|
Page 3 Environmental
and Occupational Lung Diseases
Cobalt-related lung disease Cobalt exposure occurs during the production of hard metal (cobalt and tungsten carbide) cutting tools and jet engine parts and during the polishing of diamonds with an abrasive grit of pure cobalt (30). Cobalt is highly soluble in lung tissue and may be absent in a lung biopsy analysis after exposure has ceased, but the biopsy specimen may show tungsten, which remains indefinitely. There are four types of cobalt disorders. First, asthma may occur. Second, an acute illness of fever, anorexia, malaise, and dyspnea resembling a viral illness may occur with crackles on examination, small nodules radiographically, and abnormal physiologic studies. The third disorder is interstitial pneumonitis of the usual interstitial pneumonia type, although this is rare. It is not responsive to cortico-steroid therapy and can be progressive. The fourth disorder, giant cell interstitial pneumonitis is slightly more responsive to corticosteroid therapy. A study of 513 employees indicated an increased frequency of cough and sputum, of abnormal vital capacity and diffusing capacity measurements, and of abnormal chest radiographs (36). Maintenance of strict dust level controls and regular supervision of workers must continue. Manufactured fibers Manufactured vitreous fiber products include mineral wool, glass fiber and ceramic fiber. Mineral wool refers to slag wool and rock wool produced by melting and fiberizing iron ore furnace slag or siliceous limestone. Glass fiber includes glass wool such as the fiberglass used in home insulation, continuous glass filament, and special purpose glass fiber. Refractory ceramic fiber is characterized by the ability to resist very high temperatures and is produced from kaolin clay, alumina/silica, or alumina/silica/zirconia. The commonly used glass wool as in home insulation has the lowest health risk and may be a skin irritant. The potential risks associated with slag and rock wool are somewhat higher, and that associated with special purpose glass fiber and refractory ceramic fiber even higher (37). Extensive monitoring of individuals exposed to these agents continues to examine the carcinogenic risk, occurrence of airway dysfunction, and the presence of interstitial disease and pleural effects. Toxic Fume Exposures Toxic fume exposures often result from accidents involving gas tanks, trucks or tank cars carrying ammonia, chlorine, or other toxic agents, or from explosions in chemical plants, pulp mills, or at missile sites, Table 9. The first described accident involved broken nitric acid containers in 1804 (38). Silo gas exposure may occur as a result of repairing the ventilation system or during the retrieval of a farmer's jacket (29). Mixing household substances such as four types of drain declogging agents can also be dangerous. The type of injury and eventual outcome is related to the nature of the fume and quantity of exposure. The amount of exposure is usually related to the distance from the source (40,41). Death may occur instantly from asphyxiation or within a few minutes from massive pulmonary edema. A small percentage of exposed individuals may experience no pulmonary symptoms, but breathlessness, cyanosis, and pulmonary edema may develop 8 to 12 hours later. Corticosteroid therapy is important at this stage and may prevent subsequent airway scarring (42). In rare situations, individ-uals who survive the diffuse alveolar damage phase may develop irreversible con-strictive bronchiolitis obliterans 10 to 14 days after initial exposure. This latter complication generally does not develop after chlorine or ammonia exposure but can develop after exposure to sulfur dioxide released in a missile site explosion (41). The catastrophic event in Bhopal, India, involving bronchiolitis obliterans probably resulted from hydrogen cyanide that was released from the explosion caused by water leaking into the 41,000 kg tank of methyl isocyanate at midnight. By morning, 1000 deaths and 200,000 injuries had been reported (43). Safety measurements and preventive programs are the management of choice for such disorders. Hypersensitivity Pneumonia Hypersensitivity pneumonitis or allergic alveolitis occurs in susceptible individuals exposed and sensitized to suspended bacterial or fungal spores and mycelia, animal proteins, or chemicals that cause a granulomatous lung reaction. Farmers, grain operators, wood workers, and bird breeders are at risk in an occupational setting. Office workers and home owners are at risk from birds as pets and from contaminated air conditioning and humidifier units, Table 10 (44). Acute hypersensitivity pneumonitis begins with fever and chills in the form of a flu-like illness within 4 to 6 hours after exposure once sensitization has occurred and lasts for about 18 hours. The leukocyte count is often increased. The chest roentgenogram may show bilateral patchy infiltrates. The vital capacity and diffusing capacity are decreased. Usually, the illness responds quickly and completely to cessation of exposure or to a brief course of corticosteroid therapy. However, a study of acute-stage hypersensitivity pneumonitis in Finnish farmers showed an initial corticosteroid response but no influence on long-term results (45). The chronic form of disease occurs in less than five percent of patients but is often characterized by irreversible pulmonary damage. Progressive dyspnea, crackles on examination, radiographic honeycombing, and abnormal diffusing capacity occur in this late stage. Some initial improvement may occur with corticosteroid therapy, but therapy or avoidance of antigen does not affect the permanent changes. With early recognition, the overall prognosis of hyper-sensitivity pneumonitis is excellent, but a fatal case has been reported from prolonged exposure to one parakeet kept in the home (46). Occupational Asthma Occupational asthma will probably be the most common workplace dis-order in future years especially with the development and use low molecular weight chemical agents that are capable of causing asthma. The list of etiologic agents responsible for occupational asthma is more than 200 items long (47, 48). Agents can be categorized as microbial products, animal, bird, or arthropod products, plant products, or chemicals Table 11. High molecular weight compounds, such as animal or bird proteins, probably represent an IgE-induced asthma reaction. Low molecular weight compounds, such as chemicals, may elicit immunologic responses by acting as a hapten to form an allergen, but non-IgE mechanisms are most likely involved in the pathogenesis (49). It is also possible that both mechanisms are involved, i.e., such agents initially cause an irritant reaction and an immunologic response develops over time. The diagnosis is usually established by obtaining the appropriate historical information and chronological occurrence of symptoms. Often, symptoms subside or improve after weekends and during vacations. The employee is well for the initial two or three hours during Monday, after which chest tightness and wheez-ing develops. The low molecular agents such as the isocyanates may have a two-phase response. There is improvement in the afternoon, but an inflammatory phase of the illness recurs in the evening. By Friday, the worker is generally stable, but the pattern repeats itself the next week. The chest roentgenogram is usually normal. Some type of specific radio-allergosorbent (RAST) tests may be helpful. Inhalation challenge studies can be specific, but these are labor intensive, time consuming, and may be hazardous. Vital capacity and FEV1 are obtained before the challenge and every 10 to 15 minutes thereafter. A positive test is defined as a 20% decrease in the FEV1. Methacholine challenge may serve as a non-specific test to identify individuals with reactive airways. Monitoring and recording portable worker-directed peak flow measurements for two weeks at home and two weeks at the workplace may offer a helpful alternative. Treatment by avoidance of the agent and the use of bronchodilators is usually effective early, but if begun too late, persistent symptoms and permanent bronchial hyperresponsiveness may occur. Occupational Pulmonary Infections Occupational-related infections may develop in pet shop owners, abattoir workers, farmers, tannery workers, archaeologists, or health care workers (50). The microbial agents include bacteria causing disorders such as anthrax, brucel-losis, tularemia, or plague. Chlamydia produces pneumonia and psittacosis. The fungi include blastomycosis, coccidioidomycosis, and histoplasmosis. Myco-bacterial infections may occur in health care workers. Rickettsia can cause Q fever. Viruses such as adenovirus, influenza, rubeola, and varicella may be responsible for work-related or military infectious outbreaks. The symptoms and the radiographic findings reflect the causative agent. Treatment is directed toward the specific agent (50). Occupational lung cancer Occupational lung cancer has been reported in selected workplace situations; however, cigarette smoking remains the most important preventable cause of lung cancer (51). Workers exposed to arsenic during copper or other smelting processes are at higher risk for lung cancer. Radon exposure in the form of alpha-particle emitting radon prodigy as a cause of lung cancer has been reported in miners and may be a factor in homes with high radon gas levels. Chromium and nickel exposures during the roasting, smelting, and electrolysis processes may result in lung cancer in exposed workers. Coke oven fumes have also resulted in an increased risk of lung cancer. Workers exposed to fumes of chloromethyl ethers that are used as a chemical intermediate are at risk for lung cancer, but since 1971, the entire process has been maintained within a closed system, almost eliminating worker exposure (51). Other agents, such as beryl-lium, cadmium, formaldehyde, silica, and welding fumes, are being intensively monitored for confirmation of a cause of lung cancer in exposed workers. Prevention is the key to future work-related lung cancers. Because of the interaction of exposures and cigarette smoke, cessation of cigarette smoking in the workplace is essential. If possible, hazardous exposures should be eliminated or decreased by engineering advances, i.e., ģengineer outī the exposure. Animal exposure studies are virtually of no value, but new chemicals, fumes, and dusts can be tested in multiple cell culture systems for potential carcinogenic effects. Retrospective studies may provide guidance for future work but, by themselves, are fraught with inconclusive results and may be an overestimation of the cause and effect relationship. Case control or prospective studies taking into account the effects of cigarette smoking are preferred to establish cause and effect between exposures and lung cancer. Selected Occupations Workers in selected occupations are at risk for several types of occupational lung diseases. Farm workers are at risk for the development of acute and chronic hypersensitivity pneumonitis (farmer's lung); asthma due to grain dust, rust fungi, mites, pollens, and even excreta from rodents; silo-filler's disease; adult resp-iratory distress syndrome; neuromuscular failure from certain types of pesticides; organic dust toxic syndrome and even asphyxiation and death from liquid manure systems (52). Other special working environments with a potential for multiple hazardous exposures include welding, the cement industry, the rubber industry, and the pulp and paper industries. Disability Evaluation Definitions are necessary for a discussion of disability (53-56). Impairment is a medical term for an anatomic or functional abnormality-an objective, meas-urable loss of function. Impairment may be either temporary or permanent. The degree of impairment varies in severity from mild to moderate, which precludes some types of labor, to severe, which precludes any type of gainful employment. Disability is a general term defined as the inability to work because of physical impairment. Age, education, and economic and social environments affect disability. It is categorized as partial or total. In the adjudication of disability by judicial panels and compensation boards, medical information, the degree of impairment, and social factors are weighed. The WHO classifications differ: Impairment is defined as loss of lung function, disablement is defined as dim-inished exercise capacity, and handicap is the total effect on the person's life. The disability evaluation consists of obtaining information concerning symptoms, cigarette use, and occupational and environmental exposure, the performance of a physical examination of the chest, pulmonary function studies, and chest radiography, Table 12. The degree of impairment is determined by pulmonary function testing, Table 13. Screening studies, including the vital capacity, FEV1, and diffusing capacity, should be performed to determine mild, moderate, or severe impairment. Exercise oxygen uptake studies can be performed to confirm the category or to determine whether the dyspnea is out of proportion to the results of ventilatory studies. The mild impairment category (especially near the normal category) is often not related to pulmonary symptoms, and individuals in such a category can perform virtually all types of work. Individuals with moderate pulmonary impairment usually can perform some types of work. Persons with severe pulmonary impairment are usually precluded from gainful employment. Situations involving asthma, occupational-related disorders, and lung cancer require special consideration (53-56). Conclusion It is important to understand the dose-response information and the clinical, radiographic and physiological features. Most importantly, prevention remains the fundamental element for managing the occupational and environmental lung disorders. |
