This cross-sectional study observed the association of smoke exposure and tuberculosis-related outcomes in Saskatchewan by individuals who had been exposed to someone with infectious TB. This study is unique in that we were quantifying the amount of smoke exposure that increases susceptibility to TB infection and/or active TB. Subjects who were at least 18 years old were enrolled into the study because they were contacts to infectious tuberculosis. The study involved a detailed interview. This interview involved questions on demographics, hair treatment (specifically, hair dying), tobacco smoke exposure, co-morbidities/risk factors, and alcohol consumption. After the interview was conducted, a small 10mg sample of hair was collected from each individual. This was to ensure a more accurate level of smoke exposure was attained. In total, 104 individuals were recruited to participate in this study. Linear regression analysis was used to compare cigarette consumption and nicotine concentration. A quadratic term was added to the linear model and the result was that reported cigarette consumption per day (x) was significantly associated with nicotine concentration (y) where y=0.91+1.35x-0.25x2 (p=0.001). A Fisher’s exact test was conducted to see if there was a relationship between smoking and TB disease; there was no statistically significant association between TB disease and smoking (OR= 3.28, 95%CI 0.37-29.1, p = 0.24). Logistic regression analysis was used to see if there was a relationship between smoking and TB infection. Of the five predictor variables, none were statistically significant. Smokers had an association with higher odds of TB infection (OR=2.03, 95%CI 0.71-5.80, p=0.19). Canadian-born Aboriginals had an association with lower odds of TB infection (OR=0.52, 95%CI 0.18-1.46, p=0.21). The results from this study could provide insight into creating a larger, more complex study involving TB and smoking.

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.

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)

BACKGROUND: Results of the Global Adult Tobacco Survey in Kerala, India found that 42 % of adults were exposed to second hand smoke (SHS) inside the home. Formative research carried out in rural Kerala suggests that exposure may be much higher. Numerous studies have called for research and intervention on SHS exposure among women and children as an important component of maternal and child health activities. METHODS: Community-based participatory research was carried out in Kerala. First, a survey was conducted to assess prevalence of SHS exposure in households. Next, a proof of concept study was conducted to develop and test the feasibility of a community-wide smoke free homes initiative. Educational materials were developed and pretested in focus groups. After feasibility was established, pilot studies were implemented in two other communities. Post intervention, surveys were conducted as a means of assessing changes in community support. RESULTS: At baseline, between 70 and 80 % of male smokers regularly smoked inside the home. Over 80 % of women had asked their husband not to do so. Most women felt powerless to change their husband's behavior. When women were asked about supporting a smoke free homes intervention, 88 % expressed support for the idea, but many expressed doubt that their husbands would comply. Educational meetings were held to discuss the harms of second hand smoke. Community leaders signed a declaration that their community was part of the smoke free homes initiative. Six months post intervention a survey was conducted in these communities; between 34 and 59 % of men who smoked no longer smoked in their home. CONCLUSIONS: The smoke free homes initiative is based on the principle of collective efficacy. Recognizing the difficulty for individual women to effect change in their household, the movement establishes a smoke free community mandate. Based on evaluation data from two pilot studies, we can project that between a 30 and 60 % reduction of smoking in the home may be achieved, the effect size determined by how well the smoke free home steps are implemented, the characteristics of the community, and the motivation of community level facilitators.

Polycyclic aromatic hydrocarbons (PAHs) are environmental and occupational carcinogens that are produced by the incomplete combustion of organic material, such as from the burning of tobacco, coal, and petroleum products. In addition to causing cancer, exposure to PAHs is hypothesized to contribute to atherosclerosis and to lead to increased incidence rates of cardiovascular disease in populations. Considering the number of deaths attributable to tobacco smoke exposure, ambient air pollution, and occupational hazards, PAHs may be a significant contributor to the prevalence of cardiovascular disease in human populations. However, a clear exposure-response relationship between PAHs and measures of cardiovascular disease has not been demonstrated. While PAH exposure has been shown to be associated with indicators of cardiovascular disease in research animals, this relationship has not been studied comprehensively in human populations. Using data from the continuous National Health and Nutrition Examination Surveys (NHANES) 1999 - 2004 of a representative sample of the entire US civilian population, this study investigated predictors of total body burden of PAHs and associations between urinary metabolites of PAHs and biomarkers of cardiovascular disease in 4,492 study participants aged 20 years and older. Using various analytic approaches, this research project identified tobacco smoke exposure as a significant predictor of urinary levels of low molecular weight PAHs but not as a predictor of urinary levels of high molecular weight PAHs in a large population of individuals without known occupational exposure to PAHs. Worker occupational category was not associated with urinary levels of any PAH metabolites. The results of this study also indicate a possible association between exposure to PAHs and the development of cardiovascular disease in humans. Levels of multiple metabolites of specific PAHs, naphthalene, fluorene, and phenanthrene were significantly associated with increases in total cholesterol, triglycerides, WBC count, and C-reactive protein levels. Additionally, this study examined the utility of factor analysis for data reduction of 23 urinary PAH metabolites to two latent factors representing low and high molecular weight PAHs to streamline investigations of the associations of PAH exposures with various health outcomes. Results of this study suggest mechanisms by which PAH exposure contributes to the burden of cardiovascular disease on human populations and the methods by which human body burden on PAHs can be measured.

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Introduction. La fumée secondaire est considérée comme un agent neurotoxique. À ce jour, la littérature traitant des liens entre l’exposition à la fumée secondaire à l’enfance et les comportements antisociaux repose majoritairement sur des devis transversaux ou porte sur la période développementale de l’enfance. Objectif. D’une part, nous souhaitons repousser l’âge auquel les comportements antisociaux sont mesurés en le portant à la préadolescence. De plus, nous souhaitons utiliser des données autorapportées afin d’utiliser une mesure possiblement plus valide des comportements antisociaux. Finalement, nous souhaitons confirmer les résultats longitudinaux précédemment rapportés par les parents ou les enseignants à l’âge de 10 ans. Méthode. Les parents de 1035 enfants ayant participé à l’Étude longitudinale des enfants du Québec ont rapporté si au moins un individu fumait au domicile (entre l’âge d’un an et demi et sept ans). Les variables dépendantes autorévélées (mesurées à douze ans) comprenaient les problèmes de conduite, l’agressivité proactive, l’agressivité réactive, l’indiscipline scolaire et le risque de décrochage. Résultats. Après l’inclusion des variables de contrôle, nous avons observé que l’exposition à la fumée secondaire est prospectivement associée aux problèmes de conduite, l’agressivité proactive, l’agressivité réactive, l’indiscipline scolaire et le risque de décrochage autorévélés. Discussion. Les jeunes exposés à la fumée secondaire à l’enfance rapportent avoir plus de comportements antisociaux. Nos résultats corroborent les recommandations du American Surgeon’s General indiquant qu’aucune exposition à la fumée secondaire ne peut être considérée sécuritaire à l’enfance. / Introduction. Secondhand smoke is considered a developmental neurotoxicant. Up to this day, research on secondhand smoke and later antisocial behavior has remained cross-sectional or in the developmental period of childhood. Objective. We sough to extend previous research by extending to age 12 our prospective associational model. Also, we use self-reported data for validity reasons and to cross-match previous research using parent and teacher-rated data at age 10. Method. Parents reported the amount of household smoke exposure (between ages 1.5 and 7) for 1035 children from the Quebec Longitudinal Study of Child Development. Main outcome measures include self-reported conduct problems, proactive aggression, reactive aggression, dropout risk, and school indiscipline at age 12. Results. After adjusting for potential confounders, we observed that secondhand smoke is prospectively associated to conduct problems, proactive and reactive aggression, school indiscipline, and dropout risk. Discussion. Children exposed to household smoke reported increased risks of reporting antisocial behavior at age 12. Our findings corroborate the recommendation of the American Surgeon’s General that no smoke exposure can be considered safe.

Cigarette smoking is a complex mixture of many constituents identified, among them reactive substances (reactive oxygen and nitrogen species), which are capable of initiating or promoting oxidative damage. Lungs and brain are affected by cigarette smoke exposure. Exposure to cigarette smoke is related to development of diseases in children and adults. However, children are more susceptible than adults to damage caused by cigarette smoke. Thus, the use of antioxidants is a good alternative to protect tissues of oxidative damage caused by cigarette smoke exposure. Diphenyl diselenide [(PhSe)2] is an organoselenium compound that presents pharmacological effects, among them the antioxidant effect. Nevertheless, the mechanism involved in antioxidant effect of (PhSe)2 was not been elucidated. Therefore, this study was performed to study the effects of cigarette smoke passive exposure in lungs and brain of rat pups in two experimental protocols of oxidative stress. Moreover, the antioxidant effect of (PhSe)2 in these experimental protocols was studied. Besides, the mechanisms involved in the antioxidant effect of (PhSe)2 were investigated. Rat pups that were exposed to two experimental protocols were used. In a first experimental protocol (P1), the effect of exposure to one, two and three cigarettes during the first, second and third weeks of live, respectively, was studied. In a second experimental protocol (P2), the effect of exposure to four, five and six cigarettes during the first, second and third weeks of life, respectively, was carried out. The duration of each exposure was 15 min. Animals were exposed to cigarette smoke during 20 days (3 weeks). Immediately before each exposure, animals that were treated with (PhSe)2 received daily an oral dose of 0.5 mg/kg. At the end of the experimental exposure period (3 weeks), rat pups were euthanized, and lungs and brain were removed for analyses of lipid peroxidation, enzymatic antioxidant defenses (superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione S-transferase (GST) activities) and non-enzymatic defenses (non-protein thiols (NPSH) and ascorbic acid levels). Rat pups were daily weighed, before each exposure. The weight of animals was not changed after cigarette smoke exposure neither to P1 nor to P2. In both experimental protocols, animals that were exposed to cigarette smoke showed an increase in lipid peroxidation in lungs. In brain, an increase in thiobarbituric acid reactive species (TBARS) was observed only in P2. Levels of non-enzymatic antioxidant defenses decreased in lungs of animals exposed to P1 and P2. In brain, exposure to P1 increased ascorbic acid levels and exposure to P2 reduced NPSH and ascorbic acid levels. Enzymatic antioxidant defenses changed in P2 in lungs of rat pups. In brain, the activity of CAT was reduced after exposure to P1, while SOD and CAT activities were decreased after exposure to P2. Treatment with (PhSe)2 restored the oxidative damage caused by cigarette smoke exposure in lungs and brain of rat pups. Moreover, NPSH levels, ascorbic acid content and GST activity showed an increase per se in lungs of animals treated with (PhSe)2. The mechanisms involved in antioxidant effect of (PhSe)2 (1 - 50 μM) were studied. To this end, dehydroascorbate (DHA) reductase and GST activities were determined. (PhSe)2 at concentration of 5 μM demonstrated DHA reductase and GST-like activities. Furthermore, the scavenger effect of 2,2 -diphenyl-1-picrylhydrazyl (DPPH ) radical and 2,2 -azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS +) radicals, and the protection of Fe2+ autooxidation were studied. However, the compound had no scavenger effect or protected Fe2+ autooxidation, discarding that these mechanisms are involved in the antioxidant effect of (PhSe)2. Synthesis of glutathione (GSH) was also studied as a possible mechanism involved in antioxidant effect of (PhSe)2. For this, buthionine sulfoximine (BSO), a substance that inhibits γ-glutamilcystheine synthase activity, an enzyme involved in the synthesis of GSH was used. BSO blocked the protective effect of (PhSe)2 in reducing NPSH levels caused by cigarette smoke passive exposure in lungs and liver of rat pups. In this study it was concluded that (PhSe)2 had antioxidant effect by different mechanisms. The action of (PhSe)2 to increase NPSH and ascorbic acid levels, and GST activity is one of mechanisms of the antioxidant effect of this compound. (PhSe)2 presented DHA reductase and GST-like activities, demonstrating a new mechanism of antioxidant effect of the compound. Furthermore, the synthesis of GSH is involved in the antioxidant role of (PhSe)2, since blocking the synthesis of GSH, presented the antioxidant effect of this compound. / A fumaça do cigarro é uma mistura complexa de diversos constituintes identificados, entre eles, substâncias reativas (espécies reativas de oxigênio e nitrogênio), as quais podem estar relacionadas com o desenvolvimento de várias doenças em adultos e crianças. Os pulmões e cérebro estão entre os órgãos mais afetados pela exposição à fumaça do cigarro. Entretanto, as crianças são mais suscetíveis aos danos causados pela exposição passiva à fumaça do cigarro do que os adultos. Para proteger os tecidos do dano oxidativo causado por esta exposição são utilizados antioxidantes. O disseleneto de difenila [(PhSe)2] é um composto orgânico de selênio que apresenta diversos efeitos farmacológicos descritos, entre eles, o antioxidante. Entretanto, o mecanismo pelo qual este composto exerce seus efeitos antioxidantes ainda não foi elucidado. Portanto, o presente trabalho visa estudar os efeitos da exposição passiva à fumaça do cigarro nos pulmões e no cérebro de ratos jovens, em dois protocolos experimentais de estresse oxidativo, e verificar o papel protetor do (PhSe)2 nestes protocolos. Além disso, investigaram-se os mecanismos envolvidos no efeito antioxidante desse composto. Para isso, foram utilizados ratos jovens que foram submetidos a dois protocolos experimentais de estresse oxidativo. Em um primeiro protocolo experimental (P1) verificou-se o efeito da exposição passiva à fumaça de um, dois e três cigarros nas primeira, segunda e terceira semanas de vida, respectivamente. Em um segundo protocolo experimental (P2) foi verificado o efeito da exposição passiva à fumaça de quatro, cinco e seis cigarros nas primeira, segunda e terceira semanas de vida, respectivamente. Todos os animais em ambos os protocolos experimentais foram expostos à fumaça do cigarro diariamente, 15 minutos cada exposição, por um período de 20 dias. O animais que foram tratados com o (PhSe)2, receberam diariamente pela via oral a dose de 0,5 mg/kg, imediatamente antes de cada exposição. No 21° dia, os animais foram eutanasiados e os pulmões e cérebro foram retirados para a análise da peroxidação lipídica (níveis de espécies reativas ao ácido tiobarbitúrico TBARS), das defesas antioxidantes enzimáticas (atividade das enzimas superóxido dismutase (SOD), catalase (CAT), glutationa redutase (GR), glutationa peroxidase (GPx) e glutationa S-transferase (GST)), das defesas antioxidantes não-enzimáticas (níveis de tióis não-protéicos (SHNP) e ácido ascórbico) e da atividade da δ-aminolevulinato desidratase (δ-ALA-D). Os animais foram pesados diariamente, antes de cada exposição. O peso dos animais não alterou após a exposição à fumaça do cigarro em nenhum grupo experimental, em nenhum dos protocolos. Nos P1 e P2, os animais que foram expostos à fumaça do cigarro apresentaram um aumento da peroxidação lipídica no pulmão. Entretanto no cérebro, o aumento no TBARS foi verificado apenas no P2. Em relação às defesas antioxidantes não-enzimáticas, foi observado uma redução nos níveis dos parâmetros estudados nos animais expostos ao P1 e P2. Enquanto no cérebro, a exposição ao P1 aumentou os níveis de ácido ascórbico e a exposição ao P2 reduziu os níveis de SHNP e de ácido ascórbico. Quanto às defesas antioxidantes enzimáticas, elas alteraram no pulmão apenas no P2. No cérebro, a atividade da CAT reduziu após a exposição ao P1, e a exposição ao P2 reduziu a atividade da CAT e da SOD. A atividade da δ-ALA-D foi alterada no P1 no pulmão e no P2 no cérebro. O tratamento com (PhSe)2 restaurou os danos causados pela exposição passiva à fumaça do cigarro nos pulmões e cérebro dos ratos jovens. Além disso, os níveis de SHNP, o conteúdo de ácido ascórbico e a atividade da GST apresentaram um aumento per se nos pulmões dos animais tratados com (PhSe)2. Para estudar o mecanismo pelo qual o (PhSe)2 apresentou efeito antioxidante, verificou-se o efeito mimético in vitro deste composto orgânico de selênio (1 - 50μM) na atividade das enzimas dehidroascobato (DHA) redutase e GST. O (PhSe)2 a partir da concentração de 5μM apresentou efeito mimético da atividade destas enzimas. Além disso, estudou-se o efeito do (PhSe)2 (10 - 50μM) como scavenger dos radicais 1,1-difenil-2-picril-hidrazil (DPPH ) e 2,2 -azino-bis(3-etilbenztiazolina-6-ácido sulfônico) (ABTS +), e na proteção da auto-oxidação do Fe2+. Entretanto, o composto não apresentou efeito scavenger, nem protegeu da auto-oxidação do Fe2+, descartando que esses mecanismos estariam envolvidos na ação antioxidante do composto. O envolvimento na síntese da glutationa (GSH) também foi estudado na tentativa de explicar os mecanismos pelos quais o (PhSe)2 apresenta efeito antioxidante. Para isso, foi utilizado a butionina sulfoximina (BSO), uma substância que inibe a γ-glutamilcisteína sintetase, uma enzima envolvida na síntese da GSH. Verificou-se que o BSO bloqueou o efeito protetor do (PhSe)2 na redução dos níveis de SHNP provocada pela exposição passiva à fumaça do cigarro no pulmão e fígado de ratos jovens. Com o presente trabalho conclui-se que o (PhSe)2 apresenta efeito antioxidante por diferentes mecanismos. A ação do (PhSe)2 em aumentar os níveis de SHNP, ácido ascórbico e a atividade da GST é um dos mecanismos do efeito antioxidante deste composto. O (PhSe)2 apresentou atividade DHA redutase e GST-like, demonstrando um novo mecanismo do efeito antioxidante do composto. Além disso, a síntese da GSH está envolvida no efeito antioxidante do (PhSe)2, uma vez que, bloqueando a síntese da GSH, ocorre um bloqueio no efeito antioxidante do composto.