Asbestos-related diseases constitute a major health problem due to the great number of workers exposed to asbestos.

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Diagram showing Pathogenesis of Pneumoconiosis

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Asbestos includes heterogeneous group of hydrated fibrous silicates.

They conduct heat poorly and are thus important in insulation.

The three major forms of asbestos are crocidolite, which comes mainly from South Africa ; chrysotile, the most common form of asbestos, most of which is mined in Quebec, and amosite.

If coal is the classic example of much dust and little fibrosis, asbestos is the prototype of little dust and much fibrosis.

Most clinically obvious cases occur as a result of the processing and handling of asbestos, rather than in mining, which is a surface operation. Exposure starts with the baggers who package asbestos and continues with those who modify or use it , such as workers who make asbestos products (tiles, cement, insulation material) and those in the construction and shipbuilding industry.           

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Asbestosis:

Classic asbestosis is an interstitial fibrosis of the lung.

The features are in general similar to those in fibrosing alveolitis (usual interstitial pneumonias).

The first lesion is an alveolitis that is directly related to asbestos exposure. Asbestos fibers are long (up to 100 micrometer) but thin (0.5 micrometer to 1 micrometer), so that their aerodynamic particle diameter is small.

They deposit particularly at the bifurcations of alveolar ducts.

The smallest particles are engulfed by macrophages, but many submicroscopic particles lie free in the interstitium of the lung.

The most diagnostic structure is the asbestos body, which consists of an asbestos fiber (10 micrometer to 50 micrometer in length) that has beaded aggregates of iron along its length.

By light microscopy it is golden brown with hematoxylin and eosin and stains strongly for iron. The iron staining derives from hemoglobin liberated from microhemorrhages.     Image Link

The fibers are only partly engulfed by macrophages because they are too large for a single macrophage. The macrophages coat the asbestos fiber with protein, mucopolysaccharides, and ferritin.

The macrophages also release a fibroblast-stimulating factor that promotes fibrogenesis.

In the early stages, asbestosis differ from usual interstitial pneumonia in that the fibrosis occurs in and around alveolar ducts, as well as in the periphery of the acinus.

As the lesion progresses, honeycombing (end-stage lung) results, as in terminal usual interstitial pneumonia.

Asbestosis is usually more severe in the lower zones of the lung.

Pleural thickening is often conspicuous.

Asbestos Bronchiolitis:

Asbestos fibers that deposit in the bronchioles and respiratory bronchioles incite a fibrogenic response in these locations and lead to mild airflow obstruction.

Thus, asbestos produces an obstructive as well as a restrictive defect, the latter being more serious.

At tissue is whether such patients should be regarded as having asbestosis, a term that is usually confined to alveolar wall fibrosis.

The term asbestos respiratory bronchiolitis recognizes this variant.

Pleural Plaques:

Pleural plaques are nodular, localized thickening (2 mm to 3 mm) of the pleura, most often found in the parietal pleura.

The margins are irregular and the size varies from a few millimeter to several centimeters across.

Microscopically they are densely collagenous, with interwoven bands of collagen  (“basket-weave” pattern), and are sometimes calcified.

Pleural plaques are usually an incidental finding in patients with occupational exposure to substantial amounts of asbestos, but such plaques are not uncommon in people with casual exposure.

Asbestos-Induced Pleural Effusion:

In some instances a pleural effusion is the only manifestation of asbestos exposure.

By definition it is not associated with mesothelioma, is benign and self-limiting, and heals up by fibrosis.

Such effusions are clinically significant because the are frequently mistaken as evidence of cancer.

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Carcinoma of the Lung and Other Organs:

Carcinoma of the lung has been reported to be about three to five times more common in nonsmoking asbestos workers than in nonsmoking workers not exposed to asbestos.

In asbestos workers who smoke, the incidence of carcinoma of the lung is vastly increased, the risk being 60 to 80 times greater than in the general nonsmoking population.

 It is claimed by  some that the incidence of carcinoma of the stomach and perhaps the colon is increased by asbestos exposure because fibers are not only inhaled but ingested. 

It has been reported that asbestos may be a possible major cause of malignant lung tumours (including small cell carcinoma, adenocarcinoma ) and brain tumours (i.e. astrocytoma & glioblastoma multiforme).

Asbestos Bodies

Since there are no associated pulmonary lesions, the incidental finding of asbestos bodies in autopsies does not warrant a diagnosis of pneumoconiosis.  Examination of lung tissue reveal that asbestos bodies occur in the lungs in virtually all autopsies.

A revision of criteria for diagnosis of asbestos-related pathological conditions was performed studying specially asbestosis, pleural plaques and malignant mesothelioma, also taking into account the problems connected with histopathology. As regards the histological diagnosis of asbestosis, it requires the presence of diffuse interstitialfibrosis in a well inflated tissue remote from the site of a tumour or other large lesion, plus the presence of two or more asbestos bodies in a 1 cm2 section. As regards the imaging diagnosis, the HRTC 4-point scale proposed by Paris et al. (2004) has been adopted:--0 images not suggestive of interstitial pneumonia;--1 modest unilateral or bilateral interstitial abnormalities, involving restricted areas if bilateral;--2 interstitial abnormalities of limited extent, but consistent with a diagnosis of asbestosis, i.e. honeycombing, even without other parenchymal changes and even though unilateral, or else any two abnormal findings among thickened interlobular septa, intralobular lines or subpleural curved lines;--3 numerous bilateral changes on several slices involving more than 2/3 of the posterior third of each hemi thorax. Only points 2 and 3 were considered consistent with the diagnosis of lung fibrosis. Such HRCT findings are not specific for asbestosis, changes in the pleural wall such as diffuse plaques and thickenings contribute to the diagnosis of asbestosis. As regards the pleural plaques and asbestos bodies we remark that they are merely exposition markers. We also discussed the problems the pathologist may encounter in diagnosing mesothelioma; in this field the prospects are encouraging as microarray analysis are beginning to identify new molecular markers for mesothelioma.

Histopathological diagnosis of pneumoconiosis. J Bras Pneumol. 2006 May;32 Suppl:S99-S112

Asbestos-related diseases constitute a major health problem due to the great number of workers exposed to asbestos over the past 50 years. Personal injury lawsuits against industries that deal with asbestos number in the hundreds, and new cases continue to be filed. The scientific issues related to asbestos are complex, and, although the broad outlines of asbestos-related diseases have been well-established, many significant aspects (such as the pathology involved) are poorly understood. In Brazil, asbestos has been mined commercially since 1940, with production levels recently approaching 200,000 tons/year, resulting in the asbestos exposure of approximately 10,000 workers in the mining activity, and an unknown number of workers in asbestos-cement industry, primarily roofers and concrete rooftop water tank installers. One study, using appropriate methods of scientific investigation to evaluate the effects of such exposure on the health of asbestos mine workers in Brazil was conducted as part of a multicenter study and entitled "Morbidity and Mortality Among Workers Exposed to Asbestos in Mining Activities, 1940-1996". Drawing upon the experience acquired during the course of that study, the objective of the current report was to give an overview of asbestos-related diseases, with a special focus on the difficulties involved in establishing the histopathological diagnosis.

Asbestos as a possible major cause of malignant lung tumors (including small cell carcinoma, adenocarcinoma & mesothelioma), brain tumors (i.e. astrocytoma & glioblastoma multiforme), many other malignant tumors, intractable pain including fibromyalgia, & some cardio-vascular pathology: safe & effective methods of reducing asbestos from normal & pathological areas.Acupunct Electrother Res. 2006;31(1-2):61-125.

High incidences of Small Cell Carcinoma & Adenocarcinoma of the lung, Astrocytoma & Glioblastoma Multiforme of the brain and Mesothelioma of the lung were found in those who had a high accumulation of Asbestos in the eyes and upper respiratory system (nose, larynx, trachea, etc.). When measured non-invasively using the Bi-Digital O-Ring Test (BDORT), brain tumors had the highest concentration of Asbestos (0.2 approximately 2.1 mg BDORT units). Relatively high levels of Asbestos (0.2 approximately 0.6 mg BDORT units) were found in: Squamous Cell Carcinoma of the lungs & esophagus, Adenocarcinoma of the larynx & breast, myelogenic leukemia, arteries of these cancers, left ventricle of failing heart, myocardial infarction, some of the narrowed arteries, varicose veins, cataracts, balding heads, hot flashes, Alzheimer's Disease and Autism. A small, round or ellipsoidal area, with diameter of 5 mm or less, was found near the center of every cancer tissue with a higher level of Asbestos (1 approximately 3 mg), As, Zn, Cr and Se, than in the rest of the tumor; this small area may be where the cancer initiated. Among areas of intractable pain with frequent recurrence and gradual worsening, about 0.2 approximately 0.5 mg BDORT units (or higher) of Asbestos were found. The author found that in the Astrocytoma and many other cancer patients, the optimal dose of DHEA produced very significant reductions of cancer cell telomere from over 1400 ng in the brain tumors (and over 900 ng in other cancers) to close to or less than 1 yg (=10(-24) g), with circulatory improvement by reduction of TXB2. Unlike the standard, widely used treatment with DHEA 25 approximately 50 mg daily, which is an overdose; we only gave one optimal dose (1.5 approximately 12.5 mg) and the beneficial effects usually lasted anywhere between 3-6 months, unless inhibiting factors were introduced. In addition, once one optimal dose of DHEA was given, the amount of Asbestos from these tumors decreased very significantly (30 approximately 99% reduction) with marked increase in urine Asbestos. One optimal dose of special Cilantro tablet reduced more Asbestos than DHEA or (+) Qi Gong Energy Stored Paper. In addition, the application of (+) Solar Energy Stored Paper often reduces 70 approximately 99% of the Asbestos, while (+) Qi Gong Energy Stored Paper reduces 50 approximately 99% of the Asbestos.

Asbestosis. An Sist Sanit Navar. 2005;28 Suppl 1:37-44.

Asbestosis is a diffuse interstitial pulmonary fibrosis, secondary to the inhalation of asbestos fibres. There is a dose-response relationship between exposure to asbestos and the risk of developing asbestosis, in such a way that the greater the exposure, the greater the risk of developing the disease. The time of clinical latency is inversely proportional to the level of exposure. Dyspnoea upon exertion and a dry cough together with end-inspiratory crackles are the most frequent symptoms and signs. Chest radiography is a basic tool in identifying the disease, however high resolution CAT has added greater sensitivity. Tests of the respiratory function show alterations and restrictive ventilations with a reduction of pulmonary spread. Determination of asbestos bodies in BAL is an indicator of exposure, although their absence does not rule out the disease. A histopathological diagnosis is the most reliable, although in the majority of cases the diagnosis is established on the basis of the existence of an antecedent of exposure to asbestos together with suggestive clinical, radiological and functional findings, and a suitable time of latency, without having recourse to a pulmonary biopsy.

Asbestosis. Rev Mal Respir. 1999 Dec;16(6 Pt 2):1294-307.

Asbestosis is a rare pneumoconiosis secondary to inhalation of asbestos fibers. It follows sufficient professional exposures (more than 25 fibers x years/ml). The mean latency is 20 years. Clinical symptoms include exertion dyspnea, crackles and clubbing. Chest radiography the performances of which have been enhanced by the use of the ILO score shows fine reticular or reticulonodular opacities which predominate in pulmonary bases often in association with benign pleural abnormalities. An ILO score equal or higher than 1/1 is suggestive of asbestosis in the context of a compatible professional history. Pulmonary function is typical of diffuse interstitial lung disease. High resolution CT is the most performance investigation in particular in presence of asbestosis either minimal or of recent origin. The diagnosis of asbestosis is based on the professional exposure, a compatible interstitial lung and pleural disease and the exclusion of alternative hypothesis. The diagnosis can be comforted by bronchoalveolar lavage (cytology and biometeorology). Various evolutions are possible: stability, progression to respiratory insufficiency, increased incidence of bronchial carcinoma. Life expectancy is reduced in severe cases. There is no efficient medical treatment. Asbestosis is recognized as a professional disease. A better recognition of asbestosis necessitates a performance policy of depistage in populations with significant present or past exposure and an appropriate diagnostic strategy including high-resolution-CT.

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