In Australia, the use and importation of asbestos was prohibited on 31 December 2003, though it had been progressively phased out of use since the 1980s in most work contexts. The researchers conducted a review of published literature, including available grey literature, and also relevant Australian and international bodies with interests in this area were contacted for information. Annual lung cancer screening should be considered for patients 55 to 80 yr with a history of asbestos exposure and a smoking history of ≥ 30 pack-years who are currently smoking or have quit within the past 15 years.The Asbestos Safety and Eradication Agency ( ASEA) commissioned the Monash Centre for Occupational and Environmental Health (MonCOEH), School of Public health and Preventive Medicine, Monash University, to undertake a literature review to identify best practice advice for individuals who may have been exposed to asbestos and the benefit of post exposure medical surveillance. Smoking cessation is particularly important in light of the multiplicative risk of lung cancer in patients who have both tobacco smoke and asbestos exposures. read more and influenza vaccine Influenza Vaccine Based on recommendations by the World Health Organization and the Centers for Disease Control and Prevention (CDC), vaccines for influenza are modified annually to include the most prevalent. read more, and vaccination with pneumococcal vaccine Pneumococcal Vaccine Pneumococcal disease (eg, otitis media, pneumonia, sepsis, meningitis) is caused by some of the > 90 serotypes of Streptococcus pneumoniae (pneumococci). Effective interventions include cessation counseling and drug treatment, such as varenicline, bupropion, or a nicotine. Preventive measures include eliminating exposure, asbestos abatement in occupational and nonoccupational settings, smoking cessation Smoking Cessation Most smokers want to quit and have tried doing so with limited success. CT is also superior to chest x-ray in identifying pleural abnormalities. Chest x-ray is insensitive high-resolution (thin-section) chest CT is useful when asbestosis is a likely diagnosis. Hilar and mediastinal adenopathy and nodular opacities are uncharacteristic and suggest a different diagnosis. In contrast to silicosis, asbestosis produces reticular opacities with a lower lobe predominance. As with silicosis, severity is graded on the International Labor Organization scale ( International Classification of Radiographs of Pneumoconioses) based on size, shape, location, and profusion of opacities. Honeycombing signifies more advanced disease, which may involve the mid and lower lung fields. read more -pleural plaques are virtually pathognomonic of a previous exposure to asbestos. Opacities are often bilateral and are often accompanied by pleural changes Asbestos-Related Pleural Disease Pleural disease, a hallmark of asbestos exposure, includes formation of pleural plaques, calcification, thickening, rounded atelectasis, adhesions, effusion, and mesothelioma. Chest x-ray shows linear reticular opacities signifying fibrosis, usually in the peripheral lower lobes. Pathophysiology referenceĭiagnosis of asbestosis is based on history of exposure to asbestos and chest x-ray or high-resolution CT and only rarely requires lung biopsy for confirmation. Diagnosis is based on history and chest x-ray or CT findings. read more ( 1 Pathophysiology reference Asbestosis is a form of interstitial pulmonary fibrosis caused by asbestos exposure. Symptoms and signs develop over months to years and include. Recent advances suggest there may be a common genetic predisposition between asbestosis and other fibrosing lung diseases, specifically idiopathic pulmonary fibrosis Idiopathic Pulmonary Fibrosis Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, causes progressive pulmonary fibrosis. Risk of disease is generally related to the duration and intensity of exposure and the type, length, and thickness of inhaled fibers. Asbestos fibers may also be directly toxic to lung tissue. Alveolar macrophages attempting to engulf inhaled fibers release cytokines and growth factors that stimulate inflammation, oxidative injury, collagen deposition, and ultimately fibrosis.
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