Air Pollution, the Automobile, and Public Health (1988) / Chapter Skim
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Relation of Pulmonary Emphysema and Small Airways Disease to Vehicular Emissions
Relation of Pulmonary Emphysema and Small Airways Disease to Vehicular Emissions
Pages 441-464
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From page 441... ...
Relation of Pulmonary Emphysema and Small Airways Disease to Vehicular Emissions JOANNE L WRIGHT University of British Columbia Lung Anatomy and Defense Mechanisms / 442 Airway Cells / 442 Alveoli / 443 Deposition of Particulates / 443 Pathologic Conditions: Concepts and Quantification / 443 Emphysema / 443 Small Airways Disease / 446 Mucus Hypersecretion / 446 Animal Models of Human Disease / 446 Emphysema / 448 Small Airways Disease / 449 Emphysema and Small Airways Disease: Relations to Vehicular Emissions / 449 Lung Disease Produced in Animals by Vehicular Emissions / 449 Animal Exposure to Diesel Exhaust / 454 Summary / 454 Summary of Research Recommendations: Discussion / 455 Pathogenesis of Pulmonary Disease / 455 Pathobiology / 457 Animal Studies / 457 Human Studies / 458 Summary of Research Recommendations: Priorities / 458 In Vitro Experiments / 458 In Vivo Experiments / 459 Human Studies / 460 Air Pollution, the Automobile, and Public Health.
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From page 442... ...
The lesions of emphysema and small airways disease produced by tobacco smoke inhalation in humans are similar to those that appear in animals experimentally exposed to emissions. To investigate the effects of emissions on human lungs it is necessary to use animal models.
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From page 443... ...
Alveoli There are two types of alveolar epithelial cells. Type I are attenuated cells covering 93 percent of the alveolar surface.
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This is not surprising, since macrophages in the lumens of respiratory bronchioles are a prominent feature in young healthy cigarette smokers (Niewoehner et al.
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However, elastin peptides in human blood have been shown to separate nonsmokers from smokers, and measurements of lysyl oxidase as an indicator of elastin synthesis have shown that cigarette smoke inhibits elastin repair after initial damage with instilled elastase Janoffl985~.
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~ Recommendation 7. Some of the more detailed pulmonary function tests should be used to identify progressive dysfunction.
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Comparisons of animal and human lung structure have concentrated on two areas: airway structure and airway surface epithelial cells and glands. The casts of the tracheobronchial trees of humans have a distinctive, almost spherical shape with a relatively symmetrical branching pattern.
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Protein/ calorie starvation produces enlargement of the airspaces, but physiological alterations are different from those seen in human emphysema Janoff 1985~. When exposed to cigarette smoke, experimental animals with elastase-induced emphysema show a greater degree of lung destruction.
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This model suggests that any inhaled substance that results in an inflammatory response is capable of causing airflow obstruction. These data are similar to those obtained from human studies of the association between inflammation and airflow obstruction in cigarette smokers.
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Physiological Charges. Pulmonary function tests in animals exposed to NO2 con
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1976~. An early study concluded that the pulmonary function changes in the rabbit model were due to bronchiolitis (Davidson et al.
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· Recommendation 12. Short-term animal experiments to determine pathobiology of disease related to emissions should be designed to measure biochemical parameters in lung tissue and to count and type inflammatory cells in ravage or tissue.
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1978) showed decreased alveolar surface density with airspace enlargement, as well as an increase in the size and number of the alveolar pores, centered on the respiratory bronchioles and alveolar ducts in the groups treated with NOX and sulfur oxides (SOx)
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Studies should be undertaken to determine whether the effects of diesel exhaust are different from the effects of gasoline exhaust in regard to disease progression, the effects of age at exposure, and additional applied stress. Summary It is apparent that exposure to gasoline or diesel emissions or their components has the potential to produce disease.
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From page 455... ...
Measurement of elastase and antiproteinases in ravage fluids has been useful in investigating damage related to tobacco smoke and to the adult respiratory distress syndrome, and the feasibility of using this procedure to analyze proteolysis/antiproteolysis imbalance is an important subject for further research (Recommendation 2~. The inflammatory cells stimulated by cigarette smoke are a source of proteinases and represent a possible mechanism for lung destruction.
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This localiza tion might be expected to occur also during pollutant-induced lung destruction, where the respiratory bronchioles do appear to be abnormal, and there is an inflammatory infiltrate of macrophages. What is the balance between fibrosis and destruction, and is this related to particu lates rather than oxidants (Recommenda tion 10~?
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Epithelial cells could then be examined for damage and production of inflammatory cell chemotactic factors. The inflammatory cells could also be examined for evidence of activation with production of oxygen radicals.
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In Vitro Experiments HIGH PRIORITY Recommendation 1 Pollutant constituents should be introduced to cell cultures of epithelial and/or inflammatory cells. MEDIUM PRIORITY Recommendation 3 Cell damage and its relation to inflammation should be studied through further research on exposure-related increases in neutro phils and macrophages, including collagen and elastin biomechan ics, and the dose/time relationship between exposure and neutro phil and macrophage increase.
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Recommendation 15 Long-term, multidisciplinary animal studies should be designed to document abnormalities produced by exposure to emissions at various points in the lifespans of subjects. MEDIUM PRIORITY Recommendation 9 Pollutant interference with lysyl oxidase and impairment of elastin resynthesis should be investigated.
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From page 460... ...
Recommendation 16 Experiments should be conducted to analyze the effects of nutrition, stress, infection, exercise, and co-contaminants such as diesel particulates and cigarette smoke on pulmonary disease. Recommendation 17 Short-term and long-term studies should be undertaken to determine whether the effects of diesel exhaust are different from the effects of gasoline exhaust in regard to disease progression, the effects of age at exposure, and additional applied stress.
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1980. Effects of pulmonary function of low-level nitrogen dioxide exposure, In: Nitrogen Oxides and Their E.~ects on Health (S.
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1974. Pathologic changes in the peripheral airways of young cigarette smokers, N
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1984. The relationship of the peripheral leukocyte count and cigarette smoking to pulmonary function among adult men, Chest 86:38~386.
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