Dissertations / Theses on the topic 'Childhood smoking'

This study explores how young people conceptualise addiction to smoking and, also the relationship between young people's addiction beliefs and intentions to smoke cigarettes. Addiction to smoking is a major health problem, not just for adults, but also for young smokers, up to 60% of whom are dependent on nicotine. However, anti-smoking prevention efforts targeted at young people generally emphasise ill-health effects and little attention is paid to addiction education which is generally considered relevant only to adult smoking and cessation efforts. Perhaps as a consequence, young people appear to have many misconceptions and unrealistic ideas about addiction, and these may possibly have influenced initial decisions to take up smoking. For example, between 50% and 60% of young smokers believe that it would be easy or very easy to stop smoking altogether if and when they choose to and the majority of daily smokers mistakenly believe that they will not be smoking for more than five years. For these young smokers, becoming addicted is often an unforeseen consequence and most are surprised to find that they cannot give up smoking as easily as they thought. The majority of addicted smokers regret ever taking up smoking but nevertheless continue to smoke cigarettes for perhaps 30 to 40 years because they find it very difficult to stop. This backdrop provides the impetus for the present study.

This study explores how young people conceptualise addiction to smoking and, also the relationship between young people's addiction beliefs and intentions to smoke cigarettes. Addiction to smoking is a major health problem, not just for adults, but also for young smokers, up to 60% of whom are dependent on nicotine. However, anti-smoking prevention efforts targeted at young people generally emphasise ill-health effects and little attention is paid to addiction education which is generally considered relevant only to adult smoking and cessation efforts. Perhaps as a consequence, young people appear to have many misconceptions and unrealistic ideas about addiction, and these may possibly have influenced initial decisions to take up smoking. For example, between 50% and 60% of young smokers believe that it would be easy or very easy to stop smoking altogether if and when they choose to and the majority of daily smokers mistakenly believe that they will not be smoking for more than five years. For these young smokers, becoming addicted is often an unforeseen consequence and most are surprised to find that they cannot give up smoking as easily as they thought. The majority of addicted smokers regret ever taking up smoking but nevertheless continue to smoke cigarettes for perhaps 30 to 40 years because they find it very difficult to stop. This backdrop provides the impetus for the present study.

While research has indicated that impaired mental health partially mediates the relationship between adverse childhood experiences (ACEs) and alcohol and illicit drug use, little research has examined potential mediators in the relationship between ACEs and smoking, the number one cause of preventable mortality in the United States. Accordingly, this study examined the potential mediating effect of psychological distress on the relationship between ACES and smoking using data from Wave II of the ACE Study, a cross-sectional study completed between June and October of 1997 on a sample of adult health maintenance organization members (N = 7,211). The theoretical underpinnings for this study were grounded in the developmental psychopathological perspective which examines both environmental and biological influences as they interact to promote or impede social, emotional, and behavioral development. Mediation modeling employing both linear and logistic regression techniques indicated that, after adjusting by select covariates, psychological distress (as assessed using the SF-36 Mental Component Summary score) partially mediated the relationship between several of the ACEs examined and smoking in women. These same relationships were not found in men. This research contains several key findings with social change implications. First, additional research should be conducted to examine the causes, developmental paths, and critical points that link ACEs and psychological distress to smoking among women. Second, given the gender differences in the association between ACEs and smoking, gender-specific intervention programs that build resiliency, increase positive social support, and provide tools for developing alternative coping strategies may be important adjuncts to smoking cessation programs, particularly for women with a history of ACEs.

Background A significant proportion of children are exposed to environmental tobacco smoke (ETS) throughout the world. This is mainly because of exposure to parental smoking. It is unknown to what extent the negative effects of ETS on respiratory symptoms track from childhood into adulthood. Methods TESAOD (Tucson Epidemiologic Study of Airway Obstructive Disease) is a large population-based prospective study that was initiated in 1972. Participants were followed prospectively with questionnaires and pulmonary function tests (PFTs) completed about every two years in 12 follow-up surveys up to 1996. Skin prick tests and blood samples for IgE measurements were collected at surveys 1, 6, and 11. We identified subjects who entered the study as children (<15 years old) and were followed to adulthood (>18 years) during the study follow-up. Based on questionnaire data, active asthma, wheeze, cough, and chronic cough (cough for three consecutive months) were coded as never (never reported in childhood or adulthood), incident (never reported in childhood, but ≥ one positive report in adulthood), remittent (≥ one positive report in childhood, but not in adulthood), and persistent (≥ one positive report both in childhood and adulthood). PFTs measurements included forced expiratory volume in 1 second, forced vital capacity, and forced expiratory flow at 25-75%. Parent information on smoking status was collected simultaneously at child visits. ETS exposure status was assessed as “ever” or “never” between birth and 15 years. Results Information on parental ETS exposure in childhood and outcomes in adulthood was available for 444 non-Hispanic white participants (51.4% male) with mean age at initial survey of 7.7 years. Total mean follow-up time was 19.0 years (8.8 years in adulthood). Between birth and 15 years, 53.4% of children were exposed to ETS. After adjusting for sex, age at enrollment, years of follow-up, and personal smoking status (assessed at age 15 and above), combined parental ETS exposure in childhood was significantly associated with persistent wheeze (RR(adj) 1.9, p=0.026), persistent cough (RR(adj) 5.9, p<0.001), and persistent (RR(adj) 3.7, p=0.030) and incident chronic cough (RR(adj) 2.3, p=0.040). Paternal ETS exposure in childhood was associated with persistent wheeze (RR(adj) 2.3, p=0.002), persistent cough (RR(adj) 3.9, p<0.001), persistent (RR(adj) 4.8, p=0.004) and incident chronic cough (RR(adj) 2.2, p=0.031), and persistent asthma (RR(adj) 2.3, p=0.016). Maternal ETS exposure was associated with persistent (RR(adj) 1.9, p=0.029) and incident cough (RR(adj) 2.5, p=0.006). Maternal ETS exposure was associated with an increased percent predicted FVC in adulthood (coefficient, 3.75; p=0.019). No other effects on lung function were seen. There were no effects of ETS exposure on total serum IgE or allergic sensitization. ETS exposure was associated with respiratory symptoms in adulthood among both never and current smokers. Conclusions ETS exposure in childhood has long term health effects on lung function and respiratory symptoms. These effects do not appear to be IgE-mediated. ETS exposure, especially paternal ETS exposure, seems to influence the persistence of respiratory symptoms from childhood to adulthood and to affect women more than men. These effects are independent of personal smoking and also seen in never smokers. Both smoking mothers and fathers should be targeted when attempting to reduce ETS exposure among children.

Background and objectives: Childhood sexual abuse (CSA) is a substantial public health and human rights problem, as well as a growing concern in sub-Saharan Africa (SSA). It has both short and long term effects on girls: physical and psychological, including negative sexual outcomes. Up to one-third of adolescent girls report their first sexual experience as being forced. Despite growing evidence supporting a link between contextual factors and violence, no studies have investigated the connection between CSA and contextual factors. It is therefore important to identify the extent of CSA and understand factors associated with it in SSA in order to develop interventions aimed to address the scale of the problem. Aim: The overall aim of this thesis is to assess the individual and contextual factors associated with CSA. In addition, the thesis aims to quantify the magnitude of CSA and describe the factors associated with CSA among women from SSA (Study I). This thesis also examines the independent contribution of individual and community socio-economic status on CSA (Study II). Moreover, it scrutinises the effect of social disorganisation on CSA (Study III) and explores the relationship between CSA and sexual risk behaviours as well as potential mediators (Study IV). Methods: This thesis used the Demographic and Health Survey (DHS) datasets conducted between 2006 and 2008 from six SSA countries. The thesis used multiple logistic regression models to describe and explore factors associated with CSA among 69,977 women (Study I).  It used multivariable multilevel logistic regression analysis to explore the effect of contextual level variables (neighbourhood socio-economic status) on CSA among 6,351 girls (Study II). Neighbourhood socio-economic status was operationalized with a principal component analysis using the proportion of respondents who were unemployed, illiterates, living below poverty level and rural residents. Study III applied multivariable multilevel logistic regression analysis on 6,351 girls and considered five measures of social disorganisation at the community level: neighbourhood poverty, female-headed households, residential mobility, place of residence, population density, and ethnic diversity. In study IV, 12,800 women from the Nigerian DHS were used. Structural equation modelling was applied using a two-step approach. The first step used a confirmatory factor analysis to develop an acceptable measurement model while the second step involved modifying the measurement model to represent the postulated causal model framework. Results: In study I, the reported prevalence of CSA ranged from 0.3% in Liberia to 4.3% in Zambia when the prevalence was based on all respondents aged between 15 and 49 years and who were present during the survey. None of the socio-economic factors were associated with CSA. In study II, where the data was restricted to permanent residents aged between 15 and 18 years, the prevalence ranged between 1.04% in Liberia to 5.8% in Zambia. At the individual level, there was no significant association between CSA and wealth status while at the community level, there was no significant association between CSA and socio-economic position. However, 22% of the variation in CSA was attributed to the community level factors. In study III, there was significant variation in the odds of reporting CSA across the communities, with community level factors accounting for 18% of the variation. In addition, respondents from communities with a high family disruption rate were 57% more likely to have reported sexual abuse in childhood. Study IV showed that there was a significant association between CSA and sexual risk behaviours and the association was mediated by alcohol and cigarette use. Conclusions: The study provides evidence that adolescents in the same community were subjected to common contextual influences. It also highlighted the significance of mediators in the relationship between CSA and sexual risk behaviours. It is therefore important that effective preventive strategies are developed and implemented that will cut across all socio-economic spheres in a context that both permits and encourages disclosure as well as identifying predisposing circumstances for recurrence.

Le but de cette thèse était d’analyser les associations entre plusieurs facteurs environnementaux (consommations maternelles de tabac, d’alcool et de boissons caféinées pendant la grossesse) et médicaux (antécédents d’asthme ou d’eczéma) et les leucémies aiguës de l’enfant, et d’étudier des polymorphismes génétiques susceptibles de modifier ces associations. Les analyses ont été réalisées à partir de l’étude cas-témoins nationale ESCALE réalisée en population générale en 2003 et 2004. Les données sur les antécédents médicaux et les consommations maternelles pendant la grossesse ont été recueillies au cours d’un entretien téléphonique standardisé des mères. Les polymorphismes génétiques d’intérêt ont été sélectionnés suivant une approche candidate sur leur fonctionnalité, dans des gènes impliqués dans le métabolisme du tabac (CYP1A1*2, CYP2E1*5, NQO1*2, EPHX1 et NAT2*5), de l’alcool (CYP2E1*5, ADH1C*2) et de la caféine (NAT2*5), et dans l’allergie (IL4, IL4R, IL10 et IL13). Les données génétiques ont été obtenues à partir de prélèvements de sang chez les cas et de salive chez les témoins, par génotypage de 370 000 SNPs chez les cas et sur puce à façon de 4 500 SNPs chez les témoins, complété par des imputations génotypiques lorsque les polymorphismes candidats n’étaient pas disponibles au génotypage. Au total, les données étaient disponibles pour 493 cas de leucémie aiguë et 442 témoins d’origine européenne.La consommation maternelle de café pendant la grossesse était positivement associée aux leucémies aiguës de l’enfant dans cette étude. Aucune association significative n’était observée avec le tabagisme maternel ou la consommation d’alcool pendant la grossesse. La présence de deux allèles NAT2*5 était associée aux leucémies aiguës lymphoblastiques (Odds Ratio OR=1.9 [1.3-2.7]), mais les analyses ne montraient pas d’association avec les autres polymorphismes des enzymes du métabolisme. Aucune interaction significative n’a été observée entre les polymorphismes candidats et le tabagisme maternel ou les consommations d’alcool ou de boissons caféinées pendant la grossesse. Cependant, les allèles candidats de CYP2E1, NQO1 et EPHX1, trois enzymes impliquées dans le métabolisme du benzène, semblaient interagir entre eux.Les allèles variants dans les gènes IL13, IL4, IL10 et IL4R n’étaient pas associés au risque de leucémie de l’enfant. Les antécédents d’asthme ou d’eczéma étaient plus fréquemment retrouvés chez les témoins que chez les cas (OR=0.7 [0.6-0.9]). Cette association inverse était essentiellement retrouvée chez les enfants porteurs d’un haplotype variant régulant l’expression de l’IL10 (p interaction=0.08) et porteurs de deux allèles de référence pour IL13-rs20541 (p interaction=0.06).En conclusion, ces résultats suggèrent un rôle de la consommation de café dans le risque de leucémie, déjà observé dans la précédente étude de l’équipe, qui devra être répliqué et approfondi. En revanche, aucune association n’a été observée avec la consommation maternelle de tabac ou d’alcool, même en tenant compte des polymorphismes génétiques candidats. L’interaction gène-gène des trois enzymes impliquées dans le métabolisme du benzène est intéressante et devra être explorée dans d’autres études. Enfin, l’association inverse entre le risque de leucémie aiguë et les antécédents d’asthme ou d’eczéma semble limitée aux enfants porteurs de certains polymorphismes des interleukines IL10 et IL13, ce qui pourrait refléter des mécanismes biologiques sous-jacents. Ces hypothèses pourront être testées d’autres études, et en particulier dans l’étude ESTELLE, récemment réalisée par l’équipe
The aim of this thesis was to analyze the associations between several environmental (maternal consumption of tobacco, alcohol or caffeinated drinks during pregnancy) and medical (history of asthma or eczema) factors and childhood acute leukemia, and to study genetic polymorphisms suspected to modify those associations.The analyses were performed using data from the national population-based case-control ESCALE study conducted in 2003 and 2004. Information about medical history and maternal consumptions during pregnancy was obtained through a standardized telephone interview with the mothers. The genetic polymorphisms were selected using a candidate approach based on their functionality, in genes involved in the metabolism of tobacco (CYP1A1*2, CYP2E1*5, NQO1*2, EPHX1 and NAT2*5), alcohol (CYP2E1*5, ADH1C*2) or caffeine (NAT2*5), and in allergy (IL4, IL4R, IL10 and IL13). Biological samples consisting of blood for cases and saliva for controls allowed for the genotyping of 370,000 SNPs in the cases and 4,500 SNPs in the controls. Where the candidate polymorphisms were not available from the genotyping, genotypic imputation was used to infer those. In total, data was available for 493 acute leukemia cases and 442 controls of European origin. Maternal coffee drinking during pregnancy and, to a lesser extent, cola soda drinking, was positively associated with childhood leukemia in the ESCALE study. No significant association was observed with maternal smoking or alcohol consumption during pregnancy. Carrying two NAT2*5 alleles was associated with acute lymphoblastic leukemia (Odds Ratio OR=1.9 [1.3-2.7]), although the analyses showed no association with the other candidate alleles involved in metabolism. There was no significant interaction between the candidate genetic polymorphisms and maternal consumptions of tobacco, alcohol or caffeinated drinks during pregnancy. However, the candidate alleles of CYP2E1, NQO1 and EPHX1, three enzymes involved in benzene metabolism, seemed to interact together.The variant alleles in IL13, IL4, IL10 and IL4R genes were not associated with childhood leukemia. A history of asthma or eczema was more frequently reported in controls than in cases (OR=0.7 [0.6-0.9]). This inverse association was mostly observed in children carrying a variant haplotype regulating the expression of IL10 (p for interaction=0.08), and carrying two reference alleles for IL13-rs20541 (p for interaction=0.06).As a conclusion, these results suggest a role of maternal coffee drinking during pregnancy in childhood leukemia that had already been reported in a previous French study of the same research team, and needing in-depth study and replication. However, no association was observed with maternal smoking or alcohol drinking, even after taking into account the candidate genetic polymorphisms. The gene-gene interaction of the three enzymes involved in benzene metabolism is interesting and needs to be investigated in other studies. Finally, the inverse association between childhood acute leukemia risk and medical history of asthma or eczema seems to be limited to the children with specific polymorphisms of interleukins IL10 and IL13, which could reflect underlying biological mechanisms. Those hypotheses should be further tested in other studies, such as the ESTELLE study, that has been recently conducted by the team

The effects of household exposure to cigarette smoke on the incidence of respiratory illness were examined among 1007 18 month old children at Lu-wan District, Shanghai City, People's Republic China. The passive smoking quantity was estimated by summing the total daily cigarette consumption of family members. No mothers who smoked were found. A significant dose-response relationship of passive smoking to hospitalization for respiratory illness during the children's first 18 months of life was found, for which no confounding factors were discovered. The relative risk was 2.4 for children living in families including people who smoked 20 or more cigarettes a day compared with those living in nonsmoking families. The children who were boys or artificially (bottle) fed were more affected than those who were girls or breast fed. The cumulative incidence of bronchitis and pneumonia increased significantly with increasing cigarette smoking of family members, that did not change when sex, birth weight, type of feeding, coal for cooking, or parental education were taken into account. Family smoking status was not found to be significantly associated with the cumulative incidence of asthma, whooping cough, sinusitis or measles.
Graduation date: 1993

Trajectoires développementales de l’IMC durant l’enfance: Une étude longitudinale sur 8 ans. Introduction : L’obésité infantile, origine de nombreux problèmes de santé, représente un grand défi en santé publique. Récemment, l’importance d’étudier l’évolution du surpoids durant l’enfance ainsi que les facteurs de risques précoces pour l’obésité a été reconnue. Les trajectoires développementales d’indice de masse corporelle (IMC) chez les jeunes représentent une approche innovatrice qui nous permet de mieux comprendre cette problématique importante. Objectifs: 1) Identifier des trajectoires développementales distinctes de groupes d’enfants selon leur IMC durant l’enfance, et 2) Explorer les facteurs de risques précoces qui prédisent l’appartenance de l’enfant à la trajectoire d’IMC le plus élevé Hypothèses: 1) On s’attend à retrouver un groupe d’enfants qui suit une trajectoire d’IMC élevée durant l’enfance. 2) On s’attend à ce que certaines caractéristiques de la mère (ex : tabac pendant la grossesse et IMC élevé), soient associées à l’appartenance de l’enfant au groupe ayant la trajectoire «IMC élevé ». Méthodes: Estimation des trajectoires développementales d’IMC d’enfants, dans un échantillon populationnel (n=1957) au Québec (ELDEQ). Les IMC ont été calculés à partir de données fournies par les mères des enfants et recueillis chaque année sur une durée de 8 ans. Des données propres à l’enfant sa mère, ainsi que socioéconomiques, ont étés recueillies. Une régression logistique multinomiale a été utilisée pour distinguer les enfants avec un IMC élevé des autres enfants, selon les facteurs de risques précoces. Les programmes PROC TRAJ (extension de SAS), SPSS (version 16), et SAS (version 9.1.3) ont été utilisés pour ces analyses. Résultats: Trois trajectoires d’IMC ont étés identifiées : IMC « bas-stable » (54,5%), IMC « modéré » (41,0%) et IMC « élevé et en hausse » (4,5%). Le groupe « élevé et en hausse » incluait des enfants pour qui l’IMC à 8 ans dépassait la valeur limite pour l’obésité. Les analyses de régression logistique ont révélé que deux facteurs de risques maternels étaient significativement associés avec la trajectoire “en hausse” par rapport aux deux autres groupes : le tabac durant la grossesse et le surpoids maternel. Conclusions: Des risques d’obésité infantile peuvent êtres identifiés dès la grossesse. Des études d’intervention sont requises pour identifier la possibilité de réduire le risque d’obésité chez l’enfant en ciblant le tabac et le surpoids maternelle durant la grossesse. Mots clés: Indice de masse corporelle (IMC), obésité infantile, trajectoires développementales de groupe, facteurs de risque précoce, étude populationnelle, tabac pendant la grossesse, obésité maternelle.
Developmental Trajectories of Body Mass Index in Early Childhood: An 8-Year Longitudinal Study. Introduction: Childhood obesity has become one of the greatest Public Health challenges this century, affecting not only developed nations, but increasingly low- and middle-income countries as well. Estimating developmental trajectories of Body Mass Index (BMI) during early childhood represents an innovative approach towards a better understanding of the development of this health problem. Objective: To identify groups of children with distinct developmental trajectories of Body Mass Index (BMI) between the ages of five months and eight years, and to identify early-life risk factors that distinguish children in an atypically elevated BMI trajectory group. Methods: Group-based developmental trajectories of BMI were estimated from annual maternal assessments (5 months to 8 years) in a large population sample (n=1957). Measures of height and weight, as well as family and child characteristics were obtained yearly from mothers. Multivariate logistic regression was used to distinguish children with elevated BMI from other children, using pre and early post-natal risk factors. Results: Three trajectories of BMI were identified: low-stable BMI (54.5%), moderate BMI (41.0%) and high-rising BMI (4.5%). The high-rising group included children whose BMI, at eight years of age, exceeded the cut-off value for obesity. Multinomial logit regression analyses revealed that two maternal risk factors were significantly associated with the high-rising BMI trajectory group as compared to both the low and moderate groups: smoking during pregnancy and maternal overweight. Conclusions: Antecedents of childhood obesity can be identified during pregnancy. Intervention studies are needed in order to test the possibility that targeting maternal smoking and maternal obesity during pregnancy would reduce the risk of childhood obesity in the offspring. Keywords: Body Mass Index (BMI), child obesity, Group-based developmental trajectories, early life predictors, population-based study, maternal smoking, maternal obesity.