The purpose of this study is to assess whether or not enforcement of the Minors and Tobacco Laws in the form of a citation had an impact on the knowledge, attitudes, practices and policies of over-the-counter tobacco retailers in Oregon. Demographic factors, such as store type, store size, ownership type, and location of the store that may contribute to the retailers response to receiving a citation for selling tobacco to a minor, were examined. The study examines two randomly selected groups of over-the-counter tobacco retailers in Oregon. The treatment group received a citation selling tobacco products to a minor while the control did not. A mail survey was sent to retailers selected for the study. The survey instrument measured the characteristics in each group, representing knowledge, attitudes, practices, and policies relating to the Oregon Minors and Tobacco Laws. The unit of analysis was owners or managers of retail stores. Cross-tabulation and a chi-square test statistic was used to assess and determine if there was a significant association between selected variables. Multiple regression was employed to determine if there is a relationship between composite dependent variables representing retailers' attitudes and practices and several demographic variables. Stores that had received a citation were more vigilant in compliance practices and perceptions than stores that had not received a compliance check and citation. Retailers' believe that both negative and positive strategies are necessary to achieve retailer compliance, retailers need more educational materials for training employees, and that a training video and a device to help clerks calculate the age on a minors ID would be useful. Retailers in both groups opposed the licensing of retailers to sell tobacco. Owners and owner operated stores in country settings were found to be resistant to policies aimed at reducing minors' access to tobacco products. / Graduation date: 1997

Smoking in youth continues to be an important public health issue. Because adolescence is the key period for smoking initiation, prevention efforts need to take place before the adolescent years. Little is known about parental smoking prevention interventions. The purpose of this study, therefore, was to understand parental approach to the topic of smoking with school-age pre-adolescent children within the context of local policies and programs concerning smoking. The study was carried out using the grounded theory method of Strauss and Corbin (1998). The sample was purposive and consisted of 38 parents who had at least one child ranging in age from 5 to 12 years and 9 professionals whose work involved youths or smoking prevention. Data consisted of interviews with the parents and professionals and information obtained about smoking-specific public policies and programs that were relevant locally. The data from the parents were analyzed to construct a theory and from the professionals to generate themes. The findings represent a substantive theory that explains how parents communicated with their children about smoking. Parents perceived smoking to be a latent danger for their children. That meaning was shaped by their knowledge of the health effects of smoking and their knowledge of the nature of youth smoking. They did not want their children to smoke and to deter it they communicated with them by taking action in the form of having a no-smoking rule and verbally interacting on the topic. Their verbal interaction consisted of discussing smoking with their children by intentionally taking advantage of opportunities, telling their children about the health effects of smoking and their opposition to it by responding on the spur-of-the-moment if their attention was drawn to the issue by external cues, or acknowledging to their children the negative effects of smoking by responding only when their children brought it up. Their action and verbal interaction produced outcomes for them in the form of feelings and thoughts. The study has implications for further theory development and research. The understanding gained from the theory may be used in practice to guide interventions with parents about child smoking prevention.

Concern is mounting over the increase in prevalence and severity of overweight and obesity in children worldwide. Intrauterine life has been identified as a critical period for the development of overweight or obesity and other related chronic diseases. Prenatal exposure to maternal cigarette smoke (PEMCS) has consistently emerged as an important risk factor for excess weight in the offspring and is a targetable behaviour for prevention strategies. This study examines first the relationship between PEMCS and overweight status of children at 10 years of age and second, whether PEMCS is associated with distinct longitudinal BMI trajectories. Analyses include multivariate and multinomial logistic regression and longitudinal group based modeling methods. PEMCS was found to be a significant risk factor for overweight in children independent of birth weight and catch-up growth. However, PEMCS was not associated with BMI trajectory membership. Our results lend support to the paradigm of in-utero excess weight prevention.

Objective: To explore the role of interprofessional collaboration in the delivery of team-based tobacco dependence treatments within primary care. Methods: A narrative review of the literature was completed to examine FHT team functioning in Ontario, followed by a single, multi-site qualitative exploratory case study. Results: Interprofessional collaboration contributed to changes in tobacco dependence treatment through the initiation of system-wide change, cultivation of collective action, and supporting enhanced quality of smoking cessation care. Conclusion: Interprofessional collaboration can enhance the comprehensive delivery of evidence-based treatments for individuals trying to quit smoking. Supportive public policy, education for patients and providers, and evaluation research is needed to advance FHT functioning.

Purpose: The purpose of this research program was three-fold. First it aimed to determine the effectiveness of smoking cessation interventions in increasing cessation rates in smokers with cerebrovascular disease and whether smoking cessation reduces stroke recurrence. Second it aimed to determine the prognostic influence of smoking and its association with stroke severity, disability, length of stay in hospital and mortality. Third it aimed to identify multi-level correlates of smoking cessation in Canadians who reported stroke symptoms in a large population based survey. Methods: Two systematic reviews and meta-analyses were performed to achieve the first objective. For the second objective, a retrospective cohort study was undertaken using variables from the Registry of the Canadian Stroke Network. Finally, the third objective was achieved by analyzing respondents from the Canadian Community Health Survey. Results: There is a paucity of intervention studies examining the effectiveness of smoking cessation in smokers with cerebrovascular disease. Most intervention studies that were found, failed to employ evidence-based approaches to smoking cessation. No evidence was found in regards to the effect of smoking cessation on stroke recurrence. We found smokers had strokes at a younger age compared to non-smokers. We found that in transient ischemic attacks and intracerbral haemorrhage, smoking was a significant predictor of stroke severity, disability, length of stay in hospital and 1 year mortality. Correlates of smoking cessation among Canadians who have experienced symptoms of a stroke included: higher education and income, implementation of household and vehicle smoking restrictions, access to a general practitioner and the use of smoking cessation pharmacotherapies and counselling support. Co-morbidities such as depression and alcohol consumption reduced the likelihood of successful cessation. Conclusions: This three-phase research program elucidated the gaps in intervention research for this population along with co-morbidities that hinder success in cessation. Smoking negatively impacted outcomes such as disability, hospital length of stay and mortality in patients with transient ischemic attacks and intracerebral haemorrhage strokes. Future interventions should take into account modifiable smoking cessation correlates in order to increase cessation rates in smokers with cerebrovascular disease.

Smoking patterns were described and compared retrospectively for 5395 participants in the Lung Health Study at 12 and 24 months. 3592 participants were assigned to a special intervention (SI) group that received a counseling assisted smoking cessation intervention that included nicotine gum and 1803 participants were assigned to a usual care (UC) group that received no assistance in quitting smoking. Participants were smokers diagnosed with mild to moderate chronic obstructive pulmonary disease (COPD) and averaged 31.4 cigarettes/day at entry. Significant differences were found regarding smoking outcomes and smoking patterns between groups as well as within each group. Counseling assisted participant's continuous abstinence rate at 24 months was 25.1% compared to 3.5% for unassisted smokers. Counseling assisted men were more successful at remaining abstinent at 24 months (27.1%) compared to (21.8%) for counseling assisted women. No gender differences were found for unassisted smokers. Abstinence rates were biochemically validated. Differences were also found in smoking patterns between groups for those unable to achieve continuous abstinence at 24 months. Counseling assisted participants smoked fewer cigarettes, made more quit attempts, smoked fewer months and stayed quit longer. Mixed results were found for baseline demographic and smoking history variables. Age started smoking, other smokers in the household, education and social support were not significant. Cigarettes smoked per day, previous quit attempts, longest period quit and alcoholic drinks per week were significant. / Graduation date: 1992

Background: Schizophrenia is associated with deficits in decision-making. Aim: To determine the effects of smoking status on delay discounting in schizophrenia in comparison to non-psychiatric controls. Method: Cross-sectional comparison of delay discounting across smoking and psychiatric status. Hypotheses: Individuals with schizophrenia were hypothesized to have higher rates of delay discounting than controls; Non-smokers with schizophrenia would have higher rates of delay discounting than smokers. Control smokers would discount future rewards more than non-smokers. Results: No significant differences in delay discounting were observed between psychiatric groups. Smokers with schizophrenia exhibited more delay discounting than non-smokers. Within the psychiatric group, former smokers discount rates were similar to current smokers. Conclusion: Delay discounting deficits in schizophrenia and modulation by cigarette smoking were not supported; our pattern of results in schizophrenia does suggest that deficits in delay discounting in these patients appears to be a trait rather than a state-dependent phenomenon.

The enzyme CYP2D6 can metabolize many centrally acting drugs and endogenous neural compounds (e.g. catecholamines); it can also inactivate neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1,2,3,4-tetrahydroisoquinoline (TIQ) and β-carbolines that have been associated with Parkinson’s disease (PD). CYP2D6 is ideally situated in the brain to inactivate these neurotoxins. The CYP2D6 gene is also highly polymorphic, which leads to large variation in substrate metabolism. Furthermore, CYP2D6 genetically poor metabolizers are known to be at higher risk for developing PD, a risk that increases with exposure to pesticides. Conversely, smokers have a reduced risk for PD and smokers are suggested to have higher brain CYP2D6 levels. Our studies furthered the characterization and involvement of CYP2D6 in neuroprotection against PD. METHODS: We investigated the effects of CYP2D6 inhibition on MPP+-induced cell death in SH-SHY5Y human neuroblastoma cells. We compared levels of brain CYP2D6, measured by western blotting, between human smokers and non-smokers, between African Green monkeys treated with saline or nicotine, and between PD cases and controls. In addition, we assessed changes in human brain CYP2D6 expression with age. RESULTS: Blocking CYP2D6 activity in SH-SY5Y cells with four diverse inhibitors significantly increased MPP+-induced neurotoxicity. Smokers have higher brain CYP2D6 compared to non-smokers. In monkeys, basal expression of CYP2D6 varied across brain regions and was increased by chronic nicotine treatment in select regions (notably the basal ganglia) and specific cell types. Expression of human brain CYP2D6 increased from fetal to 80 years of age in the frontal cortex; the influence of age on CYP2D6 expression was brain region specific. Compared to age-matched controls, PD cases had ~40% lower CYP2D6 levels in the frontal cortex, cerebellum and hippocampus consistent with lower CYP2D6 increasing the risk for PD. In the caudate and substantia nigra, CYP2D6 levels were similar between PD case and controls using Western blotting. This is likely due to the increase in CYP2D6-expressing astrocytes and much higher cellular CYP2D6 in PD affected areas as observed with immunocytochemical staining. CONCLUSIONS: Brain CYP2D6 can meaningfully inactivate neurotoxins, and it can be increased by nicotine in brain regions of interest to PD. These findings support the contention that higher brain CYP2D6 is protective and lower levels may contribute to increased risk for PD.

Background: Schizophrenia is associated with deficits in decision-making. Aim: To determine the effects of smoking status on delay discounting in schizophrenia in comparison to non-psychiatric controls. Method: Cross-sectional comparison of delay discounting across smoking and psychiatric status. Hypotheses: Individuals with schizophrenia were hypothesized to have higher rates of delay discounting than controls; Non-smokers with schizophrenia would have higher rates of delay discounting than smokers. Control smokers would discount future rewards more than non-smokers. Results: No significant differences in delay discounting were observed between psychiatric groups. Smokers with schizophrenia exhibited more delay discounting than non-smokers. Within the psychiatric group, former smokers discount rates were similar to current smokers. Conclusion: Delay discounting deficits in schizophrenia and modulation by cigarette smoking were not supported; our pattern of results in schizophrenia does suggest that deficits in delay discounting in these patients appears to be a trait rather than a state-dependent phenomenon.

The enzyme CYP2D6 can metabolize many centrally acting drugs and endogenous neural compounds (e.g. catecholamines); it can also inactivate neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1,2,3,4-tetrahydroisoquinoline (TIQ) and β-carbolines that have been associated with Parkinson’s disease (PD). CYP2D6 is ideally situated in the brain to inactivate these neurotoxins. The CYP2D6 gene is also highly polymorphic, which leads to large variation in substrate metabolism. Furthermore, CYP2D6 genetically poor metabolizers are known to be at higher risk for developing PD, a risk that increases with exposure to pesticides. Conversely, smokers have a reduced risk for PD and smokers are suggested to have higher brain CYP2D6 levels. Our studies furthered the characterization and involvement of CYP2D6 in neuroprotection against PD. METHODS: We investigated the effects of CYP2D6 inhibition on MPP+-induced cell death in SH-SHY5Y human neuroblastoma cells. We compared levels of brain CYP2D6, measured by western blotting, between human smokers and non-smokers, between African Green monkeys treated with saline or nicotine, and between PD cases and controls. In addition, we assessed changes in human brain CYP2D6 expression with age. RESULTS: Blocking CYP2D6 activity in SH-SY5Y cells with four diverse inhibitors significantly increased MPP+-induced neurotoxicity. Smokers have higher brain CYP2D6 compared to non-smokers. In monkeys, basal expression of CYP2D6 varied across brain regions and was increased by chronic nicotine treatment in select regions (notably the basal ganglia) and specific cell types. Expression of human brain CYP2D6 increased from fetal to 80 years of age in the frontal cortex; the influence of age on CYP2D6 expression was brain region specific. Compared to age-matched controls, PD cases had ~40% lower CYP2D6 levels in the frontal cortex, cerebellum and hippocampus consistent with lower CYP2D6 increasing the risk for PD. In the caudate and substantia nigra, CYP2D6 levels were similar between PD case and controls using Western blotting. This is likely due to the increase in CYP2D6-expressing astrocytes and much higher cellular CYP2D6 in PD affected areas as observed with immunocytochemical staining. CONCLUSIONS: Brain CYP2D6 can meaningfully inactivate neurotoxins, and it can be increased by nicotine in brain regions of interest to PD. These findings support the contention that higher brain CYP2D6 is protective and lower levels may contribute to increased risk for PD.