For a more detailed discussion, see Balmes JR, Speizer FE: Occupational and Environmental Lung Disease, Chap. 256, p. 2121, in HPIM-18.
The susceptibility to develop many pulmonary diseases is influenced by environmental factors. This chapter will focus on occupational and toxic chemical exposures. However, a variety of nonoccupational indoor exposures such as environmental tobacco smoke exposure (lung cancer), radon gas (lung cancer), and biomass fuel cooking (chronic obstructive pulmonary disease [COPD]) also should be considered. Particle size is an important determinant of the impact of environmental exposures on the respiratory system. Particles >10 μm in diameter typically are captured by the upper airway. Particles 2.5–10 μm in diameter will likely deposit in the upper tracheobronchial tree, while smaller particles (including nanoparticles) will reach the alveoli. Water-soluble gases like ammonia are absorbed in the upper airways and produce irritative and bronchoconstrictive responses, while less water-soluble gases (e.g., phosgene) may reach the alveoli and cause a life-threatening acute chemical pneumonitis.
APPROACH TO THE PATIENT Environmental Lung Diseases
Because there are many types of occupational lung disease (pneumoconiosis) that can mimic diseases not known to relate to environmental factors, obtaining a careful occupational history is essential. In addition to the types of occupation performed by the pt, the specific environmental exposures, use of protective respiratory devices, and ventilation of the work environment can provide key information. Assessing the temporal development of symptoms relative to the pt’s work schedule also can be very useful.
The chest x-ray is helpful in the assessment of environmental lung disease, but it may over- or underestimate the functional impact of pneumoconioses. Pulmonary function tests should be used to assess the severity of impairment, but they typically do not suggest a specific diagnosis. Changes in spirometry before and after a work shift can provide strong evidence for bronchoconstriction in suspected occupational asthma. Some radiologic patterns are distinctive for certain occupational lung diseases; chest x-rays are widely used, and chest CT scans can provide more detailed evaluation.
In addition to exposures to asbestos that may occur during the production of asbestos products (from mining to manufacturing), common occupational asbestos exposures occur in shipbuilding and other construction trades (e.g., pipefitting, boilermaking) and in the manufacture of safety garments and friction materials (e.g., brake and clutch linings). Along with worker exposure in these areas, bystander exposure (e.g., spouses) can be responsible for some asbestos-related lung diseases.
A range of respiratory diseases has been associated with asbestos exposure. Pleural plaques indicate that asbestos exposure has occurred, but they are typically not symptomatic. Interstitial lung disease, often referred to as asbestosis, is pathologically and radiologically similar to idiopathic pulmonary fibrosis; it is typically accompanied by a restrictive ventilatory defect with reduced diffusing capacity for carbon monoxide (DLCO) on pulmonary function testing. Asbestosis can develop after 10 years of exposure, and no specific therapy is available.
Benign pleural effusions can also occur from asbestos exposure. Lung cancer is clearly associated with asbestos exposure, but does not typically present for at least 15 years after initial exposure. The lung cancer risk increases multiplicatively with cigarette smoking. In addition, mesotheliomas (both pleural and peritoneal) are strongly associated with asbestos exposure, but they are not related to smoking. Relatively brief asbestos exposures may lead to mesotheliomas, which typically do not develop for decades after the initial exposure. Biopsy of pleural tissue, typically by thoracoscopic surgery, is required for diagnosing mesothelioma.
Silicosis results from exposure to free silica (crystalline quartz), which occurs in mining, stone cutting, abrasive industries (e.g., stone, clay, glass, and cement manufacturing), foundry work, and quarrying. Heavy exposures over relatively brief time periods (as little as 10 months) can cause acute silicosis—which is pathologically similar to pulmonary alveolar proteinosis and associated with a characteristic chest CT pattern known as “crazy paving.” Acute silicosis can be severe and progressive; whole lung lavage may be of some therapeutic benefit.
Longer-term exposures can result in simple silicosis, with small rounded opacities in the upper lobes of the lungs. Calcification of hilar lymph nodes can give a characteristic “eggshell” appearance. Progressive nodular fibrosis can result in masses >1 cm in diameter in complicated silicosis. When such masses become very large, the term progressive massive fibrosis is used to describe the condition. Due to impaired cell-mediated immunity, silicosis pts are at increased risk of tuberculosis, atypical mycobacterial infections, and fungal infections. Silica may also be a lung carcinogen.
Occupational exposure to coal dust predisposes to coal worker’s pneumoconiosis (CWP), which is less common among coal workers in the western United States due to a lower risk from the bituminous coal found in that region. Simple CWP is defined radiologically by small nodular opacities and is not typically symptomatic; however, an increased risk of COPD may occur. The development of larger nodules (>1 cm in diameter), usually in the upper lobes, characterizes complicated CWP. Complicated CWP is often symptomatic and is associated with reduced pulmonary function and increased mortality.
Beryllium exposure may occur in the manufacturing of alloys, ceramics, and electronic devices. Although acute beryllium exposure can rarely produce acute pneumonitis, a chronic granulomatous disease very similar to sarcoidosis is much more common. Radiologically, chronic beryllium disease, like sarcoidosis, is characterized by pulmonary nodules along septal lines. As in sarcoidosis, either a restrictive or obstructive ventilatory pattern with reduced DLCO on pulmonary function testing can be seen. Bronchoscopy with transbronchial biopsy is typically required to diagnose chronic beryllium disease. The most effective way to distinguish chronic beryllium disease from sarcoidosis is to assess for delayed hypersensitivity to beryllium by performing a lymphocyte proliferation test using blood or bronchoalveolar lavage lymphocytes. Removal from further beryllium exposure is required, and corticosteroids may be beneficial.
Dust exposures occur in the production of yarns for textiles and rope-making. At the early stages of byssinosis, chest tightness occurs near the end of the first day of the workweek. In progressive cases, symptoms are present throughout the workweek. After at least 10 years of exposure, chronic airflow obstruction can develop. In symptomatic individuals, limiting further exposure is essential.
Farmers and grain elevator operators are at risk for grain dust–related lung disease, which is similar to COPD. Symptoms include productive cough, wheezing, and dyspnea. Pulmonary function tests typically show airflow obstruction.
Exposure to moldy hay containing spores of thermophilic actinomycetes can lead to the development of hypersensitivity pneumonitis. Within 8 h after exposure, the acute presentation of farmer’s lung includes fever, cough, and dyspnea. With repeated exposures, chronic and patchy interstitial lung disease can develop.
Many toxic chemicals can affect the lung in the form of vapors and gases. For example, smoke inhalation can be lethal to firefighters and fire victims through a variety of mechanisms. Carbon monoxide poisoning can cause life-threatening hypoxemia. Combustion of plastics and polyurethanes can release toxic agents including cyanide. Occupational asthma can result from exposure to diisocyanates in polyurethanes and acid anhydrides in epoxides. Radon gas, released from earth materials and concentrated within buildings, is a risk factor for lung cancer.
Treatment of environmental lung diseases typically involves limiting or avoiding exposures to the toxic substance. Chronic interstitial lung diseases (e.g., asbestosis, CWP) are not responsive to glucocorticoids, but acute organic dust exposures may respond to corticosteroids. Therapy of occupational asthma (e.g., diisocyanates) follows usual asthma guidelines (Chap. 138), and therapy of occupational COPD (e.g., byssinosis) follows usual COPD guidelines (Chap. 140).
For a more detailed discussion, see Balmes JR, Speizer FE: Occupational and Environmental Lung Disease, Chap. 256, p. 2121, in HPIM-18.