Diss. med. dent. Zürich. / Sonderdruck aus: Schweizer Monatsschrift für Zahnmedizin. Bd. 118, Nr. 6, 2009. Literaturverz.

The purpose of this study was to investigate the prevalence of smoke-free environment polices throughout the Commonwealth of Virginia at worksites employing fifty or more workers. Specifically, this study assessed policy prevalence, development, implementation, and enforcement. In addition, this study assessed smoke-free environment policy effectiveness. The population for this investigation consisted of telephone surveys of 374 worksites located throughout the Commonwealth of Virginia. Of these worksites, 340 (91%) completed the telephone survey. The population (n = 340) was spread throughout five health regions, Northern, Northwest, Central, Southwest, and East. Descriptive analysis and One-way Analysis of Variance (ANOVA) were applied to investigate differences between these five health regions. An alpha of .05 was selected for this study. Based on the findings, the following conclusions were drawn: (1) Fifty-percent of the worksites located throughout the Commonwealth of Virginia have some form of smoke-free environment policies; (2) The smoke-free environment policy constructs used in the telephone survey guide were statistically significant in identifying differences between the five health regions; (3) Smoke-free environment policies at the worksite are dependent upon health region; (4) Implementation of smoke-free environment policies is dependent upon health region; (5) Enforcement of smoke-free environment policies is dependent upon health region, and (6) Effectiveness of smoke-free environment policies is dependent upon health region. The following recommendations were suggested: (1) Further studies assessing smoke-free environment policy enforcement should be conducted annually; (2) Studies incorporating a qualitative research methodology regarding smoke-free environment policy prevalence should be conducted; (3) Studies involving common smoke-free environment policies at different states should be investigated, and (4) Additional in-depth surveys should be conducted to evaluate health outcomes associated with the implementation of smoke-free environment policies. / Ph. D.

Environmental tobacco smoke (ETS) has been well established as a danger to children. Exposure to secondhand smoke can cause coughing and wheezing, bronchitis, pneumonia, ear infections, asthma, and sudden infant death syndrome (SIDS). Childhood exposure to ETS may also increase the risk of developing leukemia and lymphoma in childhood (Mitchell, 1997) as well as developing lung cancer as an adult (Glantz, 1992). Despite the great strides recently made in the implementation of regulatory measures to safeguard children from ETS in public places like schools, there remains significant concern regarding children's exposure at home and in their out-of-home care facilities (Ashley and Ferrence, 1998, Jarvis, 2000). In 1996, the Centers for Disease Control and Prevention estimated that there were 336,749 Virginia youth exposed to ETS in the home (State Tobacco Control Highlights, 1999). The purpose of this study was to ascertain the number of family day home providers who allow smoking in their home and/or those that have some type of smoking policy. The sample consisted of 746 licensed, registered or locally approved family day home providers through the Department of Social Services. Of these childcare providers, 81.5% (n=608) completed a questionnaire about their tobacco use policy and its effects. An overwhelming majority (94.7%) of providers reported having a tobacco use policy in their family day home. Most of the providers, 67.6% indicated that smoking was allowed outdoors only while 26.3% noted that smoking was not allowed anywhere at any time, indoor or outdoor. Other policy specifics and background information are discussed in the study. The implications of these findings and recommendations for future training and educational programs for family day home providers are also reviewed. / Master of Science

Thesis (MPH.) -- University of Limpopo, 2016. / Introduction: Annually, hundred thousands of people worldwide die as a result of second hand smoke (SHS) exposure. There is no safe exposure level to SHS yet in Bulawayo, smokers have been observed smoking without restraint thus exposing non-smokers to SHS. The purpose of this study was to establish the prevalence and contributing factors of SHS exposure among adults in Bulawayo, Zimbabwe. Methods: A cross sectional study was conducted and participants were randomly selected from residents who visited the 13 municipal revenue halls. A structured questionnaire was used to collect data from respondents. Descriptive and multivariate logistic regression analyses were performed. Results: Home SHS exposure prevalence was 22% and females were 2.11 times more likely than males to be exposed at home. Prevalence of SHS exposure in public transportation, health facilities, educational and food premises was 40.9%, 26.3%, 42,9% and 36.8% respectively. Conclusion: SHS exposure in Bulawayo was high and there is need to reduce SHS exposure to non-smoking adults. Keywords: Second hand smoke (SHS), Bulawayo, Prevalence, Exposure, Adult

Environmental tobacco smoke (ETS) is a serious public health threat. Residual ETS in vehicles unknowingly exposes future occupants to environmental tobacco smoke. Reducing or removing exposure to ETS has been proven to reduce long-term health complications. This quasi-experimental study investigated 5 cleaning methods and their effect on air particulate matter2.5 (PM2.5) along with the correlation between air nicotine levels and PM2.5 levels. Study variables included cleaning methods as the independent variable, and changes in air nicotine and PM2.5 levels as the dependent variables. This study is framed within primary prevention and risk reduction based on the harm reduction theory. The harm reduction theory professes that when a hazard cannot be completely removed, methods to reduce the social and personal costs associated with the hazard should be developed. Fifty vehicles were placed in 5 groups: car wash vacuumed, shop vac vacuumed, air change, hand held vacuumed, and Hepa filtration air cleaned. Nicotine and PM2.5 levels were measured before and after cleaning. A Wilcoxon ranked test analysis of the data showed all methods of cleaning studied had a statistically significant decrease in both air nicotine (Z = -6.154, p < .001) and PM2.5 levels (Z = -5.934, p < .001). Kruskall-Wallis analysis showed no statistical significance between cleaning methods. Correlation analysis determined no correlation between nicotine and PM2.5 (r value = <.3). Results of this study provides public health program professionals with information linking cleaning methods to reduction of exposure to ETS. Positive social change comes when programs are developed to training and education people to reduce their exposure, resulting in an increase in health and a decrease in medical costs.

Thesis (Ph.D.)--McGill University (Canada), 1998. / Adviser: Mark Goldberg. Includes bibliographical references.

Despite extensive research, the mechanisms behind cardiovascular effects of subchronic environmental tobacco smoke (ETS) remain unclear, but may be related to ETS-induced inflammation and oxidative stress. Additionally, the protective role of resveratrol (RES), a natural antioxidant available in red grapes, is controversial. We hypothesized that the polycyclic aromatic hydrocarbon (PAH) component of ETS is responsible for causing adverse cardiovascular effects. We also hypothesized that the administration of RES is protective against the adverse cardiovascular effects of ETS. In order to address these hypotheses, male juvenile pigs (4-weeks old) were exposed to ETS or ambient air for 28 consecutive days (1 hr/day) and effects compared to 7 days of i.v. injection of the PAH, benzo-a-pyrene (BAP; 5 mg/kg daily). In another experiment, pigs were sham-exposed or ETS-exposed, with or without oral RES treatment (5mg/kg daily). In all experiments, endothelial and left ventricular function were assessed by flow mediated dilation (FMD), and echocardiography, respectively, while blood pressure was evaluated by oscillometry. At the termination of each experiment, serum nitrotyrosine, total nitrate/nitrite (NOx) and C-reactive protein (CRP) were measured as well as hepatic and pulmonary ethoxyresorufin-o-deethylase (EROD) activity to indicate cytochrome P450 1A1 (CYP1A1) expression. Finally, the correlation between pulmonary inflammation and adverse cardiovascular effects was investigated by measuring total and differential white blood cell (WBC) count as well as leukocyte elastase activity in bronchoalveolar lavage fluid at the termination of each experiment. ETS exposure, but not BAP treatment, resulted in a significant impairment of FMD (P<0.0001) and increased left ventricular end diastolic volume (P=0.0032). Cotreatment with RES failed to restore the ETS induced impairment of FMD (P>0.05). However, a trend pointing to an increase in ejection fraction (EF) was noted (P=0.072). ETS, BAP and RES treatments failed to have any effect on blood pressure (P>0.05). BAP injection caused a significant increase in serum nitrotyrosine (P=0.0146) and CRP (P=0.012), but not serum NOx levels (P>0.05). In contrast, ETS exposure resulted in a significant increase in CRP serum levels (P=0.0092), a trend pointing to increased serum nitrotyrosine (P=0.105), and no change in serum NOx levels (P>0.05). The increased nitrotyrosine and CRP with ETS exposure was not reversed by RES administration (P>0.05). ETS exposure increased EROD activity in the lung (P=0.0093), but not the liver (P=0.12). In contrast, BAP treatment had the opposite effect (lung EROD: P=0.621, liver EROD: P=0.01), while RES administration had no effect (P>0.05). ETS exposure (P=0.0139), but not BAP treatment (P=0.723), resulted in increased WBC count in BAL fluid which was not affected by RES administration (P>0.05). These results show that ETS exposure causes lung inflammation, systemic inflammation, oxidative stress-mediated inactivation of nitric oxide and impaired endothelial function. In contrast, BAP failed to alter endothelial function, downstream of the lung, despite systemic inflammation and increased oxidative stress. Furthermore, RES failed to restore endothelial function, or decrease systemic inflammation and oxidative stress. Taken together, these results suggest either that pulmonary inflammatory responses or pulmonary increases in CYP1A1 activity may be more important links to endothelial dysfunction than systemic inflammation and nitric oxide bioactivity. The beneficial effects of RES by itself are manifested only at the cardiac level by improving the ejection fraction, but the work in this thesis failed to detect any ability of RES to ameliorate ETS cardiovascular effects.

This study explored how cultural heritage might affect peoples beliefs, attitudes, and behaviors toward Environmental Tobacco Smoke (ETS), which in turn affected actual ETS exposure. It used data from the 2001 National Survey on Environmental Tobacco Smoke in the Home. It compared two cultural groups: Francophones and the rest of the Canadian population (RCP), and found that Francophone nonsmokers had a significantly higher ETS exposure than the RCP (19.3% vs. 8.5%). The difference was much greater than the difference in smoking prevalence for the two groups (26.2% vs. 22.4%). </p>The study found Francophones scored lower than the RCP in almost every aspect of ETS-related beliefs, attitudes, and behaviors. They were less likely to believe ETS to be harmful and less supportive of ETS-control policies. They were less likely to have done something that reduced ETS exposure at home. In both cultural groups, smokers scored lower than nonsmokers in ETS-related beliefs and attitudes. However, the difference between the two groups remained significant even if the comparisons were done within smokers and nonsmokers. </p>The most significant finding of the study was that Francophones were more likely to trust those so-called ETS-reduction strategies that appeared to be effective but were not in reality (e.g., opening the window when someone smokes). Moreover, there was a statistically significant interaction between smoking status and cultural heritage: fewer nonsmokers than smokers within each cultural group believed that these strategies were really effective, but the difference between the nonsmokers and smokers was significantly smaller for Francophones than that for the RCP. Therefore, the tendency to trust ineffective ETS-reduction strategies, especially among the nonsmokers, explained why Francophones were significantly less likely to adopt strategies that would actually reduce ETS exposure. </p>These results suggest that in order to move ETS policies forward and to effectively reduce ETS exposure among Canadian nonsmokers, the key strategy is to mobilize the nonsmokers to be less tolerant of ETS and more persistent in only allowing smoking to occur outdoors. This will not only help protect nonsmokers from the harm of ETS, but will eventually help smokers to quit smoking.

This study explored how cultural heritage might affect peoples beliefs, attitudes, and behaviors toward Environmental Tobacco Smoke (ETS), which in turn affected actual ETS exposure. It used data from the 2001 National Survey on Environmental Tobacco Smoke in the Home. It compared two cultural groups: Francophones and the rest of the Canadian population (RCP), and found that Francophone nonsmokers had a significantly higher ETS exposure than the RCP (19.3% vs. 8.5%). The difference was much greater than the difference in smoking prevalence for the two groups (26.2% vs. 22.4%). </p>The study found Francophones scored lower than the RCP in almost every aspect of ETS-related beliefs, attitudes, and behaviors. They were less likely to believe ETS to be harmful and less supportive of ETS-control policies. They were less likely to have done something that reduced ETS exposure at home. In both cultural groups, smokers scored lower than nonsmokers in ETS-related beliefs and attitudes. However, the difference between the two groups remained significant even if the comparisons were done within smokers and nonsmokers. </p>The most significant finding of the study was that Francophones were more likely to trust those so-called ETS-reduction strategies that appeared to be effective but were not in reality (e.g., opening the window when someone smokes). Moreover, there was a statistically significant interaction between smoking status and cultural heritage: fewer nonsmokers than smokers within each cultural group believed that these strategies were really effective, but the difference between the nonsmokers and smokers was significantly smaller for Francophones than that for the RCP. Therefore, the tendency to trust ineffective ETS-reduction strategies, especially among the nonsmokers, explained why Francophones were significantly less likely to adopt strategies that would actually reduce ETS exposure. </p>These results suggest that in order to move ETS policies forward and to effectively reduce ETS exposure among Canadian nonsmokers, the key strategy is to mobilize the nonsmokers to be less tolerant of ETS and more persistent in only allowing smoking to occur outdoors. This will not only help protect nonsmokers from the harm of ETS, but will eventually help smokers to quit smoking.

Despite extensive research, the mechanisms behind cardiovascular effects of subchronic environmental tobacco smoke (ETS) remain unclear, but may be related to ETS-induced inflammation and oxidative stress. Additionally, the protective role of resveratrol (RES), a natural antioxidant available in red grapes, is controversial. We hypothesized that the polycyclic aromatic hydrocarbon (PAH) component of ETS is responsible for causing adverse cardiovascular effects. We also hypothesized that the administration of RES is protective against the adverse cardiovascular effects of ETS. In order to address these hypotheses, male juvenile pigs (4-weeks old) were exposed to ETS or ambient air for 28 consecutive days (1 hr/day) and effects compared to 7 days of i.v. injection of the PAH, benzo-a-pyrene (BAP; 5 mg/kg daily). In another experiment, pigs were sham-exposed or ETS-exposed, with or without oral RES treatment (5mg/kg daily). In all experiments, endothelial and left ventricular function were assessed by flow mediated dilation (FMD), and echocardiography, respectively, while blood pressure was evaluated by oscillometry. At the termination of each experiment, serum nitrotyrosine, total nitrate/nitrite (NOx) and C-reactive protein (CRP) were measured as well as hepatic and pulmonary ethoxyresorufin-o-deethylase (EROD) activity to indicate cytochrome P450 1A1 (CYP1A1) expression. Finally, the correlation between pulmonary inflammation and adverse cardiovascular effects was investigated by measuring total and differential white blood cell (WBC) count as well as leukocyte elastase activity in bronchoalveolar lavage fluid at the termination of each experiment. ETS exposure, but not BAP treatment, resulted in a significant impairment of FMD (P<0.0001) and increased left ventricular end diastolic volume (P=0.0032). Cotreatment with RES failed to restore the ETS induced impairment of FMD (P>0.05). However, a trend pointing to an increase in ejection fraction (EF) was noted (P=0.072). ETS, BAP and RES treatments failed to have any effect on blood pressure (P>0.05). BAP injection caused a significant increase in serum nitrotyrosine (P=0.0146) and CRP (P=0.012), but not serum NOx levels (P>0.05). In contrast, ETS exposure resulted in a significant increase in CRP serum levels (P=0.0092), a trend pointing to increased serum nitrotyrosine (P=0.105), and no change in serum NOx levels (P>0.05). The increased nitrotyrosine and CRP with ETS exposure was not reversed by RES administration (P>0.05). ETS exposure increased EROD activity in the lung (P=0.0093), but not the liver (P=0.12). In contrast, BAP treatment had the opposite effect (lung EROD: P=0.621, liver EROD: P=0.01), while RES administration had no effect (P>0.05). ETS exposure (P=0.0139), but not BAP treatment (P=0.723), resulted in increased WBC count in BAL fluid which was not affected by RES administration (P>0.05). These results show that ETS exposure causes lung inflammation, systemic inflammation, oxidative stress-mediated inactivation of nitric oxide and impaired endothelial function. In contrast, BAP failed to alter endothelial function, downstream of the lung, despite systemic inflammation and increased oxidative stress. Furthermore, RES failed to restore endothelial function, or decrease systemic inflammation and oxidative stress. Taken together, these results suggest either that pulmonary inflammatory responses or pulmonary increases in CYP1A1 activity may be more important links to endothelial dysfunction than systemic inflammation and nitric oxide bioactivity. The beneficial effects of RES by itself are manifested only at the cardiac level by improving the ejection fraction, but the work in this thesis failed to detect any ability of RES to ameliorate ETS cardiovascular effects.