Marcadores biológicos de tabagismo : determinação de cutoff points

VII - CONSIDERAÇÕES FINAIS Este estudo desenvolveu-se devido facto de tanto quanto nos é dado a conhecer não terem sido determinados cutoff points de diferenciação entre fumadores e não fumadores em Portugal. Segundo vários autores é importante que estes valores sejam determinados em cada país devido às suas particularidades de prevalência do tabagismo e exposição involuntária ao fumo do tabaco. Foram também estudadas as variáveis que estão associadas e que influenciam os níveis do COex, da COHb, da cotinina plasmática e da cotinina urinária. De forma a cumprir os objectivos definidos, utilizou-se uma amostra de 102 indivíduos (53 fumadores e 49 não fumadores), tendo sido o tipo de amostragem não probabilística de conveniência. A dimensão da amostra e o tipo de amostragem são duas das limitações do estudo, uma vez que esta amostra não é representativa da população fumadora e não fumadora portuguesa, o que impede de generalizar os resultados nela obtidos à totalidade da população. Outra limitação identificada é o facto de não se terem encontrado estudos nacionais de características semelhantes a esta investigação, o que faz com que não seja possível comparar os resultados obtidos com estudos que tivessem utilizado amostras idênticas. Por essa razão a discussão de resultados foi efectuada considerando estudos internacionais cujas suas amostras para além de serem de maior dimensão os seus indivíduos possuem características particulares (prevalência do tabagismo e exposição involuntária ao fumo do tabaco) que dificultam a comparação dos resultados. Nos estudos internacionais muitas vezes não são estudadas as variáveis caracterizadoras dos hábitos tabágicos, o que leva mais uma vez à impossibilidade de relacionar correctamente os nossos resultados com outros obtidos por diferentes autores. Devido ao interesse dos resultados obtidos, seria importante que este estudo, tivesse continuidade, mas com algumas modificações que foram impossíveis de realizar no contexto em que se desenvolveu esta investigação. De forma a generalizar os resultados seria ideal utilizar uma amostra representativa da população fumadora e não fumadora nacional, o que permitiria ficar a conhecer mais fidedignamente os cutoff points de diferenciação entre fumadores e não fumadores em Portugal. Esta informação seria de grande utilidade para caracterizar correctamente os hábitos tabágicos dos indivíduos, permitindo reconhecer em que casos é necessário intervir para cessar os hábitos tabágicos e ainda nas consultas de cessação tabágica para um apropriado follow-up dos sujeitos. Outro aspecto em que esta investigação poderia ser complementada, diz respeito às variáveis caracterizadoras dos hábitos tabágicos, isto porque de acordo com a análise de regressão linear multivariada, através do modelo proposto, uma grande percentagem da variabilidade dos marcadores biológicos de tabagismo ficou por explicar, assim sendo seria importante estudar também outras variáveis, e construir outro modelo que explicasse de forma ainda mais expressiva a variabilidade dos biomarcadores. Sugerem-se como outras variáveis a ser estudas aquelas que estão relacionadas com as características inalatórias de cada indivíduo (número, frequência, profundidade, duração e percentagem de cigarros consumido e desperdiçado). Também a exposição involuntária ao fumo do tabaco deveria ser melhor caracterizada, acrescentando às variáveis analisadas neste estudo, outras que caracterizassem de forma mais precisa o tipo de exposição a que os indivíduos podem estar sujeitos no seu dia a dia (domiciliária, laboral e ambiental). Idealmente deveriam conhecer-se o número de cigarros que são fumados na proximidade dos indivíduos, assim como saber quais as características dos espaços fechados sobretudo no que respeita às condições de ventilação. É importante que surjam trabalhos a nível nacional relacionados com os marcadores de tabagismo, porque o tabagismo representa um problema de saúde pública sobre o qual é necessário intervir. É importante caracterizar correctamente os biomarcadores de tabagismo de forma a determinar a real prevalência do tabagismo e avaliar medidas preventivas e políticas de saúde pública. Actualmente decorridos 3 anos da aprovação da Lei 32/2007 em que foram aprovadas as normas de protecção dos cidadãos da exposição involuntária ao fumo do tabaco, a avaliação dos marcadores biológicos pode desempenhar um papel preponderante para caracterizar o impacto da implicação da Lei, uma vez que estes reflectem a exposição activa e passiva ao fumo do tabaco.

Reflexão sobre Riscos, Asma e Tabagismo

O impacto da asma brônquica nas últimas décadas, nomeadamente em idade pediátrica, associando prevalências significativas a uma tendência, gravidade e custos crescentes, tem levado a que se efectuem múltiplos estudos para esclarecer causas, avaliando riscos, permitindo a elaboração de programas de prevenção. Estudos epidemiológicos bem desenhados, aplicados a amostras populacionais significativas, permitem identificar determinantes independentes da asma, viabilizando a actuação. Se muito se tem avançado no conhecimento das bases fisiopatológicas da doença alérgica, é com alguma preocupação que sentimos que a comunidade médica, mesmo a especializada, não sente as evidências epidemiológicas como aplicáveis à sua população de asmáticos. “Precisamos de mais estudos”, é declaração comum. Com este trabalho, centrado em três rastreios efectuados com a coordenação dos autores, pretendemos demonstrar que existem factores preveníveis, moduláveis, que podem permitir reduzir a morbilidade da doença asmática. Entre estes, o tabagismo passivo assume uma relevância ímpar, por ser o principal factor de risco para a gravidade da asma pediátrica em Portugal.

Estudo sobre o consumo de tabaco entre os adolescentes da Ilha Terceira

RESUMO - O objetivo deste estudo foi conhecer o comportamento face ao consumo de tabaco reportado pelos adolescentes escolarizados da ilha Terceira e caracterizar alguns fatores associados. O estudo realizado assumiu uma metodologia de investigação observacional, descritiva, quantitativa e de carácter transversal. Os dados foram recolhidos no ano letivo 2012/2013, nos alunos do 9.º ano de escolaridade, através da aplicação de um questionário de autopreenchimento, anónimo e voluntário, em contexto de sala de aula. A amostra foi constituída por 323 adolescentes, 142 do sexo masculino e 181 do sexo feminino, com idade média de 14,71 anos. Verificou-se que cerca de 16,9% dos adolescentes consome tabaco regularmente, 6,6% ocasionalmente e 76,6% não fuma. Mais de metade dos adolescentes já experimentou fumar tabaco (56%), sendo a idade média de experimentação de 12,49 anos. A maioria dos adolescentes que experimentaram fumar referiram tê-lo feito por curiosidade (84,7%) e, sobretudo, na companhia dos amigos (83,1%). As variáveis associadas ao comportamento tabágico foram: o desempenho escolar, os hábitos tabágicos dos amigos, a permissividade dos pais para se fumar em casa, a frequência à exposição ao tabaco em casa, os conhecimentos da “impotência sexual” como consequência do consumo de tabaco, conhecimento dos danos na saúde em frequentar ambientes com fumo e a crença de que os jovens fumadores são mais atraentes. Os resultados mostram a elevada necessidade de serem desenvolvidas estratégias de prevenção e controlo do tabagismo entre os adolescentes da ilha Terceira.

Aromatic amines sources, environmental impact and remediation

Aromatic amines are widely used industrial chemicals as their major sources in the environment include several chemical industry sectors such as oil refining, synthetic polymers, dyes, adhesives, rubbers, perfume, pharmaceuticals, pesticides and explosives. They result also from diesel exhaust, combustion of wood chips and rubber and tobacco smoke. Some types of aromatic amines are generated during cooking, special grilled meat and fish, as well. The intensive use and production of these compounds explains its occurrence in the environment such as in air, water and soil, thereby creating a potential for human exposure. Since aromatic amines are potential carcinogenic and toxic agents, they constitute an important class of environmental pollutants of enormous concern, which efficient removal is a crucial task for researchers, so several methods have been investigated and applied. In this chapter the types and general properties of aromatic amine compounds are reviewed. As aromatic amines are continuously entering the environment from various sources and have been designated as high priority pollutants, their presence in the environment must be monitored at concentration levels lower than 30 mg L1, compatible with the limits allowed by the regulations. Consequently, most relevant analytical methods to detect the aromatic amines composition in environmental matrices, and for monitoring their degradation, are essential and will be presented. Those include Spectroscopy, namely UV/visible and Fourier Transform Infrared Spectroscopy (FTIR); Chromatography, in particular Thin Layer (TLC), High Performance Liquid (HPLC) and Gas chromatography (GC); Capillary electrophoresis (CE); Mass spectrometry (MS) and combination of different methods including GC-MS, HPLC-MS and CE-MS. Choosing the best methods depend on their availability, costs, detection limit and sample concentration, which sometimes need to be concentrate or pretreated. However, combined methods may give more complete results based on the complementary information. The environmental impact, toxicity and carcinogenicity of many aromatic amines have been reported and are emphasized in this chapter too. Lately, the conventional aromatic amines degradation and the alternative biodegradation processes are highlighted. Parameters affecting biodegradation, role of different electron acceptors in aerobic and anaerobic biodegradation and kinetics are discussed. Conventional processes including extraction, adsorption onto activated carbon, chemical oxidation, advanced oxidation, electrochemical techniques and irradiation suffer from drawbacks including high costs, formation of hazardous by-products and low efficiency. Biological processes, taking advantage of the naturally processes occurring in environment, have been developed and tested, proved as an economic, energy efficient and environmentally feasible alternative. Aerobic biodegradation is one of the most promising techniques for aromatic amines remediation, but has the drawback of aromatic amines autooxidation once they are exposed to oxygen, instead of their degradation. Higher costs, especially due to power consumption for aeration, can also limit its application. Anaerobic degradation technology is the novel path for treatment of a wide variety of aromatic amines, including industrial wastewater, and will be discussed. However, some are difficult to degrade under anaerobic conditions and, thus, other electron acceptors such as nitrate, iron, sulphate, manganese and carbonate have, alternatively, been tested.

Développement d'indicateurs pour le contrat de prestations 2008 entre le Cipret et le Département de l'économie et de la santé (DES) : élaboration d'une théorie d'action du Cipret Genève selon le Modèle de catégorisation des résultats de Promotion Santé Suisse

[Table des matières] 1. Introduction. 2. Méthode. 3. Théorie d'action et plan de monitorage des résultats des activités du Cipret (Centre d'information et de prévention du tabagisme) : priorités pour l'année 2008: Axe 1: Informer sur les conséquences de la consommation de tabac et sur la promotion de la santé. Axe 2: Contribuer à la cohérence de la politique de santé publique en matière de tabac. Axe 3: Diminuer le nombre de nouveaux fumeurs. Axe 4: Aider au sevrage du tabac. Annexes.

Aspects génétiques de la consommation de tabac et prise en charge clinique [Genetic aspects of smoking and impact on clinical care]

Tobacco smoking is a major public health issue and a better understanding of tobacco addiction represents an important challenge. Many factors are involved in tobacco addiction, including genetic factors. Taking them into account in smoking cessation programs would allow to better adapt these programs to individual characteristics and improve their rate of success. Given enzymatic induction by tobacco smoke, smoking cessation can nevertheless have important consequences on the metabolism of some drugs, that have to be taken into consideration. Here we present different clinical and genetic aspects of smoking and of smoking cessation. A dose adjustment of drugs influenced by tobacco smoke is proposed when quitting smoking.

Clinical and pharmacogenetic study on smoking and smoking cessation

Currently, smoking cessation represents one of the main strategies to reduce the incidence of tobacco-related diseases in the population. Smoking can also influence pharmacotherapy through several pharmacokinetic or pharmacodynamic interactions. Some of the most concerned drugs are those metabolized by the cytochrome P450 (CYP) 1A2 enzyme (e.g. caffeine, theophylline, clozapine, olanzapine, duloxetine), whose activity is induced by the polycyclic aromatic hydrocarbons found in tobacco smoke. This can result in a clinically significant decrease in the pharmacological effect of the drugs and the need of higher doses in smokers. Conversely, upon smoking cessation, toxic plasma levels of the drugs can be reached. The main objective of this thesis was to study the interindividual variability in CYP1A2 induction in a large cohort of smokers, by measuring CYP1A2 activity before smoking cessation and one month later in continuously abstinent subjects. For this purpose, a clinical study was conducted, including 194 smokers from the general population who wished to participate in a smoking cessation program and therefore received medical counseling and substitution therapy (nicotine or varenicline). An analytical method for the simultaneous quantification of nicotine, its metabolites and varenicline in plasma was developed and validated using ultra performance liquid chromatography coupled with tandem mass spectrometry. This method was used to confirm abstinence at different time points during the follow-up. Moreover, it was used to determine plasma levels of the smoking cessation drugs, to be used in the study of their pharmacogenetics, which was the secondary objective of this thesis. High interindividual variability in CYP1A2 induction by smoking was observed, ranging from no change to approximately 7 times decreased CYP1A2 activity after smoking cessation. Several clinical and genetic factors were investigated in an attempt to explain this variability. Firstly, a significant influence of CYP1A2*1F and *1D alleles, of contraceptive use and of the number of cigarettes smoked per day on CYP1A2 induced activity was observed, and of CYP1A2*1F and the use of contraceptives on the basal activity. But no influence of these factors was found on CYP1A2 inducibility. Given that known genetic polymorphisms in CYP1A2 gene were shown to explain only poorly the observed variations in activity, additional genetic factors were studied. SNPs in the CYP oxidoreductase (POR) gene were found to influence CYP1A2 basal activity, but not the induction. Finally, a pathway-based approach allowed to identify SNPs in genes coding for nuclear receptors (CAR, RXRa, VDR, PXR) and induction-mediating receptors (AhR), which significantly influenced CYP1A2 inducibility and basal activity (SNPs in the gene coding for CAR and RXRa). As secondary objective of the study, the pharmacogenetics of nicotine and varenicline is being investigated. Therefore, the nicotine metabolite ratio is used in the attempt to better explain nicotine dependence and the failure/success of quitting smoking. A population pharmacokinetic model is being developed for varenicline, integrating clinical and genetic factors (genes coding for its metabolizing enzymes and transporters), with the purpose of trying to predict efficacy and side effects. These findings suggest that the influence of smoking on pharmacotherapy could be better managed by including clinical and possibly in the future genetic factors, in the assessment of the adaptations needed when a person starts or stops smoking.  - L'arrêt du tabac représente une des principales stratégies pour diminuer l'incidence des maladies causées par celui-ci. Le tabagisme peut influencer la thérapie médicamenteuse par des interactions pharmacocinétiques ou pharmacodynamiques. Parmi les médicaments concernés, il y a ceux métabolisés par le cytochrome P450 (CYP) 1A2 (caféine, théophylline, clozapine, olanzapine, duloxétine, etc), dont l'activité enzymatique est induite par les hydrocarbures aromatiques polycycliques présents dans la fumée de cigarette. Ceci peut se traduire par une diminution de l'effet pharmacologique du traitement et la nécessité d'augmenter les doses d'entretien chez les fumeurs. Au contraire, à l'arrêt de la cigarette, les taux plasmatiques des médicaments peuvent devenir toxiques. L'objectif principal de cette thèse était d'étudier la variabilité interindividuelle dans l'induction du CYP1A2 dans une large cohorte de fumeurs, par la mesure de l'activité du CYP1A2 avant l'arrêt de la cigarette, ainsi qu'un mois après chez les sujets abstinents. Pour ce faire, une étude clinique a été conduite, incluant 194 fumeurs de la population générale dans un programme d'arrêt du tabac offrant des consultations spécifiques et un traitement pharmacologique (nicotine ou varénicline). Une méthode analytique pour la quantification simultanée de la nicotine, ses métabolites et la varénicline dans le plasma par chromatographie liquide couplée à la spectrométrie de masse en tandem à été développée et validée. Cette méthode a été utilisée pour confirmer l'abstinence pendant l'étude et déterminer les taux plasmatiques des médicaments, dans le but d'étudier leur pharmacogénétique. Une grande variabilité interindividuelle dans l'induction du CYP1A2 par la fumée a été observée, parfois sans changement et pouvant aller jusqu'à une diminution d'environ 7 fois l'activité du CYP1A2 après l'arrêt de la cigarette. Plusieurs facteurs cliniques et génétiques ont été étudiés pour essayer d'expliquer cette variabilité. Tout d'abord, on a observé une influence significative: des allèles CYP1A2*1F et *1D, des contraceptifs et du nombre de cigarettes fumées par jour sur l'activité induite du CYP1A2, ainsi que l'influence de l'allèle *1F et des contraceptifs sur l'activité basale. Cependant, aucune influence de ces facteurs n'a été démontrée sur l'inductibilité du CYP1A2. Étant donné que les polymorphismes génétiques du CYP1A2 apportent peu de renseignements sur la variabilité de son activité, des facteurs génétiques supplémentaires ont été étudiés. Des polymorphismes dans le gène POR (CYP oxidoreductase) ont été associés à l'activité basale du CYP1A2, mais pas à l'induction. Finalement, une approche basée sur la voie de signalisation du CYP1A2 a permis d'identifier des polymorphismes dans des gènes codant pour des récepteurs nucléaires (CAR, RXRa, VDR, PXR) et d'autres liés à l'induction (AhR) qui influencent significativement l'inductibilité et l'activité basale (les SNPs du CAR et RXRa). L'objectif secondaire de cette étude était d'investiguer la pharmacogénétique de la nicotine et de la varénicline. Le ratio métabolique de la nicotine est utilisé pour mieux expliquer la dépendance à la nicotine et le succès/échec de l'arrêt de la cigarette. Un modèle pharmacocinétique de population est en cours de développement pour la varénicline, intégrant des facteurs cliniques et génétiques (gènes codant pour ses enzymes de métabolisme et transporteurs), pour tenter de prédire son efficacité et ses effets secondaires. Les résultats de cette thèse suggèrent que l'influence du tabagisme sur la pharmacothérapie serait mieux gérée par l'inclusion des facteurs cliniques et peut-être, dans le futur, génétiques, dans l'évaluation des adaptations nécessaires lorsqu'une personne fume ou arrête de fumer.  - l'arrêt du tabac représente une des principales stratégies pour diminuer l'incidence des maladies causées par celui-ci dans la population. Le tabagisme peut influencer les traitements médicamenteux, soit en modifiant leur élimination par l'organisme, soit en agissant sur leur mode d'action. Parmi les médicaments les plus concernés, on retrouve par exemple: la caféine, la théophylline, la clozapine, l'olanzapine, la duloxétine, dont l'élimination est accélérée par la fumée de cigarette (induction enzymatique). Ceci peut se traduire par une diminution de l'effet du traitement et la nécessité d'en augmenter les doses chez les fumeurs. Au contraire, à l'arrêt de la cigarette, on observe un ralentissement de la fonction enzymatique, qui a pour conséquence une augmentation du taux de médicament dans le sang, pouvant devenir toxique. L'objectif principal de cette thèse était d'étudier comment cette induction par le tabac varie dans une population de fumeurs, par la mesure de l'activité de l'enzyme avant l'arrêt de la cigarette, ainsi qu'un mois après chez les sujets abstinents. Pour ce faire, une étude clinique a été conduite, incluant 194 fumeurs de la population générale dans un programme d'arrêt du tabac offrant des consultations spécifiques et un traitement médicamenteux (nicotine ou varénicline). Une méthode analytique a été mise au point pour mesurer la quantité de nicotine, de ses produits de dégradation et de la varénicline dans le sang des participants à l'étude. De plus, cette méthode a été utilisée pour confirmer l'abstinence pendant l'étude. Une grande variabilité interindividuelle a été observée dans l'induction de l'enzyme par la fumée; il en résulte aucun changement d'activité chez certains sujets après l'arrêt de la cigarette, alors que pour d'autres elle peut être diminuée jusqu'à 7 fois. Plusieurs facteurs cliniques et génétiques ont été étudiés pour essayer d'expliquer cette variabilité. Premièrement, une influence sur l'activité de l'enzyme a été observée pour les contraceptifs hormonaux et le nombre de cigarettes fumées par jour, ainsi que pour certaines variations génétiques dans le gène codant pour l'enzyme d'intérêt, mais il η y a pas eu d'influence sur l'induction. Par la suite, des variations génétiques dans d'autres gènes influençant le fonctionnement de l'enzyme ont été associées soit avec son activité, soit avec son induction par le tabac. Finalement, l'étude propose également d'investiguer si le métabolisme de la nicotine a une influence sur la dépendance, les symptômes de sevrage et le succès/échec de l'arrêt de la cigarette. Des variations génétiques dans les gènes du métabolisme de la varénicline sont également étudiées en lien avec les quantités de varénicline mesurées dans le sang ainsi que les effets du médicament. Ceci permettra peut-être de prédire son efficacité et ses effets secondaires. Les résultats de cette thèse suggèrent que l'influence du tabagisme sur la thérapie médicamenteuse serait mieux gérée en tenant compte des facteurs cliniques et peut-être, dans le futur, de la génétique dans l'adaptation des traitements, que la personne soit fumeuse ou en phase d'arrêt.

Effect of a smoking ban on respiratory health in nonsmoking hospitality workers: a prospective cohort study

OBJECTIVE: The aim of this study was to examine the effect of a smoking ban on lung function, fractional exhaled nitric oxide, and respiratory symptoms in nonsmoking hospitality workers. METHODS: Secondhand smoke exposure at the workplace, spirometry, and fractional exhaled nitric oxide were measured in 92 nonsmoking hospitality workers before as well as twice after a smoking ban. RESULTS: At baseline, secondhand smoke-exposed hospitality workers had lung function values significantly below the population average. After the smoking ban, the covariate-adjusted odds ratio for cough was 0.59 (95% confidence interval, 0.36 to 0.93) and for chronic bronchitis 0.75 (95% confidence interval, 0.55 to 1.02) compared with the preban period. CONCLUSIONS: The below-average lung function before the smoking ban indicates chronic damages from long-term exposure. Respiratory symptoms such as cough decreased within 12 months after the ban.

Exposition au fumage involontaire dans l'air intérieur des locaux. Problèmes liés aux mesures de l'exposition à la fumée de tabac

A brief and critical review of the physical and chemical markers of ETS was made as well as the techniques which were used to measure their concentrations in indoor air. Despite the existing data, more investigations and measurements are needed to characterize the exposure to ETS and their health effects.

Naissances vaudoises 1993-1994: caractéristiques et facteurs de risque pour une affection chronique: rapport EDEN no 1

Une cohorte de 6477 nouveau-nés de mères résidant dans le Canton du Vaud a été recrutée pendant une année (1993-1994) dans les 18 maternités vaudoises et celle de Châtel-St-Denis. L'objectif de l'étude EDEN (Etude du DEveloppement des Nouveau-nés) est de calculer l'incidence et la prévalence des affections chroniques de toute étiologie et pour toutes les catégories de poids de naissance, à 18 mois et à 4 ans. Ce rapport présente la méthode de l'étude et l'état de santé à la naissance. Cinq critères de sélection non exclusifs ont permis de cibler un groupe de nouveau-nés à haut risque de développer une affection chronique (12% des nouveau-nés, n=760): (1) le petit poids de naissance (n=408, 6.5% des naissances vivantes); (2) une malformation congénitale ou une maladie génétique (n=157, 2.4% des naissances vivantes); (3) une affection susceptible de devenir chronique liée à une utilisation importante des services de soins au cours de la petite enfance (n=61, 0.9% des naissances vivantes); (4) le transfert aux soins intensifs (n=287, 4.4% des naissances vivantes); (5) des difficultés sociales importantes (n=105, 1.6% des naissances vivantes). Le taux d'acceptation de l'étude par les parents est bon (90%). En tout 5.9% des enfants étaient prématurés et 2.2 pour mille sont décédés à < ou = à 7 jours de vie. Selon les indicateurs à disposition, le réseau vaudois répond efficacement aux besoins en soins obstétricaux et néonatals La durée moyenne du séjour hospitalier était de 7 jours, avec des variations importantes. L'influence néfaste du tabagisme pendant la grossesse se manifeste par un doublement du risque de poids de naissance < ou = à 2500g chez les fumeuses; 24% des femmes ont fumé pendant leur grossesse, pour les trois quarts jusqu'à l'accouchement. Un grand potentiel de prévention subsiste dans ce domaine. L'examen des enfants à 18 mois, terminé fin mai 1996, ainsi que celui des 4 ans, permettront de valider les critères de sélection à la naissance comme indicateurs précoces de problèmes de santé chroniques dans la petite enfance. Les nouveaux cas d'affection chronique seront alors signalés par les pédiatres et les médecins spécialistes. [Auteurs, p. 9]

Smokefree legislation consultation response (UK)

The Institute of Public Health was established in 1999 to promote co-operation for Public Health on the island of Ireland. It aims to improve health across the island of Ireland by working to combat health inequalities and influence public policies in favour of health. The remit includes; providing public health information and surveillance; strengthening public health capacity; and advising on policy. The Institute of Public Health welcomes the consultation on the Smokefree Elements of the Health Improvement and Protection Bill. The Institute strongly supports a total ban on smoking in all enclosed workplaces and public places.  A total ban on smoking in all enclosed public places and workplaces is the only way to adequately protect the health of all workers and contribute to reducing the prevalence of smoking within the population. The exemptions within the proposed Health Improvement and Protection Bill will fail to protect many workers particularly in the hospitality industry. These workers are often at greatest risk from Environmental Tobacco Smoke (ETS) due to the extent of their exposure.

For your heart's sake stop smoking

On World Heart Day, 29 September 2011, the Public Health Agency is urging all smokers to stop smoking and reduce their risk of developing heart disease (cardiovascular disease - CVD) or suffering a stroke or a heart attack.Heart disease is one of the leading causes of death and illness in the UK. Research shows that smoking is one of the main contributors of the disease, causing around 25,000 deaths a year in the UK. Cigarette smokers are two times more likely than non-smokers to suffer a heart attack.The majority of people who suffer a heart attack before the age of 50 are smokers. Cigarette smoke causes heart disease by:· reducing oxygen to the heart;· increasing blood pressure and heart rate;· increasing blood clotting;· damaging cells that line coronary arteries and other blood vessels, causing narrowing of the arteries.From the moment smoke reaches your lungs, your heart is forced to work harder. Your pulse quickens, forcing your heart to beat an extra 10 to 25 times per minute, as many as 36,000 additional times per day. Because of the irritating effect of nicotine and other components of tobacco smoke, your heartbeat is more likely to be irregular. This can contribute to cardiac arrhythmia and many other serious coronary conditions, such as heart attack.For smokers who already suffer from heart problems, quitting will dramatically help. Many heart patients notice an almost immediate improvement when they stop smoking. Often, they need less medication and can cope better with physical exertion.Gerry Bleakney, Head of Health and Social Wellbeing Improvement, PHA, said: "Smoking is one of the major causes of cardiovascular disease and smokers are almost twice as likely to have a heart attackas someone who has never smoked. One in every two long-term smokers will die prematurely from smoking-related diseases, many suffer very poor health before they die. However one year after successfully quitting smoking, an individual will have reduced their risk of having a heart attack to half that of a person continuing to smoke."Across Northern Ireland, there are over 600 support services for people who wish to stop smoking, based in GP surgeries, community pharmacies, hospitals, community centres and workplaces. I would encourage everyone who is thinking about quitting to log on to our Want 2 Stop website: www.want2stop.info and order a 'Quit Kit' free of charge alternatively contact the Smokers' Helpline on 0808 812 8008."

Indoor air quality in a public building following smoking bans

Introduction: Exposure to environmental tobacco smoke (ETS) is a major environmental risk factor. Indoor contaminants come from a variety of sources, which can include inadequate ventilation, volatile organic compounds (VOCs), biological agents, combustion products, and ETS. Because ETS is one of the most frequent causes of IAQ complaints as well as the high mortality of passive smoking, in June 2004 the University of Geneva made the decision to ban smoking inside the so called "Uni-Mail" building, the biggest Swiss University human science building of recent construction, and the ordinance was applied beginning in October 2004. This report presents the finding related to the IAQ of the "Uni-Mail" building before and after smoking bans using nicotine, suspended dust, condensate and PAHs level in air as tracers to perform an assessment of passive tobacco exposure for non-smokers inside the building. Methods: Respirable particles (RSP) A real time aerosol monitor (model DataRAM)was place at sampling post 1, level ground floor. Condensate It consists in extracting any organic matter taken on the glass fibre filters by MeOH, and then measuring the total absorbent of the MeOH extract to the UV wavelength of 447 nm. Nicotine Nicotine was taken by means of cartridges containing of XAD-4 to the fixed flow of 0.5 L/min. The analytical method used for the determination of nicotine is based on gas chromatography with Nitrogen selective detector GC-NPD. Results: Figure 1 shows the box plot density display of 3 parameters before and after smoking bans for all 7 sampling posts: dust, condensate and nicotine in air in μg/m3. Conclusion: Before the smoking ban, the level of the concentrations of respirable particles (RSP) is raised more, average of the day 320 μg/m3, with peaks of more than 1000 μg/m3, compared with the values of the surrounding air between 22 and 30 μg/m3. The nicotine level is definitely more important (average 5.53 μg/m3, field 1.5 to 17.9 μg/m3). Once the smoking bans inside the building were applied, one notes a clear improvement in terms of concentrations of pollutants. For dust, the concentration fell by 3 times (average: 130 μg/m3, range: 40 to 160 μg/m3) and that of nicotine by 10 times (average: 0.53 μg/m3, range: 0 to 1.69 μg/m3) compared to that found before smoking bans. The outdoor air RSP concentration was 22 μg/m3 or 10 times lower. Nicotine seems to be the best tracer for ETS free of interference, independent of location or season.

Smoking in prisons: the need for effective and acceptable interventions.

Tobacco-smoking prevalence has been decreasing in many high-income countries, but not in prison. We provide a summary of recent data on smoking in prison (United States, Australia, and Europe), and discuss examples of implemented policies for responding to environmental tobacco smoke (ETS), their health, humanitarian, and ethical aspects. We gathered data through a systematic literature review, and added the authors' ongoing experience in the implementation of smoking policies outside and inside prisons in Australia and Europe. Detainees' smoking prevalence varies between 64 per cent and 91.8 per cent, and can be more than three times as high as in the general population. Few data are available on the prevalence of smoking in women detainees and staff. Policies vary greatly. Bans may either be 'total' or 'partial' (smoking allowed in cells or designated places). A comprehensive policy strategy to reduce ETS needs a harm minimization philosophy, and should include environmental restrictions, information, and support to detainees and staff for smoking cessation, and health staff training in smoking cessation.