The diagnosis of pneumoconiosis and novel therapies.
Wilt JL; Parker JE; Banks DE
Occupational lung disease. Banks DE, Parker JE, eds. New York: Chapman & Hall Medical, 1998 Apr; :119-138
Pneumoconioses are lung diseases which result from mineral dust deposition in the lung and the subsequent host response. This term is derived from the Greek language (pneumo, the Greek root for lung and konis, the root for dust) and has been applied in clinical medicine since the early 19th century (Meiklejohn, 1951). These are illnesses rooted in antiquity, which have had their highest human toll during the industrial age, yet it remains a tragedy of our time that these preventable diseases have not disappeared. A number of respiratory manifestations associated wit the inhalation, retention and tissue reaction to mineral dusts have been described and reflect the different effects of these dusts on the lung (Ballan et al., 1993). Although a wide variety of mineral dusts are implicated in disease, all share common diagnostic criteria. The focus of this report is the description of diagnostic criteria for the most frequently occurring disorders. These are illnesses attributable to coal dust inhalation [coal workers' pneumoconiosis (CWP)], inhalation of dusts containing crystalline silica (silicosis), and inhalation exposure to asbestos fibers (asbestosis and other asbestos-related pulmonary disorders). Novel, but unproven, therapeutic approaches which may alter the natural history of pneumoconioses will also be considered. There are three major criteria for the diagnosis of pneumoconiosis. The first is a sufficient exposure to a mineral dust known to cause pneumoconiosis with an appropriate latency period. Exposures to silica, coal or asbestos occur most commonly in an occupational setting. The second criteria is the recognition of a characteristic chest radiograph which meets published standards for the diagnosis of pneumoconiosis. Although respiratory symptoms and impairment in lung function commonly occur in workers diagnosed to have pneumoconiosis, neither is requisite for the diagnosis. The third is the absence of an illness which might mimic pneumoconiosis. Disseminated mycobacterial or fungal disease might mimic CWP or silicosis, as may sarcoidosis. Asbestosis is not infrequently confused with idiopathic pulmonary fibrosis, bronchiolitis obliterans with organizing pneumonia, or interstitial lung disease associated with collagen vascular disease (Bands et al., 1993; Wilt and Banks, 1995). The diagnosis of pneumoconiosis, therefore, is a clinical one and only in the very unusual situation is a lung biopsy indicated to make the diagnosis.
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