Asbestos-related diseases

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Asbestos-related disease
Asbestos effect.jpg
Figure A shows the location of the lungs, airways, pleura, and diaphragm in the body. Figure B shows lungs with asbestos-related diseases, including pleural plaque, lung cancer, asbestosis, plaque on the diaphragm, and mesothelioma.
Specialty Respirology

Asbestos-related diseases are disorders of the lung and pleura caused by the inhalation of asbestos fibres. Asbestos-related diseases include non-malignant disorders such as asbestosis (pulmonary fibrosis due to asbestos), diffuse pleural thickening, pleural plaques, pleural effusion, rounded atelectasis and malignancies such as lung cancer and malignant mesothelioma.

Contents

People who worked in jobs with high asbestos dust exposure are at the highest risk of developing asbestos-related disease. However, exposure to asbestos may also occur in the worker's home due to dust that has accumulated on the worker's clothing (para-occupational exposure). Asbestos-related diseases can also occur as a result of non-occupational, environmental exposure. Asbestos was extensively used in many building materials, therefore large quantities of asbestos still remain in buildings that were built prior to the restriction of asbestos use that applies in many countries. The weathering and aging of such buildings may cause asbestos fragments to be released in the air and create a potential hazard. Anyone who disturbs the asbestos-containing material during home maintenance and renovation can be affected, [1] although the exact risks are difficult to quantify.

Pathophysiology

Inhaled asbestos fibres enter the upper and lower respiratory tracts when asbestos is released into the air. Some of the inhaled fibers are cleared by the mucociliary clearance mechanism but long thin asbestos fibers may reach the lower airways and alveoli, and can be retained in the lungs for many years. Amphibole fibers are not cleared as effectively as serpentines and therefore accumulate more readily in the distal lung parenchyma. [2] Asbestos fibres are recognised by the lungs as foreign bodies and cause the activation of the lung's local immune system leading to inflammation, cell and tissue damage. In the long term, this can lead to fibrosis, or rarely to malignancy. From the lungs, some asbestos fibres (mainly short fibres) can also migrate to pleural and peritoneal (abdominal) spaces. [3]

Benign asbestos-related pleural abnormalities encompass four types of pleural changes:

The pleura appears to be more sensitive than the lung parenchyma to the effects of asbestos fibres. [4] Thus asbestos-related pleural diseases can result from much lower doses than the fibrotic changes in the lung.

Pleural plaques

Pleural plaques are the most common manifestation of asbestos exposure, affecting up to 58% of asbestos-exposed workers. The prevalence among the general population exposed environmentally ranges from 0.53 to 8%. [4] Pleural plaques are discrete circumscribed areas of hyaline fibrosis (patches of thickening) of the parietal pleura and rarely the visceral pleura that develop 20 to 40 years after first exposure. Over time, usually more than 30 years, they often become partly calcified. They consist of mature collagen fibers arranged in an open basket-weave pattern and are covered by flattened or cuboidal mesothelial cells. [5] They have a white or pale yellow shaggy appearance and are typically distributed on the posterolateral chest wall, diaphragm, and mediastinal pleura. [6] The number and size varies. Pleural plaques are typically asymptomatic, however, there is still some controversy on this topic. An association between pleural plaques and chest pain has been reported, [7] but this has not been confirmed in more recent studies. [8] Similarly, an association between pleural plaques and a restrictive impairment with diminished diffusing capacity on pulmonary function testing has been described. [9] This has not been a consistent finding and it has been postulated that this might be related to undetected early fibrosis. [5] The pathogenesis of pleural plaques remains uncertain. The most likely explanation is that asbestos fibres reach the parietal pleura by passage through lymphatic channels where they excite an inflammatory reaction. [4] The chest X-ray is the usual tool for diagnosing pleural plaques but chest CT scan is more sensitive and specific in this regard. Pleural plaques are evidence of past asbestos exposure and indicate an increased risk for the future development of other asbestos-related diseases. Pleural plaques in themselves are not pre-malignant. Individuals with pleural plaques are usually not compensated in most compensation systems.

Diffuse pleural thickening

Diffuse pleural thickening (DPT) is non-circumscribed fibrous thickening of the visceral pleura with areas of adherence to the parietal pleura and obliteration of the pleural space. [10] It often extends over the area of an entire lobe or lung, with fibrotic areas involving costophrenic angles, apices, lung bases, and interlobar fissures. The thickness ranges from less than 1 mm up to 1 cm or more and may extend for a few millimeters into the lung parenchyma. [5] Fibrous strands ("crow's feet") extending from the thickened pleura into the lung parenchyma can be often detected on CT scan. Diffuse pleural thickening develops 20 to 40 years after first exposure. [11] All types of asbestos can cause diffuse pleural thickening and a dose-related relationship has been described. [6] It is thought that asbestos fibres that reach the pleura induce subpleural fibroblasts and mesothelial cells to produce scar tissue and collagen deposition, resulting in subpleural thickening. [6] Pleural plaques often coexist with DPT although the latter is rare compared with pleural plaques. According to the Australian Surveillance of Australian Workplace Based Respiratory Events (SABRE) scheme, DPT accounted for 22% of all asbestos-related diseases. [12] It usually begins with an inflammation of the pleura that is accompanied by a pleural effusion. Most patients complain of exertional breathlessness, however, chest pain has been also associated with this disorder. [10] [11] DPT has a significant impact on pulmonary function, causing a decrease in forced vital capacity, reducing total lung capacity and diffusing capacity. [10] [13] The restrictive impairment is a result of adhesions of the parietal with the visceral pleura as well as possible diaphragmatic involvement. Medical imaging is needed for diagnosis of diffuse pleural thickening. The appearance on a postero-anterior chest radiograph is of a continuous, irregular pleural shadowing. In accordance with the International Labour Organization (2000) classification, diffuse pleural thickening is considered to be present if there is obliteration of the costophrenic angle in continuity with ≥3 mm pleural thickening. [14] CT scanning is more sensitive than chest radiography and can detect early pleural thickening (i.e. 1-2mm in thickness). [6] The most commonly used classification system defines diffuse pleural thickening as a continuous sheet of pleural thickening more than 5 cm wide, more than 8 cm in craniocaudal extent, and more than 3 mm thick. [15] Most patients are only mildly impaired by diffuse pleural thickening. Treatment options are limited but any new onset or severe pain should be investigated to exclude malignancy. In most compensation systems, patients are eligible for compensation which corresponds to the severity of disability.

Benign asbestos pleural effusion

Benign asbestos pleural effusion is an exudative pleural effusion (a buildup of fluid between the two pleural layers) following asbestos exposure. It is relatively uncommon and the earliest manifestation of disease following asbestos exposure, usually occurring within 10 years from exposure. Effusions may be asymptomatic but rarely, they can cause pain, fever, and breathlessness. [5] Effusions usually last for 3–4 months and then resolve completely. They can also progress to diffuse pleural thickening. Diagnosis relies on a compatible history of asbestos exposure and exclusion of other probable causes.

Rounded atelectasis

Rounded atelectasis (also known as Blesovsky's or folded lung syndrome) develops from infolding of thickened visceral pleura with collapse of the intervening lung parenchyma. [5] It presents radiographically as a mass and may be mistaken for a tumour. On a CT scan of the chest it appears as a rounded mass like opacity in the peripheral lung adjacent to thickened pleura and with curvilinear opacities which are the bronchi and vessels (comet tail). [16] Rounded atelectasis is the least common asbestos-related benign pleural disease. Exposure to asbestos is the most likely cause today but it can occur following other medical conditions. It is a chronic condition and usually asymptomatic.

Asbestosis

Asbestosis is a chronic lung disease caused by scarring of lung tissue, which results from prolonged exposure to asbestos. It is defined as diffuse interstitial pulmonary fibrosis secondary to asbestos exposure. It initially affects the lung bases and usually manifests after 15 or more years from initial exposure. It occurs after high intensity and/or long-term exposure to asbestos. Asbestos-related fibrosis is progressive because it continues to progress in the lung even if no further asbestos is inhaled. The scar tissue causes the alveolar walls to thicken, reducing the lung capacity which leads to the patient experiencing shortness of breath (dyspnea). Those affected are at an increased risk for heart failure and certain malignancies.

Malignant mesothelioma

Malignant mesothelioma is an aggressive and incurable tumour caused by asbestos arising from mesothelial cells of the pleura, peritoneum (the lining of the abdominal cavity) and rarely elsewhere. Pleural mesothelioma is the most common type of mesothelioma, representing about 75 percent of cases. Peritoneal mesothelioma is the second most common type, consisting of about 10 to 20 percent of cases. Mesothelioma appears from 20 to 50 years after the initial exposure to asbestos. The symptoms include shortness of breath, chronic chest pain, cough, and weight loss. Diagnosing mesothelioma is often difficult and can include physical examination, chest X-ray and lung function tests, followed by CT scan and MRI. A biopsy is needed to confirm a diagnosis of malignant mesothelioma. Mesothelioma has a poor prognosis, with most patients dying within 1 year of diagnosis. The treatment strategies include surgery, radiotherapy, chemotherapy or multimodality treatment. Several tumour biomarkers (soluble mesothelin-related protein (SMRP), [17] osteopontin [18] and fibulin3 [19] ) have been evaluated for diagnostic purposes to allow early detection of this disease. Novel biomarkers such as volatile organic compounds measured in exhaled breath are also promising. [20]

Asbestos can cause lung cancer that is identical to lung cancer from other causes. Exposure to asbestos is associated with all major histological types of lung carcinoma (adenocarcinoma, squamous cell carcinoma, large-cell carcinoma and small-cell carcinoma). The latency period between exposure and development of lung cancer is 20 to 30 years. It is estimated that 3–8% of all lung cancers are related to asbestos. [21] The risk of developing lung cancer depends on the level, duration, and frequency of asbestos exposure (cumulative exposure). Smoking and individual susceptibility are other contributing factors towards lung cancer. Smokers who have been exposed to asbestos are at far greater risk of lung cancer. Smoking and asbestos exposure have a multiplicative (synergistic) effect on the risk of lung cancer. Symptoms include chronic cough, chest pain, breathlessness, haemoptysis (coughing up blood), wheezing or hoarseness of the voice, weight loss and fatigue. Treatment involves surgical removal of the cancer, chemotherapy, radiotherapy, or a combination of these (multimodality treatment). Prognosis is generally poor unless the cancer is detected in its early stages. Out of all patients diagnosed with lung cancer, only 15% survive for five years after diagnosis.

History

Thousands of scientific and medical articles have chronicled human understanding of the hazards of asbestos to human life. [22] This understanding paralleled the growth of the industrial revolution, particularly in the textile factories and mines of Great Britain. This body of knowledge is frequently referred to in litigation as the state of the art or the benchmark for determining if a company acted within the bounds of negligent behavior. The following is a chronological list of some of the major pre-1950 scientific and medical articles relating to the knowledge of the medical and scientific communities regarding asbestos and disease in humans:

YearPublication
1898 "Annual Report of the Chief Inspector of Factories and Workshops, Part II". H.M. Stationery Office. 1898: 171–172.{{cite journal}}: Cite journal requires |journal= (help)
1912 "Effect of Asbestos Dust on Workers Health in Asbestos Mines and Factories". The Labour Gazette: 761–762. 1912.
1918Hoffman, F.L. (1918). Mortality from Respiratory Diseases in Dusty Trades (Inorganic Dusts). U.S. Dept. of Labor, Bureau of Labor Statistics. pp. 35–47, 163–181.
1924Cooke, W.E. (July 26, 1924). "Fibrosis of the Lungs due to the Inhalation of Asbestos Dust". British Medical Journal . 2 (3317): 147–140.2. doi:10.1136/bmj.2.3317.147. PMC   2304688 . PMID   20771679.
1928Editorial (1928). "Pulmonary Asbestosis". JAMA. 90 (2): 119–120. doi:10.1001/jama.1928.02690290049014.
1928Simpson, F.W. (1929). "Pulmonary Asbestosis in South Africa". British Medical Journal . 1 (3516): 885–887. doi:10.1136/bmj.1.3516.885. PMC   2455583 .
1929Haddow, A.C. (August 3, 1929). "Asbestosis". The Lancet . 214: 231. doi:10.1016/s0140-6736(01)04102-2.
1929Wood, W. Burton (May 1929). "Pulmonary asbestosis: Radiographic appearances in skiagrams of the chests of workers in asbestos". Tubercle. 10 (8): 353–363. doi:10.1016/S0041-3879(29)80024-4.
1930Correspondence, Foreign Letters (June 28, 1930). "Compensation Act to be Extended to Asbestosis". JAMA . 94 (26): 2078. doi:10.1001/jama.1930.02710520044016.
1930Mills, R.G. (June 28, 1930). "Report of a Case". Minnesota Medicine: 495–499.
1930Editorial (1930). "Current Comment, Pulmonary Asbestosis". JAMA. 95 (19): 1431. doi:10.1001/jama.1930.02720190042014.
1930Merewether, E.R.A. (May 1930). "The Occurrence of Pulmonary Fibrosis and Other Pulmonary Afflictions in Asbestos Workers". J. Ind. Hyg. 5. 12: 198–257.
1930"Health and Industrial Hygiene - Pulmonary Asbestosis". Monthly Labor Review. 31: 74–76. 1930.
1930Encyclopedia of Hygiene, Pathology and Social Welfare: Occupation and Health, Vol. I, A-H. Geneva: International Labor Office. 1930. pp. 189–181.
1930Gardner, L.U. (1931). "Studies on Experimental Pneumonoconiosis: VI. Inhalation of Asbestos Dust, Its Effect Upon Primary Tuberculosis Infection". J. Ind. Hyg. 2. 13: 65–114.
1930Gordon, B (June 1931). "Pulmonary Asbestosis". Penn.Med.J. 35: 637–639.
1934Woods, W.B.; Gloyne, S.R. (1934). "Pulmonary Asbestosis". Lancet. 2 (5808): 1383–1385. doi:10.1016/s0140-6736(00)43332-5.
1938Dreesen (August 1938). "A Study of Asbestos in the Asbestos Textile Industry". U.S. Treasury Dept., Public Health Bulletin: 1–126.
1941Dublin (1941). "Occupational Hazards and Diagnostic Signs, Bulletin". U.S. Dept. Of Labor, Div. Of Labor Standards. 41: II, IV, V and 25.
1942Holleb, H.B. (1942). "Bronchiogenic Carcinoma in Association with Pulmonary Asbestosis". American Journal of Pathology: 123–131.
1944Wedler, H.W. (1944). "Asbestosis and Pulmonmary Carcinoma". Bulletin of Hygiene. 19: 362.
1944Editorial (November 25, 1944). "Environmental Cancer". JAMA . 126 (13): 836. doi:10.1001/jama.1944.02850480036012.
1944Hutchinson (1944). "Dust as an Industrial Health Hazard". Heating and Ventilating. 41 (6): 57–61.
1946Fleischer, W.F. (1946). "Health Survey of Pipe Covering Operations in Constructing Naval Vessels". Journal of Industrial Hygiene and Toxicology. 1: 9–16. PMID   21016030.
1948Lynch, K.M. (1948). "Asbestosis IV: Analysis of Forty Necropsied Cases, Diseases of the Chest": 79–81.{{cite journal}}: Cite journal requires |journal= (help)
1949Merewether (1949). "Annual Report of the Chief Inspector of Factories for 1947". London: H.M. Stationary Ofc.: 79–81.{{cite journal}}: Cite journal requires |journal= (help)
1949Wyers (1949). "Asbestosis". Postgraduate Medical Journal. 25 (290): 631–638. doi:10.1136/pgmj.25.290.631. PMC   2530167 . PMID   15396262.

Related Research Articles

<span class="mw-page-title-main">Pleural cavity</span> Thin fluid-filled space between the two pulmonary pleurae (visceral and parietal) of each lung

The pleural cavity, pleural space, or interpleural space is the potential space between the pleurae of the pleural sac that surrounds each lung. A small amount of serous pleural fluid is maintained in the pleural cavity to enable lubrication between the membranes, and also to create a pressure gradient.

<span class="mw-page-title-main">Mesothelioma</span> Cancer associated with asbestos

Mesothelioma is a type of cancer that develops from the thin layer of tissue that covers many of the internal organs. The area most commonly affected is the lining of the lungs and chest wall. Less commonly the lining of the abdomen and rarely the sac surrounding the heart, or the sac surrounding the testis may be affected. Signs and symptoms of mesothelioma may include shortness of breath due to fluid around the lung, a swollen abdomen, chest wall pain, cough, feeling tired, and weight loss. These symptoms typically come on slowly.

<span class="mw-page-title-main">Pleurisy</span> Disease of the lungs

Pleurisy, also known as pleuritis, is inflammation of the membranes that surround the lungs and line the chest cavity (pleurae). This can result in a sharp chest pain while breathing. Occasionally the pain may be a constant dull ache. Other symptoms may include shortness of breath, cough, fever, or weight loss, depending on the underlying cause. Pleurisy can be caused by a variety of conditions, including viral or bacterial infections, autoimmune disorders, and pulmonary embolism.

<span class="mw-page-title-main">Pleural effusion</span> Accumulation of excess fluid in the pleural cavity

A pleural effusion is accumulation of excessive fluid in the pleural space, the potential space that surrounds each lung. Under normal conditions, pleural fluid is secreted by the parietal pleural capillaries at a rate of 0.6 millilitre per kilogram weight per hour, and is cleared by lymphatic absorption leaving behind only 5–15 millilitres of fluid, which helps to maintain a functional vacuum between the parietal and visceral pleurae. Excess fluid within the pleural space can impair inspiration by upsetting the functional vacuum and hydrostatically increasing the resistance against lung expansion, resulting in a fully or partially collapsed lung.

<span class="mw-page-title-main">Asbestosis</span> Pneumoconiosis caused by inhalation and retention of asbestos fibers

Asbestosis is long-term inflammation and scarring of the lungs due to asbestos fibers. Symptoms may include shortness of breath, cough, wheezing, and chest tightness. Complications may include lung cancer, mesothelioma, and pulmonary heart disease.

<span class="mw-page-title-main">Atelectasis</span> Collapse or closure of a lung resulting in reduced or absent gas exchange

Atelectasis is the collapse or closure of a lung resulting in reduced or absent gas exchange. It is usually unilateral, affecting part or all of one lung. It is a condition where the alveoli are deflated down to little or no volume, as distinct from pulmonary consolidation, in which they are filled with liquid. It is often called a collapsed lung, although that term may also refer to pneumothorax.

<span class="mw-page-title-main">Chest radiograph</span> Projection X-ray of the chest

A chest radiograph, called a chest X-ray (CXR), or chest film, is a projection radiograph of the chest used to diagnose conditions affecting the chest, its contents, and nearby structures. Chest radiographs are the most common film taken in medicine.

<span class="mw-page-title-main">Respiratory disease</span> Disease of the respiratory system

Respiratory diseases, or lung diseases, are pathological conditions affecting the organs and tissues that make gas exchange difficult in air-breathing animals. They include conditions of the respiratory tract including the trachea, bronchi, bronchioles, alveoli, pleurae, pleural cavity, the nerves and muscles of respiration. Respiratory diseases range from mild and self-limiting, such as the common cold, influenza, and pharyngitis to life-threatening diseases such as bacterial pneumonia, pulmonary embolism, tuberculosis, acute asthma, lung cancer, and severe acute respiratory syndromes, such as COVID-19. Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.

<span class="mw-page-title-main">Pleural thickening</span> Medical condition

Pleural thickening is an increase in the bulkiness of one or both of the pulmonary pleurae.

Occupational lung diseases are work-related, lung conditions that have been caused or made worse by the materials a person is exposed to within the workplace. It includes a broad group of diseases, including occupational asthma, industrial bronchitis, chronic obstructive pulmonary disease (COPD), bronchiolitis obliterans, inhalation injury, interstitial lung diseases, infections, lung cancer and mesothelioma. These diseases can be caused directly or due to immunological response to an exposure to a variety of dusts, chemicals, proteins or organisms.

Restrictive lung diseases are a category of extrapulmonary, pleural, or parenchymal respiratory diseases that restrict lung expansion, resulting in a decreased lung volume, an increased work of breathing, and inadequate ventilation and/or oxygenation. Pulmonary function test demonstrates a decrease in the forced vital capacity.

Malignant pleural effusion is a condition in which cancer causes an abnormal amount of fluid to collect between the thin layers of tissue (pleura) lining the outside of the lung and the wall of the chest cavity. Lung cancer and breast cancer account for about 50-65% of malignant pleural effusions. Other common causes include pleural mesothelioma and lymphoma.

Pleural disease occurs in the pleural space, which is the thin fluid-filled area in between the two pulmonary pleurae in the human body. There are several disorders and complications that can occur within the pleural area, and the surrounding tissues in the lung.

<span class="mw-page-title-main">Lung nodule</span> Medical condition

A lung nodule or pulmonary nodule is a relatively small focal density in the lung. A solitary pulmonary nodule (SPN) or coin lesion, is a mass in the lung smaller than three centimeters in diameter. A pulmonary micronodule has a diameter of less than three millimetres. There may also be multiple nodules.

<span class="mw-page-title-main">Fibrothorax</span> Medical condition involving fibrosis of the pleural space

Fibrothorax is a medical condition characterised by severe scarring (fibrosis) and fusion of the layers of the pleural space surrounding the lungs resulting in decreased movement of the lung and ribcage. The main symptom of fibrothorax is shortness of breath. There also may be recurrent fluid collections surrounding the lungs. Fibrothorax may occur as a complication of many diseases, including infection of the pleural space known as an empyema or bleeding into the pleural space known as a haemothorax.

<span class="mw-page-title-main">Solitary fibrous tumor</span> Medical condition

Solitary fibrous tumor (SFT), also known as fibrous tumor of the pleura, is a rare mesenchymal tumor originating in the pleura or at virtually any site in the soft tissue including seminal vesicle. Approximately 78% to 88% of SFT's are benign and 12% to 22% are malignant. The World Health Organization (2020) classified SFT as a specific type of tumor in the category of malignant fibroblastic and myofibroblastic tumors.

Tumor-like disorders of the lung pleura are a group of conditions that on initial radiological studies might be confused with malignant lesions. Radiologists must be aware of these conditions in order to avoid misdiagnosing patients. Examples of such lesions are: pleural plaques, thoracic splenosis, catamenial pneumothorax, pleural pseudotumor, diffuse pleural thickening, diffuse pulmonary lymphangiomatosis and Erdheim–Chester disease.

Hyperthermic intrathoracic chemotherapy (HITOC) is part of a surgical strategy employed in the treatment of various pleural malignancies. The pleura in this situation could be considered to include the surface linings of the chest wall, lungs, mediastinum, and diaphragm. HITOC is the chest counterpart of HIPEC. Traditionally used in the treatment of malignant mesothelioma, a primary malignancy of the pleura, this modality has recently been evaluated in the treatment of secondary pleural malignancies.

David John Sugarbaker was an American physician who was chief of the division of general thoracic surgery and the director of the Baylor College of Medicine Lung Institute at CHI St. Luke's Health–Baylor St. Luke's Medical Center in Houston, Texas. He was an internationally recognized thoracic surgeon specializing in the treatment of mesothelioma, the surgical management of malignant pleural mesothelioma, and treatment of complex thoracic cancers.

References

  1. ↑ Olsen NJ, Franklin PJ, Reid A, et al. (2011). "Increasing incidence of malignant mesothelioma after exposure to asbestos during home maintenance and renovation". Medical Journal of Australia. 195 (5): 271–274. doi: 10.5694/mja11.10125 . PMID   21895596.
  2. ↑ Kamp D.W. (2009). "Asbestos-induced lung diseases: an update". Translational Research. 153 (4): 143–52. doi:10.1016/j.trsl.2009.01.004. PMC   3544481 . PMID   19304273.
  3. ↑ Broaddus VC (May 2001). "Apoptosis and asbestos-induced disease: Is there a connection?". The Journal of Laboratory and Clinical Medicine. 137 (5): 314–5. doi: 10.1067/mlc.2001.115172 . PMID   11329527.
  4. 1 2 3 Peacock, C., S.J. Copley, and D.M. Hansell, Asbestos-related benign pleural disease. Clinical Radiology, 2000. 55(6): p. 422-32.
  5. 1 2 3 4 5 American Thoracic Society. Diagnosis and Initial Management of Nonmalignant Diseases Related to Asbestos" American Journal of Respiratory and Critical Care Medicine 2004;170:691-715
  6. 1 2 3 4 Miles SE, Sandrini A, Johnson AR, Yates DH Clinical consequences of asbestos-related diffuse pleural thickening: A review" Journal of Occupational Medicine and Toxicology 2008;3:20
  7. ↑ Mukherjee S, de Klerk N, Palmer LJ, et al. (2000). "Chest pain in asbestos-exposed individuals with benign pleural and parenchymal disease". American Journal of Respiratory and Critical Care Medicine. 162 (5): 1807–1811. doi:10.1164/ajrccm.162.5.9912012. PMID   11069817.
  8. ↑ Park EK, Thomas PS, Wilson D, et al. (2011). "Chest pain in asbestos and silica-exposed workers". Occupational Medicine. 61 (3): 178–183. doi: 10.1093/occmed/kqr011 . PMID   21406408.
  9. ↑ Oliver LC, Eisen EA, Greene R, Sprince NL. Asbestos-related pleural plaques and lung function" American Journal of Industrial Medicine 1988;14:649–656.
  10. 1 2 3 Yates D.H.; et al. (1996). ""Asbestos-related bilateral diffuse pleural thickening " natural history of radiographic and lung function abnormalities". American Journal of Respiratory and Critical Care Medicine. 153 (1): 301–6. doi:10.1164/ajrccm.153.1.8542134. PMID   8542134.
  11. 1 2 Jeebun V, Stenton SC (2012). "The presentation and natural history of asbestos-induced diffuse pleural thickening". Occupational Medicine. 62 (4): 266–268. doi: 10.1093/occmed/kqs028 . PMID   22539640.
  12. ↑ Hannaford-Turner K, Elder D, Sim MR, Abramson MJ, Johnson AR, Yates DH (Aug 2010). "Surveillance of Australian workplace Based Respiratory Events (SABRE) in New South Wales". Occupational Medicine. 60 (5): 376–82. doi: 10.1093/occmed/kqq011 . PMID   20308261.
  13. ↑ Kee ST, Gamsu G, Blanc P. Causes of pulmonary impairment in asbestos- exposed individuals with diffuse pleural thickening" American Journal of Respiratory and Critical Care Medicine 1996;154:789–793
  14. ↑ International Labor Office International, Classification of Radiographs of Pneumoconioses. Geneva, Switzerland: International Labour Organization; 2011.
  15. ↑ Lynch, DA; Gamsu, G; Aberle, DR (1989). "Conventional and high resolution computed tomography in the diagnosis of asbestos-related diseases". Radiographics. 9 (3): 523–51. doi: 10.1148/radiographics.9.3.2727359 . PMID   2727359.
  16. ↑ Batra, P., et al., Rounded atelectasis. Journal of Thoracic Imaging, 1996. 11(3): p. 187-97.
  17. ↑ Park EK, Sandrini A, Yates DH, et al. (2008). "Soluble mesothelin-related protein in an asbestos-exposed population: the dust diseases board cohort study". American Journal of Respiratory and Critical Care Medicine. 178 (8): 832–837. doi:10.1164/rccm.200802-258oc. PMID   18583574.
  18. ↑ Park EK, Thomas PS, Johnson AR, Yates DH (2009). "Osteopontin levels in an asbestos-exposed population". Clinical Cancer Research. 15 (4): 1362–1366. doi: 10.1158/1078-0432.ccr-08-0360 . PMID   19174489.
  19. ↑ Pass HI, Levin SM, Harbut MR, et al. (2012). "Fibulin-3 as a blood and effusion biomarker for pleural mesothelioma". The New England Journal of Medicine. 367 (15): 1417–1427. doi:10.1056/nejmoa1115050. PMC   3761217 . PMID   23050525.
  20. ↑ Chapman EA, Thomas PS, Stone E, et al. (2012). "A breath test for malignant mesothelioma using an electronic nose". The European Respiratory Journal. 40 (2): 448–54. doi: 10.1183/09031936.00040911 . PMID   22183490.
  21. ↑ McCormack V.; et al. (2012). "Estimating the asbestos-related lung cancer burden from mesothelioma mortality". British Journal of Cancer. 106 (3): 575–84. doi:10.1038/bjc.2011.563. PMC   3273352 . PMID   22233924.
  22. ↑ Lemen, Richard; Dement (Feb 1980). "Epidemiology of asbestos-related diseases". Environ. Health Perspect. 34: 1–11. doi:10.1289/ehp.80341. PMC   1568524 . PMID   6993197.
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