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Clin Chest Med 25 (2004) 467– 478

Occupational interstitial lung disease

Craig S. Glazer, MD, MSPHa,

  • *

    , Lee S. Newman, MD, MAb,c

aDivision of Pulmonary and Critical Care Medicine, University of Texas Southwestern, 5323 Harry Hines Boulevard, Dallas, TX 75390-9034, USA bDivision of Environmental and Occupational Health Sciences, Department of Medicine, National Jewish Medical and Research Cente , 1400 Jackson Street, Room G212, Denve , CO 80206, USA cDepartment of Preventive Medicine and Biometrics, and Division of Pulmonary Sciences and Critical Care Medicine, Department of Medicine, University of Colorado Health Sciences Cente , 4200 East 9th Avenue, Campus Box C272, Denve , CO, 80262, USA

Interstitial lung diseases (ILDs) caused by expo- sure to agents encountered in the workplace (occupa- tional ILD) are an important and preventable group of illnesses. Many different agents are reported to cause occupational ILD, some well described and others poorly characterized, and the list of causative agents continues to expand. Once thought of as the ‘‘pneu- moconioses,’’ the list of known causes of occupational ILD extends well beyond coal, asbestos, and silica. The clinical, radiologic, and pathologic presentations of occupational ILD are similar to nonoccupational variants because of the lung’s limited repertoire of responses to injury (Table 1) [1]. The clinician must maintain a high degree of suspicion and perform a thorough occupational history to search for potential exposures whenever confronted with a patient who suffers from ILD. Recognition of occupational ILD is especially important because of the implications with regard to primary and secondary disease prevention in exposed co-workers. This article reviews occupational ILDs caused by exposure to metals and inorganic fibrous and nonfibrous dusts, with emphasis on sev- eral disorders of high continued clinical relevance: silicosis, asbestosis, and chronic beryllium disease (CBD). Hypersensitivity pneumonitis, an ILD caused by exposure either in the workplace or home to organic antigens and certain reactive chemicals is covered elsewhere in this issue.

  • *

    Corresponding author.

E-mail address: Craig.Glazer@utsouthwestern.edu (C.S. Glazer).


The epidemiology of occupational ILD remains poorly understood. Limitations to the epidemiologic data include nonstandardized diagnostic criteria, var- ied physician awareness and training, limitations inherent to the various data sources (eg, death certifi- cates, hospital discharge data, surveillance or report- ing systems), and the long latency period of many agents. It is clear, however, that occupational expo- sures can cause ILD directly and influence the risk of developing idiopathic pulmonary fibrosis (IPF). Demedts et al [2] recently reviewed the latter. Several authors investigated patients with IPF and the risk of prior exposure to various occupational agents [3–7]. Mainly composed of case control studies, the literature has several limitations; however, metal dust exposure consistently emerges as a risk factor for IPF develop- ment. Workers exposed to wood dust and beauticians also were at significant risk in some studies.

Other authors investigated what proportion of ILD is occupational (including hypersensitivity pneumo- nitis). In a population-based study, Coultas et al [8] found that 14% of prevalent and 12% of incident cases of ILD were occupational. In data from European Registries, occupational ILD accounts for 4% to 18% of prevalent and 13% to 19% of incident cases of ILD [9]. Occupational ILD accounted for a greater propor- tion of ILD in the European disease registries than connective tissue disease, drugs or radiation, and vas- culitis combined. In the US population-based study by Coultas et al, occupational ILD accounted for only

slightly less than those three categories combined

0272-5231/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved. doi:10.1016/j.ccm.2004.04.004

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