Evaluation and Prevention of Occupational and Environmental Lung Disease PDF

Chapter 39 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. Air pollution causing toxic environmental exposures is increasingly recognized as a major car...

Chapter 39 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. Air pollution causing toxic environmental exposures is increasingly recognized as a major cardiopulmonary morbidity and mortality risk factor. 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 respiratory tract (URT) and lower respiratory tract (LRT) and cause vascular injury. 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 to proper diagnosis and treatment. Continued exposure often results in needless irreversible physiologic abnormalities and the development of chronic and even fatal lung disease as well as adverse cardiovascular consequences. Copyright © 2020. Wolters Kluwer Health. All rights reserved. OCCUPATIONAL LUNG DISEASE (1–19) Epidemiology In the United States and other developed countries, work-related 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. The most common cause of pneumoconiosis is asbestos. Mortality data collected by the Centers for Disease Control and Prevention (CDC) from 1999 to 2015 revealed an increase in annual deaths from malignant mesothelioma, from 2,479 in 1999 to 2,597 in 2015. Included among these deaths are family members exposed as a result of the carry home of asbestos Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 11:47:40. dust 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 two to three times greater than that of malignant mesothelioma. The prevalence of coal workers’ pneumoconiosis (CWP) is tracked by the Coal Workers’ Health Surveillance Program (CWHSP) administered by the federal government. Although the prevalence of CWP has been highest in the central Appalachian region of the United States (10%), an enhanced CWHSP from 2005 to 2015 targeting areas outside central Appalachia with historically low participation rates found a prevalence range of 0.8% in interior regions to 3.4% in the eastern region. 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 CDC estimates that 2 million US workers are potentially exposed to respirable crystalline silica, many at concentrations in excess of the existing federal exposure limit. The substance is found in concrete, brick, mortar, and other construction materials, quartz being the most common. Stone cutters working in granite quarries and workers involved in ceramics or pottery are at particular risk. Risk of lung cancer is increased with exposure. 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 non-occupational 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 chronic beryllium disease (CBD), in persons living in proximity to beryllium plants. Low dose exposure may cause disease, as is the case with asbestos and malignant mesothelioma. Pathophysiology and Clinical Presentation Copyright © 2020. Wolters Kluwer Health. All rights reserved. Both exposures and host factors contribute to the clinical expression of occupational lung disease. Exposures Inhaled vapors, gases, dusts, and fumes (VGDF) 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. Inflammation of the URT characteristically causes cough with or without excessive mucus secretion. Irritant-induced LRT responses include airway hyper-reactivity with chest tightness, wheezing, and shortness of breath, in some cases caused by pulmonary edema or chemical pneumonitis. Fixed obstructive lesions may ensue in small airways as a consequence of a fibrotic response to the insult. Clinical manifestations may be immediate or Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 11:47:40. delayed, for example, a delay of 12 to 24 hours may precede development of pulmonary edema caused by exposure to nitrogen dioxide or phosgene. Immunologic mechanisms include IgE- and T-cell mediations. Sensitization is important etiologically in hypersensitivity pneumonitis (HP), occupational asthma (OA) with latency, and CBD. 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. Host Factors There is increasing evidence of genetic influences on the risk of developing certain occupational lung diseases, such as diisocyanate-induced asthma and CBD. 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. Cigarette smoke acts supra-additively with asbestos to increase the risk for lung cancer and with VGDF to increase the risk for chronic obstructive pulmonary disease (COPD). Smoking appears to increase 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. Copyright © 2020. Wolters Kluwer Health. All rights reserved. Obstructive Airway Disease Work-related airway disease may be acute or chronic and associated airway obstruction, reversible or irreversible. The nature of the exposure and duration of exposure after onset of symptoms are important variables in determining outcome. OA is characterized by reversible airway obstruction and COPD, by irreversible obstruction. Occupational Asthma OA is the most common occupational lung disease in developed countries. It includes newonset asthma and work-exacerbated asthma (WEA) (preexisting or concurrent asthma worsened by workplace exposures). About 25% of working adults with asthma have WEA. At least 250 agents have been reported to cause OA, classifiable as asthma with latency Goroll, Allan. Primary Care Medicine, Wolters Kluwer Health, 2020. ProQuest Ebook Central, http://ebookcentral.proquest.com/lib/bgu-ebooks/detail.action?docID=6743419. Created from bgu-ebooks on 2024-02-18 11:47:40. (immunologically-mediated) and asthma without latency (irritant-induced). High-molecularweight (HMW) agents cause asthma with latency that is IgE-mediated. Low molecular weight (LMW) agents (