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.

Background: Tobacco smoke exposure (TSE) is unequivocally harmful to children's health, yet up to 48% of children who visit the pediatric emergency department (PED) and urgent care setting are exposed to tobacco smoke. The incorporation of clinical decision support systems (CDSS) into the electronic health records (EHR) of PED patients may improve the rates of screening and brief TSE intervention of caregivers and result in decreased TSE in children. Objective: We propose a study that will be the first to develop and evaluate the integration of a CDSS for Registered Nurses (RNs) into the EHR of pediatric patients to facilitate the identification of caregivers who smoke and the delivery of TSE interventions to caregivers in the urgent care setting. Methods: We will conduct a two-phase project to develop, refine, and integrate an evidence-based CDSS into the pediatric urgent care setting. RNs will provide input on program content, function, and design. In Phase I, we will develop a CDSS with prompts to: (1) ASK about child TSE and caregiver smoking, (2) use a software program, Research Electronic Data Capture (REDCap), to ADVISE caregivers to reduce their child's TSE via total smoking home and car bans and quitting smoking, and (3) ASSESS their interest in quitting and ASSIST caregivers to quit by directly connecting them to their choice of free cessation resources (eg, Quitline, SmokefreeTXT, or SmokefreeGOV) during the urgent care visit. We will create reports to provide feedback to RNs on their TSE counseling behaviors. In Phase II, we will conduct a 3-month feasibility trial to test the results of implementing our CDSS on changes in RNs' TSE-related behaviors, and child and caregiver outcomes. Results: This trial is currently underway with funding support from the National Institutes of Health/National Cancer Institute. We have completed Phase I. The CDSS has been developed with input from our advisory panel and RNs, and pilot tested. We are nearing completion of Phase II, in which we are conducting the feasibility trial, analyzing data, and disseminating results. Conclusions: This project will develop, iteratively refine, integrate, and pilot test the use of an innovative CDSS to prompt RNs to provide TSE reduction and smoking cessation counseling to caregivers who smoke. If successful, this approach will create a sustainable and disseminable model for prompting pediatric practitioners to apply tobacco-related guideline recommendations. This systems-based approach has the potential to reach at least 12 million smokers a year and significantly reduce TSE-related pediatric illnesses and related costs.

Exposure to environmental tobacco smoke (ETS) has been recognized as a significant health risk for adults and children. In adults, ETS exposure has been linked to increased incidences of cardiovascular disease and dementia. In children, exposure has been linked to behavioral and cognitive deficits. Studies on the effects of ETS in the brain have been largely epidemiological, and have lacked a defined explanation of the molecular/biochemical effects of ETS. The present dissertation aims to test whether ETS exposure leads to altered biochemistry in the adult and developing mammalian brain. A rat ETS exposure model was employed to investigate changes at the molecular and cellular level. In an adult ETS exposure study, we focused on markers of astrogliosis , oxidative stress, and cell death. We observed altered GFAP suggestive of reactive astrogliosis. Yet, markers of oxidative and cell stress were unaffected by ETS exposure in the brain regions examined. Increased degradation of αII-spectrin and dephosphorylation of serine116 on PEA-15 indicated greater apoptotic cell death signaling in the brains of ETS exposed animals. β-synuclein was greatly upregulated by ETS, a neuroprotective protein previously reported to exhibit anti-apoptotic and anti-fibrillogenic properties. We next employed a rodent model of postnatal ETS exposure to investigate effects on developing cerebellum using a system biology approach involving mass spectrometry (MS). Proteins at statistically different abundance between groups were correlated with relevant biochemical processes and pathways by bioinformatics. ETS responsive data were enriched in elements associated with all aspects of aerobic respiration. These results were substantiated by orthogonal molecular measures, along with evidence for increase mitochondrial biogenesis/fission. These findings suggest an increase mitochondrial density driven by a demand for ATP. Further exploration of the ETS responsive proteome identified statistically significant associations of the ETS with neuron projections, in particular axon associated proteins and synaptic vesicles. Immunotbloting and microscopy experiments substantiated altered process outgrowth and synaptogenic processes. The presented data depict a striking modulation in cerebellar formation consequent to ETS exposure and the energy source to allow that modulation to occur. Our findings could provide a biochemical and cellular rational for adverse neurological effects observed in ETS exposed children.

O início do desenvolvimento do sistema nervoso central (SNC) é caracterizado por diversos processos, com períodos críticos, que podem ser influenciados por xenobióticos. Este estudo teve como objetivo comparar os efeitos das diferentes concentrações de nicotina em elementos da transmissão sináptica durante o desenvolvimento de camundongos C57Bl/6. Para tanto, foram utilizados cigarros com duas diferentes concentrações de nicotina, o 3R4F (0,73 mg de nicotina/cigarro) e o 4A1 (0,16 mg de nicotina/cigarro). As exposições ocorreram diariamente a partir do 3° dia de vida (P3) até o 14° dia (P14) por duas horas, e os animais controle foram expostos somente ao ar sintético. Os animais foram eutanasiados em P15, P35 e P65 e avaliamos as seguintes proteínas: sinapsina (SYN1), sinaptotagmina (SYT), sinaptofisina (SYP), sinaptobrevina (SYB), PSD-95 e EGR-1, por Western blotting; o gene Egr-1 por PCR Real Time; MAP-2 e neurofilamentos (Neu) por imunofluorescência no hipocampo, tronco encefálico e cerebelo. Nossos resultados mostraram que na infância (P15) a fumaça do cigarro 3R4F diminuiu SYN1, assim como EGR-1, MAP-2 e Neu no cerebelo. No hipocampo houve aumento de SYN1 e MAP-2, diminuição de PSD-95, Egr-1 e Neu. No tronco encefálico esse cigarro não modificou nenhum dos parâmetros avaliados. Nessa mesma idade, a fumaça do cigarro 4A1 diminuiu MAP-2, Neu e a expressão gênica de Egr-1 no cerebelo; diminuiu MAP-2 e Neu no hipocampo e não promoveu alterações no tronco encefálico. Em P35 (adolescência) o 3R4F manteve reduzido SYN1, EGR-1, MPA-2 and Neu, e também reduziu Egr-1 no cerebelo. A diminuição de SYN1 também foi observada no hipocampo, mas nessa estrutura o 3R4F também aumentou SYT, SYP, MAP-2 and Neu; diminuiu EGR-1 e a expressão de Egr-1. No entanto, no tronco encefálico, foram observados aumento de SYN1 e MAP-2, e uma diminuição de Neu. Em relação à fumaça do 4A1, em P35, nossos resultados mostraram diminuição de SYB, Egr-1, MAP-2 and Neu no cerebelo; aumento de Egr-1, MAP-2 e diminuição de Neu no hipocampo; no tronco encefálico houve aumento de SYB, Egr-1, Neu e diminuição de MAP-2. Na fase adulta (P65) as únicas diferenças estatísticas encontradas foram: no cerebelo: diminuição de SYB pelos cigarros 4A1, aumento de EGR-1 pelo 3R4F e aumento de Egr-1 e MAP-2 por ambos os cigarros; no hipocampo: aumento de Neu por ambos os cigarros; tronco encefálico: aumento de SYB e EGR-1 e diminuição de SYT pelo 4A1, diminuição de SYN1, aumento de EGR-1, Egr-1 e MAP-2 pelo 3R4F. Nossos resultados indicam que a exposição à fumaça do cigarro nos primeiros dias de vida de camundongos, mesmo que em baixas concentrações de nicotina, podem acarretar em alterações em elementos da transmissão sináptica em várias regiões encefálicas durante a infância, adolescência e na fase adulta. / The initial steps of the development of the central nervous system are characterized by several critical processes, which can be affected by xenobiotics. The present study aimed to compare the effect of two different nicotine concentrations in cigarettes on synaptic transmission elements during the development of C57/Bl6 mice. To reach this aim we exposed C57Bl/6 mice to smoke from two different cigarettes - 3R4F (0.73mg of nicotine/cigarette) or 4A1 (0.16mg of nicotine/cigarette), from the third day of life (P3) until the fourteenth (P14) for a period of 1h, twice a day (at 8am and at 3pm). The control animals were exposed only to synthetic air. At P15, P35 and P65, the animals were submitted to euthanasia and different encephalic areas were collected (cerebellum, hippocampus and brainstem); quantification of synapsin (SYN1), synaptotagmin (SYT), synaptophysin (SYP), synaptobrevin (SYB), PSD-95 and EGR1 protein expression was assessed by Western blotting, gene expression of Egr-1 by was assessed by RT-PCR and MAP-2 and neurofilaments (Neu) were assessed by immunofluorescence. Our results showed that exposure to 3R4F smoke decreased the quantification of SYN1 at infancy (P15), as well as EGR-1, MAP-2 and Neu at cerebellum. At hippocampus, there was an increase of SYN1 and MAP-2, decrease of PSD-95, Egr-1 and Neu. At brainstem, 3R4F smoke did not modify any parameter. At the same age, 4A1 smoke decreased the quantification of MAP-2, Neu and the expression of Egr-1, at cerebellum; decreased MAP-2 and Neu at hippocampus and did not alter any parameter at brainstem. At P35 (adolescence) 3R4F smoke still reduced SYN1, EGR-1, MAP-2 and Neu, and reduced Egr-1 at cerebellum. The reduction of SYN1 quantification was also observed at hippocampus, but at this area, 3R4F smoke also increased the quantification of SYT, SYP, MAP-2 and Neu and decreased EGR-1 and the expression of Egr-1. However, at the brainstem, an increased quantification of SYN1 and MAP-2 and a decrease of Neu were observed. Regarding 4A1 smoke, at the same age, our results showed a decreased quantification of SYB, Egr-1, MAP-2 and Neu at cerebellum; increase of Egr-1, MAP-2 and decrease of Neu at hippocampus; and at brainstem, increase of SYB, Egr-1, Neu and decrease of MAP-2. At adulthood (P65) the only statistical differences were: at cerebellum - decreased quantification of SYB by 4A1 cigarette smoke, increase of EGR-1 by 3R4F and increase of Egr-1 and MAP-2 by smoke of both cigarettes; at hippocampus - increase of Neu by smoke of both cigarettes; at brainstem - increase of SYB and EGR-1 and decrease of SYT by 4A1 smoke, decrease of SYN1, increase of EGR-1, Egr-1 and MAP-2 by 3R4F smoke. Thus, we can conclude that exposure to cigarette smoke early in life, even at low nicotine concentrations can modify elements of synaptic transmission, compromising such transmission at several encephalic areas.

O início do desenvolvimento do sistema nervoso central (SNC) é caracterizado por diversos processos, com períodos críticos, que podem ser influenciados por xenobióticos. Este estudo teve como objetivo comparar os efeitos das diferentes concentrações de nicotina em elementos da transmissão sináptica durante o desenvolvimento de camundongos C57Bl/6. Para tanto, foram utilizados cigarros com duas diferentes concentrações de nicotina, o 3R4F (0,73 mg de nicotina/cigarro) e o 4A1 (0,16 mg de nicotina/cigarro). As exposições ocorreram diariamente a partir do 3° dia de vida (P3) até o 14° dia (P14) por duas horas, e os animais controle foram expostos somente ao ar sintético. Os animais foram eutanasiados em P15, P35 e P65 e avaliamos as seguintes proteínas: sinapsina (SYN1), sinaptotagmina (SYT), sinaptofisina (SYP), sinaptobrevina (SYB), PSD-95 e EGR-1, por Western blotting; o gene Egr-1 por PCR Real Time; MAP-2 e neurofilamentos (Neu) por imunofluorescência no hipocampo, tronco encefálico e cerebelo. Nossos resultados mostraram que na infância (P15) a fumaça do cigarro 3R4F diminuiu SYN1, assim como EGR-1, MAP-2 e Neu no cerebelo. No hipocampo houve aumento de SYN1 e MAP-2, diminuição de PSD-95, Egr-1 e Neu. No tronco encefálico esse cigarro não modificou nenhum dos parâmetros avaliados. Nessa mesma idade, a fumaça do cigarro 4A1 diminuiu MAP-2, Neu e a expressão gênica de Egr-1 no cerebelo; diminuiu MAP-2 e Neu no hipocampo e não promoveu alterações no tronco encefálico. Em P35 (adolescência) o 3R4F manteve reduzido SYN1, EGR-1, MPA-2 and Neu, e também reduziu Egr-1 no cerebelo. A diminuição de SYN1 também foi observada no hipocampo, mas nessa estrutura o 3R4F também aumentou SYT, SYP, MAP-2 and Neu; diminuiu EGR-1 e a expressão de Egr-1. No entanto, no tronco encefálico, foram observados aumento de SYN1 e MAP-2, e uma diminuição de Neu. Em relação à fumaça do 4A1, em P35, nossos resultados mostraram diminuição de SYB, Egr-1, MAP-2 and Neu no cerebelo; aumento de Egr-1, MAP-2 e diminuição de Neu no hipocampo; no tronco encefálico houve aumento de SYB, Egr-1, Neu e diminuição de MAP-2. Na fase adulta (P65) as únicas diferenças estatísticas encontradas foram: no cerebelo: diminuição de SYB pelos cigarros 4A1, aumento de EGR-1 pelo 3R4F e aumento de Egr-1 e MAP-2 por ambos os cigarros; no hipocampo: aumento de Neu por ambos os cigarros; tronco encefálico: aumento de SYB e EGR-1 e diminuição de SYT pelo 4A1, diminuição de SYN1, aumento de EGR-1, Egr-1 e MAP-2 pelo 3R4F. Nossos resultados indicam que a exposição à fumaça do cigarro nos primeiros dias de vida de camundongos, mesmo que em baixas concentrações de nicotina, podem acarretar em alterações em elementos da transmissão sináptica em várias regiões encefálicas durante a infância, adolescência e na fase adulta. / The initial steps of the development of the central nervous system are characterized by several critical processes, which can be affected by xenobiotics. The present study aimed to compare the effect of two different nicotine concentrations in cigarettes on synaptic transmission elements during the development of C57/Bl6 mice. To reach this aim we exposed C57Bl/6 mice to smoke from two different cigarettes - 3R4F (0.73mg of nicotine/cigarette) or 4A1 (0.16mg of nicotine/cigarette), from the third day of life (P3) until the fourteenth (P14) for a period of 1h, twice a day (at 8am and at 3pm). The control animals were exposed only to synthetic air. At P15, P35 and P65, the animals were submitted to euthanasia and different encephalic areas were collected (cerebellum, hippocampus and brainstem); quantification of synapsin (SYN1), synaptotagmin (SYT), synaptophysin (SYP), synaptobrevin (SYB), PSD-95 and EGR1 protein expression was assessed by Western blotting, gene expression of Egr-1 by was assessed by RT-PCR and MAP-2 and neurofilaments (Neu) were assessed by immunofluorescence. Our results showed that exposure to 3R4F smoke decreased the quantification of SYN1 at infancy (P15), as well as EGR-1, MAP-2 and Neu at cerebellum. At hippocampus, there was an increase of SYN1 and MAP-2, decrease of PSD-95, Egr-1 and Neu. At brainstem, 3R4F smoke did not modify any parameter. At the same age, 4A1 smoke decreased the quantification of MAP-2, Neu and the expression of Egr-1, at cerebellum; decreased MAP-2 and Neu at hippocampus and did not alter any parameter at brainstem. At P35 (adolescence) 3R4F smoke still reduced SYN1, EGR-1, MAP-2 and Neu, and reduced Egr-1 at cerebellum. The reduction of SYN1 quantification was also observed at hippocampus, but at this area, 3R4F smoke also increased the quantification of SYT, SYP, MAP-2 and Neu and decreased EGR-1 and the expression of Egr-1. However, at the brainstem, an increased quantification of SYN1 and MAP-2 and a decrease of Neu were observed. Regarding 4A1 smoke, at the same age, our results showed a decreased quantification of SYB, Egr-1, MAP-2 and Neu at cerebellum; increase of Egr-1, MAP-2 and decrease of Neu at hippocampus; and at brainstem, increase of SYB, Egr-1, Neu and decrease of MAP-2. At adulthood (P65) the only statistical differences were: at cerebellum - decreased quantification of SYB by 4A1 cigarette smoke, increase of EGR-1 by 3R4F and increase of Egr-1 and MAP-2 by smoke of both cigarettes; at hippocampus - increase of Neu by smoke of both cigarettes; at brainstem - increase of SYB and EGR-1 and decrease of SYT by 4A1 smoke, decrease of SYN1, increase of EGR-1, Egr-1 and MAP-2 by 3R4F smoke. Thus, we can conclude that exposure to cigarette smoke early in life, even at low nicotine concentrations can modify elements of synaptic transmission, compromising such transmission at several encephalic areas.

No description available.

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.

No description available.

Background: Tobacco use exacerbates diseases, including tuberculosis (TB) and interferes with recovery from such outcomes. However, there is sparse research on the integration of tobacco cessation into TB programs. Moreover, there is limited evidence on how mHealth solutions for tobacco can enhance cessation among TB patients. This study aimed to assess the impact of a training program to integrate tobacco cessation in TB program on the knowledge of health workers. Methods: In June 2017, a 5-day training about tobacco use and control and the use of mHealth solutions to improve tobacco cessation and enhance adherence to TB treatment was conducted in Uganda. A comparison of percent of participants reporting knowledge on selected health outcomes of tobacco use and secondhand tobacco smoke (SHS) exposure was conducted. Knowledge was assessed on a 21-outcome-item before and after training. A non-parametric test, signrank for comparison of paired observations was conducted. The changes were considered statistically significant if the p-value was less than 5%. Results: Twenty three trainees from across the country attended (13 females, 10 males), with median age of the trainees was 39 years. Pre-training knowledge about tobacco use (66.6%) was higher than SHS exposure (45%). Following the training, both sets of knowledge significantly improved (median 100%). Pre-training knowledge about health effects of tobacco use was particularly low for diabetes (27%), meningitis (9.5%), ear infection (43%), impotence (47.6%), and fibrosis (30%). Except heart attack (76%), lung illness among children (91%), lung cancer (81%), and chronic lung disease (81%), pre-training knowledge about SHS was low for all other disease outcomes. Conclusions: Healthcare providers play critical role in preventing and reducing tobacco use. The low pre-training knowledge of the TB health workers suggests the critical need for training health providers in Uganda and elsewhere in Africa in order to curtail the increasing trend in usage.

Current methods for the risk assessment of environmental exposures commonly involve questionnaires, stationary monitoring, and personal air sampling. However, as these approaches do not capture the body's internal response, they lend minimal understanding to the biologic consequence of exposure. In order to address the unmet need of connecting external exposure measurements with signatures of internal exposure, this thesis examines the overarching hypothesis that transcriptomic changes in the human airway epithelium can serve as indicators of physiologic responses to inhaled pollutants. This is an extension of previous work that has demonstrated an airway ''field of injury'' effect where cigarette smoke exposure alters gene-expression in epithelial cells lining the respiratory tract. Specifically, I examine transcriptomic changes and the biologic responses associated with exposure to the following pollutants: environmental tobacco smoke (Aim 1), household air pollution from smoky coal combustion (Aim 2), and electronic cigarette vapor (Aim 3). First, I performed whole-genome transcriptional profiling of the nasal epithelium in children and adults and detected gene-expression changes associated with exposure to environmental tobacco smoke. Next, I employed similar approaches to detect a signature of coal smoke exposure in the buccal epithelium of healthy, non-smoking females exposed to household air pollution Xuanwei, China. The findings from these studies suggest that upper airway gene-expression can reflect the host response to prolific sources of environmental exposures that are major risk factors for chronic lung disease. Lastly, I examine the cellular and physiologic consequences of electronic cigarette (ECIG) aerosol exposure by analyzing transcriptomic profiles of human bronchial epithelial cells that have either been (1) differentiated and exposed in vitro or (2) acquired via bronchoscopy from the airway epithelium of ECIG users. The studies detailed in this dissertation offer valuable insight that will accelerate the efforts to evaluate the health effects of both well-established and emerging types of inhaled exposures in large-scale population studies. Furthermore, the transcriptomic strategies woven throughout the following chapters push for a novel assessment paradigm that may enable the public health community to rapidly characterize the physiologic host response to inhalation exposures of different sources, and to evaluate the biologic consequences of exposure-reduction initiatives. / 2017-05-01T00:00:00Z