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Tobacco Worker's Lung

  • Author: Roger B Olade, MD, MPH; Chief Editor: Ryland P Byrd, Jr, MD  more...
Updated: Jun 03, 2014


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.

It 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.[3]

In addition, smoking can potentiate the effects of tobacco dust.[4]

Recent studies have shown that there might 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.[5]




Data are not available.


Because of the excellent prognosis, little documented evidence of long-term illness or death from tobacco worker’s lung exists.


Although no documented evidence indicates a sex predilection, tobacco worker’s lung is more common in males, probably because most tobacco workers are men. However, recent data show that female tobacco workers are more prone to respiratory symptoms and lung impairments despite working in an environment with lower levels of pollution.[4]


Tobacco worker’s lung occurs in adults of working age but not in children or retired people.

Contributor Information and Disclosures

Roger B Olade, MD, MPH Medical Director, Genesis Health Group

Roger B Olade, MD, MPH is a member of the following medical societies: American College of Occupational and Environmental Medicine, American College of Physicians

Disclosure: Nothing to disclose.


Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Jazeela Fayyaz, DO Pulmonologist, Department of Pulmonology, Unity Hospital

Jazeela Fayyaz, DO is a member of the following medical societies: American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.


Gregg T Anders, DO Medical Director, Great Plains Regional Medical Command , Brooke Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio

Disclosure: Nothing to disclose.

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High-resolution CT scan of lungs shows ground-glass opacification seen in an acute phase of tobacco worker's lung.
Giant cells are a characteristic feature of acute tobacco worker's lung, which is a form of hypersensitivity pneumonitis.
High-resolution CT (HRCT) scan shows a ground-glass appearance and reticulonodular opacities in subacute phase of hypersensitivity pneumonitis (HP) secondary to moldy hay.
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