Fibrogenic Reactions

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Fibrotic processes affecting the lung and other tissues are characterized by stimulation of fibroblast proliferation and connective tissue deposition. Conventional therapy, consisting of glucocorticoids or cytotoxic agents, is usually ineffective in blocking progression of disease.

Pneumoconiosis (Silicosis)

Pneumoconiosis is the general term for lung disease caused by inhalation of mineral dust. Thus, silicosis is a fibronodular lung disease caused by inhalation of dust containing crystalline silica (a-quartz or silicon dioxide), which is distributed widely, or its polymorphs (tridymite or cristobalite), which are distributed less widely. Workers with potential for exposure are miners, sandblasters, foundry workers, tunnel drillers, quarry workers, stone carvers, ceramic workers, and silica flour production workers.

Although silicosis has been recognized for many centuries, its prevalence increased markedly with the introduction of mechanized mining. In recent decades the high prevalence has declined in developed countries because of effective industrial hygiene measures. The disease is caused by small particles (< 1 mm) deposited distally in the respiratory bronchioles, alveolar ducts, and alveoli. The surface of these particles generates silicon-based radicals that lead to the production of hydroxyl and other oxygen radicals as well as hydrogen peroxide. These oxygen free radicals damage cell membranes by lipid peroxidation and inactivate essential cell proteins.

Alveolar macrophages ingest the silica particles, become activated, and release cytokines, including tumor necrosis factor, interleukin-1, and leukotriene B4, as well as chemo-tactic factors that recruit other inflammatory cells. The ensuing inflammation damages resident cells and the extracellular matrix. Transforming growth factor-a induces proliferation of type 2 pneumocytes and stimulates synthesis of other cytokines (e.g., platelet-derived growth factor, insulin-like growth factor) and activates fibroblasts to proliferate and produce collagen; fibrosis results. Silica particles outlive the alveolar macrophages that ingest them, thereby continuing the cycle of injury.

Exposure to silica can lead to one of three disease patterns: (1) chronic simple silicosis, which usually follows more than 10 years of exposure to respirable dust with less than 30 percent quartz; (2) subacute or accelerated silicosis, which generally follows shorter, heavier exposures (i.e., 2 to 5 years); and (3) acute silicosis, which is often seen following intense exposure to fine dust of high silica content over a several-month period.

There are few symptoms and signs attending chronic simple silicosis. The diagnosis is usually made by chest radiographs, which reveal small round opacities (less than 10 mm in diameter) in both lungs, with a predilection for the upper lung zones. If an adequate occupational history is obtained from the patient along with a thorough review of the chest radiographs, the diagnosis of silicosis should not present any great difficulty. Pulmonary function tests in patients with simple silicosis usually are normal, but a mild obstructive impairment is occasionally found because of chronic dust-induced bronchitis. With complicated silicosis involving progressive fibrosis (nodules more than 10 mm in diameter), increasing dyspnea is noted, initially with exertion and progressing to dyspnea at rest. Complicated chronic silicosis is associated with reduced lung volumes, decreased diffusing capacity, and hypoxemia with exercise.

There is an increased incidence of mycobacterial disease, both typical and atypical, in silicosis. Fungal diseases (especially cryptococcosis, blastomycosis, and coccidioidomycosis) are also seen with greater frequency. The mechanism by which immune-inflammatory responses to inhaled silica lead to the increased incidence of mycobacterial and fungal infections is not clearly understood.

No treatment for silicosis is known, so management is directed toward the prevention of progression and complications. Continued exposure should be avoided and surveillance for tuberculosis should be instituted. In tuberculin skin-test positive (more than 10 mm induration) silicotic workers, treatment of latent tuberculosis infection with iso-niazid for 9 months is recommended. In acute silicosis, therapeutic whole-lung lavage has been employed to physically remove silica from the alveoli.

The prognosis for patients with chronic silicosis is good, especially if they are removed from exposure. Mortality remains high, however, in those who develop progressive massive fibrosis (PMF) [8].


Pulmonary fibrosis caused by asbestos inhalation is called asbestosis. Asbestos is the name for the fibrous forms of a group of mineral silicates including chrysolite, amosite, anthophyllite, and crocidolite. The word asbestos is derived from Greek and means "inextinguishable," and asbestos is a group of naturally occurring, heat-resistant fibrous silicates. Asbestosis is another example of a pneumoconiosis caused by inhalation and deposition of mineral dust.

Major occupational exposures occurred with asbestos mining and milling, manufacture or installation of insulation for ships or buildings, manufacture of friction materials for brake linings and clutch facings, asbestos cement manufacture, asbestos textile manufacture, and asbestos-containing spray products for decorative, acoustical, and fireproofing purposes.

Asbestosis refers to the diffuse interstitial pulmonary fibrosis caused by inhalation of asbestos fibers. Many factors are believed to play a role in disease initiation and progression, including the type and size of fiber, the intensity and duration of exposure, history of cigarette smoking, and individual susceptibility. A dose-response relationship exists such that asbestosis is more common in workers with a higher exposure level. Once asbestosis has begun, it may progress irrespective of removal from continued exposure. Finally, there is a considerable latency period (at least 10 years) between exposure and development of clinically apparent disease.

The diagnosis of asbestosis is made by a thorough exposure history, clinical examination, appropriate imaging studies and pulmonary function testing. The symptoms of asbestosis are indistinguishable from any other gradually progressive interstitial pulmonary fibrosing disorder, with progressive dyspnea and nonproductive cough being the most prominent. Bibasilar crackles with a "Velcro" quality can be auscultated over the posterolateral chest in the mid to late phase of inspiration. The crackles of asbestosis are unaffected by coughing.

Imaging studies that are helpful in the evaluation of asbestos-exposed patients are the chest radiograph and highresolution CT scanning. The chest radiograph shows small, irregular or linear opacities distributed throughout the lung fields but more prominent in the lower zones, a pattern similar to many other forms of interstitial lung disease. The most useful radiographic finding is the presence of bilateral pleural thickening, which does not commonly occur with other diseases causing interstitial pulmonary fibrosis. Diaphragmatic or pericardial calcification is almost a pathognomonic sign of asbestos exposure. High-resolution CT scanning is the most sensitive imaging method for detecting early asbestosis.

Depending on the severity of disease, pulmonary function testing will show varying degrees of restrictive impairment. Because asbestosis begins as a peribronchiolar process, reduced flow rates at low lung volumes, indicative of small airways obstruction, may be seen.

There is no known treatment for asbestosis. Workers with the disease should be removed from further exposure, because the risk that parenchymal scarring will progress appears to increase with cumulative asbestos exposure. Any other factors that may contribute to respiratory disease should be reduced or eliminated. This is especially true of cigarette smoking because there is some evidence that it may contribute to the initiation and progression of asbestosis.

Lung cancer, either squamous cell carcinoma or adenocarcinoma, is the most frequent cancer associated with asbestos exposure. Epidemiological studies describe a significant multiplicative effect that leads to a far greater risk of lung cancer in persons who are cigarette smokers and have asbestos exposure than would be expected from the additive risk of each factor. Mesotheliomas, both pleural and peritoneal, are also associated with asbestos exposure. These tumors do not appear associated with smoking.

The substitution of other fibrous materials for asbestos and the institution of strict environmental controls where it is still present have led to a dramatic reduction of occupational exposures to asbestos. Medical surveillance of currently exposed workers in the United States is required by OSHA regulation [9].

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