Asbestos-Related Lung Disease

Am Fam Physician. 2007 Mar 1;75(5):683-688.

  Patient information: See related handout on asbestosis, written by the authors of this article.

The inhalation of asbestos fibers may lead to a number of respiratory diseases, including lung cancer, asbestosis, pleural plaques, benign pleural effusion, and malignant mesothelioma. Although exposure is now regulated, patients continue to present with these diseases because of the long latent period between exposure and clinical disease. Presenting signs and symptoms tend to be nonspecific; thus, the occupational history helps guide clinical suspicion. High-risk populations include persons in construction trades, boilermakers, shipyard workers, railroad workers, and U.S. Navy veterans. Every effort should be made to minimize ongoing exposure. Patients with a history of significant asbestos exposure may warrant diagnostic testing and follow-up assessment, although it is unclear whether this improves outcomes. Patients with significant exposure and dyspnea should have chest radiography and spirometry. The prognosis depends on the specific disease entity. Asbestosis generally progresses slowly, whereas malignant mesothelioma has an extremely poor prognosis. The treatment of patients with asbestos exposure and lung cancer is identical to that of any patient with lung cancer. Because exposure to cigarette smoke increases the risk of developing lung cancer in patients with a history of asbestos exposure, smoking cessation is essential. Patients with asbestosis or lung cancer should receive influenza and pneumococcal vaccinations.

Asbestos, a crystalline mineral that occurs in deposits throughout the world, is the smallest naturally occurring fiber. Because of its flexibility, durability, and resistance to heat and chemical corrosion, it became widely used in industry. The inhalation of asbestos fibers was first linked to the development of lung disease in 1890, and the first deaths attributable to asbestos exposure were reported in 1907. Legislation controlling exposure was introduced in the United Kingdom in 1931, but the United States did not enact its first legislation limiting exposure until 1971.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendation Evidence rating References

Risk of asbestos exposure should be assessed with occupational history. Screening should be considered in patients with a high risk of exposure.

C

2

Chest radiography and pulmonary function testing should be performed every three to five years in patients with asbestos-related disease.

C

7

Smoking cessation should be encouraged.

A

3, 9, 12

Influenza and pneumococcal vaccines should be given to patients with asbestosis or cancer.

C

12


A = consistent, good quality patient-oriented evidence; B = inconsistent or limited quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For more information about the SORT evidence rating system, see page 603 or http://www.aafp.org/afpsort.xml.

SORT: KEY RECOMMENDATIONS FOR PRACTICE

View Table

SORT: KEY RECOMMENDATIONS FOR PRACTICE

Clinical recommendation Evidence rating References

Risk of asbestos exposure should be assessed with occupational history. Screening should be considered in patients with a high risk of exposure.

C

2

Chest radiography and pulmonary function testing should be performed every three to five years in patients with asbestos-related disease.

C

7

Smoking cessation should be encouraged.

A

3, 9, 12

Influenza and pneumococcal vaccines should be given to patients with asbestosis or cancer.

C

12


A = consistent, good quality patient-oriented evidence; B = inconsistent or limited quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For more information about the SORT evidence rating system, see page 603 or http://www.aafp.org/afpsort.xml.

The peak global incidence of asbestos-related disease is expected to occur 30 to 40 years after the period of peak usage (i.e., the 1960s and 1970s). For diffuse malignant mesothelioma, the condition with the longest latency, the incidence is expected to rise in Europe until 2020.1 The prevalence of asbestosis in the United States is not known, but in 2000, there were an estimated 20,000 hospital discharges with this diagnosis and 2,000 deaths with asbestosis as the underlying or contributing cause, and these numbers are expected to rise through this decade.2,3 The incidence of malignant mesothelioma in the United States was thought to peak at 2,000 cases per year from 2000 to 2004; another study suggested there would be a yearly average of 3,200 deaths from asbestos-related lung cancer from 1985 to 2009.4,5

Asbestos-Related Lung Disease

Inhalation of asbestos fibers can result in a number of distinct pathologic processes (Table 1).25 These include the development of pleural-based abnormalities such as benign plaques, benign pleural effusions, and malignant mesothelioma. In addition, new cases of asbestosis, an important pneumoconiosis, and many asbestos-related lung cancers continue to occur. Most patients with asbestos-related lung disease have a strong exposure history; however, significant disease can occur with minimal exposure and, rarely, with unknown exposure.

TABLE 1

Symptoms, Prevalence, and Treatment of Asbestos-Related Lung Diseases

Disease Presenting symptoms Prevalence* Treatment

Asbestosis

Dyspnea, dry cough

Approximately 200,000 patients with asbestosis and 2,000 deaths annually

No specific therapy; general measures outlined in the article; surveillance for lung cancer; smoking cessation

Lung cancer

Chest pain, cough, dyspnea, hemoptysis, weight loss, fatigue, symptoms caused by metastases and direct invasion

Estimated 2,000 to 3,200 lung cancer deaths annually related to asbestos exposure

Multimodality treatment including surgery, radiotherapy, and chemotherapy

Mesothelioma

Chest pain, cough, dyspnea, weight loss, fatigue, pleural effusion, symptoms caused by metastases, pericardial invasion, esophageal compression, superior vena caval invasion

Approximately 2,000 deaths annually; incidence and mortality rate are the same

Multidisciplinary approach focused on supportive care; multimodality treatment including surgery, radiotherapy, and chemotherapy (clinical trials ongoing); radiotherapy for localized pain and metastatic spread occurring along a biopsy tract; chemical or surgical pleurodesis for pleural effusions

Pleural plaques

Usually asymptomatic, incidental finding on chest radiography; may cause grating sensation associated with calcified plaques

Among exposed persons: 3 to 58 percent; general population: between 0.5 and 8 percent

Smoking cessation; withdrawal from further exposure; management of concurrent and other respiratory diseases


*—Prevalence varies widely in different regions and relates to individual exposure history.

Information from references 2 through 5.

TABLE 1   Symptoms, Prevalence, and Treatment of Asbestos-Related Lung Diseases

View Table

TABLE 1

Symptoms, Prevalence, and Treatment of Asbestos-Related Lung Diseases

Disease Presenting symptoms Prevalence* Treatment

Asbestosis

Dyspnea, dry cough

Approximately 200,000 patients with asbestosis and 2,000 deaths annually

No specific therapy; general measures outlined in the article; surveillance for lung cancer; smoking cessation

Lung cancer

Chest pain, cough, dyspnea, hemoptysis, weight loss, fatigue, symptoms caused by metastases and direct invasion

Estimated 2,000 to 3,200 lung cancer deaths annually related to asbestos exposure

Multimodality treatment including surgery, radiotherapy, and chemotherapy

Mesothelioma

Chest pain, cough, dyspnea, weight loss, fatigue, pleural effusion, symptoms caused by metastases, pericardial invasion, esophageal compression, superior vena caval invasion

Approximately 2,000 deaths annually; incidence and mortality rate are the same

Multidisciplinary approach focused on supportive care; multimodality treatment including surgery, radiotherapy, and chemotherapy (clinical trials ongoing); radiotherapy for localized pain and metastatic spread occurring along a biopsy tract; chemical or surgical pleurodesis for pleural effusions

Pleural plaques

Usually asymptomatic, incidental finding on chest radiography; may cause grating sensation associated with calcified plaques

Among exposed persons: 3 to 58 percent; general population: between 0.5 and 8 percent

Smoking cessation; withdrawal from further exposure; management of concurrent and other respiratory diseases


*—Prevalence varies widely in different regions and relates to individual exposure history.

Information from references 2 through 5.

Although occupational exposure is now regulated in the United States, past exposure must be recognized. It is important to take a comprehensive occupational and environmental history to identify persons at risk because of previous exposure. Factors to establish include the specific occupation (Table 2), the duration of that occupation, and the intensity of exposure (e.g., was the dust visible or not). A significant exposure can be defined as at least several months' exposure to visible dust that began more than 10 years earlier. Although much attention is focused on industrial exposure, environmental sources also play a role. These include residence near asbestos or vermiculite mines and prolonged exposure in buildings with open sources of contamination.6 Undisturbed insulation in good condition is not hazardous.7

TABLE 2

Potential Sources of Occupational and Environmental Asbestos Exposure

Asbestos-containing products

Asbestos-containing flight materials: exposed workers may include aircraft mechanics and those involved in aerospace and missile production and aircraft manufacturing

Asbestos-lined electrical products: exposed workers may include electrical workers (e.g., electricians), electrical linemen, telephone linemen, and power plant workers

Asbestos shipping materials: exposed workers may include product shipyard workers (e.g., insulators, laggers, painters, pipe fitters, maintenance workers, welders), Coast Guard personnel, merchant mariners, longshoremen, U.S. Navy personnel, asbestos manufacturing plant workers, insulators, machinists, persons working at packing and gasket manufacturing plants, pipe fitters, and power plant workers

Brake linings and clutch pads: exposed workers may include auto mechanics, those involved in brake and clutch manufacturing, and assembly workers

Building materials: exposed workers may include building engineers, cement plant production workers, building material manufacturers, construction workers (including insulators, boilermakers, steelworkers, ironworkers, plumbers, steamfitters, plasterers, drywallers, cement and masonry workers, roofers, tile/linoleum installers, carpenters, and welders)

Other asbestos-containing products: exposed workers may include railroad workers, steamfitters, refinery workers, sheet metal workers, refractory products plant workers, rubber workers, and warehouse workers

Asbestos removal

Removal of insulation, asbestos removal, and waste handling

Building demolition and ship breaking

Environmental exposure

Asbestos in public buildings (e.g., hospitals, libraries, schools); occurs when the asbestos is disturbed during building or maintenance work

Family members of persons exposed occupationally

Asbestos production

Asbestos mining; textile mill workers who weave asbestos into cloth

Asbestos transport

Packing and handling of asbestos

TABLE 2   Potential Sources of Occupational and Environmental Asbestos Exposure

View Table

TABLE 2

Potential Sources of Occupational and Environmental Asbestos Exposure

Asbestos-containing products

Asbestos-containing flight materials: exposed workers may include aircraft mechanics and those involved in aerospace and missile production and aircraft manufacturing

Asbestos-lined electrical products: exposed workers may include electrical workers (e.g., electricians), electrical linemen, telephone linemen, and power plant workers

Asbestos shipping materials: exposed workers may include product shipyard workers (e.g., insulators, laggers, painters, pipe fitters, maintenance workers, welders), Coast Guard personnel, merchant mariners, longshoremen, U.S. Navy personnel, asbestos manufacturing plant workers, insulators, machinists, persons working at packing and gasket manufacturing plants, pipe fitters, and power plant workers

Brake linings and clutch pads: exposed workers may include auto mechanics, those involved in brake and clutch manufacturing, and assembly workers

Building materials: exposed workers may include building engineers, cement plant production workers, building material manufacturers, construction workers (including insulators, boilermakers, steelworkers, ironworkers, plumbers, steamfitters, plasterers, drywallers, cement and masonry workers, roofers, tile/linoleum installers, carpenters, and welders)

Other asbestos-containing products: exposed workers may include railroad workers, steamfitters, refinery workers, sheet metal workers, refractory products plant workers, rubber workers, and warehouse workers

Asbestos removal

Removal of insulation, asbestos removal, and waste handling

Building demolition and ship breaking

Environmental exposure

Asbestos in public buildings (e.g., hospitals, libraries, schools); occurs when the asbestos is disturbed during building or maintenance work

Family members of persons exposed occupationally

Asbestos production

Asbestos mining; textile mill workers who weave asbestos into cloth

Asbestos transport

Packing and handling of asbestos

Screening for asbestos-related disease may be appropriate in persons with a history of significant asbestos exposure; however, screening of the general population is not warranted. If a person with a history of significant exposure reports exertional dyspnea, the initial assessment should include spirometry and chest radiography in addition to a history and physical examination. If there is no evidence of abnormalities, high-resolution computed tomography (CT) may be considered because this may reveal pleural-based plaques and is more sensitive than chest radiography at detecting these lesions and mild fibrosis. The presence of plaques indicates significant asbestos exposure. Full pulmonary function tests, including measurement of lung volumes and diffusion capacity, should be performed in patients with abnormal spirometry results, imaging abnormalities, or suspected asbestos-related conditions.7 Symptomatic patients may be entitled to workers' compensation if there is loss of employment or functional impairment.

The presence of asbestosis is an independent risk factor for the development of lung cancer. Thus, the appearance of symptoms such as dyspnea, cough, chest discomfort, or weight loss necessitates a prompt and full assessment. Current recommendations support lifelong surveillance for persons with a significant exposure history or ongoing exposure. The American Thoracic Society recommends performing chest radiography and pulmonary function testing every three to five years in patients with disease.7 There is no good evidence that screening improves outcomes, although it may help identify lung cancer earlier. Screening for mesothelioma is not helpful.

LUNG CANCER

Asbestos exposure significantly increases the risk of developing small cell and non–small cell lung carcinoma.8 A number of studies suggest an increased incidence of non–small cell lung carcinoma in patients with asbestosis compared with those who have been exposed to asbestos but do not have asbestosis.8 Lung cancer can occur in nonsmokers exposed to asbestos; however, the risk is magnified several-fold by smoking.911 All patients who smoke cigarettes must be warned about this risk, and every attempt should be made to assist patients with smoking cessation. Nonmesothelioma asbestos-related lung cancers are indistinguishable clinically from lung cancers related to smoking alone. Thus, evaluation of a new noncalcified pulmonary nodule is similar in patients with or without a history of asbestos exposure. Patients with lung cancer should receive influenza and pneumococcal vaccines.12

ASBESTOSIS

Asbestosis is a fibrotic lung disease, or pneumoconiosis, resulting from the inhalation of asbestos fibers. In many patients, it is characterized by a very mild and indolent fibrosis that usually produces relatively minor symptoms. In general, the latent period between the peak asbestos exposure and diagnosis is 20 to 30 years.

Complaints of exertional dyspnea associated with auscultatory crackles on physical examination should prompt further investigation. The first changes in pulmonary function may be decreased diffusion capacity and exertional oxygen desaturation. As the process becomes more advanced, pulmonary function tests will reveal a restrictive pattern with a decreased total lung capacity and vital capacity.

Chest radiography typically demonstrates increased interstitial markings, usually more prominent in the lower lobes, and often pleural plaques. Typical findings on high-resolution CT of the chest include increased interstitial markings, predominantly at the bases; later, honeycombing may be apparent (Figure 1). In many respects, asbestosis is clinically similar to idiopathic pulmonary fibrosis, but asbestosis usually progresses slowly, whereas idiopathic pulmonary fibrosis has a rapidly progressive course. No current treatment effectively alters the natural course of asbestosis. Patients will benefit from influenza and pneumococcal vaccines.12

Figure 1.

Computed tomographic scan of the chest demonstrating severe asbestosis. There is marked parenchymal remodeling and tissue destruction (“honeycombing” [arrow]), leading to restrictive lung disease (forced vital capacity: 56 percent of predicted) and decreased oxygen exchange.

View Large


Figure 1.

Computed tomographic scan of the chest demonstrating severe asbestosis. There is marked parenchymal remodeling and tissue destruction (“honeycombing” [arrow]), leading to restrictive lung disease (forced vital capacity: 56 percent of predicted) and decreased oxygen exchange.


Figure 1.

Computed tomographic scan of the chest demonstrating severe asbestosis. There is marked parenchymal remodeling and tissue destruction (“honeycombing” [arrow]), leading to restrictive lung disease (forced vital capacity: 56 percent of predicted) and decreased oxygen exchange.

Given a history of significant occupational asbestos exposure and typical high-resolution CT findings, surgical lung biopsy rarely is needed to establish a diagnosis.13 For patients in whom surgical lung biopsy is performed, the pathologic pattern is that of usual interstitial pneumonia. This is the same pathology occurring in patients with idiopathic pulmonary fibrosis and may also be seen in pulmonary fibrosis associated with collagen vascular diseases (e.g., rheumatoid arthritis).13 Asbestos bodies are identified by special iron staining of tissue, and the number of these bodies correlates with the severity of fibrosis. Their presence in the lung tissue confirms the diagnosis of asbestosis.

BENIGN PLEURAL DISEASE

The most common pathologic pulmonary response to asbestos inhalation is the development of pleural plaques (Figure 2). Over time, collagen is deposited in the pleura and may calcify. Most plaques are completely asymptomatic, and there is no evidence that plaques transform into malignant lesions. Plaques occur in approximately 50 percent of persons with heavy and prolonged exposure to asbestos and are, therefore, a marker of asbestos exposure.7 Plaques are not always visible on plain chest radiography, but high-resolution CT will identify up to 50 percent of plaques found at autopsy. However, chest radiography usually is adequate, and the use of high-resolution CT is reserved most often for diagnostic uncertainty or confirmatory testing.7

Figure 2.

Chest radiograph of a patient with previous asbestos exposure who has developed pleural plaques (arrows). These plaques are characteristically located symmetrically along the lateral chest wall but also may occur on the domes of the diaphragm.

View Large


Figure 2.

Chest radiograph of a patient with previous asbestos exposure who has developed pleural plaques (arrows). These plaques are characteristically located symmetrically along the lateral chest wall but also may occur on the domes of the diaphragm.


Figure 2.

Chest radiograph of a patient with previous asbestos exposure who has developed pleural plaques (arrows). These plaques are characteristically located symmetrically along the lateral chest wall but also may occur on the domes of the diaphragm.

Benign asbestos pleural effusions, usually unilateral, are the most common manifestation of asbestos-related pleural disease within 10 to 20 years after exposure.14 When followed over time, effusions may wax and wane. The development of any new pleural effusion mandates a thorough evaluation, including tuberculosis skin testing and diagnostic thoracentesis. Asbestos pleural effusions are exudative.7 However, in cases of exudative pleural effusions, a pleural biopsy may be needed to evaluate for tuberculosis and malignancy. Furthermore, pleural effusion with pleuritic pain may be a manifestation of malignant mesothelioma.15 Therefore, benign asbestos pleural effusion is a diagnosis of exclusion.

DIFFUSE MALIGNANT MESOTHELIOMA

Diffuse malignant mesothelioma is an aggressive tumor derived from mesothelial cells, most commonly of the pleura. It is uniformly fatal, with a median survival time of six to 18 months from diagnosis. Among persons who have worked with asbestos, the lifetime risk of developing mesothelioma is high, although the condition is relatively uncommon, with approximately 2,000 new cases per year in the United States.4 However, even relatively low-level exposure has been associated with an increased risk of developing mesothelioma.13

The presenting symptoms of malignant mesothelioma are vague (Table 1), which often leads to a delay before the patient seeks care. Similarly, the nonspecific nature of the symptoms makes the diagnosis difficult. Chest pain and dyspnea are common initial complaints.16 Chest radiography most often will reveal a large, unilateral pleural effusion. Chest CT will demonstrate the same features; however, irregular thickening of the pleura also may be visible. In more advanced disease, there may be superior vena cava syndrome, Horner's syndrome, dysphagia, or other complications resulting from the propensity of mesothelioma to invade neighboring structures. Pathologic diagnosis can prove difficult, and many cases are misdiagnosed initially.

Palliative radiation therapy can be effective in reducing symptoms, especially from metastases. Current clinical trials emphasize a combination of surgery, radiation, and chemotherapy, but no regimen has yet been clearly shown to improve survival rates. Recent study has focused on the identification of serum markers (e.g., serum mesothelin-related protein, osteopontin) that may prove useful as screening tools.17,18

The Authors

KATHERINE M.A. O'REILLY, M.D., is a pulmonologist at Southampton General Hospital, Southampton, United Kingdom. She received her medical degree from McGill University, Montreal, Quebec, Canada, and completed a residency in internal medicine and a fellowship in pulmonary and critical care medicine at the University of Rochester, N.Y.

ANNE MARIE MCLAUGHLIN, M.B., is a pulmonary fellow at St. Vincent's University Hospital, Dublin, Ireland. She received her medical degree from University College Dublin, Ireland.

WILLIAM S. BECKETT, M.D., is a professor of medicine and environmental medicine at the University of Rochester School of Medicine and Dentistry. He received his medical degree from Case Western Reserve University, Cleveland, Ohio, and completed fellowships in pulmonary medicine and occupational medicine at Johns Hopkins University, Baltimore, Md.

PATRICIA J. SIME, M.D., is an associate professor of medicine, environmental medicine, an oncology at the University of Rochester School of Medicine and Dentistry. She received her medical degree from the University of Edinburgh, Scotland, where she also completed a residency in internal medicine. Dr. Sime served a fellowship in pulmonary medicine at McMaster University, Hamilton, Ontario, Canada.

Address correspondence to Katherine M.A. O'Reilly, M.D., Respiratory Medicine Department, D Level West Wing, Mailpoint 48, Southampton General Hospital, Tremona Road, Southampton SO16 6YD, United Kingdom (e-mail: kateindub@yahoo.co.uk). Reprints are not available from the authors.

Author disclosure: William S. Beckett, M.D., is supported by NIEHS P30 ES01247 and the New York State Occupational Health Clinics Network. Patricia J. Sime, M.D., is supported by NIH RO1HL075432, NIH K08HL04492, and NIEHS P30 ES01247.

REFERENCES

1. Peto J, Decarli A, La Vecchia C, Levi F, Negri E. The European mesothelioma epidemic. Br J Cancer. 1999;79:666–72.

2. Work-Related Lung Disease Surveillance Report 2002; Division of Respiratory Disease Studies, U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, DHHS (NIOSH) number 2003–111, May 2003.

3. Centers for Disease Control and Prevention. Changing patterns of pneumoconiosis mortality—United States, 1968–2000. MMWR Morb Mortal Wkly Rep. 2004;53:627–32.

4. Price B, Ware A. Mesothelioma trends in the United States: an update based on Surveillance, Epidemiology, and End Results Program data for 1973 through 2003. Am J Epidemiol. 2004;159:107–12.

5. Lilienfeld DE, Mandel JS, Coin P, Schuman LM. Projection of asbestos related diseases in the United States, 1985–2009. I. Cancer. Brit J Ind Med. 1988;45:283–91.

6. Peipins LA, Lewin M, Campolucci S, Lybarger JA, Miller A, Middleton D, et al. Radiographic abnormalities and exposure to asbestos-contaminated vermiculite in the community of Libby, Montana, USA. Environ Health Perspect. 2003;111:1753–9.

7. American Thoracic Society. Diagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 2004;170:691–715.

8. van Loon AJ, Kant IJ, Swaen GM, Goldbohm RA, Kremer AM, van den Brandt PA. Occupational exposure to carcinogens and risk of lung cancer: results from The Netherlands cohort study. Occup Environ Med. 1997;54:817–24.

9. Boffetta P. Epidemiology of environmental and occupational cancer. Oncogene. 2004;23:6392–403.

10. Liddell FD. The interaction of asbestos and smoking in lung cancer. Ann Occup Hyg. 2001;45:341–56.

11. Berry G, Liddell FK. The interaction of asbestos and smoking in lung cancer: a modified measure of effect. Ann Occup Hyg. 2004;48:459–62.

12. U.S. Preventive Services Task Force. Counseling to prevent tobacco use and tobacco-caused disease: recommendations statement. Accessed October 3, 2006, at: http://www.ahrq.gov/clinic/3rduspstf/tobacccoun/tobcounrs.pdf.

13. Craighead JE, Abraham JL, Churg A, Green FH, Kleinerman J, Pratt PC, et al. The pathology of asbestos-associated diseases of the lungs and pleural cavities: diagnostic criteria and proposed grading schema. Report of the Pneumoconiosis Committee of the College of American Pathologists and the National Institute for Occupational Safety and Health. Arch Pathol Lab Med. 1982;106:544–96.

14. Wagner GR. Asbestosis and silicosis. Lancet. 1997;349:1311–5.

15. Robinson BW, Lake RA. Advances in malignant mesothelioma. N Engl J Med. 2005;353:1591–603.

16. Antman KH. Natural history and epidemiology of malignant mesothelioma. Chest. 1993;103(4 suppl)373S–6S.

17. Robinson BW, Creaney J, Lake R, Nowak A, Musk AW, de Klerk N, et al. Mesothelin-family proteins and diagnosis of mesothelioma. Lancet. 2003;362:1612–6.

18. Pass HI, Lott D, Lonardo F, Harbut M, Liu Z, Tang N, et al. Asbestos exposure, pleural mesothelioma, and serum osteopontin levels. N Engl J Med. 2005;353:1564–73.


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