Asbestos-related diseases constitute a major health problem due to the great number of workers exposed to asbestos.
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 workers 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.
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. This dumbbell-shaped structure 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.
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 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 are nodular, localized thickening (2mm to 3mm) 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.
Mesothelioma: Visit: Mesothelioma Online
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 and glioblastoma multiforme).
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.
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.
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