Diversos estudos relatam os efeitos da exposição à nicotina nos períodos pré e pós-natal, contudo, pouco se sabe a respeito dos efeitos da fumaça do cigarro na cascata de eventos que caracteriza o desenvolvimento do sistema nervoso central (SNC). Neste contexto, o objetivo deste trabalho foi esclarecer se a exposição à fumaça do cigarro no início do período pós-natal induz prejuízo ao desenvolvimento do SNC na infância, e as possíveis consequências na adolescência e na fase adulta. Camundongos BALB/c foram expostos a uma mistura de fumaça central e lateral do cigarro referência 3R4F (Universidade de Kentucky, EUA), desde o 3° dia de vida pós-natal (P) até P14 por duas horas diárias. Nossos resultados indicam que a exposição à fumaça do cigarro no início do período pós-natal induz prejuízo ao processo de aprendizado e memória e aumento na ansiedade em todas as idades avaliadas, além de induzir diminuição da atividade locomotora na infância e na adolescência. Ainda, observamos diminuição dos níveis de BDNF e das proteínas sinápticas sinapsina e sinaptofisina no hipocampo, cerebelo, córtex pré-frontal e estriado. A fumaça do cigarro também induz diminuição na porcentagem de fibras mielinizadas no nervo óptico e aumento da proteína básica de mielina (PBM) no cerebelo na infância, além de diminuição da PBM no telencéfalo e tronco encefálico na adolescência e no cerebelo na fase adulta. Nossos resultados sugerem que a exposição à fumaça do cigarro no início do período pós-natal causa prejuízo ao desenvolvimento do SNC, sendo que não há reversão dos efeitos observados no aprendizado e memória ou mesmo nos níveis de proteína pré-sináptica na adolescência e na fase adulta. / Several studies show the effects of nicotine exposure during pre- and postnatal period. However, little is known about the effects of environmental tobacco smoke (ETS) in the cascade of events that characterizes the brain development. Thus, the aim of this study was to evaluate the effects of ETS in early brain development. BALB/c mice were exposed to a mixture of mainstream and sidestream of tobacco smoke of reference cigarettes 3R4F (University of Kentucky, EUA) from the 3rd (P3) to the 14th (P14) day of life, during 2h/day. Our results showed that ETS induced impairment in learning and memory and increased anxiety in all the ages evaluated. In addition, there was a decrease in locomotor activity during childhood and adolescence. ETS also induced impairment in synaptic transmission, by a decrease in synapsin, synaptophysin and BDNF in hippocampus, cerebellum and prefrontal cortex as compared to the control group. The percentage of myelinated fibers in the optic nerve in childhood and in myelin basic protein (MBP) in the telencephalon and brainstem were lower in adolescents mice exposed to ETS when compared to the control group. In cerebellum, there was an increase in MBP in infants and a decrease in adults compared to the control group. Taken all together, our results suggest that the exposure to ETS in the early postnatal period induces impairment to the brain development. It is noteworthy that the effects on learning and memory or even in the presynaptic protein levels were not reversed in adolescence and adulthood.

O desenvolvimento encefálico representa um período de grande vulnerabilidade. Embora diversos trabalhos mostrem que a exposição ao fumo passivo pode levar ao desenvolvimento de sintomas psicocomportamentais da farmacodependência, ainda não está claro se a exposição à poluição tabagística ambiental (PTA) na fase inicial de formação do SNC pode levar à predisposição ao uso de drogas de abuso na adolescência. Assim, o foco deste estudo foi avaliar se a exposição à PTA no início do período pós-natal (P) contribui para a sensibilização comportamental e efeitos recompensadores ao etanol e à cocaína durante a adolescência. Camundongos machos Swiss-Webster foram expostos do 3º (P3) ao 15º (P15) dia de vida pós-natal, duas vezes por dia, à mistura da fumaça central e lateral de cigarros referência (3R4F). Na adolescência (P34-P45), foram avaliados os efeitos do tratamento repetido de etanol e cocaína (primeiro protocolo) como também o efeito do tratamento agudo com cocaína (segundo protocolo). No primeiro protocolo os animais foram desafiados com cocaína (i.p) ou etanol (i.p), para a avaliação da sensibilização comportamental (P34-P35) (n=6) e da preferência condicionada por lugar (CPP) (P36-P45) (n=6). A quantificação por Western Blotting (n=6) das proteínas marcadoras de plasticidade, como os receptores dopaminérgicos D1R e D2R, c-Fos, FRA1 e Rac1, no estriado e no córtex pré-frontal (CPF) foi realizada imediatamente após o dia do teste da CPP no P45. Já para o segundo protocolo, os animais foram desafiados com cocaína (i.p) para a avaliação da sensibilização comportamental (P34-P35) (n=12), da CPP (n=10) e a quantificação dos mesmos marcadores bioquímicos (n=6) além da dinorfina-A, nas mesmas estruturas encefálicas que no primeiro protocolo. Essas análises foram realizadas duas horas após a expressão da sensibilização comportamental (P36). O primeiro protocolo avaliou a exposição repetida ao etanol e a cocaína na adolescência na predisposição à dependência enquanto o segundo se a exposição aguda a cocaína seria capaz de levar ao mesmo efeito. No primeiro protocolo observamos sensibilização cruzada pela PTA e quanto ao teste da CPP não foi observada diferença estatística nem para o tratamento com etanol, nem para o com cocaína. Nossos resultados indicam que houve efeito estimulatório nos grupos tratados com cocaína no segundo protocolo deste estudo, representado pelo aumento da atividade locomotora após administração da droga. Por outro lado, não observamos sensibilização cruzada pela PTA, a qual foi obtida no primeiro protocolo. Já para o segundo protocolo, foi observado o condicionamento pela cocaína. Com relação à quantificação das proteínas, nosso estudo mostrou diminuição na concentração de receptores DR1 no estriado no grupo exposto à PTA e tratado com etanol em relação ao grupo controle tratado com etanol no primeiro protocolo deste estudo e sugerem que a exposição repetida ao etanol é capaz de induzir alterações nos receptores de dopamina. No segundo protocolo deste estudo observamos aumento de c-Fos no estriado e no CPF no grupo tratado com cocaína em relação ao seu controle e que a exposição aguda à cocaína é capaz de induzir aumento da dinorfina no CPF, enquanto à exposição prévia à PTA previne este aumento. Vale ressaltar que esse trabalho é inovador uma vez que avaliamos a exposição à PTA na infância e se esta poderia levar a sensibilização cruzada com a cocaína e à alterações em vias envolvidas nesse comportamento na adolescência. Em conjunto, nossos resultados sugerem que a exposição à fumaça do cigarro, mesmo gerando baixas concentrações plasmáticas de nicotina e cotinina, foi capaz de produzir alterações na expressão da sensibilização comportamental, na CPP e alterações bioquímicas, tanto no tratamento repetido de etanol e cocaína quanto na vigência da cocaína. / The brain development represents a very vulnerable period. Although multiples studies showed that exposure to secondhand smoke during the early post-natal period induces impairment in cognitive functions and predisposition to substance dependence psychobehavioral symptoms in adolescents, there is no definitive evidences that exposure to the environmental tobacco smoke (ETS) can lead to the use of drugs of abuse. We aimed to evaluate if the exposure to ETS in the early postnatal period (P) can contribute to the behavioral sensitization and rewarding effects of ethanol and cocaine during adolescence. Using reference cigarettes (3R4F), Swiss-Webster male mice were exposed from the 3rd (P3) to 15th (P15) day of age, twice a day, to the mixture of the cigarettes\' sidestream and mainstream. In adolescence (P34-P45), we evaluated the effects of repeated treatment with ethanol or cocaine (first protocol) and also the effect of acute treatment with cocaine (second protocol). On first protocol, animals were then challenged with cocaine or ethanol to evaluate evidence of behavioral sensitization (P34-P35) (n=6) and conditioned place preference (CPP) (P36-P45) (n=6). Based on Western Blotting analysis, we also quantified proteins markers of plasticity immediately after the day of CPP test (P45), in the prefrontal cortex (PFC) and striatum (dopamine receptors D1R and D2R, c-Fos, FRA1 and Rac1). On second protocol, animals were challenged with cocaine to evaluate evidence of behavioral sensitization (P34-P35) (n=12) and CPP (P36-P45) (n=10). Quantification of those markers of plasticity (n=6), plus dynorphin-A was evaluated two hours after the day of behavioral sensitization expression in P36 in PFC and striatum. The first protocol evaluated the repeated exposure to ethanol and cocaine during adolescence in the predisposition to addiction while the second protocol using acute exposure to cocaine would be able to lead to the same effect. In the first protocol we observed cross-sensitization by ETS and for CPP test, no significant difference for the treatment with ethanol and cocaine were observed. Our results indicated a stimulatory effect in animals challenged with cocaine on second protocol, represented by the increase in locomotors activity after drug administration. On the other hand, we found no cross-sensitization by ETS, which was obtained in the first protocol. As for the second protocol, it was possible to observe the conditioning for cocaine. Regarding our Western Blotting assays, we observed that the group exposed to ETS and challenged with ethanol had decreased D1R in the first protocol of this study. These results suggest that repeated exposure to ethanol could induce changes in dopamine receptors. In the second protocol was an increase of c-Fos in the striatum and the PFC compared to control and that acute exposure to cocaine can induce increase of dynoprhin-A while the prior exposure to ETS prevents this increase on PFC. It is noteworthy that this present study is innovative since it evaluated the exposure to ETS in childhood and this could lead to cross-sensitization with cocaine and changes in pathways involved in this behavior in adolescence. Taken together, our results suggest that exposure to ETS, even findings low levels of nicotine and cotinine plasmatic was able to produce changes in the expression of behavioral sensitization in the CPP and biochemical changes in both the repeated treatment of ethanol and cocaine as in the acute treatment of cocaine.

Diversos estudos relatam os efeitos da exposição à nicotina nos períodos pré e pós-natal, contudo, pouco se sabe a respeito dos efeitos da fumaça do cigarro na cascata de eventos que caracteriza o desenvolvimento do sistema nervoso central (SNC). Neste contexto, o objetivo deste trabalho foi esclarecer se a exposição à fumaça do cigarro no início do período pós-natal induz prejuízo ao desenvolvimento do SNC na infância, e as possíveis consequências na adolescência e na fase adulta. Camundongos BALB/c foram expostos a uma mistura de fumaça central e lateral do cigarro referência 3R4F (Universidade de Kentucky, EUA), desde o 3° dia de vida pós-natal (P) até P14 por duas horas diárias. Nossos resultados indicam que a exposição à fumaça do cigarro no início do período pós-natal induz prejuízo ao processo de aprendizado e memória e aumento na ansiedade em todas as idades avaliadas, além de induzir diminuição da atividade locomotora na infância e na adolescência. Ainda, observamos diminuição dos níveis de BDNF e das proteínas sinápticas sinapsina e sinaptofisina no hipocampo, cerebelo, córtex pré-frontal e estriado. A fumaça do cigarro também induz diminuição na porcentagem de fibras mielinizadas no nervo óptico e aumento da proteína básica de mielina (PBM) no cerebelo na infância, além de diminuição da PBM no telencéfalo e tronco encefálico na adolescência e no cerebelo na fase adulta. Nossos resultados sugerem que a exposição à fumaça do cigarro no início do período pós-natal causa prejuízo ao desenvolvimento do SNC, sendo que não há reversão dos efeitos observados no aprendizado e memória ou mesmo nos níveis de proteína pré-sináptica na adolescência e na fase adulta. / Several studies show the effects of nicotine exposure during pre- and postnatal period. However, little is known about the effects of environmental tobacco smoke (ETS) in the cascade of events that characterizes the brain development. Thus, the aim of this study was to evaluate the effects of ETS in early brain development. BALB/c mice were exposed to a mixture of mainstream and sidestream of tobacco smoke of reference cigarettes 3R4F (University of Kentucky, EUA) from the 3rd (P3) to the 14th (P14) day of life, during 2h/day. Our results showed that ETS induced impairment in learning and memory and increased anxiety in all the ages evaluated. In addition, there was a decrease in locomotor activity during childhood and adolescence. ETS also induced impairment in synaptic transmission, by a decrease in synapsin, synaptophysin and BDNF in hippocampus, cerebellum and prefrontal cortex as compared to the control group. The percentage of myelinated fibers in the optic nerve in childhood and in myelin basic protein (MBP) in the telencephalon and brainstem were lower in adolescents mice exposed to ETS when compared to the control group. In cerebellum, there was an increase in MBP in infants and a decrease in adults compared to the control group. Taken all together, our results suggest that the exposure to ETS in the early postnatal period induces impairment to the brain development. It is noteworthy that the effects on learning and memory or even in the presynaptic protein levels were not reversed in adolescence and adulthood.

Adverse health effects in children caused by environmental tobacco smoke (ETS) are well known. Children are primarily exposed by their parents’ smoking in their homes. A comprehensive evidence base shows that parental smoking during pregnancy and ETS exposure in early childhood are associated with an increased risk for a range of adverse health problems. Child Health Care nurses, who meet nearly all families in Sweden with children aged 0-6 years, have thus an important role in tobacco preventive work in order to support parents in their ambitions to protect their children from ETS exposure. The overall aim of this thesis was to develop, test and evaluate a new model for tobacco preventive work in Child Health Care (CHC) with special focus on areas with a high prevalence of parental smoking. In a first step CHC nurses’ and parents’ views on tobacco preventive work were analysed in two studies based on questionnaires. The intervention was performed during the second step, based on the results from nurses’ and parents’ experience of the tobacco preventive work in CHC, and with methods from Quality Improvement. An “intervention bundle” was developed which included evidence based methods for prevention of ETS exposure, and four learning sessions for the nurses. The instrument “Smoking in Children’s Environment Test” (SiCET) included in the bundle was evaluated with focus group interviews with the CHC nurses who participated in the intervention. Two urine samples were analysed to measure cotinine levels in children which provide an estimate for ETS exposure. Parents’ answers from the SiCET questionnaire, measurements of cotinine, and data from the nurses’ log-books were used in the evaluation of the effects of the intervention. In areas with a high prevalence of parental smoking 22 nurses recruited 86 families of whom 72 took part for the entire one-year period of the intervention. The results showed that parents wanted to have information on the harmful effects tobacco smoke have on their children and how they can protect their children from ETS exposure. The nurses saw tobacco preventive work as important but they experienced difficulties to reach certain groups such as fathers, foreign-born parents, and those who are socio-economically disadvantaged. The SiCET instrument provided a basis for dialogue with parents. The main results from the intervention showed that ten parents (11%) quit smoking, thirty-two families (44%) decreased their cigarette consumption in the home, and fewer children were exposed to tobacco smoke. Consequently, more children showed levels of urinary cotinine less than 6 ng/ml (base-line n=43, follow up n=54; p=0.05). The total number of outdoor smokers did not change. Seven of the nurses (30%) had successful results in their areas with a decrease of smokers in families with a child of 8 months, from 20% in 2009 to 12% in 2011. The corresponding figures for the whole county as well as the country did not decrease during the same period. The sustainability of the intervention has to be followed and thus measures should be followed prospectively over time. The SiCET instrument was found useful and might be applicable in other arenas where children’s ETS exposure is discussed. The development of an instant cotinine test using dipsticks would make it possible to give parents immediate feedback on the effectiveness of taken protective actions. This could work as a pedagogic resource in the dialogue with parents.

Smoking and environmental tobacco smoke (ETS) exposure are major risk factors for cardiovascular disease (CVD), although the exact components and pathophysiological mechanisms responsible for this association remain unclear. Polycyclic aromatic hydrocarbons (PAHs), including benzo[a]pyrene (BaP), are ubiquitous environmental contaminants that form during organic material combustion and are thus found in cigarette smoke, vehicle exhaust particles, and air pollution. We hypothesize that PAHs are key agents responsible for mediating the cigarette smoke effects in the cardiovascular system, including increased oxidative stress, inflammation, and arterial stiffness.<p> Arterial stiffness is a powerful, independent predictor of cardiovascular risk and is regulated, in part, by vasoactive mediators derived from the endothelium. The first objective of this project was to determine whether pulse wave dP/dt collected from radiotelemetry-implanted rats is a reliable indicator of changes in arterial stiffness following administration of vasoactive drugs or acute ETS exposure. Anaesthetized rats were administered a single dose of saline (vehicle control), acetylcholine, norepinephrine, and N(G)-nitro-L-arginine methyl ester (L-NAME) via the tail vein, allowing a washout period between injections. Acetylcholine decreased and norepinephrine increased dP/dt compared to saline vehicle. Injection of the nitric oxide (NO) synthase inhibitor L-NAME decreased plasma nitrate/nitrite (NOx), but transiently increased dP/dt. For the ETS experiment, rats were exposed for one hour to sham, low dose ETS, or high dose ETS. Exposure to ETS did not significantly alter dP/dt or plasma endothelin-1 (ET-1) levels, but increased plasma NOx levels at the high ETS exposure and increased plasma nitrotyrosine levels in both ETS groups. In conclusion, acute changes in NO production via acetylcholine or L-NAME alter the arterial pulse wave dP/dt consistently with the predicted changes in arterial stiffness. Although acute ETS appears to biologically inactivate NO, a concomitant increase in NO production at the high ETS exposure may explain why ETS did not acutely alter dP/dt.<p> The second objective of this project was to compare the effects of subchronic ETS and BaP exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in radiotelemetry-implanted rats. Pulse wave dP/dt was used as an indicator of arterial stiffness, and was compared to both structural (wall thickness) and functional (NO production and bioactivity, ET-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver were examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450 specifically CYP1A1). Daily ETS exposure for 28 days altered the circadian pattern of heart rate and blood pressure in rats, with a loss in the normal dipping pattern of blood pressure during sleep. Subchronic ETS exposure also increased dP/dt in the absence of any structural modifications in the arterial wall. Although NO production and ET-1 levels were not altered by ETS, there was increased biological inactivation of NO via peroxynitrite production (as indicated by increased plasma nitrotyrosine levels). Thus, vascular stiffness and failure of blood pressure to dip precede structural changes in rats exposed to ETS for 28 days. Exposure to ETS also caused increased number of lung neutrophils as well as increased CYP1A1 activity in lung microsomes.<p> Since ETS-induced increases in arterial stiffness occurred as early as day 7, radiotelemetry-implanted rats were exposed daily to intranasal BaP for 7 days. Similar to ETS, BaP exposure altered circadian blood pressure patterns and reduced blood pressure dipping during sleep. Thus, in support of part of our hypothesis, the PAH component of cigarette smoke may be responsible for the ETS-induced increase in blood pressure and the loss of dipping pattern during sleep. Increased neutrophil recruitment was observed in the lungs of both ETS- and BaP-exposed rats, suggesting that lung inflammatory reactions may be involved in the disruption of circadian blood pressure rhythms. Unlike ETS however, BaP exposure did not significantly alter pulse wave dP/dt, endothelial function, or lung CYP1A1 activity. Thus, contrary to our hypothesis, the reduction in NO bioactivity and increased arterial stiffness caused by ETS cannot be explained by BaP at the dose and length of the exposure in the current study. Production of reactive metabolites in the lung following ETS exposure may be responsible, at least in part, for the increases in oxidative stress in the vasculature, leading to reduced NO bioactivity and increased arterial stiffness. Oxidative stress caused by BaP exposure may have been insufficient to reduce NO bioactivity in the peripheral vasculature. Therefore arterial stiffness was not increased and factors other than NO may be responsible for the increase in blood pressure observed with ETS and BaP exposure.

Introduction: Despite the known consequences of cigarette smoking, almost 20% of adults in the United States smoke. Smoking has been shown to harm nearly every organ of the body. Its detrimental effects have been seen not only in smokers themselves but also in those exposed to secondhand smoke (SHS) at work and in other public places. Methodology: The purpose of this thesis was to examine compliance with the signage requirement of the Georgia Smokefree Air Act (GSAA) of 2005 among 99 hospitality venues located in Atlanta. Photographs of bars and restaurant entrances were taken and raters then classified each venue as compliant or non-compliant with smoking status signage requirements of the GSAA. Additionally, air samples were collected using Sidepak equipment from 59 venues in order to estimate the PM2.5 levels, which is a recognized measure of air quality. With Spearman’s rho correlation coefficient (r), analyses were run to determine correlations between signage compliance, number of cigarettes being smoked, and smoking permitted with air quality (PM2.5). Analyses were conducted using the Statistical Package for Social Sciences (SPSS) version 19. Results: Of the 99 venues assessed, only 21 (21.2 %) complied with the signage requirements of the GSAA. Venues that do adhere to signage requirements and indicate no smoking on their signs and at the same time via telephone stated that smoking is prohibited had the lowest PM2.5 levels =15.03. On the contrary, those venues that display signs permitting smoking and via telephone indicated smoking is allowed had the highest PM2.5 levels =230.31. It was determined that there is a strong positive correlation between PM2.5 and “number of cigarettes” (r=.611, n=59, p<.001) as well as moderate correlation between PM2.5 and “smoking permitted” as indicated from phone calls (r=.464, n=59, p<.001). However, analysis showed a weak correlation between PM2.5 and “signage compliance” in accordance with GSAA (r=.107, n=59, p>.001). Conclusions: Enforcement of GSAA must be enhanced in order to better protect workers and patrons of Atlanta’s bars and restaurants from harmful exposure to SHS. Findings from this study support that prohibiting smoking in bars and restaurants and having signs stating that smoking is prohibited would improve air quality and protect workers by eliminating their exposure to SHS while working.

Smoking and environmental tobacco smoke (ETS) exposure are major risk factors for cardiovascular disease (CVD), although the exact components and pathophysiological mechanisms responsible for this association remain unclear. Polycyclic aromatic hydrocarbons (PAHs), including benzo[a]pyrene (BaP), are ubiquitous environmental contaminants that form during organic material combustion and are thus found in cigarette smoke, vehicle exhaust particles, and air pollution. We hypothesize that PAHs are key agents responsible for mediating the cigarette smoke effects in the cardiovascular system, including increased oxidative stress, inflammation, and arterial stiffness.<p> Arterial stiffness is a powerful, independent predictor of cardiovascular risk and is regulated, in part, by vasoactive mediators derived from the endothelium. The first objective of this project was to determine whether pulse wave dP/dt collected from radiotelemetry-implanted rats is a reliable indicator of changes in arterial stiffness following administration of vasoactive drugs or acute ETS exposure. Anaesthetized rats were administered a single dose of saline (vehicle control), acetylcholine, norepinephrine, and N(G)-nitro-L-arginine methyl ester (L-NAME) via the tail vein, allowing a washout period between injections. Acetylcholine decreased and norepinephrine increased dP/dt compared to saline vehicle. Injection of the nitric oxide (NO) synthase inhibitor L-NAME decreased plasma nitrate/nitrite (NOx), but transiently increased dP/dt. For the ETS experiment, rats were exposed for one hour to sham, low dose ETS, or high dose ETS. Exposure to ETS did not significantly alter dP/dt or plasma endothelin-1 (ET-1) levels, but increased plasma NOx levels at the high ETS exposure and increased plasma nitrotyrosine levels in both ETS groups. In conclusion, acute changes in NO production via acetylcholine or L-NAME alter the arterial pulse wave dP/dt consistently with the predicted changes in arterial stiffness. Although acute ETS appears to biologically inactivate NO, a concomitant increase in NO production at the high ETS exposure may explain why ETS did not acutely alter dP/dt.<p> The second objective of this project was to compare the effects of subchronic ETS and BaP exposure on circadian blood pressure patterns, arterial stiffness, and possible sources of oxidative stress in radiotelemetry-implanted rats. Pulse wave dP/dt was used as an indicator of arterial stiffness, and was compared to both structural (wall thickness) and functional (NO production and bioactivity, ET-1 levels) features of the arterial wall. In addition, histology of lung, heart, and liver were examined as well as pulmonary and hepatic detoxifying enzyme activity (cytochrome P450 specifically CYP1A1). Daily ETS exposure for 28 days altered the circadian pattern of heart rate and blood pressure in rats, with a loss in the normal dipping pattern of blood pressure during sleep. Subchronic ETS exposure also increased dP/dt in the absence of any structural modifications in the arterial wall. Although NO production and ET-1 levels were not altered by ETS, there was increased biological inactivation of NO via peroxynitrite production (as indicated by increased plasma nitrotyrosine levels). Thus, vascular stiffness and failure of blood pressure to dip precede structural changes in rats exposed to ETS for 28 days. Exposure to ETS also caused increased number of lung neutrophils as well as increased CYP1A1 activity in lung microsomes.<p> Since ETS-induced increases in arterial stiffness occurred as early as day 7, radiotelemetry-implanted rats were exposed daily to intranasal BaP for 7 days. Similar to ETS, BaP exposure altered circadian blood pressure patterns and reduced blood pressure dipping during sleep. Thus, in support of part of our hypothesis, the PAH component of cigarette smoke may be responsible for the ETS-induced increase in blood pressure and the loss of dipping pattern during sleep. Increased neutrophil recruitment was observed in the lungs of both ETS- and BaP-exposed rats, suggesting that lung inflammatory reactions may be involved in the disruption of circadian blood pressure rhythms. Unlike ETS however, BaP exposure did not significantly alter pulse wave dP/dt, endothelial function, or lung CYP1A1 activity. Thus, contrary to our hypothesis, the reduction in NO bioactivity and increased arterial stiffness caused by ETS cannot be explained by BaP at the dose and length of the exposure in the current study. Production of reactive metabolites in the lung following ETS exposure may be responsible, at least in part, for the increases in oxidative stress in the vasculature, leading to reduced NO bioactivity and increased arterial stiffness. Oxidative stress caused by BaP exposure may have been insufficient to reduce NO bioactivity in the peripheral vasculature. Therefore arterial stiffness was not increased and factors other than NO may be responsible for the increase in blood pressure observed with ETS and BaP exposure.

A fumaça ambiental de tabaco antes de ser um problema de saúde, o qual se torna quando é inalada, é um problema de engenharia, envolvendo fenômenos de transporte e saneamento ambiental, mecânica de fluidos e qualidade do ar. Este trabalho versou o problema da qualidade do ar de ambientes onde o fumo é permitido. Objetivou compilar uma base científica sobre a questão ventilação e poluição tabagística ambiental para embasar argumentações para o estabelecimento de leis de ambientes interiores livres de fumo. Mostrou-se que a fumaça do tabaco é agente cancerígeno em humanos, não havendo nível seguro de exposição a ela, e que a ventilação não soluciona o problema da exposição, sendo a abordagem eficiente no controle da qualidade do ar de ambientes interiores a proibição do fumo. A revisão das leis e normas brasileiras referentes à qualidade do ar de ambientes interiores onde o fumo é permitido mostrou que elas não estão alinhadas à base científica sobre a questão. Por modelagem física e experimentação em escala reduzida, o sistema de separação de áreas para fumantes e não-fumantes por ventilação proposto pelo projeto Convivência em Harmonia foi analisado, e mostrou-se que tal separação por ventilação não impede a dispersão da fumaça da área para fumantes para a área para não-fumantes. As metodologias de amostragem de ar indicadas para o levantamento de dados de poluição tabagística ambiental para a mobilização para a implementação de leis de ambientes livres de fumo foram avaliadas e algumas questões técnicas foram apontadas, bem como a necessidade da especificação de um instrumento em conformidade com a norma para material particulado da Agência Nacional de Vigilância Sanitária, que pode ser considerada o processo nacional de amostragem do ar para estudos de poluição tabagística ambiental. / Environmental tobacco smoke, before becoming a health issue, which becomes when it is inhaled, is an engineering issue, involving transport phenomena and environment, fluid mechanics and air quality. This research approached the problem of air quality of places where smoking is allowed. The objective was to compile a scientific basis on the issue ventilation and environmental tobacco smoke to support arguments for the establishment of smoke-free laws. It was shown that tobacco smoke is carcinogenic to humans, with no safe level of exposure, and that ventilation does not solve the problem imposed by exposure, being the efficient approach on the control of indoor air quality the prohibition of smoking. The review of Brazilian laws and norms related to the indoor air quality of places where smoking is allowed showed that they are not aligned to the scientific basis of the issue. By physical modeling and experimentation on reduced-scale, the system of separation of smoking and non-smoking areas by ventilation proposed by the Courtesy of Choice project was analyzed, and it was shown that such separation by ventilation does not prevent the dispersion of smoke from smoking to non-smoking areas. The air sampling methodologies indicated for the collection of environmental tobacco smoke data for mobilizing the implementation of smokefree environments were evaluated and some technical issues were raised, as well as the need to specify an instrument in conformity with the particulate matter norm of the National Health Surveillance Agency, that may be considered the national air sampling process for environmental tobacco smoke studies.

A fumaça ambiental de tabaco antes de ser um problema de saúde, o qual se torna quando é inalada, é um problema de engenharia, envolvendo fenômenos de transporte e saneamento ambiental, mecânica de fluidos e qualidade do ar. Este trabalho versou o problema da qualidade do ar de ambientes onde o fumo é permitido. Objetivou compilar uma base científica sobre a questão ventilação e poluição tabagística ambiental para embasar argumentações para o estabelecimento de leis de ambientes interiores livres de fumo. Mostrou-se que a fumaça do tabaco é agente cancerígeno em humanos, não havendo nível seguro de exposição a ela, e que a ventilação não soluciona o problema da exposição, sendo a abordagem eficiente no controle da qualidade do ar de ambientes interiores a proibição do fumo. A revisão das leis e normas brasileiras referentes à qualidade do ar de ambientes interiores onde o fumo é permitido mostrou que elas não estão alinhadas à base científica sobre a questão. Por modelagem física e experimentação em escala reduzida, o sistema de separação de áreas para fumantes e não-fumantes por ventilação proposto pelo projeto Convivência em Harmonia foi analisado, e mostrou-se que tal separação por ventilação não impede a dispersão da fumaça da área para fumantes para a área para não-fumantes. As metodologias de amostragem de ar indicadas para o levantamento de dados de poluição tabagística ambiental para a mobilização para a implementação de leis de ambientes livres de fumo foram avaliadas e algumas questões técnicas foram apontadas, bem como a necessidade da especificação de um instrumento em conformidade com a norma para material particulado da Agência Nacional de Vigilância Sanitária, que pode ser considerada o processo nacional de amostragem do ar para estudos de poluição tabagística ambiental. / Environmental tobacco smoke, before becoming a health issue, which becomes when it is inhaled, is an engineering issue, involving transport phenomena and environment, fluid mechanics and air quality. This research approached the problem of air quality of places where smoking is allowed. The objective was to compile a scientific basis on the issue ventilation and environmental tobacco smoke to support arguments for the establishment of smoke-free laws. It was shown that tobacco smoke is carcinogenic to humans, with no safe level of exposure, and that ventilation does not solve the problem imposed by exposure, being the efficient approach on the control of indoor air quality the prohibition of smoking. The review of Brazilian laws and norms related to the indoor air quality of places where smoking is allowed showed that they are not aligned to the scientific basis of the issue. By physical modeling and experimentation on reduced-scale, the system of separation of smoking and non-smoking areas by ventilation proposed by the Courtesy of Choice project was analyzed, and it was shown that such separation by ventilation does not prevent the dispersion of smoke from smoking to non-smoking areas. The air sampling methodologies indicated for the collection of environmental tobacco smoke data for mobilizing the implementation of smokefree environments were evaluated and some technical issues were raised, as well as the need to specify an instrument in conformity with the particulate matter norm of the National Health Surveillance Agency, that may be considered the national air sampling process for environmental tobacco smoke studies.

A fumaça ambiental de tabaco antes de ser um problema de saúde, o qual se torna quando é inalada, é um problema de engenharia, envolvendo fenômenos de transporte e saneamento ambiental, mecânica de fluidos e qualidade do ar. Este trabalho versou o problema da qualidade do ar de ambientes onde o fumo é permitido. Objetivou compilar uma base científica sobre a questão ventilação e poluição tabagística ambiental para embasar argumentações para o estabelecimento de leis de ambientes interiores livres de fumo. Mostrou-se que a fumaça do tabaco é agente cancerígeno em humanos, não havendo nível seguro de exposição a ela, e que a ventilação não soluciona o problema da exposição, sendo a abordagem eficiente no controle da qualidade do ar de ambientes interiores a proibição do fumo. A revisão das leis e normas brasileiras referentes à qualidade do ar de ambientes interiores onde o fumo é permitido mostrou que elas não estão alinhadas à base científica sobre a questão. Por modelagem física e experimentação em escala reduzida, o sistema de separação de áreas para fumantes e não-fumantes por ventilação proposto pelo projeto Convivência em Harmonia foi analisado, e mostrou-se que tal separação por ventilação não impede a dispersão da fumaça da área para fumantes para a área para não-fumantes. As metodologias de amostragem de ar indicadas para o levantamento de dados de poluição tabagística ambiental para a mobilização para a implementação de leis de ambientes livres de fumo foram avaliadas e algumas questões técnicas foram apontadas, bem como a necessidade da especificação de um instrumento em conformidade com a norma para material particulado da Agência Nacional de Vigilância Sanitária, que pode ser considerada o processo nacional de amostragem do ar para estudos de poluição tabagística ambiental. / Environmental tobacco smoke, before becoming a health issue, which becomes when it is inhaled, is an engineering issue, involving transport phenomena and environment, fluid mechanics and air quality. This research approached the problem of air quality of places where smoking is allowed. The objective was to compile a scientific basis on the issue ventilation and environmental tobacco smoke to support arguments for the establishment of smoke-free laws. It was shown that tobacco smoke is carcinogenic to humans, with no safe level of exposure, and that ventilation does not solve the problem imposed by exposure, being the efficient approach on the control of indoor air quality the prohibition of smoking. The review of Brazilian laws and norms related to the indoor air quality of places where smoking is allowed showed that they are not aligned to the scientific basis of the issue. By physical modeling and experimentation on reduced-scale, the system of separation of smoking and non-smoking areas by ventilation proposed by the Courtesy of Choice project was analyzed, and it was shown that such separation by ventilation does not prevent the dispersion of smoke from smoking to non-smoking areas. The air sampling methodologies indicated for the collection of environmental tobacco smoke data for mobilizing the implementation of smokefree environments were evaluated and some technical issues were raised, as well as the need to specify an instrument in conformity with the particulate matter norm of the National Health Surveillance Agency, that may be considered the national air sampling process for environmental tobacco smoke studies.