SEARCH · PubMed Health

Results for “ASBESTOSIS”

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 973 records · Page 54Linked to original sources

PubMed1996

Lung cinescintigraphy in the dynamic assessment of ventilation and mucociliary clearance of asbestos cement workers.

OBJECTIVES: To verify in vivo whether lung cinescintigraphy confirms the effect of asbestos on the patency of the smallest airways and on the efficiency of mucociliary clearance in asbestos cement workers. METHODS: 39 male subjects were examined: 30 asbestos cement workers and nine workers never exposed to occupational respiratory irritants. All subjects had a chest radiograph (International Labour Organisation (ILO) 1980); standard questionnaire on chronic bronchitis; spirometry; arterial blood gas analysis; carbon monoxide transfer factor (TLcosb); pulmonary O2 and CO2 ductances (DuO2, DuCO2); electrocardiogram; and lung cinescintigraphy after radioaerosol inhalation for the measurement of mucociliary clearance time in vivo in the smallest ciliated airways and for the assessment of radioaerosol deposition in alveoli (alveolar deposition index). RESULTS: Apart from nine non-exposed subjects, the 30 asbestos cement workers were so classified on the basis of chest radiography: nine of them as healthy exposed, 10 with pleural plaques, and 11 with asbestosis. The four groups had similar ages, work seniority, and smoking habits. Exercise dyspnoea was significantly more frequent in asbestos cement workers. Lung function variables of workers with effects related to asbestos were significantly lower than the other two groups. The PaO2, TLcOsb and DuO2 mean values were significantly lower in exposed workers than non-exposed. The mean PacO2 value was significantly higher in the asbestosis group than in the other three groups. Workers with effects related to asbestos showed a significantly lower alveolar deposition index and a significantly higher mucociliary clearance time than the other two groups. Subjects with asbestosis showed similar differences from those with pleural plaques. CONCLUSIONS: Lung cinescintigraphy confirms in vivo the effects of asbestos on bronchiolar and alveolar patency and on efficiency of mucociliary clearance in the smallest ciliated airways. Finally, lung cinescintigraphic variables are able to discriminate workers with asbestosis from those with pleural plaques.

Asbestos↗

PubMed1983

Pulmonary uptake of gallium-67 in asbestos-exposed humans and sheep.

To evaluate the 67Ga lung uptake as an indicator of inflammatory activity in asbestosis, we obtained 67Ga lung scans in 58 long-term asbestos workers. The 67Ga localized excessively in the lungs of 17 of the 21 workers with asbestosis. Among workers without sufficient criteria for the diagnosis of asbestosis, the 67Ga scan index was significantly increased in 43% (16 of 37). Among the 16 with positive 67Ga scan, abnormal pressure-volume curve and/or gas exchange data were found in 87%, whereas in the 21 workers with negative 67Ga scan, similar abnormalities were found in only 29%. In the sheep model of the disease, bronchoalveolar analysis after 67Ga scan demonstrated that the excessive uptake of 67Ga in asbestosis is caused by enhanced serum protein leakage and macrophage accumulation in the lung. Thus, 67Ga scanning in asbestos workers may be a useful indicator of early lung damage.

Acquired Immunodeficiency Syndrome↗

PubMed1983

Biochemical mechanisms in asbestos toxicity.

The alarming hazardous nature of asbestos makes it the foremost among toxic fugitive dusts. The biochemical mechanisms responsible for the diverse biological effects of asbestos, such as fibrosis, asbestos bodies, pleural plaques, respiratory difficulty, cancer, and cytotoxicity, are being studied in this laboratory. As asbestosis progresses in guinea pigs, along with reticulum formation, lysosomal enzymes are released from membrane-bound latent state to active free form, initiating degradative changes. Considerable alterations take place in the pulmonary metabolic machinery. Mitochondria in lung cells were found to be important loci for the toxic effect of asbestos. A profile of mitochondrial activity, in control and asbestotic animals, revealed specific enzymic changes such as increased cytochrome c oxidase during the disease. The functional organization of mitochondria was also altered, since the organelles from asbestotic lungs were swollen as measured by spectrophotometry. Glutamate dehydrogenase activity of mitochondria became exposed in asbestosis. The maleate dehydrogenase shunt which is involved in transport of the redox potential across the membrane was enhanced in cytosol and mitochondria. The involvement of microsomal enzymes in asbestosis was indicated by alterations in glucose-6-phosphatase and tyrosine transaminase and aniline hydroxylase. Changes in the biotransformational capacity of lung, due to asbestos, could be an important aspect in toxicity, especially the carcinogenic effect. Considerable alterations were encountered in the levels of different phospholipids and in mucopolysaccharide constituents. On the basis of the above, the molecular mechanisms in asbestos toxicity are explained as an integrated model. Interactions of dust constituents with those of membranes and the ensuing metabolic adjustments are thus important in the etiology of asbestosis.

Acid Phosphatase↗

PubMed1999

A retired shipyard worker with rapidly progressive pulmonary interstitial fibrosis.

We present a case of progressive interstitial fibrosis in a retired shipyard worker who was exposed to asbestos during the postwar era of the late 1940s and 1950s, when asbestos exposures in the workplace were not regulated. Forty years later, at 63 years of age, the patient presented with restrictive lung disease. The patient was diagnosed with asbestos-related pleural disease and parenchymal asbestosis. He remained stable for the next 7 years, but then he began to manifest rapid clinical progression, which raised the possibility of an unusual variant of asbestosis, a concomitant interstitial process, or an unrelated disease. Lung biopsy was not undertaken because of the patient's low pulmonary reserve and limited treatment options. An empiric trial of oral steroids was initiated, but his pulmonary status continued to deteriorate and he died of pulmonary failure at 72 years of age. Many diseases result in pulmonary interstitial fibrosis. Ideally, open lung biopsy should be performed, but this procedure inevitably causes complications in many patients with end-stage restrictive lung disease. Furthermore, while the presence of asbestos bodies in tissue sections is a sensitive and specific marker of asbestos exposure, neither this finding nor any other charge is a marker indicative of asbestosis or the severity of asbestosis. With the enactment of the Asbestos Standard in the United States, asbestos exposures have been decreasing in this country. However, industries that produce asbestos products and wastes continue to expand in developing countries. Prevention of asbestos-related lung disease should be a global endeavor, and asbestos exposures should be regulated in both developed and developing countries.

Asbestos↗

PubMed1986

Asbestos burden and the pathology of lung cancer.

To determine whether we could distinguish asbestos-related lung cancers from unrelated ones, we typed and quantified by electron-optical methods the asbestos fibers in the lungs of 75 men with lung cancer. All but eight men had some history of asbestos exposure. On the basis of combined amosite and crocidolite (AC) concentrations, we divided the subjects into three groups (AC fibers per gram of dry lung): low (less than 10(5)); intermediate (10(5) to 10(6)); and high (greater than 10(6)). Age, smoking history, latent period, and type and location of tumors were similar in all three groups. Of 62 evaluated subjects, zero of 14 in the low group, seven of 29 in the intermediate group, and five of 19 in the high group had asbestosis. Epidemiologic studies suggest that persons exposed to concentrations of asbestos that can cause asbestosis are at increased risk for lung cancer. Thus, the subjects in our intermediate and high concentration groups may have been at increased risk for cancer, even when they did not have asbestosis. Because large burdens of asbestos do not always cause pulmonary fibrosis, asbestosis may be a poor marker of fiber-related lung cancer.

Adult↗

PubMed1990

Asbestos exposure results in increased lung procoagulant activity in vivo and in vitro.

Enhanced fibrin deposition is a common histologic finding in fibrotic lung disorders including asbestosis and may be an important mechanism by which fibroblast proliferation is modulated. Asbestos-induced activation of lung interstitial cells may result in enhanced expression of procoagulant activity which contributes to the inflammatory response resulting in subsequent fibrin deposition. The current study examines procoagulant activity in bronchoalveolar lavage fluid from patients with clinically diagnosed asbestosis, patients with asbestos exposure without asbestosis, and normal, control subjects. Results indicated that asbestos exposure resulted in increased lung procoagulant expression in vivo, and furthermore, suggested that both endothelial cells and alveolar macrophages represented lung parenchymal cells which may contribute to this activity. This imbalance in coagulation homeostasis may be important in the regulation of fibrotic responses observed in asbestosis.

Adult↗

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↗

PubMed1989

A study of magnetic field in the lung of workers in an asbestos factory.

Magnetic field at the chest in 93 male workers exposed to asbestos dust in an asbestos products factory in China was studied by local magnetization and flux-gate gradiometry. The average field intensity at 12 measurement points over the anterior chest wall was compared among workers with and without asbestosis and among workers of different working age. The field intensity in workers with asbestosis and those suspected to have asbestosis on the basis of X-ray findings was significantly higher than that in workers without asbestosis. It was also found that the field intensity increased with working age. It is suggested that dynamic measurement of magnetic field in the lung of workers exposed to dust containing ferrimagnetic particles would at least serve as a quantitative method for estimating lung dust loads and be valuable for pneumoconiosis prevention.

Asbestosis↗

PubMed2001

High-resolution computed tomography classification of lung fibrosis for patients with asbestos-related disease.

OBJECTIVES: This study tested a new high-resolution computed tomography (HRCT) scoring method for asbestos-induced parenchymal changes in the lung. METHODS: HRCT scans of 602 asbestos-exposed workers and 49 referents were reviewed by 3 radiologists. Structured forms were filled out for a semiquantitative HRCT fibrosis score based on several specified parenchymal abnormalities scored separately. Observer agreement was studied with the use of the quadratic-weighted kappa (kappaqw). The HRCT fibrosis score (from 0 to V with definitions and index images given retrospectively) was compared with the radiographic classification of the International Labour Office (ILO) for the same patients. Receiver-operating characteristic (ROC) curves were computed to compare the tests for diagnosing asbestosis. RESULTS: Good inter- and intraobserver agreements were achieved (kappaqw = 0.64 and 0.72, respectively) as regards the HRCT fibrosis score. All the specified computed tomography findings explained 86% of the variance in the HRCT fibrosis score. Age and occupational group were significant predictors of fibrosis. The area under the ROC curve was significantly greater for the HRCT fibrosis score (0.89) than for the ILO radiographic classification (0.76). The sensitivity (70%) and specificity (91%) of the HRCT fibrosis score (classes I/II-V representing asbestosis) were better than those of the classification published by the International Labour Office (51% and 89%, respectively, score > or = 1/0 representing asbestosis). CONCLUSIONS: The examined HRCT scoring method proved to be a simple, reliable, and reproducible method for classifying lung fibrosis and diagnosing asbestosis also in large populations with occupational disease, and it would be possible to use it as a part of an international classification.

Adult↗

PubMed2003

Malignant and non-malignant asbestos-related pleural and lung disease: 10-year follow-up study.

AIM: To examine the presence of radiologically visible lung and pleural changes in patients who were exposed to the asbestos dust, and to correlate the progression of these changes with the duration and intensity of exposure and smoking. We also evaluated possible correlation between non-malignant asbestos-related pleural abnormalities and the occurrence of malignant pleural mesothelioma. METHODS: Among 7,300 patients who visited our department between 1991 and 2000 due to non-specific respiratory symptoms, we selected 2,420 with chest X-rays indicating the possible existence of non-malignant asbestos-related diseases. The selected group was followed-up for progression of radiological changes and the development of malignant pleural mesothelioma, and the changes were correlated with the intensity and duration of exposure to asbestos dust and smoking. RESULTS: Radiological changes characteristic for non-malignant asbestos-related pleural disease or lung asbestosis were identified in 340 (14%) out of 2,420 examined patients, of whom 77 (22.6%) developed malignant pleural mesothelioma, as compared with 13 patients out of 2,080 (0.6%) without radiological signs of asbestosis or pleural changes. Twenty-three (29.9%) patients who presented with a progression of pleural disease and lung asbestosis had a very significant incidence of malignant pleural mesothelioma (p<0.001). We also found that 55 (71.4%) patients with the highest asbestos exposure level (grade 3) developed malignant pleural mesothelioma more often (p=0.044). No correlation was found between malignant pleural mesothelioma development and duration of asbestos exposure (p=0.149) or smoking habit (p=0.617). Professionally exposed patients were at 3.3-times higher relative risk (95% confidence interval, 2.28-4.75) than those who were not exposed to develop malignant pleural mesothelioma. CONCLUSIONS: The risk of developing lung asbestosis increased with the level of exposure to asbestos dust and smoking. The risk of developing pleural disease correlated with the intensity and duration of exposure, but not with smoking. The patients with progressive pleural and parenchymal changes are at particularly high risk of developing malignant pleural mesothelioma and must be under special surveillance.

Adolescent↗

PubMed2006

Genetic predisposition and health effect of occupational exposure to asbestos.

OBJECTIVES: As asbestos presents a direct genetic hazard for humans, a small-scale molecular epidemiological study was conducted to monitor 61 subjects long-term exposed to asbestos in comparison with 49 town controls and 21 control subjects from administration of the same factory. RESULTS: Asbestos exposed workers had significantly higher numbers of chromosomal aberrations compared with both control groups (P=0.003). Clinical examination showed that 44.3% of exposed workers developed symptoms of asbestosis. We were interested in the relationship between the risk of asbestos-coupled diseases and individual variability in biotransformation enzymes, especially in glutathione S-transferases and microsomal epoxide hydrolase. GSTP1*105Val allele appeared less in the group of workers with asbestosis compared to those without asbestosis (18.5% vs 34.7%, P=0.044), and in subjects with developed asbestosis coupled with bronchitis compared to those without bronchitis (0% vs 25%, P=0.048). Similarly, the genotype corresponding to low activity of microsomal epoxide hydrolase was significantly decreased in workers with fibrotic plaques compared to those without plaques (26.7% vs 56.3%, P=0.045). CONCLUSIONS: Our results suggest that GSTP1*105Val allele and low EPHX1 activity genotype may be protective for people occupationally exposed to asbestos. However, more extensive studies are needed to confirm our results.

Asbestos↗

PubMed1989

Correlation between lung fibre content and disease in East London asbestos factory workers.

The lungs from 36 former workers at an East London asbestos factory dying of asbestos-related disease were compared with lung tissue from 56 matched control patients operated on in East London for carcinoma of the lung. The severity of asbestosis and the presence of pulmonary carcinoma or mesothelioma of the pleura or peritoneum were correlated with an asbestos exposure index and with the type and amount of mineral fibre of the lungs. Asbestosis was associated with far heavier fibre burdens than mesothelioma. Moderate or severe asbestosis was more common among those with carcinoma of the lung than in those with mesothelial tumours. Crocidolite and amosite asbestos were strongly associated with asbestosis, carcinoma of the lung and mesothelial tumours, whereas no such correlation was evident with chrysotile or mullite. It is suggested that greater emphasis should be placed on the biological differences between amphibole and serpentine asbestos fibre.

Aluminum Silicates↗

PubMed1985

Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure.

To determine whether asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls. Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (asbestosis) occurred. It is concluded that 1) amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial fibrosis of the parenchyma (classical asbestosis); 3) asbestosis, at least that induced by amosite, commences at any site in the parenchyma to which the asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.

Animals↗

PubMed1985

Epidemiological investigations of decreased employees of the asbestos cement industry in the Federal Republic of Germany.

An epidemiological study of the causes of death was performed covering the entire German asbestos cement industry (10 plants). Of 376 workers who had died in the period of 1 January 1976 - 31 December 1980 and who had been employed for a minimum of 10 years, 314 were included; 307 of these were men. Special consideration was given to the asbestos-related diseases asbestosis, asbestosis in combination with lung cancer, and mesothelioma of the pleura or peritoneum. The relationship between lung cancer with asbestosis and lung cancer without asbestosis is nearly 1:1. From this the conclusion can be drawn that a causal relationship between asbestos exposure and lung cancer can be assumed in only half of the lung cancer cases. This is, however, an upper approximation, since 15 cases of lung cancer were found which is 1/3 less than the expected number in comparison with the normal population. This documents the relatively small excess (SPMR = 1.2) of all cases of lung cancer detected in the asbestos cement industry as compared to the expected lung cancer cases not due to asbestos.

Aged↗

PubMed1983

Projections of asbestos-related disease 1980-2009.

Approximately 19,000 cases of mesothelioma and 55,000 cases of lung cancer will arise in U.S. men with histories of nontrivial occupational exposure to asbestos. There are approximately 65,000 U.S. men now alive with clinically diagnosable asbestosis. These estimates are based, in the case of the cancer, on estimates of the effective number of asbestos-exposed workers required to produce the current national incidence of mesothelioma. The asbestosis estimates are based on a number of rough measures relating the prevalence of asbestosis to the incidence of mesothelioma, the incidence of compensable asbestosis in other countries, the prevalence of and mortality from pneumoconioses generally, and the number of workers heavily exposed to asbestos.

Asbestos↗

PubMedDate not supplied

Asbestos content of bronchoalveolar lavage fluid. A comparison of light and scanning electron microscopic analysis.

We studied the asbestos content of bronchoalveolar lavage fluid (BALF) from 9 patients with asbestosis, 17 asbestos exposed but without asbestosis, 15 with idiopathic pulmonary fibrosis (IPF) and 9 nonexposed volunteers. The cellular lavage pellet was digested and filtered for asbestos body (AB) quantification by light microscopy (LM) and analysis of numbers and types of uncoated fibers (UF) by scanning electron microscopy (SEM) and energy dispersive x-ray analysis. BALF of asbestosis patients had significantly higher AB content than that of the combined IPF and volunteer groups. The UF content as determined by SEM was similar in all four groups. Commercial amphiboles (amosite or crocidolite) were identified more frequently in BALF from patients with asbestosis than from the other groups. ABs were detected by SEM only in highly exposed individuals. We conclude that the findings of > 1 AB per 10(6) cells or 1 AB/mL BALF by LM and of ABs or commercial amphibole fibers by SEM are indicative of considerable exposure to asbestos in the majority of cases.

Adult↗

PubMed1993

[Genetic polymorphism of haptoglobin and quantitative changes in its levels during exposure to asbestos].

The polymorphism and serum levels of haptoglobin were studied in asbestosis patients, in the control and the workers exposed to asbest. Hp1-1 has the highest, Hp2-2--the lowest and Hp2-1 has the intermediate concentration of this protein. In the course of contact with asbest, and especially in asbestosis patients, the haptoglobin levels are higher (for all phenotypes). The standard deviation from the Hp concentration in asbestosis patients was significantly higher. The phenotypes Hp1-1 were found more often in asbestosis patients than among asbest-exposed workers.

Asbestos↗

PubMed1993

Enhanced IL-1 beta and tumor necrosis factor-alpha release and messenger RNA expression in macrophages from idiopathic pulmonary fibrosis or after asbestos exposure.

Idiopathic pulmonary fibrosis (IPF) and asbestosis are fibrotic interstitial lung diseases characterized by alveolar wall fibrosis with accumulation of extracellular matrix, interstitial remodeling, and increased numbers of activated alveolar macrophages. Animal models and in vitro studies have shown that macrophage cytokines, namely IL-1 beta and TNF-alpha, play significant roles in the development of fibrosis. We found significant increases for TNF-alpha release in both diseases (p < 0.01) and a significant increase for IL-1 beta release in asbestosis compared to normal controls (p < 0.01). Also, the mRNA expression of these cytokines was increased in alveolar macrophages from patients with IPF or asbestosis compared with normals. The level of TNF-alpha release in macrophage supernatants correlated with the number of neutrophils per milliliter bronchoalveolar lavage fluid returned. Chrysotile, crocidolite, amosite asbestos, and silica stimulated IL-1 beta and TNF-alpha release and up-regulated their respective mRNA in macrophages or monocytes. To evaluate the role of IL-1 beta and TNF-alpha in the accumulation of extracellular matrix, we studied collagen types I and III and fibronectin gene expression in human diploid lung fibroblasts after short term (2 h) serum-free exposure to recombinant cytokines. Both cytokines up-regulated these genes 1.5- to 3.6-fold. These cytokines have the potential to influence the remodeling and fibrosis observed in the lower respiratory tract in IPF and asbestosis.

Adult↗