What is Asbestosis?

The following article is provided as a public service of Daniel Powers, M.D.:
B-Reader, Board Certified Diagnostic Radiologist, Certified by the American Board of Radiology.

Asbestos is a naturally occurring group of magnesium silicate minerals that are made up of tiny microscopic fibers. 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.

There are six different types of asbestos: Crocidolite, Amosite, Anthophyllite, Tremolite, Actinolite and Chrysotile. However, only three have been used commercially: Amosite, Crocidolite, and Chrysotile. Chrysotile is white-colored, and mined in Canada and Russia. Crocidolite is blue-colored, while Amosite is brown-colored. Both are mined in South Africa, and Crocidolite is also mined in Australia. Chrysotile fibers are curled, relatively long, and small in diameter, and are part of a group known as serpentines, while all other types of asbestos, are part of a group known as amphiboles, which are straight needle-like crystals, varying in diameter. 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. That is the reason why Crocidolite and Amosite are more harmful than Chrysotile. The human immune system can also more easily eliminate Chrysotile.

Before the 1970’s some common products that asbestos could be found in were:

  • Asbestos cement sheets and pipe products, roofing and siding, casings for electrical wires, fire protection material.
  • Asbestos textile products, such as packing components, and heat- and fire-resistant fabrics, including blankets and curtains.
  • Automotive products, such as clutch facings, brake linings for automobiles, gaskets and high stress seals.
  • Other products, including ceiling and floor tiles; dry and compression packing materials; paints, coatings, filler in adhesives; reinforced plastic composites; filters; caulking and patching tapes; and artificial ashes and embers for use in gas- fired fireplaces.

The three primary imaging modalities utilized to evaluate the chest in asbestos disease are:

  1. The Chest X-Ray – plain chest radiograph.
  2. The spiral computerized tomographic CAT or CT Scan of the Chest without iodinated contrast done in the supine position (lying on one’s back).
  3. The high resolution, thin-slice computerized tomographic HRCT Scan of the Chest done in the prone position (lying on one’s stomach).


The PA upright chest x-ray (CXR) gives an overview of the thorax for effusions, pleural plaquing, diffuse pleural thickening, interstitial/parenchymal changes including honeycombing, plate-like atelectasis, cicatricial scarring, rounded atelectasis and nodules or other masses. However the chest wall, pleura, hila, mediastinum and lung parenchyma are superimposed and thus, findings may be missed, underestimated or overlapping and difficult to separate out from one another. Oblique views of the chest allow for additional analysis of the chest walls.

The supine computerized tomographic scan of the chest without iodinated contrast (spiral CT scan) is designed to screen for pleural plaquing and differentiate extra-pleural fat from pleural plaques. It also looks for pulmonary nodules suggestive for carcinoma, rounded atelectasis, mesotheliomas and pleural effusions. 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. Should interstitial fibrosis be a concern, then prone HRCT would be necessary because the supine spiral CT scan is performed with relatively thick slices (5 mm to 7 mm thick, 5 mm to 7 mm apart) and in the supine position, leading to dependent density from blood pooling in the posterior aspects of the lungs and from dependent atelectasis resulting in increased density in the areas most often the location of interstitial fibrosis caused by asbestosis.

The prone high resolution, thin slice computerized tomographic scan of the lungs (HRCT) is designed to evaluate the chest for interstitial fibrosis, given its thin slices (1.0 mm to 1.25 mm thick). There is improved resolution, but lesser screening for pleural plaque and nodule formation due to skipped areas to lessen radiation dosage. Improved pulmonary nodule characterization, if specifically scanned, is afforded by this technique.


Asbestos is a fiber-like group of minerals found in nature with very good insulating and heat resistant properties. These are fibrous silicate minerals and are divided into two basic groups: the serpentines, having long curly fibers which includesChrysotile (90% of asbestos used in the United States) and amphiboles, having straight, short, needle-like fibers which includes Crocidolite, Amosite, Anthophyllite and Tremolite. Unfortunately, asbestos has a fiber-like shape and when thin and small enough can penetrate the breathing passages to lodge in the lungs. The body tries to destroy these foreign objects, but the fibers are relatively indestructible and thus, tissue damage and resultant lung tissue scarring occurs from the fiber irritation, foreign body fighting responses and chemical releases by the body. The fibers also penetrate the lung tissue and travel to distant locations or remain local and irritate the adjacent linings (pleura) of the lungs (visceral pleura) and the chest walls, diaphragms and mediastinum (parietal pleura). The serpentines tend to cause more plaquing and the amphiboles tend to cause more lung fibrosis. Asbestos fibers can be caught in the lung mucous and coughed up, but are often swallowed 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 lining of the abdominal cavity (peritoneum). Irritation and others factors still unknown, can result in the evolution of cancer of the lung or pleura (lining of the lung and chest wall) as well as potentially other abdominal organs and the lining of the abdominal (peritoneal) cavity and the lining of the heart (pericardium). Asbestosis is a term most frequently referring to diffuse, fine and widespread linear irregular/reticular scarring of the lung tissue also calledparenchymal or interstitial fibrosis. The term pleural asbestosis is not often used anymore, but rather the term asbestos-related disease including such findings as pleural plaquing, diffuse pleural thickening, pleural effusions, rounded atelectasis and cicatricial scarring are more frequently used.

The following are major findings looked for in asbestos-caused diseases:

    1. Transient Pleural Effusions: Fluid on the lung.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 period 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 which does cause some restrictive impairment in pulmonary function, but which is not usually progressive over time.
    1. Pleural Plaquing: Scarring of the chest wall.The chest wall and lungs have a lining called the pleura, which is like cellophane wrap. The lining covers the inner sides of the ribs (the chest wall), diaphragms and mediastinum and is called the parietal pleura. There is also lining covering the lungs themselves, called the visceral pleura. The two linings result in a space between them, which has lubrication and allows the lungs to move in and out and up and down with breathing, sliding back and forth, separate from the ribs.
      1. Parietal Plaquing – Means scarring to the parietal pleura in profile (along the lateral chest wall) or en face (on end or face on) involving the anterior or posterior chest walls. Such circumscribed plaquing can also be seen on top of the diaphragms (diaphragmatic plaquing); along the heart border (pericardial plaquing) – most often on the left side; or near the midline along the spine (paravertebral plaquing) – most often on the right side. These are the most common visualized radiographic manifestations of asbestos exposure. The incidence increases with dose. They usually take 20 to 30 years from initial exposure to be first identified. The apices, costophrenic angles or sulci and mediastinal surfaces are generally spared. Because asbestos bodies are identified in parietal plaques, this speaks for a transpleural migration of fibers. Chrysotile is 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 the greater frequency of pleural plaques initially detected prior to or without interstitial fibrosis. En face plaquing can have one ill-defined margin – where the plaque merges into the normal pleura. En Face calcifications have been described as being “holly leaf” or “lace-like”.
      1. Visceral “Diffuse Pleural Thickening” – Means scarring to the visceral pleura, but in addition, fusion often occurs across the space between the parietal and visceral pleura. This usually occurs secondary to chronic, recurrent asbestos-caused pleural effusions (but can also occur with infections or chest trauma). It can involve a lung fissure (the space between two sections of a lung). The lungs are composed of different sections or lobes and each lobe is covered with visceral pleura – like birthday presents wrapped in colorful paper, stacked on top of each other – meaning that between the two lobes there is a fissure or space with visceral pleura on either side of the space. The visceral pleural surfaces can become scarred and thickened – either on one side or the other or both and the scarring on both sides may fuse across the fissure or space. The ILO defines diffuse pleural thickening 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 is if it involves ¼ of the chest wall length or more (taken from chest x-ray observations); another is if involvement is greater than 8 cm craniocaudally, 5 cm in width and 3 mm in thickness. Visceral pleural thickening on CT/HRCT is associated with fibrous strands extending into the underlying lung, giving it a blurred or fluffy margin (compared to the sharply defined margins of parietal plaquing). Coalesced subpleural nodules in silicosis and coal workers’ pneumoconiosis can form pseudoplaques and can mimic visceral pleural thickening. Diffuse visceral pleural thickening is frequently associated with restrictive pulmonary function changes, unlike most parietal circumscribed pleural plaques.
    1. Interstitial (or Parenchymal) Fibrosis – Scarring of the lung tissue.This occurs as fine linear, irregular or reticular lung scarring (small irregular opacities) involving initially the posterior aspects of the mid and lower lung zones – classified on the ILO (International Labor Organization) form 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 is classified as either “s”;, “t” or “u”, depending on the thickness of the linear densities. The location is noted – most frequently in the middle and lower lung zones. When recording affected zones, all zones with interstitial changes are recorded, regardless of profusion. Theprofusion or number of linear lines noted per visual unit area is determined by comparison to a standard reference set of 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 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 of the reading physician, i.e., 1/2 means that the physician feels that the primary diagnosis is mild disease, but on second thought, it is tending towards moderate disease. The calculation of the overall profusion on a 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 3 sub-categories lower than the 2/2 zone of greatest/highest profusion or because there are 2 sub-categories between 1/1 and 2/2. The overall averaged 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 dust exposure. The time interval between the initial exposure and visual radiographic manifestation is variable, usually taking 20 to 30 years to occur, but has been reported as short as 3 years. Crocidolite, an amphibole, is the most fibrogenic form of asbestos fibers. Intralobular Interstitial Thickening begins adjacent to the respiratory bronchioles (subpleural dots and branching structures representing peribronchiolar fibrosis) and spreads to the alveolar walls, septa and then throughout the entire secondary pulmonary lobule (as hazy or ground glass opacities). Fibrosis may progress 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 lowered diffusion capacity.
    1. Rounded Atelectasis – An ovoid or rounded mass, often 3.5 cm to 7 cm in diameter – a pseudo-tumor, meaning not really a cancer, usually abutting upon a thickened pleural surface. It is caused by pleural and/or chest wall scarring, grabbing onto, pulling in and collapsing adjacent lung tissue.These lesions most commonly occur due to visceral pleural thickening associated with adjacent coarse parenchymal (lung tissue) scarring which grabs and folds in the adjacent lung tissue and gives the appearance of a rounded or ovoid mass, which is pleural based, often with a whorled appearance also known as the Comet-Tail Sign = curving of pulmonary vessels or bronchi into the edge of the lesion. Unlike many cancers, there is associated volume loss (including fissural displacement). Less frequently these lesions can be associated with parietal pleural thickening or more atypically without pleural thickening, separated from the chest wall by lung tissue. These lesions are benign and do not require surgery. They may be single or multiple, most often in the posterior lower lobes. Although often radiographically stable, they seldom if ever, spontaneously resolve. They show homogeneous enhancement with iodinated CT contrast.
    1. Lung Carcinoma – 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. The asbestos exposure cancer rate is approximately 5 to 7 times the normal non-smoking population. Smoking also can cause lung cancer, but asbestos exposure and smoking together are much more deadly and can cause cancer rates 50 to 100 times the normal non-smoking population.
    2. Mesothelioma – Diffuse Malignant Mesothelioma is a deadly cancer involving the pleura (lining of the chest wall and lungs) the pericardium (the lining of the heart) and the peritoneum (the lining of the abdominal [peritoneal] cavity). There is often lobulated, marked thickening of the pleura associated with a pleural effusion. Latency is usually greater than 10 years (with one series reporting 14 to 72 years). Apparently the patients 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 associated with a 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. A malignant mesothelioma can extend into the interlobular fissures, interlobular septa, pericardium, lung parenchyma and abdominal cavity.
      1. Plain Chest X-rays:The ILO classification of pneumoconioses is used worldwide for epidemiologic research, screening and surveillance and it is based solely upon the PA upright (“posteroanterior” or frontal) chest radiograph. Its purpose is to codify plain radiographic abnormalities of pneumoconioses (occupational dust and fiber exposure) in a simple reproducible manner. The ILO provides a set of standard radiographs showing various disease states and their classification as well as a written definition of abnormalities and symbols, which were most recently updated in 2000. It does not take into account the lateral or oblique chest x-ray views. These views however, add to the verification of pleural plaquing and improved visualization of the calcifications in them and to the localization and verification of parenchymal nodules. The chest x-ray is the number one screening tool for asbestos disease, when appropriate exposure levels and duration, plus time from exposure has occurred.Problems with Interpretation of Chest Radiographs include:
          1. Variations in Technique Can Affect Readings:Overexposure (dark images) can under-estimate lung disease and underexposure (light images) can over-estimate lung disease and obscure in-profile pleural plaquing.
          1. Both Intra- and Inter-Observer Errors are Frequent:This is especially true in low profusion disease. Intra-observer error is where the same doctor reads the film at two different times and gives two different opinions. Inter-observer error is where two separate doctors read the film differently. Experienced B-readers (individuals who have trained and passed the federally administered examination on pneumoconiosis) tend to be less influenced by changes in radiographic technique and be more consistent over time from reading to reading. Thus, inter-observer error would presumably be less with experienced B-readers interpreting chest x-rays on individuals with moderate to severe disease. Unfortunately, with low profusion disease, there is much intra- and inter-observer error regardless of the experience of the individual although, experienced individuals tend to be more consistent and less problematic.
          1. Inaccuracy of the Chest Radiograph Due to Overlapping Structures:The chest radiograph is a composite of the entire thickness of the chest and thus, overlapping breasts, other chest wall soft tissues, poor inspiratory effort with crowding of vascular structures, muscle slips around the lateral chest wall, etc., can all influence the appearance and interpretation of plain radiographs. Plaquing and interstitial fibrosis can be missed or not seen. Supine spiral CT is more accurate in diagnosing pleural plaques and their calcifications and in identifying pulmonary nodules/cancers because the overlapping structures are not a consideration. Prone HRCT is more accurate at showing low profusion interstitial disease. CT or HRCT however, do not provide the overview that plain radiographs render, are more costly and result in a higher radiation dose to the patient.
          1. Chest Wall Thickening is Non-Specific:Muscle slips, extra-pleural chest wall fatty deposition and plaquing can all look similar. Calcification makes for a more definitive diagnosis of plaquing. Focal and asymmetric appearances are more probably due to be plaquing, although fat can look similar. CT or HRCT can in most cases differentiate fat from plaques and are more sensitive to detecting calcium deposits within the plaques.
          1. Confusion and Limitations to the ILO Classifications of Plaques:Classification of plaquing under the ILO system is very confusing to the individual reader and has been inconsistently applied. On one hand, it is very detailed, asking whether the disease is in-profile, en face or diffuse and whether or not calcified or non-calcified plaques exist. On the other hand, it is non-specific and confusing in that it is difficult to judge from the answers where exactly the plaques are and to what extent they are influencing the patient’s physiology.
          1. Non-Specificity of Interstitial Patterns:Interstitial disease can be acute or chronic and due to multiple causes. Multiple sequential chest x-rays and/or the patient’s history are necessary to determine if the interstitial changes are chronic suggesting fibrosis and whether or not progression, i.e., an increased profusion of the interstitial findings has occurred over time. Asbestosis – scarring of the lung tissue (interstitial or parenchymal fibrosis) is frequentlybilateral, linear and irregular (not nodular) and most frequently involves the posterior mid and lower lung zones. This diagnosis is more definitive, when there are pleural plaques (scarring of the chest walls and lung surfaces – pleural fibrosis) present. However, at the recent 2004 ACR Symposium on Radiology of the Pneumoconioses, it was stated that 11 to 14% of patients with a clinical diagnosis of asbestosis, having evidence for interstitial fibrosis on plain radiographs did not have associated pleural plaques on chest x-rays. Other authors have put this figure as high as 20%. Included in the differential diagnosis is Idiopathic Pulmonary Fibrosis. Also, diffuse lung fibrosis occurs in 10 – 20% of coal miners. A reticular, coarse interstitial fibrotic pattern occurs at the lung bases often associated with honeycombing, volume loss and traction bronchiectasis. This entity may or may not be associated with small rounded opacities (centrilobular and subpleural) and has a higher incidence of lung carcinoma.
        1. Emphysema Can Mimic Asbestosis on Chest X-rays:Mild to moderate interstitial disease appearance on chest x-rays in smokers can represent emphysema(lung holes) rather than lung scarring. Often when these holes expand, the lung tissue about their perimeters becomes compressed and thus, more dense (or alternatively the holes become less dense and the surrounding normal lung looks more dense). The collapsed areas of lung tissue found along the perimeter of the emphysematous holes are additive and on the chest x-ray and appear as fine linear stranding which can lead to a false positive reading on chest x-rays for asbestosis. Spiral CT can easily demonstrate emphysematous holes and prone HRCT can separate out emphysematous holes from fibrotic interstitial changes as the cause of the perceived linear densities on plain radiographs. Of course, both emphysematous holes and interstitial fibrosis due to asbestosis may co-exist and thus, the need for prone HRCT.
      2. Computerized Tomographic Scan Without Iodinated Contrast (Supine Spiral CT):
        Computerized tomographic scanning of the chest without iodinated contrast (supine Spiral CT) is more sensitive than plain radiographs in detecting the presence or absence of plaquing with or without calcification and in judging whether or not emphysema or lung cancers are present. Increased accuracy concerning smaller anatomy including the interstitium can be obtained by utilizing a high-resolution software image-processing program called a high spatial frequency algorithm (“bone” algorithm on the General Electric System Scanners). Today multi-detector scanners allow very rapid acquisition of the image data, lessening the chance for respiratory motion artifact, blurring the images or non-sequential (not in continuous order) image slice presentation.Usually plaquing vs. fat is easy to distinguish, although occasionally subtle thickened normal variant endothoracic fascia, internal intercostal muscles or the fatty deposition’s inner edge artifact are hard to fully differentiate from thin plaquing. Thin plaquing is best identified along the inner margin of a rib (rather than between ribs where the endothoracic fascia or internal intercostal muscle can be confused for plaquing). To the untrained reader, paravertebral vascular structures (blood vessels) can appear as plaques as well. The CT scan, however, is more sensitive than plain chest x-rays in the detection of plaque calcifications, which are more definitive, if not close to pathopneumonic for plaquing (Exceptions include plaquing with or without calcifications caused by non-asbestos fibrous minerals including Erionite from Turkey and Sepiolite from Bulgaria, pleural scarring with or without dystrophic calcifications from a prior infectious empyema and/or rib fractures, and pseudo- plaquing with or without calcifications caused by the coalescence and fusion of subpleural nodules found in silicosis and coal workers’ pneumoconiosis). Also, the axial cross sections of CT allow for identification of the number of plaques present, and their size and locations – including chest wall, diaphragmatic, paravertebral, pericardial, mediastinal and interlobular fissure based.In regard to lung cancers, oftentimes, small nodular lesions are missed or obscured on plain chest radiographs, which are better identified by CT. This means that CT can detect early lung cancers better than chest x-rays and hopefully result in more rapid treatment and a prolongation of the patient’s life. Unfortunately, however, CT is so sensitive that it often picks up very small nodular densities that can represent most often granulomas (scars due to old infections) or normal variant intrapulmonic lymph nodes (structures that help fight infections). This becomes problematic, since a small nodular lesion in an individual exposed to asbestos could theoretically represent an early cancer and thus, more and more sequential CT and/or HRCT follow-up is often obtained for 3 to 5 years, to rule out slow growing cancers. The initial recommendation of scanning every three months has been modified by some, due to the great expense (20 scan over 5 years) and the substantial radiation dose, which has its own cancer risks.

Problems with Supine Spiral CT

      1. :
        1. Dependent Density Prevents the Evaluation of the Lung Parenchyma (Tissue) for Interstitial Fibrosis: When the patient lies supine (on his/her back) the blood tends to pool or collect along the back of the lungs and the lungs in part can minimally collapse (dependent atelectasis), causing a hazy density similar to lung fibrosis. Since most of the asbestosis scarring, is in the posterior mid and lower lung zones, the patient must lie prone to take this haze (false positive) effect away.
        2. Thick Slices Limit the Evaluation of the Lung Parenchyma (Tissue) for Interstitial Fibrosis: The slice thickness is most commonly 5 mm to 7 mm on today’s spiral CT scanners. This compares with the thinner slices of HRCT which are usually 1 mm to 1.25 mm thick – corresponding to a cut section of lung looked at visually in a laboratory. Thus, thicker slices volume average, overlap and merge findings making them harder to see.
        3. No Iodinated Contrast Utilized: The use of such contrast is usually not necessary for the purposes of the identification of plaques, emphysema, nodules and other lung and chest wall masses. In addition, iodine contrast can result in allergic reactions, as severe as death. Abnormal masses or fullness in size to the lymph nodes in the hilum or mediastinum, should they occur, would need follow-up and at that time in such a situation, a contrast study could be obtained.
      1. High Resolution, Thin-Slice Computerized Tomographic Scanning (Prone HRCT):This study is utilized primarily to evaluate the interstitium (lung tissue) usually in the prone non-dependent position. This allows for visualization of the posterior lung bases – the area of interstitial fibrosis (lung tissue scarring) location most common in asbestosis, without interference from gravitational dependent density – from blood pooling or dependent atelectasis. It is also better than supine spiral CT in the identification and classification of emphysema. Thin collimation 1.0 mm to 1.25 mm thickness and high spatial frequency algorithm give more detail than thicker standard supine spiral CT images.
    1. CT/HRCT Findings Related to Interstitial (Parenchymal) Fibrosis (Lung Scarring) include:
      1. Intralobular Interstitial Thickening(also called and composed of intralobular/core changes, subpleural dots or branching structures, centrilobular thickening or nodules, intralobular lines, pleural based nodular irregularities, subpleural hazy densities, patchy areas of ground glass opacity or hazy patches of increase attenuation)
      2. Interlobular Septal Thickening(also called Thickened Interstitial Short Lines)
      3. Non-dependent Curvilinear Subpleural Line Formation
      4. Parenchymal Banding
      5. Cicatricial Scarring (also called Focal or Benign Fibrotic Masses)
      6. Rounded Atelectasis
      7. Honeycombing

      Secondary findings include volume loss, distortion of intrathoracic contents, plate-like atelectasis and traction bronchiectasis.

Emphysema is also better identified. The high resolution, thin-slice CT or CAT Scan (HRCT) utilizes thinner slices, i.e., a 1.0 mm to 1.25 mm slice thickness compared to a standard CT or CAT Scan image utilizing a 5 mm to 7 mm slice thickness. Also, high resolution software processing gives sharper images (“bone” algorithm on the GE system). These thin slices are spaced over the entire lung. The study is done in the prone position to look at the posterior lung bases without dependent density (increased density caused by gravitational accumulation of blood and dependent atelectasis – collapse of lung).

The HRCT study is more definitive at showing plaquing with and without calcifications. However, given the potential of a higher radiation dose when utilizing markedly more slices, spacing is used between the thin slices (for example: 1 mm or 1.25 mm thick slices, 10 mm to 15 mm apart) to limit the radiation dose and as such, not all of the lung and chest wall are imaged and skip areas result. Significant plaques or nodules can therefore be overlooked. The HRCT study is also very useful for viewing of lung masses in evaluating the contour of the mass and whether or not visible calcification can be identified (central, ring-like or homogenous – throughout the nodule calcification usually represents a benign – non-harmful scar/granuloma rather than a malignant – harmful cancer). However, to be effective, it is important that the nodule location be known, to obtain specific slices over the suspect nodule (rounded lung shadow).

  1. Problems with HRCT:
  2. No Firm Agreement on a Grading System: There is no agreement how to quantitate and whether or not a certain concentration (profusion) or visual amount of interstitial findings are necessary to be indicative of a significant anatomic or physiologic disease state.
  3. Non-Specificity of Interstitial Findings: Many diseases cause interstitial fibrosis. The fine irregular (linear) interstitial changes seen at the posterior lung bases most commonly occur with asbestosis in the properly exposed individual, however, other etiologies are possible, the most common of which is idiopathic pulmonary fibrosis (IPF) – scarring of unknown cause. The presence of pleural plaques makes more probable an asbestos cause.

Smoking is a controversial area. “Dirty Lungs” have been described in smokers and scattered, very low profusion (low amount) of visualized interstitial changes have been seen in individuals that have smoked, that have not been exposed to asbestos. However, the etiology of these interstitial changes and their relationship to smoking is often not clearly linked. The study groups of smokers without asbestos exposure were not always historically reliable (meaning asbestos exposure may have occurred due to having worked doing demolition/construction or being homeless, at times sleeping under insulated pipes (in which the insulation was torn open) or being exposed to airborne asbestos fibers around industry, the military or at construction sites).

Multiple Disease States Can Cause Interstitial Thickening Including, but Not Limited To:

  1. Pulmonary Fibrosis (lung scarring) – as seen with asbestosis, which is frequently associated with pleural plaques.
  2. Pulmonary Edema – as seen with congestive heart failure resulting in interstitial pulmonary edema.
  3. Lymphangitic Metastases – metastatic spread of disease within the lymph vessels as seen with breast carcinoma.
  4. Lymphedema – weeping of fluid from the lymph system, as seen with congenital lymph vessel hypoplasia.


The chest x-ray is the most often used screening tool for evaluating individuals exposed to asbestos. One can look for pleural effusions, pleural plaques, costophrenic angle blunting and diffuse pleural thickening, cicatricial scarring, rounded atelectasis, interstitial fibrosis, lung cancers and/or mesotheliomas. Limitations include poor exposure techniques which can be problematic; the training of the individual reader can have significant impact on the consistency and quality of interpretations; findings can be misleading, i.e., emphysema can give the appearance of interstitial fibrosis; intra- and inter-observer errors are increased with low profusion disease; non-calcified plaquing is difficult in many cases to differentiate from extra-pleural chest wall fatty deposition and many findings are non-specific, occurring in many disease states.

Utilization of both supine spiral CT and prone HRCT has significantly impacted the credibility of interpreting images in those patients exposed to asbestos. These studies are invaluable in differentiating fat from plaques which often cause false positive results on chest x-rays, in showing the location and size of the plaques which are often overlooked on chest x-rays (false negative result), in having enhanced ability to identify calcifications within the plaques which are even more specific for asbestos-related disease, in identifying small lung cancers otherwise overlooked on chest x-rays, in differentiating a lung cancer from rounded atelectasis, in identifying emphysema often causing false positive results on chest x-rays mimicking interstitial fibrosis, in identifying low profusion interstitial changes often not seen on chest x-rays leading to a false negative result in an asbestos exposed and often functionally impaired patient and in further visualizing the extent and effect of moderate to severe profusion interstitial changes, including the identification of honeycombing in the lungs, compatible with asbestosis. Interstitial fibrosis of the lungs includes intralobular interstitial thickening (also called and composed of intralobular/core changes, subpleural dots or branching structures, centrilobular thickening or nodules, intralobular lines, pleural based nodular irregularities, subpleural hazy densities, patchy areas of ground glass opacity or hazy patches of increased attenuation), interlobular septal thickening (also called thickened interstitial short lines), non-dependent curvilinear subpleural line formation, parenchymal banding, cicatricial scarring (also called focal or benign fibrotic masses), rounded atelectasis and honeycombing. Secondary findings of volume loss, distortion of the intrathoracic contents and traction bronchiectasis occur usually with more advanced disease. Supine spiral CT has also been valuable, in most cases, at being able to differentiate a lung cancer from rounded atelectasis, which frequently has a comet-tail sign. Biopsy or PET scanning may be needed in difficult cases. Limitations of CT/HRCT include the lack of an accepted classification system regarding the amount of interstitial disease present and the amount necessary to be physiologically significant on prone HRCT, that many individuals remain untrained as to scan interpretation, that the temporal relationship of interstitial changes cannot always be determined on a single scan and that the interstitial findings are non-specific, although when coupled with asbestos-related findings such as calcified pleural plaquing, a more definitive diagnosis can usually be made.

My Training and Acknowledgements:

The above diagrams and article are based upon my education and training, multiple peer review journal articles and textbooks, as well as lectures.

My initial training for chest disease was at L.A. County/USC Medical Center. In private practice, I self-studied and passed the Federal B-Reader Certification testing in 1984 and re-certified every four years thereafter. I also independently tutored with Dr. Gordon Gamsu at the University of California at San Francisco, when he was first publishing his articles on the CT and HRCT findings in pneumoconioses. Based upon his training and my understanding of his information, I began performing large-scale CT/HRCT imaging studies utilizing terminology learned through him and from various course lectures, journal articles and textbooks. Multiple other authors and educators have contributed to my understanding as have their lectures, articles and textbook chapters. Recent experiences have included the latest American College of Radiology Symposium on Radiology of the Pneumoconioses, presented between March 5-8, 2004, and re-certification as a Federal Government “B-Reader” during that same period. Also included in the review were the “Guidelines for the Use of the ILO International Classification of Radiographs of Pneumoconiosis”, Revised Edition 2000, booklet #22 from the International Labor Office in Geneva. I also attended the Radiological Society of North America’s 90th Scientific Assembly and Annual Meeting, November 28 – December 3, 2004 and Chest Imaging for the Clinician and Radiologist, 2005, presented by the American College of Chest Physicians, June 10 – 12, 2005, in which multiple lecturers contributed information including Theresa McCloud, M.D., David P. Naidich, M.D., and W. Richard Webb, M.D. There was a syllabus with that course. Other texts utilized included The CIBA Collection of Medical Illustrations, Volume 7, Respiratory System, illustrated by Frank Netter, M.D. (1979); Diseases of the Lung, Radiologic and Pathologic Correlations, by Muller, Fraser, Lee and Johkoh, published by Lippincott, Williams, and Wilkins, in 2003; Thoracic Imaging, by W. Richard Webb and Charles B. Wiggins, published by Lippincott, Williams and Wilkins, in 2005; and the Fourth Edition, Imaging of Diseases of the Chest, by Hansel, Armstrong, Lynch and McAdams, published by Elsevier Mosby, in 2005. Additional anatomic texts included, Clinically Oriented Anatomy, Fourth Edition by Moore and Dalley, published by Lippincott, Williams and Wilkins in 1999 and Chest Atlas, Radiographically Correlated Thin-Section Anatomy in Five Planes by Littleton and Durizch, published by Springer-Verlag in 1994. Special thanks to Justin Foust, who helped research initial portions of this text and who digitized, cleaned up, annotated and stacked many of the images, Jeff Miller who helped put my ideas for the modified ILO-like forms into Microsoft Publisher®, to Hide Konishi who worked with me on making the visual diagrams come into reality on Adobe Illustrator® and Bill Malin who completed the web presentation.

My Thoughts and Wisdom:

Medicine is an “art” based upon “science.” We as educators and clinicians are constantly learning and updating our teachings and knowledge base. Certainly, by my presentation, I have added addition “art” (the visual diagrams) to this science with the hope that it will help further clarify the learner’s understanding of what Radiologists look for when observing emphysema.

Unfortunately, many authors use individualized coined terms, many of which overlap and some with the same name, that mean different things to different people. There is no easy fix. I have tried to standardize the language.

Regarding measurements and statistics – It must be remembered that common sense must prevail when using numbers and that there are false positive (overcalls) and false negatives (undercalls), plus there are always exceptions to the rules. There is no absolutely correct statistic, since involved study groups and technology change and individual patients have their own select responses to insults. The quoted statistics are for understanding general concepts only. The bottom line is, that imaging studies are part of the Sherlock Holmes investigation of a patient’s disease – identifying if the anatomy is normal or abnormal and trying to direct one to a specific diagnosis when possible. Classifications of emphysema visually overlap both visually and in terms of originating insult and thus, the significance and type of emphysema observed is made based upon the patient’s history including whether he or she smoked, the clinical examination, pulmonary function testing and imaging findings, taken all together.

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 powersmd@breader.com.

Thank you.

Daniel Powers, M.D.
Diagnostic Radiologist
American Board of Radiology Certified
Federal Government Certified “B-Reader”