SEARCH · PubMed Health

Results for “ASBESTOS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources

PubMed1990

Asbestos-related benign disease and cancer: symptoms and treatment.

Long lasting occupational exposure to asbestos dust may cause skin corns, benign pleural effusion, hyaline plaques of the parietal pleura, diffuse thickening of the pulmonary pleura, and asbestosis, i.e. diffuse interstitial pulmonary fibrosis. Malignant disorders include lung cancer and mesothelioma of the pleura, peritoneum and pericardium. In general, many years elapse from first exposure to the appearance of symptoms. Almost all these diseases are the result of dusty working conditions more than 20 years ago. In spite of the fact that the general public is invariably exposed to small amounts of the material, asbestos is not a public health problem. Even living in a building containing sprayed asbestos is calculated to produce a lifetime risk of death which is negligible. There is no evidence to indicate that ingested asbestos fibres represent a major health problem.

Aged↗

PubMed1992

Biomarker assessments in asbestos-exposed workers as indicators for selective prevention of mesothelioma or bronchogenic carcinoma: rationale and practical implementations.

In the first part of this study we have shown how the serum levels of four selected tumour markers, namely tissue polypeptide antigen (TPA), carcino-embryonic antigen (CEA), hyaluronic acid (HA) and ferritin, display patterns characteristic of mesothelioma (M) or bronchogenic carcinoma (BC) in asbestos-exposed workers, and we hypothesize that the differences in marker patterns correspond to differences in carcinogenesis mechanisms. In a preliminary study, we found these specific marker patterns in 5/19 exposed workers of whom only one demonstrated any radiological signs of disease. Thus these specific marker patterns may be early events, occurring long (possibly years) before the classical radiological signs of exposure to asbestos. Accordingly they afford an optimal opportunity for prevention which should be adapted to the carcinogenesis mechanism as it is revealed by the marker pattern; it is aimed at antagonizing free radical carcinogenesis in all persons with TPA levels in excess of 100 U/l or Ferritin in excess of 400 ng/ml, and at inhibiting chemical carcinogenesis in those having elevated CEA levels (over 3 ng/ml). The mechanisms involved in these inhibitory processes are described and discussed, as well as the practical implementations that proceed from them. A prevention trial is now being started among 300 active and retired workers of an asbestos-cement works in northern France; the design of the study is presented. This prevention programme should be maintained over many years and holds a strong potential for reducing the untoward effects of exposure to asbestos.

Acetylcysteine↗

PubMed1990

Epidemiological evidence indicates asbestos causes laryngeal cancer.

A variety of opinions have been expressed in the literature concerning asbestos and laryngeal cancer. This paper presents an analysis of epidemiological studies based on criteria that prioritized the most heavily exposed cohorts. Emphasis was given to the six cohorts or subcohorts with lung cancer relative risk estimates of 2 or more. The two groups of workers with the highest lung cancer relative risk estimates (4.06 and 3.28) both gave strong support for a causal association of asbestos and laryngeal cancer, with relative risk estimates of 1.91 (90% confidence limits 1.00 to 3.34) and 3.75 (90% confidence limits 1.01 to 9.68), respectively. Confounding with cigarette smoking or alcohol consumption does not explain the findings. Case-control studies gave mixed results, but generally supported the hypothesis. It was concluded that asbestos is a probable cause of laryngeal cancer in view of the reasonable consistency of the studies, the strength of the association in key studies, the evidence for dose-response relationships, and the biological plausibility for asbestos being a cause of laryngeal cancer.

Alcoholic Beverages↗

PubMed2000

Circulating natural killer cells in retired asbestos cement workers.

The effect of past exposure to asbestos on natural killer (NK) cell number and activity is uncertain. We measured NK cell number and activity in 1052 retired asbestos workers without symptomatic lung disease, lung cancer, or mesothelioma and with a long latency period from exposure; results were compared with those for 100 healthy age-matched controls. The exposed workers showed a decreased NK cell activity and increased NK cell number, yielding a 10.8 higher odds ratio for low NK activity per cell compared with controls (95% confidence interval 6.4 to 18.4), which was due to both a decrease in NK cell activity and an increase in NK cell number. Asbestos exposure of 10 years or more increased the risk of low NK activity per cell. We conclude that exposure to asbestos is associated with diminished effectiveness of NK cells and a concomitant increase in the number of NK circulating cells.

Aged↗

PubMed2002

Exposure to asbestos and lung and pleural cancer mortality among pulp and paper industry workers.

We studied the mortality from lung and pleural cancers in a cohort of 62,937 male workers employed for at least 1 year in the pulp and paper industry in 13 countries during 1945 to 1996. Mill departments were classified according to probability and level of exposure to asbestos on the basis of available dust measurements and mill-specific information on exposure circumstances. Thirty-six percent of workers were classified as ever exposed to asbestos. Standardized mortality ratios of lung cancer were 0.99 (95% confidence interval [CI], 0.90 to 1.08) among unexposed and 1.00 (95% CI, 0.90 to 1.11) among ever exposed workers. The number of pleural cancer deaths among unexposed workers was 10; that among exposed workers was 14, most of which occurred among maintenance workers. In internal analyses, a trend in mortality from either neoplasm was suggested for estimated cumulative exposure to asbestos, weighted for the individual probability of exposure within the department and for duration of exposure (relative risk for lung cancer for 0.78+ f/cc-years, as compared with < or = 0.01 f/cc-years: 1.44; 95% CI, 0.85 to 2.45; corresponding relative risk for pleural cancer: 2.43; 95% CI, 0.43 to 13.63). Despite a possible nondifferential misclassification of exposure and outcome, this study suggests that the carcinogenic effect of asbestos can be detected among workers employed in industries such as the pulp and paper industry, in which it is not considered to be a major hazard.

Air Pollutants, Occupational↗

PubMed2004

Asbestos exposure, manganese superoxide dismutase (MnSOD) genotype, and lung cancer risk.

To assess whether differences in genetic susceptibility to oxidative stress modify asbestos-related lung cancer risk (caused by lung inflammation, free radical production), we examined possible interactions between manganese superoxide dismutase (MnSOD) genotypes and asbestos in a hospital-based case-control study of 811 white lung cancer cases and 957 friend/spouse controls. Cumulative lifetime asbestos exposure score (AES) was calculated from self-reported duration and intensity of occupational and nonoccupational exposures. A total of 13.5% of cases and 10% of controls had "high" AES (determined by a priori cut point). The homozygous variant MnSOD genotype was associated with increased lung cancer risk among individuals with zero or "low" AES (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.52-3.01) and no association (OR = 1.00; 95% CI = 0.36-2.73) among the "high" AES group. We observed no statistically significant interaction between MnSOD genotype and asbestos exposure for lung cancer risk.

Adolescent↗

PubMed2004

The asbestos case: a comment on the appointment and use of nonpartisan experts in world trade organization dispute resolution involving health risk.

The World Trade Organization is currently evolving its approach to incorporating scientific and technological evidence into its dispute-resolution process. In European Communities-Measures Affecting Asbestos and Asbestos-Containing Products, the Panel was faced with a large amount of complex and conflicting scientific evidence presented by the partisan experts. The Asbestos Panel's solution was to appoint independent, nonpartisan experts to help it understand and evaluate the scientific evidence. While this was far better than trying to unravel the conflicting scientific evidence on its own, two aspects of the Panel's adopted procedure merit scrutiny. First, the expert-selection process used by the Panel may not assure that the collective expertise of the appointed experts is broad enough when the dispute involves multidisciplinary scientific issues. Second, the process adopted by the Panel for consulting the appointed experts-which involved individual consultation rather than a consensus process-may leave a panel with a distorted or confused picture of the science. A consensus approach is the best means of obtaining scientific advice from appointed experts; it is most calculated to provide a clear and accurate report of the scientific information needed by a panel to make a fair and informed decision on the dispute before it. The underlying principle of world trade agreements is that it is beneficial to all of us to have free trade. Among other things, this requires an effective means of resolving disputes, and increasingly that includes disputes involving complex scientific and technological issues. This can be achieved only if the parties have confidence that their disputes will be decided in a fair and informed manner, based on the best science available. To achieve this goal, we suggest that future WTO panels depart in certain respects from the procedures utilized by the Asbestos Panel.

Asbestos↗

PubMedDate not supplied

Malignant peritoneal mesothelioma in a 76-year-old woman with a history of asbestos fiber ingestion.

We report on a woman with malignant mesothelioma of the peritoneum. This is the first report of a subject with this disease who revealed a history of asbestos ingestion by asbestos-contaminated food. She presented with episodes of sweating and fever, ascites, and weight loss. At laparotomy, small tumor deposits were noted on the peritoneum. The omental cake was removed, together with the uterus, ovaries, and tubes which were all macroscopically normal. The diagnosis was established by immunohistochemistry and electron microscopy. Postoperatively, her complaints of fever and sweating disappeared. She refused further chemotherapy. After questioning her for asbestos exposure, she told us that, years ago, she used to prepare vegetables for cooking in rain water collected from a roof made of asbestos.

Aged↗

PubMed2006

Asbestos-related disease from recycled hessian superphosphate bags in rural Western Australia.

OBJECTIVES: To describe the dissemination of asbestos fibres within the Western Australian community. METHODS: A case report. RESULTS: A 60-year-old female was referred for investigation of calcified pleural plaques. On questioning, she recalled exposure to asbestos as a child on the family farm. She had shaken hessian bags prior to recycling to the fertiliser supplier. Her father survived to 90 years. Her mother died from malignant pleural mesothelioma. Four of five siblings had shaken the bags, two had radiographic evidence of pleural plaques while two others had not had recent chest x-rays. CONCLUSIONS: It appears that the use of recycled hessian bags for the fertiliser industry was endemic in the State during the period 1943-66. It is possible that many farmers and their families have had similar exposure to asbestos. IMPLICATIONS: The risk of developing an asbestos-related disease is not restricted to any specific social or employment groups within the Australian community.

Asbestos↗

PubMed1990

Interpretation of airborne asbestos measurements.

Transmission electron microscopy (TEM) is the preferred method of measuring airborne asbestos in buildings, but TEM measurements cannot be used directly in the existing equations relating risk to exposure because the equations are based on measurements made with a different technique--phase contrast microscopy (PCM). Comparison between measurements made by different methods is not simple because the methods differ in the size of particles they can detect, and the relationship between exposure and disease is thought to depend on, among other things, asbestos fiber size. Previous suggestions for converting TEM measurements to PCM equivalents lack generality because they fail to take into account the size distribution of the asbestos particles and the expectation that fiber-size distributions in current nonoccupational environments could differ from the workplaces of the past on which the risk equations are based. A mathematical model is presented for investigating the conversion of airborne asbestos measurements made by one method to an equivalent measurement made by another method. "Equivalent" means having the same potential to cause disease. The model clarifies the issues of concern and suggests approaches for obtaining meaningful conversion factors that will allow TEM measurements to be used in PCM-based risk equations.

Air Pollutants↗

PubMed2001

Chrysotile asbestos fibers mediate transformation of Escherichia coli by exogenous plasmid DNA.

The ability of chrysotile asbestos fibers to introduce the exogenous plasmid pUC18 into Escherichia coli JM109 cells was tested. Cells were transformed with pUC18 DNA although the frequency of transformation was quite low: 759+/-301 transformants were obtained per microgram of pUC18. Plasmids were purified from E. coli which had been transformed by mediation with chrysotile asbestos. Following this, the plasmids were confirmed to be pUC18 by Southern hybridization. This asbestos-mediated transformation was optimal within 5 min when 10 mg ml(-1) of asbestos was used. Plasmids up to 7.69 kb were introduced by this method.

Asbestos, Serpentine↗

PubMed1991

Asbestos-associated pleural mesothelioma in school teachers: a discussion of four cases.

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.

Adult↗

PubMed1984

Malignant mesothelioma: incidence, asbestos exposure, and reclassification of histopathology.

The Los Angeles County Cancer Surveillance Program abstracts records on almost all cases of cancer occurring in the county. In a study of those cases of pleural and peritoneal malignant mesothelioma (MM) that occurred from 1972 to 1979 occupational histories were obtained during interviews, and histopathology of the tumours was reviewed and classified by a member of a mesothelioma reference panel who was unaware of the exposure histories. About half the cases reviewed had likely exposure to asbestos at work. The greatest proportion of cases designated as MM by the pathologist occurred among individuals likely to have had the heaviest exposure of asbestos (42%). No upward trend of incidence over time was apparent among cases designated as MM. The age adjusted incidence rates for designated MM were lower than in other studies. The well recognised interobserver variability in diagnosing MM apparently produces raised estimates of incidence and an overestimate of trends of incidence. The interobserver variability may result from different awareness of MM occurrence, a lack of precise histopathological criteria for the diagnosis, or the influence of a history of exposure to asbestos on the interpretation. A history of exposure to asbestos may bias interpretation of histopathology and should not be used to make the histological diagnosis.

Asbestos↗

PubMed1985

Relations between asbestos exposure and lung cancer SMRs in occupational cohort studies.

It has long been accepted that excessive exposure to asbestos may produce lung cancer but not that there is a consistent "biological gradient." This can only be evaluated reliably in studies where, for every individual, exposure has been measured in terms of both duration and intensity. Even now, there are only at most eight such cohort studies of asbestos workers, while femoral methods of analysis have been available only recently. These methods, applied in these studies, yield good evidence that the "exposure-response" relation between accumulated exposure to asbestos and standardised mortality ratios (SMRs) for lung cancer may be taken as linear, but that at zero exposure the lung cancer SMR is not always unity--not surprising, because of well known difficulties with the choice of reference population and selection problems. This leads to a concept of "relative slopes" that take account of the background mortality in the cohort and make what appears to be the best use of the available data. Other approaches to the same data, and indeed to all cohort data known, are also considered. Each study is examined as closely as is possible in a short review, and the concepts of linearity and relative slopes appear justified. The relative slopes (b/a) in the line SMR = a[1 + (b/a) . (exposure)] vary much more widely than can be accounted for by differences in epidemiological methodology; as discussed elsewhere, reasons for the variation seem to lie rather in type and dimensions of asbestos fibre, industrial process, etc. Slopes in the line SMR = 1 + b1 . (exposure) vary about twice as much as do the relative slopes.

Asbestos↗

PubMed1985

Modified nucleosides in asbestos workers at high risk of malignant disease: results of a preliminary study applying discriminant analysis.

Patients with asbestos related malignant mesothelioma excrete high levels of modified nucleosides in their urine. The purpose of the present report was to explore further the usefulness of measuring these breakdown products of transfer RNA (tRNA) in male asbestos insulation workers who are at high neoplastic risk but without clinical signs of malignancy. Modified nucleoside levels (psi, m'A, m'I, m2G, and ac4C) were used as discriminator variables in a computer generated discriminant function in which 96% of the controls and 95% of the insulation workers were correctly classified. It was also found, using a similar multiple regression model, that 10 of 13 were correctly classified as having normal chest radiographs and 27 of 30 asbestos exposed subjects as exhibiting alterations in either the parenchyma, pleura, or both. The results suggest that measuring modified nucleosides levels in the urine of asbestos exposed workers, and perhaps others exposed to carcinogenic agents, has the potential for identifying, through multivariate statistical techniques, individuals who are at high neoplastic risk.

Adult↗

PubMed1987

Development, radiological zone patterns, and importance of diffuse pleural thickening in relation to occupational exposure to asbestos.

The radiographic appearance of the lateral pleura was divided into an upper, a middle, and a lower zone. Bilateral changes of the pulmonary layer of the pleura (diffuse pleural thickening) within the upper pleural zones were found in 863 (71%) of 1204 workers exposed to asbestos and in 249 (40%) of 622 non-exposed controls. Downwards along the chest wall this ratio of 7:4 increased progressively up to 10:1 at the lower parts of the pleura. Bilateral diffuse pleural thickening in at least two adjacent zones on each side was found in 652 (54%) of exposed and in only 86 (14%) of unexposed subjects. The difference was even more striking when comparing bilateral involvement of all three zones (28% and 3% respectively). Unilateral change was rare (4.8% and 7.8% respectively) and often due to causes other than exposure to asbestos. Pleural findings were the earliest radiographic features detectable associated with former exposure to asbestos. Bilateral diffuse thickening in at least two adjacent zones on each side seems to be a striking feature and an early indication of former occupational asbestos damage. Modifications of the International Labour Organisation 1980 classification are proposed.

Adolescent↗

PubMed1987

Possibility of inducing glandular stomach cancer in rats exposed to asbestos.

The possibility of glandular stomach cancer being induced was studied in 75 random bred white rats exposed to chrysotile asbestos. A perforated polyethylene capsule containing 100 mg asbestos and filler (beef fat and natural wax mixture 1:1) was introduced in an artificial bag placed on the greater curvature of the stomach. A capsule containing filler only was introduced in a similar way in 40 control rats. In the following 25 months, 18 tumors of the stomach and abdominal cavity were found in the rats treated with asbestos (eight adenomas, two adenocarcinomas, one carcinosarcoma, one forestomach cancer, one intestinal adenocarcinoma, two peritoneal mesotheliomas, and three abdominal lymphoreticulosarcomas.) Among the control rats no such tumors were found. The results of the experiment are discussed in connection with epidemiological data on stomach cancer in asbestos workers.

Abdominal Neoplasms↗

PubMed1987

Mortality of workers employed in two asbestos cement manufacturing plants.

In a study of the mortality experience of 6931 employees of two New Orleans asbestos cement products manufacturing plants over 95% were traced. Chrysotile was the primary fibre used in both plants. Plant 1 also used small amounts of amosite and, later, crocidolite irregularly whereas plant 2 used crocidolite steadily in pipe production. Previously reported exposure concentration estimates were revised, based on additional air sampling data and re-evaluation of these data. Workers in the two plants had similar duration of employment (overall, a mean of 3.8 years) and estimated exposure concentration (a mean of 7.6 million particles per cubic foot (mppcf)). Mortality was similar for these plants and comparable with Louisiana rates for all causes combined, nonmalignant causes, and primary cancers of specified sites other than lung. Short term workers from both plants showed raised and similar risk of lung cancer, but risk among longer term workers differed--for example, for workers employed over one year there was no excess in plant 1 (16 observed, 17.2 expected) but a significant excess in plant 2 (52 observed, 28.9 expected, p less than 0.001). After excluding short term workers, risk of lung cancer in plant 2 showed a significant trend with estimated cumulative asbestos exposure; using a conversion of 1.4 fibres/ml = 1 mppcf, the slope of the line was 0.0076. The slope for plant 1 was 0.0003. Among all workers (the 6931, plus 167 early employees) ten mesotheliomas had occurred up to 1984: two from plant 1, eight from plant 2. In plant 2 a case-control analysis found a relation between risk of mesothelioma and duration of employment (p less than 0.01) and proportion of time spent in the pipe area (p less than 0.01), thus adding to the evidence of a greater risk of mesothelioma from crocidolite than chrysotile asbestos. A review of the mortality findings of eight cohorts of asbestos cement workers is presented.

Adult↗