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physiologic pattern with slow clinical course, occu- pational history of exposure, and exclusion of other causes of ILD.

tobacco products because of the multiplicative risk for lung cancer in such patients.

Twenty percent to 40% of patients with asbestosis progress. Progression is typically slower than that which occurs with IPF. Having old radiographs that show a prolonged course (eg, 5–20 years) of gradu- ally increasing lung fibrosis helps exclude most forms of ILD and points the finger at dust-related illness. Risk factors for progression include cumulative ex- posure, severity of disease at diagnosis, and possibly fiber type [50,51]. There is no known pharmacologic treatment for asbestosis. No studies have demon- strated efficacy for corticosteroids or immunosup- pressant medications. Rather, therapy focuses on removal from exposure and supportive care, including pneumovax and influenza vaccinations, treatment of intercurring respiratory infections, supplemental oxy- gen to treat resting or exercise-induced hypoxemia, diuretics for cor pulmonale, pulmonary rehabilitation, and counseling to eliminate future exposure and avoid

Nonfibrous dust

The best characterized occupational ILD second- ary to nonfibrous inorganic dust exposure is silicosis (Table 3). Silicosis occurs after inhalational exposure to crystalline silica (eg, quartz, cristobalite, tridymite) or silicate-containing dusts [52,53]. Industries asso- ciated with silica exposure are shown in Table 3. Silica-related ILD presents in three ways. The most common—chronic simple silicosis—occurs after a latency period of at least 10 years and as long as 40 years [27]. The second presentation—accelerated silicosis—occurs with higher exposures. The clinical phenotype of accelerated silicosis is similar to chronic simple silicosis, but the latency period is only 5 to 10 years and the disease is usually more severe. When individual silicotic nodules coalesce, the dis- ease is referred to as complicated silicosis. Progres-


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

Chest Med 25 (2004) 467–478

Table 3 Inorganic nonfibrous dust pneumoconiosis

Agent Well described

Select exposure scenarios

Radiographic pattern

Crystalline silica

Coal dust

Hard rock mining, construction, road work, tunneling, sandblasting, foundry work, granite/stone work, silica flour production/use, ceramics, glass manufacture Exposure to coal mine dust

Upper zone predominant nodular infiltrates; may develop progressive massive fibrosis; hilar adenopathy +/calcification may occur

Upper zone predominant nodular infiltrates; may develop progressive massive fibrosis, emphysema

Less well characterized Other carbon compounds

(graphite, carbon black, oil shale) Mica



Diatomaceous earth


Tires, pigments, paints, pencils, foundry linings, mining, metallurgy, carbon electrodes, plastics Boiler and furnace lining, electronics industry, building materials (tiles, cements), acoustic products, grinding Kaolin mining, paper product manufacture, ceramics, refractory materials, ceramics, plastics

Nepheline mining, pottery, paint filler

Foundries, filter production, abrasives, dry lubricant; when heated above 450C it converts to crystalline silica Numerous uses: paint, paper, cosmetics, roofing products, rubber, dry lubricant, textile manufacture

Upper zone predominant nodular infiltrates; may develop progressive massive fibrosis

Mid-lower zone predominant reticular opacity; honeycombing may occur

Mid-lower zone predominant with rounded and irregular opacities; progressive massive fibrosis may occur; associated pleural disease is reported Reticular opacity, hilar adenopathy, atelectasis Identical to silicosis

Reticular and nodular opacities, possible midzone predominance; may depend on degree of contamination with asbestos/silica

Data from references [62,92,93].

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