Air Pollution, the Automobile, and Public Health (1988) / Chapter Skim
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Asthma and Automotive Emissions
Asthma and Automotive Emissions
Pages 465-498
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(it) 1988 by the Health Effects Institute.
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1983~. In this chapter, the clinical forms of asthma and their pathogenesis are described, and the results from controlled exposure studies of the effects of inhalation of pollutant gases relevant to automotive emissions on normal and asthmatic subjects are summarized.
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. Nonspecific bronchial hyperreactivity to various challenges is an index of the intrinsic responsiveness of elements in the airway wall (smooth muscle, submucosal blood vessels and glands, afferent nerve endings and efferent nerve ganglia, mast cells, and possibly neuroendocrine cells)
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They also may have a modest increase in nonspecific bronchial reactivity to histamine or methacholine. Indeed, Fish and Norman (1985)
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Bronchial Hyperreactivity Late reactions following antigen challenge in asthmatic subjects are associated with enhancement of nonspecific bronchial hyperreactivity. Marked enhancement of bronchial hyperreactivity may last for weeks and is associated with the emergence of more severe clinical manifestations of asthma.
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that increases nonspecific bronchial reactivity should also enhance reaction to inhaled antigen, even in the absence of any change in immunologic status. Furthermore, to the extent that air pollutants can provoke bronchoconstriction in a "nonspecific" manner, highly bronchoreactive asthmatics should be more .
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The uptake profiles should be examined for their ability to account for some of the variability in vital capacity response to O3 exposure observed among individuals. Asthmatic Subjects Ozone.
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challenged ragweed-sensitive asthmatic subjects with specific antigen immediately and 24 hr after a 1-fur exposure to 0.1 ppm. No effect of the exposure on specific bronchial reactivity was found, but the exposure conditions were extremely mild.
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In addition, increased epithelial permeability would allow egress of submucosal albumin onto the airways surface where it could alter the viscoelastic properties of the surface liquid and impair mucociliary clearance. Some important effecter mechanisms in asthma involve stimulation of sensory nerves and neurally mediated reflexes; release of chemical mediators, including arachidonate metabolites, from mast cells and possibly other cells; recruitment of inflammatory cells to the airways; and damage to airways epithelium.
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1986~. This factor will need to be considered in assessing bronchial reactivity.
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. Little or no attempt has been made in ' studies of pollutant effects in asthmatic subjects to fractionate airways resistance changes or, more specifically, to examine small airways function.
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Bronchoconstriction evoked by histamine or antigen challenge is partially blocked by atropine pretreatment, indicating a significant role for reflex mechanisms as well as for more direct, chemically mediated effects on smooth muscle. Atropine pretreatment will block bronchoconstriction evoked by O3 exposure (Beckett et al.
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Animals prepared so as to render their airway C-fiber systems nonfunctional should be used to examine the role of this sensory system in O3 effects on epithelial permeability, mucous secretion, epithelial ion transport, bronchial reactivity, and airways inflammation. Chemical Mediators.
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Indirect effects on mast cells by mediators released from pollutant-exposed airway epithelial cells or nerves are also possible. Although an important role of the airways mast cell in allergic asthma is generally conceded, it has been difficult to demonstrate the release of all the mediators in viva in allergen- or hyperventilation-provoked reactions (Deal et al.
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Whether this response is essential to the development of bronchial hyperreactivity in O3-exposed normal human subjects is not known. Whether asthmatic subjects would exhibit a similar or altered inflammatory response to O3 inhalation, and what effect this response may have on bronchial reactivity to specific as well as nonspecific challenge, is not known.
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The effect of expenmenta~ pollutant exposures on airways function should be measured in patients with COPD (for example, nonspecific chronic bronchitis, cystic fibrosis) , in whom increased bronchial reactivity is present.
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to specific antigen challenge should be ascertained. Respiratory Epithelium: Asthma and Ozone It is apparent why efforts to understand the pathophysiology of asthma have focused on the components of airway walls, including mast cells, smooth muscle, inflammatory cells, and neural elements.
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Abundant horseradish peroxidase has been observed between epithelial cells in suitably prepared trachea from O3-exposed guinea pigs. However, this marker has also been observed intracellularly, suggesting that intracellular penetration may also occur (V.
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in sputum from asthma patients is also well established (Naylor 1962~. Exposed sensory nerve endings and mast cells have also been noted by Laitinen and coworkers (1985)
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These membrane regions are functionally isolated from one another by the tight junctions near the apical margins of the epithelial cells. The active ion transports generate transepithelial electrical potentials and currents that can be measured in viva (Knowles et al.
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The effects of exposure to 03, or O3 plus other air pollution components, on respiratory epithelial cell function should be probed in greater detail. These functions include mucociliary clearance, permeability to molecules including albumin and antigens, secretion of mucins and of other specific macromolecules, airway surface liouid composition and volume control, and release of mediator substances.
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To the extent that an animal model of asthma fails to exhibit baseline bronchial hyperreactivity or to manifest smooth muscle hypertrophy and chronic inflammatory changes in the airways, the model is not faithful to human asthma. The fact that many cases of asthma do not appear to involve extrinsic antigens may reduce the applicability of animal models in which bronchoconstriction is acutely evoked by antigen challenge.
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Cultured pulmonary endothelial cells, alveolar macrophages, and epithelial cells could be used. Such studies would be particularly useful if they could be correlated to specific pollutant effects on the system under study.
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Even if no relation to asthma were to emerge, a better understanding of this issue is essential to a rational health policy. Some of these mechanistic studies can be performed in human subjects (for example, mucociliary clearance, airways surface liquid composition and volume, analysis of bronchial washes or of bronchoalveolar ravage samples for mediators and macromolecules)
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, in whom increased bronchial reactivity is present. Recommendation 15 The effect of oxidant pollutant exposures of asthmatics on bronchial reactivity to stimuli such as SO2, cold dry air, noniso tonic aerosolized solutions, and certain mast cell-derived mediators should be explored.
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Highly sensitive neuropeptide assays will be required, and rapid inhibition of peptidase activity may also be necessary to prevent hydrolysis of peptides in the sample. Recommendation 6 Animals prepared so as to render their airway C-fiber systems nonfunctional should be used to examine the role of this sensory system in O3 effects on epithelial permeability, mucous secretion, epithelial ion transport, bronchial reactivity, and airways inflam mation.
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1982. Effect of 0.1 ppm NO2 on bronchial reactivity in normals and subjects with bronchial asthma, Am.
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1985. Effects of short-term exposure to ambient nitrogen dioxide concentrations on human bronchial reactivity and lung function, Eur.
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1985. Respiratory epithelium inhibits bronchial smooth muscle tone, J
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A 1983 Effects of 0.1 ppm nitrogen dioxide on airways of normal and asthmatic subjects, J
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1982. Pulmonary function and bronchial reactivity in human subjects with exposure to ozone and respirable sulfuric acid aerosol, Am.
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1970a. The effects of ozone, nitrogen dioxide, and sulfur dioxide on the experimentally induced allergic respiratory disorder in guinea pigs.
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1984. Mast cells in bronchoalveolar lumen of patients with bronchial asthma, Am.
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1986. In vitro differentiation of airway epithelial cells, In: In Vitro Models of Respiratory Epithelium (L.
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