Epidemiological studies have shown strong and consistent associations between exposure to air pollution and increases in morbidity and mortality. Key air pollutants that have been identified include fine particulate matter (PM) and ozone (O3), both major contributors to smog. However, there is a lack of understanding of the mechanisms involved and the relative contributions of individual pollutants. A controlled human exposure facility was used to carry out inhalation studies of concentrated ambient fine particles (CAP), O3, CAP+O3 and filtered air following a randomized design. Exposures were 2 hrs in duration at rest. Subjects included mild asthmatics and non-asthmatics. This thesis focuses on acute cardiovascular responses including blood pressure (BP), brachial artery reactivity (flow-mediated dilatation [FMD]) and markers of systemic inflammation (blood neutrophils and interleukin [IL]-6). Results showed that for CAP-containing exposures (CAP, CAP+O3) there were small but significant transient increases in diastolic BP (DBP) during exposures. Furthermore, neutrophils and IL-6 increased 1 - 3 hrs after and FMD decreased 20 hrs after CAP-containing exposures. Responses to O3 were smaller, comparable to filtered air. The data suggests that adverse responses were mainly driven by PM. The DBP increase was rapid-developing and quick to dissipate, which points to an autonomic irritant response. The magnitude of the DBP increase was strongly negatively associated with the high frequency component of heart rate variability, suggesting parasympathetic withdrawal as a mechanism. In comparison, IL-6, neutrophil and FMD responses were slower to develop, indicative of an inflammatory mechanism. An intriguing finding was that IL-6 increased 3 hrs after CAP, but not after CAP+O3. Further investigation revealed that exposure to CAP+O3 in some individuals may trigger a reflex inhibition of inspiration, decreasing their tidal volume and inhaled pollutant dose, leading to a reduction in systemic IL-6, a potential protective mechanism. Together the findings support the epidemiological evidence of adverse fine PM health effects. Many questions remain to be answered about the health effects of air pollution including a better understanding of how inhaled pollutants result in cardiovascular effects. It is hoped that the insights gained from this thesis will advance the understanding of air pollution health effects.

Epidemiological studies have shown strong and consistent associations between exposure to air pollution and increases in morbidity and mortality. Key air pollutants that have been identified include fine particulate matter (PM) and ozone (O3), both major contributors to smog. However, there is a lack of understanding of the mechanisms involved and the relative contributions of individual pollutants. A controlled human exposure facility was used to carry out inhalation studies of concentrated ambient fine particles (CAP), O3, CAP+O3 and filtered air following a randomized design. Exposures were 2 hrs in duration at rest. Subjects included mild asthmatics and non-asthmatics. This thesis focuses on acute cardiovascular responses including blood pressure (BP), brachial artery reactivity (flow-mediated dilatation [FMD]) and markers of systemic inflammation (blood neutrophils and interleukin [IL]-6). Results showed that for CAP-containing exposures (CAP, CAP+O3) there were small but significant transient increases in diastolic BP (DBP) during exposures. Furthermore, neutrophils and IL-6 increased 1 - 3 hrs after and FMD decreased 20 hrs after CAP-containing exposures. Responses to O3 were smaller, comparable to filtered air. The data suggests that adverse responses were mainly driven by PM. The DBP increase was rapid-developing and quick to dissipate, which points to an autonomic irritant response. The magnitude of the DBP increase was strongly negatively associated with the high frequency component of heart rate variability, suggesting parasympathetic withdrawal as a mechanism. In comparison, IL-6, neutrophil and FMD responses were slower to develop, indicative of an inflammatory mechanism. An intriguing finding was that IL-6 increased 3 hrs after CAP, but not after CAP+O3. Further investigation revealed that exposure to CAP+O3 in some individuals may trigger a reflex inhibition of inspiration, decreasing their tidal volume and inhaled pollutant dose, leading to a reduction in systemic IL-6, a potential protective mechanism. Together the findings support the epidemiological evidence of adverse fine PM health effects. Many questions remain to be answered about the health effects of air pollution including a better understanding of how inhaled pollutants result in cardiovascular effects. It is hoped that the insights gained from this thesis will advance the understanding of air pollution health effects.

Many serious illnesses are linked to everyday exposures to toxic chemicals. In the U.S., most chemical exposure comes from common consumer products such as pesticides, fragranced products, cleaning supplies, and building materials--products so widely used that people consider them "safe." As the links between everyday toxic exposures and potential health effects become better understood, evidence increasingly shows that reducing exposures can create a healthier society. Although some individuals may choose to build a healthy home and maintain a healthy household, they are still exposed to pollutants at their residences from the actions of others, such as to pesticides that are used by neighbors, businesses, and governments. They need healthy residential developments in environmentally healthy communities. This research investigates "healthy residential developments," defined as a property that aims to reduce pollutant exposures to the extent required by vulnerable populations, which for this research are individuals with multiple chemical sensitivities (MCS). Through a case study approach, this research investigates two exemplars of healthy residential developments, and explains how and why they form and continue. It also examines their implementation methods, and implications for planning and policy. Primary data collection methods included in-person interviews, telephone interviews, and site visits. Research strategies included the analysis of interview data, and categorical aggregation using thematic categories within and across cases. The categories focused on factors of formation and continuation for the two healthy residential developments. Findings include the challenges of people disabled with MCS to find safe housing; the importance of planning to address these challenges; the role of individuals, funding, and zoning in the formation of healthy residential developments; the role of funding, safe maintenance, and property management in their continuation; and, the need for affordable and safe housing for vulnerable populations. Future research can address the need to develop methods to create and sustain healthy residential developments, understand and reduce sources of exposure that initiate and trigger chemical sensitivity, and investigate experiences and implementation strategies in other countries.