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Asbestos Related Diseases

Asbestos is a naturally occurring fibrous silicate that was widely used in the past for commercial applications because of its heat-resistance properties. Asbestos exists in several forms. The 2 primary groups of asbestos comprise amphibole and serpentine fibers. Chrysotile (white asbestos) is serpentine and the only form of asbestos that is used commercially at this time, and it accounts for more than 90% of asbestos used in the United States.

For the most part, asbestos exposure has been industrial or occupational and primarily affects workers involved in mining or processing asbestos or those involved in the use of asbestos in the shipbuilding, construction, and textile- and insulation-manufacturing industries. About 2-6 million people in the United States are estimated to have had significant levels of exposure. High exposures ceased in the United States in the late 1970s because of governmental legislation passed after the adverse effects became recognized. However, because the latency period between an initial exposure and the development of most asbestos- related disease is 20 years or longer, asbestos-related disease remains an important public health issue.

The spectrum of asbestos-related thoracic diseases includes benign pleural effusion, pleural plaques, diffuse pleural thickening, rounded atelectasis, asbestosis, mesothelioma, and lung cancer. Asbestosis is defined as diffuse lung fibrosis due to the inhalation of asbestos fibers, and it is one of the major causes of occupationally related lung damage. Mesothelioma is a malignant pleural or peritoneal tumor that rarely occurs in patients who have not been exposed to asbestos.

The diagnostic approach to asbestos-related intrathoracic disease is different from that of other diffuse lung diseases because of the medico-legal implications. The likelihood of asbestos-related disease should be determined, and other possible causes should be eliminated. An assessment of the extent of disease is used to calculate compensation. Therefore, imaging plays a pivotal role in the diagnosis and management of asbestos-related disease.


Fiber size matters. Fibers of 5 μm or more in diameter tend to become deposited in larger airways, in which they are effectively cleared through mucociliary action. In comparison, fibers that are more slender tend to be deposited in small airways or airspaces, from which only a proportion of them are cleared. The effect of fiber length is less certain, but straight fibers that are approximately 5-20 μm long, such as crocidolite fibers, are not cleared as effectively as others are, and they can cause intense inflammation and fibrogenic changes within the interstitium. Crocidolite fibers are the most carcinogenic of all asbestos fibers and had been used in construction prior to the 70’s.

The pleura (outside lining of the lungs) are more sensitive than pulmonary parenchyma (internal lung tissue) to the effects of the fibers. Thus, pleural plaques develop after low, intermittent exposure, whereas asbestosis is associated with cumulative, high-level, long-term, continuous exposure in association with a definite dose-effect relationship. Nonmanual workers in industries involving asbestos, inhabitants of areas immediately surrounding asbestos mills, and families of asbestos workers have an increased incidence of mesothelioma. However, even with significant industrial exposure, asbestosis is unusual.

Pleural plaques are the most common manifestation of asbestos exposure, occurring after a latent period of approximately 20-40 years. A history of exposure can be elicited in more than 80% of patients. The precise pathogenesis of pleural plaques remains undetermined. That they were caused by the mechanical effect of asbestos fibers piercing the visceral pleura (the scratching theory) was assumed. Currently, however, the fibers are believed to be transported to the parietal pleura via lymphatic channels, where they incite an inflammatory response. Plaques slowly grow over time, even after cessation of exposure, but they are not considered premalignant. Asbestosis is rarely seen in the absence of plaques.

Benign asbestos-related pleural effusions are often the earliest manifestation of asbestos-related disease, typically occurring within 10 years of exposure. The effusions are exudative. Occasionally, they are hemorrhagic, but otherwise, their features are nonspecific. Effusions tend to be self-limiting, with a duration of a few months, but they can be chronic or recurrent. The presence of the effusion has been postulated to cause passive atelectasis, with in-folding of the lung resulting in invagination of the adjacent pleura. This process causes tethering, which prevents re-expansion of the lung upon resolution of the effusion and which causes round atelectasis.

Asbestosis is usually seen when levels reach 10 million asbestos fibers per gram of pulmonary tissue. Asbestosis characteristically occurs following a latent period of 15-20 years, with a progression of disease even after exposure has ceased. Fibrosis first arises in and around the respiratory bronchioles, predominating in the subpleural portions of the lung in the lower lobes. This progresses to involve the alveolar walls, eventually causing honeycombing in a minority of patients.

Folded lung (also termed round atelectasis, pulmonary pseudotumor, or Blesovsky syndrome) specifically refers to an area of atelectatic lung adjacent to pleural thickening, with characteristic in-drawing of bronchi and vessels. Blesovsky first reported folded lung in 1966. Although folded lung is strongly associated with asbestos exposure, it may also be seen as a consequence of any inflammatory or infective organizing pleural exudate.

Malignant pleural mesothelioma is a rare neoplasm, accounting for less than 5% of pleural malignancies. Malignant pleural mesothelioma is strongly associated with asbestos exposure, particularly crocidolite exposure, although the association does not appear to be dose- related because significant numbers of cases occur after trivial environmental or household exposure. No relevant history of any asbestos exposure is found in 20% of patients. The disease is frequently seen in the absence of any other manifestations of asbestos exposure and usually develops after a long latent period of 35-40 years.

Mesothelioma is 80% pleural and 20% peritoneal in origin. Pleural effusions are not a precursor of mesothelioma, but they often antedate development of malignancy. A confident diagnosis is often difficult to make and usually requires ultrastructural analysis and histochemical and immunohistochemical tests. Histologically, 3 forms of malignant mesothelioma are recognized: epithelial, mixed, and sarcomatous or mesenchymal. These must be differentiated from mesothelial hyperplasia and metastatic adenocarcinoma. The most common histologic subtype is epithelial, accounting for 50% of cases.

Bronchogenic carcinoma is estimated to develop in 20-25% of heavily exposed asbestos workers. Smoking has a cumulative effect, further increasing the risk of lung cancer to a factor of 90 versus a factor of 5 in exposed nonsmokers. Often, asbestos-related interstitial disease is associated; however, no correlation exists between the severity of asbestosis and the development of lung cancer. Furthermore, lung cancer has been reported in individuals without interstitial lung disease who are exposed to asbestos. A latency period of 25-35 years is usual. Histologically, the predominant subtype is bronchoalveolar cell carcinoma, but adenocarcinoma and squamous cell carcinoma also occur.

Associations between asbestos exposure and other cancers have been reported anecdotally but have not been conclusively determined to be causative. Carcinomas of the larynx, esophagus, stomach, colon, and a variety of lymphoid malignancies have been described.


The number of individuals affected by asbestos- related disease is slowly increasing. However, whether this is secondary to a true increase in incidence or due to increased recognition is debated. The prevalence of benign pleural plaques in the non-asbestos-exposed general population is extremely low. The prevalence in environmentally exposed general populations in industrial societies is approximately 0.5-8%. Frequencies in exposed individuals are 3- 58%, depending on occupation. The development of plaques depends on the length of exposure or the time from first exposure, as opposed to a threshold dose, which is the case for asbestosis. The prevalence of pleural plaques is 10% in exposed individuals 20 years after exposure, rising to 50% after 40 years.

The frequency of benign asbestos-related pleural effusions in exposed individuals is reported to be 3-7%. However, this number may be an underestimate because most patients are asymptomatic; therefore, effusions are subclinical and undetected. The incidence rises with increasing levels of asbestos exposure. Asbestosis is reported to develop in 49-52% of adults with industrial asbestos exposure, after a latency period of 40-45 years. A minimum latency period of 8-10 years is required for an asbestos-related pleural effusion to develop; this is usually the earliest manifestation of asbestos-related disease. Similarly, a latency period of more than 20 years is required for the development of asbestosis. As a result, most patients with asbestos- related disease are older than 40 years. Mesothelioma usually is seen after a longer latency period, with most patients in the sixth-to-eighth decades of life.

Approximately 2000-3000 cases of malignant mesothelioma are diagnosed annually in the United States, or 7-13 cases per million general population. Lung cancer develops in as many as 25% of asbestos workers. In asbestos- exposed nonsmokers, the incidence of lung cancer is 5 times that of the general population. In exposed individuals, smoking further increases the risk of bronchogenic carcinoma by 80-90 fold.

Regarding mortality and morbidity, after the onset of symptoms, severe asbestosis may lead to respiratory failure and death over 12-24 years. Respiratory failure may be accelerated by the development of pulmonary hypertension or malignancy, including lung cancer or mesothelioma. No treatment for asbestosis is effective. The primary strategy is prevention, with the worldwide elimination of asbestos use and with the replacement of asbestos by safe synthetic products. Mesothelioma tends to appear late and is usually associated with an extremely poor prognosis. The median survival is 10 months or less, and most patients die within 2 years.


The clinical picture in benign asbestos-related pleural effusion varies from asymptomatic patients to patients with an acute episode of pleuritic chest pain and pyrexia. Pleural plaques do not cause symptoms per se. However, asbestosis may cause an insidious onset of progressive dyspnea in addition to a dry cough. Clinical findings of basal inspiratory crackles associated with reduction in vital capacity and diffusion capacity are also seen.

Asbestosis is usually diagnosed on the basis of certain clinical, functional, and radiographic findings outlined by the American Thoracic Society (ATS). However, these guidelines have not been updated since the routine clinical use of high- resolution CT (HRCT) scanning began in the early 1990s. Findings based on the ATS criteria include the following: reliable history of nontrivial asbestos exposure; Appropriate interval between exposure and detection (usually >10 y); abnormal chest radiographic findings; restrictive lung disease as indicated by pulmonary function test results; abnormal diffusing capacity; bilateral crackles at the lung bases that are not cleared by coughing. Regarding malignant mesothelioma, clinical symptoms are frequently present 6-8 months prior to diagnosis. Symptoms include localized chest wall pain and weight loss. Cough and dyspnea may also be present.

Staging of Malignant Mesothelioma:

Stage Ia – T1a, N0, M0

Stage Ib – T1b, N0, M0

Stage II – T2, N0, M0

Stage III – Any T3, M0; any N1, M0, any N2, M0

Stage IV – Any T4, any N3, any M1

T means tumor location and degree of tissue involvement.

N means lymph node involvement, which ones, how many.

M means metastases or not.

Imaging and Other Testing:

HRCT (high resolution CT of the chest) plays an increasingly important role in the diagnosis of diffuse interstitial lung disease. CT is now established as the criterion standard in the evaluation of pleural disease. Recent developments in HRCT have made it an invaluable tool in the assessment of asbestosis. Scanning the patient in both the prone and supine positions increases sensitivity and specificity.

Plain chest radiography, however, is the initial modality for the detection and characterization of pleural and parenchymal disease. The limitations of chest radiography in the diagnosis and evaluation of asbestos-related disease are well recognized. The quality of the radiograph and the size, shape, position, and degree of calcification determine whether the radiologist can detect pleural plaques on the image. While the identification of bilateral scattered calcified costal and diaphragmatic pleural plaques is virtually diagnostic of asbestos exposure, studies have shown an 11% false-positive rate with chest radiographs. In particular, extrapleural fat mimics pleural thickening and is a significant cause of false-positive readings. Conversely, a high false-negative rate has also been reported. CT scans has long been known to be more sensitive and specific than chest radiographs for the diagnosis of asbestos-related pleural disease.

Medical Care:

Control of asbestos in the workplace is the most effective method for preventing asbestos-related diseases. Cessation of further exposure to asbestos once the diagnosis of asbestosis is made is imperative because further exposure increases the rate of progression. A small minority of people (10-20%) have progressive disease after cessation of exposure. Smokers should be advised to quit smoking. Patients should be informed on the work-related causation of the disease (potentially compensable) and report it to appropriate state or federal agencies.

Assessment of disease severity and functional impairment are important in tailoring a treatment and follow-up plan (i.e.: frequency of clinic visits, chest radiographs, pulmonary function testing). Treatment requires prompt attention to respiratory infections and immunizations against influenza and pneumococcal pneumonia. Antibiotics should be used when appropriate and supplemental oxygen should be added as needed. In advanced cases palliative care should be provided for the relief of distressing symptoms. Because of the likelihood of bronchogenic carcinoma, the patient should consult a thoracic surgeon if a solitary pulmonary nodule develops in a patient with asbestosis.

Complications of include: pulmonary hypertension, cor pulmonale, right heart failure, progressive respiratory insufficiency, and malignancy. It is important to keep in mind that there is a higher risk of lung carcinoma in patients with asbestosis. Patients with asbestosis are also at higher risk for malignant mesothelioma and carcinomas of upper respiratory tract, esophagus, biliary system, and kidney.

Medical/Legal Concerns:

The association between exposure and disease is the essential factor in establishing causation. Diagnosis, causation, and impairment are the major issues with regard to establishing medical negligence.

Determining the cause depends on assessment of the levels and duration of exposure and on knowledge of occupational epidemiologic studies. Assessment of impairment, which is a key ingredient in determining disability, is based mainly on pulmonary function studies. One important caveat is that no evidence exists to confirm that small airway disease, which is detected by flow volume curves, progresses to asbestosis. Also, pleural plaques may coexist with asbestosis, but pleural plaques alone are usually not associated with impaired pulmonary function. Nonetheless, pleural plaques are a reliable indicator of asbestos exposure.

Physicians often make the diagnosis without histopathologic confirmation. Errors may occur because other more common interstitial diseases (e.g.: idiopathic pulmonary fibrosis) mimic the clinical, radiologic, and pulmonary functional features of asbestosis. Bear in mind the long latency period between patient exposure and the manifestation of symptoms and signs of asbestosis. When lung tissue is available for histopathologic examination, confirmation of diagnosis requires both fibrosis and accumulation of asbestos bodies or fibers.

Compensation for asbestos-related diseases is frequently awarded for bilateral diffuse pleural thickening, asbestosis, malignant mesothelioma, and bronchogenic carcinoma in the presence of asbestosis.

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