Air Pollution, the Automobile, and Public Health (1988) / Chapter Skim
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Motor Vehicle Emissions: A Strategy for Quantifying Risk
Motor Vehicle Emissions: A Strategy for Quantifying Risk
Pages 17-36
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From page 17... ...
BATES ANN Y WATSON Health Effects Institute Automotive Emissions: A Brief Perspective / 19 Understanding the Components of Risk / 19 Chemical and Physical Properties of Pollutants / 20 Pollutant Exposure and Dose to Biological Tissues / 22 Biological Responses to Pollutants / 23 Sensitive Individuals / 24 Research Approaches / 24 Epidemiology / 24 Experimental Methods / 25 Mathematical Models / 26 Physical Models / 26 Pursuing Quantitative Toxicology: A Strategy for Research / 26 Highlights of the Authors' Recommendations / 27 Criteria for Prioritization / 27 A Proposed Research Strategy / 28 Summary 1 34 Conclusion / 34 Air Pollution, the Automobile, and Public Health.
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From page 18... ...
One's perception of, and response to, the environment may be just as significant for the "health" of society as clinical presentations of organic disease. Thus, this book examines the existing evidence about risks from automotive emissions and evaluates the methodologies presently available to quantify human risks.
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Finally, after having carefully read the authors' suggestions, we conclude with an attempt to translate their individual priorities into a feasible, cross-disciplinary research strategy. Automotive Emissions: a Brief Perspective Motor vehicles contribute significantly to .
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Upon their release, emitted substances are transformed by complex atmospheric chemical reactions. Airborne pollutants, therefore, consist of primary tailpipe emissions (for example, carbon monoxide, nitric oxide)
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fore, is intimately associated with the physical properties of the airborne contaminants. Because chemical structure and physical characteristics are important determinants of toxicity, an improved understanding of these properties is essential.
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Obtaining such information from laboratory animals or tissue cultures is not trivial and is seldom feasible in living human beings. Instead, for most practical purposes, we must rely on some surrogate measurement of dose-to-target sites.
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In contrast, some other manifestations of toxicity are highly indirect and, hence, poorly understood; this is frequently true of chronic or delayed effects of toxicity. In these cases, the initial interaction of the toxic chemical with a target site receptor may trigger a cascade of molecular and cellular events that ultimately damage tissue other than the original target site.
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Sensitive Individuals The ability to identify population subgroups particularly vulnerable to health effects induced or exacerbated by hazardous substances is a critical aspect in the assessment of human exposure to automotive emissions. In particular, the young or the elderly may be especially susceptible to deleterious effects; persons with asthma may experience aggravated symptoms upon exposure.
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It is highly desirable, therefore, to determine that adducts or other proposed molecular dosimeters are indeed reliable indices of exposure and to identify early markers of chronic disease. People who should be examined in epidemiologic studies include those with well-defined exposures, specific diseases, or inherent factors of susceptibility.
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In addition, predictions of noncriteria pollutant concentrations could be improved if better mathematical descriptions of atmospheric chemical reactions were used. With respect to dosimetry models, reactive gas uptake in the upper respiratory tract and particle deposition In regional areas are inadequately developed.
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Each subset might then be more fully investigated. It is possible, however, to speculate on directions of research that may eventually lead to improved quantification of human exposure and risk.
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Analytical techniques for the nondestructive, nonintrusive, in situ study of transformation products of gaseous as well as particle-associated chemical species should be improved. or government agencies formulate regula tory policies, certain scientific knowledge may be desirable.
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It is becoming increasingly apparent, however, that exposure estimation is not as straightforward as initially supposed and may have uncertainties as great as, or greater than, those associated with dose/response estimates. We need more information about environmental levels of most unregulated pollutants, indoor exposure levels, and how to integrate indoor and outdoor levels into a comprehensive picture of human exposure.
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· More emphasis should be placed on the upper respiratory tract, including the development of dosimetry models for this region. · Description of the liquid lining of the lung in humans and laboratory animals is needed.
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· Experiments should be undertaken in cells cultured from the upper respiratory tract to determine the mechanisms by which aldehydes exert pathological changes. Kaufman Hecht Marnett (Table continued next page.)
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Other Coronary heart disease · Using ongoing cohort studies or other existing data bases, increased risk of heart disease should be evaluated in persons exposed to varying levels of automotive emissions. · The effect of automotive emissions on various components of atherogenesis should be evaluated in animal studies that use cynomolgus monkeys.
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Thus, real progress in defining human risks is not likely to occur until the cellular and biochemical mechanisms of various diseases are better characterized. Early events of many respiratory diseases involve damage to epithelial tissues; altered epithelial permeability is implicated in the etiology of an asthmatic attack; damaged epithelial cells release biochemical signals for inflammatory cells, which in turn appear to regulate interstitial cell function; and proliferation of damaged cells is associated with cancers of the respiratory tract.
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Knowing biological markers and factors that deter mine individual sensitivity will not only provide better extrapolations from animals to humans, but will also improve the feasibility of using epidemiologic approaches. Ideally, a comprehensive research strategy would link molecular dosimetry to disease in laboratory animals and finally to exposure in humans.
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These comments were balanced by another statement: "The impact of ambient air pollutants on the total respiratory disease burden in the United States must be small relative to the impact of cigarette smoking, and occupational exposures might also have greater effects than pollution of ambient air" (National Research Council 1985~. Motor vehicle emissions are responsible for a substantial proportion of atmospheric exposure to carbon monoxide, nitrogen oxides, volatile organic compounds, and, in urban areas, total suspended particulate matter.
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From page 36... ...
1984. National Emissions Report, 1981, National Emissions Data System of the Aeromatic and Emissions Re porting System, Report EPA-450/4-83-022, Research Triangle Park, N.C.
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