ASBESTOSIS

ASBESTOSIS - Ruben Peralta, MD, FACS; Sarah Guzofski, MD
BASICS
DESCRIPTION
• Slowly progressive lung disease caused by inhalation of dust from the fibrous silicate asbestos
• Asbestos is used in insulation and other building products, cement, and textiles.
• Nodular interstitial fibrotic lung disease caused by cascade of inflammatory responses to inhaled asbestos fibers. Pleural fibrosis, pleural plaques and interstitial fibrosis develop. Lung cancer risk is increased.
• Synonym(s): Asbestos pneumoconiosis
GENERAL PREVENTION
• Asbestos has been federally regulated by the Occupational Health and Safety Administration since 1972. Primary responsibility of employers to provide safe work environment.
• Exposure control: Substitution of safer material or adoption of control technologies
• During high-exposure periods such as building repair, use fit-tested personal respirators for workers.
• World Health Organization (WHO) recommendations for regular health screening of exposed workers
- Chest radiograph film at baseline
- For workers with 10 years since 1st exposure: Chest radiograph every 3-5 years
- >10 years: Chest radiograph every 1-2 years
- >20 years: Chest radiograph annually
- All workers: Annual respiratory symptom questionnaire, physical examination, and spirometry (alternatively can be done on chest radiograph schedule)
• Reporting of new cases to health authorities
EPIDEMIOLOGY
• In the US, an estimated 1.3 million people who work in maintenance and construction are at risk for exposure (1)[B].
• Predominant age: Middle age (40-75 years)
• Predominant sex: Male > Female, owing to exposure pattern
RISK FACTORS
• Professional exposures most common in construction; those who mine, mill, or remove asbestos; ship builders; textile workers; railroad workers
• Office workers, teachers, and students in buildings with asbestos in place have exposure orders of magnitude below those of construction workers.
• Cigarette smoking markedly increases risk of radiographic changes and eventual lung cancer risk, thought to be due to decreased clearance of asbestos fibers.
Genetics
No known genetic pattern
ETIOLOGY
• Asbestos fibers are inhaled. Macrophages engulf the fibers and release inflammatory mediators. Inflammatory mediators cause fibroblast proliferation, leading to fibrosis and remodeling of interstitial lung tissue, including intra-alveolar fibrosis and loss of alveolar capillary units (1)[B].
• Disease continues to slowly progress over the course of years, even if exposure is not ongoing.
• The degree of fibrosis depends on amount of asbestos exposure.
• Symptoms may be related to impaired gas exchange and/or a pattern of restrictive lung disease.

DIAGNOSIS
• Credible history of exposure (ask about intensity and duration of exposure).
• Delay from exposure to detection (typically becomes clinically apparent 10-15 years after exposure).
• Typical radiographic findings
• Restrictive pattern of lung disease
• Impaired diffusion capacity
• Lung biopsy or bronchoalveolar lavage (BAL) can reveal asbestos fibers or asbestos bodies. May help diagnostically in cases with history of minimal exposure or with atypical clinical or radiographic features. Transbronchial biopsy is less reliable than BAL or open lung biopsy in establishing diagnosis (1)[B].
SIGNS AND SYMPTOMS
• Insidious onset
• Progressive dyspnea is the most common symptom.
• Dry cough
• Progressive exercise intolerance
• Pleuritic chest pain
• Inspiratory crackles (may be best heard laterally)
• Wheeze with forced exhalation
• Digital clubbing and cyanosis in advanced disease
• Right-sided heart failure
TESTS
Pulmonary function test
• Not diagnostically specific
• Useful for following level of impairment
• Restrictive, mixed, or obstructive pattern
• Reduction in diffusing capacity to carbon monoxide (2)[B]
Lab
No pathognomonic lab findings
Imaging
• Chest radiograph (sensitivity 90%, specificity 93%) (1)[B]
- Most common findings are bilateral pleural thickening and circumscribed calcified pleural plaques.
- Pleural plaques usually posterior-lateral, may also involve diaphragm (3)[B]
- As disease progresses, irregular, linear opacities most often in middle or lower lung fields
- Less common: Rounded atelectasis (Blesovsky syndrome) when fibrosis of visceral pleura extends into parenchyma (4)[B]
- Classification scheme available through International Labour Office
• High-resolution CT may increase sensitivity to near 100%; improves detection of interstitial fibrosis.
Pathological Findings
Pleural plaques are found in parietal pleura; made up of collagen bundles with rare inflammatory cells. Pleural thickening involves the visceral pleura (3)[B].
DIFFERENTIAL DIAGNOSIS
Other pneumoconioses
• Idiopathic pulmonary fibrosis
• Hypersensitivity pneumonitis
• Sarcoidosis
• Other pneumoconiosis, including mixed exposures
TREATMENT
STABILIZATION
GENERAL MEASURES
• No effective treatment to reverse course
• Approach directed at elimination of progression, amelioration of symptoms, reduction of risk of associated disorders
• Withdrawal from exposure (3)[B]. Workers with no symptoms and only chest radiographic changes may make an informed choice to continue employment using maximum environmental and personal protection.
• Pneumococcal and influenza vaccines
• Chest physiotherapy
• Home oxygen
• Smoking cessation: Cigarette smokers have more radiographic signs of disease and have a significantly increased risk for lung cancer.
Diet
High calorie, high protein with advanced disease
Activity
Graded exercise
MEDICATION (DRUGS)
First Line
• No specific pharmacologic treatment
• Oxygen
• Bronchodilators for pulmonary toilet
Second Line
• Antibiotics for respiratory infections
• Diuretics if cor pulmonale develops
FOLLOW-UP
PROGNOSIS
• Severity depends on duration and intensity of exposure.
• Lung disease irreversible
• Increased risk for lung cancer (synergistic increase with cigarette smoking) and mesothelioma (2)[B]
COMPLICATIONS
• Mesothelioma
- Related to dose, time elapsed from exposure (usually 25-40 years after exposure).
- Risk is higher with exposure to amphibole fibers rather than chrysotile fibers.
- Insidious but progressive. Median survival for mesothelioma is 8-18 months (5)[B]
- Pleural effusion in 80-95% (4)[B]
• Lung cancer risk is associated with asbestos exposure whether asbestosis is present or not; synergistically increased risk in asbestos workers who smoke.
• Gastrointestinal cancer risk may be increased
PATIENT MONITORING
• Chest radiograph
• Occasional pulmonary function tests
• Prompt treatment of infections
REFERENCES
1. American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med 2004;170:691-715.
2. Glazer CS, Newman LS. Occupational interstitial lung disease. Clin Chest Med 2004;25.
3. Huggins JT, Sahn SA. Causes and management of pleural fibrosis. Respirology 2004;9:441.
4. Cugell DW, Kamp DW. Asbestos and the pleura. Chest, 2004;125:1103-1117.
5. Martino D, Pass HI. Integration of multi-modality approaches in the management of malignant pleural mesothelioma. Clin Lung Cancer 2004;5:290-298.
6. www.atsdr.cdc.gov/medical_community/working_with_patients/_downloads/overviewclin_32205_hi.pdf (accessed 5/25/2006) (C)