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PubMed1987

[Effects of smoking on asbestos-related pulmonary and pleural changes].

A radiologic study was made on 184 male asbestos workers in order to determine the effects of smoking on asbestos-related pulmonary and pleural changes. The effects of smoking on the prevalence of pleural changes could not be demonstrated, but the prevalence of pulmonary changes significantly increased with length of smoking history (p less than 0.01). It was found that smoking elevated the prevalence of asbestos-related pulmonary changes. These findings are of great importance in the health management of asbestos workers.

Asbestos↗

PubMed1993

[Study on the relationship between appearance of autoantibodies and chest X-ray findings of asbestos plant employees].

Antinuclear factor (ANA) and rheumatoid factor (RF) were determined in 220 employees of an asbestos plant. The relationship of the appearance of the two factors to sex, age, smoking habit, duration of asbestos exposure and asbestos exposure level was studied. In 207 employees who had chest roentgenograms, the relationship of these two factors to pulmonary lesions and pleural lesions was examined. Of the 220 employees, 33 (15%) had ANA and 7 employees (3.2%) had RF. ANA positive rate in the asbestos plant employees was significantly higher than in the control. Factors significantly correlated to their appearance could not be demonstrated. With the progress of pulmonary lesions the ANA positive rate significantly elevated, but ANA positive rate was not significantly correlated with pleural lesions. RF did not show any significant correlation with any of the factors.

Adult↗

PubMed2003

Identification of rounded atelectasis in workers exposed to asbestos by contrast helical computed tomography.

Rounded atelectasis (RA) is a benign and unusual form of subpleural lung collapse that has been described mostly in asbestos-exposed workers. This form of atelectasis manifests as a lung nodule and can be confused with bronchogenic carcinoma upon conventional radiologic examination. The objective of the present study was to evaluate the variation in contrast uptake in computed tomography for the identification of asbestos-related RA in Brazil. Between January 1998 and December 2000, high-resolution computed tomography (HRCT) was performed in 1658 asbestos-exposed workers. The diagnosis was made in nine patients based on a history of prior asbestos exposure, the presence of characteristic (HRCT) findings and lesions unchanged in size over 2 years or more. In three of them the diagnosis was confirmed during surgery. The dynamic contrast enhancement study was modified to evaluate nodules and pulmonary masses. All nine patients with RA received iodide contrast according to weight. The average enhancement after iodide contrast was infused, reported as Hounsfield units (HU), increased from 62.5+/-9.7 to 125.4+/-20.7 (P < 0.05), with a mean enhancement of 62.5+/-19.7 (range 40 to 89) and with a uniform dense opacification. In conclusion, in this study all patients with RA showed contrast enhancement with uniform dense opacification. The main clinical implication of this finding is that this procedure does not permit differentiation between RA and malignant pulmonary neoplasm.

Asbestos↗

PubMed1981

Asbestos and cancer in the Sennan District of Osaka.

The cancer incidence among asbestos workers in the Sennan District and its surrounding of Osaka Prefecture, Japan, and the results of a mass survey in the above area since 1957 were evaluated from view points of epidemiology. During the period from 1953 to 1979, 107 patients with asbestosis were admitted to this Hospital. Twenty-six (24%) of them died of various carcinoma; 21 had lung cancer, 2 pleural mesothelioma and 3 had stomach cancer. Respiratory insufficiency due to pulmonary asbestosis was responsible for 41 deaths (38%). by a cohort survey of the 297 asbestos workers in the same district, 4 cases of lung cancer, and 3 cases of gastric cancer were detected and cases of cohort survey were followed up for 19 years. Fifty-seven (10%) of 556 cases of silicosis and 14 (11%) of 125 cases of pneumoconiosis other than silicosis or asbestosis were found to have lung cancer, but no mesothelioma. These results indicate that lung cancer and mesothelioma are associated more frequently with asbestosis than with non-asbestos pneumoconiosis (p less than 0.001 as tested by chi2-test). The standardized mortality ratio of lung and stomach cancer among the inhabitants of the Sennan District was calculated based on the statistics during the period of 10 years (1968-1977). the ratio of observed death to expected death of both cancers was smaller than 1.1, and there was no significant increase of death of lung and stomach cancer, although the risk of lung cancer tended to increase among male inhabitants. Discussions were made on the problems related to asbestos industry.

Adult↗

PubMed1999

A clinicopathological study of lung cancer patients with occupational exposure to chrysotile asbestos fibers.

OBJECTIVE: To summarize the features of asbestos-related lung cancer. PATIENTS: Thirty-one lung cancer patients with occupational exposure to chrysotile asbestos fibers. They worked or had worked in one asbestos factory or its subcontracters. RESULT: All patients were male with mean age of 60.6 when diagnosed, and all except one were current or ex-'heavy' smokers. Histological types were fairly evenly divided into adeno-, squamous and small cell carcinoma and 24 (78%) of patients showed 'peripheral type' lung cancers. Regarding clinical stages, 20 patients (65%) were classified as III or IV (advanced stage). Tumor shadow(s) was detected on chest X-ray in 22 patients (71%), and in 5 patients with 'negative' chest X-ray, chest CT was necessary to recognize a primary tumor. Seventeen patients (55%) did not undergo periodical check-ups. CONCLUSION: Occupational asbestos exposure is interpreted as one of the important risks for lung cancer and frequent and accurate observation is necessary.

Adult↗

PubMedDate not supplied

Pleural mesothelioma after neighborhood exposure to asbestos during childhood.

A 38-year-old woman with pleural mesothelioma who had a history of neighborhood asbestos exposure during her childhood was demonstrated. She had no known history of occupational asbestos exposure. This is the first case of mesothelioma with neighborhood asbestos exposure reported in Japan. Previously-reported cases of mesothelioma with neighborhood asbestos exposure in the English language literature were reviewed.

Adult↗

PubMed1988

Asbestos-related pleural disease and asbestosis: a comparison of CT and chest radiography.

High-resolution CT (HRCT) has the ability to demonstrate both asbestos-related pleural disease and parenchymal abnormalities consistent with asbestosis. The role of CT in the diagnosis of asbestosis can be defined by comparing it with radiography. We evaluated 60 men who had a history of occupational exposure to asbestos and whose outside chest radiographs were considered abnormal. Chest radiographs (inside films) and HRCT were performed in all patients at our institution and were interpreted independently by experienced radiologists. Outside film results were compiled from the submitted reports. The final conclusion regarding the interpretation of the radiologic examinations was determined by consensus when disagreements existed. Positive predictive values (the likelihood that a positive report is correct) for pleural disease were: outside films 56%, inside films 79%, HRCT 100%. The positive predictive values for parenchymal disease were: outside films 51%, inside films 83%, HRCT 100%. The addition of HRCT to chest radiography is most useful in eliminating false-positive diagnoses of asbestos-related pleural disease caused by subpleural fat and false-positive diagnoses of parenchymal asbestosis in patients with extensive plaques or emphysema obscuring lung detail. The interpretation of chest radiographs in patients exposed to asbestos is often extremely difficult and subjective, and we recommend that positive findings (except calcified plaques) be confirmed with HRCT.

Asbestos↗

PubMed1999

A historical cohort mortality study of workers exposed to asbestos in a refitting shipyard.

To investigate the risks of developing asbestos-related diseases we conducted a historical cohort mortality study on 249 ship repair workers (90 laggers and 159 boiler repairers) in a single U.S. Navy shipyard in Japan. We successfully identified the vital status of 87 (96.7%) laggers and 150 (94.3%) boiler repairers, and, of these, 49 (56.3%) and 65 (43.3%) died, respectively, during the follow-up period from 1947 till the end of 1996. Our in-person interviews with some of the subjects clarified that asbestos exposure was considered to be substantially high in the 1950-60s, decreased thereafter gradually but remained till 1979 in the shipyard. The laggers, who had handled asbestos materials directly, showed a significantly elevated SMR of 2.75 (95% C.I.: 1.08-6.48) for lung cancer. The risk developing the disease was greater in the laggers after a 20-year latency (SMR = 3.42). Pancreatic cancer yielded a greater SMR than unity (7.78, 90% C.I.: 2.07-25.19) in a longer working years group. Four laggers died from asbestosis. The boiler repairers, who had many chances for secondary exposure to asbestos and a few for direct exposure, showed no elevation of the SMR of lung cancer overall, but there was a borderline statistically significant SMR of 2.41 (90% C.I.: 1.05-5.45) in a longer working years group. One boiler repairer died from mesothelioma and four from asbestosis.

Adult↗

PubMed2002

Assessment of the mutations of p53 suppressor gene and Ha- and Ki-ras oncogenes in malignant mesothelioma in relation to asbestos exposure: a study of 12 American patients.

In our previous study, we found no genetic alteration in exons 1 and 2 of Ha- and Ki-ras oncogenes nor in exons 5 to 9 of the p53 suppressor gene in seven Japanese malignant mesothelioma patients exposed to asbestos. To examine further whether malignant mesothelioma due to asbestos has genetic alterations in the p53 suppressor gene and in Ha- and Ki-ras oncogenes, we analyzed point mutations of these genes in paraffin embedded operative open biopsied samples of the primary tumor of malignant mesothelioma in twelve American patients. The genetic analysis was conducted by the PCR-SSCP (polymerase chain reaction single-strand conformation polymorphism) method in all patients and by sequencing analysis of DNA bases in the two patients with suspected gene mutation. The analysis of the p53 suppressor gene showed an amino acid converting mutation of exon 7 in one patient and a polymorphism of exon 6 in another patient; the former patient was a heavy smoker with a biphasic cell type. No genetic alteration was found in exons 1 and 2 of Ha- and Ki-ras oncogenes in any of the patients. The results suggest that the effects of asbestos on the p53 suppressor gene and Ha- and Ki-ras oncogenes in malignant mesothelioma are negligible. Further studies are needed to examine whether the observed mutation of the p53 suppressor gene is due to the combined effects of asbestos and smoking or to other unknown factors.

Aged↗

PubMed1987

Asbestos-induced fibrosis in rats: increase in lung mast cells and autacoid contents.

Adult male Wistar rats were treated with one tracheal instillation of 5 or 10 mg chrysotile B asbestos fibers in 0.5 ml saline, or 0.5 ml saline only (controls). Rats were killed at 1, 3, and 6 months postinstillation. Serotonin and histamine were quantitated in lung tissue homogenate using high-performance liquid chromatography with electrochemical and fluorometric detection, respectively. Serotonin was also quantitated in the cytoplasm of grouped (NEB) and individual (NEC) neuroendocrine cells and in mast cells using formaldehyde vapor-induced fluorescence and microspectrofluorometry, and density indices of NEBs, NECs, and mast cells were determined. Tissue edema, fibrotic lesions, and medial hypertrophy of pulmonary arterioles were assessed morphometrically. Test rats had higher pulmonary serotonin and histamine levels than controls at 1, 3, and 6 months. They also had higher cellular serotonin in NEBs at 1 month, but not in NECs, and tended to have higher serotonin levels in mast cells at 6 months. Mast cell numbers were higher among tests at 1 and 3 months, whereas NEBs and NECs were unchanged by asbestos. There was no difference between tests and controls in the amount of tissue edema at any time. However, all test rats had distinct lung lesions characterized by peribronchiolar fibrosis and bronchiolitis obliterans. No such lesions were present among control rats. Typically, mast cells were located immediately beneath the epithelial basal lamina of the bronchiolar fibrotic projections and at their stalks, whereas no mast cells were noted beneath normal epithelium, indicating a role of mast cells in asbestos-induced peribronchiolar fibrosis. Moreover, arteriolar medial hypertrophy at all three ages in conjunction with the increased levels of serotonin was an index of putative chronic pulmonary hypertension. Our results suggest that asbestos-induced rises in serotonin and histamine are due primarily to increased numbers of mast cells.

Animals↗

PubMed1990

Association between exposure to asbestos and pleural effusion. Results from a questionnaire study of 31,000 persons.

All visitors to a general health survey in 1979, 17,140 men and 14,371 women, completed a questionnaire on smoking habits, exposure to asbestos, silica and welding fumes, and diseases such as pleural effusion, pneumonia, cough, asthma and diabetes. Seven per cent of the men reported exposure to asbestos, 10% to welding fumes, and 6% to silica. Among those who reported work related dust exposure there was a higher proportion of smokers, and smokers exposed to dust smoked more tobacco per day than non exposed smokers. In the group of men 30-59 years of age, who did not indicate exposure to occupational pollutants 2.7% reported previous pleural effusions. However, among asbestos exposed men of the same ages, the prevalence was more than doubled (5.7%, p less than 0.01). This finding was highly significant in a logistic regression model where age and smoking habits were included. The data indicate that 10% or more of diagnosed cases of pleurisy could be associated with previous asbestos exposure.

Adult↗

PubMed1992

Synchronous double malignancy: adenocarcinoma of lung and malignant astrocytoma induced by asbestos exposure.

A 54-year-old male died of cerebellar herniation induced by brain tumor. Radiological examination of this case showed two separate tumorous lesions in the brain and lung. Autopsy proved malignant astrocytoma in the brain and coincidental alveolar cell carcinoma in the lung. He had a history of asbestos exposure for 8 years doing piping work in a shipyard. Furthermore, we detected a large number of asbestos bodies in the lung and one asbestos body in the brain. Therefore, this rare case of double cancer (malignant astrocytoma and lung cancer) might have been induced by asbestos exposure.

Adenocarcinoma↗

PubMed1978

The effects of asbestos on macrophages.

The exact role of the alveolar macrophage in the pathogenesis of asbestosis is not known. Most studies of the effect of asbestos on macrophages have been concerned with the in vitro biochemical or cytotoxic properties of the dust and have made use of peritoneal macrophages. In general, chrysotile had a toxic effect on the macrophages, whereas amphibole varieties did not. Most forms of absetos, however, are actively fibrogenic in man and animals, and there is no clear correlation between in vitro cytotoxicity of various forms of asbestos and their fibrogenicity. Recent experiments in which animals are exposed to asbestos in vivo provide evidence of alteration of macrophage activity, as demonstrated by changes in surface morphology and IgG receptor sites, as well as released of various secretory products. Deposition of complement components found on the surface of alveolar marcophages from animals exposed to asbestos could be a manifestation of a humoral immune response directed against an altered cell. The capacity of macrophages to participate in inflammation, tissue repair, and immunity suggests an immunopathogenic concept for the development of asbestosis.

Animals↗

PubMed1985

Lung response to particulates with emphasis on asbestos and other fibrous dusts.

Many theories have been proposed to explain asbestosis and asbestos-related pulmonary disease. However, none of the theories give a completely plausible explanation for the pathogenesis. Recently, attention has been drawn to a theory that the fibrogenicity or carcinogenicity of fibrous dust particles is related to fiber diameter and length rather than to chemical properties. This theory may help partially elucidate the disease process but is still far from solving the enigma of pulmonary fibrosis or carcinogenesis. The theory cannot explain the absence of these pathological effects among fiberglass workers or experimental animals exposed by inhalation (even though mesotheliomas are induced by intrapleural implantation and fiber dimension-related fibrogenicity is demonstrated by intratracheal injection). Little information regarding the pulmonary response to manmade fibrous particles is available in animals following inhalation exposure. Attempts should be made to confirm the absence of adverse effects using animal inhalation experiments even though to this point there is no conclusive evidence that either lung cancer or pulmonary diseases can be produced among employees in manmade fiber industries. A new research trend seems concentrated on testing the durability of asbestos or manmade fibers. This is based on the concept that biological effects of fibrous particles are the result of relative durability and that particles which can be fragmented or shortened may be less pathogenic. In the last two decades, considerable understanding about pulmonary fibrosis and carcinogenesis of asbestos has been achieved by clinical and animal experiments. In vitro tests including cytotoxicity, hemolysis, immunology, and enzyme biochemistry have provided important information on the interrelationships among these various biological effects of asbestos.

Animals↗

PubMed2002

Oxidant-mediated increases in redox factor-1 nuclear protein and activator protein-1 DNA binding in asbestos-treated macrophages.

Alveolar macrophages have been implicated in the pathogenesis of a number of acute and chronic lung disorders. We have previously shown that normal human alveolar macrophages exhibit decreased DNA binding activity of the transcription factor, AP-1, compared with monocytes. Furthermore, this decrease in AP-1 DNA binding appears to be due to a decrease in the redox active protein, redox factor (Ref)-1. Ref-1 is an important redox regulator of a number of transcription factors, including NF-kappaB and AP-1. In this study we evaluated the role of asbestos, a prototypic model of chronic fibrotic lung disease, in Ref-1 expression and activity. We found that incubation with low concentrations of crocidolite asbestos (0.5-1.25 microg/cm(2)) resulted in an increase in nuclear Ref-1 protein after 5 min, with a persistent elevation in protein up to 24 h. Additionally, an increase in nuclear Ref-1 could be induced by treating the cells with an oxidant-generating stimulus (iron loading plus PMA) and inhibited by diphenyleneiodonium chloride, an inhibitor of NADPH oxidase. The asbestos-induced accumulation of nuclear Ref-1 was associated with an increase in AP-1 DNA binding activity. These findings suggest that an exposure associated with fibrotic lung disease, i.e., asbestos, modulates accumulation of nuclear Ref-1 in macrophages, and that this effect is mediated by an oxidant stimulus.

Animals↗

PubMed1994

Mechanisms of the combined effect of asbestos and smoking in the etiology of lung cancer.

The joint effects of exposure to two known lung carcinogens, tobacco smoking and asbestos, are reviewed. The variable pattern of interaction--ranging from supramultiplicative to less than additive--may reflect the fact that both asbestos and smoking are complex carcinogens which can affect more than one stage of lung carcinogenesis. The joint effect of two such agents will depend on the relative magnitude of the effects at each stage. The epidemiologic evidence from studies of insulation workers with high exposures suggests an interaction that approximates the multiplicative model, indicating that each of the two factors has an independent action on the multistage process of carcinogenesis. Very limited information is available on the interaction between these two agents in causing specific histological types of lung cancer. Both tobacco smoke and asbestos fibers can be genotoxic and cytotoxic and cause proliferative lesions in the lungs. Tobacco smoke is known to contain carcinogens that bind to critical genes in DNA (deoxyribonucleic acid) and cause mutations. Asbestos fibers may cause chronic inflammation of the lungs, which releases various cytokines and growth factors, and therefore may provide a possible selective growth advantage for mutated cells.

Asbestos↗

PubMed1990

Smoking habits and lifetime occupational exposure to gases or dusts, including asbestos and quartz, in a Norwegian community.

Past or present occupational airborne exposure was recorded with a self-administered questionnaire sent to a random sample (N = 4992) of the 15- to 70-year-old population of Hordaland County, Norway. Completed questionnaires were returned by 90% of the sample. The respondents comprised 39% smokers, 20% ex-smokers, and 41% nonsmokers. Altogether 46% of the men and 12% of the women had a history of occupational gas or dust exposure. Occupational asbestos exposure was reported by 10% of the men and 0.4% of the women, and quartz exposure had been experienced by 8% of the men and 0.4% of the women. Smokers with a history of asbestos exposure represented 5% of the male population. Thirty percent of the smokers reported having been advised to stop smoking by a physician. The asbestos-exposed smokers had not received such advice more often than the smokers not exposed to asbestos. The findings indicate that airborne occupational exposure is widespread in the Norwegian County of Hordaland.

Adolescent↗

PubMed1984

Occupational asbestos exposure, lung-fiber concentration and latency time in malignant mesothelioma.

Mineral fiber concentration in lung tissue was analyzed by scanning electron microscopy in 73 males with malignant mesothelioma and in 36 referents who died of cardio- or cerebrovascular diseases. The investigation showed apparent differences in the median lung-fiber concentration between occupational groups with different levels of asbestos exposure, as judged from their occupational history. Thus the mineral fiber content in human lung tissue provides a useful indicator of cumulative asbestos exposure. There was also a statistically significant difference between the median lung-fiber concentration among mesothelioma cases with unlikely or unknown occupational asbestos exposure and the reference group. The latency times in 42 of the cases with definite or probable occupational asbestos exposure showed a log-normal distribution with a median of 37 years and a range of 19-68 years. No statistically significant correlation was found between the logarithm of the latency time and the logarithm of the lung-fiber concentration.

Aged↗