Following the implementation of the smokefree law in 2006, which formed part of the Smoking, Health and Social Care (Scotland) Act 2005, smoking in enclosed public spaces has been prohibited in Scotland. The law has led to a number of improvements in public health but does not cover homes and cars where children are primarily exposed. Secondhand smoke (SHS) exposure is associated with particularly significant risks to child health, yet few studies have explored children’s perspectives on SHS and smoking in the home and car. Comprising a qualitative exploration of the views and experiences of 38, 10- to 15-year-olds of SHS in the home and car, this thesis begins to address this gap. It addresses the nature and extent of children’s involvement in negotiating smoking restrictions, compares the understandings, experiences and involvement among participants living in communities of contrasting socioeconomic profiles and considers the implications for health promotion interventions aimed at reducing children’s exposure to SHS in the home and car. Informed by a Childhood Studies perspective, the study focuses, both in methods and content, on the voices and agency of the participants. Recruited from two Edinburgh communities with contrasting socioeconomic profiles, the participants were interviewed either individually, in pairs or in small focus groups about their understandings of SHS, smoking restrictions in their homes and cars and their role in negotiating them. Home floor plans constructed by the participants were used to prompt discussion and also served to identify spatial and temporal home smoking restrictions. Both discursive and thematic techniques were used in analysis. The thesis details the participants’ overt and covert strategies to resist family members’ smoking, demonstrating the active roles that participants describe in their accounts. While acknowledging SHS as a health risk and using an embodied language of disgust to describe it, the participants’ main concern was for their smoking family members’ health, rather than their own. Many participants also challenged the stigma surrounding smoking parents by detailing the ways in which their parents restricted where, how much and with whom they smoked. Parents were described as especially careful in protecting small children from SHS. While most participants described such protective practices, those from the disadvantaged area reported less stringent smoking restrictions that were more challenging to negotiate. Participants’ resistant (to smoking) and defensive (of parents who smoke) accounts may stem from the growing stigma associated with smoking, particularly smoking in the presence of children. Such findings highlight the importance of a sensitive and asset based public health response that acknowledges parents’ attempts to protect their children from SHS and recognises the potential of the active role of children in family negotiations around smoking in the home and car.

The dangers of secondhand smoke (SHS) exposure on the human body were initially reported in 1972, just eight years after the negative effects of smoking on smokers was reported. The Surgeon General of the United States systematically expanded (and continues to expand) the warnings over time, as new scientific evidence becomes available. Warnings, which began to incorporate youths in 1975, emphasized the need to pay particular attention to fetuses, newborns, infants, children, adolescents, and young adults since they rely on parents, guardians, and other adults to keep them safe. Although fewer in number than adults, the diseases that are causally linked to smoking and exposure to SHS in youths are also complex and can result in death (i.e., sudden infant death syndrome). The introduction of new tobacco products, such as low nicotine cigarettes and electronic cigarettes, prompted the Surgeon General to release additional warnings. In 2016, the Surgeon General advised the nation that more information will become available as the electronic cigarette manufacturers comply with new Tobacco Control Act requirements to report harmful vapor constituents. Physicians need to keep abreast of the vast and growing body of knowledge related to the biological and chemical components of SHS and vapor, as well as the dangers that SHS and vapor cause. To ease the burden on physicians, the federal government and medical professional societies created clinical practice guidelines which summarize the literature related to the dangers of SHS and make recommendations for medical management. Guidelines recommend that physicians and other clinicians should offer smoking cessation advice and intervene to limit youth exposure to SHS. Although the approach recommended for use with patients in a physician’s office is clear and attempts to streamline the processes have been made, the identification and counseling process for smoking cessation and eliminating SHS exposure remains time consuming. Barriers to payment make it difficult for physicians to be adequately reimbursed for their efforts to keep their patients safe from the dangers of SHS and vapor exposure. More work is needed to be able to continue to reduce the percentage of youths exposed to SHS in their environments. Additional attention is needed to address the racial and ethnic disparities that are evident in the scientific literature.

No description available.

No description available.

The lungs represent one of the earliest interfaces for pathogens and noxious stimuli to interact with the body. As such, careful maintenance of the permeability barrier is vital in providing homeostasis within the lung. Essential to maintaining this barrier is the tight junction, which primarily acts as a paracellular seal and regulator of ionic transport, but also contributes to establishing cell polarity, cell-to-cell integrity, and regulating cell proliferation and differentiation. The loss of these tight junctions has been documented to result in alterations in inflammation, and ultimately the development of many respiratory disorders such as COPD, Asthma, ARDS, and pulmonary fibrosis. One critical contributor that creates this permeability barrier is the tight junctional protein Claudin. While studies have begun to elucidate the various functions and roles of various Claudins, our understanding is still limited. To initially investigate these proteins, we looked at both temporal and spatial expression patterns for family members during development. A consistent pattern was demonstrated in mRNA expression for the majority of Claudin members. In general, Claudin expression underwent rapid increase during time periods that correlate with the pseudoglanduar/canalicular periods. One notable exception was Claudin 6 (Cldn6), which demonstrated decreasing levels of mRNA expression throughout gestation. We also sought to understand expression dynamics during the addition of maternal secondhand smoke (SHS) which resulted in an almost universal decrease in Claudin proteins. To more fully explore expression mechanisms that affect Claudin-6 (Cldn6), we exposed pulmonary alveolar type II (A549) cells to cigarette smoke extract (CSE) and found that it transcriptionally regulated Cldn6 expression. Using a luciferase reporter, we determined that transcription was negatively regulated at multiple promoter response elements by CSE, and transcription was equally hindered by hypoxic conditions. These findings identified Cldn6 as a potential target of SHS and other respiratory irritants such as diesel particulate matter (DPM). We next sought to assess whether an increase in Cldn6 was sufficient to provide a protective advantage against harmful exogenous exposure. To test this, we utilized a doxycycline induced Cldn6 over-expressing mouse, and subjected it to SHS for 30 days to stimulate an inflammatory state. Our findings demonstrated that Cldn6 transgenic animals have decreased inflammation as evidence by decreased total cell infiltration into the airways, decreased polymorphonuclocyte (PMNs) extravasation, total protein in bronchoalveolar lavage fluid (BALF), and decreased cytokine secretion. Anti-inflammatory advantages were also discovered during experiments involving acute exposure to DPM. In both cases, while stimulation of transgenic mice with SHS or DPM diminished Cldn6 expression, anti-inflammatory evidence emerged suggesting that genetic up-regulation of Cldn6 likely causes the recruitment of other tight junctional components during an organism's response to environmental assault.

Introduction: The purpose of this study is to examine the change in smoking policy status among bars and restaurants since the Georgia Smokefree Air Act of 2005 was implemented and identify restaurant and bar characteristics that are associated with allowing smoking. Methods: Data was obtained from similar Georgia indoor air surveys conducted in 2006 and 2012. Both surveys were designed to gather information about restaurant and bar smoking policies and examine owner and manager perceptions of the Georgia Smokefree Air Act. Descriptive analysis and paired sample t-tests were performed to identify changes in smoking policy status and other variables over time. Chi-square and logistic regression analysis were used to test for significant associations between establishment smoking policy status and other characteristics. Results: The percent of restaurants and bars in Georgia allowing smoking nearly doubled from 9.2% in 2006 to 18.2% in 2012. The analysis showed a statistically significant increase in the percentage of establishments allowing smoking when minors are present. After adjusting for the effects of other variables, three variables were significant predictors of allowing smoking: having seats for drinking outdoors, having a liquor license, and generating greater than or equal to 25% of gross sales from alcohol. Conclusions: The Smokefree Air Act was enacted to protect the health and welfare of Georgia citizens, but the percentage of establishments allowing smoking has risen since it was implemented. These results suggest that policy makers should reevaluate the law and consider strengthening it to make restaurants and bars 100% smokefree without exemptions.

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)

No description available.

No description available.

Introduction: Multiple sclerosis (MS) is a chronic inflammatory disease which affects approximately 2.5 million people worldwide, including approximately 7,000 children. The etiology of MS is unclear, although researchers generally agree that both environmental and genetic factors are involved. It is also unclear why some patients may only have one demyelinating event (acquired demyelinating syndrome, or ADS) and others develop chronic demyelinating disease (MS). Recent evidence suggests an association between smoking and multiple sclerosis (MS) in adults. A question remains if there is a similar association between secondhand tobacco smoke exposure and MS in children. The purpose of this study is to explore the association between tobacco smoke exposure (TSE) and MS risk in a cohort of children with demyelinating disease. Methods: Data was obtained from the Canadian National Demyelinating Disease Study. This study included two disease groups, which are distinguished by a single (ADS) versus chronic demyelinating attacks (MS). Parents’ self-report of their child’s exposure to smoke in the home, as well as biomarker verification by serum cotinine, classified a child as exposed or not exposed. Logistic regression models were created to determine the association between TSE and the odds of MS compared to healthy controls, the odds of ADS compared to healthy controls, and the odds of MS compared to patients with ADS. In order to determine factors and exposures which distinguish MS from ADS, an assessment of interaction was performed to examine the relationship between TSE and MS risk genes, TSE and serum vitamin D levels, and TSE and prior Epstein Barr Virus exposure on the odds for developing MS compared to ADS patients.. Finally, serum cotinine levels were compared to neurologic functional scores in order to assess if a dose response mechanism exists creating impaired function for pediatric MS. Results: TSE was not significantly associated with increased odds for MS compared to healthy controls (OR= 1.84; 95%CI 0.86, 3.95) but was significantly associated with higher odds of monophasic ADS compared to healthy controls (OR=2.24; 95%CI 1.08, 4.63). TSE alone was not associated with increased odds for MS compared to ADS; however, the presence of both TSE and HLA alleles increased the odds for MS by 3.2 (95%CI 1.04, 9.79) when compared to ADS patients. An additive effect was also found between TSE and lower vitamin D, which together increased the odds for MS compared to patients with monophasic ADS (OR=2.89; 95%CI 1.21, 7.46). EBV was individually associated with MS compared to ADS (OR=4.12; 95%CI 1.62, 10.9) and odds for MS appeared to increase further with the addition of TSE (OR=5.13; 95%CI 1.79, 14.9), however sample size limited interpretation of the interaction analysis. TSE had minimal impact on neurological functional score measures, although long-term follow up with regard to exposure could not be properly assessed. Conclusion: Exposure to tobacco smoke through secondhand sources was not related to MS but TSE may increase the odds of monophasic demyelinating disease occurrence (ADS). The finding of additive effects between TSE and other disease modifying factors (HLA, vitamin D) may provide valuable insight into why some children have only one demyelinating attack (monophasic ADS) while others have multiple attacks and are diagnosed with MS. These effects should be further explored in a larger population of pediatric patients and compared to healthy children. Intervention methods should be tailored to help explain to parents the benefits of reducing their child’s exposures to environmental tobacco smoke. / Public Health