Chest X-Rays (Plain Radiographs):
The ILO (International Labor Organization) 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 on the ILO form. The ILO provides a set of standard radiographs showing various profusion (quantity) amounts of small irregular opacities (most often seen in asbestosis) and small rounded opacities (most often seen in silicosis and coal workers’ black lung aka coal workers’ pneumoconiosis), examples and grading of the various sizes alone and as a composite of large opacities of progressive massive fibrosis and examples of pleural changes, as well as a written definition of abnormalities and symbols. 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 improve visualization of the calcifications in them and to the localization and verification of parenchymal nodules/cancer or metastases. The chest x-ray is the entry screening tool for asbestos disease, when appropriate exposure levels or duration, plus time from exposure has occurred.
Problems with interpretation of chest radiographs, include:
a) 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 plaquing. However, with digital imaging these issues are diminished. Also, even though overexposure can under estimate lung disease, it can often improve the visualization of plaques. Digital images can be flawed in heavyset individuals, if the penetration ability of the equipment is limited. To better visualize findings, a more contrasty set of images are often produced or worse, “vessel-edge enhancement” may occur, where the vessel margins are enhanced and thickened making separation of blood vessels from interstitial disease, impossible.
b) Both Intra and Inter-Observer Errors Occur: This is especially true in low profusion disease. Intra-observer error is where the same doctor reads the images at two different times and gives two different opinions. Inter-observer error is where two separate doctors read the same images 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 is presumably less with experienced B-Readers interpreting chest x-rays on individuals with moderate-to-severe disease. Unfortunately with low profusion/mild disease, there is much intra- and inter-observer error, regardless of the experience of the individual, although experienced B-Readers tend to be more consistent and less problematic. In all cases but especially low profusion cases, correlation with prone HRCT without contrast is more ideal especially if there is significant disparity amongst readers.
c) Inaccuracy of the Chest Radiograph due to Overlapping Structures: The chest radiograph is a composite of the entire thickness of the thorax and thus, overlapping breasts, the thickness of the body fat, overlapping structures, such as a pacemaker, poor inspiratory effort with crowding of vascular structures, muscle slips around the lateral chest wall, etc., can all influence the appearance in interpretation of chest radiographs. 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. It is also useful to show moderate to severe interstitial disease having the appearance and distribution of asbestosis and in defining emphysema in most cases. Prone HRCT is more accurate at showing low profusion interstitial disease at the lung bases with interference from gravitational dependent density occurring in the supine position. CT or HRCT, however, cannot provide the overview that the plain radiographs render, are more costly and result in a higher radiation dose to the patient. Plaquing and interstitial fibrosis can be missed on chest x-rays. Peer-reviewed textbook descriptions of plaquing, both calcified and not calcified indicate that chest x-rays have a limited ability to see plaquing, with 40% to 90% of plaques being missed. CT or HRCT substantially improves identification of plaques. CT with contiguous slices is the ideal screening tool for plaquing. However, HRCT with thinner slices may show calcifications or some plaques better than CT, although the prone HRCT often has skipped spaces between slices, where plaques can be missed. Nonetheless, with modern technology the supine spiral CT can often be reformatted as a supine HRCT with thin slices, making plaque detection even more sensitive. CT and HRCT also separate non-calcified plaques from chest wall fat and help separate out non-asbestos disease processes that may look similar to asbestosis on chest x-rays, but are not. Low profusion interstitial lung disease is often overlooked on chest x-rays, but can be identified in some individuals on prone HRCT. The converse is also true in that the chest x-ray may appear to show interstitial fibrosis when in fact due to overlapping structures, technical interference and other medical conditions, prone HRCT demonstrates that no asbestos type interstitial changes are present.
d) Non-calcified Chest Wall Thickening Can Be Non-Specific: Muscle slips, extra-pleural chest wall fatty deposition and plaquing can all look similar. Calcification makes a more definitive diagnosis of plaquing on chest x-ray. Focal and asymmetric appearances are more probably due to plaquing, although fat can on occasion, look similar. CT or HRCT, can, in most cases, differentiate fat from plaques and are more sensitive to detecting calcium deposits within the plaques.
e) Confusion and Limitations to the ILO Classifications of Plaques: The ILO system is very detailed, asking whether the pleural abnormalities are in-profile, face-on, diaphragmatic, at other sites including paravertebral and pericardial or diffuse and whether or calcified or non-calcified. On the other hand, it is non-specific and confusing in that it is often difficult to judge from the answers to what extent, area-wise, they are covering the chest cavity and how they are influencing the individual’s physiology.
f) Non-specificity of Interstitial Patterns: Interstitial disease can be acute or chronic and due to multiple causes. Multiple sequential x-rays and/or the individual’s history, if accurate, can be helpful in focusing on a particular diagnosis and definitely multiple sequential chest x-rays over time are often necessary to demonstrate that the interstitial changes are chronic suggesting fibrosis (although certain features of chronicity can be seen on a single dated chest x-ray) and whether or not progression, i.e., an increased profusion of interstitial findings has occurred over time. Chest x-rays may show other lung disease processes that look like asbestosis, but on CT or HRCT are shown not to have the pattern and distribution of asbestosis. Asbestosis – scarring of the lung tissue (interstitial or parenchymal fibrosis, scarring affecting the interstitium or parenchyma) is frequently bilateral, somewhat horizontally linear and irregular (not nodular) and most frequently involves the posterior mid and lower lung zones early on. This diagnosis is more definitive when there are pleural plaques (scarring of the chest wall lining – pleural fibrosis), although asbestosis occurs both with and without associated plaquing and rarely, even with plaquing, the interstitial fibrosis can be due to other causes. At the 2004 ACR Symposium on Radiology of Pneumoconiosis, 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%. It may be even more, since 40% to 90% of plaques can be missed by chest radiographs. Included in the differential diagnosis of asbestosis are other Usual Interstitial Pneumonias (UIP) including Idiopathic Pulmonary Fibrosis (IPF), autoimmune or collagen vascular disease disorders affecting the lungs, most frequently, rheumatoid arthritis and scleroderma, medication-caused fibrosis often from chemotherapeutic agents or anti-arrhythmic drugs and extremely rare congenital/familial pulmonary fibrosis. Also in some circumstances depending upon the appearance and distribution of the disease, smoking-related processes such as Respiratory Bronchiolitis – Interstitial Lung Disease (RB–ILD) and its variants can be considered. With advanced disease, chronic hypersensitivity pneumonitis and sarcoidosis are considerations. Also, 10% to 20% of coal miners can have a variant presentation, where a reticular, coarse interstitial fibrotic pattern occurs at the lung bases, which in advances stages can be associated with honeycombing, volume loss and traction bronchiectasis.
g) Emphysema can Mimic Asbestosis on Chest X-Rays: Mild-to-moderate interstitial lung disease appearance on chest x-rays in smokers can represent emphysema (lung holes) rather than lung scarring when such is advanced involving the mid and especially the lower lung zones. Emphysema is usually in the upper to mid lung zones, sparing the lower lung zones, in most individuals. In advanced disease there is more involvement of the mid lung zones with extension into the lower lung zones. When emphysematous holes expand, the lung tissue around 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-rays appear as fine horizontal linear stranding, which may lead to a false-positive reading on chest x-rays for asbestosis. Supine spiral CT or even better, supine or prone HRCT can demonstrate emphysematous holes. Prone HRCT can separate out emphysematous holes from fibrotic interstitial changes at the posterior lung bases. Of course, both emphysematous holes and interstitial fibrosis due to asbestosis may coexist.
Computerized Tomographic Scan of the Chest Without Iodinated Contrast (Supine Spiral CT):
The computerized tomographic scan of the chest without iodinated contrast (supine spiral CT aka the standard or routine CAT scan) 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 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 imaging data, lessening the chance for respiratory motion artifact e.g., blurring the images. Also reformatted supine, thin slice, high-resolution (supine HRCT) images can be generated from the standard supine spiral CT acquisition. Usually plaquing versus fat is easy to distinguish, although occasionally with very thin plaquing, subtle thickened normal variant endothoracic fascia, internal intercostal muscles or the fatty deposition’s inner edge artifact are hard to fully differentiate. Thin plaquing is best identified along the inner margin of a rib (rather than between the ribs where the endothoracic fascia or internal intercostal muscles can be confused for plaquing). To the untrained reader, paravertebral or posterior rib adjacent vascular structures (blood vessels) can appear as plaques as well, especially if iodinated contrast is utilized. To the trained reader, occasionally punctate calcified plaquing can be mimicked by contrast enhancement of vascular structures, if the vessel is curving on-end adjacent to the chest wall. That is why a non-contrast CT is preferred. The CT scan, however, is more sensitive than plain radiographs in the detection of plaque calcification, which are more definitive, if not close to pathognomonic of asbestos exposure (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 calcification 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 – in-profile; anterior and posterior face-on; diaphragmatic, paravertebral; pericardial; mediastinal and inter-lobular fissure based. In regards to lung cancers, oftentimes, small nodular lesions are missed on plain radiographs, which are better identified by CT. This means if CT can detect early cancers better than chest x-rays and hopefully result in more rapid treatment and prolongation of the individual’s life. That is why aggressive low-dose CT scanning in high risk individuals has been implemented in recent years. Unfortunately, CT is so sensitive that it often picks up very small nodular densities that can represent, most often granulomas, scars from old tuberculosis or fungal infections – common in the general population or normal variant intrapulmonic lymph nodes (structures that help fight infections) or localized thickening or densities extending from or within the interlobular fissures. This becomes problematic since a small nodular lesion in an individual exposed to asbestos can theoretically represent an early cancer and thus, sequential CT follow-up is often obtained sometimes for up to 3 to 5 years to rule out slow-growing cancer. Older recommendations of scanning every three months have been modified due to the great expense and the substantial radiation dose, which has its own cancer risk. Today, there are guidelines for follow-up CT based upon nodule size, but even these guidelines, although useful, are not designed for higher risk asbestos-exposed individuals and as such tweaking of the recommendations – often prolonging the sequential scanning time frame, is often necessary.
Problems with the interpretation of supine spiral CT, include:
a) Dependent Density Prevents 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 or density) causing a hazing density similar to lung fibrosis at the posterior subpleural lung bases. Since most of the early asbestosis scarring occurs in the posterior subpleural lung bases, the individual must lie prone to take the haze caused by gravity’s dependent blood pooling and atelectasis (false-positive effect) away. The dependent density shifts to the anterior lung bases when lying prone, but that is not a problems as asbestosis most commonly begins in the posterior lung bases, the areas now free of gravitational interference.
b) Slice Thickness Limits Evaluation of the Lung Parenchyma (tissue) for Interstitial Fibrosis: The slice thickness of the supine spiral CT is commonly 3 to 10 mm, most often 5 mm thick. This compares with thinner slices of HRCT, which are 0.625 mm to 2.5 mm thick, most often 1.0 or 1.25 mm thick. Understand that even thin HRCT slices correspond to looking at cut sections of the lung visually in the laboratory and are not microscopic analyses. Thus, thicker slices are volume averaged, overlapping and merging findings to make small interstitial details harder to see. Modern CT scanners can reformat standard supine spiral CT images into supine HRCT images that eliminates the disadvantage of thick slices, but does not take away from the dependent density problems seen when individuals are in the supine position.
c) Iodinated Contrast Can Interfere with Thin Plaque Identification: The use of Iodinated contrast is usually not necessary for the purposes of identification of plaques, emphysema, nodules or other lung and chest wall masses. In addition, iodine contrast can result in allergic reactions as severe as death. Abnormal masses or fullness in the size to the lymph nodes in the hilum or mediastinum should they occur, can be followed up with a contrast study or alternatively and often better yet, if a malignancy is suspect, with a PET/CT. Contrast iodinated contrast can result in false-positive appearances to the chest wall mimicking plaques with on-end vascular enhancement looking like small punctate calcified pleural plaques.
Prone High Resolution, Thin Slice, Computerized Tomographic Scanning of the Chest (Prone HRCT):
The prone HRCT is utilized primarily to evaluate the interstitial (lung tissue) in the prone non-dependent position for the identification of early/low profusion/mild asbestosis. This allows for visualization of the posterior lung bases – the area of interstitial fibrosis (lung tissue scarring), most common in early asbestosis without interference from gravitational dependent density caused by the supine positioning, i.e., without blood pooling or dependent atelectasis. It is also better than the supine spiral CT in the identification and classification of emphysema, although reformatted supine HRCT images can give similar results. The supine or prone HRCT scans are more definitive at showing plaquing with and without calcifications, however, if only prone HRCT is utilized, given the thinner slices acquired for this scan, contiguous slices would result in a high radiation dose and, therefore, skip spacing is utilized, which can lead to missing small plaques and/or small nodules. This can be overcome by utilizing the high resolution lung algorithm on a reformatted supine HRCT study obtained from the supine spiral CT acquisition. The supine or prone HRCT study can be useful at viewing lung masses and in evaluating the contours of the mass and whether or not visible calcification can be identified. Central, ring-like, homogeneous or irregular/ popcorn appearing calcifications commonly represent benign calcifications, although asymmetric calcifications can be present in a malignancy especially if the malignancy is adjacent to or encasing a calcified granuloma or other calcified benign mass.
Problems with the interpretation of prone HRCT, include:
a) Skipped Spacing Can Result in Missed Plaquing and Nodule Identification: The prone HRCT is most often acquired with skip spacing, which can lead to the missing of small plaques or small nodules. That is why the contiguous slice supine CT and/or reformatted supine HRCT are necessary in conjunction with the prone HRCT study.
b) No Firm Agreement on Grading System: There is no agreement on how to quantitate and whether or not a certain quantity (profusion) or visual amount of interstitial findings are necessary to be indicative of a significant physiologic disease state. Although no standard images are made available at this point by the ILO, most peer-reviewed articles and textbooks show examples of normal lung parenchymal anatomy, mild, moderate and severe interstitial disease, having the appearance and distribution of asbestosis or other visually like diseases within the differential diagnosis.
c) Non-specificity of Interstitial Findings: Many diseases cause interstitial fibrosis. The 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 are those having a histologic appearance of Usual Interstitial Pneumonia (UIP), which include Idiopathic Pulmonary Fibrosis (IPF) – scarring of unknown cause, Collagen Vascular/Autoimmune Lung Diseases including Rheumatoid Arthritis and Scleroderma, medication related lung fibrosis including those from chemotherapeutic agents and/or anti-arrhythmic drugs and rarely congenital/familial pulmonary fibrosis. Occasionally other disease states can also overlap including smoking-related interstitial lung disease from Respiratory Bronchiolitis – Interstitial Lung Disease (RB-ILD) and/or its variants. The presence of pleural plaquing makes for a more probable diagnosis of asbestosis, however, there are many cases in which asbestosis occurs in the absence of pleural plaques (and as I have said in deposition when taking the recent B-Reader recertification examination several of the examples of asbestosis type conditions showing moderate or severe disease did not have associated plaquing).
d) Smoking is a Controversial Area: “Dirty lungs” have been described on chest x-rays, in smokers and scattered very low profusion (low quantity) visualized interstitial changes have seen in individuals that have smoked that have not been exposed to asbestos. However, the etiology of these interstitial changes in the 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 and/or at construction sites). In addition, described earlier, is the fact, that advanced emphysema can give the appearance of interstitial lung disease on plain radiographs, which is usually easily excluded on CT and especially on prone HRCT.
e) Multiple Disease States can Cause Interstitial Thickening: These can have various pattern recognition, be acute or subacute rather than chronic and are not always that of asbestosis. Some of these diseases include:
Pulmonary Fibrosis – lung scarring can present with various shapes, patterns and locations.
Pulmonary Edema – often seen with congestive heart failure, resulting in interstitial pulmonary edema, which can have interlobular septal thickening and often patchy areas of ground-glass opacities sometimes forming a bat wing configuration about the hila or rarely with Lymphedema – weeping of fluid from the lymph system, as seen with congenital lymph vessel hypoplasia.
Lymphangitic Metastases – metastatic spread of disease within the lymph vessels sometimes seen with breast carcinoma and often appearing as a “string of pearls” or linear areas of densities with nodular bumps within the linear extension.
Prone HRCT Finding in Asbestosis:
a) Intralobular Interstitial Thickening – (previously called by some, “Core” changes): These findings have been described by various authors to include subpleural dots or branching structures, centrilobular thickening or nodules, interlobular lines, pleural-based nodular irregularities, subpleural hazy densities, patchy areas of ground-glass opacity or hazy patches of increased attenuation. In simple terms, I use three main findings: subpleural hazy densities (which I do not call ground-glass opacities and reserve such term for more centralized larger areas of hazy changes), small linear, perpendicular “short lines” and subpleural punctate dot-like densities. The overwhelming appearance of such findings are as subpleural hazy densities.
b) Traction Bronchiolectasis – pulling apart or dilatation of the small bronchioles in the peripheral lung caused by the adjacent interstitial fibrosis. These little black dots or air tube identifications are often significant markers in identifying chronic fibrosis involving the lung periphery.
c) Interlobular Septal Thickening – these represents slightly longer and more thickened linear perpendicular lines, which are more commonly seen in other disease state such as congestive heart failure. This can, however, occur in asbestosis especially in more advanced states. The intralobular scarring occurs within the lobule and the interlobular scarring is scarring involving the perimeter or margin of the lobule, separating one lobule from another (like the fence surrounding a person’s property).
d) Non-Dependent Curvilinear Subpleural Line Formation – dependent subpleural line formation can be an anatomic variant often due to lymphatic filling. However, non-dependent curvilinear subpleural line formation is abnormal. At times, this is just an optical illusion that is related to the tops of sequentially arranged areas of bronchiolectasis, which have denser scarred lung tissue about them.
e) Parenchymal Banding – non-specific, representing thicker more elongated oblique or perpendicular lines extending from the chest wall. These are most common associated with diffuse pleural thickening, but can occur with plaquing and/or are commonly seen with more moderate-to-advanced interstitial lung disease. When clustered and extending in a radial fashion/fan-shaped they are have the appearance of a crow’s foot, which is more likely to cause the evolution of rounded atelectasis.
f) Honeycombing – areas of destroyed lung with fibrotic surrounds often multi-layered and of varying hole sizes.
g) Benign Fibrotic/Cicatricial Mass Formation – triangular and rectangular areas of thickened scarring, abutting upon the chest wall and extending into the lung parenchyma.
h) Rounded Atelectasis – in-folding of parenchymal bands, grabbing and pulling into their center, adjacent lung tissue causing a rounded soft tissue mass that can have a comet-tail sign of whirling or spiraling vessels and/or bronchioles extending into the mass. They are most often pleural based and most commonly associated with diffuse pleural thickening. However, they may mimic a cancer because of the rounded appearance, especially if not pleural adjacent and without the comet-tail sign, in which case, PET/CT or biopsy may be necessary to exclude a lung cancer.
i) Secondary Findings – these findings, occurring in more advanced disease, include volume loss, distortion of intrathoracic contents, traction bronchiectasis and centrally extending areas of ground glass opacities.
The chest x-ray is the most often used entry screening imaging study for the evaluation of individuals exposed to asbestos. One can look for pleural effusions, pleural plaques, costophrenic angle blunting, diffuse pleural thickening, benign fibrotic/cicatricial scarring, rounded atelectasis, interstitial fibrosis/asbestosis, lung cancers or mesotheliomas. Limitations include, but are not limited to, poor exposure techniques, which can be problematic; large individual patient size with contrast overcompensation by the machinery resulting in vessel-edge enhancement or inadequate penetration resulting in a patchy or pixely salt and pepper appearance; the lack of training of the individual reader having a significant impact on the consistency and quality of interpretations; misleading findings, i.e., other lung diseases, looking like interstitial fibrosis, but separated out on CT or HRCT; false positives, i.e., emphysema giving the appearance of interstitial fibrosis or extra-pleural chest wall fatty deposition looking like non-calcified pleural plaques; false negatives, i.e., missed plaquing and small nodules and intra- and inter-observer errors increased with low profusion disease.
Utilization of both supine spiral CT and supine and prone HRCT scanning has significantly impacted the credibility of and improved the interpretation of images on those exposed to asbestos. These studies are invaluable in differentiating fat from non-calcified plaques, which often causes false-positive results on chest x-rays; in showing the location of plaques, which are often overlooked on chest x-rays (false-negative result on chest x-rays); 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 lung cancer from rounded atelectasis; in identifying emphysema, which with advanced disease can cause false-positive results on chest x-rays mimicking interstitial fibrosis; in identifying low profusion interstitial changes, having the appearance and distribution of asbestosis, often not seen on chest x-rays leading to a false-negative result in an asbestos exposed individual who can be functionally impaired and in further visualizing the extent and appearance of moderate-to-severe profusion asbestosis including the identification of honeycombing in the lungs.
The interstitial fibrosis findings in the lungs that have the appearance and distribution of asbestosis include intralobular interstitial thickening (previously called “Core” changes), which include most commonly hazy subpleural patchy areas of increased attenuation, subpleural dots and perpendicular vertical short lines, together when more moderate in profusion, often associated with traction bronchiolectasis, non-dependent curvilinear subpleural line formation, parenchymal banding and benign fibrotic/cicatricial mass formation and with more advanced disease with interlobular septal thickening, longer and more prominent parenchymal band formation, intrathoracic distortion, volume loss, rounded atelectasis, honeycombing and on occasion more centralized and advanced ground-glass opacities and traction bronchiectasis.
Supine spiral CT has been valuable in some cases at being able to differentiate lung cancer from rounded atelectasis where the rounded atelectasis has a “comet-tail sign” and is pleural based. Biopsy or PET/CT scanning may be needed in difficult cases. Limitations of CT and HRCT include the lack of accepted classification system regarding the amount of interstitial profusion, although this is pretty much covered by academic journals and peer-reviewed textbooks; the amount of profusion and its distribution necessary to be physiologically significant; that many individuals remain untrained as to CT/HRCT interpretation in asbestos and other occupational dust and fiber cases; that the temporal relationship of interstitial changes cannot always be determined on a single scan (although the appearance, distribution and presence of bronchiolectasis and, if present, intra-thoracic distortion with parenchymal bands can often make such chronic changes probable) and that the interstitial findings have a differential diagnosis – meaning several diseases can look similar, although when of a specific pattern and distribution is coupled with a history of asbestos exposure and if possible, with the presence of non-calcified or calcified pleural plaquing, a more definitive diagnosis can be made.
My training acknowledgments: The above article is based upon my education, training, experience and from multiple peer-reviewed journal articles, textbooks and lectures.
My initial training for chest disease was at LA County/USC Medical Center. In private practice, I self-studied and passed the Federal Government B-Reader Certification examination in 1984 and recertified every four years thereafter, the latest being in 2016. I also independently tutored with Dr. Gordon Gamsu at the University of California at San Francisco when he was first publishing his articles on CT and HRCT findings in pneumoconiosis. Based upon his training and my understanding of this information, I began performing CT/HRCT imaging studies utilizing terminology learned through him and his colleagues as well as from various course lectures, journal articles and textbooks in the late 1980s and early 1990s. Multiple other authors and educators have contributed to my understanding, as have their lectures, articles and textbook chapters. Experiences have included the American College of Radiology Symposium on Radiology of Pneumoconiosis, recertification review for the Federal Government “B-Reader” certification exams, review of the guidelines for the use of the ILO International Classification of Radiographs of Pneumoconioses, revised edition, 1980 and 2000. I have also attended courses at the Radiological Society of North America (RSNA), courses by the American College of Chest Physicians and the Society of Thoracic Radiologists, reviewed multiple textbooks including the CIBA Collection of Medical Illustrations, Volume 7, Respiratory Disease Illustrated by Frank Netter, M.D., multiple textbooks by Richard Webb, Nestor Müller and David Naidich as well as other textbooks by Hansell, Armstrong, Lynch and McAdams to name a few.
Medicine is an “art” based upon “science.“ We as educator and clinicians are constantly learning and updating our teachings and knowledge base. There are three areas of diagnosis a) the Clinical Diagnosis – e.g., from the history, physical exam, blood work and pulmonary function testing; b) the Pathologic/Histologic Diagnosis, based on the autopsy, pathologic specimen, gross microscopic or electron microscopic findings and c) the Imaging Diagnosis based upon the pattern and appearance of both interstitial and pleural findings. By my presentation, I hope that it will further clarify the learner’s understanding of what Radiologists look for when searching for asbestos markers on imaging studies. Unfortunately, many authors use individualized coined terms, many of which overlap and some terms with the same name, mean different things to different authors. There is no easy fix. I have tried to standardize the language and understanding of this information. It must be remembered that common sense must prevail when using measurements and statistics and that there are false-positives (over-calls) and false negatives (under-calls) plus there are always exceptions to the rules. There is no absolutely correct statistic, since involved study groups and technologies change and individual patients have their own select responses to insults. 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.
This article is provided as a public service by Daniel Powers, M.D.: B-Reader and 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 in general, please do e-mail them to me at firstname.lastname@example.org.