Black carbon, a proxy for woodsmoke was measured indoors and outdoors for an occupied residence in Cambria, CA during the winter months of 2009. The purpose was to investigate the infiltration parameters: air exchange rate, deposition rate, and penetration factor. The second part of this study investigated the light absorption properties of organic carbon from residential wood combustion, the dominant fraction of woodsmoke. To assess woodsmoke variation, a study conducted parallel to the one presented in this thesis (Ward, 2009), a grid array of personal emission monitors (PEMS) and aethalometers were placed in a small area, approximately one square kilometer, within a community in Cambria, California between the months of November 2008 and March 2009. In this study, PEMS were used to collect particles on filters, which were analyzed for tracers for woodsmoke, including levoglucosan, elemental carbon, and organic carbon. Aethalometers measured black carbon, an indicator of carbon combustion. Additional PEMS and aethalometers were placed inside one residential home to better understand infiltration of woodsmoke. To model the infiltration of woodsmoke, the Lawrence Berkeley National Laboratory Air Infiltration Model was used. The home of interest was chosen such that indoor sources of particulate matter (PM) were minimal. This insures that all PM measured indoors was from outdoor sources, namely household chimneys. While indoor sources such as indoor fires and resuspension of particles were of concern, homes were chosen to minimize these sources. To investigate the infiltration parameters, four different solution techniques were used. Two of the solution techniques used SOLVER, a Microsoft Excel program, to minimize the sum of squared differences between calculated indoor concentrations and measured indoor concentrations, with all three parameters (air exchange rate, penetration, and deposition) as independent variables. The other two solution techniques used the Air Exchange Rate (AER) model from Lawrence Berkeley National Laboratory (LBNL) (Sherman & Grimsrud, 1980) and then used SOLVER to calculate deposition rate and penetration factor. Solution techniques 1 and 3, which used SOLVER to find all three parameters, had average penetration factors of 0.94 and 0.97 respectively, while solution techniques 2 and 4, which used the LBNL AER model had average penetration factors of 0.85 and 0.78 respectively. The deposition rates for solution techniques 1,2,3, and 4 were 0.10, 0.07, 0.08, and 0.04 hr-1 respectively. The air exchange rates varied throughout the study and ranged from 0.1 to 0.7 hr-1. The average indoor/outdoor ratio was also found to be 0.75. The aerosols derived from the study samples were found to have light absorption properties that were heavily spectrally dependent, which is consistent with expectations for wood combustion aerosols. Conversely, traffic derived aerosols are not found to be heavily spectrally dependent and follow the power law relationship of λ-1 whereas our samples followed λ-1.7 across all wavelengths and λ-2.25 for wavelengths less than 600 nm. The reason for the difference in spectral dependence is the presence of light absorbing organic carbon in wood smoke that is not found in diesel aerosols. The optical absorbances were also calculated for our samples and average values were found to be 3 and 1 m2/g for 370 and 450 nm wavelengths respectively.

Background Anthropogenic air pollution is a global health problem estimated to contribute to millions of premature deaths. Exposure to biomass smoke is common due to varying sources, such as wildfires, indoor cooking over open fires, and residential heating from wood stoves. In urban environments transportation and industry rely heavily on the combustion of fossil fuels yet environmental policies increasingly support a shift to renewable fuels such as biodiesel. It has not been investigated how either wood smoke or biodiesel exhaust affect human health in general or the cardiovascular system in particular. We hypothesized that wood smoke exposure would induce acute cardiovascular impairment via similar underlying mechanisms as have been established for petrodiesel exhaust exposure. We also hypothesized that replacing petrodiesel with biodiesel, as a blend or pure biodiesel, would generate an exhaust profile with a less harmful effect on the cardiovascular system than petrodiesel exhaust. Methods In four separate studies healthy non-smoking subjects were exposed to different air pollutants in controlled exposure chambers followed by clinical investigations of the cardiovascular system. All studies were performed as randomized controlled trials in a crossover fashion with each individual acting as her own control. In study I healthy volunteers were exposed to wood smoke at a target concentration of particulate matter (PM) 300 µg/m3 for three hours followed by measures of blood pressure, heart rate variability and central arterial stiffness. In study II subjects were exposed to wood smoke at a target concentration of PM 1000 µg/m3 for one hour followed by measures of thrombus formation using the Badimon technique and vasomotor function using forearm venous occlusion plethysmography. In study III subjects were exposed to petrodiesel exhaust and a 30% rapeseed methyl ester (RME30) biodiesel blend for one hour at a target concentration of PM 300 µg/m3. Following exposure, thrombus formation and vasomotor function were assessed as in study II. In study IV subjects were exposed to petrodiesel exhaust at a target concentration of PM 300 μg/m3for one hour and pure rapeseed methyl ester (RME100) exhaust generated at identical running conditions of the engine. Following exposure, thrombus formation and vasomotor function were assessed as in study II and III. Results In study I fourteen subjects (8 males) were exposed to wood smoke at P M 294±36 μg/m3. Compared to filtered air exposure, measures of central arterial stiffness were increased and heart rate variability was decreased following wood smoke exposure. No effect was seen on blood pressure. In study II sixteen males were exposed to wood smoke at PM 899±100 μg/m3. We found no evidence of increased thrombus formation or impaired vasomotor function following wood smoke exposure. In study III sixteen subjects (14 males) were exposed to petrodiesel exhaust (PM 314±27 µg/m3) and RME30 exhaust (PM 309±30 µg/m3). Thrombus formation and vasomotor function were equal following either exposure. In study IV nineteen males were exposed to petrodiesel exhaust (PM 310±34 µg/m3, 1.7±0.3 x105 particles/cm3) and RME100 exhaust (PM 165±16 µg/m3, 2.2±0.1 x105 particles/cm3). As in study III, thrombus formation and vasomotor function were identical following both exposures. Conclusions We have for the first time demonstrated that wood smoke exposure can increase central arterial stiffness and decrease heart rate variability in healthy subjects. We did not, however find evidence of increased thrombus formation and impaired vasomotor function following wood smoke exposure at a higher concentration for a shorter time period. We have, for the first time, demonstrated that exhaust from RME biodiesel induced acute adverse cardiovascular effects of increased thrombus formation and impaired vasomotor function in man. These effects are on par with those seen following exposure to petrodiesel exhaust, despite marked physicochemical differences of the exhaust characteristics.