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C.S. Glaze , L.S. Newman / Clin

sive massive fibrosis, in which large masses of dense fibrosis develop (usually in the upper lung zones), can complicate chronic simple and accelerated silico- sis (see later discussion). Finally, high exposures over a period of months to 2 years can cause acute sili- coproteinosis, a disease that is similar clinically and pathologically to alveolar proteinosis [54,55].

In addition to ILD, silica exposure increases the risk for developing various pulmonary and nonpul- monary illnesses. Silica exposure markedly increases the risk of developing active tuberculosis and other mycobacterial disease. The risk increases with ex- posure and severity of disease on chest radiograph [56]. The incidence of chronic bronchitis and chronic obstructive pulmonary disease (COPD) also increases in workers with silica exposure independent of to- bacco use and even in the absence of radiographically detectable silicosis [57,58]. The risk of emphysema increases in silica-exposed smokers (compared with smokers without silica exposure) and persons with progressive massive fibrosis [27,59]. Silica exposure also increases the risk for developing chronic renal insufficiency and autoimmune diseases, particularly scleroderma, rheumatoid arthritis, and Wegener’s granulomatosis [27,60]. Silica is a human carcinogen that is especially associated with risk for lung cancer independent of tobacco exposure [27,58,61].

Patients with chronic simple silicosis are fre- quently asymptomatic unless COPD also is present. Symptoms develop as the disease progresses, particu- larly when complicated by progressive massive fibro- sis [62]. Symptoms include dyspnea on exertion and productive cough. Both symptoms are of gradual onset and progress slowly. Pulmonary function tests typically reveal a mixed pattern of obstruction and restriction with a reduced diffusion capacity. Symp- toms often correlate best with the obstructive abnor- malities [63,64]. When complicated by severe progressive massive fibrosis, restriction predominates. Direct measures of gas exchange by arterial blood gases, especially during exercise testing, provide the most sensitive indication of physiologic impairment.

The typical radiographic finding in silicosis is upper lobe predominant nodular opacities. Hilar adenopathy also is seen, and in approximately 10% of cases a characteristic pattern of ‘‘eggshell’’ or peripheral calcification occurs. Such calcifications are neither sensitive nor specific. The pulmonary nodules of silicosis are typically less than 5 mm in diameter and are well circumscribed. The nodules may coalesce to form masses, which are known as progressive massive fibrosis. The International Labor Organization defines a progressive massive fibrotic lesion as a mass larger than 1 cm in diameter, whereas

Chest Med 25 (2004) 467–478


the Silicosis and Silicate Disease Committee uses a size parameter of 2 cm [55]. As with asbestosis, HRCT is more sensitive than chest radiography [65]. CT is also superior at detecting coalescent nodules and the typical, well-circumscribed upper lobe pre- dominant individual nodules. The nodules are primarily posterior and central in distribution. Sub- pleural nodules are also common, but centrilobular nodules are unusual [66,67]. Progressive massive fi- brotic lesions are usually posterior and bilateral. Unilateral lesions occur rarely, predominantly on the right side. Rapid changes in the size of masses or the presence of cavitation should prompt a search for alternative or secondary diagnoses, particularly mycobacterial disease and lung cancer.

The diagnosis of silicosis usually does not require a lung biopsy. When a biopsy is performed, the pathognomonic finding is a round, hyalinized nodule known as a silicotic nodule [50]. Silicotic nodules are found in the lung parenchyma and hilar lymph nodes. Diffuse interstitial fibrosis also occurs in a small number of patients [50,68]. Early silicotic nodules are highly cellular, with scattered, disorganized deposi- tion of collagen. In later stages, the nodules form the typical ‘‘onion skin’’ appearance, with little or no cen- tral cellularity.

Several therapies have been tried, including corti- costeroids and whole lung lavage, but none is of pro- ven benefit. Therapy focuses on removal from exposure and supportive care. One also should screen patients with silicosis for tuberculosis with purified protein derivative skin tests. All patients with a posi- tive test result ( > 10 mm of induration) should receive treatment [69,70]. Other considerations for case man- agement are as described previously for asbestosis.


The best characterized occupational ILD second- ary to metal dust and fume exposure is CBD (Table 4). CBD is a granulomatous disease similar to sarcoid- osis that occurs after exposure and subsequent sensi- tization to beryllium. Like sarcoidosis, the lung is the primary organ involved, but the skin, liver, spleen, myocardium, skeletal muscle, salivary glands, and bones also may be affected. Exposure to dust or fumes of pure beryllium metal, low percentage be- ryllium alloys (with copper, nickel, magnesium, or aluminum), or beryllium oxides can cause CBD [71,72]. Industries that use beryllium are shown in Table 4. Current data based on workforce screenings indicate that beryllium sensitization or CBD develops in 2% to 10% of persons exposed [72], with higher rates found associated with certain job titles and

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