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.
key facts
Prevalence
Estimated 200,000+ deaths per year from asbestos-related diseases globally (WHO 2024); asbestosis itself accounts for roughly 16,000-25,000 of these annually
Demographics
Men affected 6-8x more often than women because of historical occupational exposure patterns; rising rates in women reflect secondary (household) exposure
Avg. age
Diagnosis typically age 55-75 because of the 10-40 year latency between first exposure and clinical disease
Global cases
Approximately 125 million people still occupationally exposed worldwide; 70+ countries have banned all forms of asbestos but use continues in Russia, China, India, Brazil, and parts of South-East Asia
Specialist
Occupational Medicine
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How you might notice it
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..
01Progressive exertional dyspnea developing gradually over months to years, initially with strenuous activity and later at rest.
02Dry, nonproductive cough that persists for months without an identifiable infectious cause.
03Fine bibasilar inspiratory crackles (so-called 'Velcro rales') heard on auscultation, sometimes the earliest objective finding.
04Chest discomfort or tightness, often dull and posterior, that may reflect underlying pleural thickening.
05Reduced exercise tolerance — climbing one flight of stairs becomes difficult, then walking on level ground.
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How it’s diagnosed
diagnosis
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.
Key tests
01
Detailed occupational and exposure historyEstablishes credible asbestos exposure with adequate latency, the cornerstone of diagnosis
02
High-resolution CT chest (HRCT)Definitive imaging for asbestosis; identifies subpleural reticulation, honeycombing, and pleural plaques
03
Pulmonary function tests (spirometry, lung volumes, DLCO)Quantifies physiologic impairment and tracks progression
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Treatment & cost
medical treatments
✓Complete cessation of asbestos exposure
✓Smoking cessation with pharmacotherapy
✓Pulmonary rehabilitation programme (8-12 weeks)
✓Long-term ambulatory oxygen therapy
surgical options
Lung transplantation5-year survival approximately 50-60% in interstitial-lung-disease transplant cohorts; selection is stringent given limited donor availability
Pleurectomy and decorticationSymptomatic improvement in approximately 60-70% of selected patients; physiological gains are modest
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Causes & risk factors
known causes
Occupational inhalation of asbestos fibers
Mining, milling, insulation work, shipbuilding, boiler-making, demolition, asbestos cement manufacturing, automotive brake and clutch work, and construction trades carried the highest historical exposures. Cumulative exposure (fiber-years) predicts asbestosis risk more strongly than peak exposure intensity.
Secondary (household) exposure
Family members exposed to asbestos brought home on a worker's clothing, hair, or skin developed asbestosis and mesothelioma at rates well above the unexposed population. Women laundering contaminated workwear are a recognized affected group.
Environmental exposure
Communities living downwind of asbestos mines, factories, or processing plants and those near naturally occurring asbestos outcrops (Libby, Montana; parts of Turkey, Cyprus, Corsica, and India) develop asbestos-related disease without occupational exposure.
Demolition and renovation of asbestos-containing materials
Older buildings constructed before national asbestos bans contain asbestos in insulation, roofing, floor tiles, and pipe lagging. Demolition, renovation, or fire disturbance releases fibers into the air; tradespeople and DIY renovators sustain new exposures decades after primary industrial use ended.
Inadequate respiratory protection
Use of no respirator, dust masks insufficient for asbestos, or improperly fitted half-mask respirators allowed fibers to penetrate the airways. Workplace safety improvements since the 1970s have reduced but not eliminated exposures.
01Comply with national bans on asbestos use and avoid disturbing asbestos-containing materials in older buildings.
02Use NIOSH-approved P100 or equivalent respirators when work brings any possibility of asbestos exposure (renovation, demolition, plumbing, electrical work in older buildings).
03Engage licensed asbestos abatement professionals for removal of identified materials; do not attempt DIY removal.
04Workplaces must comply with national exposure limits (US OSHA permissible exposure limit 0.1 fiber/cc 8-hour TWA), provide fit-tested respirators, change out of work clothing on site, and shower before leaving work.
05Stop smoking and avoid second-hand smoke — interaction with asbestos multiplies lung cancer risk 28-50-fold.
06Document any work-related asbestos exposure in writing for future medical and compensation purposes.
recommended foods
•Adequate caloric intake to maintain body weight; weight loss accelerates breathlessness in chronic lung disease
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When to seek help
why see an occupational medicine
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.
01Asbestos-related lung cancer — risk 5-fold higher than the general population in heavy asbestos exposure, 50-90-fold higher when combined with smoking; surveillance with low-dose CT may be reasonable in high-risk groups.
02Malignant pleural or peritoneal mesothelioma — peak incidence 30-45 years after first exposure; new pleural effusion or chest wall pain warrants urgent imaging and pleural biopsy.
03Progressive respiratory failure with chronic hypoxemia, eventually requiring long-term oxygen and sometimes non-invasive ventilation.
04Cor pulmonale and right-sided heart failure from chronic pulmonary hypertension.
05Recurrent benign asbestos pleural effusions, sometimes complicated by trapped lung requiring decortication.
Asbestosis (parenchymal fibrosis)Bilateral, lower-lobe predominant, subpleural interstitial fibrosis with reticulation, traction bronchiectasis, and honeycombing on HRCT. The cardinal asbestos-related parenchymal disease and the subject of this page.
Pleural plaquesDiscrete fibrocollagenous thickening of the parietal pleura, often partially calcified, mostly asymptomatic. Marker of asbestos exposure rather than fibrotic disease; present in 20-60% of exposed workers.
Diffuse pleural thickeningConfluent visceral pleural fibrosis that may cause restrictive lung function impairment and pleuritic chest pain. Distinct from pleural plaques and from mesothelioma.
Benign asbestos pleural effusionExudative effusion appearing 5-15 years after exposure. Self-resolving but often recurrent; must be distinguished from mesothelioma effusion by pleural biopsy if clinically warranted.
Rounded atelectasis (Blesovsky syndrome)Folded lung adjacent to pleural thickening producing a pseudo-tumor appearance on imaging. The 'comet tail' of vessels and bronchi entering the lesion confirms the diagnosis.
Living with Asbestosis
Timeline
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.
Lifestyle
01Stop smoking permanently with pharmacotherapy and behavioral support.
02Receive annual influenza and current pneumococcal vaccination schedules.
03Participate in pulmonary rehabilitation and continue home exercise after the formal programme ends.
04Avoid further occupational or hobby-related dust exposure (silica, mold spores, organic dusts).
05Maintain a healthy body weight to reduce additional respiratory load.
06Document all known asbestos exposures with employer name, dates, and job title to support future compensation claims.
Daily management
01Take prescribed medications and use oxygen as directed; check oxygen saturation regularly if a home pulse oximeter is available.
02Track symptoms (cough, breathlessness, weight, sleep quality) and report any rapid change to the pulmonology team.
Complementary approaches
Comprehensive pulmonary rehabilitation including breathlessness coping strategiesPursed-lip breathing, paced activity, energy conservation techniques, and psychological support address the symptomatic burden when no disease-modifying therapy is available.
Palliative care integration in advanced diseaseEarly palliative care involvement for symptom control of severe breathlessness, anxiety, and reduced quality of life. Low-dose opioids and benzodiazepines reduce distressing dyspnea in advanced interstitial lung disease.
Choosing a doctor
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.
Mesothelioma Applied Research Foundation →Patient organization focused on mesothelioma but useful for asbestos-exposed individuals; clinical trial finder and support groups.
WHO Asbestos Fact Sheet →Global statistics, current production patterns, and elimination strategy for asbestos-related diseases.
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Frequently asked
What is asbestosis?▾▴
Asbestosis is a chronic scarring of the lungs caused by inhaling asbestos fibers. It develops 10-40 years after first exposure and causes progressive breathlessness, dry cough, and reduced lung function. There is no cure; treatment focuses on stopping further exposure, slowing decline, and managing symptoms.
What are the first signs of asbestosis?▾▴
The earliest signs are gradually worsening shortness of breath on exertion and a dry cough that persists for months. Doctors often hear fine crackles at the base of both lungs on examination. Pulmonary function tests show reduced lung volumes and reduced diffusion capacity before significant changes appear on imaging.
How long after asbestos exposure does asbestosis develop?▾▴
Asbestosis typically appears 10-40 years after first significant exposure. Mesothelioma, another asbestos-related disease, can develop 30-45 years after exposure. Risk and latency depend on cumulative exposure (fiber-years) and the type of fiber (amphibole forms are far more dangerous than chrysotile).
Is asbestosis the same as mesothelioma?▾▴
No. Asbestosis is scarring of the lung tissue itself caused by asbestos fibers. Mesothelioma is a cancer of the pleura (lung lining) or peritoneum (abdominal lining) caused by asbestos. Both come from the same exposure but they are different diseases with different clinical features, imaging, and treatment.
How is asbestosis diagnosed?▾▴
Diagnosis requires a credible history of significant asbestos exposure with adequate latency, characteristic findings on high-resolution CT (subpleural fibrosis, honeycombing, often with pleural plaques), restrictive pulmonary function, and exclusion of alternative causes. The Helsinki Criteria and ATS 2004 statement guide diagnosis worldwide.
Can asbestosis be cured?▾▴
No. The fibrosis is irreversible. Treatment focuses on stopping further exposure, smoking cessation, pulmonary rehabilitation, oxygen therapy when needed, vaccinations, and managing complications. Antifibrotic drugs (nintedanib, pirfenidone) may slow progression in selected progressive cases but do not reverse existing scarring.
What is the life expectancy with asbestosis?▾▴
Median survival ranges 9-15 years in lighter disease and 5-7 years in advanced disease with hypoxemia. The main causes of death are respiratory failure, cor pulmonale, infection, and asbestos-related lung cancer or mesothelioma. Smoking cessation and avoidance of further exposure significantly improve outcomes.
Who is at risk of asbestosis?▾▴
Workers in shipbuilding, insulation, demolition, construction, automotive brake repair, asbestos mining, boiler-making, and naval service before 1990 carry the highest risk. Family members exposed to fibers brought home on workwear (secondary exposure) and residents near asbestos mines or natural deposits are also at risk.
Does asbestos exposure always cause asbestosis?▾▴
No. Risk depends on cumulative dose, fiber type, and individual susceptibility. Brief or low-intensity exposures rarely cause asbestosis, though they can still cause pleural plaques and modestly raise mesothelioma risk. Heavy occupational exposure over years is the typical setting for clinical asbestosis.
Should I get tested if I worked with asbestos?▾▴
Workers with documented significant exposure should have a baseline chest X-ray, pulmonary function tests, and a low-threshold approach to HRCT if respiratory symptoms develop. The American Thoracic Society recommends periodic surveillance for exposed workers; specific schedules vary by jurisdiction and employer scheme.
Can asbestos still be present in older homes?▾▴
Yes. Homes built before national asbestos bans (1999 in the UK, partial bans in the US since 1989) may contain asbestos in insulation, floor tiles, roofing, pipe lagging, and textured ceilings. Undisturbed material is generally safe; renovation or demolition requires licensed assessment and abatement.
Does smoking make asbestosis worse?▾▴
Smoking accelerates lung function decline in established asbestosis and dramatically multiplies the risk of asbestos-related lung cancer — 28-50-fold higher than smoking or asbestos alone. Smoking cessation is the single most important intervention for any asbestos-exposed person, regardless of asbestosis status.
Are pleural plaques the same as asbestosis?▾▴
No. Pleural plaques are localized thickening of the pleura (lung lining) caused by asbestos exposure and are usually asymptomatic. They are a marker of exposure rather than fibrosis. Asbestosis is fibrosis of the lung tissue itself and causes breathlessness and reduced lung function.
Is there compensation for asbestosis?▾▴
Yes, in most industrialized countries. Workers' compensation, government schemes (UK Pneumoconiosis Etc. Act, US state and federal funds), and asbestos trust funds established through industry bankruptcies provide payments for diagnosed cases. Documentation of exposure history is essential — keep employment records, photos, and witness statements.
What is the difference between asbestosis and silicosis?▾▴
Asbestosis is caused by asbestos fibers and produces lower-lobe predominant interstitial fibrosis with honeycombing, often with pleural plaques. Silicosis is caused by crystalline silica (sandblasting, mining, stone fabrication) and produces upper-lobe nodules and progressive massive fibrosis. Exposure history distinguishes them.
Can asbestosis be passed to family members?▾▴
Asbestosis itself is not contagious or genetic. However, asbestos fibers brought home on workwear, hair, or skin can be inhaled by family members and cause asbestosis or mesothelioma in them. Showering and changing clothes at work before going home are essential to prevent secondary exposure.
Does asbestosis cause cancer?▾▴
Asbestosis is not cancer, but the same asbestos exposure that causes asbestosis greatly raises the risk of lung cancer and mesothelioma. Patients with established asbestosis carry the highest individual cancer risk of any asbestos-exposed group. Surveillance and prompt investigation of new respiratory symptoms are critical.
What is the treatment for breathlessness in asbestosis?▾▴
Pulmonary rehabilitation, breathlessness coping techniques, and inhaled bronchodilators (when concomitant airflow obstruction) all help. Long-term oxygen therapy is indicated when resting blood oxygen falls below 55 mmHg or 60 mmHg with cor pulmonale. Low-dose opioids reduce severe breathlessness in advanced disease.
Can asbestosis cause heart problems?▾▴
Yes. Long-standing low oxygen levels raise pulmonary artery pressure, eventually causing right-sided heart failure (cor pulmonale) with peripheral edema, raised jugular venous pressure, and reduced exercise capacity. Early recognition and oxygen therapy slow this progression.
Is there a lung transplant for asbestosis?▾▴
Yes, in carefully selected patients under approximately age 65 with end-stage asbestosis, no asbestos-related malignancy, and acceptable comorbidities. Five-year survival after lung transplantation in interstitial lung disease is approximately 50-60%. Mesothelioma or active lung cancer disqualifies a patient.
How is asbestosis monitored over time?▾▴
Patients with asbestosis attend pulmonology clinic every 6-12 months for symptom review, pulse oximetry, spirometry, and DLCO. HRCT is repeated every 1-2 years or sooner if symptoms change. Low-dose CT screening for lung cancer is reasonable in heavy smokers with asbestos exposure aged 50-80.
Finger clubbing developing late in the disease in roughly 30-40% of patients.
07Fatigue, weight loss, and reduced appetite as the disease advances.
08Cyanosis of the lips and fingertips in advanced disease with chronic hypoxemia.
09Right-sided heart failure features (peripheral edema, raised jugular venous pressure) in cor pulmonale.
10Recurrent chest infections that are slow to clear because of impaired mucociliary clearance.
early warning signs
•Subtle, progressive shortness of breath on exertion in a former or current asbestos-exposed worker
•Bibasilar end-inspiratory crackles on routine examination in an asymptomatic exposed worker
•Falling forced vital capacity (FVC) on serial spirometry without another explanation
•Reduced diffusing capacity (DLCO) below 80% predicted on pulmonary function testing
•Pleural plaques noted incidentally on a chest radiograph or CT during workup for another condition
● emergency signs
•Sudden worsening of breathlessness, fever, and cough — possible acute exacerbation requiring hospitalization and high-dose corticosteroids
•Sudden pleuritic chest pain with breathlessness — exclude pneumothorax, pulmonary embolism, and acute pleural effusion
•Hemoptysis or cough productive of significant blood — exclude superimposed lung cancer, pulmonary embolism, or tuberculosis
•New unilateral chest wall pain that is dull, persistent, and not relieved by routine analgesia — exclude mesothelioma
•Acute hypoxemia with SpO2 below 88% on room air — admit for oxygen therapy and evaluation
04
Chest radiograph with ILO classificationDocuments pneumoconiosis findings using a standardized international system for surveillance and medico-legal purposes
05
Bronchoalveolar lavage (BAL)Demonstrates asbestos bodies and excludes alternative causes of interstitial disease when imaging is equivocal
06
Surgical lung biopsy (rarely needed)Reserved for cases where HRCT and clinical features cannot exclude an alternative diagnosis
07
Six-minute walk test and pulse oximetryQuantifies exercise capacity and detects exertional desaturation to guide oxygen prescription
Outlook
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.
Risk rises monotonically with cumulative exposure. Workers with more than 25 fiber-years of exposure carry substantially elevated risk; clinically apparent asbestosis usually requires more than 25 fiber-years and a latency over 10 years.
Amphibole fibers are biopersistent and far more pathogenic than serpentine chrysotile per unit mass. Industries using crocidolite (blue asbestos) or amosite (brown asbestos) have the highest asbestosis and mesothelioma rates.
Long latency since first exposurenon-modifiable
Asbestosis develops 10-40 years after first exposure. Mesothelioma latency averages 30-45 years. Most new diagnoses in 2025 reflect exposures occurring in the 1960s-1990s.
Cigarette smokingmodifiable
Smoking does not cause asbestosis directly but multiplies the risk of asbestos-related lung cancer 28-50x relative to non-smokers without exposure, and accelerates decline in lung function in established asbestosis.
Male sexnon-modifiable
Men sustained the majority of historical occupational exposures and account for 80-90% of asbestosis diagnoses. Women's share is rising with recognition of secondary exposure and changing workforce patterns.
Working in older buildings or shipyardsenvironmental
Construction trades, shipyard work, naval service, and railway work between 1940 and 1990 in industrialized countries carried particularly high cumulative exposures.
Underlying interstitial disease may accelerate clinical progression of asbestosis. The distinction from idiopathic pulmonary fibrosis can be radiologically subtle and requires careful history-taking.
Protein-rich foods (lean meat, fish, eggs, legumes) to preserve respiratory muscle mass
•Fruit and vegetables rich in antioxidants (vitamins C and E, carotenoids) to support antioxidant defenses
•Omega-3-rich oily fish twice weekly for general anti-inflammatory benefit
foods to avoid
•Alcohol excess — interacts with sleep, immunity, and medication tolerance
•Highly processed foods and sugary drinks that contribute to weight loss in cachectic patients but provide little nutrition
•Tobacco in any form, including smokeless tobacco and waterpipes
•Unproven 'detox' supplements marketed for asbestos exposure — none have evidence of benefit
Acute exacerbations of fibrosis presenting with rapid breathlessness, fever, and ground-glass change on HRCT — high mortality despite treatment.
choosing the right hospital
01Thoracic radiology service with HRCT and expert interstitial lung disease reporting
02Pulmonary function laboratory offering full lung volumes and DLCO
03Pulmonary rehabilitation programme on site or in network
04Multidisciplinary interstitial lung disease and mesothelioma teams
05Access to long-term oxygen and lung transplantation services
03Maintain home environment free of irritants (smoke, strong cleaning agents, indoor wood fires).
04Attend follow-up appointments at 6-12 month intervals with pulmonary function testing.
05Plan rest periods through the day to manage breathlessness; use a wheeled walker if needed for mobility outdoors.
06Stay current on influenza and pneumococcal vaccinations and seek early care for any chest infection.
Exercise
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.