Occupational lung disease can affect any part of the respiratory tract, including sinuses, airways, the lung parenchyma, and the surrounding pleura. As a result, signs and symptoms associated with occupational exposure include rhinitis, reactive airways disease, COPD, pleural disease, diffuse parenchymal lung disease, and malignancy. Occupational lung diseases can present acutely, subacutely, or slowly after many years of exposure. As a result, these diseases require that clinicians maintain suspicion for and obtain a careful history of occupational exposures. Clinical presentations related to silica and asbestos exposures are well characterized and recognized. However, new agents that may lead to respiratory diseases are frequently introduced in industry. Factors suggesting an underlying occupational lung disease include patient concerns about an exposure, a temporal association with an exposure, unexplained signs or symptoms, and evidence of coworkers with similar symptoms (Table 17). In addition, patients may experience relief of symptoms when away from the work environment and recurrence of symptoms upon their return. For the patient with occupational lung disease, similar to diffuse parenchymal lung disease, cough and dyspnea on exertion are common.
The time course from exposure to the development of signs and symptoms of occupational lung disease is highly variable. Therefore, it is essential to obtain a complete history, including employment history. Exposures within the same industry can vary based on use of best practices and on the type of workplace. For example, coal worker's pneumoconiosis in the United States has substantially decreased since the institution of federal safety standards. However, rates of coal worker's pneumoconiosis are higher for individuals who work for companies with fewer than 50 employees, and for those who work in thin-seam mines. Thin-seam mines appear to have higher crystalline silica exposure and pose greater risk. More than 95% of these mines are located in Kentucky, West Virginia, and Virginia. Adequate determination of exposure requires a clear description of job duties and determination of the extent of dust exposure. Clinicians should also obtain a history of additional exposures from hobbies or the home environment (see Table 17).
When an occupational lung disease is suspected, clinicians should request Material Safety Data Sheets (MSDSs) from the employer, which detail chemical properties and known health risks associated with substances within the workplace. The U.S. Occupational Safety and Health Administration (OSHA) requires that this information is available upon request for employees who work with potentially harmful materials.
For individuals who have undiagnosed disorders, persistent unexplained symptoms, or permanent impairment possibly due to an occupational lung disease, referral to an occupational and environmental lung disease specialist is appropriate.
The key to management of occupational lung disease is removal of the offending agent from the workplace or the worker from the offending agent. Because workers typically have colleagues in a similar environment, further investigation of the workplace to ensure identification of all affected individuals is essential. Beyond one specific patient, prevention through mitigation of further exposures in the workplace is best practice.
Workers' compensation often becomes an issue during medical management. It may be difficult to define the degree of impairment resulting from the exposure, and the determination of disability related to the impairment may require referral to a specialist with expertise in occupational lung disease.
For individuals at high risk for the development of pulmonary disease, the use of health questionnaires and pulmonary function screening is appropriate; such screening can also identify a new exposure and any associated risk of disease development. Surveillance systems that catalogue sentinel cases of disease can help identify clustering of cases. However, one major limitation of these databases is the failure of physicians to report events.
Asbestos includes a group of minerals that, when crushed, will break into fibers. These fibers are chemically heterogeneous hydrated silicates that are used in industry because of their high tensile strength, heat resistance, and acid resistance. In the past, asbestos fibers were widely used in insulation, brake linings, flooring, cement paint, and textiles. Because of the known toxicities associated with asbestos, these compounds are used far less frequently today.
Asbestos-associated diseases have a prolonged latency period (15 to 35 years), resulting in continued identification of new cases despite the decreased use of asbestos in the United States. Continued exposures within the United States and the developed world occur through updating, demolition, and abatement of older construction. Asbestos exposure remains an occupational hazard for workers in developing nations.
Duration and extent of exposure are key risk factors for the development of disease. Asbestos-related lung diseases are common in mine workers who procure the asbestos and in industries that make use of the products. In the United States, workers in construction, naval shipyards, and the automotive service industries are particularly at risk. Exposure is also possible in areas where manufacturing of asbestos leads to environmental contamination. Similarly, there are reports of people who develop asbestos-related lung diseases after exposure to asbestos dust from family members working in an asbestos-related industry.
Inhaled asbestos fibers deposit deep within the lung, reaching airway bifurcations; respiratory bronchioles; and the alveolus, where they promote alveolitis. Type I alveolar epithelial cells take up the fibers, which migrate to the interstitium. Lymphatic channels transport asbestos fibers to the pleural surface. Although activated macrophages phagocytose and remove fibers, remaining fibers stimulate the macrophage to produce inflammatory mediators. These and other cell mediators stimulate fibroblast proliferation and chemotaxis, resulting in collagen deposition and development of fibrosis.
Asbestos exposure increases the risk for development of lung cancer regardless of smoking status, but the risks are substantially higher in smokers. This risk of cancer is apparent when any form of asbestos-related lung disease is present; however, for those with a history of asbestosis (that is, diffuse parenchymal lung disease secondary to asbestos), the risk of lung cancer is 36 times higher than in those with no history of smoking. Smoking cessation is essential. Findings of parietal pleural calcifications or plaques on chest radiograph should alert the clinician to the possibility of asbestos exposure. Although most patients with pleural plaques are asymptomatic, the most common symptom is exertional dyspnea. Additional evaluation including evaluation for lung cancer or mesothelioma should be considered.