Evaluation and Prevention of Occupational and Environmental Lung Disease
L. Christine Oliver
Occupational lung disease is among the 10 leading causes of work-related illness in the United States. Toxic environmental exposures are increasingly recognized as an important cause of pulmonary disease. Causal agents in both the workplace and the general environment include irritant and/or sensitizing chemical vapors and gases, organic and inorganic dusts, mold, and toxic fumes. These can adversely affect the upper and lower respiratory tracts.
Prevention of exposure is key to reducing morbidity and mortality from occupational and environmental lung disease. Knowledge about and familiarity with these diseases is critically important for the primary care physician, who is often the first health care provider to see individuals with occupational/environmental lung disease. Because respiratory symptoms caused by toxic exposures are nonspecific, recognizing their potential relationship to a toxic agent or agents is essential for proper diagnosis and treatment. Continued exposure often results in needless irreversible physiologic abnormalities and the development of chronic and even fatal lung disease.
In the United States and other developed countries, workrelated asthma is the leading cause of occupational lung disease, having supplanted the pneumoconioses, or dust diseases, of the lung. An estimated 15% to 26% of newly diagnosed cases of asthma in adults are the consequence of occupational exposures. Exposure to cigarette smoke in the workplace represents a major risk factor for persons with preexisting asthma and also contributes to risks of cardiovascular disease, lung cancer, and premature death.
The most common cause of pneumoconiosis is asbestos. The National Occupational Respiratory Mortality System (NORMS) reveals a 20-fold increase in the number of deaths due to asbestosis in the United States from the 1960s to the late 1990s, with a plateau at approximately 1,500 deaths per year between 2000 and 2005. The prevalence of coal workers’ pneumoconiosis (CWP) is tracked by the Coal Workers’ Health Surveillance Program (CWHSP) administered by the federal government. The most recent CWHSP prevalence data show variation by region, with highest prevalence in the central Appalachian region of the United States (10% observed vs. 4.2% predicted [PR 2.4; p < 0.001]). Important contributing variables are number of employees per mine, with smaller mines being at greater risk; lower height of the coal seam, associated with greater silica exposure; and longer length of the workday. The National Institute of Occupational Safety and Health (NIOSH) has estimated that 1.7 million US workers are potentially exposed to respirable silica, many at concentrations in excess of existing or recommended federal standards. With regard to malignancy, the NORMS data reveal that the annual number of deaths in the United States from malignant mesothelioma, a sentinel for asbestos exposure, increased from 2,485 in 1999 to 2,704 in 2005 without evidence of a plateau. Included among these deaths are family members exposed to asbestos dust carried home on work clothes. The number of asbestos-related lung cancers is difficult to quantify because of smoking attribution; but it has been estimated to be at least twice that of malignant mesothelioma.
These figures underestimate the true occurrence of occupational lung disease because the diagnosis is often missed. Physicians for the most part lack adequate training in occupational medicine. Clinical findings in patients with work-related lung disease resemble those in persons with nonoccupational lung disease. The latency period between exposure and manifestation of disease may be long, obscuring the causal relationship. The association may be further obscured by the fact that occupational disease is often caused by bystander and household exposures and/or by residential proximity to a toxin source. For example, asbestos-related disease has been reported in family members of asbestos workers and in persons living close to shipyards and pulmonary beryllium disease (PBD), in persons living in proximity to beryllium plants. Low-dose exposure may cause disease, as is the case with asbestos and malignant mesothelioma.
Inhaled vapors, gases, dusts, and fumes exert their effects on the respiratory tract in several ways. The basic pathophysiologic mechanism is inflammation caused by direct irritation and/or an immunologic response with the development of sensitization. Such reactions have been documented in workers, both asthmatic and nonasthmatic, exposed passively to cigarette smoke in the work environment. Inflammation of the upper respiratory tract (URT) characteristically causes cough with or without excessive mucus secretion. Lower respiratory tract (LRT) responses include airway hyperreactivity with chest tightness, wheeze, and shortness of breath; chemical and hypersensitivity pneumonitis; and pulmonary edema. Clinical manifestations may be immediate or delayed; for example, a delay of 12 to 24 hours may precede the development of pulmonary edema caused by exposure to nitrogen dioxide or phosgene.
Immunologic mechanisms include IgE and T-cell mediation. Sensitization is important etiologically in hypersensitivity pneumonitis, occupational asthma (OA) with latency, and PBD. For agents such as diisocyanates and formaldehyde, mechanisms are less clearly understood. In the case of diisocyanate-induced asthma, diisocyanate-specific IgE may be elevated and appears to correlate with disease, while IgG is an indicator of exposure.
Dusts such as silica and asbestos and metals such as beryllium are retained in the lungs over time and provoke a fibrotic response or, in the case of beryllium and inorganic dusts, granuloma formation. Particle size and dimensions determine distribution within the lung; particles with a diameter of ≤5 µm reach the LRT. Larger particles impact the mucosa of the URT. Latencies may be as long as 20 to 25 years or as short as a few months if there is sensitization. Elevated circulating levels of immunoglobulins, rheumatoid factor, antinuclear antibody, and α1-antitrypsin have been observed in dust-induced lung diseases.
As noted, passively inhaled cigarette smoke acts on the lung in a manner similar to other irritant gases; it is a potent risk factor for development of chronic obstructive pulmonary disease (COPD) and lung cancer (see Chapters 47, 48, and 53). In addition, exposure to its toxic components triggers mechanisms leading to vascular injury (see Chapters 18, 31, and 54) and a host of extrapulmonary cancers, such as those of the GI tract and breast (see Chapters 76 and 122).
There is increasing evidence of genetic influences on the risk of developing certain occupational lung diseases, such as diisocyanate-induced asthma and PBD. As is the case with many other diseases, it is likely that interaction between genes and the environment is a critical variable in the development of occupational lung disease. Cigarette smoking is also important. Asbestos acts synergistically with cigarette smoke to increase the risk for lung cancer. Smoking appears to increase the risk for IgE-mediated OA in individuals exposed to platinum salts and tetrachlorophthalic anhydride. The prevalence of bronchitis and airway obstruction is increased in welders and coal miners who smoke compared to their nonsmoking coworkers. Social and economic variables often determine geographic proximity of home to industrial sources of air pollution. Work practices affect the likelihood that family members bring workplace toxins home on their work clothes.
Categories of occupational and nonoccupational lung disease are similar: obstructive airway disease, interstitial lung disease, pneumonitis, noncardiogenic pulmonary edema, and cancer (Table 39-1).
