Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASBESTOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 1,333 records · Page 74Linked to original sources
PubMed1986

Fibronectin and procollagen 3 levels in bronchoalveolar lavage of asbestos-exposed human subjects and sheep.

To evaluate the potential interest of levels of fibronectin and procollagen 3 in bronchoalveolar lavage fluid as markers of fibrogenic activity, we characterized the time course of changes in fibronectin and procollagen 3 levels in the tracheal lobe of sheep exposed to nonfibrogenic and fibrogenic materials. We correlated these observations with those of bronchoalveolar lavage in long-term asbestos workers in various stages of disease activity. Following studies before exposure, the tracheal lobe of three groups of 24 sheep were exposed once to 100 ml of phosphate-buffered saline solution (PBS), to 100 mg of latex beads in 100 ml of PBS, or to 100 mg of chrysotile fibers in 100 ml of PBS. Bronchoalveolar lavages were obtained at 0, 1, 2, 4, 8, and 12 months after exposure, and four or five sheep per group were killed after each lavage for histopathologic analysis. Fibronectin in bronchoalveolar lavage fluid increased significantly only in the asbestos-exposed sheep to values two to three times above controls or latex-exposed sheep and remained elevated during the 12 months of the study. Levels of procollagen 3 in bronchoalveolar lavage fluid were increased significantly only during the first two months following exposure in the asbestos-exposed sheep only. In the asbestos workers without disease, levels of fibronectin and procollagen 3 in bronchoalveolar lavage fluid were comparable to controls, but these levels were significantly elevated in those with asbestos-associated alveolitis or asbestosis. This study documents that the measurement of levels of fibronectin and procollagen 3 in bronchoalveolar lavage fluid assesses fibrogenic activity of alveolitis and should be useful to predict its progression in a fibrotic process. In asbestos workers the potential use of these markers is primarily related to early detection of asbestos-induced pulmonary injury.

Adult↗
PubMed1987

Measurement of lung density by x-ray computed tomography. Relation to lung mechanics in workers exposed to asbestos cement.

We measured lung density by means of x-ray computed tomography and lung mechanics in 33 workers exposed to asbestos cement and in 39 normal subjects. The exposed group showed evidence of lung fibrosis with reduced static lung volumes and lung compliance, although only three subjects had signs of interstitial fibrosis at standard chest radiography. Lung density was significantly increased in the exposed workers compared to control subjects, with greater differences between nonsmokers than between smokers. Lung density correlated inversely with static lung volumes. There was no appreciable difference in the regional distribution of lung density between exposed workers and control subjects. We conclude that lung density is often increased in workers with mild asbestosis, even in the presence of a normal chest radiograph. Measurement of lung density may be of value in the evaluation of asbestos-exposed workers for assessment of the extent of parenchymal disease.

Asbestosis↗
PubMed1990

Rounded atelectasis complicated by obstructive pneumonia and pulmonary arterial thrombosis.

A patient with a history of asbestos exposure developed rounded atelectasis. The mass was associated with local bronchial obstruction, obstructive pneumonia and arterial thrombosis. Autopsy demonstrated marked pleural thickening and radiographically inapparent asbestosis. This is the first reported case in which seemingly benign rounded atelectasis not only increased morbidity, but also contributed to mortality through airway obstruction and local arterial thrombosis.

Aged↗
PubMedDate not supplied

Asbestos toxicity: an immunologic perspective.

Asbestos has long been associated with a number of life threatening pulmonary diseases, including asbestosis and mesothelioma. While the lung is the primary target organ for asbestos toxicity, a number of clinical and experimental studies over the past 30 years have shown that the immune system may also be altered by exposure to asbestos at occupationally relevant concentrations. Whereas early clinical studies generally focused on systemic observations of immune alteration, more recent studies have assessed the immunological changes occurring in the lung, the primary target organ of asbestos. This review will focus on the investigations that examine the influence of asbestos on systemic and local immunity, as well as the role that the immune system may play in asbestos-related disease.

Antibody Formation↗
PubMed2004

[Talc pneumoconiosis among soapstone handicraft workers in a rural area of Ouro Preto, Minas Gerais, Brazil].

Talc pneumoconiosis in Brazil has received little research attention to date. The disease was investigated in Mata dos Palmitos, a district of Ouro Preto, Minas Gerais State, among soapstone handicraft workers. The district has some 180 inhabitants, of whom 108 are engaged in handicrafts production, while 15 alternate handicrafts production with work in the soapstone quarries. A clinical and occupational investigation was conducted, along with a respiratory symptoms standardized questionnaire, chest x-ray (ILO standard), and spirometry. Clinical data showed a low prevalence of respiratory complaints. Dyspnea was the most frequent symptom. Chronic bronchitis was identified in 12 adult workers. Chest x-rays showed evidence of small lung opacities in 5 workers, and in 11 there was suspicion of the same opacities. One worker showed a plaque-shaped pleural thickening. Seven workers showed abnormal spirometry. The soapstone dust composition showed breathable asbestos fibers from the amphibole group (tremolite-actinolite). The results suggest talc asbestosis occurrence among soapstone handicraft workers.

Adolescent↗
PubMed2004

Effect of platelet-derived growth factor on the development and persistence of asbestos-induced fibroproliferative lung disease.

Platelet-derived growth factor (PDGF) isoforms and PDGF receptor-alpha are upregulated in fibroproliferative lesions in response to asbestos exposure. To examine the functional role of PDGF in asbestos-induced lung disease, we have evaluated the impact of PDGF-B overexpression in the lung on the development of pulmonary fibrosis induced by asbestos inhalation. Transgenic mice expressing PDGF-B from the surfactant protein C promoter and wild-type C57BL/6 mice were exposed to aerosolized chrysotile asbestos fibers via three different exposure regimens: 3 consecutive days to 9 mg/m(3), once a week for 5 weeks to 12 mg/m(3), or once a week for 8 weeks to 11 mg/m(3). The 3-day exposure did not produce fibroproliferative lesions in SPC-PDGFB or wild-type mice, indicating that PDGF expression did not increase susceptibility to a subthreshold dose of asbestos. Transgenic and wild-type mice subjected to the 5-week exposure protocol exhibited similar fibrogenic lesions histologically 48 hours and 8 weeks postexposure, but lungs from transgenic mice had elevated lung hydroxyproline content 8 weeks postexposure relative to wild-type mice. In addition, SPC-PDGFB transgenic mice developed pronounced thickening of arterioles following the 5-week exposure regimen. Mice exposed to asbestos for 8 weeks and examined 10 months later showed pronounced, diffuse fibrotic lesions of terminal bronchioles and alveolar ducts, but no histological differences between transgenic and nontransgenic mice were observed. These results indicated that PDGF-B overexpression can stimulate increased collagen deposition and vascular smooth muscle hyperplasia following asbestos inhalation and that a limited exposure (8 times) to chrysotile aerosol can produce long-lasting fibrotic lesions. The 8-week exposure regimen provides an animal model that encompasses an important aspect of human asbestosis-i.e., persistence of fibrosis for long periods after cessation of asbestos exposure.

Animals↗
PubMed1985

Asbestos disease in family contacts of shipyard workers.

Radiologic signs of pulmonary asbestos disease were found in 11.3 per cent of 274 wives of shipyard workers who were 20 or more years from initial hiring-on in shipyards in Los Angeles County. Asbestosis was also found in 7.6 per cent of 79 sons and 2.1 per cent of 140 daughters of these workers. The wives, sons, and daughters were without occupational exposure. Comparable radiographic signs were not found in comparison groups. It is probable that asbestos exposure in the household places these family members at risk for mesothelioma and lung cancer.

Adolescent↗
PubMed1986

Asbestos disease screening by non-specialists: results of an evaluation.

We performed a medical audit of an asbestos disease screening program offered to New York City sheet metal workers by a corporate medical service. The screening program purported to evaluate the health status of workers exposed to asbestos in the past and present during construction and renovation of commercial buildings. Using current Occupational Safety and Health Administration (OSHA) regulations as a benchmark, medical records for more than 800 workers who took the examination between 1982-83 were reviewed; x-ray interpretations of the staff radiologist were compared with the interpretations of specialists in occupational lung diseases. The audit found inadequate record-keeping procedures, a lack of a comprehensive occupational history, poor notification and absence of any form of health education. Further, there was an extreme lack of concordance between the staff radiologist and the specialist readers in the interpretation of x-rays (kappa = .14 for pleural disease and .26 for asbestosis). To an increasing extent, occupational clinical services are being provided by corporate medical groups; such groups may not be familiar with occupational health problems.

Adult↗
PubMed1985

Diffuse pleural thickening in an asbestos-exposed population: prevalence and causes.

Two types of pleural reaction have been described in association with asbestos exposure: pleural plaques and diffuse pleural thickening. This study was undertaken to determine the prevalence and causes of diffuse thickening in asbestos-exposed persons. Serial chest radiographs in 1373 exposed individuals and 717 controls were interpreted according to the ILO scheme by two B readers. Diffuse pleural thickening was defined as a smooth, noninterrupted pleural density extending over at least one-fourth of the chest wall, with or without costophrenic angle obliteration. Among the exposed group, plaques and diffuse thickening occurred with almost equal frequency, 16.5% and 13.5%, respectively. Of the 185 cases with diffuse thickening, the radiographic appearance was most often due to the residual of a benign asbestos effusion (31.3%) or confluent plaques (25.4%). The most commonly held explanation of diffuse thickening, an extension of pulmonary fibrosis to the visceral and parietal pleura, was actually infrequent (10.2%). Among the group with diffuse thickening without asbestosis, the forced vital capacity and single-breath diffusing capacity were significantly lower than those of comparable normal persons and those with confluent plaques.

Asbestosis↗
PubMed1999

The hazards of chrysotile asbestos: a critical review.

Chrysotile, or "white", asbestos is the dominant form of asbestos in international commerce today. It accounts for 99% of current world asbestos production of 2 million tonnes. Chrysotile is an extremely hazardous material. Clinical and epidemiologic studies have established incontrovertibly that chrysotile causes cancer of the lung, malignant mesothelioma of the pleura and peritoneum, cancer of the larynx and certain gastrointestinal cancers. Chrysotile also causes asbestosis, a progressive fibrous disease of the lungs. Risk of these diseases increases with cumulative lifetime exposure to chrysotile and rises also with increasing time interval (latency) since first exposure. Comparative analyses have established that chrysotile is 2 to 4 times less potent than crocidolite asbestos in its ability to cause malignant mesothelioma, but of equal potency of causation of lung cancer. The International Agency for Research on Cancer of the World Health Organization has declared chrysotile asbestos a proven human carcinogen. Sales of chrysotile asbestos have virtually ended in Western Europe and North America, because of widespread recognition of its health hazards. However, asbestos sales remain strong in Japan, across Asia and in developing nations worldwide. The claim has been made that chrysotile asbestos can be used "safely" under "certain conditions" in those nations. That claim is not accurate. The Collegium Ramazzini, an international learned society in environmental and occupational medicine, has called for an immediate worldwide ban on all sales and uses of all forms of asbestos, including chrysotile. The rationale for this ban is threefold: (1) that safer substitute materials are readily available, (2) that "controlled" use of asbestos is not possible, and (3) that the health risks of asbestos are not acceptable in either the industrialized or the newly industrializing nations.

Asbestos↗
PubMedDate not supplied

Human alveolar macrophage cytokine release in response to in vitro and in vivo asbestos exposure.

The lung macrophage is proposed to be involved in the development of asbestos-induced pulmonary fibrosis. Knowledge of the effects of long-term asbestos exposure on lung macrophage cytokine release should better define the role of the macrophage in fibrogenesis. This study examines the effects of acute in vitro asbestos exposure and chronic in vivo asbestos exposure on human alveolar macrophage cytokine release. As indicators of asbestos-induced macrophage activation, the cellular release of IL-1 beta, TNF-alpha, IL-6, GM-CSF, and PGE2 was measured during a 24-h in vitro culture. Alveolar macrophages from normal volunteers were cultured in vitro with chrysotile asbestos. Of the factors measured, only TNF-alpha was elevated in response to asbestos exposure. Alveolar macrophages from asbestos-exposed individuals were placed into one of two groups based on their exposure history. These two groups were matched for age, smoking history, and diagnosis; none met the criteria for asbestosis. Cells isolated from subjects that had been exposed to asbestos for more than 10 years secreted enhanced basal amounts of IL-1 beta, TNF-alpha, IL-6, and PGE2, while those who had been exposed for less than 10 years did not. The results indicate that while asbestos had minimal acute effects on cytokine production by the human alveolar macrophage, intense, chronic exposure to asbestos leads to the enhanced basal release of significant amounts of several cytokines that have activity for the fibroblast, even in the absence of overt fibrosis.

Aged↗
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↗
PubMed2003

Asbestos exposure and antineutrophil cytoplasmic Antibody (ANCA) positivity.

The authors used indirect immunofluorescence to examine the association of antineutrophil cytoplasmic antibodies (ANCAs) with exposure to asbestos among 61 asbestos-exposed patients (mean exposure = 24.6 yr) and 39 nonexposed controls. ANCA positivity was detected significantly more frequently (p = 0.034) in the asbestos-exposed group (21.3%) than in the control group (5.1%). ANCA-associated diseases did not occur more frequently among subjects exposed previously to asbestos than among unexposed controls. These findings confirmed that exposure to asbestos is another occupational factor, as is silica exposure, that is associated with ANCA positivity. The influence of asbestos appears stronger than that of silica because ANCA positivity was found among subjects who had histories of exposure to asbestos but who did not exhibit typical radiographic signs of asbestosis on their chest x-rays. Additional stimuli may be necessary to induce systemic vasculitis in asbestos-exposed persons.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2003

Occupational lung disease. Part 2. Discovering the cause of diffuse parenchymal lung disease.

Diffuse parenchymal lung disease (also known as interstitial lung disease) and acute irritant reactions are much less commonly managed by primary care physicians than asthma. Acute irritant reactions are typically readily recognized because of the immediate exposure-response relationship. As with asthma, a diagnosis of diffuse parenchymal lung disease should prompt a careful review of the patient's work history. Findings from history taking and radiography provide most of the data needed to establish a diagnosis of asbestosis or silicosis. A pulmonologist should be consulted about lung disease that eludes diagnosis. In cases in which a link between work and illness is strongly suspected, an occupational medicine specialist may be consulted for assistance with preparing reports for a workers' compensation claim as well as characterizing and quantifying impairment. Various government agencies provide extensive information about specific toxic exposures and occupational lung diseases by telephone and on the World Wide Web.

Air Pollutants, Occupational↗
PubMed2002

Does asbestos exposure cause non-Hodgkin's lymphoma or related hematolymphoid cancers? A review of the epidemiologic literature.

Asbestos exposure has been linked to non-Hodgkin's lymphoma (NHL) and other types of hematolymphoid cancer (HL-CA) in several case reports and epidemiologic studies. This review covers the scientific and medical literature on the issue of whether asbestos exposure is a cause of NHL or other HL-CAs. Studies of animals exposed to asbestos have not shown an increase in NHL or other types of HL-CA. Although some patients with asbestosis have mild immunologic abnormalities, 32 of 35 epidemiologic studies of asbestos exposure in humans are negative for NHL or other HL-CAs. Therefore, it can be concluded that there is no increased risk of NHL or other HL-CAs associated with asbestos exposure.

Adult↗
PubMed1998

Radiographic abnormalities among Finnish construction, shipyard and asbestos industry workers.

OBJECTIVES: The prevalence of asbestos-related radiographic abnormalities was surveyed among Finnish construction, shipyard, and asbestos industry workers. METHODS: The radiographic screening focused on active and retired workers who were under the age of 70 years and had been employed for at least 10 years in construction or for at least 1 year in shipyards or in the asbestos industry. In 1990-1992, 18,943 people participated in an X-ray examination of the lungs and an interview on work history and exposure. The criteria for a positive radiological finding were (i) small irregular lung opacities clearly consistent with interstitial pulmonary fibrosis (ILO 1/1 or higher), (ii) lung opacities indicating mild pulmonary fibrosis (ILO 1/0) with unilateral or bilateral pleural plaques, (iii) marked adhesions with or without thickening of the visceral pleura, or (iv) findings consistent with bilateral pleural plaques. RESULTS: Fulfilling the criteria were 4133 workers (22%) (22% from construction, 16% from shipyards, and 24% from the asbestos industry). The radiological findings included signs of pulmonary fibrosis (3%), changes in the visceral pleura (7%), bilateral plaques (17%), and unilateral plaques (10%). Occupational disease was diagnosed according to the Finnish insurance regulations for three-fourths of those referred for further examinations, 96% being abnormalities in the pleura and 4% being asbestosis. CONCLUSIONS: Exposure to asbestos dust has been common in ordinary construction work, and, consequently, radiographic abnormalities (mostly pleural) occur frequently among active and retired construction workers.

Adult↗
PubMed1983

Indications of an increase of occupational pleural mesothelioma in Japan.

In order to obtain an epidemiological picture of occupational pleural malignant mesotheliomas in Japan, the author surveyed the Annual of Pathological Autopsy Cases (published by the Japanese Pathological Society) from 1974 through 1980. Two hundred and twenty-two malignant mesotheliomas (0.114% of all autopsy cases) were found in that period. One hundred and forty-five cases (0.074%) of them were of pleural origin. Until 1977, there were no pleural malignant mesotheliomas associated with asbestosis, but there were one in 1978, three in 1979 and two in 1980. Two of them were housewives and the others were a ship builder, a welder, a ceramist and a steel factory worker. Two lived in Sakae City, and the others in Kure City, Kaizuka City, Nagasaki City and Kanagawa Prefecture, where large shipyards are located. Compared to the Western countries, there is a time lag of 10 to 20 years in the increase of consumption of asbestos in Japan, where the increase has occurred rapidly after World War II. The epidemiological picture obtained by this study clearly states that the number of occupational pleural malignant mesotheliomas began to increase in the past few years in Japan.

Adult↗
PubMed1999

[Asbestos exposure and pleuropulmonary cancer].

Pleuropulmonary cancers are recognized asbestos-related diseases. Mesothelioma occurs almost uniquely in individuals exposed to asbestos whereas lung cancer is strongly associated with smoking. If the asbestos exposure is sufficient however, the incidence of lung cancer is higher than would be expected from the smoking effect alone. For lung cancer in asbestos workers, asbestosis is not a prerequisite for recognition as an occupation related disease. The intensity and duration of exposure to asbestos are factors associated with higher risk of lung cancer. These factors can be estimated on the basis of the work history or, when necessary, by analyzing mineral dust from available lung tissues.

Asbestos↗