Air Pollution, the Automobile, and Public Health (1988) / Chapter Skim
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Effects of Automotive Emissions on Susceptibility to Respiratory Infections
Effects of Automotive Emissions on Susceptibility to Respiratory Infections
Pages 499-518
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Effects of Automotive Emissions on Susceptibility to Respiratory Infections JAMES E PENNINGTON Brigham and Women's Hospital and Harvard Medical School The Hypothesis / 500 Background / 501 Determinants of Susceptibility / 501 Occurrence of Respiratory Infections / 501 Lung Defense Mechanisms / 502 Long-Term Effects of Infection / 503 Epidemiologic Approach / 503 Documentation and Measurement of Respiratory Infection / 503 Other Epidemiologic Variables / 505 Experimental Approach / 506 Experimental Infections / 506 Studies of Lung Defense Mechanisms / 507 Gaps in Knowledge and Research Recommendations / 508 Epidemiologic Study Design / 508 Experimental Studies / 510 Summary / 513 Summary of Research Recommendations / 514 Air Pollution, the Automobile)
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From page 500... ...
Thus, prevention of respiratory infections associated with automotive emissions might reduce subsequent noninfectious pulmonary diseases. In organizing a method for assessment of the basic hypothesis, a natural starting point is agreement about the constituents of automotive emissions and about the concentration ranges relevant to human expo sures; some components (for example, nitrogen dioxide, acrolein)
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For example, is ciliary dysfunction with associated bronchitis/sinusitis a major determinant, or is the alveolar parenchymal region more prone to infection if stressed by automotive emissions? Naturally, if certain locations in the respiratory tract appear to be more susceptible, then research could be directed at analysis of the most relevant local defense mechanisms.
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Host Defense Mechanisms in the Human Respiratory Tract Upper airways Nasopharyngeal filtration Mucosal adherence Bacterial "interference" Saliva (proteases, lysosome) Secretory IgA Epiglottis Lower airways and alveoli Cough reflex Mucociliary clearance Humoral factors Immunoglobulins Complement Cells and cell products Bronchus-associated lymphoid tissue Lymphocytes Alveolar macrophages Polymorphonuclear leukocytes Cytokines (interleukin-1, interleukin-2, interferons)
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compared respiratory symptoms of a group of urban traffic police exposed to automotive emissions with symptoms of a group
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Hematologic or radiographic tests do not provide conclusive evidence of respiratory infection. An elevated white blood cell count may suggest bacterial infection, and infiltrative patterns on chest x rays may suggest lung infection (among other possibilities)
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Serologic Diagnosis of Common Respiratory Infections Agent Tests Viral Respiratory syncytial virus Influenza A and B Parainfluenza Adenovirus (group) Mycoplasma pneumonias Legionella sp.
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Experimental Approach Experimental Infections A link between respiratory mucosal damage from inhalation of O3 and increased susceptibility to localized infections was postulated by Miller and Ehrlich (1958~. They reasoned that mucous membranes, known to be important in antiinfective defenses, might be damaged by O3 during high-altitude flight.
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Studies of Lung Defense Mechanisms Careful analysis of past studies describing the importance of specific lung defense components in resistance against specific types of infection is critically important to test the hypothesis that automotive emissions impair lung defenses. For example, careful epidemiologic studies such as those discussed above may demonstrate that individuals working or living in urban areas with high levels of ambient NO2 have an increased risk for viral respiratory infection but not bacterial infections.
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The most direct method to prove this hypothesis would be to demonstrate clearly that individuals exposed to higher levels of automotive emissions experience more frequent and/or more severe respiratory infections than individuals exposed to lower levels. Reliance on symptoms (cough, sore throat, "colds going to chest," sputum production)
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· Recommendation 1. Epidemiologic survey in high-risk populations exposed to varying levels of automotive emissions should be conducted.
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Despite the large body of information regarding susceptibility to infection in animals exposed acutely or chronically to inhaled NO2 or O3, questions regarding lung defenses during experimental infection remain unanswered. For example, little or no information exists about defenses against several extremely common respiratory pathogens, including mycoplasma, respiratory syncytial virus, Legionella s p., S
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Survival or lung clearance during experimental infections could be evaluated as well as the additive influences of gas exposure plus underlying host defect on lung defense components (for example, alveolar macrophages, inflammatory reaction in airways after infection, bacterial adherence to respiratory mucosa)
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Recommendation 5. Animal and/or human lung cell populations should be evaluated for the effect of inhaled gases on the production of interleukin-1 by alveolar macrophages, interleukin-2 by T lymphocytes, and the production of various interferons by alveolar macrophages and lymphocytes.
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Mucosal cell binding affinity for respiratory pathogens should be studied after exposure to relevant concentrations of emission components. Summary The basic hypothesis under consideration is that exposure to automotive emissions results in increased susceptibility to respiratory infections.
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This analysis could be done in humans or animals exposed to emission components under controlled conditions. Studies most likely to yield useful new information would be numbers and function of pulmonary NK cells and cytotoxic lymphocytes; interferon production by alveolar macrophages and lymphocytes; and antibody-dependent cellular cytotoxic activity of Fc receptor bearing lung cells (that is, alveolar macrophages and K lympho cytes)
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1978. Effects of NO2 on the response of baboon alveolar macrophages to migration inhibitory factor, J
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1979. Defective oxidative metabolic responses in vitro of alveolar macrophages in chronic granulomatous disease, Am.
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1984. The accessory cell function of human alveolar macrophages in specific T cell proliferation, [.
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1972. Influence of nitrogen dioxide on the uptake of parainfluenza-3 virus by alveolar macrophages, J
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