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Home , Occupational asthma

IsIs YourYour Patient’sPatient’s WWorkplaceorkplace CausingCausing LungLung Disease?Disease?

Occupational lung diseases not only have a significant impact on the affected individual, but they often result in workplace changes and significant socio-economic impact.

By Susan M.Tarlo, MB, BS, FRCPC

he range and relative frequency of blasting underground. Conversely, the T occupational lung diseases has diagnosis of occupational caused changed significantly in Canada over the by workplace sensitizers has risen, and past 30 years. Occupational lung diseases this is now the most common chronic that were relatively common before, such occupational lung disease in Canada.1,2 as and coal miners’ pneumoco- It is estimated that occupational asthma niosis, are now uncommon conditions in (usually due to an immunologic response Canada. Although silicosis can still be to a work agent) accounts for about 7% of caused by sandblasting and occasionally all adult-onset asthma,3 and occupational by other types of exposures, it has become factors may play a role in up to 30% of uncommon in Canadian underground min- adult asthma.4 There has been increased ers. This is due to much improved dust- recognition of the role of workplace irri- control measures, such as spraying water tants in aggravating asthma and even, at to keep dust down while drilling and times, causing asthma due to very high

74 The Canadian Journal of Diagnosis / July 2001 Lung Disease

respiratory irritant exposures (termed reactive airways dysfunction syndrome [RADS], or irritant-induced asthma).5,6 Besides causing asthma in some patients, workplace respiratory irritant exposures in accidental high levels (such as nitrogen oxides from silage, or spills of in chemical plants), can also induce other acute respiratory effects in any part of the respiratory tract.7 These can include acute respiratory distress syn- drome, pneumonitis, bronchiolitis, bron- chiolitis organizing pneumonia (BOOP), bronchiectasis, bronchitis, tracheitis, laryngitis and . Figure 1. Acute pneumonia or hypersensitivity pneumonitis? The effects are determined by several Bilateral interstitial lung disease in a worker cleaning carrots. factors, including the odor threshold, sol- ubility and hydrogen ion concentration effects. In contrast, nitrogen oxides are (pH) of the irritant, the inhaled particle odorless and poorly soluble. The effects size, the duration and concentration of the are less immediately apparent and occur exposure, and the presence or absence of mainly in the bronchoalveolar regions. underlying respiratory disease. For exam- Unless a clear exposure history is ple, ammonia has a strong odor, which obtained, the physician may find it diffi- alerts the worker to relatively low expo- cult to determine whether the indiviudal is sure conditions, and is water soluble. The suffering from the effects of an irritant or effects are, therefore, usually upper air- from coincidental non-occupational caus- way effects rather than lower airway es of respiratory disease, such as viral pneumonia or laryngitis. Another source of respiratory symp- toms in the workplace is endotoxin air- borne exposure, which can be caused by Dr. Tarlo is professor of gram-negative bacteria contaminating medicine and sciences, University of organic dusts on farms or in animal feed. Toronto, and respiratory Endotoxin exposure also can occur from physician, University Health Network, Gage Occupational contaminated cutting oils (i.e., metal and working fluids) in factories and humidi- Unit, Toronto, Ontario. fiers in buildings. This exposure can result in such flu- like symptoms as , chills, fever,

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malaise and chest pain, which are usually such as pleural plaques, pleural calcifica- self-limited.8 Contamination of the same tion and , are relatively easy materials with organisms, such as fungi, to attribute correctly to exposure, can cause a similar self-limiting syn- some manifestations may mimic other drome, or may cause an immunoglobulin lung diseases, (e.g., pleural effusions, E (IgE) antibody-mediated response, lead- interstitial fibrosis and lung cancer). Lung ing to either new- cancer also can be caused by other occu- Asbestos-related onset asthma or an pational exposures, such as chromium exacerbation of pre- salts, radon, coke production, arsenic, manifestations existing asthma. IgE beryllium and nickel refining. continue to and immunoglobulin The above examples illustrate that G (IgG) antibody- occupational lung diseases may present in increase in mediated allergic many different forms beyond the more prevalence due to bronchopulmonary traditional pneumoconioses. Often now, their long latency mycoses (e.g., aller- these diseases present to physicians in gic bronchopul- ways that mimic non-occupational lung period. monary aspergillo- diseases. Without an accurate occupation- sis) also may present al history in all patients with respiratory initially as an exacerbation of asthma. disease, the correct diagnosis will easily Thermophilic actinomycetes or fungi also be missed. can cause a Type IV hypersensitivity The importance of a missed occupa- response (T-lymphocyte-mediated), tional diagnosis can have implications, resulting in hypersensitivity pneumonitis not only for the individual patient, whose (e.g., farmer’s lung), which may clinically condition may worsen if he/she continues mimic pneumonia.9 to work in the same conditions, but also True respiratory infections may have for co-workers. Medical screening of an occupational cause, such as tuberculo- other workers after diagnosis of an “index sis in health-care workers; legionnella case” may lead to earlier diagnosis and pneumonia from contaminated workplace treatment. Awareness of the “index case” humidification systems; anthrax in farm- and sending notification to the Provincial ers; and respiratory viral infections spread Ministry of Labour and/or workplace by close contact among office workers. occupational hygienist, as appropriate Asbestos-related manifestations con- with the consent of the patient, also may tinue to increase in prevalence due to their allow preventive measures to be taken in long latency period, despite the reduced the workplace. use of asbestos—especially the reduced The following cases illustrate the use of the most hazardous types of importance of thinking and asking about asbestos: crocidolite, amosite and antho- workplace exposure in all patients, but phyllite. Although most manifestations, especially in those with lung disease.

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Case 1 Recurrent viral infections, humidifier fever or mass psychogenic illness? Eight out of 40 underground nickel min- ers, seen by the same local family physi- cian, presented with recurrent cough, chest discomfort, difficulty breathing, chills and malaise. These symptoms occured within a few hours of working underground, and improved away from work within hours. No abnormalities were found on physical examination, chest radiographs or pulmonary function test- ing, although all tests were performed several hours after leaving the mine. Peak Figure 2. Sarcoidosis or ? Bilateral hilar lymphadenopathy and right lower lobe infiltrate. expiratory flow (PEF) readings were slightly reduced underground, but would ed by the miners were initially elevated, be expected to fall somewhat due to though later samples collected in a sterile underground pressure manner were normal. Mold counts under- Without an changes. Some miners ground were significantly higher than out- accurate had a mild neutrophil- door levels.10 ia on blood counts It was considered most likely that symp- occupational performed a few hours toms were due to “humidifier fever,” history of patients after mining. The min- induced by endotoxin and/or mycotoxins, or ers attributed their other fungal irritants, such as beta 1-4 glu- with respiratory symptoms to diesel cans from fungal walls. However, viral disease, the fumes underground. infections or mass psychogenic illness could Subsequent investiga- have caused symptoms in some of the min- correct diagnosis tions at the mine ers. changes in the will be missed. showed that water was mine were associated with resolution of sprayed underground symptoms. to reduce levels of silica and other dust, especially when blasting. The water had Case 2 been obtained from a tailings pond produced by damming a river. The surrounding area Pneumonia or hypersensitivity pneu- had been used as a sewage dump site, and the monitis? water was treated to kill bacteria (but this A 24-year-old-man worked for five years would not destroy endotoxin). Measured lev- in a plant where carrots and onions were els of endotoxin in the water sample collect- cleaned and packed. He was seen in the

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Figure 3. Left upper lobe lung cancer, due to smoking or chromium?

emergency department with a three-day history of dry cough, dyspnea and mild fever. He was found to have severe hypox- ia and bilateral infiltrates on his chest radiograph (Figure 1). He was admitted to Figure 4. Left upper lobe lung cancer, due to smoking or chromium? the intensive care unit and rapidly improved with supplemental oxygen. Five no symptoms, except when he re-visited days later, he was discharged after treat- the onion room, where symptoms would ment with intravenous fluids and antibi- recur three hours after even short visits. otics, showing a clear chest radiograph. Pulmonary function tests at the time of He was readmitted two days later with symptoms showed restrictive changes similar findings. His white blood count with reduced diffusing capacity, clearing was 27.9 x 103, with a marked neutrophil- between episodes. Serum precipitins (lgG ia and leftward shift. He improved with- antibodies) were identified from the out antibiotics, with only supportive treat- patient against Aspergillus flavus and ment (fluids and supplemental oxygen). Aureo pullulans. Fungal culture from Episodes had occurred on both occa- uncleaned onions from the workplace sions eight hours after working in the showed a heavy growth of A. fumigatus, onion room, soon after plastic curtains various penicillin species, and a lighter had first been erected to prevent cold air growth of A. flavus and A. Fusarium from entering the area. He returned to species. work in the separate carrot room and had

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Adiagnosis of onion worker’s hyper- electronics, metal extraction, dental alloys sensitivity pneumonitis was made, due to and sporting goods, such as golf clubs. If fungal exposure at work. The patient beryllium is suspected as a cause because moved to a different workplace. The plas- of the patient’s tic sheeting at work was removed and the history, then a Chronic beryllium other 40 workers had no ill effect. beryllium lym- disease can Case 3 phocyte transfor- mation test is exactly mimic Sarcoidosis or beryllium lung disease? appropriate. This A 39-year-old woman worked for six is performed on sarcoidosis. years in a company casting and grinding blood or bron- aluminum alloys. Her job was to clean the choalveolar lavage fluid lymphocytes, and castings. She presented with a six-month is only available in a few specialized cen- history of dry cough and exertional dysp- ters. nea. Chest radiograph showed mediastinal lymphadenopathy and a lower lobe infil- Case 4 trate (Figure 2). Biopsy showed non- caseating granulomas, and bronchoalveo- Lung cancer: Caused by cigarette lar lavage showed mainly lymphocytes— smoking or occupation? especially T cells suggestive of sarcoido- A 60-year-old man died within six weeks sis. The workplace material safety data after diagnosis of oat cell carcinoma of sheets showed that the aluminum alloys the lung (Figures 3 and 4). He had a 40- included small amounts of zinc, copper, year history of smoking one pack per day. beryllium and other metals. Her sister, He had worked for 17 years in the aircraft who also worked there, had similar find- industry with exposure to spray paint, alu- ings.11 Both were found to have a positive minum, lubricants and small amounts of serum beryllium lymphocyte transforma- an anticorrosive spray, which contained tion test, supporting a diagnosis of beryl- hexavalent chromium. He had no history lium lung disease. They were removed of skin rash or nasal septal preparation. from further exposure and treated with Did hexavalent chromium exposure con- oral . Other workers under- tribute to his lung cancer? went a medical surveillance program for Hexavalent chromium has been recog- berylliosis, as is recommended in Ontario. nized as a carcinogen since 1948 on the Chronic beryllium disease can exactly basis of animal studies and human epi- mimic sarcoidosis. A genetic component demiologic studies. As with other occupa- has been recognized. Exposure to berylli- tional carcinogens, there is a latent period um may occur in metal working, especial- between exposure and cancer (i.e., the can- ly in the manufacture of aerospace com- cer appears many years after the exposure). ponents, nuclear energy applications, The risk increases with the extent of expo-

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sure (duration and exposure concentration), 24 hours of a working day due to a and the history is essential in assessing markedly reduced forced expiratory vol- 12 this. Cigarette smoking can be synergistic ume in one second (FEV1). Specific chal- for cancer risk with occupational carcino- lenge testing with the glue was positive, gens, and smoking further confirming the diagnosis of true Early referral to an alone increases the rel- occupational asthma due to sensitization occupational ative risk of lung can- to the pine in the glue.13 cer 10- to 100-fold. In He moved to a different workplace and medicine or calculating the relative his asthma markedly improved, but did respiratory risk of an occupational not completely resolve. carcinogen contribut- Conclusion specialist with ing to lung cancer one expertise in must consider the These cases illustrate how occupational occupational lung above factors and pub- lung disease can very closely resemble lished epidemiologic non-occupational lung diseases. Unless a disease is helpful. studies. careful occupational history is taken, the diagnosis will likely be missed.14 Case 5 Important aspects of the history’s occupa- tional component include: Occupational asthma or asthma coinci- 1. Details of workplace exposure at the dental to the workplace and aggravated time of symptom onset and during by work? symptom exacerbations (especially for A 45-year-old man had a history of nasal diseases, such as asthma, where symp- polyps, but no asthma symptoms until five toms relate to exposures in the preced- years after he began working in a rubber ing minutes to hours); tire manufacturing plant. His job involved 2. Details of previous workplace expo- working with a heated glue containing sures (especially for conditions, such pine resin. The man described his work- as lung cancer- or asbestos-related dis- place as dusty and smoky. He said there eases, which have a long latency peri- was no respiratory protection at work, and od); that he noted an improvement in his 3. Understanding the job description and symptoms on weekends and during holi- exposure by supplementing the history days. with information from workplace Serial PEF readings and materials safety data (MSDS) sheets, were worse at work, as compared to peri- which are available from the employ- ods off work. Methacholine challenge er; while away from work confirmed the 4. For diseases, such as asthma, obtain- presence of airway hyper-responsiveness, ing a history of the timing of symp- but this test could not be repeated within toms in relation to workplace expo-

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sures versus periods off work; and Acknowledgements 5. Assessing non-occupational factors in The author wishes to thank Dr. Ken the history, which may contribute to, Roberts for permitting the report of Case or completely account for, the respira- 2, which he astutely diagnosed, and Dr. tory disease (e.g., smoking, atopy, Gary M. Liss for his helpful review of this hobbies). article. Occupational lung diseases not only References have a significant health impact on the 1. Provencher S, Labreche FP,Guire L: Physician based sur- affected individual, but they often result veillance system for occupational respiratory diseases: the experience of PROPULSE, Quebec, Canada. Occup in workplace changes and significant Environ Med 1997; 54:272-6. 2. Liss GM, Ellinson L: Recognition of occupational asth- socio-economic impact. These patients ma. Pract Allergy Immunol 1994; 9(6):252-60. often will be considered for workers’ 3. Blanc P,Toren K: How much asthma can be attributed to occupational factors? Am J Med 1999; 107:580-7. compensation. Early referral to an occu- 4. Johnson AR, Dimich-Ward HD, Manfreda J, et al: Occupational asthma in adults in six Canadian com- pational medicine or respiratory specialist munities. Am J Resp Crit Care Med 2000; 162:2058-62. with expertise in occupational lung dis- 5. Brooks SM,Weiss MA, Bernstein IL:Reactive airways dys- function syndrome (RADS): Persistent asthma syn- ease will help provide an accurate diagno- drome after high level irritant exposure. Chest 1995; 88:376-84. sis and assist the patient in appropriate 6. Tarlo SM, Broder I: Irritant induced occupational asth- disease management. This should include ma. Chest 1989; 96:297-300. 7. Tarlo SM:Workplace respiratory irritants and asthma. In: decisions about appropriate future work- Banks D,Wong ML (eds.):: State of the Art Review. Hanley and Belfor, Philadelphia, 2000, pp. place conditions and workers’compensa- 471-83. tion, if applicable. For diseases where 8. Clapp WD, Thorne PS, Frees KL, et al: The effects of inhalation of grain dust extract and endotoxin on there is a potential acute ongoing effect at upper and lower airways. Chest 1993; 104:825-30. 9. Pickering CAC, Newman Taylor AJ: Extrinsic allergic work, as in the case of asthma and other bronchioloalveolitis (hypersensitivity pneumonitis). In: allergic responses, it is important, where Parkes WR (ed.): Occupational Lung Disorders. Third Edition. Butterworth-Heinemann Ltd., London, 1994, possible, to refer the patient while he/she pp. 667-709. 10. Summerbell RC, Staib F, Ahearn DG, et al: Household is still working. This will allow the work- hyphomycetes and other indoor fungi. J Med Vet place relationship to be objectively inves- Mycology 1994; 32S:277-86. 11. Tarlo SM, Rhee K, Powell E, et al: Marked tachypnoea in tigated further, as recommended by siblings with chronic beryllium disease due to copper- 14 beryllium alloy. Chest 2001; 119:647-50. Canadian guidelines. In addition, diag- 12. Begin R, Christman JW: Detailed occupational history: nosis of occupational lung disease should The cornerstone in diagnosis of asbestos-related lung disease. Am J Resp Crit Care Med 2001; 163:598-9. be considered to be a “sentinel event,” 13. Tarlo SM: Occupational asthma induced by tall oil in the rubber tyre industry. Clin Exp Allergy 1991; 22:99- which should lead to a review of the risks 101. for similar exposure and disease in co- 14. Tarlo SM, Boulet LP, Cartier A, et al: Canadian Thoracic Society Guidelines on Occupational Asthma. Can Resp workers by the provincial Ministry of J 1998; 5:289-300. Labour, or by the workplace physician, as appropriate. Dx

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