eMedicine Specialties > Pulmonology > Occupational Lung Diseases

Tobacco Worker's Lung

Roger B Olade, MD, MPH, Medical Director, Providence Health Group
Jazeela Fayyaz, DO, Senior Fellow, Department of Pulmonology, Lenox Hill Hospital; 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

Updated: Sep 17, 2009

Introduction

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. The clinical features and natural history are akin to hypersensitivity pneumonitis of other causes.

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.

In addition, smoking can potentiate the effects of tobacco dust.^{[2 ]}

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.^{[2 ]}

Age

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

Clinical

History

• A comprehensive history of exposure to tobacco mold and leaves should be obtained.
  • Workers not using masks during their working period are 5 times more likely to develop this disease.^{[3 ]}
  • Longer duration of work is associated with an increased risk of disease. In a 2009 study, those working with tobacco for more than 10 years were twice as likely to develop the disease compared with those working in the field less than 5 years.^{[3 ]}
• Tobacco worker’s lung, as with most hypersensitivity pneumonitis syndromes, has acute, subacute, and chronic presentations.
  • In acute presentations, patients develop abrupt onset of fever, cough, chills, myalgias, headache, and malaise about 4-6 hours following exposure to tobacco plants and molds. These symptoms are self-limited, resolving in 12 hours to several days once the patient avoids the inciting agent. The symptoms may recur with reexposure.
  • Patients who have had long-term exposure to tobacco plantations usually have insidious onset of cough, exertional dyspnea, fatigue, and weight loss. Disabling and irreversible respiratory findings due to pulmonary fibrosis may occur late in the course of the disease. Removing patients from tobacco exposure results in only partial improvement.

Physical

Physical examination reveals the following:

• Tachypnea
• Diffuse fine rales
• Wheezing
• Weight loss
• Digital clubbing
• Fever
• Evidence of cor pulmonale

Causes

Major causative antigens include the following:

• Aspergillus species
• Scopulariopsis brevicaulis
• Rhizopus nigricans^{[4 ]}

Differential Diagnoses

Other Problems to Be Considered

Inhalation fever (Monday illness)
Organic-dust toxic syndrome
Allergic bronchopulmonary aspergillosis
Pneumoconiosis
Bagassosis
Byssinosis

Workup

Laboratory Studies

• No specific tests exist for tobacco worker's lung (TWL); the diagnosis is established with a history of exposure and possibly with the support of the following tests.
  • Elevated serum levels of angiotensin-converting enzyme (ACE), N- acetyl-beta-glucosaminidase (NAG), and beta-glucuronidase (beta-GLU) may be present. Elevation of these enzymes does not have a high sensitivity or specificity.
  • Bronchoalveolar lavage (BAL) may show lymphocytosis, neutrophilia or eosinophilia, and reversal of CD4/CD8 ratio.
  • Immunoglobulin G, immunoglobulin M, and immunoglobulin A serum antibodies to causative antigens may be present.
  • Nonsmoking tobacco harvesters may have cotinine and nicotine levels as high as active smokers in the general populations.^{[5 ]}
• Nonspecific markers of inflammation are elevated.
  • Elevated erythrocyte sedimentation rate
  • Elevated C-reactive protein
  • Positive rheumatoid factor
  • Elevated serum lactate dehydrogenase (LDH)

Imaging Studies

• Chest radiograph: No distinctive changes are noted on chest radiography, but it might show progressive fibrotic changes associated with upper lobe volume loss or diffuse reticulonodular infiltrates in chronic exposure. In acute exposure, the infiltrates are usually more prevalent in the lower lobes.
• High-resolution computed tomography (HRCT) scan: This may show a ground-glass appearance, prominent medium-sized bronchial walls, parenchymal micronodules, and absence of hilar adenopathy.

High-resolution CT scan of lungs shows ground-glass opacification seen in an acute phase of tobacco worker's lung.

Other Tests

• Pulmonary function testing shows mostly restrictive patterns with occasionally mixed restrictive and obstructive patterns, impaired diffusion capacity, and lung volume loss. Peak expiratory flow rates also are reduced.^{[6 ]}
• Arterial hypoxemia with hypocapnia reflecting an increased A-a oxygen gradient commonly occurs at rest, with further worsening on exercise.

Procedures

• 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.

Histologic Findings

Samples from lung biopsies show chronic interstitial inflammation with infiltration of plasma cells, mast cells, macrophages, and lymphocytes, usually with poorly formed nonnecrotizing granulomas. The granulomas are loosely formed and tend to occur in proximity to the bronchioles. Cholesterol clefts and giant cells also are observed within and outside the granulomas.

Giant cells are a characteristic feature of acute tobacco worker's lung, which is a form of hypersensitivity pneumonitis.

Treatment

Medical Care

• No medical treatment is available for tobacco worker's lung (TWL).
• The major treatment strategy is elimination of exposure to tobacco molds or leaves.
• Systemic glucocorticoids have been used to treat patients with tobacco worker’s lung but without any good evidence of effectiveness, especially in patients with chronic exposure.
• Removal from exposure to the offending agents usually leads to symptom resolution.
• Also see the clinical guideline summary from the American College of Chest Physicians (ACCP), Cough: occupational and environmental considerations: ACCP evidence-based clinical practice guidelines.^{[7 ]}

Consultations

• Pulmonologist

Medication

• No medications are available.

Follow-up

Further Outpatient Care

• Tobacco worker's lung (TWL) patients should receive supportive follow-up care at a chest clinic.

Deterrence/Prevention

• 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.^{[8 ]}

Complications

• Some patients have irreversible lung damage progressing to pulmonary fibrosis with resultant cor pulmonale.

Prognosis

• The prognosis is excellent if exposure to tobacco plants is curtailed before permanent damage occurs.

Patient Education

• Inform tobacco workers about the possible risk of chronic lung damage from continuous exposure and that they should seek medical attention if certain symptoms are noted.

Miscellaneous

Medicolegal Pitfalls

• Medicolegal issues could ensue if the physician fails to recognize the relationship between occupational exposure and symptoms. Workers' compensation usually covers treatment if the exposure was at work.

Multimedia

Media file 1: High-resolution CT scan of lungs shows ground-glass opacification seen in an acute phase of tobacco worker's lung.

Media file 2: Giant cells are a characteristic feature of acute tobacco worker's lung, which is a form of hypersensitivity pneumonitis.

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

3. 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.

4. 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].

5. 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].

6. 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].

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

8. 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].

9. Bhisey RA, Bagwe AN, Mahimkar MB, Buch SC. Biological monitoring of bidi industry workers occupationally exposed to tobacco. Toxicol Lett. Sep 5 1999;108(2-3):259-65. [Medline].

10. Ghosh SK, Parikh JR, Gokani VN, Kashyap SK, Chatterjee SK. Studies on occupational health problems during agricultural operation of Indian tobacco workers: a preliminary survey report. J Occup Med. Jan 1979;21(1):45-7. [Medline].

11. 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].

12. Kusemamariwo T, Neill P. Carcinoma of the bronchus in tobacco farm workers. An unrecognised high risk group. Trop Geogr Med. Jul 1990;42(3):261-4. [Medline].

13. McBride JS, Altman DG, Klein M, White W. Green tobacco sickness. Tob Control. Autumn 1998;7(3):294-8. [Medline].

14. Mustajbegovic J, Zuskin E, Schachter EN, Kern J, Luburic-Milas M, Pucarin J. Respiratory findings in tobacco workers. Chest. May 2003;123(5):1740-8. [Medline].

Keywords

tobacco worker's lung, hypersensitivity pneumonitis, HP, extrinsic allergic alveolitis, EAA, TWL, parenchymal lung diseases, tobacco molds, Aspergillus species, interleukin-1, tumor necrosis factor-alpha, interleukin-6, IL-1, IL-6, pulmonary inflammation, Scopulariopsis brevicaulis

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, Senior Fellow, Department of Pulmonology, Lenox Hill 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 Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: sepracor Ownership interest None

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gregg T Anders, DO, Medical Director, Great Plains Regional Medical Command , Brook 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.

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint 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, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
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.

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