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474

C.S. Glaze , L.S. Newman / Clin Chest Med 25 (2004) 467–478

Table 4 Metal induced pneumoconiosis

Agent

Select exposure scenarios

Radiographic pattern

Well described Beryllium

Cobalt

Nuclear weapons, electronics, aerospace, ceramics, metal recycling, dental prostheses, alloy machining, defense industries, automotive Hard metal production, grinding, use and maintenance of hard metal tools, diamond polishing

Middle and upper zone predominant nodular infiltrates; hilar adenopathy in 20%– 30%

Mid-lower lung zone predominant reticulonodular opacities

Less well characterized Aluminum

Titanium

Zirconium

Rare earths (lanthanides)

Numerous uses: abrasives, metals, alloys, explosives (pyro powder), building materials, glass manufacture, ceramics, welding Numerous uses: metal products, paints, aerospace, defense industry, electronics Foundry sands, refractory bricks, abrasives, optical lens polishing, ceramics, nuclear reactors Glass manufacturing, photoengraving, lens polishing, electronics, carbon arc lamp exposure

Upper zone predominant reticulonodular infiltrates; upper lobe bullae and ground-glass appearance also reported Poorly described but probably reticulonodular infiltrates; pleural disease may occur Irregular and nodular opacities have been reported Lower lung zone predominant irregular opacities

Benign pneumoconiosis Iron (siderosis)

Iron welding, metal polishers

Tin (stannosis)

Tin production: smelting and bagging

Barium (baritosis)

Inhalation of fine ground barium sulfate: paint, paper, textile, vinyl, rubber, and glass manufacture, medical diagnostics

Upper zone predominant or diffuse nodular opacities Upper zone predominant or diffuse nodular opacities Diffuse nodular opacities

Data from references [71,74,94].

tasks, such as machining of beryllium. In addition to CBD, beryllium exposure can cause tracheobronchi- tis, acute toxic pneumonitis (when inhaled at high levels), and increased risk of lung cancer. Researchers currently estimate that approximately 1 million cur- rent and former workers in the United States have been exposed to beryllium, and cases are being iden- tified in other industrialized countries [73].

Unlike asbestosis and silicosis, the pathogenesis of CBD involves activation of the adoptive immune response and the innate (inflammatory) immune re- sponse. As a result, although cumulative dose seems to play a role in disease risk, the dose response re- lationship is probably less linear than in other in- organic dust-induced diseases, such as silicosis and asbestosis [74]. This has several important implica- tions. First, the latency period varies greatly, ranging from 2 months to more than 40 years [75,76]. Second, even seeming ‘‘minimal’’ exposures can be clinically significant, as illustrated by reported cases of CBD in security guards, secretaries, and residents living near beryllium production facilities [77,78].

Activation of the adoptive immune system also can be detected with the beryllium lymphocyte prolifera- tion test (BeLPT) [74]. This test is performed on either blood or bronchoalveolar lavage fluid and quantifies the beryllium-specific cellular immune re- sponse based on cell uptake of radiolabeled DNA precursors [74]. It measures the ability of T lympho- cytes to ‘‘recognize’’ beryllium as an antigen and their proliferative response. In addition to its use as a clinical diagnostic tool, the BeLPT has been used successfully to conduct surveillance for disease in many exposed workers [77,79]. It has become a stan- dard tool in the clinical screening of suspected cases (eg, ‘‘sarcoidosis’’ patients exposed to metals) and in workplaces in which beryllium contamination has occurred.

CBD that is detected through workplace surveil- lance programs is often asymptomatic. When symp- toms occur, they include insidious onset of dyspnea on exertion and dry cough. Constitutional symptoms, including fatigue, weight loss, fever, night sweats, arthalgias, and myalgias, also occur. Physical exami-

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