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

gens or haptens and lead to immune sensitization. Once sensitized, individuals are susceptible for pro- gression to immune-mediated inflammation and sub-

patient qualify for worker’s compensation or other compensation and insurance programs.

sequent fibrosis. Beryllium is the best understood example of this group of agents and is discussed in more detail later. For other exposures (eg, asbestos, coal, silica), the cumulative exposure dose is the most important disease determinant for fibrosis [23]. The size, solubility, durability, oxidation/reduction, and charge of the inhaled agent are also important [24]. For fibers, pathogenic potential is also related to the fiber dimensions (length:diameter) because longer, thinner fibers are more fibrogenic [25]. This group of agents activates a complex inflammatory cascade through direct oxidant effects, activation of alveolar macrophages, alveolar epithelial cells, and other mechanisms [26]. Persistent inflammation and injury that begin with alveolar type I epithelial cell injury then progress to fibrosis [24,25].

Management

The management of occupational ILD is similar to the nonoccupational variants, with two important caveats. First, a physician should recommend reduc- tion or removal from exposure for any patient diag- nosed with ILD secondary to an occupational or environmental agent. For some of the better charac- terized agents (eg, asbestos and silica), this recom- mendation is based on the association between disease progression and cumulative exposure dose [27,28]. For the less well characterized agents, removal from exposure is considered medically prudent, even in the absence of strong scientific support. Second, a diagnosis of occupational ILD is a sentinel health event [29,30]. In other words, each new diagnosis suggests the possibility of other workers having the same disease. An index case of occupational ILD represents an opportunity for primary and secondary disease prevention in exposed co-workers. The Na- tional Institute of Occupational Safety and Health’s SENSOR program uses this concept to identify prob- lem worksites where improved exposure controls can prevent disease [31,32]. Like nonoccupational ILD, no pharmacologic treatment has proven efficacy for most occupational ILDs. In addition to reduction or removal from exposure, management is primarily supportive and includes pulmonary toilet, oxygen to treat hypoxemia, antibiotics for intercurrent infection, diuretics if cor pulmonale is present, pulmonary re- habilitation, psychosocial counseling, and assistance in providing a clear report that can be used to help a

Specific agents

Numerous agents are reported to cause occupa- tional ILD. Some of these agents are well described and others are poorly characterized. The descriptions of the poorly characterized agents are limited to case series or reports with incomplete clinical, radiologic, and pathologic correlation. This section discusses the best described example of inorganic fibrous and nonfibrous dusts and metals known to cause ILD.

Fibrous dust

Asbestosis is the best characterized occupational ILD caused by inorganic fibers (Table 2). Asbestosis is defined as interstitial fibrosis caused by asbestos fibers [33,34]. There are several different types of asbestos fibers, including serpentine (eg, chrysotile) and amphibole (eg, crocidolite, amosite, tremolite) fiber types. In addition to interstitial fibrosis, asbestos exposure causes various pleural diseases, including benign pleural effusions, pleural and diaphragmatic plaques, and diffuse pleural thickening. Asbestos exposure also increases one’s risk of several malig- nancies, most prominently lung cancer and mesothe- lioma [35]. All fiber types have the potential to cause asbestosis (and the other health effects noted) pro- vided the individual has sufficient exposure [34]. Fiber burden studies suggest that the dose required to cause asbestosis is the highest of all the asbestos- related health effects [36]. The classic teaching is that at least 25 fibers/mL/year of exposure are required to develop asbestosis [24]. Recent studies have shown, however, that lower levels can cause disease in some workers [37]. Such information is rarely available when clinically evaluating individual patients. It also is important to realize that disease after short but intense exposure is well reported [16]. The latency between exposure onset and disease is wide, ranging from 15 years to more than 40 years [38].

The primary symptom of asbestosis is dyspnea on exertion [34]. Patients also note a dry cough. Physical examination reveals bibasilar dry crackles. Hyper- trophic osteoarthropathy (clubbing) also can occur. Cor pulmonale may complicate advanced disease. Pulmonary function abnormalities include reduced lung volumes or a reduced diffusion capacity for carbon monoxide (DLCO). Large airway function, as shown by the FEV1/FVC ratio, is usually pre- served, but small airways obstruction is an early

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