjects. Occupational asbestos exposure was certain in 51 cases, including 44 shipyard workers, probable in six and undetermined in 13. Asbestos fibres were found in tissue from 32 of 34 subjects examined, and crocidolite was present in three. Among 40 shipyard workers, exposure usually lasted more than 25 years, and latency exceeded 25 years in all but six. The shortest latency, 11 years, was in a lagger's son exposed as a child. The authors feared that mesothelioma frequency would remain high in the years to come.

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Mesothelioma registries in identifying asbestos hazards. A.D. McDonald. 1979;330:441-54. PubMed · Publisher

Summary

The author examined methods of finding and registering cases of malignant mesothelioma, a rare tumour, as a way of monitoring asbestos hazards and detecting other possible causes. The paper reviewed experience with such surveys and made recommendations. The methods considered were published case series, statutory notification, cancer registries, workmen's compensation and pneumoconiosis panels, the Third National Cancer Survey (United States, 1969-71), registration through pathologists (four rounds in Canada and one in the United States in 1972) and death certificates. The Third National Cancer Survey gave an incidence per million people aged 45 and over of 11.20 in males and 3.53 in females. These rates were higher than those found in the pathologist surveys, except in Quebec. In California, only 31 of 60 deaths certified as mesothelioma were confirmed by pathologists. The author concluded that registration through pathologists gave the most complete and unbiased ascertainment, with death certificates the next best approach. Registration in Canada led to the discovery of crocidolite exposure in gas mask manufacture. Among 199 exposed workers, there were nine mesothelioma cases, 16% of 56 deaths. A rising trend was seen in Canadian males but not in females. In the case-control analyses, insulation work carried by far the greatest risk. In 344 case-control pairs, eight cases and two controls had domestic exposure. The author recommended continuing ascertainment through pathologists, followed by case-control studies with standardized diagnosis and methods.

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Mortality among shipyard workers in Genoa, Italy. R. Puntoni, M. Vercelli, F. Merlo, et al. 1979;330:353-77. PubMed · Publisher

Abstract

The dockyards of Genoa are exposed to many known or suspect carcinogenic agents, namely, asbestos, silica, polycyclic aromatic hydrocarbons, and halogenated hydrocarbons; other possibly harmful substances are trace amounts of aromatic amines, welding smokes, paints, and lipid-removing solvents. A cohort study of causes of death of 2190 dockyard workers in Genoa was conducted between January 1, 1960 and December 31, 1975. Mortality rates were calculated for 20 different occupational categories, for which there exist different levels of exposure to noxious substances. Two control groups were selected: the general male population of Genoa and all male employees (462) of San Martino Hospital, Genoa for the same period of time. Causes of death that demonstrated significant excesses for both control groups were: cancer of the colon, excluding the rectum; cancer of the larynx; cancer of the lung, bronchus, and trachea; cancer of the kidney, urinary bladder, and other urinary organs; respiratory diseases; and cirrhosis of the liver. The data obtained from these 20 job categories revealed different types and levels of risk for various carcinogenic agents.
Mortality experience of insulation workers in the United States and Canada, 1943--1976. I.J. Selikoff, E.C. Hammond, H. Seidman. 1979;330:91-116. PubMed · Publisher

Summary

This study examined mortality among asbestos insulation workers in two cohorts. One comprised the 632 men in two New York-New Jersey union locals on January 1, 1943, followed to December 31, 1976, plus 833 men who joined these locals in 1943-1962. The other comprised all 17,800 members of the insulation workers' union in the United States and Canada on January 1, 1967, followed to December 31, 1976. Observed deaths were compared with those expected from U.S. white male age-specific death rates. Causes of death were assigned from death certificates and also from review of the best available evidence (autopsy, surgical, clinical). By 1976, 478 of the 632 men had died, including 93 of lung cancer (13.3 expected), 38 of mesothelioma and 41 of asbestosis. Among the 17,800 men, 2271 died (1658.9 expected), including 486 of lung cancer (105.6 expected), 175 of mesothelioma and 168 of asbestosis. Little increase in cancer or asbestosis deaths was seen less than 15-19 years from onset of exposure. Death certificates listed 49 pancreatic cancer deaths, but review confirmed 23. They listed 78 asbestosis deaths, against 168 after review. The authors concluded that insulation workers had an extraordinary increased risk of death from cancer and asbestosis, and that studies should observe workers 30-40 or more years from onset. They also concluded that adding amosite to chrysotile did not demonstrably alter the resulting diseases.

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Mortality experience of residents in the neighborhood of an asbestos factory. E.C. Hammond, L. Garfinkel, I.J. Selikoff, et al. 1979;330:417-22. PubMed · Publisher

Summary

The authors asked whether very light, non-occupational exposure to amosite asbestos dust from a factory in Paterson, New Jersey, which operated during 1942-54, caused measurable harm to men living nearby. Dust from the factory was vented outdoors and blew through open windows. No air measurements were made at the time, but settled attic dust collected years later from houses near the factory still contained appreciable amosite fibers, and houses farther away contained fewer. Using annual city directories, the authors identified male residents of Riverside, the area within one half mile of the factory, and of Totowa, a similar Paterson neighborhood several miles away. Factory workers were excluded. Tracing began in 1968. The analysis included 5,550 men aged 35 or older who were alive on January 1, 1962 (1,779 from Riverside and 3,771 from Totowa), followed to December 31, 1976. Age distributions were nearly identical, and age standardization had virtually no effect. In Riverside, 780 men (43.8%) died, compared with 1,735 (46.0%) in Totowa. Cancer deaths were 9.2% versus 9.4%, and lung cancer deaths were 2.3% versus 2.6%. No peritoneal mesothelioma occurred. One pleural mesothelioma death occurred in a Riverside electrician in 1966. The authors called this the only hint of a fatal effect, but noted that its timing, in the first rather than the last five-year period, detracted from that conclusion.

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Mortality in Canadian miners and millers exposed to chrysotile. J.C. McDonald, F.D. Liddell. 1979;330:1-9. PubMed · Publisher

Summary

This paper reviewed how mortality findings developed over four stages of follow-up in a cohort study of the chrysotile asbestos mines and mills at Asbestos and Thetford Mines, Quebec. The study began in 1966. From a register of 28,000 employees, the cohort comprised persons born 1891-1920 and employed at least one month. After revision it numbered 11,379 (10,939 men, 440 women). By the end of 1975, 90.1% had been traced and 4547 had died. Dust exposure was estimated for each subject in millions of particles per cubic foot (mpcf), and smoking was assessed by questionnaire. Analyses used man-years methods with Quebec death rates and a matched case-control approach. In 1926-75 there were 4350 male deaths against 4107 expected (SMR 1.06). Relative risks for respiratory cancer rose with accumulated dust exposure to 2.9-3.2 in the highest category and were similar at each stage. In men employed 20 years or more with very heavy exposure, the SMR for respiratory cancer was 265. Dust and smoking fitted a multiplicative model. Ten male mesothelioma deaths occurred in the cohort against about 2 expected. The authors concluded that respiratory cancer and pulmonary fibrosis were the major hazards, that the exposure-response relationship might be linear, and that mesothelioma risk appeared much lower than with crocidolite.

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Netherlands mesothelioma register. H.T. Planteydt. 1979;330:467-71. PubMed · Publisher

Summary

This article described the Netherlands Mesothelioma Register, started in 1969, to which all Dutch pathologists were asked to report histologically verified pleural and peritoneal mesotheliomas. The register held 419 cases. Of the 294 recorded from 1969 through 1975, most were pleural tumours in older men, with the largest concentration (77 cases) in Rotterdam and smaller ones around Amsterdam, Haarlem and Walcheren Island. National mortality statistics recorded 332 deaths from primary pleural tumours in 1969-72. The overall frequency was 6.2 per million inhabitants, but it exceeded 20 per million in Rotterdam and neighbouring towns and 40 per million in Flushing. These are river-mouth areas with heavy industry, especially shipyards. Detailed work histories of 67 cases and 67 matched controls showed definite or probable asbestos exposure in 72% of cases (84% from Rotterdam, 61% elsewhere) and definite exposure in 18% of controls. Three cases illustrated unexpected exposure routes: home renovation work, a laundry with asbestos-covered ironing equipment, and handling asbestos-covered stage props. Electron microscopy of lung tissue found chrysotile in all 28 mesothelioma patients and amphibole fibres in 25. Among 10 controls from an agrarian region, chrysotile was found in all and amphiboles in seven. The author named the register's goals as discovering unknown exposure sources and determining the presence, quantity and kind of asbestos in patients' lungs.

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Observer variation and reliability of the histopathological diagnosis of mesothelioma. H.T. Planteydt. 1979;330:761-4. PubMed · Publisher
Patterns of mortality in asbestos factory workers in London. M.L. Newhouse, G. Berry. 1979;330:53-60. PubMed · Publisher

Summary

The authors reported mortality among workers at an East London asbestos factory, open from 1913 to 1968, which made asbestos textiles and later insulation and other products using crocidolite (until the late 1950s), chrysotile and amosite. The cohorts were 4600 men who began work between 1933 and 1964 and 922 women first employed between 1936 and 1942. Vital status was traced through national registers, and follow-up ran to 31 December 1975. Jobs were graded as low-moderate or severe exposure, and laggers were analysed separately. Among men there were 775 deaths, including 46 from mesothelial tumours (19 pleural, 27 peritoneal) and 103 from lung carcinoma. Laggers had 25 deaths from cancers of the lung and pleura against 5.6 expected. Lung and pleural cancer SMRs generally rose with length of follow-up and with exposure. Among women, 77% were traced; 225 had died, including 13 pleural and 8 peritoneal mesothelial tumours. Severely exposed women with long employment had excess breast (6 observed, 2.1 expected) and ovarian (3 observed, 0.74 expected) cancer, which the authors interpreted cautiously. Mesothelioma death rates related clearly to the length and severity of exposure. A 1971 smoking survey suggested that smoking explained only a small part of the lung cancer excess. The results were consistent with asbestos and smoking combining multiplicatively. The authors concluded that, under past conditions, workers starting in their early twenties would have markedly diminished life expectancies.

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Periodic examination of asbestos and coal miners. G.K. Sluis-Cremer. 1979;330:541-3. PubMed · Publisher
Pleural plaques and neoplasia in Finland. R. Kiviluoto, L.O. Meurman, M. Hakama. 1979;330:31-3. PubMed · Publisher

Summary

The authors studied whether pleural plaques, which can be caused by asbestos, were linked with cancer in Finland, using two approaches. In the first, chest photofluorographs of 6000 adults from a 1962 mass x-ray survey in Tuusniemi commune were re-examined for calcified pleural plaques. Tuusniemi lies near two open asbestos mines at Paakkila, worked from 1918 to 1977. Plaques were found in 700 people. Controls without plaques came from Maaninka commune, where asbestos is not used in industry or present in soil. Cancers reported to the Finnish National Cancer Registry in 1962-77 were identified. There were 60 neoplasms in the plaque group and 53 among controls, including 13 and 14 lung cancers respectively. In the second approach, chest x-rays of 69 lung cancer cases recorded at Turku City Hospital in 1963-77 (after exclusions) and 69 age-matched controls were examined for pleural plaques and pulmonary fibrosis. Both plaques and fibrosis were present in 25 cases and 11 controls. Neither plaques nor fibrosis alone seemed linked with lung cancer, but the combination seemed to increase cancer risk 2.8-fold, which was statistically significant. The authors suggested that slight asbestos exposure causes plaques while heavy exposure leads to plaques and lung fibrosis. They considered the results in accord with the general view of the association between plaques and asbestos exposure.

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Preparation of extrapulmonary tissues and body fluids for quantitative transmission electron microscope analysis of asbestos and other mineral particle concentrations. P.M. Cook. 1979;330:717-24. PubMed · Publisher
Prevalence of radiographic abnormalities among Northern California shipyard workers. P.L. Polakoff, B.R. Horn, O.R. Scherer. 1979;330:333-9. PubMed · Publisher

Summary

The authors measured how common chest X-ray changes compatible with asbestos exposure were among shipyard workers in Northern California. They took posterior-anterior chest radiographs of 359 male volunteers who were present or former workers at the Mare Island and Hunter's Point Naval Shipyards in the San Francisco Bay Area. All had at least 10 years since first exposure to asbestos. The article does not state when the study was done. At least two of the authors read each film using the ILO-U/C classification. Later, 311 workers completed a questionnaire on occupation, smoking, respiratory symptoms and medical history. The data were analysed by chi-square. Normal films were found in 147 workers (40.9%) and abnormal films in 213 (59.1%). Of these, 36.2% were mildly and 19.8% moderately abnormal. Parenchymal changes were found in 158 workers (44%) and pleural changes in 94 (26%). Pleural changes became more common with age and with time since first exposure: 18% among those who started after 1953 and 43% among those who started before 1953. Ten workers (2.8%) had pleural calcification. Overall parenchymal changes did not vary with age or time since exposure. Only 12 workers (3.3%) had changes of 1/2 or greater. Seven workers had mass lesions, four known to be lung carcinoma. Abnormalities were spread evenly across occupations. Eighty-five percent of respondents were smokers or ex-smokers. The authors concluded that all past shipyard workers, regardless of craft, are at risk of asbestos-related disease and recommended medical surveillance.

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Proper compensation for the damaged worker. J.A. Adam. 1979;330:597-600. PubMed · Publisher
Public health control of environmental asbestos disease: consumer products. B.H. Franklin. 1979;330:497-501. PubMed · Publisher
Public health significance of smoking-asbestos interactions. A.L. Frank. 1979;330:791-4. PubMed · Publisher
Radiographic progression of asbestosis: preliminary report. A. Gregor, R.W. Parkes, R. du Bois, et al. 1979;330:147-56. PubMed · Publisher

Abstract

In a collaborative study with the Pneumoconiosis Medical Panel, 232 asbestos workers were seen between 1967 and 1975. During this time, 50 of the 232 (21.5%) workers dies, 33 (13.8%) from respiratory disease probably related to asbestos exposure [10 (4.3%) pleural mesothelioma, three (1.3%) peritoneal mesothelioma, 10 (4.3%) asbestosis, 10 (4.3%) carcinoma of the lung]. Of the 182 survirors, 119 were recalled for other studies, and follow-up data were obtained as additional information at the same time, over a 1--7 year period. Paired radiographs were read, and 21 patients (17.6%) had worsened. As expected, the frequency of progression increased with a longer follow-up time, so that about one third of the subjects displayed progression after a minimum follow-up of 6 years. Ten of 73 patients (13.6%) had progressed in 3 years or less and may be defined as rapid progressors. No particular clinical feature distinguished clearly between progressors and nonprogressors, but there was a trend toward a greater frequency and higher titer of ANA among the progressors in this group. There was also a higher frequency of progression in those who were initially classified radiographically as 1/1 of 1/2 than in those with other initial radiographic appearances. This pilot study is now forming the basis for a larger, longer-term comprehensive survey.
Radiographic search for asbestos-related disease in a naval shipyard. J.S. Felton. 1979;330:341-52. PubMed · Publisher

Abstract

The Long Beach Shipyard underwent a chest x-ray survey of 6640 employees, or 88.6% of the total shipyard population, to determine the level of asbestotic changes. For computer classification purposes, the findings were divided into five groups: abnormal findings consistent with inhalation of asbestos fiber; normal; pulmonary fibrosis, nonspecific, questionable; and other findings not related to asbestosis. Asbestos-related abnormal findings, were encountered in 1061 workers, or 16.0%. No change was noted in 4806, or 72.4%. Pulmonary fibrosis was encountered in 140, or 2.1%. Other abnormalities not related to the inhalation of free asbestos fiber were encountered in 624, or 9.4%. The interpretation was questionable in nine individuals, or 0.1%. Of the male employees, 17.2% were positive for asbestos-related chest x-ray changes, and four women, or 0.8%, showed comparable findings. Of the men, 71.5% had normal chest x-rays, and 83.3% of the 402 women demonstrated normal films. Positive x-ray changes for asbestosis were encountered in a linear relationship when viewed by age of the worker. Employees aged 25--29 years exhibited 1.3% positive findings, and this level increased to a maximum of 38.2% positives among workers aged 65 years and over. Normal chest films descended, conversely, in a linear relationship. Similarly, the percentage of positive findings for asbestos-related disease increased in a linear configuration with length of service. Persons with 2--6 years of asbestos contact displayed 12.4% positive findings, while individuals with 22-26 years of work at the shipyard manifested 37.0% positive chest film findings. Although the shipyard was operational between 1943 and 1949, the system of allocation of badge numbers precludes the inclusion of these 7 years of work among persons who had had at least 26 years of service. When studied by work site, dividing the subjects into production and nonproduction personnel, it was found that production workers accounted for 74.5% of the asbestos-positive films. Overall, the 780 production workers manifested 11.8% of the positive findings of all persons studied, while nonproduction employees accounted for 4.1% of the positives out of the population studied. A figure that approximates the total finding of asbestos-related disease is 16.0%.
Radiologic and surgical aspects of the diaphragm in asbestos exposure. L. Di Menza, A. Hirsch, M. Mangold, et al. 1979;330:787-9. PubMed · Publisher
Radiologic changes after cessation of exposure among chrysotile asbestos miners in Italy. G.F. Rubino, M. Newhouse, R. Murray, et al. 1979;330:157-61. PubMed · Publisher

Summary

The authors noted that no published report had described whether asbestosis progresses after exposure stops. As a preliminary part of a morbidity study of chrysotile asbestos miners in Balangero, northern Italy, they examined whether radiologic changes appeared or progressed in retired workers. Of 473 men who had left employment between 1946 and 1975, 265 responded to an invitation for clinical examination, chest x-ray and lung function tests. Fifty-six were included. Each had left exposure more than 3 years earlier, had a comparable film from the end of exposure, and had no radiologic changes from other chest conditions. Pairs of films, taken on average about 12 years apart, were read side by side in chronological order by three experienced readers using the ILO/UC classification. Mean exposure was 23.4 years. At the end of exposure, 32.1% had irregular opacities of category 1/0 or higher and 19.6% had pleural changes. Of the 18 men with abnormal first films, 7 (38.9%) showed progression after an average of 8 years. Of the 38 men with normal first films, 3 (7.9%) developed opacities after an average of 14 years. All previously observed pleural thickening progressed. Duration of exposure and smoking showed no clear effect on appearance or progression. The authors suggested that individual susceptibility plays a role. They concluded that men with radiologic signs should not be permitted to work where asbestos exposure exists.

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Risk of asbestosis in crocidolite and amosite mines in South Africa. L.M. Irwig, R.S. du Toit, G.K. Sluis-Cremer, et al. 1979;330:35-52. PubMed · Publisher

Abstract

X-rays of all while and mixed-race men employed in crocidolite and amosite mines and mills were read independently by three experienced readers according to the ILO U/C classification. Abnormality was regarded as present if reported by two or more readers. Parenchymal abnormality, defined as the presence of small irregular opacities of profusion 1/0 or greater, was found in 7.3% of the workers. Pleural thickening was found in 4.5% of the workers, costophrenic angle obliteration in 3.2%, and pleural calcification in 1.7%. The prevalences of both pleural and parenchymal abnormality were strongly related to the duration of exposure to asbestos at work. The overall prevalence of abnormality increase from 4.0% in men with exposure for 1 year or less to 47.9% in men with more than 15 years of exposure. After taking into account the effects of age and duration of asbestos exposure, the prevalence of pleural abnormality was not predicted by fiber concentration. However, white men working with amosite tended to develop a higher prevalence of pleural abnormality than did those working with crocidolite. Compared to whites, men of mixed race, who only work with crocidolite, had a high prevalence of pleural abnormality in each exposure duration category. In contrast to pleural abnormality, the prevalence of parenchymal abnormality, after taking into account the effects of age and duration of exposure, was significantly predicted by fiber concentration but not by race or asbestos type. Our results suggest that parenchymal abnormality in workers in South African asbestos mines could be largely prevented by reducing exposure to fibers visible under the light microscope. However, this may not be the case for pleural abnormality.
Short-term asbestos work exposure and long-term observation. H. Seidman, I.J. Selikoff, E.C. Hammond. 1979;330:61-89. PubMed · Publisher

Summary

The authors examined how the duration of work exposure to amosite asbestos related to later mortality, extending earlier follow-up of a factory cohort to 35 years. Between June 1941 and December 1945, 933 men were recruited to an amosite asbestos insulation factory in Paterson, New Jersey, that supplied the U.S. Navy. Many worked only briefly. After exclusions, 820 men were studied. Twenty were excluded for prior asbestos work, and 93 because they took asbestos work elsewhere, died, or were lost to follow-up within 5 years. Using generation life table methods, the authors compared observed cumulative probabilities of death from 5 through 35 years after onset of work, through 1977, with those expected from New Jersey white male rates, by length of time worked. Causes were coded from death certificates and from 'best evidence'; additional information was obtained for 413 (78%) of 528 deaths. Men who worked under one month had favorable all-cause mortality. In the other groups excess mortality appeared later, and was smaller, the shorter the work. There were 30 asbestosis deaths and 7 each of pleural and peritoneal mesothelioma. Among men aged 40-59 who had worked 9 months or more, lung cancer was about 10 times expected within 5-14 years. The authors concluded that lower dosage lengthened latency and reduced excess mortality, and that latency also depended on age at exposure.

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Significance of aspect ration in regulation of asbestos fiber exposure. A.M. Langer. 1979;330:601-4. PubMed · Publisher

Summary

This article introduced a workshop on the significance of aspect ratio in regulating asbestos fiber exposure and set out the participants' recommendations. The author recalled that a 1964 New York Academy of Sciences conference on the biological effects of asbestos had stressed an interdisciplinary approach. That conference had only peripherally addressed the physical-chemical nature of asbestos fibers, the properties that give them biological activity, and their relationship with fibrous rock-forming silicates that are not asbestos. The workshop was shaped with the Office of Environmental Assessment of the US Bureau of Mines. It had three sections: physical and biological properties of asbestos and acicular mineral fragments; the role of regulatory agencies; and aspect ratio and health hazards of asbestos fibers. Afterwards, T. Zoltai and the author drafted what they believed was a consensus of the participants. The recommendations were:
(1) use standard mineralogical terminology, such as US Bureau of Mines Information Circular No. 8751 (1977).
(2) use the term asbestos only when the source or megascopic characteristics are known; otherwise describe fibers as indistinguishable from asbestos or use general mineralogical terms.
(3) study the chemical, physical and crystallographic properties of asbestiform fibers, including fiber dimension (aspect ratio), alongside biological and medical studies.
(4) stop limiting "asbestos" to the 5 (or 6) commercial minerals, study fibrous rock-forming silicates, and control them like asbestos until safety is demonstrated.
(5) collect more data on inorganic fibers in human tissues.

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Silica and asbestos: contrasts in tissue response. A.G. Heppleston. 1979;330:725-44. Review PubMed · Publisher
Surveillance of high-risk groups exposed to asbestos in the United States. H.C. Lewinsohn. 1979;330:533-40. PubMed · Publisher
Surveillance of high-risk groups--a survey of asbestos workers: the present position in the United Kingdom. W.J. Smither. 1979;330:525-32. PubMed · Publisher
The contamination of Lake Superior with amphibole gangue minerals. A.M. Langer, C.M. Maggiore, W.J. Nicholson, et al. 1979;330:549-72. PubMed · Publisher

Abstract

Iron ore called taconite is mined in the Biwabik Iron Formation in the Eastern Mesabi region of the Mesabi Range, in eastern Minnesota. After mining, ore is shipped to Silver Bay, Minnnesota for processing and wet magnetic extraction. Tailings from the process are dumped, as a slurry, into a man-made containment delta constructed in Lake Superior. Submicroscopic amphibole fibers and/or cleavage fragments, a component of the gangue, apparently escape from the delta at Silver Bay, and enter Lake Superior. These particles contaiminate the potable water supplies of municipalities drawing directly from the lake. One of the gangue minerals is the amphibole grunerite, whose asbestiform variety is called amosite. Major emphasis of this study was directed at identification of submicroscopic particle pollutants, based on morphology, structure and chemical composition. Quantitative determination of fibrous amphibole phases, present in a range of water samples, was undertaken. Transmission electron microscopy, selected area electron diffraction, and an electron microprobe technique was used for identification and enumeration and this information was compared with data sets determined from standards. Grunerite fiber and/or acicular cleavage fragments, in some instances indistinguishable from asbestiform grunerite, are present in the tailings, lake water and drinking water of a number of municipalities, a result of contamination of the lake at the Silver Bay milling operation. This amphibole is found in drinking water in concentrations which range from 0.6 to 2.8 X 10(6) fiber/liter. The risk to health, associated with direct ingestion of grunerite fiber is unknown and is extrapolated from the asbestiform grunerite (amosite) data base. The biological activity of other fibrous amphiboles observed, unrelated to any asbestiform silicate variety, is presently unknown and warrants investigation.
The use of animal models for studies on asbestos bioeffects. J.M. Davis. 1979;330:795-8. PubMed · Publisher
United States regulations for control of asbestos exposure. E.M. Fenner. 1979;330:179-83. PubMed · Publisher
What to do about the asbestos currently in ships and industry?. A.A. Cross. 1979;330:379-81. PubMed · Publisher
What to do about the asbestos currently in ships and industry?. G.W. Wright. 1979;330:383-6. PubMed · Publisher
Case study 1: asbestos--the TLV approach. W.J. Nicholson. 1976;271:152-69. PubMed · Publisher

Abstract

A review of the control of carcinogenic exposures using the TLV approach presents a prospect of limited effectiveness. With asbestos, as with any carcinogen, no threshold is known below which no health effect may be manifest. At best, we have only limited dose-response information at levels much above those of practical concern. In the case of asbestos, current exposures can only be described crudely at any level of exposure, and health effects are only known for past high, but ill-defined, exposures. Limited information exists on the effects of synergistic interactions with other materials. The current U.S. TLV, based on data concerned with occurrence of asbestosis, has not been evaluated with regard to possible effectiveness in the prevention of asbestos cancer. Yet cancer is the heart of the asbestos-hazard problem. Finally, enforcement of the existing TLV, especially for asbestos has been limited, frequently absent, and often ineffective. Workers are exposed in many situations to levels much above the current standard. As discouraging as this picture may seem, a TLV can be useful for stimulating the development and application of engineering-control procedures. The application of these procedures, however, must be specified and mandated in future standards to lower worker exposures to the minimum commensurate with existing technology. As technology is developed that makes lower exposure levels possible in a large part of the industry, TLVs should be reduced to take advantage of that technology.
Discussion paper: asbestos fiber exposures in a hard rock gold mine. J.M. Dement, R.D. Zumwalde, K.M. Wallingford. 1976;271:345-52. PubMed · Publisher

Summary

This discussion paper described the laboratory analyses NIOSH used to characterize airborne fiber exposures in a hard rock gold mine in Lead, South Dakota. A companion mortality study by Gillam et al. had reported increased respiratory disease among the mine's workers. In 1974, the U.S. Bureau of Mines' Mining Enforcement and Safety Administration (MESA) collected about 200 air samples. Phase-contrast optical microscopy gave an average of 0.25 fibers longer than 5 µm per cm³, with a highest single value of 2.8 fibers/cm³, but the fibers were not identified. NIOSH selected the 25 underground personal samples with the highest fiber counts and analyzed them by transmission/scanning electron microscopy with electron diffraction and energy-dispersive x-ray analysis. About 250 fiber analyses were done, and 2111 fibers were counted and sized. Of the airborne fibers, 80-90% showed an amphibole diffraction pattern. Of these amphiboles, 60-70% had compositions identical to fibrous grunerite (amosite), 1-2% were cummingtonite and 10-15% were hornblende. Mean concentrations were 0.36 fibers/cm³ longer than 5 µm and 4.82 total fibers/cm³. Median fiber diameter was 0.13 µm and median length 1.1 µm, and 94% of fibers were shorter than 5 µm. The authors concluded that the 1976 OSHA standard of 2.0 fibers/cm³ may not protect against asbestos-induced respiratory cancer. They also concluded that fibers shorter than 5 µm need more attention and better sampling methods, and that noncommercial asbestos present as a contaminant can cause disease.

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Household-contact asbestos neoplastic risk. H.A. Anderson, R. Lilis, S.M. Daum, et al. 1976;271:311-23. PubMed · Publisher

Summary

The authors investigated whether disease among household contacts of asbestos workers was common or rare. They studied household contacts of the 1664 workers employed between 1941 and 1954 at a factory producing amosite asbestos products. Contacts who had lived with the workers during their employment were being traced for a mortality study and invited for medical examination. Each examinee gave an occupational, medical, smoking and respiratory history and had a physical examination, posteroanterior and oblique chest x-rays, and screening pulmonary function tests. Five experienced physicians read the x-rays blind using the ILO/UC Pneumoconiosis Classification, and the consensus reading was used. Of 354 people examined, 326 had lived in the household during the worker's employment and had no occupational asbestos exposure of their own. Of these, 114 (35%) had chest x-ray abnormalities: pleural thickening in 69 (21%), pleural calcification in 19 (6%) and irregular opacities in 62 (19%). Pleural changes alone were more frequent than parenchymal changes alone (52 versus 35), the reverse of the pattern seen in the workers. Four pleural mesotheliomas were identified among household contacts, two of them fatal. The authors concluded that significant household contamination with asbestos from industrial sources can and does commonly occur. They stated that it may cause characteristic x-ray changes and, less frequently, asbestos-associated cancer.

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Lung cancer and mesothelioma during prospective surveillance of 1249 asbestos insulation workers, 1963-1974. I.J. Selikoff. 1976;271:448-56. PubMed · Publisher
Mortality patterns among hard rock gold miners exposed to an asbestiform mineral. J.D. Gillam, J.M. Dement, R.A. Lemen, et al. 1976;271:336-44. PubMed · Publisher

Summary

This study examined whether exposure to cummingtonite-grunerite, an amphibole mineral, was linked to excess mortality among hard rock gold miners in Lead, South Dakota. The cohort comprised 440 white men examined in a 1960 U.S. Public Health Service silicosis survey who had at least 60 months of underground mining at the mine and had never mined underground elsewhere. They were followed from April 1960 to December 31, 1973, with none lost to follow-up. Observed deaths were compared with those expected from South Dakota white male rates. There were 71 deaths against 52.9 expected. Respiratory cancer deaths numbered 10 against 2.7 expected, eight of them bronchogenic carcinomas. Nonmalignant respiratory deaths numbered 8 against 3.2 expected, and this excess appeared 20 or more years after first underground work. Surveys found free silica exposures below the OSHA standard, no detectable radon daughters, and trace arsenic, chromium and nickel. In 1974 about 200 personal samples averaged 0.25 fibers longer than 5 µm per cm3 by phase-contrast microscopy. Electron microscopy of selected samples showed that 80-90% of airborne fibers were fibrous amphiboles, mostly fibrous grunerite (amosite), and that about 94% were shorter than 5 µm. The authors attributed the respiratory cancer excess to asbestos, alone or with cigarette smoking. They attributed the nonmalignant excess to asbestos, possibly with free silica. They called for reevaluation of asbestos standards and sampling methods.

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Occupational asbestos exposure, smoking, and laryngeal carcinoma. R.W. Morgan, P.T. Shettigara. 1976;271:308-10. PubMed · Publisher

Summary

This study asked whether cancer of the larynx is related to occupational asbestos exposure. Smoking habits were also measured, mainly as a control variable. The cases were 54 men who had been treated for laryngeal cancer at the Toronto General Hospital and were alive on May 1, 1974. They represented all of the patients available. Each case was matched with one male control of similar age (within 5 years) who lived four or more doors to the right of the case. The same interviewer questioned all cases and controls using a mostly yes/no questionnaire, chosen to reduce interviewer bias. Telephone clerks later recontacted 51 cases and 52 controls to check the original answers. They took occupational histories, which were classified blind into three categories of probable asbestos exposure. Matched pairs were analysed with the McNemar test. In 13 pairs only the case reported asbestos exposure, and in 1 pair only the control did (relative risk 13; p<.001). Time from asbestos exposure to diagnosis ranged from 5 to 55 years, with a mean of 28.6 years. Risk rose with the number of cigarettes smoked, reaching a relative risk of 21.00 at 40 or more cigarettes. The asbestos risk appeared confined to smokers. The occupational histories appeared to confirm the interview data. No case-control differences were found for alcohol, uranium, chromium, cobalt, nickel, arsenic or medical irradiation. The authors concluded that laryngeal cancer must now be included among presumptive asbestos diseases unless evidence to the contrary is presented.

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Occupational carcinogenesis. High-risk industrial groups: identification, education, and surveillance. Tyler Asbestos Workers Program. S.D. Greenberg, G.A. Hurst, W.T. Matlage, et al. 1976;271:353-64. PubMed · Publisher

Abstract

It is concluded that sputum cytopathology is an excellent, simple, noninvasive, painless, and inexpensive means for early detection of malignant and premalignant lesions of the lung, and that no special techniques are necessary for the identification of ferruginous bodies.
Pathogenic effects of inhaled particles and antigens. A.C. Allison. 1974;221:299-308. Review PubMed · Publisher

Summary

This review, presented as a symposium paper, summarized evidence on how inhaled particles and antigens damage the lungs, with emphasis on the role of macrophages. The author described how particle size and shape govern deposition. A rat study using radioactive UICC crocidolite found that an average of 35% of inhaled asbestos was deposited, and about 30% of deposited fibre remained in the lungs after 30 days. The author outlined a proposed mechanism of phagocytosis. In the author's experiments with mouse peritoneal macrophages, short chrysotile and crocidolite fibres (<5 µm) were rapidly and completely ingested, while long fibres (>20 µm) were never completely ingested. The review covered how silica and asbestos kill macrophages, linking asbestos toxicity to fibre magnesium content. Animal studies of intrapleural injection indicated that all asbestos types, and some non-asbestos fibres, induced mesotheliomas at about equal frequency if they were in the correct size range. This suggested that fibre dimensions mattered more than chemical composition. The paper discussed fibroblast anchorage dependence and direct stimulation of collagen synthesis by chrysotile in cultured fibroblasts. It also discussed the interaction of asbestos with cigarette smoking in lung cancer. The author reported that immune complexes, at as little as 5 µg/ml, induced selective release of lysosomal enzymes from macrophages. The author speculated that this might help explain fibrosis in extrinsic allergic alveolitis.

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Electron microscopic findings in the lungs of miners. G. Harrison, N.L. Lapp. 1972;200:73-93. PubMed · Publisher

Abstract

Portions of four lungs were prepared for study by electron microscopy. Three were obtained at autopsy from underground coal miners and one at biopsy from a boiler repairman at a power plant that burned bituminous coal. All four lungs contained large amounts of collagen and elastic fibers. The autopsy specimens showed changes such as membrane disruption and vesiculation, probably resulting from postmortem autolysis. All four lungs contained a number of particles of various types. Four were common to all of the lungs: (1) hard, dense needle-like material, (2) smooth, angular pieces, (3) larger rectangular chunks with chatter marks, and (4) granular aggregates that often contained some of the other types of particles. In addition, a variety of round and square particles were seen, and in one case asbestos bodies were noted. Positive identification of the types of particles seen was not possible; thus, their specific role in producing the pathological changes observed is uncertain.

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Interactions of mineral fiber surfaces with cells in vitro. R.J. Schnitzer, G. Bunescu, V. Baden. 1972;172(23):759-71. PubMed
Investigative techniques in the laboratory study of coal workers' pneumoconiosis: recent advances at the cellular level. J.S. Harington. 1972;200:816-34. Review PubMed · Publisher

Summary

This paper set out problems and priorities for laboratory research on coal workers' pneumoconiosis, focusing on how coal dust behaves towards macrophages in cell culture. The author noted that few such studies had been done and drew on earlier silica and asbestos work. Two laboratory-milled coal dusts were tested, one from a South Wales colliery (SWS 3) and one from a Nottinghamshire colliery (NT 1). Both were tested native and after benzene extraction, which removed 1.5% and 0.7% organic material respectively. Hemolytic activity was measured on human and sheep erythrocytes. Cytotoxicity was assessed in hamster peritoneal macrophages, with Fransil silica and UICC chrysotile as cytotoxic standards and rutile as a control dust. Native NT 1 was strongly hemolytic to human erythrocytes (70%), falling to 29% after extraction. Fresh serum increased hemolysis, but not significantly. SWS 3 was weakly hemolytic, and the extracts alone were inactive on sheep erythrocytes. Neither coal was toxic to macrophages, whereas silica and chrysotile caused marked degeneration. The author then reviewed how methods varied between laboratories: animal species, type of macrophage, culture media, incubation conditions, measures of cytotoxicity and dusts. He reported conflicting published results for asbestos. He concluded that coal itself is the most variable factor and recommended international working parties to standardize coal samples and techniques, as the 1965 UICC asbestos working parties had done.

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In plain English

This 1972 paper from a South African cancer research unit discussed problems and priorities in laboratory research on coal workers' pneumoconiosis. It reviewed how other studies had tested silica and asbestos on cells, and it reported the author's own tests on two laboratory-milled coal dusts: one from a South Wales colliery (SWS 3) and one from a Nottinghamshire colliery (NT 1). Native NT 1 coal released 70% of the hemoglobin from human red blood cells. After its organic matter was removed with benzene, this fell to 29%. Native and extracted SWS 3 were weakly hemolytic. In cultured hamster macrophages, neither coal, native or extracted, was found toxic. Silica and chrysotile asbestos, used as toxic standards, damaged and destroyed the cells. Because airborne dust was not used, the author did not relate the results to miners. He described published cell-culture results on asbestos as somewhat confusing. He concluded that working parties should study the many variables, with international agreement on criteria and standard coal samples.

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Pathologica, physiological, and radiological correlations in the pneumoconioses. E.A. Gaensler, C.B. Carrington, R.E. Coutu, et al. 1972;200:574-607. PubMed · Publisher
Interactions of mineral fiber surfaces with cells in vitro. R.J. Schnitzer, G. Bunescu, V. Baden. 1971;172(23):759-72. PubMed

1960s

A biopsy series of mesotheliomata, and attempts to identify asbestos within some of the tumors. D.O. Hourihane. 1965;132(1):647-73. PubMed · Publisher
A comparison of impinger and membrane filter techniques for evaluating air samples in asbestos plants. H.E. Ayer, J.R. Lynch, J.H. Fanney. 1965;132(1):274-87. PubMed · Publisher
Asbestos and neoplasia: diffuse mesothelial tumors. Criteria for diagnosis of diffuse mesothelial tumors. W.T. McCaughey. 1965;132(1):603-13. PubMed · Publisher

Summary

The author, a pathologist at Queen's University, Belfast, set out criteria for diagnosing diffuse mesothelial tumors (diffuse mesothelioma) and distinguishing them from metastatic tumors of the serosal membranes. He drew on a review, with colleagues from other United Kingdom centers, of their combined experience of 124 autopsied cases and many surgical specimens. Grossly, the tumors infiltrated the serosa extensively, often encasing the lung, but this appearance alone did not exclude metastatic tumor, and diagnosis at autopsy rested largely on excluding other primary sites. Histologically, structure varied greatly within and between tumors. More specific patterns included tubulopapillary structures lined by uniform cubical or flattened cells, sheets of spheroidal cells with a pericellular reticulin network, and distinctive patterns of hyaline collagen. A mixed structure was noted in close on half of the author's autopsied cases, so he stressed sampling many areas. The periodic acid-Schiff reaction was nearly always negative. A colleague found hyaluronidase-removable acid mucopolysaccharide in all 17 mesotheliomas examined and in none of 20 adenocarcinomas. However, the author had seen an identical reaction in pleural metastases from pancreatic adenocarcinoma. He considered effusion cytology and hyaluronic acid only a guide. He concluded that the diagnosis should be reserved for growths with an unequivocal predilection to spread along a serosal membrane and a certain serosal origin.

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Asbestos and the urban dweller. J.G. Thomson. 1965;132(1):196-214. PubMed · Publisher

Abstract

The extent of inhalation of asbestos fibers by urban dwellers was investigated by counting asbestos bodies in smears from the lung bases from 500 consecutive autopsies in subjects over the age of 15 in Cape Town, South Africa, and 500 in Miami, Florida. The results were similar in the two cities, and no less than 30 per cent of the males and 20 per cent of the females showed asbestos bodies. In 85 per cent of the positive cases the bodies were scanty, were not associated with pulmonary changes, and were regarded as the result of contamination of the urban atmosphere. In six per cent of all the males examined the bodies were numerous and were presumably of occupational origin.

The tendency for asbestos fibers too long to be phagocytosed to move downwards by gravity before they become asbestos bodies leads to concentration at the lung bases, and small doses can have a cumulative effect. An increase in the amount of urban air contamination would seem inevitable in view of the increasing consumption and diversity of uses of asbestos and of its virtual indestructibility, and an increase in basal asbestosis is suggested as a possible future development. As a limited basal asbestosis may be associated with malignant mesothelioma of pleura and peritoneum an increase in this tumour is forecast as the main ground for regarding asbestos as a potential urban hazard. While that view is conjectural, the finding of abundant asbestos bodies in the lung bases of 1 in 17 of the male hospital population suggests that the occupational hazard from asbestos is greater and more diversified than is at present realized.

The main object of this work is to draw attention to the effects of a relatively new development, the widespread use of asbestos in cities, and to stimulate the obtaining of comparable figures from other parts of the world, to establish the baselines of urban asbestos inhalation of today, and enable us to detect increases in the future.

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Asbestos dust deposition and retention in rats. J.C. Wagner, J.W. Skidmore. 1965;132(1):77-86. PubMed · Publisher
Asbestos-induced tumors in White Leghorn fowls. P.R. Peacock, A. Peacock. 1965;132(1):501-6. PubMed · Publisher

Summary

The authors, at the Cancer Research Department of the Royal Beatson Memorial Hospital in Glasgow, studied how the air-sac and lung tissues of line-bred White Leghorn fowls react to asbestos, and whether tumors develop. Finely ground fibers suspended in tributyrin were injected into the axillary air sac. The fibers spread over the air-sac mesothelium and reached the pulmonary alveoli. Macrophages engulfed them and carried them to subepithelial lymphoid follicles. In a first experiment, six birds aged 2 to 6 years received 0.5 ml of "asbestos" of unknown origin. The six-year-old bird died a year later with a massive tumor of the right lung that had invaded neighbouring organs. In further experiments, 12 three-month-old pullets received 1 ml of amosite and 12 received 1 ml of crocidolite. In the amosite group, one bird killed at 42 months had a pleomorphic tumor involving the axillary air sac, pectoral muscles and left lung; it was grafted successfully into one of three pullets. In the crocidolite group, one bird killed at 40 months had a tumor classified as reticulosarcoma, possibly of mesothelial origin. Another bird had a granulomatous, non-neoplastic mass containing abundant fibers, and asbestos bodies were found in its lung. No such tumors had been seen in some hundreds of control birds over 36 years. The authors considered that, although the numbers were small, the findings seemed likely to have some significance.

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Asbestosis and primary intrathoracic neoplasms. W.D. Buchanan. 1965;132(1):507-18. PubMed · Publisher

Abstract

The findings of a continuing study by the Medical Branch of H.M. Factory Inspectorate, Ministry of Labour, of information recorded on death certificates of persons dying with asbestosis are presented. Arrangements are in force whereby copies of all such certificates are received routinely by the Medical Branch. It is considered, for reasons outlined, including the high proportion of such cases coming to autopsy, that this method is a reasonably accurate one of assessing both the incidence of all recognized cases as asbestosis and of complications ensuing.

A review of the literature indicates that the possibility of carcinoma of the lungs or bronchi as a complication had been expressed prior to 1947. Nevertheless, it is believed that the first series in which the incidence of lung carcinoma had been related to a sizeable group of asbestosis deaths was that published in the 1947 Annual Report of the Chief Inspector of Factories. Similar reports followed in 1954 and 1955.

Up to the end of 1963, 584 death certificates recording the presence of asbestosis have been obtained and the annual totals of such certificates are currently increasing. The proportion recording a thoracic tumor is also in both sexes continuing to increase disproportionately to the total number, so that currently over 50 per cent of males dying with asbestosis present have also a neoplasm. Data on the mean age at death over various periods of time of male and female asbestosis cases indicate an improving prognosis where the asbestosis is uncomplicated but no significant improvement where complicated by cancer. Suggestions to account for this and also the yearly increasing total of recorded cases of asbestosis are put forward.

The conclusion of the study is that even when viewed against the steadily rising incidence of lung cancer in the population as a whole, there seems little doubt that there is a special risk of an intrathoracic tumor if asbestosis is also present in the lungs.

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Asbestosis in Great Britain. J.C. McVittie. 1965;132(1):128-38. PubMed · Publisher

Summary

This paper reviewed the history of asbestosis in Great Britain and described cases diagnosed by the Ministry of Pensions and National Insurance's Pneumoconiosis Medical Panels. The author traced knowledge of the disease from Montague Murray's 1906 evidence and the 1930 Merewether and Price report, and the compensation and regulatory measures that followed. Between 1931 and December 1963, 748 cases of asbestosis were diagnosed in life under the compensation and industrial injuries legislation. The average of 45 new cases a year over the last five years suggested an incidence of at least five per thousand exposed. Four Panels (London, Manchester, Newcastle and Sheffield) diagnosed 247 new cases, including 34 women, in the nine years to 1963. Insulation work accounted for 41 per cent of these cases. More than half came to light through claims for benefit. Sixty-six per cent of the workers had entered the industry in 1933 or later, and in almost every occupation asbestosis had developed after less than 10 years' exposure. Disablement at diagnosis was slight in 140 cases, moderate in 81 and severe in 26. Of the 247, 59 had died, at an average age of 57. These deaths included 21 from lung cancer, two from pleural mesothelioma and one from peritoneal mesothelioma. The Panels accepted lung cancer as a sequela of asbestosis. The author concluded that there was no room for complacency. He questioned whether periodic examinations prevented disease and noted that some employers had greatly improved working conditions.

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Asbestosis in South Africa--certain geographical and environmental considerations. G.K. Sluis-Cremer. 1965;132(1):215-34. PubMed · Publisher

Summary

The author asked why pleural mesothelioma had been reported often from the North West Cape (N.W.C.) crocidolite mining area of South Africa but never from the Transvaal (TVL) asbestos field, where amosite and Transvaal crocidolite are mined. He compared the two areas on medical services, production history, dust counts, ore constituents, neighbourhood pollution, a field survey and post-mortem findings. In the field survey (1960 to 1962), the Pneumoconiosis Research Unit examined a random sample of households: 1904 persons aged 20 and over from the N.W.C. asbestos area, 485 from the TVL, and residents of a control N.W.C. town with no asbestos industry. The survey used questionnaires, clinical examination, chest X-rays read blind, and single sputum samples. Mines and mills in the N.W.C. were about twice as dusty as in the TVL during the 1940s and 1950s. Asbestos bodies were found in sputum in both asbestos areas, including in people with no occupational exposure, but not in the control town. Among exposed people, bodies were found in 35% of males in the N.W.C. versus 10% in the TVL, and in 20% versus 7% of females. Fibre prevalence was similar in the two areas. Post-mortem reports on 87 N.W.C. and 64 TVL Bantu miners (1959 to 1964) showed no significant difference in the frequency or severity of asbestosis. The author concluded that there appears to be a real difference between N.W.C. crocidolite and TVL amosite in producing mesothelioma, not explained by environmental differences.

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Association of pulmonary tumors with asbestosis in Piedmont and Lombardy. E.C. Vigliani, G. Mottura, P. Maranzana. 1965;132(1):558-74. PubMed · Publisher

Abstract

In Piedmont and Lombardy, there are at present about 4,000 asbestos workers employed in mining, and in textile and asbestos products factories. From 1943 to 1964, 879 cases of asbestosis were certified in the above regions: 830 cases in Piedmont and 49 in Lombardy. Of these, 172 died and 707 are still alive. The ultimate cause of death of the 172 subjects who died was in 15 cases carcinoma of the lung and in three cases mesothelioma of the pleura. One lung carcinoma and two pleural mesotheliomas were found among the 707 living subjects.

The incidence of death from thoracic malignancy among subjects with asbestosis has been compared with that found among workers with silicosis. Among 172 fatal cases of asbestosis, 15 carcinomas of the lung and three mesotheliomas of the pleura were found, that is 10.5 per cent of all cases. No case of mesothelioma and 25 cases of carcinoma of the lung, that is 1.8 per cent, were found among 1,459 fatal cases of silicosis. Carcinoma of the lung therefore accounts for death in subjects with asbestosis five times more frequently than in subjects with silicosis.

The rate of death from carcinoma of the lung and from mesothelioma has been studied in 24,700 necropsies performed on people over 40 years of age in Turin, Milan and Pavia. In Turin and Milan, carcinoma of the lung accounts roughly for 4 per cent of the necropsies (5.3 per cent of men and 1.8 per cent of women) ; this is half the rate found among all subjects with asbestosis and one-fourth the rate among those who came to post-mortem.

Mesotheliomas, either pleural or peritoneal, were found in 76 out of a total of 24,700 necropsies (0.3 per cent) of subjects over 40 years of age. Three cases of mesothelioma (all pleural) were found among the 172 fatal cases of asbestosis. Altogether, six cases of mesothelioma of the pleura occurred in people occupationally exposed to asbestos dust ; three of them had worked with crocidolite and amosite besides chrysotile. In 10 cases of mesothelioma, not occupationally exposed to asbestos dust, where a lung specimen was available for study, no asbestos bodies were found.

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Chemical studies of asbestos. J.S. Harington. 1965;132(1):31-47. PubMed · Publisher

Abstract

Further chemical studies of the three main types of asbestos, crocidolite, amosite and chrysotile, have been made.

The origin of the primary oils associated with crocidolite and amosite has been discussed. By suitable methods 0.32 per cent of extractable material can be removed from crocidolite and 0.28 per cent from amosite. A sample of commercial amosite known to be carcinogenic yielded 0.76 per cent of extractable material. Chemical investigations have been made of the oils from crocidolite and amosite by various techniques. Low levels of polycyclic aromatic hydrocarbons were detected.

In addition to the primary oils, asbestos may contain secondary oils derived from contamination or from the intentional application of oil during processing in industry. Up to 80 per cent of the jute oil in the jute bags used for storing asbestos may be absorbed by the asbestos fiber. This could explain why chrysotile, which apparently has no primary oils, may contain, after milling and other industrial treatment, yields of from 0.1 per cent to 0.4 per cent. Insulation materials also contain significant amounts of extractable material.

Finally, studies have been made to assess, wherever possible, the part which metals and metal complexes may play in the carcinogenic action.

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Cohort analysis of changes in incidence of bronchial carcinoma in a textile asbestos factory. J.F. Knox, R.S. Doll, I.D. Hill. 1965;132(1):526-35. PubMed · Publisher

Summary

The authors examined whether the lung cancer risk among workers in a large British asbestos textile factory, where chrysotile was predominantly used, had changed since dust-control regulations made in 1931 took effect at the start of 1933. They extended an earlier study (Doll, 1955) to the end of 1961. From personnel records they identified 198 men who had completed at least 20 years in the regulated 'scheduled areas'. These men were divided into four groups by their length of experience before 1933. A further group of 427 men and 175 women was first employed on or after 1 January 1933 and completed at least 10 years. Observed deaths were compared with numbers expected from England and Wales rates. Among men with over 10 years' experience before 1933 (57 men), there were 15 deaths from lung and pleural cancer against 0.94 expected. There were 41 deaths from all causes against 15.00 expected. Men with 5-10 years' pre-1933 experience had 5 lung cancer deaths against 0.81 expected. The remaining male groups showed no excess. Women had 8 deaths against 4.02 expected (P=0.052), including one lung cancer. The risk rose with age and fell with shorter exposure before 1933. The authors concluded that the risks were much reduced, mainly because of the improved working conditions. They stated that complete elimination of the hazard could not yet be asserted.

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Developments in dust sampling and counting techniques in the asbestos industry. S. Holmes. 1965;132(1):288-97. PubMed · Publisher
Differential diagnosis in the pathology of asbestosis. J. Gough. 1965;132(1):368-72. PubMed · Publisher

Abstract

Asbestosis occurs in two anatomical forms - diffuse and solid fibrosis. The diffuse form leads to honeycomb (cystic) lung. In the diagnosis, distinction is made from other forms of honeycomb lung. Differentiation of asbestosis from fibrosis due to other silicates is not difficult. Hemosiderosis of elastic tissue (elastosis bodies) may mimic asbestos bodies.

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Dust measurement and monitoring in the asbestos industry. C.G. Addingley. 1965;132(1):298-305. PubMed · Publisher
Economics of dust control. D.W. Hills. 1965;132(1):322-34. PubMed · Publisher
Electron-microscope studies of asbestosis in man and animals. J.M. Davis. 1965;132(1):98-111. PubMed · Publisher
Epidemiology of diffuse mesothelial tumors: evidence of an association from studies in South Africa and the United Kingdom. J.C. Wagner. 1965;132(1):575-8. PubMed · Publisher

Summary

This conference paper reviewed evidence linking asbestos exposure to diffuse mesothelioma in South Africa and the United Kingdom. In South Africa, the first case of pleural mesothelioma with asbestos bodies in the lung was diagnosed in Johannesburg in 1956, after patients in Kimberley were found to have pleural malignancy rather than tuberculosis. Detailed life histories were taken from patients and relatives. By 1959 an association with the Cape asbestos fields or industrial asbestos use was established in 32 of 33 proven pleural cases. The average time from first exposure to tumor was 40 years. By the end of 1961, 87 pleural and two peritoneal mesotheliomas had been diagnosed. Only two lacked a history of asbestos exposure, and only one lacked definite crocidolite exposure. Twelve had industrial exposure. The rest came from the Cape asbestos fields region, many through environmental exposure from living near mills and dumps. No cases were reported from the amosite or chrysotile mining areas. The total later exceeded 100. In Britain, thoracic surgery and pathology departments examined lung tissue, sputum and occupational histories. Asbestos exposure was found in 5 of 6 cases in Cardiff, 11 of 13 in Newcastle and 2 of 3 in Portsmouth. The author concluded that the association was with asbestos exposure, sometimes slight, rather than with asbestosis. He reported that crocidolite exposure was established in most British cases and that no indisputable pure chrysotile case had been found.

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Epidemiology of mesothelial tumors in the London area. M.L. Newhouse, H. Thompson. 1965;132(1):579-88. PubMed · Publisher

Abstract

Two groups of patients who have attended a large hospital in the East End of London have been examined to determine their exposure to asbestos. The first consisted of 83 patients in whom the diagnosis of mesothelioma had been confirmed at autopsy or by biopsy. In all but seven, past occupational and domestic histories were obtained. In 22 patients the tumor was peritoneal in origin, in 61 pleural. The earliest recorded death was 1917, but only 10 of the series died before 1950. Fifty-five per cent of the males and 42 per cent of the females died under the age of 55. The interval between first exposure and development of terminal illness ranged between 16 and 55 years (mean 37 years). The second group consisted of 76 patients of the same hospital, matched by sex and date of birth with those traced in the first series. Of the patients suffering from mesotheliomata 52.6 per cent had been exposed to asbestos, as compared to 11.8 per cent of the control series. The difference in the proportion of patients with known exposures in the two series is highly significant (χ2 = 29.1, P <.001). Three main types of exposure were recognized: work in factories manufacturing asbestos textiles, insulating materials, and other products; employment as laggers or insulators; and exposure to dust brought home by relatives working with asbestos. Eighteen of those employed in factory work and four whose relatives were working with asbestos were employed at one factory. This factory opened in 1913 and was, until recent years, a heavy user of crocidolite; all those whose records could be traced worked with this type of asbestos. Among the 36 patients with mesotheliomata, with no positive occupational history and no relatives living at home who worked with asbestos, there were 11 who lived within half a mile of an asbestos factory; five of the control series also lived in the same area. The difference in the proportion of patients in the two series is also statistically significant (χ2 = 7.85, P <.01).

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Experimental asbestosis with four types of fibers: importance of small particles. P.F. Holt, J. Mills, D.K. Young. 1965;132(1):87-97. PubMed · Publisher
Histological characteristics of mesothelioma associated with asbestos. J. Churg, S.H. Rosen, S. Moolten. 1965;132(1):614-22. PubMed · Publisher

Abstract

Cytological and histological features in 30 cases of mesothelioma associated with asbestos exposure are presented. All cases conform to the gross and microscopic criteria for this type of tumor. There were 13 pleural and 17 peritoneal cases. The cytological and histological features were identical in both types. Two variants of tumor cells were seen; epithelium-like and mesenchymal. Epithelium-like cells were found in all 30 cases. In nine of these mesenchymal tumor elements were also present. Several histological patterns could be recognized : papillary, tubular, tubulopapillary, solid, nodular, and sheet-like. In the majority of cases several patterns coexisted. Demonstration of acid mucopolysaccharides in association with epithelium-like cells was of diagnostic value.

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Human exposure to asbestos: dust controls and standards. The inhalation of fibrous dusts. V. Timbrell. 1965;132(1):255-73. PubMed · Publisher
Measurement of airborne asbestos dust by instruments measuring different parameters. S.A. Roach. 1965;132(1):306-15. PubMed · Publisher
Mesothelial tumors and exposure to asbestos dust. W.G. Owen. 1965;132(1):674-9. PubMed · Publisher

Summary

The author looked for evidence of asbestos exposure in recorded cases of diffuse mesothelioma from Liverpool and neighbouring towns of the Merseyside area of North West England. The area is industrial, with shipbuilding, ship repairing and asbestos processing factories. Thirty cases were reviewed over a ten-year period from 1953 onwards. In each, a diagnosis of diffuse mesothelioma had been suggested at some time. The author re-examined clinical histories, post-mortem records and the available tissue, examined lung tissue for asbestos bodies, and took detailed occupational histories from patients or their nearest relatives. Seventeen cases were accepted as diffuse mesothelioma: 16 pleural and one peritoneal, in 12 men and 5 women with an average age of 68 years. Evidence of asbestos exposure was found in 14 (82 per cent). Twelve had been exposed at work, including five laggers, two boiler makers, two asbestos factory workers and two sack repairers. One typist had been exposed through cement dust at her workplace. Asbestos bodies were found in 7 of the 10 confirmed cases with lung sections available, compared with 18 (9 per cent) of 200 consecutive lung specimens. Exposure lasted 5 to 45 years. In all but two cases, more than 20 years passed between first exposure and the tumour. The author concluded that asbestos exposure is a major factor in causing this tumour.

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Mesotheliomatous tumors in South Africa: pathology and experimental pathology. I. Webster. 1965;132(1):623-46. PubMed · Publisher

Summary

This article reviewed the pathology of mesotheliomatous tumors in South Africa and the evidence linking them with asbestos. Of 169 primary mesotheliomas diagnosed in South Africa, 125 had been examined at the Pneumoconiosis Research Unit, Johannesburg. The description of malignant tumors was based mainly on 41 cases confirmed at post-mortem. The tumors varied in cell type and often had a dense collagen stroma. In 16 autopsy cases a primary multicentric bronchiolar carcinoma could not be excluded. Hyaluronic acid in the tumor or pleural fluid was judged a useful guide but not an absolute diagnostic criterion. Pleural biopsy and exfoliative cytology results were also reported. Specimens from a Northern Cape tuberculosis hospital showed a significantly higher incidence of mesotheliomatous tumors than those from a Southern Transvaal hospital. Of 41 cases examinable for asbestosis, 9 showed none, although 6 of these had some connection with the Northern Cape. In 350 Miners' Medical Bureau records from asbestos areas, malignancy was increased in cases with asbestosis, but mesothelioma was not more common with marked than with slight asbestosis. No mesothelioma was found in people exposed to Transvaal blue asbestos or amosite. In animals, 6 of 177 inoculated intrapleurally with crocidolite developed mesotheliomatous tumors, but such tumors also occurred occasionally after chrysotile, silica and carbon. The author concluded that these tumors appeared related to asbestos inhalation, particularly crocidolite, but that other factors could not yet be excluded.

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Mortality among asbestos products workers in the United States. P.E. Enterline. 1965;132(1):156-65. PubMed · Publisher

Summary

The author examined whether men who worked in the asbestos products industry in the United States had higher mortality, particularly from respiratory cancer. The cohort was 2,833 white men aged 15 to 64 who worked at some time during 1948-1951 for nine producers of asbestos textiles and one producer of asbestos friction materials. For comparison, 6,242 white men from three cotton textile plants were studied. Workers were identified from social security tax returns, and deaths through June 1963 from Social Security death claims. Death certificates were coded to the seventh revision of the International Classification of Diseases. Expected deaths were calculated from U.S. white male death rates. All-cause mortality among asbestos products workers was about 12 per cent above the U.S. rate (SMR 112.4). Among cotton textile workers it was about 12 per cent below (SMR 88.4). Asbestos products workers had significant excesses of respiratory cancer (24 observed, 11.9 expected), hypertensive heart disease and respiratory diseases. The respiratory disease excess was due entirely to 18 deaths from asbestosis. The respiratory cancer SMR rose to 258.6 in 1958-1963. When cotton textile workers' rates were used as the comparison, the SMRs were 130.8 for all causes, 219.7 for cancer and 438.6 for respiratory diseases. The author concluded that the data were consistent with an important past health hazard in the asbestos products industry, shown as increased cancer and asbestosis. He noted that smoking and length of exposure could not be assessed and called the results preliminary.

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Neoplasia among insulation workers in the United States with special reference to intra-abdominal neoplasia. E.C. Hammond, I.J. Selikoff, J. Churg. 1965;132(1):519-25. PubMed · Publisher

Summary

The authors reviewed early reports on asbestos workers, who were heavily exposed and often died young of tuberculosis and pneumonia, and argued that such deaths may have prevented cancers from appearing after their long latent period. They then reported mortality among asbestos insulation workers, whose exposure they described as light and intermittent, for deaths after 1942, when antibiotics were available. In a first group of 632 men, all members of New York Local 12 and Newark Local 32 of the International Association of Heat and Frost Insulators and Asbestos Workers on January 1, 1943, followed through December 31, 1962, there were 255 deaths against 203.5 expected from US white male death rates. There were 45 deaths from cancer of the lung and pleura against 6.6 expected, 29 from cancer of the stomach, colon and rectum against 9.4 expected, and 12 deaths from asbestosis. An extended group of 1,522 men was traced through August 1964. Of their 307 deaths, 124 (40.4%) were from cancer, including 53 bronchogenic carcinomas, 10 mesotheliomas (4 pleural, 6 peritoneal) and 34 gastrointestinal cancers, and 17 (5.5%) were from asbestosis. None of 57 lung and pleura cancer deaths occurred less than 20 years after first exposure. The authors did not draw conclusions on gastrointestinal cancer. They concluded that, with light exposure and antibiotics available, neoplasia is a major cause of death in such workers.

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Observations an atmospheric air pollution caused by asbestos. A. Laamanen, L. Noro, V. Raunio. 1965;132(1):240-5. PubMed · Publisher
Occupational and nonoccupational exposures to asbestos. W.C. Hueper. 1965;132(1):184-95. PubMed · Publisher

Summary

This narrative review described the sources and types of occupational and nonoccupational exposure to asbestos and the groups of people exposed. It drew on published reports from many countries. The author cited an estimated 700 cases of asbestosis among about 8,000 asbestos industry employees in Germany in 1946, and 125 cases among 476 workers of one company in Finland. Among 132 workers examined by Bohme, 29 per cent had radiologic signs of asbestosis, rising from 5 per cent with less than three years' exposure to 79 per cent with over 10 years. A table compiled a total of 240 reported cases of lung carcinoma in people with asbestosis from several countries. World asbestos production was reported to have risen from 500 tons in 1880 to over 2,000,000 tons in 1958, with chrysotile making up about 95 per cent. The review covered exposures in ore mining and milling, asbestos cement production and use, textile manufacture and other products, as well as exposure of residents near plants and in homes. The author estimated that 50,000 to 100,000 people in the United States had contact with asbestos. He concluded that rising production had widened exposure, that reports of asbestosis and asbestos cancer came from a growing number of countries, that information on exposed workers and disease was fragmentary, especially in the United States and Canada, and that workmen's compensation laws in many places gave inadequate protection.

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Pleural plaques and asbestos: further observations on endemic and other nonoccupational asbestosis. R. Kiviluoto. 1965;132(1):235-9. PubMed · Publisher

Summary

The author reported further observations on pleural plaques in people in Finland who did not work with asbestos. Anthophyllite asbestos had been mined there since 1918. Several hundred cases of pleural calcification had earlier been found in non-miners near two open asbestos mines, termed 'endemic asbestosis'. Slight pulmonary fibrosis was visible on X-ray in about 14% of 150 such cases. Heart volume, measured on X-ray in 130 plaque cases, was 18% greater than in controls of similar age taken from the X-ray file. In 38 plaque cases and 23 controls, diffusing capacity was reduced in nine and two respectively, a difference that was not statistically significant. Mean vital capacity was 3600 versus 4000, which was significant. The author considered positive conclusions impossible. Of 216 histologically proven lung carcinomas in Northern Karelia in 1958-61, all in men, the cases were not more frequent around the mines. Twenty-one of them also had endemic asbestosis. One pleural mesothelioma, with lifelong environmental exposure, was recorded in 1959-62. Among 35,000 routine chest X-rays in 1963-64, 77 plaque cases were found, and 68 were questioned about exposure. Bricklayers had dyspnea and definite fibrosis. Cases without detectable dust exposure had slight or no lung changes. The author concluded that plaques develop slowly, and that even slight, brief exposure may cause pleural changes decades later. Plaques, though not pathognomonic, were judged useful for industrial hygiene and epidemiology.

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Preparation of asbestos fibers for experimental use. M.S. Badollet, W.A. Gantt. 1965;132(1):451-5. PubMed · Publisher
Present threshold limit value in the U.S.A. for asbestos dust: a critique. E.L. Schall. 1965;132(1):316-21. PubMed · Publisher

Summary

This paper critically examined the scientific basis of the United States threshold limit value for asbestos dust. That value was 5.0 million particles per cubic foot of air (mppcf) for an eight-hour day, 40-hour week, and was adopted by the American Conference of Governmental Industrial Hygienists and reaffirmed in April 1964. The author traced the value to the 1938 Public Health Service study by Dreessen and colleagues of workers in asbestos textile plants using chrysotile. That study found only three doubtful cases of pneumoconiosis below 5 mppcf. The author identified several limitations of the study. It considered only asbestosis and only American textile plants. Dust counts included all particles, such as cotton and rock dust, and did not separate asbestos fibers. Fibers made up 1 to 8 per cent of particles in most operations and 12 to 26 per cent in weaving. Average counts hid peaks as high as 211 mppcf. The workforce was young and short-term: 333 of 511 employees had worked less than five years, and only 66 more than ten years. The 76 "controls" were themselves exposed to dust. The author concluded that the 5 mppcf value could not be presumed to be a safe limit for asbestos in all applications. The author also noted that the original investigators had offered it only tentatively, "until better data are available."

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Problems and perspectives: the changing hazards of exposure to asbestos. J.C. Gilson. 1965;132(1):696-705. PubMed · Publisher
Pulmonary function in asbestosis: serial tests in a long-term prospective study. M.E. Bader, R.A. Bader, A.S. Tierstein, et al. 1965;132(1):391-405. PubMed · Publisher
Abstract

SUMMARY AND CONCLUSIONS
1. In 1954-1955, pulmonary physiological studies in 17 asbestos workers revealed the characteristic pattern of alveolar-capillary block syndrome. These patients were withdrawn from industrial exposure.
2. Of these 17 patients, 13 were available to follow-up study up to 10 years after the initial observation. Eight are now dead -one of cor pulmonale, two of carcinoma of the lung, two of carcinoma of the stomach, one of asbestosis, one of coronary occlusion, and one of mesothelioma. Of the living, six are working, one had surgery for carcinoma of the lung, one had a coronary occlusion and is unable to work.
3. Follow-up measurements were made in 13 patients. These included vital capacity, maximum breathing capacity, arterial oxygen saturation at rest and with exercise, and arterial pCO2 and pH.
4. During the period of the study, vital capacity was found to be reduced significantly in 12 of the 13 patients. There was also a fall in maximum breathing capacity, but in general they remained relatively well preserved. Air velocity indices showed an upward trend in more than half, and in only one was the air velocity index slightly less than one.
5. There was no significant trend in the arterial oxygen saturation at rest or on exercise. Arterial pCO2 and pH remained essentially unchanged.
6. The fall in vital capacity correlated well in about half of the cases with progression of X-ray findings and progression of dyspnea on exertion. In the remainder, vital capacity fell in almost all, without significant progression of radiological features or clinical symptoms.
7. The reduction in vital capacity correlated well with reduction in pulmonary compliance in 30 observations on 21 patients with asbestosis. This would indicate that the reduction in vital capacity is not a consequence of poor patient performance.
8. While diffusing capacity was not measured, the arterial O2 saturation on exercise did not demonstrate changes parallel to the fall in vital capacity observed.
9. It is concluded that of the parameters here studied, vital capacity was the most sensitive index of progression of the disease. Its ease of application, availability, and repeatability all recommend it for use in the frequent assessment of workers exposed to asbestos dust.
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Pulmonary neoplasia among Dresden asbestos workers. G. Jacob, M. Anspach. 1965;132(1):536-48. PubMed · Publisher

Abstract

Analysis of experiences among workers in the Dresden asbestos industry has been completed from 1952 to September 15, 1964. This progress report summarizes these observations with special reference to neoplasia observed among these workers. Lung cancer and neoplasms of the pleura are significantly increased among asbestos workers in the Dresden area when compared with the general population of this area of corresponding age and sex. Neoplasms of the lung and pleura were found to have increased both in relative incidence and in absolute numbers, with increasing duration of the latent period from first exposure. Thus, while an increased incidence of statistical significance was not observed in the period 1952-1957, a sharp increase was noted in lung cancer among men from 1958 to 1964, and in both lung cancers and pleural tumors among women from 1958 to 1964.

Right heart failure (cor pulmonale) is no longer the leading cause of death among Dresden asbestos workers, a position it held from 1952 to 1957. In the period 1958-1964, it has been replaced by neoplasms of the lung and pleura as the most common cause of death among these asbestos workers. Data are presented which indicate that the reduction in deaths due to cor pulmonale is a consequence of improved industrial hygiene measures. However, since the latent period from onset of exposure to death from cor pulmonale is considerably shorter (25.7 years) than the latent period of lung cancer associated with asbestos exposure (30.7 years), it is suggested that this has been a factor in the observed increased incidence of lung cancer. More asbestos workers are surviving long enough to reach the period in which the lung cancer rate is important.

Analysis of the lung cancer deaths has been undertaken and several features associated with asbestos lung cancers are documented. The remarkable increase of lung cancer among female asbestos workers is detailed, as is the preponderance of lower lobe localization of the observed tumors. The high incidence of pleural neoplasms is noteworthy. We observed six cases of pleural tumors, all in women. We have also observed one peritoneal tumor.

These observations are presented as a progress report and investigations continue. Among current studies are investigations of serosal neoplasms and an analysis of our data with reference to the “inverse association” proposed by Peller. These studies will be subsequently reported.

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Radiological and pathological correlations in asbestosis in the Republic of South Africa and the United Kingdom. I. A proposed radiological classification of asbestosis. G.K. Sluis-Cremer, C.P. Theron. 1965;132(1):373-8. PubMed · Publisher

Summary

The authors proposed a modification of the I.L.O. international classification of radiological opacities in pneumoconiosis for use in asbestosis. The linear opacity category was expanded into coarse (more than 1 mm wide) and fine markings, with extent graded by lung area. Calcified pleural plaques and pleural thickening were brought into the classification, with codes for their anatomical sites. Symbols were added for bronchial carcinoma, mesothelioma and cystic changes. The code was tested on four groups: 155 cases diagnosed radiologically in a population survey in the asbestos areas of the Cape and Transvaal; 120 cases certified by the Miners' Medical Bureau, Johannesburg; 50 post-mortem proven South African mining cases; and 64 post-mortem proven United Kingdom industrial cases. Single postero-anterior chest films were read by two or more readers. For the post-mortem cases, films were exchanged between the two countries, and disagreements were resolved by discussion. In the survey group, calcified plaques were seen in 82% of Cape cases (mainly crocidolite) and 76% of Transvaal cases (mainly amosite), and parenchymal changes in 40% and 84%. Certified cases showed a similar trend toward parenchymal changes in the Transvaal. In the UK cases, calcified plaques were found in 18% and parenchymal changes in 92%. The authors concluded that the code was workable, but that a standard set of films should be made available if it were widely used.

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Radiological and pathological correlations in asbestosis in the Republic of South Africa and the United Kingdom. II. A preliminary study of observer variation in the classification of radiographs of asbestos-exposed workers and the relation of pathology and x-ray appearances. A. Caplan, J.C. Gilson, K.F. Hinson, et al. 1965;132(1):379-86. PubMed · Publisher
Radiological classification of pulmonary asbestosis. H. Bohlig. 1965;132(1):338-50. PubMed · Publisher

Abstract

Every classification is imperfect, even more so regarding asbestosis. The classifications now in use are not quite identical, but they mainly divide the radiological appearances into three fluently changing stages, of which especially the second is illogically defined and not to be produced efficiently. Because of the national differentiation between the compensation rules only a mere radiological classification can be taken into consideration for international agreement. The fact of a conference taking place at all proves that new international agreements about a practicable classification for pulmonary asbestosis are necessary. If experts agree, that linear opacities are also disseminated shadows and that the radiological appearances of pneumoconioses can be either disseminated or squared opacities, it would seem appropriate to adopt these two kinds of appearances as a base for new classification. Doing so, considerable approximation to already existing classifications (Sydney, 1950 ; Geneva, 1958) would be gained as well. For intensifying the reproducibility of the X-ray film and, on the other hand, enlarging the distinctness of the codified X-ray findings, we suggest not to use the unalterable symbol “L” (Geneva, 1958), but to introduce another symbol “f” for linear patterns, chiefly occurring in asbestosis, and to combine it with the quantitative categories for small opacities. The large opacities might be characterized by the symbol “A” for beginning confluence and by “B” and “C” for opacities having a longer diameter than 5 cm. The additional symbols (Geneva, 1958) would be welcome for further accommodation of the findings code to individual, local or national peculiarities. Extensive reconstruction of the radiological appearances, even without the film in question, would be possible when adopting the symbol suggested. It is unimportant whether this proposition is adopted or not ; it is exceedingly important, that some international agreement should be attained, which would be really practicable.

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Relationship between exposure to asbestos and pleural malignancy in Belfast. P.C. Elmes, O.L. Wade. 1965;132(1):549-57. PubMed · Publisher

Abstract

A study of 43 cases in Belfast has revealed a relationship between exposure to asbestos at work and the development of mesothelial tumor of the pleura.

Evidence has been produced which indicates that the exposure associated with this tumor need not be severe or prolonged, and that as many as a quarter of the male population of this area may have received sufficient exposure.

Among asbestos workers carcinoma of the lung is at least as frequent a cause of death as mesothelioma but the increasing widespread use of asbestos may be exposing a wide section of the population to the risk of secondary neoplasia.

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Report and recommendations of the working group on asbestos and cancer; convened under the auspices of the Geographical Pathology Section of the International Union against Cancer. 1965;132(1):706-21. PubMed
Rheumatoid factor in serum of individuals exposed to asbestos. B. Pernis, E.C. Vigliani, I.J. Selikoff. 1965;132(1):112-20. PubMed · Publisher
Routine lung function studies on 830 employees in an asbestos processing factory. R. Hunt. 1965;132(1):406-20. PubMed · Publisher

Summary

This interim report described the use of routine lung function tests to screen prospective employees and to assess workers exposed to chrysotile asbestos dust in an asbestos textile factory in the north of England. Testing began in 1960. The aims were to see whether asbestosis could be detected by lung dysfunction before X-ray or clinical changes appeared, whether X-ray evidence correlated with impaired function, and whether the tests could screen new employees. Normal values were derived from 260 males and 120 females not exposed to asbestos. The tests included gas transfer factor (10-second breath-holding), vital capacity, residual volume, functional residual capacity, timed vital capacity and other measures. By May 1964, 450 exposed men had been examined. Of these, 340 showed little or no departure from expected normal values. The other 110 showed a decreased gas transfer factor with falls in other measures, and 36 of them had a gas transfer factor below 60 per cent of predicted. Sixteen men and two women whose X-rays had been considered negative, but whose tests since 1960-61 had suggested interstitial fibrosis, were later diagnosed with asbestosis. Five were certified by the Pneumoconiosis Panel, and four died from asbestosis with associated lung neoplasms. The author concluded that lung function studies can detect asbestosis before it appears on X-ray and are valuable for pre-employment screening and for monitoring exposed workers.

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Secular changes in asbestosis in an asbestos factory. W.J. Smither. 1965;132(1):166-81. PubMed · Publisher

Summary

The author examined how asbestosis had changed over about 30 years in a single London East End factory that had made asbestos products since 1913. He compared earlier published series from this factory (Hunter, 1930-34; Wyers, 1949; Williams and Hugh-Jones, 1958-59; Thomson et al.) with 26 new cases certified since 1960. He also compared 71 post-mortem examinations since 1957, 51 attended by the writer, with Wyers' 115 post-mortem cases. Mean exposure before certification rose from 7 years (Hunter) to 10.4, then 14.5, and 17.5 years in the present series (range 4-35), although many present cases were found early through lung function testing. Breathlessness was reported by 69 per cent of new cases, against nearly all earlier cases. Mean DLCO was 19.3, against 13.9 in the Thomson series. Among deaths, mean age rose from 40.8 to 56.5 years and mean duration of disease from 6.4 to 7.25 years. Tuberculosis at death fell from 31.3 per cent to four cases, all with old healed lesions. Lung carcinoma rose from 14.8 to 36.6 per cent, and there were two pleural mesotheliomas or endotheliomas (2.8 per cent). Smoking habits were not recorded, so the author stated that the link between these cancers and asbestos could not be indicated. He concluded that better working conditions had lengthened exposure before certification despite earlier case finding.

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Some observations of the dust content and composition in lungs with asbestosis, made during work on coal miners pneumoconiosis. G. Nagelschmidt. 1965;132(1):64-76. PubMed · Publisher
Statistical tables--asbestos. T.C. May. 1965;132(1):745-65. PubMed
Studies of carcinogenesis of asbestos fibers and their natural oils. J.S. Harington, F.J. Roe. 1965;132(1):439-50. PubMed · Publisher
Tests for carcinogenicity of asbestos. W.E. Smith, L. Miller, R.E. Elsasser, et al. 1965;132(1):456-88. PubMed · Publisher

Summary

The authors tested whether asbestos causes tumors in animals. They used male golden Syrian hamsters, about two months old at the start, at the Health Research Institute, Fairleigh Dickinson University, New Jersey. Samples of harsh chrysotile, soft chrysotile and amosite were prepared to remove rock dust. In Experiment A, 60 hamsters were divided into four groups of 15. Three groups each received a single intrapleural injection of 25 mg of one sample plus one per cent asbestos in the diet: soft chrysotile for the two chrysotile groups and amosite for the amosite group. The fourth group was an untreated control. Animals lived out their natural lives unless sacrificed, and all were examined at necropsy. The injections produced granulomatous inflammation, necrosis, calcification and thick fibrous pleural adhesions. Pleural mesotheliomas were found at 244, 358 and 482 days after amosite and at 419 and 527 days after harsh chrysotile, but not after soft chrysotile. A sarcoma arose around a subcutaneous deposit of soft chrysotile. No tumors were found in the controls. Gastric ulcers, a lymphoma and a cholangiocarcinoma in asbestos-fed animals may have been spontaneous. In Experiments B and C, repeated weekly intratracheal injections produced lung lesions resembling asbestosis but, so far, no respiratory tumors, and many animals were still alive. The authors concluded that asbestos can induce mesotheliomas in hamsters. They questioned whether this reflects a primary carcinogenic action or a nonspecific effect of fibrosis.

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Tests for effect of asbestos on benzo[a]pyrene carcinogenesis in the respiratory tract. L. Miller, W.E. Smith, S.W. Berliner. 1965;132(1):489-500. PubMed · Publisher
The detection and localization of mineral fibers in tissue. C. Berkley, J. Churg, I.J. Selioff, et al. 1965;132(1):48-63. PubMed · Publisher
The discriminant value of pulmonary function tests in asbestosis. M.L. Thomson, A.M. Pelzer, W.J. Smither. 1965;132(1):421-36. PubMed · Publisher

Abstract

A clinical and pulmonary function field survey was made of 28 factory workers who had been exposed to asbestos dust for an average of 14 years. In certifying 19 of these as having asbestosis, the British Pneumoconiosis Board relied mainly on radiological abnormality and the presence of dyspnea and rales, in that order. Finger clubbing came next in importance and cyanosis, productive cough and wheeze were of relatively minor value.

The power of 11 pulmonary function indices to discriminate between the certified and uncertified workers, estimated by the U/Umax test, was greatest for inspiratory capacity (IC), vital capacity (VC), diffusing capacity for carbon monoxide (DCO) and compliance. These indices therefore supported the Board's selection. The discriminant value was lower in forced expiratory volume (FEV) and pulmonary capillary blood volume (Vc), and poor in membrane diffusing capacity (DM), airway conductance (AWC), peak flow rate (PFR), residual volume/total lung capacity (RV/TLC) and FEV/VC.

The influence of the reduced lung volume found in asbestosis on the more specialized tests has been considered, and an attempt made to determine whether they provide significant extra information.

The VC or IC alone correctly classified all but a few individuals. In some certified workers, however, these volumes were normal but the DCO and compliance were low.

Abnormality in the arterial blood oxygen saturation (by ear oximeter) was present in seven workers; it was usually, but not invariably, associated with a low DCO.

Severe obstructive defect was rare in these workers. The mean FEV/VC ratio was within 10 per cent of normal; this small reduction appeared to be due mainly to dynamic factors other than airway obstruction. This was borne out by the airway conductance (by body plethysmograph) and by the PFR, which on the average were better than might have been anticipated in view of the reduction in lung volume. The AWC was low in workers with wheeze and high in the remainder. Of the two simpler indices, PFR correlated more highly with conductance than FEV. Perhaps the main value of the AWC and, to a lesser extent, of the PFR was in excluding airway obstruction in a proportion of workers with asbestosis, and enabling greater precision in its diagnosis and evaluation.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.
The occurrence of asbestosis among insulation workers in the United States. I.J. Selikoff, J. Churg, E.C. Hammond. 1965;132(1):139-55. PubMed · Publisher

Abstract

An investigation involving 1522 asbestos insulation workers in the New York-New Jersey metropolitan area has been conducted. Among 392 individuals examined more than 20 years from onset of exposure, radiological evidence of asbestosis was found in 339. In half of these, the asbestosis was moderate or extensive. In individuals with less than 20 years of exposure, radiological evidence of asbestosis was less frequent and when present, much less likely to be extensive.

Neoplastic complications of asbestos exposure were studied among 307 consecutive deaths in this group of men. Lung cancer was found to be at least seven times as common as expected and cancer of the gastrointestinal tract three times as common as expected. There were 10 instances of mesothelioma of the pleura or peritoneum.

Of the 1258 men alive at the start of this survey, 1117 were examined. Eleven cancers of the lung or pleura were found during this survey of the living members, all among the 392 men with more than 20 years from onset of exposure. No cancers were found in those men, the onset of whose work experience was less than 20 years.

We may conclude that asbestosis and its complications are significant hazards among insulation workers in the United States at this time.

PubMed has no abstract for this study. This is the authors' abstract, copied from the article.
The occurrence of pleural calcification among asbestos insulation workers. I.J. Selikoff. 1965;132(1):351-67. PubMed · Publisher
Abstract
1. Roentgenographic study of 1,117 asbestos insulation workers showed pleural calcification to be a common finding. Altogether, 150 instances of such calcification were present.
2. Data is presented which demonstrates that pleural calcification among workmen exposed to asbestos in this trade rarely occurs in less than 20 years from onset of exposure. Pleural calcification was found in 5 of 725 asbestos insulation workers with less than 20 years from onset of exposure but in 145 of 392 men examined more than 20 years from beginning work with asbestos. Similarly, the extent of calcification also increased with duration of exposure.
3. Available data suggests that both total amount of exposure as well as lapsed time from onset of exposure are of importance. In this group of men, the earliest case seen was in a man examined 12 years from onset of exposure. Elsewhere, somewhat shorter periods from onset of exposure have been noted, but such cases are rare.
4. Approximately half the cases were bilateral. In unilateral cases, involvement of the left hemithorax predominated. Extensive calcification was usually bilateral.
5. Bilateral pleural calcification is almost pathognomonic of pleural disease associated with pneumoconiosis. Asbestos is by far the most common industrial dust involved and bilateral pleural calcification in the absence of evidence of traumatic or infectious pleural disease can usually be considered to be due to asbestos exposure.
6. In half the cases, the calcification found was unilateral. The appearance and location of such calcification is described and no portion of the pleura was found to be immune. The diagnostic importance of such unilateral calcification is stressed since even unilateral calcification is uncommon in the general population and when it occurs, a traumatic or infectious history can generally be obtained. When the calcification is idiopathic, it should strongly suggest asbestosis and the presence of unilateral pleural calcification is almost as strongly diagnostic of asbestosis as is bilateral calcification.
7. The pleural calcification is primarily found in the parietal pleura, more heavily in the lower portions of the chest. Data concerning correlations with pleural fibrosis and asbestotic parenchymal fibrosis is given. Pleural calcification not infrequently is present in the absence of visible pleural fibrosis and occasionally may be present in the absence of radiologically visible parenchymal fibrosis.
8. In addition to standard posteroanterior films, it has been found advantageous to use two additional simple techniques; a second posteroanterior film taken with a slightly more penetrating technique and the use of oblique projections.
9. At the present time, it is likely that asbestos exposure is the most common cause of pleural calcification. The finding of such calcification as described here generally indicates asbestos exposure more than 20 years before.
PubMed has no abstract for this study. This is the authors' abstract, copied from the article.
The physical and molecular structure of asbestos. R. Gaze. 1965;132(1):23-30. PubMed · Publisher

Summary

This article, by an author from The Cape Asbestos Company Limited, London, was written as an introduction to a monograph on the biological effects of asbestos. It described the physical and molecular structure of the commercially important asbestos minerals and highlighted features the author considered significant for biological and pathological study. The author defined asbestos as any mineral that breaks down into fibers when crushed or processed. Unlike man-made inorganic fibers, asbestos can go on subdividing into fibers almost to molecular dimensions. Chrysotile (white asbestos) accounted for over 90 per cent of world usage. Crocidolite (blue asbestos), amosite and anthophyllite were described as amphiboles, and tremolite and actinolite were mentioned as of little commercial interest. Tables gave typical chemical analyses and physical properties. Summarizing published electron-optical and structural studies, the author reported that chrysotile fibers are hollow tubes formed from rolled-up sheets, with the finest fibers normally 150 to 400 Å in diameter. The smallest amphibole fibers, usually 800 to 1000 Å, are solid. Fiber lengths ranged from 2 inches or more down to barely more than the diameter, and many fibers in asbestos dust were too small to be resolved by optical microscope. The author stated that this must be taken into account in assessing dust-counting methods. He also described the unpredictable behavior of fibers in air, including agglomeration into balls of fluff and the formation of "parachutes", and suggested research on their electrical and surface properties.

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.
The sequelae of exposure to asbestos dust. J.C. Wagner. 1965;132(1):691-5. PubMed · Publisher

Summary

This paper summarized the main points of a conference on the biological effects of asbestos, covering the inhalation, deposition and retention of asbestos dust and their consequences. The author stressed that the effects of different types of exposure should be distinguished, taking account of the mineral variety of asbestos and its contaminants. He reported that the presence of long fibers in small air spaces had now been explained, with emphasis on fiber diameter. The primary site of lodgment was described as the alveoli arising directly from the respiratory bronchioles. In experimental animals, the amount of chrysotile retained clearly differed from that of amosite and crocidolite at equal doses. Asbestos bodies and fibers in sputum were described as evidence of exposure, not of asbestosis, and the author called for agreed identification methods in post-mortem prevalence surveys. Asbestosis was described as a slow, insidiously progressive fibrosis that begins as a focal lesion at the respiratory bronchioles. Four theories of how the disease develops were reviewed, and the author preferred the stagnation of phagocytes theory. Lung carcinoma was described as strongly supported as occurring in cases with significant asbestosis. Mesotheliomas, at first linked to crocidolite, had also been reported with chrysotile and possibly anthophyllite. Gastrointestinal tumors and preliminary animal tumor experiments were noted. The author called for standard reference dusts, comparative surveys in asbestos-producing areas, and coordinated international 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.
Trends in the health of the asbestos worker. K.W. Smith. 1965;132(1):685-90. PubMed · Publisher

Summary

In this conference paper, the author, from the Johns-Manville Corporation, commented on the health of asbestos workers and on how asbestos-related disease had been reported. He argued that the term "asbestos worker" was used too loosely. Insulation union members might have applied amosite, chrysotile, cristobalite-containing diatomaceous earth or glass fibre, and asbestos-cement products typically contained 50 per cent cement, 25 per cent quartz silica and 25 per cent asbestos. He called for surveys to record the fibre types and other dusts involved. He described calcified pleural plaques in four of seven Thetford mines in Quebec. He reported none in over 100,000 chest films at the company's Jeffrey Mine at Asbestos, and plaques in only one of four US plants using that chrysotile. He suggested that plaques might have causes other than chrysotile alone. Company tests of brake-lining dust from test vehicles after 5,000, 10,000 and 15,000 miles identified no chrysotile fibres, and he questioned whether asbestos bodies in lung juice were always due to asbestos. He pointed to coal tar products in the brake lining industry and to air pollution in a New Jersey city as other possible causes of cancer. Citing Knox, he noted that lung cancer in English asbestos workers had fallen from 15 times the expected rate 30 years earlier to the expected level, which he attributed to dust control. He urged support for a nationwide US Public Health Service study.

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.

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