Asbestos are naturally occurring fibers that are extremely heat resistant and have superb insulating properties. For decades, these two properties of asbestos have led to its widespread use in the home and industry. Microscopically, asbestos fibers vary from 1-12 microns in size and may be curved (serpentine asbestos) or straight (amphibole). Over the years several subtypes of amphibole fibers have been recognized, namely actinolite, anthophyllite, crocidolite, amosite and tremolite. Of these, chrysotile is by far the most common type of asbestos fiber produced and used in the manufacturing industry. Asbestos was widely used in the industry until reports started to appear in the late 60s that people who were exposed to it were developing severe restrictive lung disease, lung cancer and mesotheliomas. It was not until a decade later that it was finally concluded that asbestos exposure was not benign and hence, its use started to decline in most western countries. In the manufacturing industry, strict guidelines were introduced to limit the levels of asbestos in the environment. Further workers were asked to wear proper garments and masks when working with asbestos related product. The use of asbestos as insulation in the home continued until the late 80s but sporadic reports exist that asbestos can be found in dry wall made in china .
Asbestos exposure in most countries occurs during manufacture of the following products:
Occupations with high risk of asbestosis include the following:
• Car mechanics who work on brake linings and clutches
• Insulation workers
When there is uncontrolled removal of asbestos from the environment studies show that even within a few months, individuals can have very high levels of asbestos fibers in the airways.
Asbestos exposure was significant nearly half a century ago. Almost every country was using asbestos related products and hence many people were exposed to it. By the 1980s, there was awareness of the dangers of asbestos, and thus, the use of asbestos products declined gradually in most western countries. At present, there are no solid data on the number of people somehow exposed to asbestosis. In the USA, experts indicate that there may be less than a few hundred cases of patients presenting with asbestos related lung disease. Strict governmental regulation of use of asbestos products in the home and better means of protecting the worker has significantly reduced the risk of asbestosis development. However, individuals who have been exposed to asbestos in previous decades continue to be at risk for the pneumoconiosis and other related disorders.
In most western countries, the use of asbestosis is strictly regulated. However in developing countries there is evidence that the use of asbestos is not regulated and in fact asbestos related health disease is rapidly increasing. The reason why asbestos continues to be used in developing countries is because it is cheap, readily available and has exceptional insulating properties.
The incidence of asbestosis is variable and greatly dependent on the cumulative dose of inhaled fibers over many years. Those individuals who have high and prolonged exposure tend to have a higher incidence of asbestosis. Every single type of asbestos fiber studied so far has been shown to induce fibrosis of the lung. Inhalation of the crocidolite fibers are also known to cause malignant lesions of the lung and pleura. Fibers which are less than 3 microns tend to induce fibrosis as they are able to penetrate the cell lining. Thicker fibers are incompletely phagocytised and remain in the lung where they continue to generate an inflammatory reaction. Besides influx of inflammatory cells, there is generation of oxygen free radicals which damage the lung enzymes, proteins and endothelial cell lining .
The ability of asbestosis fibers to induce inflammation depends on individual susceptibility, immunological factors and respiratory clearance. Overall, people who tend to smoke have poor airway clearance and are more likely to see progression of disease with asbestosis. Asbestos leads to development of intense fibrosis of the lung, which is most common at the bases. In addition, the ongoing inflammation initiates pleural thickening and plaques.
There is also evidence that some people who are exposed to asbestos fibers of the amphibole type may develop an autoimmune reaction, with generation of autoantibodies. Further research shows that asbestos related lung disease is slightly more common in people who have positive serology for antinuclear antibodies. These patients were also more prone to developing more intense fibrosis of the lung and large pleural plaques, then individuals who were seronegative for anti nuclear antibodies.
The prognosis for most individuals after prolonged exposure to asbestos has to be guarded. The symptoms of asbestosis are not immediate and often present after several decades. However, once the symptoms start, they are progressive and can be debilitating. The majority of patients will develop lung related complications such as:
Risk factors for chronic respiratory insufficiency include:
• Duration and intensity of asbestosis exposure
• Degree of shortness of breath
• Continued use of tobacco
• Combined pulmonary and pleural involvement
• Chest X-ray and CT scan imaging showing honeycombing
• Bronchoalveolar lavage with high number of inflammatory cells
Prolonged exposure to asbestos is known to cause lung cancer and mesotheliomas of the upper respiratory tract (pharynx, larynx), esophagus, kidney and biliary tract. The combination of tobacco and asbestos has a synergistic effect on the development of lung cancer. Individuals who smoke and have asbestosis exposure are at a very high risk for development of lung cancer than people who do not smoke .
Asbestosis, when it coexists with other lung disorders like COPD, emphysema, bronchitis, bronchiectasis or idiopathic fibrosis, can severely worsen the symptoms and worsen the quality of life. Most of these patients develop severe dyspnea and have no exercise tolerance. Asbestosis also worsens the symptoms of asthma and over time, even bronchodilators do not have an effective response.
Many studies have shown that asbestosis has a high morbidity and mortality rate. The disorder leads to premature termination of employment and numerous visits to the hospital.
The presentation of patients after asbestos exposure is not immediate. The symptoms often do not appear for several decades after exposure. This latency may be shortened if the intensity of exposure to asbestosis is high .
The most common presenting feature of asbestosis is dyspnea on exertion, which once started is progressive in nature. Other may also complain of a dry non-productive cough. Presence of a productive cough indicates a concomitant respiratory tract infection. Vague chest pain or discomfort is also a common complaint in patients with advanced disease.
Physical exam may reveal rales which are primarily heard at the lung bases and in the lower posterior area beneath the scapula.
Clubbing of the digits may be seen in 50% of patients but has no correlation to the severity of the disease.
With advanced disease, there will be decreased expansion of the chest that clinically correlates with restrictive ventilatory impairment and reduced vital capacity. Patients with Cor pulmonale may have varying degrees of cyanosis, hepatojugular reflux, jugular venous distension and pedal edema. Most patients with end stage lung disease appear cachectic, out of breath and moribund.
The diagnosis of asbestosis is based on the following:
Pulmonary Function Test
Pulmonary function tests are performed in patients with asbestosis but are not specific. The CO diffusing capacity is decreased and may be the earliest abnormality seen. As the disease advances, the patient will develop reduction in total lung capacity and vital capacity. However, these features are nonspecific and can be seen in many other restrictive lung disorders.
Pulse oximetry will usually reveal hypoxia which may be exacerbated in the presence of right heart failure and cor pulmonale. In the clinic, the pulse oximetry can be performed at rest and during exercise and can quickly reveal the severity of hypoxemia
Bronchoalveolar Lavage and Bronchoscopy
The role of bronchoscopy and bronchoalveolar lavage in making the diagnosis of asbestosis is limited. It is only helpful when trying to make a diagnosis of an infection or determining the cause of a sudden wheeze in an elderly individual. During bronchoscopy, the airways can be lavaged and the fluid is collected to assess the number of asbestos fibers. If there is more than one asbestos body/ml of lavage from the airways, then the probability of high exposure to asbestos is likely. Bronchoscopy should not be used to perform a lung biopsy as the tissue yield is inadequate and false negatives are high.
Lung biopsy is necessary to make the diagnosis of asbestosis and rule out other disorders. In addition, the lung biopsy may reveal the absence or presence of a malignancy. The biopsy specimen is usually viewed under light and electron microscopy and reveal presence of fibrosis and asbestosis bodies. A grading system has been developed to assess the severity of asbestosis related fibrosis. It is important to note that presence of asbestosis bodies alone is not diagnostic for the disorder because sometimes the pathologist may observe these bodies in individuals who have had no exposure or have had only a transient exposure to asbestos
Biopsy of the pleura
Pleural thickening can occur with asbestosis and it is difficult to know if this is a benign or malignant lesion. Hence a biopsy is required. This is usually done in the operating room via an open procedure because the yield from a needle biopsy is not sufficient to make the diagnosis of a malignancy. Even though pleural plaques can occur with several other medical disorders, the presence of plaques and dyspnea should be a good indicator of prior exposure to asbestos.
To prevent asbestosis, one needs to restrict the use of asbestos in the home and workplace. Anyone exposed to asbestos must discontinue all further exposure by either changing the job or home. This is to prevent further exposure and decrease the risk of developing asbestos related lung disease. Unfortunately, once asbestos exposure has occurred, the disease continues even though the exposure had discontinued. Smoking cessation is highly recommended.
Asbestos was a common product once used in the home and manufacturing industry to make a variety of products. However, because of the risk of developing severe lung disease and cancer, the use of asbestos has declined in most western countries. Today, people who work in the manufacturing industry are at the highest risk, but because of awareness and use of appropriate garments and masks, there has been a significant decrease in asbestos associated lung disease. When uncontrolled asbestos exposure occurs, the inhaled fibers can cause severe lung fibrosis and increase the risk of lung and pleural cancer. The patients usually present several decades after the initial exposure. Treatment is immediate cessation of exposure. Besides oxygen, there is no definitive therapy for asbestosis. Patients need to be monitored for life as some may develop right heart failure, severe lung fibrosis and even cancer.
1. Cullinan P, Reid P Pneumoconiosis. Prim Care Respir J. 2013 Jun;22(2):249-52.
2.Gulati M, Redlich CA. Asbestosis and environmental causes of usual interstitial pneumonia. Curr Opin Pulm Med. 2015 Mar;21(2):193-200.
3.Norbet C, Joseph A, Rossi SS, Bhalla S, Gutierrez FR. Asbestos-Related Lung Disease: A Pictorial Review. Curr Probl Diagn Radiol. 2014 Oct 30. pii: S0363-0188(14)00117-0.
4.Bernstein DM. The health risk of chrysotile asbestos. Curr Opin Pulm Med. 2014 Jul;20(4):366-70.
5.Liu G, Cheresh P, Kamp DW. Molecular basis of asbestos-induced lung disease. Annu Rev Pathol. 2013 Jan 24;8:161-87.
6.Campbell K, Brosseau S, Reviron-Rabec L, Bergot E, Lechapt E, Levallet G, Zalcman G. Malignant pleural mesothelioma: 2013 state of the art]. Bull Cancer. 2013 Dec;100(12):1283-93.
7. Dang GT, Barros N, Higgins SA, Langley RL, Lipton D. Descriptive review of asbestosis and silicosis hospitalization trends in North Carolina, 2002-2011. N C Med J. 2013 Sep-Oct;74(5):368-75.
8. Donaldson K, Poland CA, Murphy FA, MacFarlane M, Chernova T, Schinwald A. Pulmonary toxicity of carbon nanotubes and asbestos - similarities and differences. Adv Drug Deliv Rev. 2013 Dec;65(15):2078-86.
9. Prazakova S, Thomas PS, Sandrini A, Yates DH. Asbestos and the lung in the 21st century: an update. Clin Respir J. 2014 Jan;8(1):1-10.