Diss. (sammanfattning) Stockholm : Karolinska institutet, 2005. / Härtill 4 uppsatser.

Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1993. / Vita. Abstract. Includes bibliographical references (leaves 121-123). Also available via the Internet.

Thesis (M.S.)--Københavns universitet, 1996. / Title from title screen (viewed on July 9, 2008). Title from document title page. Includes bibliographical references. Available in PDF format via the World Wide Web.

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Thesis: M.S., Massachusetts Institute of Technology, Department of Mechanical Engineering, 1981 / Includes bibliographical references. / by Mark Charles Sellnau. / M.S. / M.S. Massachusetts Institute of Technology, Department of Mechanical Engineering

Call number: LD2668 .T4 1984 T78 / Master of Science

Published Article / Air pollution, just like any other type of pollution, produces harmful effects to man and his environment. In spite of knowing this, many less industrialised countries of the world have no air quality monitoring strategies in place. Consequently, documented evidence of air pollution studies in such countries is scarce. This is the case in Tanzania. This scenario is made worse by lack of scientific tools which could aid in identifying air pollution-prone areas with a view to aiding town planners in locating safe sites for schools, hospitals and residential areas as well as parks. In this paper, we present results of a study carried out in the city of Dar-es-Salaam, Tanzania on air pollution in residential areas. Results show significant air pollution in the studied areas. Moreover, both adults and children are at risk due to lead pollution in the air.

Exposure to air pollution, particularly fine and ultrafine particulate matter derived from combustion sources, has been consistently associated with increased cardiovascular morbidity and mortality. Recent controlled exposure studies demonstrate that short-term exposure to diesel exhaust, which can contribute up to 40% of urban particulate air pollution, results in impaired vascular endothelial and fibrinolytic function in healthy volunteers, and increased exercise-induced myocardial ischaemia in patients with coronary heart disease. These observations may, in part, explain the observed increase in cardiovascular events following exposure to air pollution. Despite these observations there remain uncertainties regarding the key constituents of the air pollution mixture that mediate these adverse effects, and the underlying physiological and biological pathways involved. In these studies, using two controlled exposure facilities, I explored the vascular effects of the most prevalent gaseous component of the air pollution mixture – nitrogen dioxide – and the mechanisms responsible for impaired vasomotor function following exposure to diesel exhaust. Furthermore, I investigated the effect of acute exposure to “real-world” urban air pollution in both healthy volunteers and patients with coronary heart disease, and the effect of reducing that exposure using a simple facemask. In total, 10 healthy volunteers were exposed to nitrogen dioxide, and 29 healthy volunteers exposed to dilute diesel exhaust in a series of doubleblind randomised crossover studies. Exposure to nitrogen dioxide had no effect on either vasomotor function or endogenous fibrinolysis, providing indirect evidence that the adverse vascular effects are predominantly driven by particulate components. Following exposure to diesel exhaust there was no up regulation of endothelin-1 production, although there was increased vasoconstriction to intra-arterial infusion of endothelin-1. Following endothelin A receptor antagonism, there was attenuated vasodilatation following exposure to diesel exhaust as compared to air, an effect abrogated by endothelin B receptor antagonism. My findings suggest that the endothelin system does not play a central role in the adverse vascular effects of air pollution, but given the tonic interaction between the endothelin and nitric oxide systems, these observations could be explained by reduced nitric oxide bioavailability. Following diesel exhaust inhalation, plasma nitrite concentrations (as a marker for nitric oxide generation) are markedly increased without changes in haemodynamics or basal blood flow consistent with increased nitric oxide consumption. In the presence of a nitric oxide clamp, and without endogenous nitric oxide release, the vascular responses to vasodilators are similar. This perturbation of nitric oxide consumption and release appears to underlie the observed vascular endothelial effects. Fifteen healthy volunteers and 98 patients with coronary artery disease were recruited in Beijing, China. Subjects walked along a predefined city centre route for 2 hours in the presence and absence of a highly efficient facemask to reduce personal particulate air pollution exposure in an open label randomised crossover study. When wearing a facemask, there was an attenuation of exercise-induced increases in blood pressure, an improvement in heart rate variability, reduced myocardial ischaemia and subjects reported fewer symptoms. My findings have identified the biological mechanisms underlying the adverse vascular effects of exposure to diesel exhaust, and have helped to clarify the components responsible for these effects. Moreover, I have identified important benefits of reducing personal exposure to particulate matter using a simple facemask that have the potential to reduce cardiovascular events in patients living in urban or industrialised areas. Ongoing research in this area will provide further insight into the underlying vascular mechanisms, and the potential benefits of reducing particulate air pollution exposure, and may result in important targeted interventions to reduce the impact of air pollution on cardiovascular health.

This dissertation consists of three chapters on questions in Environmental Economics, addressing policy and health issues in indoor and outdoor environments. In the first chapter, I explores price and quantity policy solutions to externalities that arise from private decisions made over time, focusing on resource extraction as a specific example. In the U.S., mining causes more pollution than any other single industry. I show how tax policy can optimally address a flow externality associated with resource extraction when the policymaker faces asymmetric information in the short run. Chapter 2 investigates whether ordinary exposure to a common indoor air pollutant—Nitrogen Dioxide (NO₂)—affects respiratory health. About 40 percent of occupied homes in the U.S. use gas stoves for cooking, which produce NO₂ as a byproduct of combustion (US Census, 2006), and peak concentrations in homes may reach above 900 ppb when a gas stove is used for cooking (Dennekamp et al., 2001). Permanent or fatal lung damage occurs at NO₂ concentrations greater than 1000 ppb (Samet and Utell, 1990). Previous studies find mixed evidence of negative effects from indoor NO₂ (Basu and Samet, 1999), but exposure may be endogenous in these analyses. I address this problem by developing a physical model of indoor NO₂ concentrations that depends on ventilation decisions and housing characteristics and estimate it using data from the third wave of the National Health and Nutrition Examination Survey. In every model I consider, I find no significant effects of gas stoves on respiratory outcomes. In the final chapter, I combine data on state and local tobacco control ordinances from Americans for Non-smokers Rights Tobacco US Tobacco Control Laws Database with a sample of 35 million births in the U.S. to examine the impact of smoking bans on birth weight and related outcomes. Using difference-in-difference techniques, I identify the effects of state bans net of local bans, as well as the effects of local bans net of state bans. The results suggest less restrictive bans do more to improve birth outcomes than “100% smokefree” bans do, particularly in urban settings. / text