Tobacco Worker's Lung

Updated: Apr 17, 2018
  • Author: Roger B Olade, MD, MPH; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Practice Essentials

Tobacco worker's lung (TWL) is one disease in the group of parenchymal lung diseases categorized as hypersensitivity pneumonitis (United States) or extrinsic allergic alveolitis (Britain). [1] This disease entity is caused by inhalation of tobacco molds and is encountered in persons who work in tobacco fields and cigarette manufacturing plants. Increased humidity plays a major role in favoring mold growth. [2] The clinical features and natural history are akin to hypersensitivity pneumonitis of other causes. [3, 4, 5]

TWL 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 tobacco worker’s lung. Serum antibodies are present in most patients with tobacco worker’s lung, but a lack of correlation between the presence of serum antibodies and pulmonary symptoms has been noted.

In tobacco worker’s lung, the culprit antigen is the Aspergillus species, with a source in tobacco molds. The antigens induce injury by causing macrophages and polymorphonuclear leukocytes to produce substances such as proteolytic enzymes and reactive oxygen compounds. These further lead to synthesis and release of interleukin (IL)-1, tumor necrosis factor (TNF)-alpha, and IL-6 from macrophages and lymphokines from lymphocytes, which result in pulmonary inflammation. Lung biopsies in patients with long-term exposure usually demonstrate chronic interstitial inflammation and poorly formed nonnecrotizing granulomas. [6]

In addition, smoking can potentiate the effects of tobacco dust. [7]

Studies have shown that there may be a genetic predisposition to hypersensitivity pneumonitis, postulated to play a major role in determining an individual's risk of disease. It is likely that the 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 tobacco worker's lung. [8]

Major causative antigens include the following:

  • Aspergillus species

  • Scopulariopsis brevicaulis

  • Rhizopus nigricans [9]

Lung biopsies are rarely required to confirm diagnosis, because diagnosis is primarily derived from a thorough occupational history, clinical features, and radiography. Both transbronchial and video-assisted thoracoscopic lung biopsy are used to provide adequate specimens for histopathological examination. [10]

The major treatment strategy is elimination of exposure to tobacco molds or leaves. Preventing further exposure to the offending agents usually leads to symptom resolution.

Avoidance of exposure to tobacco leaves is the best prevention. Curwin et al report that washing hands in the field while harvesting significantly reduces the amount of nicotine absorbed through the skin. [11]

Devices that limit inhalation of inciting antigens is recommended for those who must continue to work on tobacco farms. Installing controls that reduce moisture and humidity in occupied buildings will prevent excessively moldy tobacco leaves.