Asbestosis

BASIC INFORMATION
Asbestosis is a slowly progressive diffuse interstitial fibrosis resulting from dose-related inhalation exposure to fibers of asbestos. Asbestos is a mixture of silicates of iron, magnesium, nickel, cadmium and aluminium, and has the unique property of occurring naturally as a fibre. It is remarkably resistant to heat, acid and alkali, and has been widely used for roofing, insulation and fireproofing. Asbestos has been mined in southern Africa, Canada, Australia and eastern Europe. Several different types of asbestos are recognized: about 90% of asbestos is chrysotile, 6% crocidolite and 4% amosite. Chrysotile or white asbestos is the softest asbestos fibre. Each fibre is often as long as 2 cm but only a few microns thick. It is less fibrogenic than crocidolite.

Crocidolite (blue asbestos) is particularly resistant to chemical destruction and exists in straight fibres up to 50 mm in length and 1-2 m in width. Crocidolite is the type of asbestos most likely to produce asbestosis and mesothelioma. This may be due to the fact that it is readily trapped in the lung. Its long, thin shape means that it can be inhaled, but subsequent rotation against the long axis of the smaller airways, particularly in turbulent airflow during expiration, causes the fibres to impact. Crocidolite is also particularly resistant to macrophage and neutrophil enzymatic destruction.

Exposure to asbestos occurred particularly in shipbuilding yards and in power stations, but it was used so widely that low levels of exposure were very common. Up to 50% of city dwellers have asbestos bodies (asbestos fibres covered in protein secretions) in their lungs at post mortem. Regulations in the UK prohibit the use of crocidolite and severely restrict the use of chrysotile. Careful dust control measures are enforced, which should eventually abolish the problem. Workers continue to be exposed to blue asbestos in the course of demolition or in the replacement of insulation, and it should be remembered that there is a considerable time lag between exposure and development of disease, particularly mesothelioma (20-40 years).
The risk of primary lung cancer (usually adenocarcinoma) is increased in people exposed to asbestos, even in nonsmokers. This risk is about 5-7-fold greater in those who have parenchymal asbestosis and about 1.5-fold in those with pleural plaques without parenchymal fibrosis. A synergistic relationship exists between asbestosis and cigarette smoking with the risk of bronchial carcinoma multiplied 5- fold above the risk attributable to smoking alone.

Diseases caused by asbestos are summarized in Table 14.18. Bilateral diffuse pleural thickening, asbestosis, mesothelioma and asbestos-related carcinoma of the bronchus are all eligible for industrial injuries benefit in the UK.
Asbestosis is defined as fibrosis of the lungs caused by asbestos dust, which may or may not be associated with fibrosis of the parietal or visceral layers of the pleura. It is a progressive disease characterized by breathlessness and accompanied by finger clubbing and bilateral basal endinspiratory crackles. Fibrosis, not detectable on chest X-ray, is often revealed on high-resolution CT scan. No treatment is known to alter the progress of the disease, though corticosteroids are often prescribed.

EPIDEMIOLOGY & DEMOGRAPHICS
• In U.S.: 5 to 10 new cases / 100,000 persons / yr
• Prolonged interval (20 to 30 yr) between exposures to inhaled fibers and clinical manifestations of disease
• Most common in workers involved in the primary extraction of asbestos from rock deposits and in those involved in the fabrication and installation of products containing asbestos (e.g., naval shipyards in World War II, installation of floor tiles, ceiling tiles, acoustic ceiling coverings, wall insulation, and pipe coverings in public buildings)
PHYSICAL FINDINGS & CLINICAL PRESENTATION
• Insidious onset of shortness of breath with exertion is usually the first sign of asbestosis.
• Dyspnea becomes more severe as the disease advances; with time, progressively less exertion is tolerated.
• Cough is frequent and usually paroxysmal, dry, and nonproductive.
• Scant mucoid sputum may accompany the cough in the later stages of the disease.
• Fine end respiratory crackles (rales, crepitations) are heard more predominantly in the lung bases.
• Digital clubbing, edema, jugular venous distention are present.
ETIOLOGY
Inhalation of asbestos fibers
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
• Silicosis
• Siderosis, other pneumonoconioses
• Lung cancer
• Atelectasis
WORKUP
Documentation of exposure history, diagnostic imaging, pulmonary function testing
LABORATORY TESTS
• Generally not helpful
• Possible mild elevation of ESR, positive ANA and RF (These tests are nonspecific and do not correlate with disease severity or activity.)
• Pulmonary function testing: decreased vital capacity, decreased total lung capacity, decreased carbon monoxide gas transfer
• ABGs: hypoxemia, hypercarbia in advanced stages
IMAGING STUDIES
Chest x-ray examination:
• Small, irregular shadows in lower lung zones
• Thickened pleural, calcified plaques (present under diaphragms and lateral chest wall)
TREATMENT
NONPHARMACOLOGIC THERAPY
• Smoking cessation, proper nutrition, exercise program to maximize available lung function
• Home oxygen therapy prn
• Removal of patient from further asbestos fiber exposure
ACUTE GENERAL Rx
• Prompt identification and treatment of respiratory infections
• Supplemental oxygen on a prn basis
• Annual influenza vaccination, pneumococcal vaccination
CHRONIC Rx
See “Acute General Rx.”
DISPOSITION
• There is no specific treatment for asbestosis.
• Death is usually secondary to respiratory failure from cor pulmonale.
• Patients with asbestosis have increased risk for mesotheliomas, lung cancer, and TB. Recent reports indicate that the risk of asbestos-induced lung cancer may
be overestimated.
• Survival in patients following development of mesothelioma is 4 to 6 yr.