The retrieval of an aerosol scattering phase function using a multi-satellite technique is proposed. A total of 33 phase functions were derived from 18 smoke cases and 15 dust cases. Each case was interrogated using four to nine satellite passes over the aerosol in a two to four hour time frame. The radiance values for the Red and Near-Infrared (NIR) channels were combined with backscattering angles to determine the shape of the scattering phase function. The radiance values were input into the Naval Postgraduate School (NPS) aerosol model to determine optical depths and sample phase functions. A comparison was made between the actual phase functions retrieved and the NPS model phase functions. It was found that the phase functions for the smoke cases more closely matched the model phase functions than in the dust cases. Some conclusions could be drawn about the actual aerosol size and density distribution based on how well it matched the model phase function. Further analysis is necessary to define the exact size and number of the aerosol particles. Fully understanding the aerosol composition is crucial in determining its effects on military sensors and impacts to operations.

A pre-flashover fire is very different from a post-flashover fire. The main difference is that in a pre-flashover fire the gas temperature and the radiation temperature differ. One thing that makes it a lot different is that the thermal exposure induced by a pre-flashover fire is largely affected by the smoke gas layer. These smoke gases can be very hot and therefore they emit heat radiation to their surroundings. The theory used, to calculate the thermal exposure of a pre-flashover fire, in this thesis relies on using thermal resistances to describe the heat transfer from the smoke gases. By doing so it is possible to calculate the temperatures of the smoke gases and the surfaces in touch with the smoke gases. Another approach is to use CFD software to numerically calculate the temperatures and in this thesis the two-zone model are compared to FDS, a CFD software. The two-zone model are also compared to a reduced-scale test. The comparisons gave good results, the two-zone model produced similar results compared to re reduced-scale test and FDS. This method of calculating thermal exposure can thereby be used to evaluate evacuation safety and save a lot of calculation time compared to calculating the thermal exposure with CFD software such as FDS.

Background: With almost 80,000 Europeans estimated to die annually from the consequences of exposure to second-hand smoke (SHS) and over a quarter of all Europeans being exposed to the toxins of cigarette smoke at work on a daily basis, SHS is a major European public health problem. Smoke-free policies, i.e. policies which ban smoking in public places and workplaces, are an effective way to reduce exposure. Policy options to reduce public exposure to SHS were negotiated by European Union (EU) decision makers between 2006 and 2009, resulting in the European Council Recommendation on smoke-free environments. A variety of stakeholders communicated their interests prior to the adoption of the policy. This thesis aims to analyse the engagement and collaboration of organisational stakeholders in the development of the Council Recommendation on smoke-free environments. Methods: The case study employs a mixed method approach to analyse data from policy documents, consultation submissions and qualitative interviews. Data from 176 consultation submissions serve as a basis to analyse the structure of the policy network using quantitative network analysis. In addition, data from these submissions, selected documents of relevance to the policy process and 35 in-depth interviews with European decision makers and stakeholders are thematically analysed to explore the content of the network and the engagement of and interaction between political actors. Results: The analysis identified a sharply polarised network which was largely divided into two adversarial advocacy coalitions. The two coalitions took clearly opposing positions on the policy initiative, with one coalition supporting and the other opposing comprehensive European smoke-free policy. The Supporters’ Alliance, although consisting of diverse stakeholders, including public health advocacy organisations, professional organisations, scientific institutions and pharmaceutical companies, was largely united by its members’ desire to protect Europeans from the harms caused by SHS and campaign for comprehensive European tobacco control policy. Seemingly coordinated and guided by an informal group of key individuals, alliance members made strategic decisions to collaborate and build a strong, cohesive force against the tobacco industry. The Opponents’ Alliance consisted almost exclusively of tobacco manufacturers’ organisations which employed a strategy of damage limitation and other tactics, including challenging the scientific evidence, critiquing the policy process and advancing discussions on harm reduction, to counter the development of effective tobacco control measures. The data show that the extent of tobacco company engagement was narrowed by the limited importance that industry representatives attached to opposing non-binding EU policy and by the companies’ struggle to overcome low credibility and isolation. Discussion: This study is the first that applies social network analysis to the investigation of EU public health policy and systematically analyses and graphically depicts a policy network in European tobacco control. The analysis corroborates literature which highlights the polarised nature of tobacco control policy and draws attention to the complex processes of information exchange, consensus-seeking and decision making which are integral to the development of European public health policy. The study identifies the European Union’s limited competence as a key factor shaping stakeholder engagement at the European level and presents the Council Recommendation on smoke-free environments as an example of the European Commission’s successful management of the policy process. An increased understanding of the policy network and the factors influencing the successful development of comprehensive European smoke-free policy can help to guide policymaking and public health advocacy in current European tobacco control debates and other areas of public health.

A gripe é causada pelo vírus Influenza e é um problema de saúde pública mundial, que pode levar a problemas sérios em idosos e crianças. O Brasil implantou a vacinação anual contra influenza a partir de 1999, como ação preventiva contra a doença. A vacina é produzida pelo Instituto Butantan e contém três cepas diferentes do vírus Influenza fragmentado para induzir resposta imune adaptativa, com produção de anticorpos específicos e neutralizantes. A literatura tem mostrado que a exposição à xenobióticos com potencial imunossupressor pode comprometer a eficácia de imunizações ativas, como a imunização contra a gripe. Nosso grupo de pesquisa tem mostrado que a exposição à hidroquinona (HQ), um composto tóxico presente em altas concentrações na fumaça do cigarro, prejudica a resposta imune inata e adquirida. Assim, este trabalho avaliou o efeito da exposição à HQ sobre a resposta imune à vacinação contra influenza. Camundongos machos da linhagem C57BL/6 foram diariamente expostos à HQ (2500 ppm) ou PBS, por 1 hora, por nebulização, por um período de 8 semanas. Durante este período, foram imunizados nas semanas 6 e 8 do início das exposições, pela injeção i.m. de 100µL da vacina. Os parâmetros tóxicos e imunológicos foram avaliados 7, 35 e 70 dias após a segunda dose da vacina. A exposição à HQ não alterou o peso corpóreo dos animais e nem causou alterações morfológicas no pulmão, fígado e rins (histologia por H&E); reduziu a frequência de hemácias (11%), hematócrito (14%), hemoglobina (14%) e volume celular (4%); causou estresse oxidativo no baço (citometria de fluxo); aumentou a área dos folículos de células B no baço e linfonodomegalia (histologia por H&E). Em conjunto, os dados aqui obtidos mostram que a exposição à HQ afetou mecanismos envolvidos na gênese da imunidade ativa contra influenza. Assim, os dados deste trabalho mostram mecanismos tóxicos ainda não descritos para a HQ, e ressalta a HQ como um poluente ambiental que deve ser considerado nas avaliações de risco. / The flu is a health problem worldwide which is caused by the Influenza virus and may result in severe illness in infants and the elderly. The annually vaccination against influenza was implemented in Brazil in 1999 as a preventive measure. The vaccine is produced by Butantan Institute and contains three different strains of the inactivated Influenza virus which induce the adaptive immune response along with production of specific and neutralizing antibodies. The literature has shown that exposure to immunosuppressive xenobiotics may compromise the efficacy of active immunizations, such as influenza. Our research group has shown that exposure to hydroquinone (HQ), a toxic constituent of cigarette smoke, impairs both innate and adaptive immune response. Thus, the aim of this work was to evaluate the effects of HQ on the immune response induced by the influenza vaccine. Male C57BL/6 mice were daily exposed to HQ (2500 ppm) or PBS by nebulization, for 1 hour, for 8 weeks. During the exposure period, the animals were vaccinated on weeks 6 and 8 with 100µL of the vaccine. Toxicologic and immunological parameters were assessed 7, 35 and 70 days after boost administration. HQ exposure did not alter body weight and did not cause morphological alterations in the lungs, liver and kidneys (H&E staining); reduced the frequency of erythrocytes (11%), hematocrit (14%), hemoglobin (14%) and cellular volume (4%) and caused oxidative stress on the spleen (Flow Cytometry); increased the area of B cell follicles in the spleen and increased the size of draining lymph nodes (H&E staining). Altogether, these data show that HQ exposure affected mechanisms involved in the genesis of the adaptive immune response. Thus, the data presented in this work show toxic mechanisms of HQ that have not yet been described, and it also points out HQ as an environmental pollutant which should be considered on risk assessments.

O anestésico local é o medicamento mais utilizado na Odontologia e sua associação com vasoconstrictores aumenta a duração da anestesia, diminuindo seus efeitos sistêmicos. A hipertensão e o tabagismo são freqüentes na população, sendo responsáveis por complicações sistêmicas. A felipressina, por não interferir com receptores simpáticos, poderia ser um vasoconstrictor indicado para pacientes hipertensos. O objetivo deste trabalho foi estudar a reatividade cardiovascular de animais simultaneamente hipertensos e fumantes passivos aos agentes vasoconstritores associados aos anestésicos locais, verificando também o efeito do tratamento com atenolol. Foram utilizados ratos Wistar machos, divididos em 5 grupos: 1) normotensos não fumantes; 2) normotensos fumantes passivos; 3) hipertensos não fumantes; 4) hipertensos fumantes passivos; 5) hipertensos fumantes passivos tratados com atenolol. A hipertensão renal foi induzida pela remoção do rim direito e instalação de clip de prata (abertura 0,25mm) na artéria renal esquerda, após anestesia com quetamina e xilazina. Os ratos fumantes passivos foram colocados diariamente por 10 minutos, durante 28 dias, em caixa de madeira de 30cmX25cmX15cm dividida em dois compartimentos. Em um deles, eram acesos 10 cigarros e no outro ficavam os animais. A tampa da caixa era fechada e um sistema de ventilação lançava fumaça dos cigarros para o compartimento dos ratos, num fluxo de 10l/min. Após medida indireta da pressão arterial, 14 dias após a cirurgia, o grupo tratado com atenolol foi medicado durante 14 dias seguintes (90 mg/Kg) por gavage. No 28o dia, todos receberam catéter de polietileno na artéria carótida esquerda (para medida de pressão) e outro na veia jugular direita (para injeção de drogas). Para os 5 grupos foram utilizadas: adrenalina (80, 160, 320, 640 e 1280ng) e felipressina (0,125, 0,25, 0,5, 1, 2 e 3 x 10-3UI). O catéter arterial era conectado a transdutor de pressão e o registro realizado por software específico. Foram analisadas: menor resposta hipotensora, maior resposta hipertensora e duração de resposta para cada dose. Os dados foram analisados por análise de variância de medidas repetidas, seguida do teste de Tuckey ou Holm-Sidack, com nível de significância de 5%. Os resultados mostraram que o fumo passivo reduziu significativamente a resposta vasodilatadora produzida pela adrenalina, em animais normotensos e hipertensos, potencializou suas respostas hipertensoras e aumentou a duração das respostas à adrenalina, ampliadas ainda mais pelo tratamento com atenolol. O tratamento com atenolol promoveu aumento adicional das respostas hipertensoras à adrenalina nos hipertensos-fumantes. A felipressina não apresentou ações vasodilatadoras e suas ações hipertensoras foram potencializadas pelo fumo passivo, em amplitude e duração. O atenolol não promoveu aumento adicional da amplitude das respostas à felipressina. Nos animais hipertensos, o tratamento com atenolol associado ao fumo passivo teve efeito expressivo, aumentando significativamente a duração total das respostas à felipressina. A felipressina, quando comparada à adrenalina, não apresentou efeitos hipotensores diretos, a resposta hipertensora máxima foi nitidamente inferior e a duração das respostas à felipressina foi o dobro da adrenalina. Dessa forma, a felipressina se torna uma droga interessante na hipertensão, devido a sua capacidade de promover vasoconstrição prolongada, sem potencializar a atividade simpática sistêmica. / The local anesthetic is the most common drug in dentistry and the associated vasoconstrictors increase the duration of anesthesia, decreasing its systemic effects. Hypertension and smoking are problems commonly found in the general population, being responsible for systemic complications. Felypressin, a vasoconstrictor that does not interact with sympathetic receptors, could be indicated to hypertensive patients. This study investigated the cardiovascular reactivity of hypertensive and passive smoker animals under atenolol treatment to epinephrine and felypressin. Male wistar rats were divided into five groups: 1) normotensive and non-smokers, 2) normotensive and passive smokers, 3) hypertensive and non-smokers, 4) hypertensive and passive smokers; 5) hypertensive, passive smokers and treated with atenolol. Renal hypertension was induced by removal of the right kidney and installation of a silver clip (with 0.25-mm opening) in the left renal artery, after anesthesia with ketamine and xylazine. The passive smoker rats were placed, 10 minutes per day, during 28 days in a 30cmX25cmX15cm wood box divided into two compartments. Ten cigarettes were lit in one compartment, and the rats were placed in the other. The box lid was closed and a ventilation system threw the cigarette smoke to the rat compartment. After indirect measurement of blood pressure, 14 days after the surgery, the group of rats treated with atenolol was medicated during the following fourteen days (90 mg/kg) by gavage. On the 28th day, a polyethylene catheter was inserted into the left carotid artery (for direct blood pressure measurements) and into the right jugular vein (for drug injection). The groups received epinephrine (80, 160, 320, 640 and 1280ng) or felypressin (0.125, 0.25, 0.5, 1, 2 and 3 x 10-3UI). The arterial catheter was connected to a pressure transducer and recording was made by a specific computer software. The following parameters were analyzed for all groups: lower hypotensive response, higher hypertensive response and duration of response for each dose. Data were statistically analyzed by repeated measures analysis of variance, followed by Tukey test or Holm-Sidack test, at a significance level of 5%. The results showed that passive smoking significantly decreased the vasodilator response produced by epinephrine in normotensive and hypertensive animals, increasing their hypertensive responses and increased the duration of response to epinephrine, that was further increased by atenolol treatment. Atenolol treatment increased the hypertensive responses in hypertensive-smokers rats. The felypressin did not show vasodilator responses and its hypertensive responses were increased by passive smoking. The atenolol did not cause additional increase in felypressin responses. In hypertensive animals, the atenolol treatment associated with passive smoking had expressive effects, significantly increasing the total duration of response to felypressin. Felypressin, when compared with epinephrine, did not show direct hypotensive effects, the higher hypertensive responses were smaller and the duration of response to felypressin was twice the epinephrine time. Then, felypressin becomes an interesting drug to hypertensive patients, due to its capacity to promote prolonged vasoconstrictor effect without increasing the sympathetic nerve activity.

Second-hand smoke exposure (SHSe) causes significant morbidity and mortality in children. A large proportion of children with smoking parents do not live in smoke-free homes, however, to date, little is known about the prevalence of partial smoking restrictions and their efficacy in reducing children’s SHSe. Given the lack of convincing evidence on how to achieve further reductions in children’s SHSe in the home, the identification of the modifiable factors associated with childhood SHSe is imperative to reduce the burden of disease resulting from childhood SHSe. Analysis of the Omnibus Survey (OS) revealed that the prevalence of smoke-free homes in England did not increase significantly between 2006 and 2008. Only 30% of smokers reported a smoke-free home in 2008. However, during the same time period, the proportion of smokers (who did not have a smoke-free home) reporting that they did not smoke when in the same room as a child increased significantly from 62.5% to 74.8%. Using the Health Survey for England, biologically validated self-reported measures of child SHSe revealed that in 2008 and 2009 approximately 50% of children living with a smoking parent were not exposed to SHSe in the home (0.30ng/ml, 95% confidence interval 0.27-0.32ng/ml). Of the 50% of children who remained exposed inside the home, 29% had a parent that smoked in one room only in the home. These children had significantly lower cotinine concentrations (1.13ng/ml, 95% CI 1.05-1.22) than the 21% of children with smoking parents who smoked in 2 or more rooms in the home (2.36ng/ml, 95% CI 2.08-2.68ng/ml). Although smoking in one room equates to lower risk it does not equate to no risk and so interventions are required to change indoor smoking to outdoor smoking. The OS data found that good knowledge of SHS-related illnesses was predictive of both full and partial smoking restrictions in the home. Increases in the proportion of respondents with good knowledge occurred during 2003-2006, a period when frequent anti-SHS mass media campaigns were aired. A case-study evaluation of a brief mass media campaign in the North West and North East of England, which aimed to move smoking parents to smoke outside, was found to have no statistically significant effect on home smoking behaviour in the short term, however knowledge that SHS caused both heart attack and Sudden Infant Death Syndrome increased in this region following the campaign whilst simultaneous decreases were found in the rest of England. Following the identification of those children most exposed to SHS, and the modifiable factors associated with this exposure, this thesis suggests that a comprehensive multi-level approach to tobacco control policy, which includes emotive media campaigns which include information on SHS-related illnesses, will contribute to the continued reduction of childhood SHSe.

Entry resistance in smoke detectors was investigated using experimental and analytical approaches. The experimental work consisted of measuring velocity inside the sensing chamber of smoke detectors with a two-component Laser Doppler Velocimeter and exposing addressable smoke detectors to four different aerosol sources. The velocity measurements and exposure tests were performed in NIST's Fire Emulator / Detector Evaluator under steady state flow conditions in the range of 0.08 to 0.52 m/s. The addressable detectors were a photoelectric and an ionization detector. A specially constructed rectangular detector model was also used for the interior velocity measurements in order to have geometry compatible with numerical approaches, such as computational fluid dynamics modeling or a two-dimensional analytical solution. The experimental data was used to investigate the fluid mechanics and mass transport processes in the entry resistance problem. An inlet velocity boundary condition was developed for the smoke detectors evaluated in this study by relating the external velocity and detector geometry to the internal velocity by way of a resistance factor. Data from the exposure tests was then used to characterize the nature of aerosol entry lag and sensor response. The time to alarm for specific alarm points was determined in addition to performing an exponential curve fit to obtain a characteristic response time. A mass transport model for smoke detector response was developed and solved numerically. The mass transport model was used to simulate the response time data collected in the experimental portion of this study and was found, in general, to underestimate the measured response time by up to 20 seconds. However, in the context of wastebasket fire scenario the amount of underprediction in the model is 5 seconds or less which is within the typically polling interval time of 5 to 10 seconds for an addressable system. Therefore, the mass transport model results developed using this proposed engineering framework show promise and are within the expected uncertainty of practical fire protection engineering design situations.

Conselho Nacional de Desenvolvimento Científico e Tecnológico / Eventos ou estímulos no início da vida podem afetar o desenvolvimento do indivíduo; dentre esses o tabagismo materno. A exposição materna isolada à nicotina, principal componente do cigarro, causa na prole alterações metabólicas, em curto e longo prazo, como aumento da adiposidade, resistência à leptina, e disfunção tireoideana e adrenal. Entretanto é sabido que na fumaça de cigarro estão presentes outros componentes com potenciais efeitos tóxicos. Assim propomos comparar o efeito de duas formas de exposição neonatal à fumaça do cigarro sobre o perfil endócrino-metabólico da prole em curto e longo prazo. Para isso, no 3 dia após o nascimento, ratos lactentes foram submetidos a dois modelos: Modelo I (exposição pelo leite materno), ninhadas separadas em: exposição à fumaça (EF; n=8) lactantes expostas à fumaça de cigarros 2R1F (1,7 mg de nicotina/cigarro por 1h, 4 vezes ao dia), separadas de suas proles e grupo controle (C; n=8), onde as mães foram separadas de suas proles e expostas ao ar filtrado; Modelo II (exposição direta à fumaça), ninhadas separadas em: exposição à fumaça (EF; n=8) mães e proles expostas à fumaça de cigarros 2R1F e controle (C; n=8) mães e proles expostas ao ar filtrado. A exposição ao tabaco ocorreu até o desmame. Mães sacrificadas aos desmame e proles aos desmame e aos 180 dias de idade. As mães lactantes expostas à fumaça (EF) apresentaram hipoleptinemia (-46%), hiperprolactinemia (+50%), hipoinsulinemia (-40%) e diminuição de triglicérides (-53%). Quanto a composição bioquímica do leite, as lactantes EF mostraram aumento de lactose (+52%) e triglicérides (+78%). No modelo I, as proles EF apresentaram ao desmame: diminuição da gordura corporal total (-24%), aumento de proteína corporal total (+17%), diminuição da glicemia (-11%), hiperinsulinemia (+28%), hipocorticosteronemia (-40%) e aumento de triglicérides (+34%). Quando adultas, as proles EF apresentaram somente alteração da função adrenal onde observou-se menor conteúdo de catecolaminas (-50%) e da expressão de tirosina hidroxilase na medula adrenal (-56%). No modelo II, as proles EF aos 21 dias exibiram diminuição da MC (-7%), do comprimento nasoanal (-5%), da gordura retroperitoneal (-59%), da área dos adipócitos viscerais (-60%) com maior área dos adipócitos subcutâneos (+95%), aumento do T4 (+59), da corticosterona (+60%), do conteúdo adrenal de catecolaminas (+58%) e hipoinsulinemia (-29%). Aos 180 dias, as proles EF apresentaram aumento da ingestão alimentar (+10%), dos depósitos de gordura visceral (~60%) e conteúdo de gordura corporal total (+50%), menor área dos adipócitos subcutâneos (-24%), aumento da leptina (+85%), glicemia (+11%), adiponectina (+1.4x), T3 (+71%), T4 (+57%) e TSH (+36,5%) com menor corticosterona (-41%) e catecolaminas adrenais (-57%) e aumento dos triglicerídeos (+65%). Somados nossos dados evidenciam o impacto negativo que a exposição à fumaça do cigarro tem sobre o desenvolvimento do neonato com o surgimento de desordens endócrinas futuras, que ocorrem pelo menos em parte devido às alterações observadas nas mães. Portanto, independente da forma de exposição, seja via aleitamento materno ou por inalação direta, é de grande importância alertar a sociedade sobre as possíveis complicações metabólicas em longo prazo decorrente da exposição involuntária do neonato ao tabagismo. / Events or stimuli during early life can affect the development; among these events, there is the maternal smoking. Children born from smoking mothers showed low birth body weight and overweight in childhood and adolescence. Maternal nicotine exposure, the main cigarette component, causes in the offspring several metabolic changes in short- and long-term, such as increase in adiposity, hyperleptinemia, leptin resistance as well as thyroid and adrenal dysfunction. However, it is known that there are other toxic components in tobacco smoke. Then, we compared the effects of two models of tobacco smoke exposure on endocrine-metabolic profile in offspring at short- and long-term. For this, in the 3rd day of birth, suckling rats were submitted to two different experiments: Model I (through breast milk exposure), in which litters were separated into, smoke exposure (SE; n=8) lactating mothers exposed to 2R1F cigarettes smoke (1.7 mg nicotine/cigarette/1h, 4 times per day) separated from their offspring; and control (C; n=8) mothers were separated of their pups and exposed to filtered air. Model II (direct exposure), in which litters were separated into: Smoke exposure (SE; n=8) lactating mothers and their offspring were exposed to 2R1F cigarettes smoke; and control (C; n=8) mothers and their pups were exposed to filtered air. The smoke exposure occurred until the weaning, when mothers and half of pups were killed. The other offspring were killed at 180 days-old. SE dams presented hypoleptinemia (-46%), hyperprolactinemia (+50%), hypoinsulinemia (-40%) and lower triglycerides (-53%). Concerning milk compositon, SE dams showed higher lactose (+52%) and triglycerides (+78%). In model I (through breast milk exposure), EF offspring showed at weaning lower total body fat (-24%) and higher total body protein (+17), lower serum glucose (-11%), hyperinsulinemia (+28%), hypocorticosteronemia (-40%) and higher triglycerides (+34%). In adulthood, these parameters were normalized, except for the adrenal function, featured by lower catecholamines content (-50%) and tyrosine hydroxylase expression in adrenal medulla (-56%). In model II (direct exposure), SE offspring (21 days-old) presented lower BW (-7%) and length (-5%), VFM (-28%) and visceral adipocytes area (-60%) with higher subcutaneous adipocytes area (+95%), higher T4 (+59%), corticosterone (+60%) and adrenal catecholamines content (+58%) and lower serum insulin (-29%). At 180 days-old, SE offspring presented higher food intake (+10%) without change in BW, higher visceral fat depots (~60) and total body fat (+50%), lower subcutaneous adipocytes area (-24%), higher serum glucose (+11%), adiponectin (+1.4x), leptin (+85%), T3 (+71%), T4 (+57%), TSH (+36.5%), lower corticosterone (-41%) and adrenal catecholamines content (-57%) and higher triglycerides (+65%). Therefore, our data evidences the negative impact that exposure to cigarette smoke can have on the development of the neonate as well as on future endocrine disorders, which occur at least in part due to the changes observed in the mothers. Therefore, independent of the kind of exposure, i.e. through breastfeeding or direct inhalation, it is of great importance warn society about the long-lasting metabolic complications resulting from involuntary exposure of newborn to smoking.

Introduction. The adverse health effects of cigarette smoking are well established, including the direct effects of nicotine on human endothelial cells and fibroblasts. However, the direct effects of nicotine in the nasal cavity remain uninvestigated. The study aim was to ascertain the direct effect of chemical components in cigarette smoke on the microbial flora or microbiota of the nasal cavity. Methods. We enrolled 40 participants from the Benson Idahosa University’s Health clinics to conduct this study. Information on demographic characteristics including age, sex, and smoking duration was obtained at baseline. We collected nasal swabs of 20 smokers and 20 non-smokers. The wool content of the swap stick was immediately stored in mac Cathy bottles containing 9 ml of normal saline and transported to the laboratory in less than 45 minutes after collection for microbiological analysis under aseptic condition. The enumeration of the microorganisms was carried out using the streak and pours plate method on Nutrient agar, Blood agar, Chocolate agar, Mac coney agar and Potato Dextrose agar (PDA). A two-sample t-test was used to determine differences in enumeration of microorganisms and isolates between smokers and non-smokers. Results. Total bacterial counts for the smokers ranged from 177 - 307 x 102 cfu/ml and 223 - 551 x 102 cfu/ml for non-smokers with (p = 0.046 Nutrient agar, and p = 0.011 PDA). The bacteria isolates were identified as Staphylococcus aureus, Escherichia coli, Klebsiella pneumonia, Proteus vulgaris and Streptococcus pneumonia, and the fungi isolates were identified as Aspergillus niger, Rhizopus stolonifer, Tricoderma viridae, respectively. The mean of nutrient agar in smokers is significantly lower (12.10) than that in nonsmokers (19.35), and the mean of PDA in smokers is significantly higher in smokers (5.75) than in nonsmokers (2.35). Higher percentages of gram-negative rods including Klebsiella pneumoniae (20%), Escherichia coli (20%) and Proteus vulgaris (20%) were identified in the smokers, which is in contrast to higher percentage of gram-positive cocci including Staphylococcus aureus and Streptococcus pneumonia identified in non-smokers. The most commonly isolated fungus in smokers was Aspergillus niger (45%) and nonsmokers was Rhizopus stolonifer (60%). Conclusions. Study findings demonstrated increased bacterial count and isolates in nasal cavity of smokers than non-smokers. Future studies should be warranted to understand the mechanistic role of nicotine in influencing microbiota of the nasal cavity.

Use of electronic cigarettes (e-cigarettes) is rapidly growing around the world. E-cigarettes are commonly used as an alternative nicotine delivery system, and have been advocated as generating lower levels of harmful chemicals compared to conventional cigarettes. Cigarette smoke-like aerosols are generated when e-cigarettes heat e-liquids. The main components of e-cigarette liquids are propylene glycol (PG) and glycerol (GL) in a varying ratio, plus nicotine and flavor chemicals. Both PG and GL are considered safe to ingest in foods and beverages, but the toxicity of these chemicals in aerosols is unknown. Current studies of e-cigarettes have mainly focused on dehydration and oxidation products of PG and GL. In this study, the other degradation products that can be generated during the vaping process are discussed. In addition, the gas/particle partitioning of chemicals in vaping aerosols is determined. This work finds that the formation of benzene in electronic cigarettes depends on the wattage, types of coils, and devices. To simulate commerical e-cigarette liquids, mixtures containing equal parts of PG and GL by volume were made with the following added components: benzoic acid (BA), benzoic acid with nicotine (Nic), benzaldehyde (BZ), band enzaldehyde with nicotine. PG only, GL only, and PG and GL mixtures were also made for comparison. The data presented here demonstrate that more benzene is generated as the wattage of a device increases. The results also seem to support the importance of ventilation in the generation of benzene. More benzene is generated from the mixtures containing benzoic acid when using the EVOD device with a smaller vent. However, benzaldehyde yields more benzene when using the Subtank Nano device with a larger vent. Findings also indicate that more benzene is produced from GL rather than PG. This thesis also addresses the chemical formation pathways of degradation compounds found in the aerosols formed from isotopically labeled e-cigarette liquids. Mixtures of both 13C-labeled and unlabeled PG as well as GL were made. The mixtures were vaped and gas-phase samples were collected to determine which chemicals were in the gas-phase portion of the aerosols. With the use of GC/MS methods, these isotopic labeling experiments provided evidence that the majority of the benzene, acetaldehyde, 2,3-butanedione, toluene, xylene, acrolein, and furan found in e-cigarette aerosols originates from GL in the PG plus GL mixtures. It was also shown that the majority of propanal is derived from PG: while hydroxyacetone can be formed from both PG and GL. Possible mechanisms for the formation of acetaldehyde, benzene, 2,3-butanedione, toluene, and xylene formation are proposed. Last, this study investigated the gas/particle partitioning of nicotine and flavor-related chemicals in e-cigarette fluids. The gas/particle partitioning behavior of chemicals in e-cigarettes fluids is highly dependent on the chemical volatility. A total of 37 compounds were examined. The target compounds were divided into 3 groups based on their vapor pressures: high, medium, and low. Headspace gas samples were collected and analyzed to determine the concentration of a compound in equilibrium with the liquid phase. The gas and liquid concentrations were used to calculate the gas/particle partitioning constant (Kp) for each compound. In an e-cigarette aerosol, volatile compounds have smaller Kp values and tend to be found in greater proportion in the gas-phase, whereas the less volatile compounds are likely to stay in the particle phase. General agreement with theory was found for compounds with known activity coefficients in PG and GL, indicating that theory can be used to predict Kp values for other compounds.