In Russia, asbestosis is managed by occupational medicines. Asbestosis is a chronic interstitial lung fibrosis caused by inhaling asbestos fibers and developing over 10-40 years after first exposure. WHO estimates that over 125 million people remain occupationally exposed to asbestos worldwide and that more than 200,000 deaths each year are attributable to asbestos-related diseases.
Asbestosis (ICD-10: J61) is a diffuse interstitial pulmonary fibrosis caused by inhalation of asbestos fibers — predominantly amphibole forms (crocidolite, amosite) and to a lesser extent serpentine chrysotile. Asbestos fibers deposit in respiratory bronchioles and alveolar ducts, are partially cleared by alveolar macrophages, and trigger ongoing oxidative injury, alveolar epithelial damage, fibroblast proliferation, and collagen deposition. The result is a slowly progressive, lower-lobe predominant fibrosing interstitial lung disease that radiologically and histologically resembles usual interstitial pneumonia. Asbestos exposure also causes a spectrum of other related diseases: pleural plaques (the most common, often asymptomatic), benign pleural effusion, diffuse pleural thickening, rounded atelectasis, malignant mesothelioma, and lung carcinoma.
The key symptoms of Asbestosis are: Progressive exertional dyspnea developing gradually over months to years, initially with strenuous activity and later at rest., Dry, nonproductive cough that persists for months without an identifiable infectious cause., Fine bibasilar inspiratory crackles (so-called 'Velcro rales') heard on auscultation, sometimes the earliest objective finding., Chest discomfort or tightness, often dull and posterior, that may reflect underlying pleural thickening., Reduced exercise tolerance — climbing one flight of stairs becomes difficult, then walking on level ground., Finger clubbing developing late in the disease in roughly 30-40% of patients., Fatigue, weight loss, and reduced appetite as the disease advances..
Diagnosis follows the Helsinki Criteria and the American Thoracic Society 2004 statement: a credible history of significant asbestos exposure with adequate latency, radiologic evidence of bilateral interstitial fibrosis predominating in the lower zones, and exclusion of alternative causes. History-taking covers all jobs held since adolescence, military service, hobby work (auto repair, home renovation), residence near asbestos sources, and possible household exposure. Examination identifies bibasilar fine inspiratory crackles, finger clubbing, and signs of pulmonary hypertension. Pulmonary function tests show a restrictive pattern with reduced FVC, preserved or reduced FEV1/FVC ratio, and reduced DLCO. High-resolution CT is the imaging modality of choice and shows subpleural curvilinear lines, parenchymal bands, reticulation, traction bronchiectasis, and honeycombing concentrated in posterior lower lobes; pleural plaques on the parietal pleura strongly support the diagnosis. Chest radiographs scored by the ILO classification document small irregular opacities and pleural changes for medical-legal purposes. Bronchoalveolar lavage may reveal asbestos bodies (ferruginous bodies), and surgical biopsy is rarely needed unless an alternative diagnosis cannot be excluded. The most important differential is idiopathic pulmonary fibrosis, distinguished primarily by the exposure history and the presence of pleural plaques.
Asbestosis progresses slowly over years to decades but does not resolve. Median survival from diagnosis ranges 9-15 years in lighter disease and 5-7 years in advanced fibrosis with hypoxemia. Mortality is driven by respiratory failure, cor pulmonale, intercurrent infection, and asbestos-related malignancy (lung cancer and mesothelioma combined account for 40-60% of deaths in long-term cohorts). Predictors of more rapid decline include continued asbestos or smoke exposure, baseline DLCO below 40% predicted, extensive honeycombing on HRCT, and a progressive fibrosing phenotype. Pulmonary rehabilitation, oxygen therapy, smoking cessation, and antifibrotic agents in progressive cases modestly improve outcomes. Quality of life is most affected by breathlessness, fatigue, depression, and the psychological burden of an irreversible occupational disease. Compensation programs in many countries (UK Pneumoconiosis Etc. (Workers' Compensation) Act, US Federal Black Lung Program limited to coal, state and federal asbestos trust funds) provide financial support.
Pulmonology and occupational medicine referral is recommended for any worker or family member with suspected asbestos-related disease. Specialists confirm the diagnosis using the Helsinki Criteria, document exposure for compensation, monitor for asbestos-related malignancy, optimize medical management, and coordinate access to pulmonary rehabilitation, oxygen, and transplantation.
Find specialists →Asbestosis does not recover. Patients can expect progressive disease over years to decades. Pulmonary rehabilitation gains plateau over 12 weeks but functional benefit persists with home exercise. Oxygen prescription is typically lifelong once initiated. Antifibrotic therapy in progressive phenotypes slows FVC decline over 1-2 years.
Begin with supervised pulmonary rehabilitation. Walking, stationary cycling, and resistance training at a perceived exertion of 3-5 out of 10 are tolerated by most patients. Use prescribed ambulatory oxygen during exertion if exercise desaturation occurs. Aim for 150 minutes of moderate aerobic activity weekly with two resistance sessions, adjusted for symptoms.
Choose a pulmonologist or occupational medicine physician with documented experience in pneumoconiosis and asbestos-related disease. Centers offering HRCT with thoracic radiologist review, full pulmonary function testing, occupational lung disease clinics, and access to mesothelioma multidisciplinary teams provide the best care. Ask about NIOSH B-reader availability for medico-legal certification.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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