Air Pollution, the Automobile, and Public Health (1988) / Chapter Skim
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Evaluation of Automotive Emissions as Risk Factors for the Development of Atherosclerosis and Coronary Heart Disease
Evaluation of Automotive Emissions as Risk Factors for the Development of Atherosclerosis and Coronary Heart Disease
Pages 605-630
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From page 605... ...
CLARKSON Wake Forest University Atherosclerosis / 606 Natural History / 606 Pathogenesis / 606 Factors that Influence Atherogenesis / 609 Age / 609 Gender / 610 Genetic Susceptibility / 610 Psychosocial Phenomena / 611 Diet / 612 Animal Models / 612 Avian Species / 612 Nonprimates / 612 Nonhuman Primates / 613 Effects of Chemicals on Atherogenesis / 613 Plasma Lipoproteins as Chemical Carriers / 613 Cigarette Smoking / 614 Carbon Monoxide / 617 Clonal Character of and Carcinogen Effects on Plaques / 619 Summary / 620 Summary of Research Recommendations / 621 Air Pollution, the Automobile, and Public Health.
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1972~. Atherosclerosis in the coronary arteries is the usual cause of coronary heart disease (a term covering the spectrum of angina pectoris, myocardial infarction, and disturbances of cardiac rhythm)
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particles by smooth muscle cells, the replication rates of these cells, and the kinds of connective tissue proteins they elaborate should be determined. Many human fibrous plaques have been found to be monotypic for one of the isozymes of glucose-6-phosphate dehydrogenase (G-6-PD)
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The general findings from these studies were that the coronary artery intima at the lesion-prone site becomes as thick as the media does in early life, and that the thickened intima is made up of smooth muscle cells, connective tissue fibers, and proteoglycans beneath an intact and normally appearing
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Platelet aggregation and fibrin thrombi may be associated with clinical symptoms of coronary heart disease and may also be involved in the progression of coronary artery atherosclerosis (Mustard and Packham 1972~. Research in the area of myocardial ischemia is advancing rapidly.
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The gender-specific differences in extent of coronary artery atherosclerosis are thought to account for the gender-specific differences in coronary heart disease morbidity and mortality, since the differential in clinical events and lesion extent is similar (Kennel et al. 1961; Cassel 1971; Armstrong et al.
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Psychosocial Phenomena There is increasing evidence that psychosocial influences might affect the development of coronary artery atherosclerosis and coronary heart disease. The most extensively studied psychosocial variable has been the Type A or "coronary-prone" behavior pattern (Glass 19771.
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Diet Dietary influences on atherogenesis and coronary heart disease have been studied extensively. The literature on the subject cannot be reviewed here, but there have been several relatively recent reviews (Gordon et al.
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Summary of Atherosclerosis Characteristics of Avian Models Potentially Useful for Studies of Automotive Emissions" Model Advantages Disadvantages Pigeonsb Lesions occur naturally and are exacerbated by dietary cholesterol, CO, polycyclic aromatic hydrocarbons (PAHs)
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A comparison of LDLs of different size and apoprotein composition relative to their ability to bind hydrocarbons and deliver them to smooth muscle cells and macrophages in culture is needed. Cigarette Smoking There is a vast literature base for the conclusion that cigarette smoking is a major cause of coronary heart disease in the United States for both men and women.
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In view of the large effect of cigarette smoking on coronary heart disease morbidity and mortality it is surprising to find that there are few data to suggest that the increased coronary heart disease events are related to more extensive coronary artery atherosclerosis. Viel and coworkers (1968)
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found that smoking enhanced ADP-induced platelet aggregation, and the latter investigator suggested that platelet aggregation might be associated with the increased coronary heart disease morbidity and mortality associated with cigarette smoking. Later, Davis and Davis (1979)
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Since HDL3, a fraction lowered by cigarette smoking, is not associated with coronary heart disease risk, the authors concluded that the effect of smoking may be mediated through mechanisms other than its effect on HDLC. In summary, there is a clear effect of cigarette smoking on plasma concentrations of HDLC, but more work needs to be done on its effect on the subfractions of HDL before conclusions can be drawn about the significance of the phenomenon to increase risk for coronary heart disease.
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Taken on balance, the epidemiologic evidence suggests that carboxyhemoglobin concentrations above about 6 percent may exacerbate coronary artery atherosclerosis, and those of around 2 percent may adversely affect the symptoms of individuals with coronary heart disease. On the basis of these data, it would seem that the present industrial standards which allow carboxyhemoglobin levels of 7.36 percent and the newly recommended standard allowing; carboxybemoglobin of 5 percent may ne inadequate.
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(1976a) studied the effect of 14 months of CO exposure on cynomolgus monkeys fed normal diets and found no effect on total serum cholesterol concentrations, on coronary artery atherosclerosis, or on the occurrence of myocardial infarction.
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points out that among the four common risk factors (hypertension, high serum cholesterol, physical activity, and cigarette smoking) only cigarette smoking fits the observed pattern of the rise and fall in mortality from ischemic heart disease.
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Emphasis was on the origin of fatty streaks, whether fatty streaks progress to fibrous plaques, and on the development of plaque complications. Age differences in susceptibility to coronary artery atherosclerosis, gender differences in the progression of coronary lesions, genetic susceptibility to coronary atherosclerosis, and psychosocial influences on plaque progression have been reviewed.
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Recommendation 12 Research to evaluate components of atherogenesis and extent of coronary artery atherosclerosis of cynomolgus monkeys exposed to varying concentrations of automotive emissions for varying .
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1980b. Myocardial infarction in a large colony of nonhuman primates with coronary artery atherosclerosis, Am.J.
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1984. Risk factors of coronary heart disease among personnel in a bus company, Int.
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1981. Platelet survival and the development of coronary artery disease in the young adult: effects of cigarette smoking, strong family history and medical therapy, Circulation 63:546-551.
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1961. Factors of risk in the development of coronary heart disease six-year follow-up experience: the Framingham study, Ann.
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41 :3179-3185. Review Panel on Coronary-Prone Behavior and Coronary Heart Disease.
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1975. Coronary heart disease in the Western Collaborative Group Study: final follow-up experience of 8~/2 years,J.
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1986. Effects of age and/or puberty on coronary artery atherosclerosis in cynomolgus monkeys, Atherosclerosis 62:137-144.
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