Asbestos-related diseases

, September, 1918. The first industry regulations did not come into effect until 1932. 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. 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. == Non-malignant asbestos-related pleural diseases ==

Benign asbestos-related pleural abnormalities encompass four types of pleural changes: • Pleural plaques • Diffuse pleural thickening • Benign asbestos pleural effusions • Rounded atelectasis (folded lung) The pleura appears to be more sensitive than the lung parenchyma to the effects of asbestos fibres. 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%. 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, but this has not been confirmed in more recent studies. Similarly, an association between pleural plaques and a restrictive impairment with diminished diffusing capacity on pulmonary function testing has been described. This has not been a consistent finding and it has been postulated that this might be related to undetected early fibrosis. 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. 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. All types of asbestos can cause diffuse pleural thickening and a dose-related relationship has been described. 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. 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. CT scanning is more sensitive than chest radiography and can detect early pleural thickening (i.e. 1-2mm in thickness). 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. 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 asbestos-related diseases ==

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), osteopontin and fibulin3) 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. Asbestos-related lung cancer 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. 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. 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: ==References==