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Class of 2012 Abstract / Specific Aims: To assess the number of patients referred to ASHLine during the health screenings performed by University of Arizona College of Pharmacy students; and to identify the comfort level of students who asked patients about their smoking status. Methods: An anonymous questionnaire was sent via electronic mail to evaluate students’ comfort levels in implementing a smoking cessation referral program and subject demographics. Chart reviews quantified the number of patients referred to a smoking cessation program. Main Results: A total of 1,147 patients were screened for smoking cessation, 85 of which said they still smoked. Of the 85 who smoked, only 2 (0.17%) were referred to ASHLine. There was no significant increase in the comfort level of students (based on three domains) who participated in a smoking cessation training program or students in different years of their professional education. It was found that more students were comfortable with completing the required smoking cessation paperwork if they attended three or more health fairs (P=0.014). Conclusions: The comfort level of students with smoking cessation education is independent of the number of patients referred to a local smoking cessation program.

A thirty year follow-up survey was carried out to determine the prevalence of adult onset wheeze in a randomly selected community cohort of 2,056 adults who had had no childhood respiratory symptoms when they were originally studied in 1964. New onset wheezing symptoms developed at a steady rate of 0.5 per 100 person years between age 15 and 14; 11.5% of subjects reported having had an attack of wheezing for the first time during this period of their lives. Adult onset disease accounted for a greater proportion (62.9%) of current wheezing in middle age than child onset disease (37.1%). The risk of adult onset wheeze among all cases who had ever wheezed since age 15 increased with low socioeconomic status, current smoking, positive atopic status and positive family history of atopic disease. Gender was not related to risk of wheeze. Vitamin C and E consumption were inversely related to the risk of current wheeze (i.e. wheeze in the previous 12 months); analyses stratified by social class and smoking habit suggested that these inverse associations were stronger in the manual compared to the nonmanual class, and among smokers compared to nonsmokers. Childhood factors, including father's social class, sibship structure and common childhood infections were not related to adult onset wheeze. The pattern of significant independent risk factors differed between three distinct subgroups of cases who reported doctor-diagnosed asthma (n=24), chronic cough and phlegm (n=31) or other wheeze (n=47). Manual social class was associated with cough and phlegm and other wheeze. Smoking was only related to cough and phlegm. Atopy was associated with doctor-diagnosed asthma and with cough and phlegm. Family history of atopic disease was related to all subgroups, suggesting that despite apparent heterogeneity in diagnostic labelling, concurrent symptoms and other risk factors, the different forms of adult onset wheeze may share a common allergic basis.

A research report submitted to the Faculty of Heath Sciences, University of the Witwatersrand, in partial fulfilment of the requirements for the degree of Master of Science in Medicine in the field of Tropical Diseases (Epidemiology & Biostatistics) Johannesburg, / Objective. The aim of this paper was to systematically evaluate available evidence on tobacco smoking as a risk factor for pulmonary tuberculosis. Methods. Relevant reports were identified by a systematic electronic search of Medline, Pubmed, Nioshtic, Toxline and Embasse. Methodological quality of all selected publications was assessed using a standardized checklist. Information was collected on all major study characteristics. Inter-study heterogeneity was examined qualitatively and statistically using the DerSimonian and Laird method. Results. Five case-control studies and 1 cohort study were included in the systematic review. All the 6 studies revealed a relationship between tobacco smoking and pulmonary tuberculosis. Heterogeneity across studies hampered overall statistical pooling of results, however pooled risk ratios for sub-groups were determined / IT2018

Cigarette smoking has been reported to be prevalent in military training populations, and associated with lower cardiorespiratory fitness and higher risk of training-related injury. However, it is unclear whether habitual smoking impairs development of physical fitness. It is possible that smoking-induced alterations in oxidative stress, inflammation and hormone balance may disrupt training adaptation in smokers. The aim of this programme of work was to identify the influences of smoking on physical performance adaptation, selected biomarkers and injury risk in a military trainee population. The first study established that habitual smokers comprised 48% of a cohort of 2087 trainees. Upon closer examination, both at entry (Study 2) and during 10 weeks of training (Study 3) smokers exhibited chronically elevated oxidative stress and, after commencement of training, evidence of significantly higher resting inflammation compared with non-smokers. Throughout the full duration of training, performance of smokers in military physical fitness tests was significantly worse than non-smokers (Study 4), but neither muscular adaptation nor physical performance improvement were impaired in smokers in the early stages (10-14 weeks) or over the full duration (26 weeks) of training. It was expected that smokers would experience greater acute inflammatory responses to exercise but neither these, nor hormonal responses, differed between smokers and non-smokers in response to consecutive days of military field exercise (Study 5). In addition to poorer physical performance in smokers, training-related injury incidence was higher in smokers than non-smokers, specifically injuries attributed to overuse (Study 6). Overall, smoking appears to cause some physiological alterations which, while not impairing adaptation to training, may have adverse implications on health outcomes. Although the specific underlying mechanisms are unclear, habitual smokers exhibit greater injury risk and typically lower physical fitness than non-smoking counterparts.

Submitted by LUCAS POSSEBON null (lucas_possebon@hotmail.com) on 2017-03-07T01:37:03Z No. of bitstreams: 1 Dissertação Mestrado Lucas Possebon.pdf: 3575174 bytes, checksum: bd6f3f0fb08741b8fd22772ba8dded60 (MD5) / Approved for entry into archive by Juliano Benedito Ferreira (julianoferreira@reitoria.unesp.br) on 2017-03-10T17:07:31Z (GMT) No. of bitstreams: 1 possebon_l_me_sjrp.pdf: 3575174 bytes, checksum: bd6f3f0fb08741b8fd22772ba8dded60 (MD5) / Made available in DSpace on 2017-03-10T17:07:31Z (GMT). No. of bitstreams: 1 possebon_l_me_sjrp.pdf: 3575174 bytes, checksum: bd6f3f0fb08741b8fd22772ba8dded60 (MD5) Previous issue date: 2017-02-20 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / O processo inflamatório causado pelo tabagismo está relacionado a diferentes tipos de doenças como enfisema pulmonar, doença pulmonar obstrutiva crônica (DPOC) e aterosclerose. Neste cenário, a proteína anti-inflamatória AnxA1 pode representar uma alternativa terapêutica. Por essas razões, o objetivo da pesquisa foi avaliar os efeitos do peptídeo mimético Ac2-26 da proteína AnxA1, em modelo de tabagismo. Ratas Wistar foram divididas em 3 grupos (n=10/grupo): expostos ao fumo não tratados (F) e tratados com o peptídeo (F+Ac2-26) e controles (C). Os grupos de animais expostos ao fumo foram colocados em um equipamento específico da Unidade Didática e de Pesquisa Experimental (UDPE) das Faculdades Integradas Padre Albino (FIPA), e expostos à queima de 10 cigarros comerciais, um após o outro, 2x/dia, por 5 semanas. O grupo C foi mantido no mesmo regime, porém na ausência da fumaça do cigarro e tratamento. Para avaliar a eficácia do Ac2-26, animais F+Ac2-26 foram administrados intraperitonealmente com o peptídeo (1mg/kg), 1x/dia, antes da primeira exposição ao cigarro. As ratas foram pesadas e tiveram a pressão arterial aferida no início e final do experimento. No período final, a ventilação pulmonar foi verificada por meio da pletismografia e também foram realizadas imagens de raios-X. Os animais foram eutanasiados e coletados o lavado bronco alveolar (LBA) para quantificações de células inflamatórias e citocinas, o sangue para dosagens bioquímicas de citocinas e hemoglobina e os órgãos, pulmão e traqueia, para os estudos histopatológicos e imuno-histoquímicos. As análises fisiológicas mostraram perda de peso, aumento da pressão arterial, reduções da frequência e ventilação pulmonares, bem como alterações macroscópicas das dimensões pulmonares por imagens de raio-X no grupo F. Enquanto, nos F+Ac2-26, esses valores foram semelhantes aos controles. As análises histopatológicas mostraram maiores espaços intra-alveolares e aumento do tecido linfoide no pulmão e perda dos cílios no epitélio da traqueia no grupo F comparado as F+Ac2-26 e C. Nas análises do LBA, foi observado aumento na quantidade de linfócitos e macrófagos em F, com redução significante dessas células promovida após o tratamento. Nas quantificações de células inflamatórias nos tecidos, os macrófagos e mastócitos foram observados aumentados no grupo F comparado aos C e F+Ac2-26. As análises imuno-histoquímicas do pulmão e da traqueia mostraram menor expressão de AnxA1, COX-2 e MMP-9 nos animais C e F+Ac2-26. As dosagens de citocinas e quimiocina indicaram aumento no sobrenadante do macerado do pulmão, plasma sanguíneo e LBA no grupo F e redução nos níveis desses mediadores em C e F+Ac2-26. Ainda, as dosagens bioquímicas do sangue mostraram que o tratamento com o peptídeo ocasionou aumento da concentração de hemoglobina e glicose e redução do colesterol total e transaminase glutâmico oxalacética (TGO) comparados aos animais não tratados. Nossos resultados evidenciaram a ação protetora do peptídeo mimético Ac2-26 no modelo de DPOC, atenuando o processo inflamatório causado pela exposição à fumaça do cigarro e abre novas perspectivas para o tratamento das doenças relacionadas ao tabagismo. / The inflammatory process caused by smoking is related to different kinds of diseases such as pulmonary emphysema, chronic obstructive pulmonary disease (COPD) and atherosclerosis. In this scenario, an anti-inflammatory protein AnxA1 may represent a therapeutic alternative. For these reasons, the objective of this research was to analyze the effects of the mimetic peptide Ac2-26 of the AnxA1 protein, in a smoking model. Wistar rats were divided into 3 groups (n = 10/group). The groups of animals exposed to smoke were placed in a specific equipment of the Didactic and Experimental Research Unit (UDPE) of the Integrated Colleges Padre Albino (FIPA), and exposed to the burning of 10 cigarettes, one after another, 2x / day for 5 weeks. To evaluate the efficacy of Ac2-26, CS+Ac2-26 animals were administered intraperitoneally with peptide (1mg / kg), 1x / day, prior to first exposure to the cigarette. Group C was maintained in the same regimen, but in the absence of cigarette smoke or treatment. The rats were weighed and had blood pressure measured at the beginning and ending of the experiment. In the final period, pulmonary ventilation was verified through plethysmography and also performed ray-X images. The animals were euthanized and collected the alveolar bronchus (BAL) for quantification of inflammatory cells and cytokines, the blood for biochemical measurements of cytokines and hemoglobin and organs, lung and trachea, for histopathological and immunohistochemical studies. The physiological analyzes showed weight loss, increased blood pressure, reductions and in the pulmonary frequency and ventilation, as well as macroscopic alternative in the lung dimensions by X-ray images in group CS. While, in CS+Ac2-26, these values were similar to controls. The histopathological analyzes showed enlargement of the intra-alveolar spaces and increased lymphoid tissue (BALT), and loss of the cilia in the epithelium of the trachea in the CS group, compared to CS+Ac2-26 and C. Numerous lymphocytes and macrophages were observed in the BAL in CS, with significant reduction of the cells after treatment. In the quantifications of inflammatory cells in the tissues, macrophages and mast cells were increased in the CS+Ac2-26 group. The immunohistochemical analyzes of the lung and trachea showed lower expression of AnxA1, COX-2 and MMP-9 in C and CS+Ac2-26 animals. The dosages of cytokines and chemokine indicated incr ease in the supernatant of lung macerate, blood plasma and BAL in the F group and reduction of these mediators levels in C and CS+Ac2-26 groups. Also, the biochemical blood measurements showed that treatment with the peptide caused an increase in hemoglobin and glucose concentrations and reduction of total cholesterol and Glutamic oxaloacetic transaminase (GOT) compared to untreated animals. Our results evidenced a protective action of the Ac2-26 mimetic peptide in the COPD model, by attenuating the inflammatory process caused by exposure to cigarette smoke, which opens new perspectives for the treatment of smoking-related diseases.

Background: Smoking contributes to health inequalities and there is a need to focus interventions on the disadvantaged. Abrupt quitting is widely advocated, but assisted ‘reduction’ may be an option for those not ready to quit. Physical activity acutely reduces cigarette cravings and withdrawal symptoms, and may increase long-term cessation and reduce weight gain. This thesis reports on the multi-method evaluation of an intervention delivered by Health Trainers (HTs) and a pilot randomised controlled trial of the Exercise Assisted Reduction then Stop (EARS) intervention for disadvantaged smokers who are not ready to quit, but do wish to reduce, without nicotine replacement therapy. This programme of research aimed to evaluate four aspects of the EARS trial: 1) Recruitment, 2) Study attrition, 3) Main quantitative outcomes, and 4) Intervention fidelity. Methods: 1) Recruitment: Smokers were recruited through mailed invitations from three primary care practices (62 participants) and one National Health Stop Smoking Service (SSS) database (31 participants). Six other participants were recruited via a variety of other community-based approaches. Data were collected through questionnaires, field notes, work sampling, and databases. Chi-squared and t-tests were used to compare baseline characteristics of participants. 2) Study Attrition: Disadvantaged smokers who wanted to reduce but not quit were randomised (N=99), of whom 61 (62%) completed follow-up assessments at 16 weeks. Univariable logistic regression was conducted to determine the effects of intervention arm, method of recruitment, and participant characteristics (socio-demographic factors, and lifestyle, behavioural and attitudinal characteristics) on attrition, followed by multivariable logistic regression on those factors found to be related to attrition. 3) Main quantitative outcomes: Data at 16 weeks were collected for various smoking and physical activity outcomes. Primary analyses consisted of an intention to treat analysis based on complete case data. Secondary analyses explored the impact of handling missing data, examining different methods including last baseline observation carried forward, last observation carried forward, and multiple imputation. 4) Intervention fidelity: Three researchers scored a total of 90 audio recorded consultations for 30 different participants split between three HTs delivering the intervention. Delivery was scored using a 0-6 likert scale for 12 different processes identified as being fundamental to the intervention. Results: 1) Recruitment: Depending on the intensity and time invested in following up those who did not initially respond to a letter, we randomised between 5.1–11.1% of those invited through primary care and SSS, with associated researcher time to recruit one participant varying from 18 –157 minutes. Recruitment rates were similar for invitations sent from primary care and SSS. Despite substantial time and effort, only six participants of our total of 99 were recruited through a wide variety of other community-based approaches, with an associated researcher time of 469 minutes to recruit one participant. Targets for recruiting a disadvantaged population were met, with 91% of the sample in social classes C2–E, and 41% reporting moderate to severe depression or anxiety. However, we under-recruited single parent smokers. Chi squared tests revealed that those recruited from the SSS database were more likely to respond to an initial letter, had used cessation aids before and had attempted to quit in the past year. Overall, initial responders were more likely to be physically active than those who were recruited via follow-up telephone calls. No other demographic or behaviour characteristics were associated with recruitment approach or intensity of effort. Qualitative feedback indicated that participants had been attracted by the prospect of being assigned to an intervention that focused on smoking reduction rather than abrupt quitting. 2) Attrition: Participants with low confidence to quit, and who were undertaking less than 150 minutes of moderate and vigorous physical activity per week at baseline were less likely to complete the 16-week follow-up assessment. Exploratory analysis revealed that those who were lost to follow-up early in the trial (i.e., by 4 weeks), compared with those completing the study, were younger, had smoked for fewer years and had lower confidence to quit in the next 6 months. Participants who recorded a higher expired air carbon monoxide reading at baseline were more likely to drop out late in the study, as were those recruited via follow-up telephone calls. Multivariable analyses showed that only completing less than 150 minutes of physical activity retained any confidence in predicting attrition in the presence of other variables. 3) Main quantitative outcomes: Compared with controls, intervention smokers made more quit attempts (36 v 10%; Odds Ratio 5.05, (95% CI: 1.10; 23.15)), and a greater proportion achieved ≥ 50% reduction in cigarettes smoked (63 v 32%; 4.21 (1.32; 13.39). Post-quit abstinence measured by exhaled carbon monoxide at 4 week follow-up showed promising differences between groups (23% v 6%; 4.91 (0.80; 30.24). No benefit of intervention on physical activity was found. Secondary analyses suggested that the standard missing data assumption of ‘missing’ being equivalent to ‘smoking’ may be conservative resulting in a reduced intervention effect. 4) Fidelity: All three HTs demonstrated high levels of skill in delivering a client-centred motivational interviewing based intervention. Processes relating to physical activity were not delivered as well as those relating to smoking behaviour. Processes related to social support were poorly delivered. There was little variation between individual HT scores and the scores of the researchers completing the scoring. Conclusions: 1) Recruitment: Mailed invitations, and follow-up, from health professionals was an effective method of recruiting disadvantaged smokers into a trial of an exercise intervention to aid smoking reduction. Recruitment via community outreach approaches was largely ineffective. 2) Study attrition: The findings indicate that those who take more effort to be recruited, are younger, are heavier smokers, have less confidence to quit, and are less physically active require more effort to be retained once recruited . 3) Main quantitative outcomes: A smoking reduction intervention for economically disadvantaged smokers which involved personal support to increase physical activity appears to be more effective than usual care in achieving reduction and may promote cessation. The effect does not appear to be influenced by an increase in physical activity. 4) Intervention fidelity was deemed to be successful overall. Key areas for improvement have been identified, including recommendations for future training as well as methodological implementation.