Tobacco Worker's Lung 

  • Author: Roger B Olade, MD, MPH; Chief Editor: Zab Mosenifar, MD   more...
 
Updated: Jan 18, 2012
 

Background

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.

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Pathophysiology

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]

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Epidemiology

Frequency

Data are not available.

Mortality/Morbidity

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

Sex

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]

Age

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

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and World Medical Association

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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

Gregg T Anders, DO is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Timothy D Rice, MD  Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, St Louis University School of Medicine

Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD  Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Professor and Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society

Disclosure: Nothing to disclose.

References

  1. Huuskonen MS, Husman K, Jarvisalo J, et al. Extrinsic allergic alveolitis in the tobacco industry. Br J Ind Med. Feb 1984;41(1):77-83. [Medline].

  2. Blanco-Romero LE, Vega LE, Lozano-Chavarría LM, Partanen TJ. CAREX Nicaragua and Panama: Worker exposures to carcinogenic substances and pesticides. Int J Occup Environ Health. Jul-Sep 2011;17(3):251-7. [Medline].

  3. Pauly JL, Paszkiewicz G. Cigarette smoke, bacteria, mold, microbial toxins, and chronic lung inflammation. J Oncol. 2011;2011:819129. [Medline]. [Full Text].

  4. Yanev I, Kostianev S. Respiratory findings in tobacco industry workers. Chest. Feb 2004;125(2):802. [Medline].

  5. Rahman M. Health Hazards And Quality Of Life Of The Workers In Tobacco Industries: Study From Three Selected Tobacco Industries At Gangachara Thana In Rangpur District Of Bangladesh. Internet J Epidemiol [serial online]. 6(2):Accessed May 2009. Available at http://www.ispub.com/journal/the_internet_journal_of_epidemiology.html.

  6. Zhang Y, Chen J, Chen Y, Dong J, Wei Q, Lou J. Environmental mycological study and allergic respiratory disease among tobacco processing workers. J Occup Health. Mar 2005;47(2):181-7. [Medline].

  7. Huuskonen MS, Jarvisalo J, Koskinen H, Kivisto H. Serum angiotensin-converting enzyme and lysosomal enzymes in tobacco workers. Chest. Feb 1986;89(2):224-8. [Medline].

  8. Swami S, Suryakar AN, Katkam RV, Kumbar KM. Absorption of nicotine induces oxidative stress among bidi workers. Indian J Public Health. Oct-Dec 2006;50(4):231-5. [Medline].

  9. Ghosh T, Barman S. Respiratory problems of workers in the zarda industry in Kolkata, India. Int J Occup Saf Ergon. 2007;13(1):91-6. [Medline].

  10. [Guideline] Tarlo SM. Cough: occupational and environmental considerations: ACCP evidence-based clinical practice guidelines. Chest. Jan 2006;129(1 Suppl):186S-196S. [Medline].

  11. Curwin BD, Hein MJ, Sanderson WT, Nishioka MG, Buhler W. Nicotine exposure and decontamination on tobacco harvesters' hands. Ann Occup Hyg. Jul 2005;49(5):407-13. [Medline].

 
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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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