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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
 

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.

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.

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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]

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]

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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, 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.

Coauthor(s)

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.

Acknowledgements

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.

References
  1. Huuskonen MS, Husman K, Jarvisalo J, et al. Extrinsic allergic alveolitis in the tobacco industry. Br J Ind Med. 1984 Feb. 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. 2011 Jul-Sep. 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. 2004 Feb. 125(2):802. [Medline].

  5. Camarena A, Juárez A, Mejía M, Estrada A, Carrillo G, Falfán R, et al. Major histocompatibility complex and tumor necrosis factor-alpha polymorphisms in pigeon breeder's disease. Am J Respir Crit Care Med. 2001 Jun. 163(7):1528-33. [Medline].

  6. 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. 6(2):[Full Text].

  7. 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. 2005 Mar. 47(2):181-7. [Medline].

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

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

  10. 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].

  11. Kokkarinen JI, Tukiainen HO, Terho EO. Effect of corticosteroid treatment on the recovery of pulmonary function in farmer's lung. Am Rev Respir Dis. 1992 Jan. 145(1):3-5. [Medline].

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

  13. Braun SR, doPico GA, Tsiatis A, Horvath E, Dickie HA, Rankin J. Farmer's lung disease: long-term clinical and physiologic outcome. Am Rev Respir Dis. 1979 Feb. 119(2):185-91. [Medline].

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