Historical Background:
Asbestos is a group of fibrous magnesium silicate minerals found in nature. These tough fibers are nearly indestructible, being resistant to heat and chemicals, and have incredible insulating characteristics as well as conferring added strength to resins and cement. Because of these characteristics, asbestos has been used extensively in building materials, as well as in heat-resisting fabrics and several different friction products.
Before the 1970’s, common products that asbestos could be found in, were:
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Asbestos cement sheets and pipe products, roofing and siding, casings for electrical wires, fire protection material.
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Asbestos textile products, such as packing components and heat-and-fire-resistant fabrics, including blankets and curtains.
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Automobile products, such as clutch facings, brake linings for automobiles, gaskets and high stress seas.
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Other products, including ceiling and floor tiles; dry and compression packing materials; paints, coatings, fillers and adhesives; reinforced plastic composites; filters; caulking and patching tapes and artificial ashes and embers for use in gas fireplaces.
Pathophysiology:
These minerals are divided into two basic groups: The serpentines, having long curly fibers, which includes Chrysotile (accounting for the majority of asbestos used in the United States) and the amphiboles, having straight, short, needle-like fibers, which include Crocidolite, Amosite, Anthophyllite, Actinolite and Tremolite. Only three have been used commercially: Chrysotile, Crocidolite and Amosite. Chrysotile is white-colored and mined in Canada and Russia. Crocidolite is blue-colored and Amosite is brown-colored, both of which are mined in South Africa and Crocidolite is also mined in Australia. Because of their shape, Crocidolite and Amosite tend to more easily become airborne, and are the smallest of the different asbestos fibers. Generally, the smaller and straighter the fiber, the deeper it can be lodged in the lungs, and the more harmful it is, in terms of causing fibrosis. That is the reason why Crocidolite and Amosite are in theory more likely to cause pulmonary tissue fibrosis than Chrysotile, however, in practice Chrysotile is commonly contaminated with Tremolite and other amphibole types of asbestosis fibers. All asbestos fibers can cause pleural plaquing and parenchymal fibrosis and lead to malignancies. When thin and small enough, the asbestos fibers penetrate the breathing passages and lodge in the lungs. The body tries to destroy these foreign objects, but the fibers, in general, are relatively indestructible (although the immune system can occasionally eliminate Chrysotile) and thus, tissue damage and resultant lung tissue scarring/fibrosis occurs from the fiber irritation, foreign bodies fighting responses and chemical releases by the body. Chromosomal and other yet unknown changes also occur to the lung tissue. The fibers also penetrate the lung tissue and travel to distant locations or remain local and irritate the adjacent linings of the chest walls, diaphragms and mediastinum (parietal pleura) causing pleural plaques. Weeping of fluid into the potential space between the lungs and chest cavity or lobes of the lung can result in pleural effusions and in some cases sticking together for the linings of the lungs and chest cavity resulting in diffuse pleural thickening. The serpentine’s tend to cause more plaquing and the amphiboles tend to cause more lung fibrosis, but either can cause one or the other or both. Asbestos fibers can be caught in the lung mucous and coughed up, but are often swallowed and/or the breathing in or drinking of liquids containing asbestos fibers can deliver these fibers to the GI tract where they can penetrate the walls and irritate the linings of the abdominal cavity (peritoneum). Irritation of the lung tissue resulting in fibrosis (asbestosis) and other factors including cell chromosomal changes without the need for fibrosis and causes still unknown, can result in the evolution of lung carcinoma (cancer of the lung) or mesothelioma (cancer of the pleura – the lining of the lung and chest cavity) as well as potentially other abdominal and retroperitoneal organs and the lining of the abdominal (peritoneal) cavity, the lining of the heart (pericardium) and the lining of the testes (tunica vaginalis). Asbestosis is a term most frequently referring to diffuse, fine, widespread linear irregular/reticular scarring of the lung tissue also called parenchymal or interstitial fibrosis. On chest x-rays, it most frequently causes small irregular opacities of the middle and lower lung zones. The term pleural asbestosis is not used anymore, but rather the term for various types of pleural related and associated scarring is asbestos-related disease including such findings as pleural effusions, pleural plaquing, diffuse pleural thickening, benign fibrotic/cicatricial masses and rounded atelectasis.
Imaging of the Chest in Asbestos Disease:
Three primary imaging modalities are utilized to evaluate the chest in asbestos disease:
1. The chest x-ray – plain chest radiograph.
2. The spiral computerized tomographic scan of the chest (routine CAT or CT scan) and the supine high-resolution, thin slice computerized tomographic scan of the chest (supine HRCT), both without iodinated contrast and both done in the supine position (lying on one’s back).
3. The prone high-resolution, thin slice computerized tomographic scan of the chest (prone HRCT), without iodinated contrast and done in the prone position (lying on one’s stomach).
PET/CT can also be utilized when there is a need to confirm a primary pleural or parenchymal malignancy and/or metastases.
Where Particular Imaging Modalities are Useful:
The PA chest radiograph (CXR) is an overview of the thorax for pleural effusions (fluid between the lungs and chest lining or between sections of the lungs known as the fissures), pleural plaquing (scarring of the chest cavity lining); diffuse pleural thickening (scarring and fusion of the chest cavity and lung linings or scarring and fusion between the divisions or lobes of the lungs, the fissure); mesothelioma (cancer of the pleural linings); asbestosis (scarring of lung tissue) and other interstitial/parenchymal changes including honeycombing, benign fibrotic/cicatricial mass formation, rounded atelectasis, carcinoma (cancer of the lung) and other nodules from metastases (spread of cancer). However, the chest wall (skin, subcutaneous fat, bones and muscles), pleura (linings of the lungs and the chest cavity), hila (chest cavity structures on either side of the heart consisting of arteries, veins and lymph nodes), mediastinum (area of the center of the chest cavity surrounding the heart including the aortic arch, pulmonary arteries, focal fat, lymph nodes and esophagus) and lung parenchyma (lung tissue) are superimposed and thus, findings may be missed due to under calls (false negatives) – such as small plaques or nodules, findings may be overestimated due to over calls (false positives) – such as chest wall fat looking like non-calcified plaques or an individual’s large size, suboptimal strength of the x-ray machine in penetrating large individuals and other artifacts causing the appearance of abnormalities that with improved chest x-ray imaging or CT/HRCT are found not to be present or overlapping structures and findings may be difficult to separate out from one another. Oblique views of the chest allow for additional analysis of the chest walls and regions of the costophrenic angles. The lateral view gives additional identification of the thoracic spine, diaphragms for calcified plaques and the location of nodules or infiltrates.
The supine computerized tomographic scan of the chest without iodinated contrast (spiral CT scan or routine CAT scan) is designed to screen for pleural plaques and their calcifications and differentiate extra-pleural fat from pleural plaques. It also looks for pleural effusions, diffuse pleural thickening, benign fibrotic/cicatricial mass formation, rounded atelectasis, moderate to severe asbestosis, emphysema, pulmonary nodules suggestive of carcinoma and mesotheliomas. Compared with plain radiographs, it is better able to separate out the chest wall, pleura, hila, mediastinum and lung parenchyma for improved delineation of individual findings. It is superior to plain radiographs for the detection of calcification within plaques and in the identification of emphysema and small pulmonary nodules. It cannot determine the presence of mid/low profusion interstitial fibrosis, having the appearance and distribution of asbestosis. Should that be a concern, then prone HRCT is necessary because the supine spiral CT is performed with relatively thick slices (3 mm to 10 mm thick, 3 mm to 10 mm apart, most often, 5 mm thick, 5 mm apart) and in the supine position, leading to dependent density from blood pooling in the posterior aspects of the lungs and dependent gravitationally-caused atelectasis resulting in increased density in the posterior subpleural (adjacent to the chest wall) aspects of the lower lung zones, most often the location of interstitial fibrosis caused by asbestosis. The supine high-resolution, thin slice, computerized tomographic scan of the chest (supine HRCT), due to its thinner slices, can further evaluate the thoracic cavity for details of pleural disease, nodules and emphysema, but still has the same issues as the supine spiral CT relative to dependent density and the resulting inability to screen for mild asbestosis.
The prone high-resolution, thin slice computerized tomographic scan of the chest (prone HRCT) is better designed to evaluate the posterior lung bases for interstitial fibrosis, having the appearance and distribution of mild/low profusion asbestosis, given its thinner slices (0.625 mm to 2.5 mm thick, most often 1.0 mm or 1.25 mm thick). There is improved resolution, but lesser screening for pleural plaques and nodule formation due to skipped areas between slices (often 5, 10 or 15 mm apart), to lessen radiation dosage. Improved emphysema and pleural plaque identification, including their calcifications and pulmonary nodule characterization, if specifically scanned, is afforded by this technique.
Imaging Findings in Asbestos-Caused Disease:
1. Transient Pleural Effusion(s): Fluid accumulates between the lung and chest wall or within the fissure separating parts of the lungs. Benign asbestos-related pleural effusion(s) are often not detected by the patient or doctor, since these can be transient (temporary) and may not cause symptoms (no chest pain or shortness of breath). This pathology, in general, has the shortest latency of the various adverse effects of asbestos exposure. The effusions can be uni or bilateral and tend to recur. This is the most common abnormality seen within 10 years of exposure, although reported up to 58 years after exposure. Its incidence has been reported to be 3% overall in asbestos-exposed individuals, but as high as 7% with heavy exposure. Approximately one half (50%) develop diffuse pleural thickening (sticking together and scarring of the opposing pleural linings), which can cause restrictive impairment in pulmonary function, but which is not usually progressive over time.
2. Pleural Plaquing: This represents scarring of the lining of the chest cavity. The chest cavity and lungs have a lining called the pleura, which is like cellophane wrap. The chest cavity lining called the parietal pleura, where pleura plaques occur, covers the inner sides of the ribs (the chest wall), the diaphragms, the spine, the heart and the mediastinum. Thus, scarring of the parietal pleura most commonly occurs on the lining of the chest walls – in-profile (along the lateral chest wall) and face-on and/or en-face (involving the anterior or posterior chest walls), as well as diaphragmatic (along the tops of the diaphragms); and at other sites including paravertebral (near the midline posteriorly along the spine) – most often on the right side and pericardial (along the heart border) – most often on the left side. Parietal plaquing is also known as circumscribed plaquing and is the most commonly visualized radiographic manifestation of asbestos exposure. The incidence of pleural plaquing supposedly increases with dose, but the type of fiber inhaled, the duration of exposure and the individual’s reaction to such fibers also alter the plaque’s time of appearance, thickness, quantity and extent. They usually take 20 to 30 years from initial exposure to be first identified. The apices, costophrenic angles and the mediastinal surfaces are generally spared. Because asbestos bodies have been identified in parietal pleural plaques, this speaks for a transpleural migration of fibers. Chrysotile is said to be particularly associated with such transpleural migration and as such, with this being the most frequently commercially utilized asbestos product in the USA, is probably the etiology of greater frequency of pleural plaques initially detected prior to or without interstitial fibrosis, although all types of asbestos fibers can cause pleural plaques. Face-on plaquing can have one ill-defined margin when looking at chest x-rays where the plaque merges into the normal pleura. When such face-on pleural plaques are calcified, they have been described as being “holly leaf” or “lace-like” in appearance on chest x-rays.
3. Diffuse Pleural Thickening: The lining covering the lungs themselves is called the visceral pleura. The two linings – the visceral (lung lining) and the parietal (chest cavity lining) pleura have a minimal/potential space between them, which has lubrication and allows the lungs to move in and out and up and down with breathing within the chest cavity, sliding back and forth separate from the ribs. Diffuse pleural thickening has been described as scarring of the visceral pleura (lining of the lung), which I consider a misnomer. In reality, it most often represents scarring and fusion of the chest wall (parietal) to the lung (visceral) pleural linings across the small/potential space between the linings, where sticky fluid from chronic, recurrent asbestos-caused pleural effusions occurred, acting as a glue. However, any sticky fluid occurring between the pleural linings can result in diffuse pleural thickening, including infections resulting in pus, called an empyema or chest trauma/surgery resulting in blood, called a hemithorax. Diffuse pleural thickening results in loss of the freedom of the lung to slide back and forth and up and down, separate from the chest wall and can cause breathing restriction without the need for asbestosis (scarring or the lung tissue and its loss of use). An analogy would be the macadamian nut. It has a hard shell with the nut in the center that freely moves around and sounds like a rattle. If the shell of the nut represents the chest wall with its inner parietal pleural lining and the nut represents the lung with its outer visceral pleural lining, then when there is diffuse pleural thickening, the analogy is that the nut now sticks to the inner wall of the shell and can now longer move freely within the shell – no more rattle – just as the lung is stuck to the chest wall and can no longer freely move up and down and back and forth. An exception to the parietal to visceral pleura fusion cause of diffuse pleural thickening occurs when such pleural effusion(s) extend from between the chest cavity and lung into the fissures (the space between two sections of the lung). Each section of lung is lined by its own visceral pleural lining and these visceral pleural surfaces on either side of the fissure can also fuse across the fissure and scar thicken, resulting in visceral to visceral pleural fusion/scarring. As an analogy, if two birthday presents are wrapped in colorful paper and stacked on top of each other – this is like the two lobes or sections of the lungs being adjacent to each other, with visceral pleura on either side of the space, like the wrapping paper around each present. There is minimal space between the two presents or the two lobes of the lungs. If glue is placed between the two presents, their wrapping paper will stick together just like when sticky pleural effusion fluid causes the two visceral pleural linings of the lobes of the lungs to stick together. The ILO defines diffuse pleural thickening on chest x-rays only when it is in the presence of and in continuity with, an obliterated costophrenic angle (the peripheral lower corner of the lower chest cavity). Costophrenic angle “blunting”, with thickening of the lateral chest wall adjacent to it, is most commonly secondary to prior pleural effusions. On CT, there are various ways of defining its presence – one method offered is if it involves one quarter of the chest wall length or more (taken from chest x-ray observations); another is if the involvement is greater than 8 cm craniocaudally, 5 cm in width and 3 mm in thickness. However, smaller focal areas of fissural or chest wall to lung pleural thickening is not uncommonly observed on CT or HRCT. Diffuse pleural thickening in many cases is associated with linear or curvilinear scar strands (parenchymal bands) extending into the adjacent lung from the pleural surface. When parenchymal bands are clustered together, they can give the visual appearance of a crow’s foot. Such may precede the development of rounded atelectasis, giving it a blurred or fluffy margin compared to the sharply defined margins of parietal plaquing in chest x-rays. Diffuse pleural thickening is frequently associated with restrictive pulmonary function changes, unlike most parietal circumscribed pleural plaques unless they are in great and widespread quantity. Also note, there are causes of visceral pleural thickening without fusion across the potential space, including irregular thickened visceral pleura in advanced interstitial fibrosis of any cause. Coalescence of subpleural nodules in silicosis and coal workers’ pneumoconiosis causes pseudo-plaques that can mimic visceral pleural thickening, but really are not.
4. Benign Fibrotic/Cicatricial Masses: These are areas of focal, thickened subpleural fibrosis, most often associated with diffuse pleural thickening, but do not have to be, are often triangular or rectangular in shape, extending from the pleural surfaces into the adjacent lung, can be singular or multiple and uni or bilateral and are usually smaller than rounded atelectasis. Smaller such scar extensions can also occur off the interlobular fissures and mimic small adjacent nodules.
5. Rounded Atelectasis: These are ovoid or rounded masses often 3.5 cm to 7 cm in diameter – a pseudo-tumor (meaning not really a cancer), usually abutting upon a thickened pleural surface. They are most often associated with diffuse pleural thickening having elongated parenchymal bands grabbing onto, pulling in and collapsing adjacent lung tissue (like extended fingers of the hand folding inward, into the palm) resulting in the appearance of a rounded or ovoid mass, which is pleural-based, often with a whorled appearance frequently called the comet-tail sign, which is the curving of pulmonary vessels and/or bronchi into the edge of the lesion. Unlike many cancers, there is associated volume loss (including fissural displacement). They may be single or multiple, most often in the posterior lower lobes. Although often radiographically stable, they seldom if ever, spontaneously resolve. Less frequently these lesions can be associated with parietal pleural thickening or more atypically without pleural thickening at all, separated from the chest wall by lung tissue. They are benign and do not require surgery and show homogeneous enhancement with iodinated CT contrast. Biopsy or PET/CT may be needed, however, to separate them from a lung carcinoma, if their appearance and location is not classic.
6. Mesothelioma: Diffuse malignant mesothelioma is a deadly cancer involving, most commonly, the pleura (lining of the chest walls and lungs), but in addition, the pericardium (the lining of the heart), the peritoneum (the lining of the abdominal cavity) cavity and the tunica vaginalis (the lining of the testes). In the chest cavity, there is often lobulated, marked thickening of the pleura, including involvement of the mediastinal pleura, associated with a pleural effusion. The pleural thickening can contiguous and encaging or can have skipped spaces between areas of involvement (pleural nodules). Chest wall invasion with rib destruction and fissure extension can also occur. Latency is usually greater than 10 years (with one series reporting 14 to 72 years). Apparently, individuals having a greater intensity of exposure can have a shorter latency time. Classic findings include nodularity to the pleural thickening, pleura that is often more than 1 cm in thickness, which can be circumferential (encasing) involving the mediastinal pleura and an associated pleural effusion. This is in contrast to classic pleural plaques, which are usually flat, 2 mm to 5 mm thick and do not often involve the mediastinal pleura.
7. Interstitial (or Parenchymal) Fibrosis/Asbestosis & the ILO Grading System: Diffuse, fine, scarring of the lung tissue from asbestos fiber exposure in the correct pattern and distribution is called asbestosis. On chest x-rays, this occurs as fine linear irregular or reticular lung scarring (small irregular opacities) involving initially the mid and lower lung zones – classified by the ILO (International Labor Organization) in terms of size and shape, location (upper, middle or lower lung zones) plus profusion (the visual amount of fibrosis per visual unit area). The shape is irregular (linear) as opposed to rounded. The size and shape is classified as either “s”; “t” or “u”, depending on the thickness of the small irregular opacities. The system of grading the size and shape of the small irregular opacities uses a numerator and a denominator, with the numerator (top number of the fraction) representing the main impression of the reading physician and the denominator (the bottom number of the fraction) representing the second choice (the in addition to) of the reading physician; i.e., s/t means that the physician interprets that the primary size and shape of the small irregular opacities as “s”, but there are in addition, but of a lesser amount, “t” small irregular opacities. Location is noted – upper, middle or lower lung zones – most frequently in the middle and lower lung zones. When recording affected zones, all zones with interstitial changes are recorded, regardless of profusion. The profusion or quantity of small irregular opacities noted per visual unit area is determined by comparison to a standard reference set of plain radiographs and is rated as either mild, moderate or severe disease by a numbering system put out by the International Labor Organization (ILO) for international epidemiological purposes – 0 for no disease, 1 for mild disease (previously stated to be associated with normal lung markings, that are still visible), 2 for moderate disease (previously stated to be associated with normal lung markings, that are partially obscured) and 3 for severe disease (previously stated to be associated with normal lung markings, that are usually obscured). The system of grading profusion also uses a numerator and denominator with the numerator (top number of the fraction) representing the main impression of the reading physician and the denominator (the bottom number of the fraction) representing the second choice (tending towards) of the reading physician, i.e., 1/2 means that the physician interprets that the primary diagnosis is mild disease, but on second thought it is tending towards moderate disease. The calculation of the overall profusion on chest x-ray involves reviewing all six lung zones for evidence of interstitial fibrosis. It requires a mental averaging of all of the affected lung zones with one caveat – that one removes from the calculation, those zones having 3 sub-categories or more lesser profusion compared to the zone of greatest/highest profusion (or put another way, those zones that have a profusion in which there are two sub-categories or more between them and the zone of greatest/highest profusion are removed from the calculation). As an example, if a patient had small irregular opacities in both mid and lower lung zones of profusion values 1/1, 1/2, 2/1 and 2/2, then the zone having a profusion of 1/1 is removed from the calculation because it is three sub-categories lower than the 2/2 zone of greatest/higher profusion or because there are two sub-categories between 1/1 and 2/2. The overall average profusion would be 2/1. Another example would be 1/1, 1/2, 2/3 and 3/3. The 1/1 and 1/2 zones would be removed and the overall average would be 3/2. The classification of mild, moderate and severe disease is a visual classification unrelated to the patient’s clinical symptoms or physiologic changes. Asbestosis is related to cumulative dusts exposure. The true interval between the initial exposure and visual radiographic manifestations is variable, usually taking 20 or 30 years to occur, but has been recorded as short as 3 years. Crocidolite, an amphibole, is the most fibrogenic form of asbestos fibers.
Prone HRCT finding begin with Intralobular Interstitial Thickening previously called “Core” changes presenting itself imaging-wise as a) subpleural dots representing peri-respiratory bronchiolar fibrosis, b) short vertical scarring or “short lines” due to scarring of the alveolar walls and septa and as c) hazy opacities, the most visually common finding, due to volume averaging of the peribronchiolar, alveolar wall and septal fibrosis and additional scarring throughout the interstitium of the secondary pulmonary lobule. These mild findings begin most frequently at the posterior lung bases and then progress as moderate disease extending initially upward along the lateral chest walls into the middle lung zones and later as more advanced disease, superiorly into the upper lung zones and finally, anteriorly and centrally. More moderate profusion HRCT findings, in addition to more extensive and denser intralobular interstitial thickening, include bronchiolectasis, non-dependent subpleural line formation, parenchymal bands and with pleural disease, benign fibrotic/cicatricial masses and/or rounded atelectasis. More advanced findings include honeycombing, intrathoracic distortion, more central areas of ground glass opacities and traction bronchiectasis. Fibrosis often progresses even after cessation of exposure. Clinical features include shortness of breath, lung crackles and clubbing. Restrictive pulmonary function deficits develop including lowered vital capacity and lower diffusion capacity.
8. Lung Carcinoma: These are cancers of the lung tissue. Lung cancers occur to a greater extent in individuals with prolonged exposure to elevated levels of asbestos fibers compared to the normal population but can occur with many different levels of exposures. There are genetic, environmental, toxic and fibrotic responses to the asbestos fibers that initiate carcinoma. Although lung carcinoma can be associated with asbestosis/fibrosis of the lung tissue, it does not have to be, as chromosomal or changes still unknown to the lung tissue can occur from the toxic effect of asbestos fibers. The asbestos exposure cancer rate is approximately 5 times the normal non-smoking population. Smoking also can cause lung cancer, but asbestos exposure and smoking exposure together are much more deadly and can cause cancer rate 50 to 100 times the normal non-smoking population.
The above article is provided as a public service by Daniel Powers, M.D.: B-Reader, Board-Certified Diagnostic Radiologist, Certified by the American Board of Radiology.
If you detect any errors, have additional information to point me to, use other useful terms or have comments, please do e-mail them to me at [email protected].
