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PubMed1991

Comparison of alveolar and interstitial macrophages in fibroblast stimulation after silica and long or short asbestos.

Pulmonary fibrosis in response to silica or asbestos has been attributed to secretion of fibroblast growth factors (FGF) by alveolar macrophages (AM). However, since fibrosis is interstitial, and is associated with particle retention by interstitial macrophages (IM), we have now compared the secretory activity of FGF by rat alveolar (AM) and IM in response to silica and to long or short asbestos fibers. AM were obtained by bronchoalveolar lavage, and IM by collecting macrophages that migrate from explants of a previously lavaged and perfused lung. Six weeks after instilling silica, isolated AM and IM from lungs secreted equal amounts of FGF. Six weeks after instilling short asbestos fibers in vivo, lavaged AM secreted FGF, but there was no change in fibroblast growth and no fibrosis in vivo. After long fibers, that reach the interstitium were instilled, isolated IM secreted FGF, and collagen levels were increased. When IM and AM were isolated from normal rats and exposed to the same silica or asbestos samples in vitro, it was found that all macrophage supernatants contained FGF, and the response of AM and IM was equal. The results indicate that the two macrophage populations respond equally to particles with respect to FGF secretion. The greater fibrotic reaction seen in vivo may be explained by the proximity of fibroblasts to particle-laden macrophages within the interstitium allowing more efficient transfer of FGF.

Animals↗

PubMed1989

[Pathological study of bronchio-alveolitis induced by xinkang short-fiber chrysotile asbestos in rats].

Eighty-four rats were exposed intratracheally to 25 mg of locally produced Xinkang short-fiber chrysotile asbestos (98% of the fibers are less than 5 microns in length). In 1 to 3 d after instillation, the pathological changes in rat lungs demonstrated that the affection was mainly acute bronchio-alveolitis characterized by acute inflammatory exudation and injuries of the small airways and alveolar structural units. The four main manifestations of alveolitis induced by the chrysotile asbestos were of the neutrophilic, serous, alveolar macrophages and granulomatous varieties. Three types of pulmonary fibrosis developed gradually from 7 to 90 d following the exposure to the asbestos, i.e. the intraluminal, murally incorporated, and interstitial fibrosis. Findings showed the complete process from the acute inflammatory exudation and the damage to lung tissue, with the following repair and proliferation of injuried lung tissue and organization of exudate, to the final fibrosis and destruction of the lung. The results suggested that the persistent and irreversible damage to the epithelial cells of respiratory bronchioles and pneumocytes, and denudation and destruction of the basement membrane played an important role in the development of pulmonary fibrosis by forming a channel for the inflammatory exudates and fibroblasts migrating into the bronchioalveolar spaces. Therefore, the experimental results have proved that Xinkang chrysotile asbestos fibers less than 5 microns in length certainly have a fibrogenic effect.

Animals↗

PubMed1989

Adsorption of polycyclic aromatic hydrocarbons on to asbestos and man-made mineral fibres in the gas phase.

The adsorption of the aromatic hydrocarbons naphthalene and phenanthrene on to 4 types of asbestos and 2 types of man-made mineral fibres in the gas phase was studied. The asbestos types were chrysotile, anthophyllite, amosite, and crocidolite and the man-made mineral fibres were rock wool and glass wool. The influence of the gas humidity on this adsorption was also studied. The experiments were performed in an open system with the continuous generation of a gas stream of constant flow rate, humidity and hydrocarbon concentration. The results show that chrysotile asbestos is an extremely good adsorbent of polycyclic aromatic hydrocarbons (PAHs) in dry gas. This material adsorbs about 100,000 times more PAH than does glass wool, which has the lowest capacity of the fibres tested. The amphibolic asbestos types lie in the upper half and the rock wool sample in the lower half of the range. However, if the gas phase is humidified to typical ambient air values, there is a dramatic decrease in the adsorption on to the highly adsorbing materials. This means that, at relevant gas-phase humidities, there will be a fairly weak adsorption of PAH of about the same order of magnitude for all the materials tested. Any enhanced biological effect of inhalation of PAH adsorbed on fibres is thus likely to be connected with properties of the fibres other than the mere amounts of PAH adsorbed.

Adsorption↗

PubMed1989

Scavengers of active oxygen species prevent cigarette smoke-induced asbestos fiber penetration in rat tracheal explants.

It was previously shown that rat tracheal explants first exposed to cigarette smoke and then to amosite asbestos take up more asbestos fibers than explants exposed to air and asbestos. To examine the mechanism of this process, the same experimental design was followed but test groups were added in which the asbestos was mixed with catalase or superoxide dismutase, scavengers of active oxygen species, or deferoxamine, an iron chelator that prevents formation of hydroxyl radical. All three agents protected against the cigarette smoke effect. Heat inactivated catalase or superoxide dismutase was not protective. These observations indicate that active oxygen species, probably derived from the cigarette smoke, play a role in smoke-mediated fiber transport into tracheobronchial epithelia.

Animals↗

PubMed1988

Issues and controversies in the plain-film diagnosis of asbestos-related disorders in the chest.

This article reviews the chest radiographic manifestations of asbestos exposure. While the chest radiograph (CXR) is a highly valuable tool in the evaluation of asbestos-related disease, there are ongoing controversies regarding the sensitivity and specificity of the plain film in diagnosing asbestos-related disorders. Autopsy series indicate that at least 60% of pleural plaques may be overlooked. Conversely, such series indicate that up to 20% of plaques are falsely diagnosed. The significance of visceral pleural thickening and the definition and positive predictive value of diffuse pleural thickening as they relate to asbestos exposure are unresolved issues. Data suggest that the CXR may fail to reflect significant asbestosis in 10% to 20% of cases. On the other hand, the presence of overlying pleural abnormalities as well as technical factors may contribute to overreading of interstitial disease. Data on the rate of false positive readings for asbestosis are limited. Considered alone, the CXR can support but not specifically establish nor exclude the diagnosis of asbestosis. In practice, an ILO grade of less than 1/0 implies that the diagnosis is unlikely. A constellation of positive CXR findings may increase specificity, although the diagnosis rests on a combination of multiple clinical criteria.

Asbestos↗

PubMed1988

Asbestos exposure and laryngeal cancer: an analysis of the epidemiologic evidence.

We conducted a critical analysis of the available epidemiologic investigations on the causal relationship between asbestos exposure and laryngeal cancer. A review of nine case-control studies indicates that the estimated risk (odds ratio) attributable to asbestos exposure alone is negligible when smoking and ethanol intake are appropriately controlled for. Six of the 12 cohort studies demonstrated no significant increase in the standardized mortality ratio due to asbestos exposure. The remaining six longitudinal studies showed an increased standardized mortality ratio from 1.91 to 5.41 but no adjustment was made for the confounding effects of smoking and ethanol consumption. In conclusion, the available epidemiologic evidence does not support a causal association between asbestos exposure and laryngeal cancer.

Alcohol Drinking↗

PubMed1988

Chronic occupational exposure to asbestos: more than medical effects?

One hundred and twenty-nine workers chronically exposed to asbestos were interviewed regarding their perceived health status and concerns, their health behaviors, particularly their smoking behavior, and their psychologic well-being. In contrast to a non-exposed comparison group of postal workers, asbestos workers exhibited significantly elevated levels of somatic concern (P less than .03), and significantly lower levels of mental health functioning only when experiencing high levels of stress (P less than .01). Despite feeling significantly more susceptible to developing cancer (P less than .0001), 34% of asbestos workers were cigarette smokers (compared to 32% of the postal group) and long-term mask usage was minimal. Asbestos workers' increased sensitivity to stress and changes in health status along with the lack of adaptation of health-promotive behaviors indicate the need for interventions to attend to the psychologic effects of increased risk status.

Asbestos↗

PubMed1977

A review of the health effects of ingested asbestos.

Occupational studies indicate that a human health hazard may exist for ingested asbestos since the death rates due to digestive system cancers are elevated in asbestos workers. This finding may be related to the swallowing of asbestos that was inhaled and cleared from the respiratory system via the respiratory clearance mechanism. Published animal ingestion experiments have serious shortcomings in their design and execution which make their interpretation very difficult. Animal ingestion and human autopsy studies suggest that asbestos fibers may penetrate the digestive tract and migrate to other locations in the body.

Administration, Oral↗

PubMed1986

[Asbestos and cancer of the larynx].

Two hundred subjects were evaluated using a standardised questionnaire in order to determine possible exposure to asbestos: 50 patients with a carcinoma of the larynx (mean age: 59.2 +/- 1.6 years), 50 patients with a carcinoma of the bronchus (mean age 61.2 +/- 1.5 years) and 100 controls. Rates concerning exposure to asbestos were 27.8%, 23.4% and 4% respectively. The difference between the carcinoma patients and the controls was significant (p less than 0.001). The mean time lapse between the first exposure to asbestos and the development of malignant disease was shorter for the larynx (28.5 +/- 4 years) than for the lung (46.2 +/- 4.2): p less than 0.01. This study confirms the aetiological role of asbestos in the pathogenesis of carcinoma of the larynx as well as carcinoma of the lung, and raises the problem of their medicolegal compensation.

Alcoholism↗

PubMed1986

Asbestos as an air pollutant and synergism with smoking.

For many years the health consequences of asbestos exposure, including an overall mortality experience of approximately 50% from cancer among occupationally exposed individuals, have been well documented worldwide. Less well appreciated are the lessons to be learned from data available concerning outdoor asbestos air pollution and, of perhaps greater concern, the risks in certain indoor environments contaminated by this useful mineral. The biologically complex issue of carcinogenic synergism has been clearly demonstrated for cigarette smoking, asbestos-exposed individuals. Prevention of cancer among those exposed to asbestos not only requires efforts to minimize such exposure, but also requires strong antismoking measures among those exposed.

Air Pollutants↗

PubMed1986

The patient with asbestos exposure.

Attention to the hazards of asbestos has aroused concern among many healthy persons who have been exposed at some time to one of the world's most versatile materials. Present standards for exposure to asbestos, however, may not fully protect workers from asbestos-induced pulmonary malignancy. To evaluate the patient who has had some asbestos exposure, the physician should focus on the pulmonary system, take a thorough occupational history, conduct a physical examination and pulmonary function studies, and obtain chest films. In managing the patient with asbestosis, removal from further occupational exposure is advisable. For workers with only pleural changes, it is unclear whether removal from the work place is of any value.

Asbestos↗

PubMed1986

Obstructive airway disease as a risk factor for asbestos-associated malignancy.

A case-control study of a heavily asbestos-exposed group was performed to determine if obstructive airway disorder is an independent risk factor for developing asbestos-associated malignancies. From a group of 1,500 asbestos workers who had previously undergone careful evaluation, 18 case employees were identified. Each case employee was matched by smoking status, pack-years, age, and years of asbestos exposure to a single referent, a member of the same exposed population known to be free of malignancy. The spirometry results, obtained prior to the clinical manifestation of the cancer, were compared. The FEV1/FVC ratio and the FEV1/height3 ratio were lower (P less than .05, P less than .10, respectively) in the case employees. These results suggest that obstructive airway disease may be an independent risk factor for cancer.

Adult↗

PubMed1985

Respiratory illness in the construction trades. I. The significance of asbestos-associated pleural disease among sheet metal workers.

To assess the rate of roentgenographic and lung function abnormalities in asbestos-exposed construction workers, the authors studied 314 white male members of a local sheet metal workers union. Health outcomes were assessed by questionnaire, simple spirometry, and chest roentgenography; data were collected and interpreted following guidelines of the American Thoracic Society and the International Labor Office. Analyses of union records showed the tested population to be representative of all those eligible for testing. Pleural abnormalities were common, increasing to a prevalence of approximately 70% in workers with more than 30 years employment. Roentgenographic evidence of pleural disease was significantly correlated with decreased forced vital capacity (p = 0.027) after controlling for the potential confounding effects of age, height, cigarette consumption history, and employment duration. In contrast, forced expiratory volume in 1 s showed a stronger association with amount smoked (p = 0.022) than with pleural abnormality (p = 0.316). Logistic regression analyses showed that cigarettes act to increase the effect of asbestos in causing pleural disease among exposed workers. Cigarettes, in the absence of significant asbestos exposure, do not appear to cause pleural disease. The authors conclude that construction workers, such as those described herein, have a considerably increased rate of pleural disease, which has functional significance in view of the correlations noted with forced vital capacity measurements. Therefore, pleural disease in asbestos-exposed workers is not only an indicator of exposure but also an indicator of early impairment of pulmonary function.

Adult↗

PubMed1979

Purification and properties of prothrombin modified by asbestos filtration of human plasma.

Filtration through asbestos filter (Seitz) of human plasma modified the prothrombin molecule as previously shown. Factor II could no longer be activated by physiological activators (Ca++ + phospholipid + V and Xa) but reacted readily with staphylocoagulase. The separation and purification of the modified prothrombin allowed allowed the preparation of two fractions: A small slightly modified accessory fraction, "prothrombin-asbestos-1", lost its ability to be activated by physiological activators, and its ability to be adsorbed by barium citrate, but retained the immunological reactivity of fragment 1, as well as the mobility and molecular weight of unmodified prothrombin. A main fraction, "prothrombin-asbestos-2" appeared to be a modified prothrombin which has lost its N-terminal extremity. It was not adsorbed by barium citrate and could not be activated by physiological activators. It possessed a reduced electrophoretic mobility, as well as a reduced molecular weight (39,000), which are properties similar to those of thrombin. Both fractions 1 and 2 were devoid of thrombin activity. Asbestos was thus able to break the prothrombin molecule non enzymatically, the amputation of the N terminal extremity being responsible for the new functional and physicochemical properties of the molecule. Staphylocoagulase appeared not to need the N terminal extremity of the molecule of prothrombin to form the active thrombin-coagulase complex.

Asbestos↗

PubMed1984

Asbestos exposure in Israel: findings, issues and needs.

In Israel, since the 1950s, at least several thousand workers, their wives and children, and possibly many others, have been or still may be exposed to hazardous amounts of airborne asbestos fibers. These are found both in asbestos-based industries (asbestos cement, textiles and brake linings) and trades with asbestos exposure (construction, shipyard repair, boiler maintenance, insulation work). These people are at increased risk for disability or illness, or for premature death from asbestosis, from lung cancer, from exacerbation of preexisting respiratory disease (especially if they smoke), from mesothelioma, from gastrointestinal cancer, and from other malignancies. Although there has been progress, much still has to be done in the areas of legislation, standard setting, exposure control, technology, surveillance, smoking cessation, and medical care and follow-up. Compensation is needed to care for those workers currently or previously exposed, as well as for their families and others at risk. A national policy for protecting and caring for those formerly or currently exposed is indicated by the review of the situation in Israel.

Asbestos↗

PubMed1984

Pulmonary macrophage accumulation and asbestos-induced lesions at sites of fiber deposition.

Inhaled chrysotile asbestos fibers are deposited at alveolar duct bifurcations and subsequently are phagocytized there by pulmonary macrophages. The characteristics of the rapid macrophage response at alveolar duct bifurcations following asbestos inhalation has been further evaluated. Significant numbers of pulmonary macrophages accumulated at sites of asbestos deposition within 48 h after a 1-h exposure, whereas duct surfaces of sham-exposed animals were essentially devoid of macrophages. The influx of macrophages was associated with a significantly increased bifurcation tissue area (p less than 0.025), and this alteration persisted for at least 1 month. Two thirds of the accumulated macrophages from alveolar duct bifurcations could be removed by bronchoalveolar lavage. Macrophages recovered by lavage had significant changes (p less than 0.01) in their morphology and in their phagocytic and chemotactic capacities. These cellular alterations could play a role in the pathogenesis of asbestos-related lung disease.

Animals↗

PubMed1983

Squamous metaplasia of the respiratory tract. Possible pathogenic role in asbestos-associated bronchogenic carcinoma.

Asbestos workers who smoke have a substantially greater risk of developing bronchogenic carcinoma than nonsmokers. Squamous metaplasia often replaces the mucociliary epithelium in the respiratory tract of chronic users of cigarettes. As a result, clearance mechanisms are altered. Using both scanning and transmission electron microscopy, we examined the interaction of chrysotile and crocidolite asbestos with the metaplastic mucosa found in the bronchi of cigarette smokers and produced in cultures of hamster trachea by enriched, serum-free medium. After deposition on the squamous epithelium, both "long" and "short" fibers were either phagocytosed by, or moved between, the cells of the mucosa. The interaction of asbestos with the mucociliary epithelium differed. Most long fibers were cleared, whereas short fibers were taken up by the mucosa. The apparent increase in uptake of long asbestos fibers by the metaplastic squamous mucosa could contribute to the synergism between this unique mineral and cigarette smoke in the causation of bronchogenic neoplasms.

Animals↗

PubMed1983

In vitro suppression of fibroblast growth inhibitory lymphokine production by asbestos.

Human peripheral blood mononuclear leucocytes (PBML) stimulated with concanavalin A (Con A) or phytohaemagglutinin (PHA) produced a soluble factor which inhibits lung fibroblast DNA synthesis and growth. Lymphocyte enriched preparations produced significant growth inhibitory activity in the presence of PHA whereas media from adherent mononuclear cells incubated in the presence of the mitogen did not contain similar activity. This fibroblast growth inhibitory factor (FGIF) was non-dialysable, heat stable and resistant to pH 5. FGIF was also resistant to treatment with chymotrypsin and phosphodiesterase but partially sensitive to treatment with trypsin. Interestingly, there was significant suppression of FGIF production by PBML cultured with PHA in the presence of low concentrations of chrysotile asbestos (5-25 micrograms/ml). In this regard, asbestos (25 micrograms/ml) was not cytotoxic for lymphocytes but had a damaging effect on monocytes as evidenced by the release of lactate dehydrogenase (LDH) a cytoplasmic enzyme, in their culture media. These findings indicate that stimulated lymphocytes have the ability to inhibit fibroblast proliferation by releasing FGIF and that asbestos interfere with this process. Thus, while FGIF may regulate the extent of connective tissue proliferation during normal repair process, suppression of its production by asbestos may contribute to excessive fibroblast accumulation and fibrosis.

Asbestos↗