Other Uncommon Pneumoconioses 263 12 Other Uncommon Pneumoconioses Masanori Akira CONTENTS including hydrogen fluoride, sulfur dioxide, metal fumes, cyanide, ozone, and aromatic hydrocarbons. 12.1 Aluminum Pneumoconiosis 263 Exposure to aluminum, alumina, and pot room 12.1.1 Prevalence 263 12.1.2 Chest X-Ray 264 fumes has been putatively associated with diffuse 12.1.3 Thin-Section Computed Tomography 265 interstitial fibrosis; however, the exact etiological 12.2 Welders’ Lung 266 agent of aluminum-induced fibrosis is uncertain 12.2.1 Prevalence 266 (Dinman 1987). 12.2.2 Chest X-Ray 266 Although exposure to aluminum metal and its 12.2.3 Thin-Section CT 267 12.3 Graphite Pneumoconiosis 268 oxides in the workplace is very common, pneumoco- 12.3.1 Prevalence 268 nioses attributable to these agents are rare. In early 12.3.2 Chest X-Ray 268 studies, pulmonary fibrosis in relation to aluminum 12.3.3 Thin-Section CT 269 exposure has been reported almost exclusively in 12.4 Talc Pneumoconiosis 270 workers involved in bauxite smelting (Shaver’s disease) 12.4.1 Prevalence 270 Shaver Riddell Wyatt Riddell 12.4.2 Chest X-Ray 271 ( and 1947; and 1948) 12.4.3 Thin-Section CT 272 or in those exposed to finely divided aluminum pow- 12.4.4 Positron Emission Tomography 272 ders, especially of the flake variety (pyro powder), in 12.5 Kaolinosis 272 the fireworks and explosives industry (Mitchell et al. 12.5.1 Prevalence 272 1961; Jordan 1961). Subsequently, diffuse interstitial 12.5.2 Chest X-Ray 273 fibrosis has been reported in workers making alumi- 12.5.3 Thin-Section CT 274 Bellot Jederlinic 12.6 Chemical Pneumonitis 274 num oxide abrasives ( et al. 1984; et 12.6.1 Ammonia 274 al. 1990) and in aluminum arc welders ( Vallyathan 12.6.2 Nitrogen Dioxide 274 et al. 1982; Herbert et al. 1982). 12.6.3 Chlorine 275 Desquamative interstitial pneumonia (Her- 12.6.4 Paraquat 275 bert et al. 1982), a granulomatous lung reaction References 277 (DeVuyst et al. 1987), and pulmonary alveolar pro- teinosis (Miller et al. 1984), which develop after exposure to fumes from aluminum welding, have 12.1 been described. Aluminum Pneumoconiosis Aluminum is derived from bauxite, an ore that con- 12.1.1 sists of alumina with iron and other minerals. The Prevalence alumina is extracted from the ore and reduced to metallic aluminum by electrolysis using large pots Shaver and Riddell (1947) found 35 cases (10%) of in the pot room. This process is carried out in large pulmonary fibrosis out of 344 aluminum pot room pots. The pot room atmosphere contains not only workers. Studies from Germany revealed that 26% of 628 alumina dust but also a variety of other substances workers had roentgenographic evidence of pneumoco- niosis (Mitchell et al. 1961). In one study, the authors reported that small irregular opacities were observed in Akira 7–8% of 788 male employees of an aluminum produc- M. , MD Townsend Jederlinic Department of Radiology, Kinki-Chuo Chest Medical Center tion company ( et al. 1988). et (former National Kinki Chuo Hospital for Chest Disease), 1180 al. (1990) found a 1% incidence of interstitial fibrosis Nagasone-cho, Sakai City, Osaka 591-8555, Japan in a factory using alumina as an abrasive. 264 M. Akira 12.1.2 The interstitial changes and honeycombing some- Chest X-Ray times shows diffuse distribution (Fig. 12.3a) (Gilks and Churg 1987; Jederlinic et al. 1990). Radiographically and pathologically, aluminum- It is reported in workers employed in the man- induced interstitial fibrosis is predominantly upper ufacture of alumina abrasives that a man leaving and mid zonal. The roentgenograms show ground- employment of the plant with a negative chest film glass or nodular opacities more pronounced in the showed evidence of disease 1 year later (Shaver upper or middle zones of both lungs and a widen- 1948). Once the disease becomes well established, ing of the mediastinal shadow (Figs. 12.1a, 12.2a). progression is often rapid, and complete disability Emphysematous change in the basal lung and dis- may result shortly thereafter. placement of the hila upwards or backwards indicat- Aluminum-associated pulmonary fibrosis is ing pulmonary contracture also characterizes the associated with a high frequency of spontaneous advanced cases (Shaver and Riddell 1947; Edling pneumothorax (Shaver and Riddell 1947; Shaver 1961; Mitchell et al. 1961; De Vuyst et al. 1986). 1948), which is life-threatening for the patient. Fig. 12.1a,b. Aluminum pneumoconiosis. (a) Numerous small nodules with upper zonal pre- dominance are seen. (b) Thin-section computed tomography scan of the same patient shows a b coalesce of small nodules a b Fig. 12.2a,b. Aluminum pneumoconiosis. (a) Fine striations, nodular, and ground-glass opacities more pronounced in the upper and middle lung zones and displacement of the hila upwards are seen. (b) Thin-section computed tomography scan of the same patient shows areas of ground-glass attenuation around the bronchovascular bundles and traction bronchiectasis Other Uncommon Pneumoconioses 265 12.1.3 section CT findings were similar to those of simple Thin-Section Computed Tomography silicosis (Akira 1995) (Fig. 12.2b). Thin-section CT is more sensitive than chest X- Thin-section computed tomography (CT) findings rays for detecting the early stage of aluminum dust- have several patterns (Figs. 12.1b–12.3b). In one study induced lung disease. Thin-section CT findings of six workers, the thin-section CT findings were of the early stage in a 40-year-old worker who had classified into three forms: predominantly reticular worked as a stamper for 14 years in a plant produc- fibrosis; predominantly nodular fibrosis; and upper ing aluminum powder were reported. The thin-sec- lung fibrosis. In two patients with predominantly tion CT findings were characterized by small, cen- reticular fibrosis, thin-section CT findings were trilobular, nodular opacities of up to 3 mm diameter similar to those of usual interstitial pneumonia, and and slightly thickened interlobular septa in all lung honeycomb formation was found (Fig. 12.3b). In one sections (Kraus et al. 2000). of these two, the distribution was different from that A case with increased CT densities of medias- of IPF in that aluminum-induced interstitial fibrosis tinal lymph nodes with histologically proven alu- had predominantly upper distribution. In one of two minum storage is reported (Vahlensieck et al. patients with predominantly nodular fibrosis, thin- 2000). The lymph nodes showed increased density section CT depicted ill-defined centrilobular nod- on native scans with values of 70–180 HU. Alumi- ules diffusely throughout both lungs. In the other num particles in such patients as well as in animals patient with predominantly nodular fibrosis, thin- experimentally exposed to aluminum-contain- ing dust are found in bronchoalveolar lavage, lung tissue, and lymph nodes up to 5 years after stop- ping the exposure (Snipes et al. 1983; Pearson et al. 1986). It is predictable that an aluminum-loaded lymph node results in increased radiographic den- sity due to metallic absorption pattern. Aluminosis is considered as differential diagnosis in patients with increased native CT densities beyond 50 HU (Vahlensieck et al. 2000). Fig. 12.3a,b. A 52-year-old man with a history of exposure to aluminum for 7 years. (a) The chest radiograph reveals reticu- lonodular opacity, predominantly distributed in the lower lung zones. (b) Thin-section computed tomography scans show dif- fusely distributed reticular hyperattenuation. Traction bron- a chiectasis and honeycombing are present b 266 M. Akira 12.2 lar markings and a generalized fine mottling or Welders’ Lung very fine nodules that are most prominent in the middle third of the lungs in the perihilar regions or Welding is the joining of metal to metal by use of in the lower two-thirds of both lungs (Fig. 12.4a). heat and/or pressure. The main fume generated by The finely nodular shadows on chest radiographs consumable electrodes is iron oxide. Cadmium, chro- disappear after removal of patients from occupa- mium, beryllium, aluminum, titanium, and nickel tional exposure (Doig and McLaughlin 1948). The may also be present. Exposure to welding fumes is micronodules do not reflect reactive fibrosis but, known to be a risk factor for chronic respiratory dis- rather, radiopaque accumulations of iron particles orders – such as pneumoconiosis, chronic bronchitis, that lie within macrophages, aggregated along the and lung cancer (Sferlazza and Beckett 1991). perivascular and peribronchial lymphatic vessels. Iron oxide is not fibrogenic in human and animal Slight fibrosis may be present, but this is not a prom- lungs. Some workers exposed to metallic iron or iron oxide fume may also have had significant exposure to other dusts such as quartz, cristobalite, or asbestos, such that siderosis may be complicated by the pres- ence of mixed dust fibrosis or asbestosis ( Harding et al. 1958; Guidotti et al. 1978). However, some authors suggested that the cause of interstitial pul- monary fibrosis seen in some welders did not appear to be coexisting silicosis (Funahashi et al. 1988). Hicks et al. (1983) and Hewitt and Hicks (1983) showed experimentally that nodular fibrosis could be produced with instillation of very large amounts of welding fumes. They concluded that most likely this was a reaction to the iron itself, although other components of the welding fume, such as chro- mium, nickel, and manganese, also accumulate in the lung. 12.2.1 a Prevalence Welder’s pneumoconiosis was first described by Doig and McLaughlin in 1936. In one study of 37 arc welders, the radiographic changes were only mini- mal (ILO category 1, type s, t, p) in the majority of the welders and had developed not only after many years of high but also after low exposure, and ILO category 2 was only found in 4 welders of the high- risk group (Spá lová and Koval 1975).