Practice Essentials
Tobacco worker's lung (TWL) is one disease in the group of parenchymal lung diseases categorized as hypersensitivity pneumonitis or extrinsic allergic alveolitis. This disease entity is caused by inhalation of tobacco molds and is encountered in persons who work in tobacco fields and in cigarette manufacturing plants. Increased humidity plays a major role in favoring mold growth. [1, 2, 3] The clinical features and natural history are akin to hypersensitivity pneumonitis of other causes. [4, 5, 6, 7]
Tobacco worker's lung can affect workers exposed to tobacco leaves and molds in the humidified environment of the tobacco production industry. Limited epidemiologic data point to a prevalence of TWL that is not negligible and probably is underestimated. As with other types of hypersensitivity pneumonitis, an acute versus a chronic presentation depends on the pattern of exposure. Therefore, the clinical presentation can vary from an acute influenza-like syndrome, most often self-limiting with removal of exposure, to an insidious onset of cough, exertional dyspnea, fatigue, and weight loss in chronic presentations, where fibrotic changes may be observed.
Causes
Tobacco worker's lung usually involves inhalation of an antigen, particularly organic ones. This leads to an exaggerated immune response, which produces a complex clinical presentation within the pulmonary parenchyma. Immune mediation plays a major pathogenetic role in TWL. Serum antibodies are present in most patients with TWL, but lack of correlation between presence of serum antibodies and occurrence of pulmonary symptoms has been noted.
Major causative antigens include the following:
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Aspergillus species
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Scopulariopsis brevicaulis
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Rhizopus nigricans [8]
In TWL, the primary culprit antigen is the Aspergillus species, with the source in tobacco molds. These antigens induce injury by causing macrophages and polymorphonuclear leukocytes to produce substances such as proteolytic enzymes and reactive oxygen compounds, further leading to synthesis and release of interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, and IL-6 from macrophages and lymphokines from lymphocytes, all of which result in pulmonary inflammation. Lung biopsies in patients with long-term exposure usually reveal chronic interstitial inflammation and poorly formed nonnecrotizing granulomas. [9]
In addition, smoking can potentiate the effects of tobacco dust. [10]
Studies have shown that there may be a genetic predisposition to hypersensitivity pneumonitis, which is postulated to play a major role in an individual's risk of disease. It is likely that immunologic abnormalities that underlie hypersensitivity pneumonitis reflect the interplay of multiple genes involved in the immune response. Genetic involvement can be extrapolated to apply to risk for TWL. [11]
Diagnosis
Lung biopsy is rarely required to confirm the diagnosis because diagnosis is primarily derived from a thorough occupational history, assessment of clinical features, and review of radiography results. Both transbronchial and video-assisted thoracoscopic lung biopsies are done to obtain adequate specimens for histopathologic examination. [12]
Treatment and prevention
The main treatment strategy consists of removal of exposure to tobacco dust and molds, and the main aim of corticosteroid therapy is to reduce morbidity and prevent complications—namely, the development of pulmonary fibrosis and permanent lung dysfunction. Preventing further exposure to offending agents usually leads to symptom resolution.
Avoidance of exposure to tobacco leaves is the best prevention. Curwin and associates reported that washing hands in the field while harvesting significantly reduces the amount of nicotine absorbed through the skin. [13]
Devices that limit inhalation of inciting antigens are recommended for those who must continue to work on tobacco farms. Installing controls that reduce moisture and humidity in occupied buildings helps to prevent excessively moldy tobacco leaves.
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High-resolution CT scan of lungs shows ground-glass opacification seen in an acute phase of tobacco worker's lung.
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Giant cells are a characteristic feature of acute tobacco worker's lung, which is a form of hypersensitivity pneumonitis.
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High-resolution CT (HRCT) scan shows a ground-glass appearance and reticulonodular opacities in subacute phase of hypersensitivity pneumonitis (HP) secondary to moldy hay.
