Enorme Mengen an Waldbrandrauch von außerordentlich starken und unkontrollierbaren Waldbränden in Kanada (2017), Sibirien (2019) und Australien (2019-2020) gelangten in den letzten Jahren in die Stratosphäre. Die Auswirkungen des Rauchs auf das Klimasystem der Erde wurden von vielen Forschungsgruppen untersucht. Mithilfe von Polarisations-Raman-Lidarmessungen wurden im Rahmen dieser Arbeit die optischen Eigenschaften des Rauchs vermessen und einige Aspekte der Auswirkungen auf das Klimasystem untersucht. Der sibirische Rauch verteilte sich über der gesamten Arktis und wurde fast ein Jahr lang während der MOSAiC-Kampagne mit einem Lidar auf dem deutschen Eisbrecher Polarstern in der Nordpolregion beobachtet. Dabei wurde eine 10km dicke Aerosolschicht (etwa zwischen 8 und 18km Höhe) in der oberen Troposphäre und unteren Stratosphäre (UTLS) detektiert. Die Schicht zeigte eindeutige Eigenschaften von Waldbrandrauch. Die Lidarverhältnisse lagen bei 55 sr (355nm Wellenlänge) und 85 sr (532nm Wellenlänge) und die optische Dicke des Aerosols (AOT) erreichte Werte bis zu 0,1 im Herbst 2019. Waldbrandrauch erreicht die Stratosphäre normalerweise nur im Zusammenhang mit Pyrokumulonimbus-Konvektion (pyroCb). Der sibirische Waldbrandrauch gelangte allerdings ohne die Hilfe von pyroCbs in die Stratosphäre, vermutlich durch sogenannte Selbsthebung, wie in der Arbeit ausgeführt wird. Demnach steigt der Rauch innerhalb von 3-7 Tagen bis zur Tropopause und in die untere Stratosphäre auf. Die Hypothese wird unterstützt durch CALIOP-Beobachtungen und ECRAD-Modellsimulationen. Während der Hauptphase der großen australischen Feuer (zwischen dem 29. Dezember 2019 und dem 4. Januar 2020) entstanden etwa 40 pyroCbs über den ausgedehnten Feuerflächen. Nie zuvor war eine derart hohe Anzahl von pyroCbs beobachtet worden. Sie verursachten eine stratosphärische Verschmutzung mit Rauch, wie sie nie zuvor beobachtet worden war. Der australische Rauch verteilte sich über der gesamten Südhemisphäre und wurde während der DACAPO-PESO-Kampagne in Punta Arenas (Chile) mit einem Lidar vermessen. Zwischen Januar 2020 und November 2021 befand sich der Rauch typischerweise zwischen 9 und 24km Höhe. Im Januar 2020 war die maximale optische Dicke des Rauchs über Punta Arenas etwa 1,0. Die Kombination von Lidar- und Photometermessungen ergab, dass das Lidarverhältnis des Rauchaerosols bei 69±19 sr (355 nm), 91±17 sr (532 nm) und 120±22 sr (1064 nm) lag. Der Rauch in der Stratosphäre hatte einen Einfluss auf die Strahlung, auf die chemische Zusammensetzung der Stratosphäre und auf die Entwicklung von Zirruswolken an der Tropopause. Herausragend starke Ozonlöcher bildeten sich teilweise (Arktis, 2020) und vollständig (Antarktis 2020 und 2021) in rauchverschmutzter Luft beider polarer Gebiete. Dabei wurden erstmals klare Hinweise auf einen Einfluss des Rauchs auf die Ozonlöcher gefunden (besonders ausgeprägt in der Antarktis 2020), wie in der Arbeit dargelegt wird. Zusammengefasst präsentiert diese Dissertation die Messungen der geometrischen, optischen und mikrophysikalischen Eigenschaften der stratosphärischen Rauchschichten über der Arktis und über Punta Arenas, sowie das Abklingverhalten dieser großen stratosphärischen Störungen in vier Publikationen. Darüber hinaus wird der Einfluss von Rauchpartikeln auf den Ozonabbau diskutiert und die Hypothese, dass Rauch von der freien Troposphäre bis zur Tropopause selbst aufsteigt wird aus der Prespektive von Beobachtungen und Modellergebnissen gezeigt.:1 Introduction 2 Measurement campaigns 2.1 DACAPO-PESO 2.2 MOSAiC 3 Stratospheric aerosol perturbations 3.1 Historical observations of aerosol in the stratosphere - an overview 3.2 Siberian wildfires 3.3 Australian wildfires 4 Instrumentation and data analysis 4.1 PollyXT 4.2 Lidar-derived optical properties 4.3 Data analysis 5 Results 5.1 First Publication: Ohneiser et al., Optical properties of Australian smoke over Punta Arenas, Chile, ACP, 2020 5.2 Second Publication: Ohneiser et al., Decay Phase of Australian wildfire smoke in the stratosphere, ACP, 2020 5.3 Third Publication: Ohneiser et al., Unexpected smoke layer in the High Arctic winter stratosphere 2019–2020, ACP, 2021 5.4 Fourth Publication: Ohneiser et al., Self-lofting of wildfire smoke in the troposphere and stratosphere, ACPD (preprint), in review, 2022 6 Summarizing discussion, conclusion, and outlook A Author’s contribution to the four publications B Lists B.1 List of Abbreviations B.2 List of Symbols B.3 List of Figures B.4 List of Tables References Acknowledgements

Cigarette smoking is a common and lethal worldwide habit, with considerable mortality stemming from its deleterious effects on heart function. While current theories posit altered blood lipids and fibrinogen metabolism as likely mediators, none have explored the role of the sphingolipid ceramide in exacerbating heart function with smoke exposure. Ceramide production is a consequence of cigarette smoke in the lung, and considering ceramide's harmful effects on mitochondrial function, we sought to elucidate the role of ceramide in mediating smoke-induced altered heart mitochondrial respiration. Lung cells were exposed to cigarette smoke extract and heart cells were exposed to the lung-cell conditioned medium. Adult male mice were exposed sidestream cigarette smoke for 8 weeks with dietary intervention and ceramide inhibition. Ceramides and heart cell or myocardial mitochondrial respiration were determined. Lung cell cultures revealed a robust response to cigarette smoke extract in both production and secretion of ceramides. Heart cells incubated with lung-cell conditioned medium revealed a pronounced inhibition of myocardial mitochondrial respiration, though this effect was mitigated with ceramide inhibition via myriocin. In vivo, heart ceramides increased roughly 600% in adult mice with long-term sidestream cigarette smoke exposure. This resulted in a significant ceramide-dependent reduction in left myocardial mitochondrial respiration, as heart mitochondria from the mice exposed to both smoke and myriocin injections respired normally. These results suggest ceramide to be an important mediator of altered myocardial mitochondrial function with cigarette smoke exposure. Thus, anti-ceramide therapies might be considered in the future to protect heart mitochondrial function with smoke exposure.

This thesis includes three studies. The first study examined how reductions in light availability and changes in soil chemistry that occur as conifers establish in aspen stands, differentially affects the regeneration success of aspen and conifers. We found that aspen were more sensitive to changes in light and soil then subalpine fir. For aspen, reduced light and conifer influenced soils significantly reduced height, biomass, photosynthesis and the production of secondary defense compounds. Subalpine fir seedlings were significantly reduced in photosynthesis, biomass and R:S under lower light conditions but showed no differences in physiology or growth when grown on the contrasting soil types. Subalpine fir seedlings were significantly reduced in photosynthesis, biomass and root:shoot ratio under lower light conditions but showed no differences in physiology or growth when grown on the contrasting soil types. Results from this study suggest that reduction in light and changes in soil chemistry associated with conifer succession place constraints on aspen growth and defense capacity, which may contribute to losses in aspen cover under longer disturbance return intervals. The second study looked at regeneration dynamics of aspen and conifers as forest stands transition from canopy gaps to aspen dominated canopies to conifer dominated canopies. We found that as overstory conifer density increases, aspen decrease in density, basal area, and seedling establishment. Conifers were shown to establish closer to aspen as the canopy increased in conifer density. As this proximity relationship extended into the canopy there is increased mortality in both aspen and subalpine fir, suggesting both facilitation and competition. Our third study looked at the physiological effects of smoke exposure on growth and primary and secondary metabolic responses of deciduous and conifer tree species. Twenty minutes of smoke exposure resulted in a greater than 50% reduction in photosynthetic capacity in five of the six species we examined. Impairment of photosynthesis in response to smoke was a function of reductions in stomatal conductance and biochemical limitations. In general, deciduous species showed greater sensitivity than conifer species. Smoke had no significant affect on growth or secondary defense compound production in any of the tree species examined.

Receptors for advanced glycation end-products (RAGE) are multi-ligand cell surface receptors of the immunoglobin family expressed by epithelium and macrophages. RAGE expression increases following ligand binding and when diverse cells are exposed to a variety of insults including cigarette smoke extract (CSE). The current research sought to characterize the pro-inflammatory contributions of RAGE expressed by alveolar macrophages (AMs) following CSE exposure. Acute exposure of mice to CSE via nasal instillation revealed diminished bronchoalveolar lavage (BAL) cellularity and fewer AMs in RAGE null mice compared to controls. Primary AMs were obtained from BAL, exposed to CSE in vitro, and RNA, DNA, and protein were analyzed. CSE significantly increased RAGE expression by wild type AMs. Employing ELISAs, wild type AMs exposed to CSE had increased levels of active Ras, a small GTPase that perpetuates pro-inflammatory signaling. Conversely, RAGE null AMs had less Ras activation compared to wild type AMs after exposure to CSE. In RAGE null AMs, assessment of p38 MAPK and NF-κB, important intracellular signaling intermediates induced during an inflammatory response, revealed CSE-induced inflammation occurs at least in part via RAGE signaling. For example, activated p38 was diminished in RAGE null AMs compared to controls and assessment of phosphorylated NF-κB in CSE exposed RAGE null AMs suggest lessened nuclear translocation of NF-κB compared to wild type AMs exposed to CSE. Importantly, quantitative RT-PCR revealed that mRNA expression of pro-inflammatory cytokines including TNF-α and IL-1β were detectably decreased and analysis of secreted proteins by ELISA displayed diminished IL-1β in RAGE null AMs exposed to CSE compared to CSE-exposed wild type AMs. These results reveal that primary AMs orchestrate CSE-induced inflammation, at least in part, via RAGE-mediated mechanisms.

The receptor for advanced glycation end-products (RAGE) has increasingly been demonstrated to be an important modulator of inflammation in cases of pulmonary disease. Published reports involving tobacco smoke exposure have demonstrated increased expression of RAGE, its participation in pro-inflammatory signaling and its role in irreversible pulmonary remodeling. The current research evaluated for the first time the in vivo effects of short-term tobacco smoke exposure in RAGE null and control mice compared to identical animals exposed to room air only. Quantitative real time PCR, immunoblotting, and immunohistochemistry revealed elevated RAGE expression in controls after four weeks of exposure and an anticipated absence of RAGE expression in RAGE null mice regardless of smoke exposure. Inflammatory cell behaviors were confirmed by measuring active Ras, NF-κB, and cytokine synthesis and secretion. Furthermore, bronchoalveolar lavage fluid (BALF) was procured from RAGE null and control animals after exposure for the assessment of total protein in order to indirectly measure vascular permeability, inflammatory cells and chemoattractant molecules involved in the inflammatory response. As a general theme, inflammation induced by tobacco smoke exposure was influenced by the availability of RAGE. These data reveal captivating information suggesting a role for RAGE signaling in lungs exposed to tobacco smoke. Furthermore, research may demonstrate RAGE signaling as an important therapeutic target capable of ameliorating cell level inflammation in those coping with exposure.

Roadway crashes related to vision obstruction due to fog/smoke (FS) conditions constitute a challenge for traffic engineers. Previous research efforts mostly concentrated on the snow and rain related crashes. Statistics show that Florida is among the top three states in terms of crashes due to vision obstruction by FS. This research culminated in a comprehensive study of fog and smoke related crashes in the state of Florida. The analysis took into account the crashes that occurred between 2003 and 2007 on Florida state roads. Spatial analysis and injury severity analysis have been conducted and significant results have been identified. The spatial analysis by GIS examines the locations of high trends of FS related crashes on state roads in the State of Florida. Statistical features of the GIS tool, which is used efficiently in traffic safety research, has been used to find the crash clusters for the particular types of crashes that occur due to vision obstruction by FS. Several segmentation processes have been used, and the best segmentation for this study was found to be dividing the state roads into 1 mile segments, keeping the roadway characteristics uniform. Taking into account the entire state road network, ten distinct clusters were found that can be clearly associated with these types of crashes. However, no clear pattern in terms of area was observed, as it was seen that the percentage of FS related crashes in rural and urban areas are close. The general characteristics of FS related crashes have been investigated in detail. For the comparison to clear visibility conditions, simple odds ratios (in terms of crash frequencies) have been introduced. The morning hours in the months of December to February are found to be the prevalent time for fog related crashes, while for the smoke related crashes the dangerous time was found to be morning to midday in the month of May. Compared to crashes under clear-visibility conditions, the fog crashes tend to result in more severe injuries and involve more vehicles. Head-on and rear-end crashes are the two most common crash types in terms of crash frequency and severe crashes. For the injury severity analysis, a random effect ordered logistic model was used. The model in brief illustrates that the head-on and rear-end crash types are the two most prevalent crash types in FS conditions. Moreover, these severe crashes mainly occurred at higher speeds. Also they mostly took place on undivided roads, roadways without any sidewalk and two-lane rural roads. Increase of average daily traffic decrease the severity of FS related crashes. Overall, this study provides the Florida Department of Transportation (FDOT) with specific information on where improvements could be made to have better safety conditions in terms of vision obstruction due to FS in the state roads of Florida. Also it suggests the times and seasons that the safety precautions must be taken or the FS warning systems to be installed, and the controlling roadway geometries that can be improved or modified to reduce injury severity of a crash due to FS related vision obstruction.

This thesis will analyze video from land-based, cooled mid-wave infrared cameras to identify temporal features indicative of a heat plume from a forest fire. Desirable features and methods will show an ability to distinguish between heat plume movement and other movements, such as foliage, vehicles, humans, and birds in flight. Features will be constructed primarily using combinations of statistics and principal component analysis (PCA) with intent to detect key characteristics of fire and heat plume: persistence and growth. Several classification systems will combine and filter the features in an attempt to classify pixels as either heat or non-heat. The classification systems will be tuned and compared with common metrics of error rate and computation time. It was found that the movement pattern of a heat plume could be distinguished from the similar movement pattern of foliage by detecting outlier movement patterns, a phenomenon associated with the growth property of fire. Outlier movement patterns were best detected by thresholding the quotient of mean and median of a set of variance measurements over time. The best tested classifier in terms of minimizing false positives without losing the heat signal came from PCA of a dual-range moving average difference.

Affecting approximately 5-6% of the primary school population, developmental coordination disorder (DCD) is a condition characterized by poor motor proficiency that interferes with a child’s activities of daily living. The cause of DCD is not yet understood; however, it is known that children with DCD are more likely to have other co-occurring developmental disorders such as attention-deficit hyperactivity disorder (ADHD). While there is a growing body of evidence linking ADHD to smoke exposure in utero, there is limited research investigating a similar link between smoke exposure in utero and DCD. The purpose of this study was to examine the effect of SHS exposure in utero in children with DCD and a group of typically developing (TD) children. Methods – A case-control study was conducted to compare children with DCD to TD children on their exposure to SHS in utero and other demographic variables. At baseline, participants included 63 DCD children and 63 healthy controls. All children were assessed for motor proficiency, intelligence, and ADHD. Mother’s SHS exposure during pregnancy and other demographic variables were obtained from a parent completed survey. Results – Multinomial logistic regression analyses revealed that children exposed to SHS in utero were significantly more likely to be at high risk for DCD than children who were not exposed to SHS in utero, even after adjusting for associated demographic variables. Furthermore, children exposed to SHS in utero were significantly more likely to be at moderate-high risk for DCD, whether or not ADHD was co-occurring. Conclusion – Results from this study suggest that exposure to SHS during pregnancy has negative effects on fetal development and appears to be a contributor for DCD. Further study is needed to examine the specific mechanisms linking SHS exposure in utero to motor coordination problems in children. / Thesis / Master of Science (MSc)

Over 1.1 billion people smoke worldwide despite the association of smoking with numerous diseases including chronic obstructive pulmonary disease (COPD). The decline in lung function observed in COPD patients is thought to be related to smoke-induced inflammation. COPD patients are also at increased risk of acquiring lung bacterial infections that are associated with exacerbations, characterized by worsened disease symptoms and inflammation. The focus of this thesis is on how cigarette smoke impacts bacterial-host interactions and bacterial community interactions to promote infection and disease. In chapter 3.1, we sought to understand how cigarette smoke primed the lungs towards an amplified inflammatory response to bacterial infection reflective of COPD exacerbations that accelerate disease progression. We present a novel finding that exacerbated neutrophilia elicited by nontypeable Haemophilus influenzae (NTHi) lung challenge in smoke-exposed mice occurred dependent on IL-1α. Smokers and patients with COPD are additionally at increased risk of acquiring bacterial infection that may be related to impaired containment of nasally colonizing pathogens. In chapter 3.2, we found that cigarette smoke predisposed mice to invasive pneumococcal disease (IPD) following nasal pneumococcal colonization associated with attenuated nasal inflammatory responses. To our knowledge, this is the first study to describe the progression from asymptomatic nasal pneumococcal colonization to the development of IPD in the context of cigarette smoking. It has been suggested that smokers have higher rates of pathogen colonization as a consequence of cigarette smoke-induced nasal microbiome dysbiosis. The last study in chapter 3.3 advanced knowledge in the field by testing this hypothesis. We observed that cigarette smoke alone did not alter the mouse nasal microbiome and concluded that microbiome dysbiosis observed in smokers likely occur as a consequence of nasal pathogen colonization. Overall, work presented in this thesis advanced our understanding of how cigarette smoking alters bacterial-host interactions to promote infection and disease. / Thesis / Doctor of Philosophy (PhD) / Over 1.1 billion people smoke worldwide and can develop chronic obstructive pulmonary disease (COPD), a serious inflammatory disease compromising lung function. Additionally, smokers and COPD patients have higher rates of bacterial infection. The goal of this thesis is to understand how smoking impacts our ability to combat infection. Lung infection in COPD patients causes exacerbation, with worsened disease symptoms. Using mouse models, we learned how smoking causes increased lung inflammation following bacterial infection, contributing to damage reflective of COPD exacerbations, and identified a potential intervention. We elucidated smokers may have increased infections due to impaired immune responses in the nose, a major pathogen entry point. It is thought smoking reduced beneficial bacteria that counter pathogen acquisition in the nose. We confirmed smoking did not impact these bacteria, directing research focus towards other ways smokers acquire pathogens. Overall, this thesis advanced knowledge and will help efforts to control disease in smokers.

Wildfires pose a significant and growing threat to human health. Current trends in climate change predict that wildfire occurrence and severity will increase in the near future, and therefore the adverse health effects associated with wildfire and its air quality effects are becoming increasingly relevant. Even with current efforts to stem future rises in temperature, wildfire activity will continue to increase due to lags in the climate system itself. Thus, in addition to the known increase in mortality, respiratory, and cardiovascular risks, there is a growing need to investigate other health outcomes associated with wildfire smoke exposure, especially their effect on pregnancy and birth outcomes. In order to provide a broad overview of the state of wildfire research on the topic of pregnancy and birth outcomes, this narrative review will summarize the existing literature on pregnancy and birth outcomes associated with wildfire smoke exposure, with consideration for the ambient air pollution literature that informs wildfire research. As research in this specific topic is still developing, a pattern of limitations to study designs is beginning to emerge, which will guide future research needs. Finally, practical considerations for implementing research findings into land management and public health policies that reduce wildfire exposure in order to mitigate the health risks associated with it will be explained.