Seminars in respiratory and critical care medicine
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Semin Respir Crit Care Med · Dec 2008
ReviewMyths and controversies in hypersensitivity pneumonitis.
Hypersensitivity pneumonitis (HP) is a pulmonary disease with symptoms of dyspnea and cough resulting from the inhalation of an antigen to which the patient has been previously sensitized. HP is an orphan disease, and current concepts on its diagnosis and management are often outdated. The objectives of this review are to summarize the modern evidence regarding the diagnostic criteria of HP, its pathophysiology, the procedures involved in the management of the disease, and its treatment strategies. Several areas for further research are identified, with priority given to (1) the establishment of a multicenter collaborative network to enhance the recognition, diagnosis, and management of the disease; (2) the development and support of population-based studies to provide additional insights into environmental and clinical characterization of HP; and (3) the exploration of the use and validity of biomarkers of both exposure and disease.
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Practicing pulmonologists are often faced with the question of whether a lung disease is related to something in the patient's workplace, home, or recreational environment. Recognizing a lung disease as exposure related creates both opportunities and obligations for clinicians. ⋯ We present five illustrative case studies of patients with diffuse lung diseases from environmental and occupational exposures in which communication between the pulmonologist, radiologist, and pathologist was essential for both medical and public health management. Diagnostic and treatment strategies as well as social and preventive interventions are reviewed, with key points for the practicing pulmonologist.
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Semin Respir Crit Care Med · Dec 2008
ReviewLung disease caused by exposure to coal mine and silica dust.
Susceptible workers exposed to coal mine and silica dust may develop a variety of pulmonary diseases. The prime example is classical pneumoconiosis, a nodular interstitial lung disease that, in severe cases, may lead to progressive massive fibrosis (PMF). Exposure to silica and coal mine dusts may also result in pulmonary scarring in a pattern that mimics idiopathic pulmonary fibrosis, and in chronic obstructive pulmonary disease (COPD), including emphysema and chronic bronchitis, that appears indistinguishable from obstructive lung disease caused by exposure to tobacco smoke. ⋯ Most physicians are aware of the nodular fibrosing pulmonary tissue reactions in response to retained dust, but they may not realize that these other reactions of the pulmonary parenchyma and airways to dust exist and can result in significant respiratory dysfunction in sensitive individuals. This article discusses current data on exposure to coal mine and silica dust in the United States, the epidemiology of the diseases caused by these exposures, and new concepts of causation and pathogenesis. We also review the patterns of pulmonary disease and impairment that may result.
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Cigarette smoking has been associated with several diffuse lung diseases in which both bronchiolar and interstitial lung inflammation appear to result from chronic tobacco smoke inhalation. These diseases occur primarily in relatively young adult smokers and include desquamative interstitial pneumonia, respiratory bronchiolitis-associated interstitial lung disease, and pulmonary Langerhans cell histiocytosis. ⋯ Although relatively uncommon, these smoking-related diffuse lung diseases should be recognized by clinicians as an important subset in the spectrum of interstitial lung diseases in which smoking cessation forms a central part of disease management. With the exception of acute eosinophilic pneumonia, which responds well to corticosteroid therapy, the role of corticosteroid and other immune-suppressive treatments in the management of smoking-related interstitial lung diseases is not entirely clear and is probably of limited utility, particularly in the absence of smoking cessation.
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Of the idiopathic lung diseases, idiopathic pulmonary fibrosis (IPF) and sarcoidosis have been the focus of a growing number of epidemiological investigations on the risk of environmental and occupational exposures. To date, the consistency of epidemiological evidence is suggestive of a causal relationship between several environmental exposures and IPF, with the strongest evidence for cigarette smoking and metal dust. Current knowledge about pathogenesis provides further support for a causal link. ⋯ Two studies provide consistent evidence for exposures to agricultural dust and musty odor/mold/mildew, and studies among military personnel and firefighters suggest mixed dust and fume exposures as risk factors for sarcoidosis. Although studies of the pathogenesis of sarcoidosis also provide evidence supporting environmental causation, more epidemiological studies are needed to establish consistency of associations, dose-response, and temporality. Future investigations, of gene-environment interaction offer the potential for strengthening the evidence of causation between several environmental and occupational exposures and idiopathic lung diseases.