RCPs can have a positive influence on patients with industrial lung diseases through knowledge of the new causes, diagnostic methods, and management tools.
Traditionally, industrial lung disease has commonly been associated with work environments in the automotive production, mining, and nuclear industries. However, some other fields of enterprise and some new industries have been associated with current incidences of industrial lung disease. RCPs need to be aware of the new causes of industrial lung disease and the methods of diagnosis and management.
In addition to the above-mentioned industries for which a time-lapse ongoing research effort may need to be made regarding industrial lung disease, there are some current environments that should also be explored and understood. Farmers, bird fanciers, flock workers, carpenters, construction workers, clutch refabricators, textile workers, and machinists may all be exposed to atmospheres where industrial lung diseases can be contracted and/or exacerbated.
In the field of agriculture a common respiratory ailment is “farmer’s lung.” This condition is a form of hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis. HP results from a hypersensitization to repeated inhalations of nonpathogenic actinomycetes present in the farm environment.1 Farmer’s lung manifests itself by a large influx of T-lymphocytes, which are mostly of the cluster of differentiation (CD)8+ T-cell subset. These T-lymphocytes gather within the alveolar structures of the lungs and may encourage tissue damage. Dakhama et al1 mention studies that have found alveolar lymphocytes can endure after a severe episode of farmer’s lung with no clinical signs of active disease in subjects with continuous exposure to irritating antigens.
Dakhama et al1 further questioned what factors could cause the alveolar lymphocytes to endure. They found evidence that linked previous episodes of farmer’s lung with interleukin-2, a major growth factor required for the differentiation, functional activation, and production of T-lymphocytes. Their research concluded that lymphocytes from both acutely ill patients and patients who previously suffered from farmer’s lung were responsive to interleukin-2. It was found that these lymphocytes can still release the cytokine after stimulation with concanavalin A. They also concluded that it is likely that interleukin-2 is a major contributor to the development of farmer’s lung by acting as a stimulus for the buildup and perseverance of lymphocytes in the lungs that are a likely source of this cytokine in vivo.
Organic Dusts
Organic dusts found in the agriculture, food packaging, and weaving industries are known to be important in the contraction and exacerbation of many respiratory diseases such as farmer’s lung, allergic alveolitis, occupational asthma, byssinosis, chronic bronchitis, chronic airflow limitation, and organic dust toxic syndrome.2 Endotoxins derived from the cell wall of gram-negative bacteria are contaminants of organic dusts. Endotoxins are potent biological agents, with much of their activity caused by the lipid A component.2 It has been found that organic dusts contaminated with endotoxins are significant in the etiology of respiratory morbidity.2
Organic dusts are a vital factor in the development of farmer’s lung. Patrick Hartley, MB, BCh, BAO, MPH, clinical assistant professor of the Division of Pulmonary, Critical Care, and Occupational Medicine, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, agrees, “Organic dusts play an essential role in the development of farmer’s lung. Organic dusts include particles of grain, mold, bacteria (or constituents of bacteria such as endotoxin), mites, animal dander, and fecal matter. Some farmers may be exposed to all of these forms of dust, which will result in a higher probability of developing farmer’s lung. The possibility of multiple different exposures and work in poorly ventilated animal confinement buildings needs to be considered when taking a medical history. In addition, grain, poultry, swine, cattle, and dairy farmers also need to be considered for exposure.” Despite recent findings, further research needs to be conducted to establish the consequences of exposure to endotoxins isolated from organic dusts and to uncover the relationship between reported symptoms and disease.2
Treating and Managing Lung Disease
Treatment of farmer’s lung is often confounded by a few factors. Hartley notes, “Obstacles to treatment include recognition of the problem, reluctance of farmers to seek medical care, and misdiagnosis. In general, farmers are less likely to be smokers than an industrial population so smoking is not as strong a confounding factor.”
Managing lung diseases and ailments found in the field of agriculture can involve many different approaches. Hartley comments, “Education regarding potential hazards in the workplace is critical. The typical hierarchy of managing approaches to hazardous exposures used in industrial settings (administrative controls, engineering controls, and personal protective equipment in decreasing order of emphasis) is applicable here also. Administrative controls would involve reducing exposure by changing farming practices and even quitting farming if exposure cannot be controlled or avoided. Engineering controls would include adequate ventilation to reduce farmers’ exposure to possible respiratory irritants and asphyxiants. Respirators and dust masks can help reduce the exposure to potentially hazardous dust, fumes, or gases, but should not be a substitute for making changes in farming practice or institution of engineering controls. Respirators must be used properly to be effective and require proper care. Gases from animal waste are especially dangerous. Hydrogen sulfide (H2S) has been identified as a fatal asphyxiant. Adequate ventilation, particularly of confined spaces during the agitation of slurry, may prevent the adverse effects of released gases such as H2S, which have resulted in human and animal fatalities. An air-supplying respirator is necessary if entering an enclosed space where there is potential for exposure to these gases.”
Bird Fanciers and Breeders
Bird fanciers and bird breeders also face respiratory ailments and diseases from their chosen hobby or occupation. These individuals commonly contract “bird fanciers’ lung” or HP in response to organic dusts.3 Pulmonary function tests (PFTs) often reveal a restrictive defect and diffusion impairment.4 In addition, high resolution computed tomography (HRCT) scans may reveal a ground glass appearance of the lung parenchyma. Desaturation may be revealed when exercise testing.4 Symptoms of bird fanciers’ lung can be acute, subacute, or chronic and may include chills, fever, myalgia, dyspnea, and cough lasting for hours or days with gradual onset ranging from days to weeks.4 Symptoms of the chronic form include cough and dyspnea, which may occur for months or years.4
Careful questions about pets—including birds, occupational status, and occupational status of family members—may help in the initial diagnosis.4 Diagnostic criteria include positive skin prick test, presence of exact antibodies to the causal antigens, resolution of symptoms after cessation of contact with the bird or birds in question, and, if required, positive specific inhalation challenge.5 Other aids in diagnosing specific antigens include IgG antibodies. However, with an IgG antibodies test immunoglobulin and complement deposition in the lung are lacking.3 The use of the wrong antigens frequently results in a lack of detecting precipitating antibodies.3 However, Rodrigo et al5 report that performing the IgG test with the ELISA (enzyme linked immunosorbent assay) method permits a more accurate measurement of the antibody response. In addition, McClellan et al3 found that including antigens from bird droppings in addition to sera antibodies from the birds in question may produce a more accurate diagnosis.
Managing bird fancier’s lung includes use of oral prednisone. However, prednisone is not an ideal long-term treatment due to potentially dangerous side effects and risk of disease progression due to continued exposure.4 In acute cases, removing patients from the work environment or removing the birds from the home environment may be needed. Thorough environmental cleanup of the bird fancier’s home is needed after the bird is removed. Cleanup should include removing the bird cage and any items used by the bird; damp mopping of all surfaces; removing or thoroughly cleaning carpets, furniture, and drapes; and vacuuming with a high efficiency particulate air filter vacuum or central vacuum with an outdoor exhaust.4 Continuously monitoring dust can reduce inhalation of particulates that may still be coated with avian particles. This can be aided by changing filters on heating and air conditioning systems regularly.4 Farrell et al4 report that the reaction to treatment and prognosis seems to be poorer in bird fanciers’ lung than in farmer’s lung.
Flock Workers
Flock worker’s lung is another current industrial lung disease. While the name may imply avian involvement, this is actually not the case. Flock worker’s lung is exclusive to employees of the rotary cut synthetic materials industry. Rotary cut nylon, polyester, rayon, textile waste, and other synthetic fibers produce a powder of short fibers that are then adhesive coated to fabrics and other objects to produce a velvety surface.6 Producing flock has been associated with an increased risk of workers developing chronic interstitial lung disease characterized by a lymphocytic bronchiolitis, bronchiolocentric nodular and diffuse lymphocytic interstitial infiltrates, and variable interstitial fibrosis.6
There are two methods for cutting flock. All but two companies, located in the United States, cut the long cables (tow) of nylon, rayon, and polyester with guillotines that produce precision-cut flock of a defined length.6 The American companies use rotary cutters that are much faster but produce less precisely cut flock.6 The 24 reported cases of identified flock worker’s lung arose among workers using rotary cutting methods.6 While guillotine blades emit a certain sound when the blade becomes dull, it is much more difficult to detect a dull blade on a rotary cutter6. Dull rotary blades are more likely to produce flock with tiny protrusions, which during further processing may be released as respirable sized particles.6 Kern et al6 refer to recent studies that suggest that respirable sized nylon particles have substantial pulmonary toxicity.
Symptoms of flock worker’s lung include a persistent dry cough and dyspnea with or without abnormal pain in the chest.6 Chest radiographs may reveal diffuse patchy infiltrates.6 HRCT scans may show scattered areas of consolidation, patchy ground glass opacity, and peripheral honeycombing.6 To date, HRCT scans are the most effective noninvasive tests when detecting flock worker’s lung in the early stages.6 PFTs may show restrictive, or occasional obstructive or normal, physiology.6 Flock exposure may cause different lung injury to different people.7 Ratios of interstitial lung disease have been reported to be 48 to 250 times greater for flock workers than for the general population.6
Kern et al6 believe that the accompanying diffuse interstitial inflammation that is presumably responsible for the severely reduced diffusing capacity and interstitial fibrosis should be included in the diagnostic criteria proposed by the National Institute for Occupational Safety and Health (NIOSH). NIOSH emphasized the central role of a lymphocytic bronchiolitis and peribronchiolitis with associated lymphoid nodules in the histopathologic recognition of flock worker’s lung.6 Kern et al,6 however, believe that the case definition for flock worker’s lung should focus on previous or ongoing work in the flock industry, constant respiratory symptoms, and histologic proof of interstitial lung disease without better explanation. Further, they propose an atypical dispersal of cell types on bronchoalveolar lavage (BAL), restrictive lung function, and HRCT findings of ground glass opacity or clear fibrosis as a substitute for the histologic standard. The efficacy of corticosteroids and other immunosuppressants remains undetermined to date. Removal from the environment is the only intervention that has been shown to make a positive and noticeable improvement.6
Contrary to Kern et al, Kuschner7 has a different belief about the requirements and efficacy of diagnosis. In an editorial responding to the research by Kern et al, Kuschner7 notes that diagnosis may be difficult because biomarkers of exposure and susceptibility and a 100% accurate flock disease marker are lacking. It is also suggested that the same criteria for diagnosis be applied to flock worker’s lung that are applied to diagnosing other industrial lung diseases. Namely, clinicians should look for evidence that helps to establish a causal association between exposure and disease by considering data representing pulmonary health before exposure to the toxicant in question, past data and industrial hygiene data that help distinguish the probable dose and extent of exposure to the toxicant, evaluation of other likely toxicants, data signifying that the inception and progression of lung damage are temporally connected to the toxicant exposure, stabilization or the end of lung disease following termination of exposure, and decline in respiratory health during an exposure-free period. Kuschner7 warns that stringent terminology used to describe health and illness may make a comprehensive understanding of such terms elusive.
Kern et al6 acknowledge that the causative role for rotary cut flock and the relatively high concentrations of air contaminants (or both) remains unclear and the possibility of rotary cut flock—specifically nylon—being a carcinogen is suggested but not proven. However, NIOSH studies appear to implicate respirable sized nylon particulates as a source for industrial lung disease.6 Kuschner agrees7 that a growing body of evidence links respirable flock exposure with disease and believes a careful medical history, PFT, physical examination, industrial hygiene data, radiographic studies, and possibly BAL should garner enough information to make a diagnosis. Further, it has been proposed that a lung biopsy may be more helpful in ruling out other lung diseases than identifying flock worker’s lung.7
To better understand flock worker’s lung and relevant terminology, Kern et al6 suggest that further laboratory and field studies are needed to assess the prevalence of this condition. This research may need to concentrate on the role that heat, dull cutting blades, and mechanical shearing play in the development of flock worker’s lung. Also of interest may be alternate current vs direct current flocking in the origination of respirable sized flock particulates. In addition, guillotine vs rotary cut flock should be examined, as well as air concentration of respirable dust. The relative toxicity of nylon, polyester, rayon, and textile waste fragments should be considered and air concentrations of respirable particulates and corresponding higher rates of interstitial lung disease should be investigated.6
Other Occupations
Carpenters, construction workers, and clutch refabricators face a well-known industrial lung disease—asbestosis. Although asbestos has been banned in new buildings, a carpenter, construction worker, or other artisan who is renovating, repairing, or demolishing an older building may be exposed to asbestos. A recent report8 also notes that automotive clutch refabricators are at risk for asbestos exposure as asbestos was used as a friction product in automobiles.
In addition to being exposed to asbestos, carpenters are also exposed to other possible respiratory hazards such as wood dust, formaldehyde, solvents, copper sulfate, iron sulfate, pentachlorophenol, phenol, glues, chromates, plaster, mineral wool, insulation, polyurethane, adhesives, varnishes, and acrylates.9 A recent study9 found that carpenters had an elevated proportionate mortality ratio in the areas of respiratory disease, including cancer, as mortality was correlated with asbestos exposure. The study also found that on-site carpenters had a higher rate of lung cancer over other carpenters. On-site carpenters had a greater potential for exposure to asbestos. Emphysema was also noted to have a higher occurrence among construction carpenters.
It has been suggested that intervention activities such as education about the prevention of lung cancer and other respiratory diseases would be helpful in this industry. Other resources that may be helpful include medical observation programs and early discovery and treatment programs. These ongoing programs would be significantly worthwhile due to the long latency period (30 years) for asbestos-related lung cancer.
Byssinosis is a current industrial lung disease associated with cotton textile workers. Workers involved in the spinning process have a higher occurrence of this disease than cotton weavers.10 Byssinosis is associated with many years of worker exposure in the textile industry.10 It has been hypothesized that a dust contaminant, or endotoxins, rather than the cotton dust itself may be responsible for the contraction of this disease.10 Chronic bronchitis has also been found in textile workers. Raza et al10 noted that smoking was the most important predictive factor in locating the presence of symptoms of byssinosis or other respiratory ailments.
Machinists or metal parts manufacturers who work with a beryllium copper alloy are also at risk for developing an industrial lung disease. Chronic beryllium disease (CBD) is a systemic granulomatous disease that affects the lungs, skin, and lymphatic system.11 CBD occurs in 1-16% of those exposed to beryllium metal, oxide, or ceramic dust.11 Workers become exposed to respirable beryllium during polishing, sanding, grinding, and other machining processes that would involve generating dust or fumes.11 Symptoms of CBD include nonproductive cough, exertional dyspnea, weight loss, and fatigue.11 Specific lung symptoms can include evidence of noncaseating granulomas, bibasilar reticular-nodular infiltrates, mild bilateral hilar lymphadenopathy, and diffuse nodularity.11 Short-term treatment with oral prednisone may be appropriate, but long-term treatment with this steroid is less appealing due to the associated side effects of this drug.
While the Occupational Safety Health Administration has placed a standard for exposure at 2 mg/m3 studies indicate that CBD is still occurring in workers exposed at this lowered threshold.11 Some researchers believe that all workers at any level of exposure should be considered at risk. It has been suggested11 that industrial measures should limit exposure to as low an amount as sensibly attainable. In the future, prevention strategies may include substitution of safer materials for beryllium copper alloys, more stringent industrial controls, screening for early detection of CBD, and educating workers about the possible risks of beryllium.11
Conclusion
The effects of previously identified industrial lung diseases are still being treated by respiratory care practitioners. Current and evolving industrial lung diseases are new ailments that require attention. Through knowledge of current industrial lung diseases, diagnostic methods, and management tools, today’s respiratory care practitioners can positively affect the lung health of patients with these diseases.
Jennifer Vavra is a contributing writer for RT Magazine.
References
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2. Simpson JCG, Niven RM, Pickering CAC, et al. Prevalence and predictors of work related respiratory symptoms in workers exposed to organic dusts. Occup Environ Med. 1998;55:668-672.
3. McClellan JS, Albers GM, Noyes BE, et al. B-lymphocyte aggregates in alveoli from a child with hypersensitivity pneumonitis (bird breeders lung). Ann Allergy Asthma Immunol. 1999;83:357-360.
4. Farrell B, Farrell K, Oken HA. Bird fanciers’ lung: a case report. Md Med J. 1999;48:174-175.
5. Rodrigo MJ, Benavent MI, Cruz MJ, et al. Detection of specific antibodies to pigeon serum and bloom antigens by enzyme linked immunosorbent assay in pigeon breeder’s disease. Occup Environ Med. 2000;57:159-164
6. Kern DG, Kuhn C III, Ely EW, et al. Flock worker’s lung: broadening the spectrum of clinicopathology, narrowing the spectrum of suspected etiologies. Chest. 2000;117:251-259.
7. Kuschner WG. What exactly is flock worker’s lung? Chest. 2000;117:10-13.
8. Levin JL, O’Sullivan MF, Corn CJ, et al. Asbestosis and small cell lung cancer in a clutch refabricator. Occup Environ Med. 1999;56:602-605.
9. Robinson CF, Petersen M, Sieber WK, et al. Mortality of carpenter’s union members employed in the US construction or wood products industries, 1987-1990. Am J Ind Med. 1996;30:674-694.
10. Raza SN, Fletcher AM, Pickering CAC, et al. Respiratory symptoms in Lancashire textile weavers. Occup Environ Med. 1999;56:514-519.
11. Balkissoon RC, Newman LS. Beryllium copper alloy (2%) causes chronic beryllium disease. J Occup Environ Med. 1999;41:304-308.
